Cholera, Chloroform and the Science of Medicine: A Life of John Snow

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Author: Peter Vinten-Johansen | Howard Brody | Nigel Paneth | Stephen Rachman | Michael Russell Rip

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Cholera, Chloroform, and the Science of Medicine: A Life of John Snow

Peter Vinten-Johansen, et al.

OXFORD UNIVERSITY PRESS

Cholera, Chloroform, and the Science of Medicine

ii

Cholera, Chloroform, and the Science of Medicine A Life of

Peter Vinten-Johansen Howard Brody Nigel Paneth Stephen Rachman Michael Rip with the assistance of David Zuck

1 2003

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1 Oxford New York Auckland Bangkok Buenos Aires Cape Town Chennai Dar es Salaam Delhi Hong Kong Istanbul Karachi Kolkata Kuala Lumpur Madrid Melbourne Mexico City Mumbai Nairobi São Paulo Shanghai Singapore Taipei Tokyo Toronto

Copyright 2003 by Oxford University Press, Inc. Published by Oxford University Press, Inc. 198 Madison Avenue, New York, New York, 10016 http://www.oup-usa.org Oxford is a registered trademark of Oxford University Press All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission of Oxford University Press. Library of Congress Cataloging-in-Publication Data Cholera, Chloroform, and the Science of Medicine: A Life of John Snow Peter Vinten-Johansen ... [et al]. p. cm. Includes bibliographical references and index. ISBN 0-19-513544-X 1. Snow, John, 1813—1858. 2. Epidemiologists—Great Britain—Biography. 3. Anesthesiologists—Great Britain—Biography. I. Vinten-Johansen, Peter. RA649.5.S66 S647 2003 617.9’6092–dc21 [B] 2002030347

246897531 Printed in the United States of America on acid-free paper

Preface

This book is the product of an ongoing scholarly collaboration among five professors at Michigan State University who share an inordinate interest in the life and work of an early Victorian physician, John Snow. Early on someone tagged us with a mildly embarrassing nickname, “The Snowflakes,” which stuck. Harmony does not always reign among five men with varied training and scholarly expertise: a European intellectual historian (Peter Vinten-Johansen), a philosopher–MD (Howard Brody), an epidemiologist–MD (Nigel Paneth), an American literary and cultural historian (Stephen Rachman), and a medical geographer–epidemiologist (Michael Rip). We began this project with very different views of Snow’s writings and his significance in the history of medicine. Because we all agreed that his investigations during the 1854 cholera epidemic in London constituted a singular achievement, our initial intent was to feature that incident in a relatively brief biographical study. Several jointly crafted articles and presentations shaped our collective sense of Snow. In the process, however, we came to believe that only an extensive, interdisciplinary biography would do him justice. In our view Snow’s accomplishments in anesthesia and epidemiology are interconnected. His medical training occurred in the 1830s, when a new generation of medical men attempted to refashion medicine as a scientific discipline with linkages to “the collateral sciences” such as chemistry and comparative anatomy. In this vision of scientific medicine, the ultimate purposes of developing a solid grounding in the collateral sciences of medicine were to enhance one’s clinical acumen and to improve the public health. Snow swallowed this intellectual regimen hook, line, and sinker and actualized the vision in his medical career. Early on he took a special interest in respiratory cases among the patients he was treating, devised animal experiments, and presented his findings and case reports at medical society meetings and in the medical press. He was already a specialist, so to speak, in respiratory physiology and clinical practice when news of inhalation ether reached London from the United States in 1846. Within two years he was arguably the most accomplished anesthetist in the British isles—perhaps even farther afield. When the second pandemic of “Asiatic cholera” reached London in the fall of 1848, his understanding of gas law, respiratory physiology, and anesthetic agents led him to question the predominant theories about the nature and transmission of this devastating disease. The following year he published two essays that outlined his views

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Preface

and offered preliminary substantiation. From then until his death, at the age of fortyfive, in June 1858, his working days were spent administering anesthesia, conducting laboratory and autoexperiments on new anesthetic agents, and tracking down information on outbreaks of cholera. Snow was a shoe-leather anesthetist and epidemiologist par excellence. It took us half a decade to develop this interpretation, but all along we were puzzled by the fractured life and legacy depicted by other scholars. We mean no disrespect. On the contrary, we acknowledge with admiration the devoted stewardship of his work undertaken by anesthesiologists and epidemiologists in Great Britain and the United States; John Snow memorial lectures are given annually in both fields. Since the mid-1980s scholars have recast our understanding of Snow’s early life; edited one of Snow’s major articles on narcotism and produced an annotated edition of his case books from the last decade of his life; self-published a biography; and written a dissertation from a historical–sociological perspective. In our view, it was time for a synthetic study of Snow as an interdisciplinary thinker and medical practitioner that integrated this recent scholarship. We wanted to produce a monograph, not an anthology, so we selected a team leader–final reviser. For various reasons that role was given to Peter Vinten-Johansen; hence, he is listed as first author. Thereafter, the list is alphabetical because the book is a collective product. We designated various members of the team “primary” writers for particular chapters, but each chapter was subjected to rigorous group editing and revision. Two years into the project we made the acquaintance, first via the internet, of David Zuck, a retired anesthesiologist but an active historian of medicine. His contributions as on-site researcher and in-house editor have been substantial, and he richly deserves the acknowledgment on the title page. However, it should be said that we were sometimes unable to accept the Britishisms he strongly suggested would improve the readability of our book, or to include the detailed discussion of anesthesia topics he recommended. Please consult the following Web site for searchable transcriptions of John Snow’s writings (eventually, all of them), samples of word analysis and chronology comparisons used in our research, as well as additional maps and images: http://www.msu.edu/unit/epi/johnsnow. East Lansing, Michigan

P.V.-J. H.B. N.P. S.R. M.R.

Acknowledgments

We have many people to thank for providing research assistance. At the Main Library of Michigan State University: Peter Berg, Special Collections; Michael McSeoin, Inter-Library Loan borrowing coordinator; Ann Silverman, cataloger (retired); and Agnes H. Widder, humanities bibliographer. Professorial assistants assigned by the Honors College at Michigan State University: Joshua Courtade, Kristin Slattery, Jeris Stueland, and Damon Williams. Also at Michigan State University, research assistance was provided by Jennifer Beggs, Lyman Briggs School; Andrew Bielaczyc, College of Arts and Letters; Dan Hesse, the Honors College; Anne Forrester Barker, PhD candidate in history; Debra Mulrooney and Talmadge Holmes, the College of Human Medicine. At the University of Michigan Libraries: Shabbir Boxwalla, Taubman Medical Library; Carol McKendry, coordinator of technical operations, Buhr Shelving Facility; and Dawn Wallace, technical library assistant, Buhr Shelving Facility. At the National Library of Medicine: Steve Greenberg and Betsy Tunis, History of Medicine Division; and Ken Niles, Collection Access Section. In Canada: Lee Perry, librarian, Woodward Biomedical Library, The University of British Columbia. In the United Kingdom: Dee Cook, archivist to the Society of Apothecaries, London; Kay Easson, librarian, Newcastle Literary and Philosophical Society; Stephen Freeth, keeper of manuscripts, Guildhall Library, London; Howard R. Hague, assistant librarian, Charing Cross Campus Library, London; Phoebe Harkins and Roy Porter (deceased), Wellcome Institute of Historical Research, London; Patricia Sheldon, assistant librarian, City Library, Newcastle upon Tyne; and Christopher Webb, archivist, The Borthwick Institute of Historical Research, University of York. We are also grateful for the assistance provided by unnamed staff members at the following institutions: the London Metropolitan Archives (formerly the Greater London Record Office); the Taubman Medical Center, University of Michigan; the Wellcome Institute of Historical Research, London; and the Central Reference Library, York. We discussed specific issues with many individuals, including Anthony Ashcroft, Frank A. Barrett, Charles Croner, Clive Davenhall, Andrew Dean, Andrew Dent, Rusty Dodson, Pamela Gilbert, Bill Henriques, William C. Hoffman, Joel Howell, Daniel Karnes, David P. Lusch, Kari McLeod, Arthur Robinson, and Catherine SchenckYglesias.

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Acknowledgments

Ralph R. Frerichs, DVM, DrPH, Department of Epidemiology, University of California, Los Angeles, School of Public Health maintains an extensive Website on John Snow and consulted with us on issues related to mapping and the location of cholera outbreaks that Snow investigated. H. Spence Galbraith, MD, an indefatigable researcher into Snow’s early life and extended family, read early drafts of several chapters and sent us manuscripts of prospective articles. Oxford University Press asked Christopher Hamlin, University of Notre Dame, to comment on a partial draft of the manuscript; he submitted an admirably detailed report that has proven helpful in our revisions. David M. Morens, MD, National Institute of Allergy and Infectious Diseases, read the drafts of several chapters and advised us on the history of cholera in the nineteenth century. Throughout this long-term project, we received intellectual, emotional, technical, and financial support from faculty and staff at the Center for Ethics and Humanities in the Life Sciences, Michigan State University, and the Department of Epidemiology, Michigan State University. An All-University Research Grant from Michigan State University in 1997–98 effectively launched our project. After two years as a research team, we were honored in 1999 with the Excellence in Interdisciplinary Scholarship Award from the Honor Society of Phi Kappa Phi at Michigan State University; we used the monetary portion to cover research expenses and various production costs incurred in the preparation of this book. In addition, the Department of Epidemiology and the Mid-West Universities Consortium for International Activities covered a portion of Michael Rip’s travel expenses for a research trip to England.

Contents

Abbreviations, xi Introduction, 1 CHAPTER

1

York and Newcastle, 1813–1833, 14 CHAPTER

2

Senior Apprentice and Assistant, 1830–1836, 39 CHAPTER

3

London Medical and Surgical Training, 1836–1838, 56 CHAPTER

4

Forging a London Career, 1838–1846, 81 CHAPTER

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Ether, 110 CHAPTER

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Chloroform, 140 CHAPTER

7

Cholera Theories: Controversy and Confusion, 165 CHAPTER

8

Snow’s Cholera Theory, 199 CHAPTER

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Professional Success, 231 ix

x

Contents

CHAPTER

10

Cholera and Metropolitan Water Supply, 254 CHAPTER

11

Broad Street, 283 CHAPTER

12

Snow and the Mapping of Cholera Epidemics, 318 CHAPTER

13

Snow and the Sanitarians, 340 CHAPTER

14

Further Developments in Anesthesia, 359 CHAPTER

15

Common Ground: Continuous Molecular Changes, 372 CHAPTER

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Snow’s Multiple Legacies, 388 Bibliography, 404 Index, 421

Abbreviations

AMJ

Association Medical Journal.

ApothAct

Holloway, Sydney W. F. “The Apothecaries’ Act, 1815: A reinterpretation.” Medical History 10 (1966): 107–29, 221–36.

BF

Galbraith N. Spence. “Dr John Watson (1790/91–1847) of Burnopfield and his assistant Dr. John Snow.” Bulletin, Durham County Local History Society 57 (1998): 32–50.

BIHR

The Borthwick Institute of Historical Research, University of York, England.

BMJ

British Medical Journal

CB

Ellis, Richard H., ed. The Casebooks of Dr. John Snow. London: Wellcome Institute for the History of Medicine, 1994.

CIC

Cholera Inquiry Committee. Report on the Cholera Outbreak in the Parish of St. James, Westminster during the Autumn of 1854. London: J. Churchill, 1855.

CMC

Snow, John. On Continuous Molecular Changes, More Particularly in their Relation to Epidemic Diseases. London: Churchill, 1853.

CSI

Committee for Scientific Inquiries.

E

Snow, John. On the Inhalation of the Vapour of Ether in Surgical Operations: Containing a Description of the Various Stages of Etherization, and a Statement of the Results of Nearly Eighty Operations in Which Ether Has Been Employed. London: Churchill, 1847.

EMSJ

Edinburgh Medical and Surgical Journal.

xi

xii

Abbreviations

GBH

General Board of Health.

GP

Loudon, Irvine. Medical Care and the General Practitioner, 1750–1850. Oxford: Clarendon Press, 1986.

GPO

Government Printing Office.

GRO

General Register Office.

HMSO

Her Majesty’s Stationery Office.

HoC

House of Commons.

JPH&SR

Journal of Public Health, and Sanitary Review. Continued as Sanitary Review and Journal of Public Health.

JS

Shephard, David A. E. John Snow, Anaesthetist to a Queen and Epidemiologist to a Nation: A Biography. Cornwall, Prince Edward Island: York Point, 1995.

JS-EMP

Snow, Stephanie J. “John Snow 1813–1858: The emergence of the medical profession.” PhD diss, University of Keele, 1995.

JS-EY

Galbraith, N. Spence. Dr John Snow (1813–1858). His early years. London: Royal Institute of Public Health, 2002.

L

Richardson, Benjamin W. “The Life of John Snow.” Introduction to John Snow, On Chloroform and Other Anaesthetics. London: Churchill, 1858.

LJM

London Journal of Medicine.

LMG

London Medical Gazette. (To avoid confusion, we cite volumes by the old series throughout.)

LRCP

Licentiate of the Royal College of Physicians.

LSA

Licentiate of the Society of Apothecaries.

MCC

Snow, John. On the Mode of Communication of Cholera. London: Churchill, 1849.

Abbreviations

xiii

MCC2

Snow, John. On the Mode of Communication of Cholera, 2d ed. London: Churchill, 1855.

M-CJ

Medico-Chirurgical Journal.

M-CR

Medico-Chirurgical Review.

MCS

Metropolitan Commission of Sewers.

M-CT

Royal Medical and Chirurgical Society, Medico-Chirurgical Transactions.

MRCS

Member, Royal College of Surgeons.

MSL

Medical Society of London.

MT

Medical Times.

MTG

Medical Times and Gazette.

Newton

Newton, John Frank. The Return to Nature, or, A Defence of the Vegetable Regimen; With Some Account of an Experiment Made During the Last Three or Four Years in the Author’s Family. London: T. Cadell & W. Davies, 1811.

OC

Snow, John. On Chloroform and Other Anaesthetics. London: Churchill, 1858.

OED

Oxford English Dictionary

ON

Snow, John. “On narcotism by the inhalation of vapours.” London Medical Gazette (1848–51).

PB

Galbraith, N. Spence. “Joseph Warburton (1786–1846) of Pateley Bridge and his assistant Dr. John Snow.” Yorkshire Archaeological Journal 71 (1999): 225–36.

PharJ

The Pharmaceutical Journal.

PMCC

Snow, John. “On the pathology and mode of communication of cholera.” London Medical Gazette 44 (1849): 745–52, 923–29.

xiv

Abbreviations

PMSJ

Provincial Medical and Surgical Journal.

RM-CS

Royal Medico-Chirurgical Society.

SCME

Select Committee on Medical Education, House of Commons, 1834.

SR&JPH

Sanitary Review and Journal of Public Health, Continuation of Journal of Public Health, and Sanitary Review.

S&V

Southwark and Vauxhall Water Company.

VCH-Y

Tillott, P. M. A History of Yorkshire. The City of York. Victoria History of the Counties of England, edited by R. B. Pugh. London: Oxford University Press, 1961.

WH

Galbraith, N. Spence. “William Hardcastle (1794–1860) of Newcastleupon-Tyne and his pupil John Snow.” Archæologia Æliana (The Society of Antiquaries of Newcastle upon Tyne) 27 (1999): 155–70.

WMS

Westminster Medical Society.


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Introduction

S

OMETIME BETWEEN 1839 and 1841, John Snow drowned a guinea pig.1 It died in two minutes. An hour after its death, Snow began dissecting. He observed that the heart was perfectly still and that the right side was swollen with blood while the left was nearly empty. As he proceeded he noted that the surface of the lungs changed color when exposed to air. Then, much to his surprise, the heart twitched in the form of “a slight vermicular motion in the right auricle.” He opened the trachea and began artificial respiration. The heart’s ventricles began to move, and through the coats of the left atrium (the chamber that receives blood from the lungs) he could see oxygen-rich, bright red blood. The heart continued to contract weakly, unable to expel blood from its chambers, but it kept beating rhythmically for forty-five minutes. What exactly was Snow up to in attempting to reactivate a guinea pigs’s dead tissue? This particular experiment took place in the course of his investigations into respiration and asphyxia, undertaken with the desire to establish the physiological basis for pulmonary resuscitation on infants. His efforts involved more unsettled questions than would William Kouwenhoven’s when he developed his cardiopulmonary resuscitation (CPR) techniques in the 1950s. In the 1840s, according to the data Snow cited, one in twenty births was stillborn, many of whom were asphyxiated at the very moment of birth. What method, based on principles rather than habit, he wondered, should be used to revive children “born in a state of suspended

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animation”?2 A number of practices were commonly used: dashing cold water in the infant’s face; immersing it in warm water; performing mouth-to-mouth resuscitation; using a bellows (and extra oxygen) to inflate the lungs; and shocking it with electricity. Snow acknowledged that each of these measures had merit, but all entailed considerable risks. For Snow respiration—“essential to the life of the whole animal kingdom”—was the fundamental physiological principle at issue, so measures that directly restored or established respiration would be most appropriate. Dashing cold water in a baby’s face, immersing it in warm water, or stimulating its skin with electroshocks might well rouse the nervous system and facilitate breathing, but these seemed indirect, risky methods compared with artificial respiration, which Snow reasoned “must be had recourse to as quickly as possible.”3 However, he worried that “breathing into the lungs of the child” would be too unnatural to facilitate regular breathing and that such air probably contained too much carbon dioxide gas to be effective, yet the ordinary bellows frequently used could overinflate and damage the newborn’s lungs. Snow delivered a paper at the Westminster Medical Society in October 1841 in which he proposed a resuscitating device constructed with newborn infants in mind. It consisted of two small syringes, one fitted over the mouth, the other fitted over the nostrils. While the syringe over the mouth drew air from the lungs, the one over the nostrils delivered fresh air. The device was as simple as a bellows but lacked its dangers: “The two pistons are held in the same hand, and lifted up and pressed down together, the cylinders being fixed side by side, and each having two valves. When the pistons are raised, one cylinder becomes filled with air from the lungs, and the other with fresh air from the atmosphere, which can be warmed on its way by passing a tube and metal coil placed in hot water.” Snow had designed a hand-held resuscitator, complete with a warmer to enhance the oxygenation of the blood.4 Snow’s plan for an artificial respirator was a practical solution to a concrete and pervasive medical and social problem, accomplished by a cogent application of physiological principles. As an understanding of diseases reveals underlying patterns of normal functions, asphyxia was important to Snow because it revealed the underlying pattern of respiration. Respiration was first and foremost a chemical exchange of gases—oxygen from the air for carbon dioxide from the blood—first shown by Lavoisier in the eighteenth century but most recently refined by the German physiologist Heinrich Magnus in 1837. Snow admired physiologists and chemists who were busy exploding the old vitalist doctrine that posited a peculiar lifeforce in living organisms, distinct from general physical and chemical forces. In Snow’s mind respiration disproved vitalism because, although crucial to life, it was based on the same principles that guided all physicochemical forces: The exchange of gases “is not strictly a vital process, but only an operation of organic chemistry, since it continues after death as well as before, when the mechanical advantages for access of air remain the same.”5 There was general agreement that asphyxiation induced a distinct sequence of symptoms in adults

Introduction

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as well as newborns, but there was considerable debate as to what caused it. Bichat had concluded that oxygen-depleted venous blood acted as a poison when it was recirculated. Was he right? Or was asphyxia the result of “the poisonous effects of carbonic acid detained in it”? If so, was carbon dioxide gas formed in the lungs or the capillaries? There were other vexing questions, too: Was circulation primarily caused by the mechanical action of the heart or by the chemical exchanges in the blood? Was animal heat derived from this chemical exchange? Why did asphyxiation occur more suddenly at higher temperatures? Snow offered answers to all these questions in his paper on newborn resuscitation at the Westminster Medical Society, citing what he deemed the most reliable studies and supplementing those findings with results from his own experiments. He thought Bichat went “rather too far” in calling venous blood a poison, because if respiration is renewed in time, no ill effects remain from the circulation of dark blood. In a series of eighteen experiments on small animals and birds, Snow had found that carbon dioxide gas’s “injurious effects seem to depend rather on its physical properties, viz. its density and solubility in the blood than on any strictly poisonous qualities.”6 Asphyxiation was caused by the absence of oxygen, because experimental animals became asphyxiated when placed in nitrogen and hydrogen gas. The bulk of evidence in experiments by Alison, Edwards, and Reid suggested, as well, that the exchange of oxygen and carbon dioxide and the generation of heat and blood flow take place in the capillaries and that higher temperatures accelerated such exchanges. So what had Snow learned by performing artificial respiration on his suffocated guinea pig? He surmised that the line between life and death was not fixed, and the heart retained its irritability (its ability to be stimulated by oxygen) beyond death. On this experimental and theoretical basis, Snow urged his colleagues to use his artificial respirator on still-born infants. The new physiology had shown that respiration was the key to life, so oxygen was the appropriate stimulant for the asphyxiated. Other measures were indirect at best, harmful at worst. Above all, he urged the avoidance of the application of warmth, despite its time-honored use in medical circles and endorsement by The Royal Humane Society. At higher temperatures and in the absence of new incoming air (as when an infant is simply placed in a warm bath to revive it), the oxygen still present in the blood would be converted to carbon dioxide more quickly, thereby accelerating the asphyxiation. In addition to questioning contemporary clinical practice, Snow’s asphyxiation research allowed him to trace respiration and its basic chemical exchanges into the womb and to the caudal brainstem.7 It also prepared him to manage clinical problems in a scientific manner. In the 1841 presentation at the Westminster Medical Society, he noted “that even a strong child does not always begin to breathe the minute when it is born; but if the umbilical cord be pressed between the fingers it will instantly draw an inspiration.”8 Seven years later, on a Wednesday morning in November 1848, he was called in to advise on a difficult delivery. Mrs. Strachan, a mother who had already given birth

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to several children in protracted, “very hard labors” was going through this ordeal again. She was distressed, tired, “out of patience,” and “wished to know if something could not be done for her relief.” Snow administered moderate doses of chloroform. The patient experienced immediate relief and remained in a light state of unconsciousness for the duration of the labor (two-and-a-half hours) until a baby girl was born, but the infant was in “a state of asphyxia, fetching a breath only at intervals of about a minute. . . . Dashing cold water on the child sometimes caused it to breathe a little sooner, & its lips remained black and limbs relaxed.” The umbilical cord, however, pulsated as far as it was exposed, and shortly before the afterbirth was delivered, Snow compressed the cord between his forefinger and his thumb; immediately the baby began breathing naturally. When he released the cord the breathing diminished. On tying the cord the child breathed well and recovered quickly. He had resolved the asphyxiation, as his physiological inquiries over the years had predicted, by stimulating the urge to breathe.9 In this way Snow’s research would become his practice. He brought a knowledge of physiology and chemistry to bear on the task of saving newborns that come into the world apparently dead. In Snow’s day the scientific practice of medicine demanded the use of techniques often at odds with convention and established authorities. It also required a worldview in which humanity had to be understood as part of animal evolution rather than distinct from it. Perhaps drawing on the comparative anatomy and physiology he had learned at the Hunterian School of Medicine in London, he concluded his 1841 presentation on asphyxia with a comparison: “Moralists have often asserted that human beings come into the world in a more puny and helpless condition than any other animals; but in this they are mistaken; for, without including marsupial animals, the young of cats, and all those that are brought forth with their eyes closed, cannot maintain life without artificial heat, which they receive from lying close to the mother: in fact they can scarcely be said to have a proper temperature of their own. A child born at the full term, on the contrary, can maintain its temperature if well protected from cold.”10 In Snow’s vision of life, newborn infants were not as defenseless as convention would have it. Our animal heat at birth was a sign of our respiratory power, our resiliency, and, to the scientific medical practitioner, our capacity for being restored to life from apparent death by the proper methods.

* * * John Snow has been called a “compleat physician,” meaning exemplary in every way, but the basis for this exemplariness has remained suggestive until now.11 Qualifying as a surgeon-apothecary at the age of twenty-five in 1838, he had already had eleven years of medical training and experience. He had served six years as an apprentice to a surgeon-apothecary who was attached to the Lying-in Hospital in Newcastle, followed by three years as an assistant to two country apothecaries whose practices also included midwifery. Then, while a medical student in London, he studied

Introduction

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medicine with a physician who had a particular interest in obstetrics, and he studied midwifery and diseases of women and children with a physician who had a practice at the Royal Lying-in Hospital. After qualifying he established a general practice in the Soho area of London that involved many deliveries. The young clinician, who in 1841 “remarked that . . . if the umbilical cord will be pressed between the fingers it will instantly draw an inspiration” from a newborn who was not breathing, had probably already attended hundreds of deliveries.12 Others at the time could equal or even surpass this clinical experience, but Snow belonged to a cadre of young medical men whose clinical practice was grounded in what was then called the collateral sciences of medicine. He chose to attend a London medical school renowned for the teaching of anatomy and staffed by instructors all of whom were keenly interested in Continental developments in physiology and chemistry and several of whom had trained in Edinburgh, who taught their students the newest ideas in comparative anatomy and Lamarckian evolutionary biology. The antivitalist philosophy Snow confronted at the Hunterian School of Medicine was cutting edge thought in the 1830s, and it contributed to his becoming an advocate of scientific medicine as distinct from a singularly experiential (bedside) medicine that was dominant among many of his older colleagues. Snow’s approach was to base clinical methods on the latest research in the sciences relevant to his chosen specialty. When confronted by a pressing medical and social concern—newborn infants were dying of asphyxiation at an alarming rate—he surveyed the literature on respiration, conducted experiments on a variety of animals, and designed a resuscitation apparatus that would perform according to scientific principles. One sees in his early research on asphyxiation the mind-set and process he would use in 1847 to base the administration of ether and chloroform on medical scientific principles rather than simple trial-and-error research. In some respects the ether inhaler he devised in 1847 permitted him to induce controlled “suspended animation” via the administration of anesthesia—in essence, the reverse of the resuscitation apparatus he designed in 1841. Like his colleagues in the Westminster Medical Society, Snow’s theoretical and research interests were always stimulated by practical problems and directed to producing results with practical applications. There was no difference in English medicine at this time between the medical researcher and the clinician. In addition to being a conduit for Continental and Scottish ideas, Snow was an exemplar of moderate medical radicalism. This movement arose in conjunction with debate on the First Reform Bill of 1831–1832, which eventuated in a modest expansion of the franchise for elections to the House of Commons (including Snow’s father, who had become a property owner by then). Medical radicals agitated to replace the three medical orders of physician, surgeon, and apothecary, then under the control of elite corporations, with a unified program of medical training, a single qualification, and a democratic professional organization.13 The Hunterian School of Medicine and the Westminster Medical Society were hotbeds for outspoken as well as moderate radicals in the 1830s. Snow’s favorite teacher had earned his MD

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in Edinburgh but refused to take a license to practice as a physician in London in protest of the power exerted by the Royal College of Physicians, but Snow was no agitator. Instead, he achieved three medical qualifications and then snubbed the corporate establishments for the rest of his career. The twenty-eight year old “Mr. Snow” who read a paper on resuscitating asphyxiated newborns at the Westminster Medical Society was a surgeon-apothecary, or general practitioner (GP) in emerging parlance, but within three years he would call himself Dr. Snow, having received the MD from the University of London. Certainly, he hoped to improve his prospects and expand his practice by becoming a physician, but the medical colleagues with whom he associated were medical radicals, and he occasionally found himself opposed to the medical establishment. Snow’s progression from animal experimentation to the invention of a device for the resuscitation of newborns exemplifies his scientific modus operandi for the work that made him famous in his lifetime—the development of scientific anesthesia. In addition, he was also profoundly interested in the public health questions of the day, and applied his scientific perspective to the major new epidemic disease of his time, cholera. Until his death in 1858 he would juggle a flourishing career as a premier anesthetist and new ventures in public health and epidemiology.

Testimony, 1855 For Snow 5 March 1855 was a typically busy Monday. His anesthesia practice brought him to Hanover Square, a few blocks north of his residence in Sackville Street, to assist a dentist with a tooth extraction. There were complications, however. The attending physician was concerned that the administration of chloroform would place his patient, a young man named Tudor with a “weak constitution,” at special risk. He reassured them both that everything would go smoothly, then took Tudor’s pulse. It was weak. When told that he would feel no pain and had nothing to fear, the young man relaxed, and his pulse improved. Shortly thereafter Snow gave him chloroform without complications or subsequent depression of his pulse, and the dentist was able to remove two teeth.14 Next he walked west toward Hyde Park but stopped in the Mayfair district to give chloroform to a middle-aged man from Staffordshire who was undergoing a second operation to remove dead bone tissue from the femur. A longtime colleague of Snow’s, Mr. Bowman, was the surgeon. The outcome seemed successful, and, from Snow’s perspective, the patient tolerated the anesthesia very well.15 His third anesthesia case of the day was near Clapham Common in South London. To get there he would have crossed the River Thames, then walked along the Wandsworth Road, where in 1849 he had investigated an epidemic outbreak featured in his first essay, On the Mode of Communication of Cholera. The uncle of yet another colleague, Dr. Spitta, was having lithotripsy, in which an instrument is inserted into the bladder to

Introduction

7

crush stones. In the first decade of anesthesia use, only the number of dental extractions exceeded lithotripsy in Snow’s caseload; third in frequency were lithotomies (surgical incision of the bladder to remove stones), followed by breast tumors, hemorrhoids, anal fistulae, harelips, and childbirth.16 Anesthesia had become routine in medical procedures, major and minor. Snow would log more than 5,000 cases in almost a dozen years and in the process was exposed to every nook and cranny of London, every walk of life, and the widest imaginable array of diseases the metropolis had to offer. Sandwiched among these visits, Snow found time on that Monday afternoon in March 1855 to testify at the Houses of Parliament, near Westminster Abbey, before the Select Committee on Public Health on the Nuisances Removal and Diseases Prevention Act. Parliamentary committees had been gathering data and hearing expert testimony for a quarter century on sanitary conditions throughout Britain, but especially in the “towns and populous districts.” The sanitary reform movement was driven by the medical opinion that poisonous vapors, whether miasmas rising from marshes or from decomposing organic matter near human dwellings, were the main cause of disease, including epidemic cholera, which had killed tens of thousands of people in England since 1831. Much of the law resulting from this movement concentrated on removing sources of filth and smoke from the environment, improving sewage disposal, and forcing private water companies to provide purer drinking water. The bill then before the select committee would grant public officials the power to regulate or eliminate the so-called offensive trades that released foul-smelling, noxious fumes: gasworks, bone boilers and merchants, soap manufacturers, tallow melters, gut spinners, dye makers, market gardeners, and manufacturing chemists who produced artificial manure for agricultural purposes. At the least, sanitation reformers wanted to keep businesses from fouling up residential neighborhoods with pollutants viewed as pathogenic for a host of constitutional diseases and contributory to the cause and spread of epidemic cholera. However, Henry Knight, a bone merchant, and the consortium of “offensive trades” he represented believed the proposed act would, in effect, put them all out of business. He submitted Snow’s name as an expert medical witness to plead their case, although he had never actually met him or discussed the matter with him. The alliance between Snow and the “offensive trades” was entirely intellectual. Knight had read On the Mode of Communication of Cholera—the second, expanded edition—in which Snow presented evidence drawn from three epidemics (1831–1832, 1848–1849, and 1853–1854) that cholera could be transmitted only by swallowing the “morbid matter” specific to that disease. He completely ruled out as a cause of cholera the inhalation of miasmas and effluvia, whether from the atmosphere or the bodies of the sick. His argument featured two landmark epidemiological studies of cholera that would secure his reputation into the twenty-first century: an analysis of the differential mortality in thirty-two London subdistricts supplied by two companies drawing water from separate stretches of the Thames, and also

8


the linkage of a lethal Golden Square outbreak to contamination of a popular pump in Broad Street. Mr. Knight had been intrigued by Snow’s view “that measures necessary to protect the public health would not interfere with useful trades.”17 Many of Snow’s contemporaries were unconvinced by his reasoning and practical recommendations, even though he was by then a forty-two-year-old physician of some gravitas (Fig. Intro.1): current president of the Medical Society of London and the leading authority on ether and chloroform in Britain, who, two years before, had given chloroform to Queen Victoria when she was delivering Prince Leopold—an event generally accepted as instigating the use of anesthesia in childbirth throughout the West. In preliminary remarks Snow stated: “I have paid a great deal of attention to epidemic diseases, more particularly to cholera, and in fact to the public health in general; and I have arrived at the conclusion with regard to what are called offensive trades, that many of them really do not assist in the propagation of epidemic diseases, and that in fact they are not injurious to the public health. I consider that if they were injurious to the public health they would be extremely so to the workmen

Figure Intro.1. Photograph of John Snow, mid-1850s.

Introduction

9

engaged in those trades, and as far as I have been able to learn, that is not the case; and from the law of the diffusion of gases, it follows, that if they are not injurious to those actually upon the spot, where the trades are carried on, it is impossible they should be to persons further removed from the spot.”18 The crux of the matter for Snow was that “offensive trades,” much as they might offend our olfactory sensibilities, would not cause illness in the general population if the workers themselves were uninjured. He knew from years of research, most recently on the properties of anesthetic agents, that gases were “injurious” to health only at close range in very high concentration, so if those closest to offensive smelling materials did not get sick, how could such trades be spreading disease-causing vapors? While some people today might quarrel with Snow’s pollution-tolerant notion of public health, his conclusion was sound: Carcass renderers and their ilk were not propagating cholera or other epidemic diseases.19 But the chair, Sir Benjamin Hall, and twelve members of the Select Committee on Nuisances Removal and Disease Prevention did not share Snow’s knowledge of gas laws and were, not surprisingly, utterly astounded by his opening statement. “Are the Committee to understand,” Hall inquired, “taking the case of bone-boilers, that no matter how offensive to the sense of smell the effluvia that comes from the boneboiling establishments may be, yet you consider that it is not prejudicial in any way to the health of the inhabitants of the district?” Snow replied, “That is my opinion.”20 The committee seemed eager to probe him, to catch him in a contradiction. If it made no difference living cheek by jowl to a knacker’s yard, were “all animal substances” harmless to humans? “No,” Snow replied, “I believe that epidemic diseases are propagated by special animal poisons coming from diseased persons, and causing the same diseases to others, and that they are extremely injurious; but that substances belonging to animals, that is to say, ordinary decomposing animal matter, will not produce disease in the human subject.”21 What about “decaying vegetable matter; do you consider that will not be productive of disease?” He did not, with the possible exception of ague (recurring fevers such as malaria), about which there was still medical uncertainty; “but in London, in any trade I am acquainted with, I do not believe that any decomposing vegetable or animal matters produce disease.”22 Chairman Hall, however, remained in disbelief about Snow’s earlier comment about the “knacker’s yard,” a slaughterhouse in which the animals are not fit for human consumption. Would the “very offensive effluvia” from a pile of rotting horse flesh “not be prejudicial to the health of the inhabitants round”? “I believe not,” Snow first reiterated and then explained in reply to another questioner: “gases produced by decomposition when very concentrated, will produce sudden death; but where the person is not killed, if the person recovers, he has no fever or illness.”23 Another member wanted additional clarification of this point, and after two brief exchanges with Snow asked him, “Do you mean to tell the Committee that when the effect is to produce violent sickness there is no injury produced to the constitution or health of the individual?” Snow’s reply was careful and discriminating: “No fever or special

10


disease.”24 But Mr. Greene did not catch his meaning: “Are you not aware that persons going into vaults where there are a number of dead bodies have suffered very severely, and that sometimes death has been produced by this cause?” “Yes, when those gases are extremely concentrated, they will actually poison and cause death.” However, the cause of death resulted from the laws of gases, not the local miasma theory of disease, because the poisons in such gases do “not cause disease;” only poisons “that reproduce themselves in the constitution” can cause disease in that person and be transmitted to others to cause an identical disease.25 Nevertheless, Snow’s explanation left yet another committee member confused: “You say that effluvia arising from living subjects are dangerous?” He replied yes, “or even from certain persons who have died from disease,” Snow added. Another committee member asked, “But not from the mere decay of animal matter?” Snow responded that that was correct.26 At this point the committee moved on to other topics, but these parliamentary exchanges offer a glimpse into Snow’s theory of disease transmission and the conceptual impasse that stood between him and those most influential in British government at midcentury. The exchanges also reveal the differences between his thinking and germ theory, which crystallized in the decades after Snow’s death in 1858. Snow’s theory of epidemic diseases was based on the communication of “special animal poisons.” As confusing as this notion was to the members of the parliamentary committee, he could not possibly have used a more precise term. In Snow’s day the agents (some called them “germs,” others an infectious “virus”) that caused cholera, typhus, and measles, for example, were unknown—unknown in the sense of not yet isolated, observed, or classified. Nevertheless, Snow believed, on medical and social evidence, that cholera and other epidemic diseases were propagated from one diseased person to another, that like caused like, and that a particular disease-causing agent could not cause a different disease in someone else. Even though the agents were unknown, the signatures of epidemic diseases were sufficiently apparent for him to hypothesize how they were communicated from one person, household, town, city, nation, and continent to the next. Moreover, the pathways were sufficiently clear for preventive public health measures to be enacted, whether or not the organized life forms that caused the disease in the human body were identified. If the members of Parliament found Snow’s theory implausible, the Lancet, a leading medical journal of the day, considered Snow a traitor to empirical medicine and a fellow-traveler with an “unsavory” consortium of profiteering businessmen. His testimony lent support to the producers “of pestilent vapors, miasms, and loathsome abominations of every kind” who fatten themselves “upon the injury of their neighbors.”27 Equally galling to the editors of the Lancet was Snow’s use of a public forum to truck his unsubstantiated theories. “Is this evidence scientific?” Lancet asked rhetorically. “Is it consistent with itself? Is it in accordance with the experience of men who have studied the question without being blinded by theories?” There was ample evidence that fumes from gas-producing trades made local people ill.

Introduction

11

And we presume that there is hardly a practitioner of experience and average powers of observation who does not daily observe the same thing. Why is it then, that Dr. Snow is singular in his opinion? Has he any fact to show in proof? No! But he has a theory, to the effect that animal matters are only injurious when swallowed! The lungs are proof against animal poisons; but the alimentary canal affords a ready inlet. Dr. Snow is satisfied that every case of cholera for instance, depends upon a previous case of cholera, and is caused by swallowing the excrementitious matter voided by cholera patients. Very good! But if we admit this, how does it follow that the gases from decomposing animal matter are innocuous? . . . If this logic does not satisfy reason, it satisfies a theory; and we all know that theory is often more despotic than reason. The fact is, that the well whence Dr. Snow draws all sanitary truth is the main sewer. His specus, or den, is a drain. In riding his hobby very hard, he has fallen down through a gully-hole and has never since been able to get out again. . . . And to Dr. Snow an impossible one: so there we leave him.28 The Lancet diatribe reverberates with the contumely that Snow’s ideas engendered when they were first proposed. The most unpleasant aspect of Snow’s thesis—that the mass of cholera victims were swallowing other people’s fecal matter—made him appear to the Lancet to be like an offensive tradesman himself.29 We part company with Snow when he argued that “ordinary decomposition” was not a source of disease, because we associate decomposition and putrefaction with the bacteria and fungi that cause them, but the “germs” involved in bone-boiling and the other “offensive trades” that Snow considered harmless will not cause cholera or any other epidemic disease. Snow was correct (or at least more correct than the Lancet) on these matters.

* * * These two snapshots of Snow—dissecting a guinea pig, then being dissected by Parliament—are illustrative of the medical road he traveled. He began his career studying the physiology of respiration and asphyxiation, which paved the way for his approach to researching and administering anesthetic agents after 1846. When a second cholera epidemic began in England in 1848, his understanding of gas law, the mechanism of respiration, and human physiology made him skeptical of the view he had once shared that this was fundamentally a febrile disease. These vignettes also show the resistance Snow encountered when he sought to clarify his “special poisons” theory and its ramifications for public health. The Lancet editorial considered his reliance on “theory” as suspect in itself, but the fundamental disagreement was over which theory to trust and whose authority to follow in the pre-germ theory era characterized by many informed and partially informed opinions along with so many unknowns. Snow lived three more years

12


after testifying before the parliamentary committee, during which time he continued to defend his sanitary ideas in the London medical press and in the medical and social circles in which he traveled. He did not succeed in his lifetime, although he would be vindicated after the fourth cholera epidemic of 1866. Even so, who could possibly have imagined that an impoverished Soho medical man and son of an unskilled Yorkshire laborer would ever have achieved such notoriety?

Notes 1. Snow mentions this in “On asphyxia and the resuscitation of still-born children,” LMG 29 (1841–42): 226. The exact date of the experiment is not known, but his interest in the subject is easily traceable through his published writings on respiration and asphyxia dating from January 1839. 2. Snow, “On asphyxia,” 224. 3. Ibid., 223, 225. 4. Snow’s device was actually an adaptation of one designed for adults by a Mr. Read of Regent Circus, who introduced the syringe method for artificial respiration at the Westminster Medical Society in 1838, coinciding with Snow’s burgeoning interest in respiration. See Snow, “On asphyxia,” 225. 5. Ibid., 221–24. Other physiologists he cited over the years were William Frédéric Edwards, John Reid, Xavier Bichat, François Magendie, Collard de Martingny, Pierre Hubert Nysten, and William Alison. 6. On Bichat, see Ibid., 223. Snow performed these experiments in March 1839, but he described them several years later; see Snow, “On the pathological effects of atmospheres vitiated with carbonic acid gas” (1846). In the same passage Snow added that “this view is supported by Nysten’s experiments of injecting it [CO2 gas] into the blood-vessels” (55) and then quotes Nysten’s article, in French. 7. In Snow’s mind there was nothing vital or special about the process: “Physiologists have amused themselves in speculating on the cause of the first respiration; but doubtless it is the same as the second and third, and all succeeding respirations; namely, a sensation or impression arising from a want of oxygen in the system, and conveyed to the medulla oblongata, either by the blood circulating in it, by the nerves in connection with it, or by both causes”; “On asphyxia,” 227. He was referring to earlier generations of physiologists. For a parallel argument that, “even a generation previously, Snow’s reasoning would have been improbable, if not impossible,” see Rosenberg, Explaining Epidemics, 118. Although Rosenberg was referring to Snow’s reasoning about cholera, he goes on to mention “advances in chemistry, in pathology, in technology, and in public health practice”; Ibid. 8. Snow, “On asphyxia,” 227. 9. Ellis, CB, 22 (1 November 1848). 10. Snow, “On asphyxia,” 227. 11. Shephard, JS, 279–94. 12. Snow, “On asphyxia,” 227. 13. Desmond, Politics of Evolution, 11–12, 102–04. 14. Ellis, CB, 360. 15. Ibid., 360, 356. 16. Ibid., 360, 596–616. The contemporary term for lithotripsy was lithotrity.

Introduction

13

17. UK HoC, “Select committees on medical relief and public health,” par. 119, p. 328. 18. Ibid., par. 120, p. 328. 19. Lilienfeld, “John Snow: The first hired gun?” 8; Vandenbroucke, “Invited commentary: The testimony of Dr. Snow,” 10, 12. 20. UK HoC, “Select committees on medical relief and public health,” par. 121, p. 328. Hall was also President of the Board of Health. 21. Ibid., par. 122, p. 328. 22. Ibid., par. 123, p. 328. 23. Ibid., par. 124, 126, pp. 328–29. 24. Ibid., par. 129, p. 329. 25. Ibid., par. 130–32, p. 329. 26. Ibid., par. 133–34, p. 329. 27. Editorial, Lancet 1 (23 June 1855): 634. 28. Ibid., 634–35. 29. A fortnight later, a medical journal that had been receptive on past occasions to Snow’s views and theories regretfully criticized his testimony before the Parliamentary Committee, albeit without the vituperative ad hominem tone used by its rival; “The Public Health Bill,” MTG 11 (1855): 12–13. A few days later, Snow published an open letter to the chairman of the committee in which he referred to the harsh criticism dished out by the newspaper and medical press for his ostensible support of noxious trades, even though “I explained the grounds of my opinions as well as the opportunity permitted”; Snow, [Open] Letter to the Right Hon. Sir Benjamin Hall (1855), 3. Snow continued, “The writers of these attacks have assumed and asserted that the opinions I have expressed on the subject of offensive trades are altogether new and peculiar”; Ibid., 4. Quite the contrary, Snow argued, and cited similar views of the non-danger attached to gases from decomposing organic matter published by Bancroft (1811) and Thomas Watson (1841–42). In mentioning Watson, Snow added that his attackers had assumed that he was drawn to his conclusions about offensive gases because of his pet theory of cholera transmission, whereas in actuality Snow had entertained his views on gases long before he began to study cholera; Ibid., 9. In an 1856 article published by the Lancet he marshaled statistics to show that workers in those trades seemed as healthy as other workers; Snow, “On the supposed influence of offensive trades on mortality” (1856).

Chapter 1

York and Newcastle, 1813–1833

A

PICTURESQUE GRAVEYARD adjacent to the church of All Saints North Street (Fig. 1.1) in the ancient English city of York contains one of the few tangible traces of John Snow’s origins: the Snow family plot with a gravestone for four members buried there just before city authorities outlawed intramural interments. The church was one of six in Micklegate Ward, an area of about forty acres south of the River Ouse. The ward included the northern part of North Street and contiguous courts, rows, and alleys, many named Tanner, indicative of a long-standing local industry, tanning (Fig. 1.2). The buildings were a mixture of residential housing, craft shops, flour mills, and warehouses. Carts from the southern and western hinterlands carrying grain and produce, cattle bound for the central market, and coaches all used the city portal at Micklegate Bar, where incoming traffic was inspected and tolls assessed. Quays along the Ouse were the unloading point for goods brought downstream by barges and small boats from the west and the north via a tributary, the River Swale, as well as from London, Newcastle, and elsewhere via the Humber inlet from the North Sea. The vessels were then refilled with cattle, agricultural produce from the Yorkshire countryside, and assorted commercial goods. Large warehouses lined the riverbank and served double duty as dikes, protecting low-lying houses in North Street from periodic flooding of the slowmoving river. Laborers were in great demand, as were transport workers such as carmen. Alleys connected the quays with North Street, which intersected Micklegate

14


15

Figure 1.1. Church of All Saints North Street, c. 1840 (F. Bedford, illustrator, from Booth, pl. 13).

near the Ouse Bridge, the only vehicular and pedestrian connection to the rest of the city lying north of the river.1 Early in the nineteenth century the city of York bore traces of a history spanning almost two millennia. It was still a walled city. The foundations of some walls erected during the Roman era for a small military outpost of the empire were extended and repaired over the centuries as York was transformed into an autonomous borough. Some street names still ended in “-gate,” medieval Danish for “street” and indicative of a ninth-century occupation by Scandinavian invaders. By the late Middle Ages, however, York had risen in significance to become a cathedral town (York Minster) and the northern capital of England by virtue of its location at the junction of two rivers and at the confluence of roads from the hinterlands. Some of the medieval quays and market squares still hummed with activity at the turn of the nineteenth century, when almost 17,000 people inhabited a contained area intended for half that many. At a time when the Industrial Revolution was transforming economic life, roiling social relations, and altering the landscape elsewhere in England, York was dominated by artisan guilds, and the mayor annually rode ceremoniously across the im-

16


➂ ① ➁ ➅

➃ ➄

Figure 1.2. Micklegate Ward: 1—All Saints North Street Church; 2—Possible location of Snow family residence and John Snow’s birthplace; 3—North Street postern by Wellington Row, to which the Snows moved in the early 1820s; 4—Micklegate Bar entrance; 5—Dodsworth School that Snow may have attended from approximately 1819 to 1827; 6—Queen Street, where the Snows moved in 1825 (adapted from Hargrove, vol. 2, between iv and 6).

mediate suburbs that were claimed by the four wards into which the city was divided for administrative purposes.2 Much of Micklegate Ward, particularly the streets near the river, was considered unsanitary, even in Snow’s day. For centuries most of the parish had drawn water for household use from the Ouse near the North Street postern. In the 1670s the city corporation commissioned the York Waterworks company to provide running water. For more than a century the company pulled relatively fresh water from the Ouse near the North Street postern, eventually serving many customers in the three northern wards with running water via taps to cisterns placed in backyards and court-


17

yards. The water company found few customers in Micklegate Ward, however, because of low pressure and intermittent supply; the hollow tree trunks that carried water under the Ouse Bridge frequently developed leaks because of the heavy traffic above. Consequently, many residents in the ward as a whole, All Saints North Street parish in particular, drew water for drinking and washing either from shallow local wells or directly from the river. Neither source was particularly salubrious. The river water below the North Street postern was frequently polluted by discharges of dung from livestock pens near the ferry crossing. Although most houses in the parish had water closets connected to basement cesspits, which night soil men emptied periodically for a fee, some householders ran drains directly into the river to avoid paying sewage rates.3 Similar violations of city regulations for the disposal of human and industrial wastes occurred north of the river. The result was that water quality gradually deteriorated as the river bisected the city and was foul when it reached the Skeldersgate postern and the southern suburbs. All wells situated in the Ouse River floodplain received episodic overflows and became contaminated. Runoff from tanneries and market squares polluted springs that supplied wells or drained through cracks in linings into the wells themselves. Water tables within the city were also tainted by seepage from cemeteries and dunghills where night soil wagons dumped their loads for use as manure in the communal vegetable gardens. Conditions for residents near the River Ouse were often unsanitary, but they were much worse in the eastern and southeastern parishes of Walmgate and Monk Wards near the River Foss. A lock near the junction with the Ouse turned the Foss into a stagnant river, with an adjoining bog into which “poured the fetid contents of the drains” from nearby houses. City authorities in the eighteenth century considered such problems with water supply and sanitation unavoidable annoyances, but they became a matter of increasing concern among the earliest sanitary reformers in the 1820s, when the population of York exceeded 22,000—an increase of twenty-five percent since 1801.4 In such an unsanitary environment, Frances Snow would give birth to seven healthy and long-lived children before the family moved to higher ground just outside the city walls in 1825, when their first-born, John, was twelve.5 Perhaps the unhealthy conditions during these formative years stimulated his later obsession with the purity of what people ingest.

The Snows in York Frances (Fanny) Askham was the “base born,” or illegitimate, daughter of John Empson and Mary Askham. Being illegitimate, she was assigned her mother’s surname. In 1792, three years after Fanny’s birth, her parents exchanged vows of marriage in the parish church of the village of Acomb, two miles west of York (Fig. 1.3).6 The couple had another daughter and three sons in the following nine years, all sur-

18


Figure 1.3. Parishes and townships around York (adapted from Tillott, 312).

named, unlike their elder sister, Empson (Fig. 1.4). During this period John Empson was a weaver, a “gentleman’s servant,” and a laborer—all “genteel occupations” in an era when self-reliance was the hallmark of respectability among the working poor and lower middle classes.7 Sometime after 1801 John and Mary Empson moved to Huntington, a farming parish on the northern outskirts of York.8 In 1812 Fanny Askham, aged 24, married William Snow, aged 29. Both were sufficiently literate to sign the marriage register, and both listed their residence as Huntington. William Snow was a laborer.9 His parents, Hannah and William Snow, are more mysterious than his in-laws. One view is that they were longtime residents of York, perhaps in the parish of All Saints North Street because their names are carved on a family tombstone in that churchyard. It is more likely, however, that they owned a farm in Upper Poppleton a few miles east of the city.10 Shortly after their marriage William and Fanny Snow moved into the city of York. They set up a household somewhere in North Street, described in an 1818 guidebook as a “narrow” street with

Askhams are recorded in Ledsham and York parish registers from 1300s.

Empsons appear in Yorkshire parish records from 1500s.

William Askham = Mary Butler of Ledsham

Lancelot Empson = Hannah ? of Strensall

Mary Askham (1769-??)

John Empson (?-1850) Weaver, gentleman’s servant, laborer, gardener, yeoman farmer

m., 1792; Acomb parish

Hannah (1792-??)

Frances Askham of Fairburn (1789-1860) Illegitimate; York

Mary Ann Empson (18??) Illegitimate

Elizabeth (1830-??) Illegitimate

Charles (1794-1861)

John (1799-??)

Adventurer, South America; in Newcastle, bookseller & stationer; in Bath, bookseller & antiquities

Gardener

Mary Ann (1838-??) Illegitimate ??

Andrew Simpson Nurseryman, York

Figure 1.4. Askham–Empson genealogy.

William = Elizabeth Cobb (1801-??) m., 1825

John Buckle of Stillingfleet, farmer. m1

m2

John Ripley = Hannah Buckle = William Snow of Whixley. (1744-1827) (1754-1815) of Poppleton, farmer.

George (??-??)

Joseph (1788-??)

William = Frances Askham (1783-1846) (1789-1860) laborer, carman, farmer

m. 1812, Huntington parish.

John (1813-58) Apothecary, Surgeon, Physician.

William (1815-??) Temperance Hotelier, tailor & hatter. Emigrated to Australia?

Charles (1817-??)

Robert (1819-85/86)

Thomas (1821-93)

Mary (1823-1911)

Hannah (1825-1904)

Occupations and residence after 1841 unknown.

Secretary, then manager of Garforth Colliery, Leeds.

Teacher; then curate, chaplain, and eventually vicar of Underbarrow.

Schoolteacher; Head, “The Mount” school for girls, York.

Schoolteacher; Head, “The Mount” school for girls, York.

Figure 1.5. Askham–Snow genealogy.

Sarah = Matthew Collier, (1827-91) farmer, Homemaker

Osbaldwick

George (1828-30) Buried, All Saints North Street, York.


21

“several good houses” remaining from the previous century, but most houses were apparently in various stages of disrepair and occupied by renters.11 Their neighbors were also general laborers, as well as watermen, cowherds, tanners, skinners, sail and flag makers, weavers, joiners, bakers, painters, merchants, and small manufacturers.12 William and Fanny Snow began their married life as a laboring family with the advantages of literacy and connections to extended families with modest resources.13 On 15 March 1813 Mr. G. Brown, the minister at All Saints North Street since 1798, baptized “John son of William & Frances Snow,” born the same day.14 John’s birth occurred ten months after his parents’ marriage; they had eight more children, three daughters and five sons, over the course of fifteen years (Fig. 1.5) and maintained attachments to their home parish throughout. They had ambitions for all their children and would provide each child with basic schooling. How an unskilled laborer accomplished this feat is unclear. They had no prospects of a substantial inheritance from the Empsons, although the Upper Poppleton farm that may have been owned by William Snow’s father would likely pass to their eldest son, but the in-laws could have provided some financial assistance during hard times. There were notable changes in the family’s circumstances by the early 1820s. The first indication was a change in William Snow’s occupation from unskilled to semiskilled laborer sometime after the birth of his third son; the baptismal registers list him as a carman from 1819 until 1828 (Table 1.1). Precisely what this occupation involved other than driving a cart is unclear. He may have worked for someone else, hauling goods from the quays on North Street to other parts of the city. He may have invested in his own rig and could have owned several. If so, he needed access to a stable for the horses. Regardless of whether he worked for someone else or was a proprietor himself, William Snow’s income increased sufficiently from 1821 to 1823 to allow him to move his family several blocks into “a row of new houses” on Wellington Row, an extension of North Street to the postern by the western wall.15 In 1824 a William Snow appears in a county property tax register for St. Mary Bishophill Junior, the parish to which Upper Poppleton belonged, as owner of land valued at

Table 1.1. William Snow’s occupational history and changes in family residence Dates

Occupation

Residence

1812–1819 1819–1821/23 1821/23–1825 1825–1830 1830–1832 1832–1846 1841–1846

laborer carman carman carman farmer farmer/landlord farmer

North Street (rental?) North Street (rental?) Wellington Row (rental?) Queen Street (property holder) Queen Street (residence unclear) Queen Street (property holder)a Rawcliffe (purchased farm in 1841)

aCollected

rents on four properties in Queen Street during this period. Source: BIHR, PR Y/ASN 4; S. Snow, JS-EMP, 37.

22


nearly thirty-eight pounds, a substantial holding at the time.16 The likelihood is strong that this person was John Snow’s father because the following year William Snow purchased a home with some adjacent land on Queen Street, just outside the wall but still on the southwestern side of the Ouse. That is, the property in Upper Poppleton was apparently transferred to William Snow, which he used to purchase a house on Queen Street rather than move his family to the farm. His listed vocation remained carman until 1832, when he registered himself as a farmer when voting in the first reform Parliament. He continued to live in Queen Street and collected rent on four properties. In 1841 he purchased a farm in Rawcliffe that he worked until his death in 1846, aged 66.17 However, if William Snow hankered to farm while he was still a carman in the 1820s, he might have done so long before he formally registered himself as a farmer. All inhabitants of Micklegate Ward had access to the ward’s “stray,” approximately 500 acres of unenclosed pasturage southwest of the city. In addition, all residents of York could apply for the privilege of grazing cattle and horses throughout the year on various moors and commons surrounding the city.18 It is entirely possible under such circumstances that before he bought property of his own on Queen Street, William Snow grazed the horses he used (or perhaps owned) as a carman on the rough pasturage in Micklegate Stray and the encircling average grounds of Nun Ings, Campleshon, and York Fields. Such an arrangement would explain an otherwise puzzling statement that John Snow, as a boy, “occasionally assisted his father in agricultural pursuits . . . [on] early winter mornings.”19

Snow’s Elementary School William Snow’s vocation changed from general laborer to carman about the time his eldest son was ready to enter an elementary school. State-subsidized, universal education did not begin in England until the 1880s, but York in 1819 had many pedagogical institutions, public and private, that catered to the poor and laboring classes.20 Public meant that a school received substantial funding and direction from external sources such as religious organizations, local government authorities, and philanthropies. In York, for example, there were day schools administered by the Church of England and a Blue Coat Charity School. Students attended such public schools either free of charge or for a very modest “school-pence.”21 There were also about fifty for-profit preparatory academies and at least thirty “private schools for the education of the poor” (common day schools) operating in York between 1819 and 1823, including two common day schools in the parish of All Saints North Street, which charged parents about six pence per week for each child enrolled.22 John Snow might have attended one of these day schools.23 However, because there were already three boys in the family queue behind John Snow and his parents were dedicated to giving all their children primary education, we think it likely that they would have


23

preferred to send him to a less expensive alternative, the Dodsworth School in a nearby parish.24 John Dodsworth, an ironmonger, founded three schools in York and established endowments that paid a teacher to instruct poor boys in reading and writing free of charge. In this respect Dodsworth Schools were philanthropic charities, but because parents paid fees for their children to be taught some subjects as well as the fact that the schools were administered locally by parish officials rather than centrally by the Anglican Church, Dodsworth Schools were private schools by contemporary standards. In short, Dodsworth Schools were curricular equivalents to common day schools, just less expensive.25 The charter for the school that had operated since 1803 in a house adjacent to the Church of St. Mary, Bishophill Junior, required “that twenty poor children from the six parishes on . . . [the Micklegate Ward] side of the river, in proportion to their sizes, should be educated therein, free of expense.”26 The allotment for All Saints North Street was three. The Snow family’s long-standing connection with the parish church would have made their eldest son a suitable candidate for admission. From 1824 to 1832 William Snow did a variety of odd jobs for the church, and he became a warden in 1836.27 Therefore, if a space was available around 1819 and the vestry recommended him for it, we believe that the “private school in York” Snow attended was the Dodsworth School at Bishophill.28 On the assumption that Snow attended this elementary school, he would have traversed the heart of the ward twice every schoolday for eight years. A short walk from home along North Street lay the Ouse Bridge at the intersection with Briggate. Across this major thoroughfare lay Skeldergate, a “narrow, and disagreeable street” along which he would have continued east for one block. At the Elephant and Castle, a “commodious and respectable inn,” he would have turned south into “a narrow dirty street” called Fetter Lane. About 150 meters west, Fetter Lane intersected Bishophill. The Dodsworth School was sixty meters straight ahead, occupying the ground floor room of a small house; the master lived above the school-room.29 The curriculum— ”reading, writing, arithmetic, and the Scriptures, Church Catechism, and the use of the Prayer Book”—was similar to that offered by the private schools in the ward, with the possible exception of the absence of Latin.30 Every pupil was required to attend Sunday school in his home parish. The rector at All Saints North Street ran “a Sunday School, supported by voluntary subscription, in which about forty-five boys are instructed,”31 so Snow’s Sunday school was independent of the Church of England.32

Apprenticeship in Newcastle-upon-Tyne As Snow approached his fourteenth birthday his parents began looking for a suitable apprenticeship for him. It is unclear who suggested the unusual route of a medical career. In Suffolk, for example, about half the apprentices came from medical

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families, while the remainder were sons of clergymen, farmers, gentlemen, and a scattering of artisans and tradesmen. Not a single apprentice was the son of a general laborer or carman. In Bristol the distribution was similar to that in Suffolk, although there were fewer sons of surgeon–apothecaries and more whose fathers were artisans; only one listed his father as a carrier.33 Similar studies do not exist for York, but by 1827 William Snow’s listed vocation no longer reflected his financial situation as a property holder.34 The Snows could probably have afforded the indenture fee required for a medical apprenticeship in a provincial town.35 William Snow reached an agreement with William Hardcastle, a surgeon–apothecary in Newcastle upon Tyne and close friend of Snow’s maternal uncle, Charles Empson. A native of York born in Micklegate Ward in 1794, Hardcastle was the son of a cobbler. In 1808, aged 14, Hardcastle had been apprenticed to a licensed surgeon, William Stephenson Clark, who expanded his premises on Micklegate, the thoroughfare that bisected the ward, to include an apothecary shop.36 When Hardcastle completed his indenture in 1814, he joined the practice of an established apothecary in Newcastle upon Tyne. Two years later he traveled to London to take the lecture courses and practical medical training necessary to become a Licentiate of the Society of Apothecaries. He continued his training for an additional six months with lectures in surgery and midwifery, as well as participating in surgical rounds at a London hospital, and then passed the examination that gave him membership to the Royal College of Surgeons of London. Dual qualification as a surgeon–apothecary made Hardcastle a general practitioner. He returned to Newcastle in the spring of 1818 and purchased the practice of his former principal. Within a few years he was appointed surgeon–apothecary to the Newcastle Lying-in Hospital, where he and two colleagues shared duties as male midwives.37

Changing Medical Orders in England Snow began his apprenticeship during a period of transition from local to national regulation of medical corporations. Medicine as a profession had been “incorporated” in England since the sixteenth century, when local authorities began delegating control of occupational training and practice to guilds, or companies. The result in London and large towns was a tripartite division of medical activities similar to, if less rigidly enforced than, many Continental versions. University-trained physicians diagnosed and prescribed for “internal” complaints (medicine, or physic). Barbers and barber–chirurgeons (surgeons) were considered the manual workers who performed venesection and treated a variety of “external” conditions. Apothecaries—originally general merchants and retailers in spices, drugs, and medicinal compounds who had become specialty shopkeepers selling medicines and filling prescriptions written by physicians—were considered tradesmen and the lowest of the three medical orders by people who believed the professions should be gentlemanly occupations.38


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Local authorities of the City of London had given physicians and barber–surgeons charters of incorporation to control their own affairs.39 Henry VIII created the College of Physicians of London, which gave its members independence from local authorities, but he refused their request for nationwide jurisdiction (Table 1.2). The Barber-Surgeons of London remained a city company after unsuccessful lobbying for parity with the College of Physicians. In the next century the apothecaries were separated from the Grocers’ Company when James I chartered the Worshipful Society of Apothecaries of London, but independence came with a proviso: London apothecaries could fill prescriptions written only by physicians licensed by the College of Physicians.40 Surgeons did not extract themselves from their corporate affiliation with barbers until the mid-eighteenth century. Their practice premises became “surgeries” to distinguish them from barber shops. They gradually replaced another corporate vestige, the apprenticeship, with formal schooling including anatomy lectures and dissections. In 1800 London surgeons shed their company status for good, becoming a royal college with authority to establish requirements for anyone who sought its diploma and a license to practice in the City of London. The college had no jurisdiction in the provinces, however, where competition with apothecaries and irregular practitioners of all types remained the norm. Surprisingly, the Worshipful Society of Apothecaries was the first of the London medical orders to achieve nationwide authority. As late as the mid-eighteenth century, the apothecary’s vocation was considered an intellectually undemanding, albeit often prosperous, trade.41 The Apothecaries’ Act of 1815 empowered a reorganized society to establish licensing requirements for all apothecaries in England and Wales, to conduct examinations, and to monitor the behavior and services of its membership. Henceforth the apothecary’s duties were legally limited to compounding medicines prescribed by a licensed physician. In the words of one angry critic, the apothecary was reduced to “the phisician’s cooke,”42 but compounding and dispensing became the exclusive purview of apothecaries under the act, which expanded prerogative distinctions among the three medical orders in London to all of England and Wales. As such, the 1815 act affirmed the physicians’ long-standing claim to exclusive treatment of internal (“constitutional”) diseases, and only licensed surgeons were supposed to treat external diseases and perform surgical procedures.43 However, the Apothecaries’ Act of 1815 was a jerry-built dike, unable to contain the tides of medical convergence that had begun a century earlier. Part of the problem was that licensed physicians, who constituted less than five percent of medical practitioners at the turn of the nineteenth century, were concentrated in London and the larger provincial towns. Apothecaries continued to advise patients on how to treat internal complaints and to charge for such advice, either separately or absorbed in the cost of the medicines they dispensed. Among the middle and upper middle classes, surgeons served similar functions. They attended patients presenting internal and external complaints alike, they occasionally cut into bodies, and increasingly

Table 1.2. English medical orders: from London medical corporations to unified medical register Surgeons

Physicians

Apothecaries

1518

1300–1540

Medieval Times

College of Physicians of London (by charter from Henry VIII). Removed physicians from control by church authorities. Privilege to give licenses and right to suppress unlicensed practitioners of physic (medicine) in London and within 7 miles of the City.

Company of barbers (incorporated 1462) and Guild of Surgeons (not incorporated), City of London

Apothecarius (Spicer or Pepperer) became part of monarch’s retinue.

1523 Royal charter reconfirmed. Authority over London apothecaries established.

13th/14th centuries 1540 Company of Barber-Surgeons, City of London (no authority beyond City). Barbers and surgeons maintained distinct functions; surgeons could operate and treat external injuries/complaints. Apprenticeship required.

Apothecaries joined Company of Grocers, City of London. Joint responsibilities for regulating the importation and sale of drugs, spices, and medicinal compounds. Apothecaries gradually specialized in preparing medicinal compounds.

1745

1523

Company of Surgeons, City of London. Anatomy schools evolved in response to the emergence of new hospitals in London. Apprenticeships gradually fell out of favor.

Apothecaries in London and within 7 miles of the City permitted to fill only prescriptions written by licensed physicians. 1617

1800–1843 Royal College of Surgeons of London, Lincoln’s Inn Fields. Apprenticeships not required. Minimal formal training until Apothecaries’ Act of 1815, after which RCS developed parallel requirements for prospective members. Lectures must be completed in London; hospital training in specified metropolitan hospitals.

Worshipful Society of Apothecaries, City of London (and 7-mile radius) (by charter from James I). Restrictions from 1523 remained in force.

Anatomy Act of 1832

1703

Medical profession permitted to use “unclaimed bodies” in dissecting rooms of medical schools.

House of Lords ruled that apothecaries could give advice on internal complaints but could not charge for it.

1832

1815

RCS recognized provincial medical schools that offered curricula similar to what was available in London, but at least six months hospital training had to be completed in specified metropolitan hospitals.

An Act for better regulating the Practice of Apothecaries throughout England and Wales (Apothecaries’ Act).

1843 Royal College of Surgeons of England. 1858 Medical Act established a unified register of licensed practitioners, specified requirements for qualification, and created the General Medical Council to investigate charges of malpractice and improper conduct.

1834 In Woodward v. Ball apothecaries could mix medicines prescribed by themselves. In Apothecaries’ Co. v. Lotinga the apothecary was defined as “one who professes to judge of internal disease by its symptoms and applies himself to cure that disease by medicine.”

Source: Adapted from Cope, Royal College of Surgeons; Copeman, Worshipful Society; Holloway, ApothAct; Porter, Greatest Benefit; SCME; Wall, London Apothecaries; Wall, Cameron, and Underwood, Worshipful Society of Apothecaries.

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they advertised as male midwives. Surgeons who wished to augment their practices with the sale of medicines continued to do so after 1815 with little fear of prosecution. Despite the provisions for distinct functions, the 1815 act actually furthered the emergence of the general practitioner by permitting dual qualification as surgeon and apothecary. When the Society of Apothecaries upgraded its curriculum for prospective licentiates in the decades after the 1815 act, the Royal College of Surgeons of London was spurred to raise its standards for membership and, eventually, work with the society in developing a complementary training scheme. By the mid-1820s there was a noticeable increase in the number of licensed surgeon–apothecaries such as Hardcastle—medical men who were Members of the Royal College of Surgeons (MRCS) as well as Licentiates of the Society of Apothecaries (LSA).44 Legal barriers to general practice in the 1815 act were eliminated by a series of judgments. By the mid-1830s surgeon–apothecaries were essentially unrestricted in their practice opportunities, fulminations from the Royal College of Physicians notwithstanding.45 However, when John Snow finished elementary school, the separation into three medical orders mandated by the 1815 act was still in force. Dispensing drugs provided the bulk of a practitioner’s income, so the prospective medical man in England and Wales normally completed the requirements for a license from the Society of Apothecaries. The Society required a five-year apprenticeship, which Snow began under Hardcastle’s tutelage in June 1827.

Life as an Apprentice It was some eighty miles from York to Newcastle, a journey of five or six days by foot, or a day by coach, in 1827. Mail coaches were the safest mode of travel available, because they carried armed guards to discourage highway robbers.46 A smooth turnpike linked York to Northallerton, a rough road traversed County Durham to Gateshead, and then a short bridge took the traveler over the River Tyne to Newcastle (Fig. 1.6). Like York, Newcastle was a walled town but had twice as many inhabitants. Hardcastle lived in a house at 52 Westgate Street, next to the Spital field by the western wall and directly opposite St. John’s Church. The accommodations were spacious, including a personal apartment, surgery, and shop and a stable off the courtyard behind the house.47 We have not located Snow’s actual indenture, but we assume it was similar to the standard version used during the reign of George IV.48 By law, all masters were required to feed their charges, while lodging, laundry, and tools of the trade were negotiable. In turn, the medical apprentice was expected to serve his master “well and faithfully,” to follow all “lawful Commandments,” to stay clear of alehouses, and to abjure from playing “Dice, Cards, [gambling] Tables, Bowls or any other unlawful Games.”48a In addition, the apprentice was expected to accommodate to his master’s domestic routine and remain a bachelor for the duration of his contract.


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Figure 1.6. Newcastle upon Tyne from the south, 1827 (Wright, 16).

Typically, apprentices rose early enough to sweep the shop floor and set up for business and were already washed and dressed for the day before eating breakfast. Shop tasks included much drudgery, such as washing bottles, maintaining an inventory of drugs, “dispensing” (filling prescriptions and running them to patients’ houses), and keeping accurate ledgers. It was not uncommon for apprentices to diagnose and dispense for anyone who could not pay for the master’s attendance. Such patients received medical advice for the cost of drugs alone. Many masters dictated information about each patient’s age, occupation, constitution, living conditions, and presenting symptoms that apprentices wrote in ledger books.49 Apprentices were also responsible for delivering drugs to patients at all hours of the day and night.50 After several years apprentices often served as unsupervised assistants, making house calls, handling emergencies, and riding to mining villages if their masters were retained by one of the local collieries. Thomas Giordani Wright, a senior apprentice from 1826 to 1829 to the surgeon James McIntyre, with premises in nearby Newgate Street, recorded in his diary that he had set fractures, lanced abscesses, undertaken postmortem dissections when the relatives would approve it, handled a bewildering array of accident injuries, pulled the occasional rotten tooth, and used a stethoscope for auscultation. Such clinical encounters were over and above his usual routine of compounding medicines, treating childhood diseases, confronting the occasional measles epidemic, and dealing with recurring bilious disorders.51

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Snow left no first-hand account of his life as an apprentice, but there is evidence that Hardcastle was a “progressive thinking” master rather than an exploiter of his young charge.52 Progressive masters permitted their apprentices access to medical books, made certain they observed and eventually treated a variety of clinical complaints, and released them from shop duties and rounds in order to receive formal training when possible. Thomas Wright’s master sent him to Edinburgh for some lecture courses, but McIntyre had a virtual stable of other apprentices to take up the slack. Hardcastle, it appears, had no apprentice other than Snow, which may explain why he did not send him to the nearest provincial medical school in Hull and Leeds, roughly 100 miles from Newcastle.53 In 1832 several Newcastle physicians and surgeons founded a medical school that eventually was accredited by the Society of Apothecaries. The founders secured the use of “a large room over the entrance of Bell’s Court, Pilgrim Street,” above the consulting rooms and surgeries of three participating practitioners. They printed a prospectus of five courses for the forthcoming winter session to begin on 1 October. Although nearly forty general practitioners worked in greater Newcastle, only eight students enrolled, Snow among them. He was a senior apprentice with five years of experience, during which he had accumulated sufficient knowledge of Latin and Greek to begin formal training. Dr. George Fife probably had the best facilities for his course on materia medica and therapeutics, because Snow and his seven classmates had access to “a large physic garden.” The other instructors were Mr. H. G. Potter, who taught chemistry; Dr. Samuel Knott, who lectured on the theory and practice of medicine; Mr. John Fife, who lectured on surgery; and Mr. Alexander Fraser, who gave lectures on anatomy and physiology. The educational premises were less than ideal; there was no library, the pathology museum contained few specimens, and there was no dissecting room. Anatomical material was, in any case, hard to come by, despite the Anatomy Act of 1832, which had “awarded the medical profession rights to ‘unclaimed bodies,’ ” usually from workhouses and hospitals. When anatomical material did become available, public lectures and demonstrations were held in Surgeons’ Hall.54 As a complement to lectures, and for an additional fee, Snow attended clinical presentations and “walked the wards” of the Newcastle Infirmary.55 In 1832–1833 this hospital contained 150 beds in renovated premises. Only patients with acute medical complaints or those requiring surgical treatment were admitted. The senior surgeon was Thomas Michael Greenhow (1792–1881), a graduate of the University of Edinburgh. He was also surgeon–apothecary at the Lying-in Hospital, where Hardcastle was on the staff. Hardcastle’s willingness to have Snow attend lectures at a nascent school of medicine and observe cases at the respected Newcastle Infirmary affirm his progressive vision of what an apprenticeship should be and his confidence in Snow’s abilities.56


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Uncle Charles Empson in Newcastle Hardcastle’s practice extended beyond the town walls to include the mining village of Killingworth connected to the West Moor colliery. For several years he was general practitioner for the family of George Stephenson, the pioneering mining and railway engineer who invented the first steam locomotive, “The Rocket.” Hardcastle developed a close friendship with Stephenson’s son, Robert, and introduced him to Charles Empson, Fanny Snow’s half-brother. The three men were urbane, cosmopolitan, and pragmatic. All were members of the Newcastle Literary and Philosophical Society.57 In 1824 a London firm asked Robert Stephenson to travel to Colombia to determine if it was feasible to reopen several derelict gold and silver mines. He, in turn, engaged Empson, who was fluent in Spanish, to serve as translator, secretary, and administrator for this exploratory venture.58 In the free time available during his South American stay, Empson observed, collected many specimens of native flora and fauna, and made notes for a comprehensive journal of his researches. On the return voyage in the summer of 1827, the ship was supposed to make a short stop in New York but capsized on the shoals off Sandy Hook, New Jersey. All hands were rescued and deposited in New York City, but Empson lost most of his naturalist collection. Because no alternative conveyance was immediately available, he and Stephenson walked to Montreal but found no ship bound for England there, either. Returning to New York, they found a packet ship bound for Liverpool, where Stephenson’s parents had moved in the interim so his father could supervise construction of the Liverpool–Manchester Railway.59 Robert Stephenson decided to return to Newcastle, and Empson also settled in the town in which his nephew had lived for half a year as an apprentice. In 1830 he became a dealer in antiques, old books, and paintings, opening a shop on Collingwood Street, just a few blocks from Hardcastle’s home. He advertised as a bookseller and stationer, and within months his shop became a virtual museum of fine art and natural history collections (Empson’s speciality was shellfish), as well as a meeting place for local literati, naturalists, gentry, professionals, and commercial folk. A dapper dresser,“He usually wore full dress-black cloth and ruffled shirt, and in warm weather he wore a white waistcoat, white trousers and a white hat” (Fig. 1.7) He was an engaging conversationalist. He actively promoted the artistic interests of local youths and offered tuition-free drawing lessons to some poor students and modest scholarships to others. Meanwhile, he prepared a series of colored sketches of Colombian life and an accompanying travel narrative.60 It is unclear how often Snow joined his uncle and two friends on social occasions during his six years as an apprentice, or how his elders responded to his increasingly independent thinking about medicine, health, and life, but it seems certain that Charles Empson provided Snow access to higher social circles than he might have

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Figure 1.7. Charles Empson (courtesy of Anthony Snow; black and white reproduction supplied by David Zuck).

expected given his mother’s illegitimacy and father’s early laboring-class occupations. Like York itself, the Snow family was in social flux in the early nineteenth century. Uncle Charles was a mysterious figure but central in expanding the Snow family’s connections, establishing them in the middle class, and facilitating his nephew’s apprenticeship with Hardcastle. In many ways, then and later, Empson may have made Snow’s medical career possible.

Notes 1. Armstrong, Stability and Change, 16–36; G. Benson, City and County of York, 88–91, 101. Hargrove, York, 2: 197–206; Tillott, VCH-Y, 256–62, 517, and S. Snow, JS-EMP, 20–21, 24. 2. The Industrial Revolution would not envelop York and the surrounding region until the 1840s, when the city became an important railway hub. Rail service to London did not commence until 1840. For administrative purposes, the city lumped parishes into four wards: Monk, Walmgate, Bootham, and Micklegate. The wards were responsible for paving, sanitation, and resolving interparochial disputes; wards were also the basic administrative unit in York’s civil government. The lord mayor regularly perambulated all lands outside the walled


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city on which York’s citizens enjoyed rights of pasturage to reconfirm the city’s “ridden boundaries”; see Tillott, VCH-Y, 315–18. On the administrative structure of York, see Tillott, VCHY, 311–15; and Hargrove, York, 1: 308–36. 3. Tillott, VCH-Y, 210–11, 281–82, and Armstrong, Stability and Change, 117–23. 4. Armstrong, Stability and Change, 117–18; Tillott, VCH-Y, 254. Information about public health and sanitation problems in York is impressionistic until the cholera epidemic of 1832, when residents of North Street were among those first affected. The earliest systematic survey of sanitary arrangements, housing, and water supply in York was undertaken by Thomas Laycock for the Commissioners Inquiring into the State of Large Towns and Populous Districts; his report was included in the Commission’s First Report (1844). See also S. Snow, JS-EMP, 22–23. 5. She gave birth to two more children, although the last died as a toddler. The survival of eight children to adult life in the first half of the nineteenth century is remarkable by any measure, but especially so in light of Laycock’s estimate that until 1831 the mortality rate for children aged 5 and under in the parish of All Saints North Street was 44%; UK Parliament, First Report 1: 106 (Table 17). In 1813 the mean age of death in York was 32 years. Mean age of death was slightly lower (29 years) in the parish of All Saints North Street. The Snows’ success in child rearing suggests a home in which breastfeeding was prolonged, postweaning nutrition more than adequate, and standards of personal hygiene exceptional. 6. We follow family custom by referring to John Snow’s mother as Fanny Snow. Her home parish of Ledsham lay twenty miles south of York. The baptismal entry for 15 February 1789 reads, “Fanny, daughter of Mary Askham of Fairbourn, base born”; cited in Galbraith, JS-EY, 8. Fairburn lies just south of Ledsham village. For the marriage entry of John Empson and Mary Acomb, a variant spelling of Askham, see H. Richardson, Parish Register of Acomb, 85. We thank Spence Galbraith for alerting us to this source. John Empson noted in his will that Fanny was “my natural daughter”; BIHR, “Last Will and Testament.” 7. Thompson, Rise of Respectable Society, 199–200. 8. For genealogical details, see Zuck, “Charles Empson,” 3; Galbraith, JS-EY, 8–9; H. Richardson, Acomb, 101, 104, 122, and 124. 9. BIHR, PR HUN 6, cited in Galbraith, JS-EY, 18. A signature is a vague indicator of literacy, but “it is usually taken to show the ability to read fluently and to write laboriously”; Digby and Searby, Children, School and Society, 3. 10. Sims, “Family history”; Leaman, “John Snow MD,” 803; S. Snow, JS-EMP, 23. However, a search of the marriage register covering 1750 to 1812 for All Saints North Street by Ms. Davison of BIHR found no entry for William and Hannah Snow; BIHR, PR Y/ASN 6. In addition, the surname Snow does not appear in All Saints North Street baptismal registers; BIHR, PR Y/ASN 2 and 3. Galbraith may have solved the mystery when he located a baptismal entry from 1788 in the register for St. Mary’s, Bishophill Junior, that listed William Snow, farmer of Upper Poppleton, and Hannah (Buckle) Snow, daughter of a farmer in Stillingfleet, as parents of Joseph Snow; JS-EY, 7; William Snow, the younger, born in 1783 (according to his gravestone), apparently had a brother named Joseph. Although S. Snow states (JS-EMP, 23) that William Snow, the younger, was baptized at All Saints North Street in 1783, neither Galbraith nor the staff at BIHR could locate such an entry in that register (PR Y/ASN 2). 11. The 1818 description of North Street is from Hargrove, York, 2: 186–87. The exact location of the Snow residence in North Street is unknown; see Galbraith, JS-EY, 22–24. For a view that it was a house by a coal yard near the present position of the Viking Hotel, see A. Leaman, “John Snow MD,” 803; and Galbraith, JS-EY, 24. 12. The baptismal register suggests that occupations associated with the respectable poor predominated in the parish; BIHR, PR Y/ASN 4. See also Ashcroft, “John Snow,” 246. How-

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ever, Baines’ Directory & Gazetteer for 1823 lists more than a score of artisans, merchants, and small manufacturers on North Street; see Galbraith, JS-EY, 61. 13. John Empson’s estate was settled in 1850 for less than £100; BIHR, “Last Will and Testament”. 14. BIHR, PR Y/ASN 4. The first page of this parish register lists eight infants born between late January and mid-March 1813; all but one were baptized on the day of or within a day of birth. No street numbers are given. 15. At Thomas’ baptism on 25 February 1821, the Snows resided on North Street; at Mary’s baptism on 2 March 1823, they resided on Wellington Row; Ibid., entries 261 and 339. The description of Wellington Row is from Hargrove, York, 2:186. 16. Galbraith, JS-EY, 24. 17. S. Snow, JS-EMP, 25. 18. There were also fields with “average,” or half-year, rights of pasturage between Michaelmas (in October) and the Annunciation (usually in late March); the rest of the time, these fields were used for crops. The York corporation administered commons and average lands through the four wards. Aldermen hired pasture-masters and set limits on “rights of stray”— whose stock, which kinds, and how many could graze in each field and moor, including those areas specifically designated as ‘strays’; Tillott, VCH-Y, 498–504; and Richardson, L, ii. 19. Richardson, L, ii, and Thompson, Rise of Respectable Society, 131. 20. In 1818 approximately one-quarter of English children were receiving some form of elementary education, and most of that was vocationally oriented; see K. Evans, English School System, 24. The percentage seems to have been higher in York, in which charitable and private institutes can be traced to the late eighteenth century and a limited manufacturing sector kept child labor to a minimum; see E. Benson, “Education in York,” 22. In 1819–1820 about 1,300 children attended day schools, whether public or private, in York; E. Benson, “Education in York,” 134–35. 21. Pedagogy in day schools administered by the Church of England National Society for Promoting the Education of the Poor (the National Schools) was based on the monitorial system, under which older pupils led younger pupils in group reading and recitation as well as circulating among the desks as “monitors” when their charges practiced penmanship and mathematics. To support National Schools throughout the country, local congregations held subscription drives, donating the proceeds to the parent societies, which in turn sponsored local schools offering basic instruction in the three Rs and religion for children from the working and lower middle classes. Because subscriptions were theoretically voluntary, recipient institutions were frequently referred to as “voluntary” schools. When imposed, the “schoolpence,” a certain amount of money per child payable in weekly or quarterly installments, was a preservative against the taint of charity; see Hurt, Education in Evolution, 14–17, and Thompson, Rise of Respectable Society, 143. In York about 440 pupils were enrolled in the Manor National School “for the education of the poor, in the principles of the church of England”; see Tillott, VCH-Y, 449, and Hargrove, York, 2: 581–82. Other schools under denominational control, such as cathedral and grammar schools, were also considered public. In York Haughton’s School was available only to pupils who resided in St. Croix parish; see E. Benson, “Education in York,” 40, and Hargrove, York, 2: 664–65. A grammar school on St. Andrew Gate, descended from the cathedral school founded in the seventh century and known today as St. Peter’s, had twenty boys enrolled in 1818 who received instruction in “‘the realm in knowledge of letters and integrity of manners’”; quoted in E. Benson, “Education in York,” 39. See also Hargrove, York, 2: 362–64. Archbishop Holgate’s grammar school had free places for some “foundation scholars,” while others paid fees; see Hargrove, York, 2: 135–36. “These two free grammar schools, which drew their pupils al-


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most entirely from within the city, were the sole representative at that time of the higher schools that taught the classics and prepared students for residence at Oxford and Cambridge”; E. Benson, “Education in York,” 40. Charity schools were financed by subscription and administered by leading men and women of a town or county. York in1818 had at least two such schools: the Blue Coat Charity School, with places for fifty-six boys, and Wilson’s Green Coat Boy’s Charity School, which boarded twenty pupils from the parish of St. Denis; see Tillott, VCH-Y, 443 and 458. See also Hargrove, York, 2: 350–54 and 289–90, and E. Benson “Education in York,” 41–49, 97–106. 22. Only one of the private academies and institutes in York, most geared for middle and upper classes, was located in Micklegate Ward; see E. Benson, “Education in York,” 107–25. The number and nature of common day schools is based on reports by parish rectors in 1818; UK House of Commons, “Digest of Parochial Returns,” Sessional Papers, 1819, vol. 9, no. 2, County of York, East Riding. Average enrollment in each school was between twenty and thirty pupils. The typical school consisted of a single room in a private house. Most offered instruction to boys and girls of varying ages, without sex segregation; only two were limited to girls. The two common day schools in the parish of All Saints North Street served a total of sixty children. 23. According to Richardson, Snow was “sent to a private school at York”; L, ii. To date no one has located his name on any list of pupils in the city. Ellis was the first to suggest that it was a “private school for the education of the poor,” otherwise known as a “common day school”; CB, xii. 24. For the alternative suggestion that Snow may have attended a Quaker school, see A. Leaman, “John Snow,” 803–04, and Shephard, JS, 17. The first Quaker school for boys in York was a private school, but it did not open until October 1822 and appears to have been limited to sons of affluent Friends. The (public) Friends’ Bootham school for boys was not founded until 1828; see E. Benson, “Education in York,” 114, 126–28. For the possibility that Snow was educated at St. Peter’s grammar school, see Ashcroft, “John Snow,” 247. But Benson states that pupils at this school were being groomed for Oxford and Cambridge; “Education in York,” 40. According to Ellis, Richardson’s assertion that Snow was privately educated “has, erroneously, been taken by some commentators to imply that Snow received an expensive education at an institution analogous to a present-day British public school”; CB, xii. 25. Lawson, Education in East Yorkshire, 9, states that contemporaries did not make sharp distinctions among endowed and private schools when the former required modest fees; see also P. Gardner, Lost Elementary Schools, 15–16. Fees at common day schools varied from 3 to 9 pence per week (1–3 shillings per month, because 12 pence ⫽ 1 shilling, 20 shillings ⫽ 1 pound); see P. Gardner, Lost Elementary Schools, 12, 16. If Snow attended the Dodsworth School, his parents paid only 2 shillings per year for instruction in mathematics plus extra fees for rudimentary training in Latin, at least. The difference was considerable, especially by the mid-1820s, when the Snows had four school-age boys. All received primary schooling. William Snow (born 1815) became a hotel keeper and a tailor/hatter, Thomas Snow (born 1817) a vicar, and Robert Snow (born 1819) a secretary/manager of a colliery. Two daughters also received an education adequate for them eventually to become heads of their own seminary for girls. S. Snow, JS-EMP, 50–58, discusses Snow’s brothers and sisters in detail. The willingness of the working poor to pay for the education of their children is also noted by Digby and Searby, Children, School and Society, 5, and is discussed in detail by Laquer, “Working-class demand and the growth of English elementary education.” 26. Hargrove, York, 2: 157. See also Tillott, VCH-Y, 445–46. 27. Churchwarden’s Accounts, All Saints North Street, 1818–45 (PR Y/ASN 12), BIHR, cited in S. Snow, JS-EMP, 48, 27.

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28. Hargrove, York, 2: 157; Lawson, Education In East Yorkshire, 12; and E. Benson, “Education in York,” 69, 93–95. There is a family story that William Snow worked in Dodsworth’s coal yard as a young man, and on this basis S. Snow thinks it possible that Snow attended a Dodsworth School, although she does not specify which one; see JS-EMP, 32. 29. Hargrove, York, 2: 186 (North Street), 168 (Skeldergate), 172 (Elephant and Castle), 172 (Fetter Lane). 30. E. Benson, “Education in York,” 94. 31. UK House of Commons, “Digest of parochial returns,” Sessional Papers, 1819, vol. 9, no. 2, 1075. 32. On the attraction of schooling in general, Sunday schools in particular, for workingclass parents “dedicated to self-respect and respectability,” see Thompson, Rise of Respectable Society, 139–41. 33. Van Zwanenberg, “Apothecaries in Suffolk,” 141, 149; Loudon, GP, 29–31. 34. S. Snow, JS-EMP, 37, 71–72. For typical occupations of the fathers of medical apprentices, see Loudon, GP, 256–59. 35. In the early nineteenth century medical indentures outside London generally cost between £100 and £200; see Loudon, GP, 41–42; Peterson, Medical Profession, 69–70; and Digby, General Practice, 43. S. Snow states that the Snows paid £100 for their son’s indenture, but the source she cites does not give a fee; JS-EMP, 72. 36. Clark had attended medical school in London and qualified as a Member of the Royal College of Surgeons in 1804; see Galbraith, WH, 155–57. 37. Galbraith, WH, 157; Society of Apothecaries, Records, Ms 8241/1, 213. 38. In the eighteenth century some provincial apothecaries were still members of mercers’ guilds (dealers in textiles); Burnby, English Apothecary, 14–15. 39. The City of London occupies about one square mile, largely within the area encompassed by the original Roman walls, including the Tower of London and St. Paul’s Cathedral. Beyond the City lay various “liberties,” such as Westminster, considered part of the metropolis. 40. Background on medical organization and care in England is derived from Webster, Caring for Health, 25–32; Clark, Royal College of Physicians, 2: 476–79; Cope, College of Surgeons; Copeman, Worshipful Society; Wall, London Apothecaries; Wall, Cameron, and Underwood, History of the Worshipful Society; Waddington, Medical Profession, 1–4; Newman, Evolution of Medical Education, 1–21; Peterson, Medical Profession, 5–21. 41. A mid-eighteenth century-commentator offered a deprecating description: “His Knowledge, by his Profession, is confined to the Names of Drugs, of which he is not so much as to understand the Etymology; he must only know that Rhubarb is not Jesuit’s Bark, that Oil is not Salt, and that Vinegar is not Spirit: He must be able to call all the Army of Poisons by their proper Heathenish Names, and to pound them, boil them, and mix them into their proper Companies; such as Pills, Bolus’s, Linctus’s, Electuaries, Syrups, Emulsions, Juleps, &c. &c. He must understand the Physical Cabala, the mysterious Character of an unintelligible Doctor’s Scrawl”; Campbell, London Tradesman, 64. The apothecary’s “profits are unconceivable; Five Hundred per Cent. is the least he receives”; Ibid., 64. 42. J. Cordy Jeaffreson, A Book about Doctors (1851), 70, quoted by Holloway, ApothAct, 127. 43. Holloway, ApothAct, 124–25. See also Newman, Evolution of Medical Education, 58–79; and Peterson, Medical Profession, 20–23. 44. Waddington, Medical Profession, 2; Loudon, GP, 13–28. Loudon also argues that surgeon–apothecaries normally served a wide range of social classes wherever physicians were not plentiful and therefore enjoyed greater incomes than pure apothecaries; GP, 114. See also


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Bishop, “Evolution of the general practitioner,” in Underwood, Science and Medicine in History, 2: 350–54; Reader, Professional Men, 1–58; and Peterson, Medical Profession, 10–11, 60–61. Apothecaries practicing before the 1815 act were exempted from qualifying examinations and called “pre-1815 medical men.” 45. Loudon, GP, 189–94; Holloway, ApothAct, 221–23; in Apothecaries Co. v. Lotinga (1834), “Justice Cresswell felt justified in defining an apothecary as ‘one who professes to judge of internal disease by its symptoms and applies himself to cure that disease by medicine’” (222). 46. In York the Wellington departed the Black Swan General Coach Office on Coney Street every evening at 9:30. A Royal Mail stage coach departed from the tavern on St. Helen’s Square every midnight. In Newcastle the private and postal coaches stopped at Loftus’ Turf Hotel and the Queen’s Head Inn, respectively. See Hargrove, York, 2: 671–74; Dyos and Aldcroft, British Transport, 76; Simmons, Transport, 38–41; Tillott, VCH-Y, 475–77. 47. Galbraith, WH, 157–60. 48. His apprenticeship began on 22 June 1827; Society of Apothecaries, Court of Examiners’ Entry Book, Ms 8241/10, 61. The standard indenture was a printed form that listed expected duties and obligations, with spaces to enter names and particular details; see Walker, “Surgical apprentice,” 68–70, and Digby, General Practice, 43. 48a. Walker, “Surgical Apprentice,” 68. 49. Loudon, GP, 39, 46–47, has generalizations about the daily routines of apprentices during this period. S. Snow, JS-EMP, 78–91, contains examples of the apprenticeship experience from several contemporaries, including James Paget. Paget’s recollections in their entirety are in S. Paget, Memoirs and Letters, 19–30. 50. Gas lamps were installed within the town walls of Newcastle in the mid-1820s, but suburban roads remained unlit; Charleton, Newcastle Town, 427. 51. See also Wright, Diary of a Doctor, containing excerpts from records kept by a senior apprentice in Newcastle from 1826 to 1829. 52. The phrase is taken from Ellis, CB, xv. See also Loudon, GP, 45. Nothing indicates that Snow fit the image of “a downtrodden, aproned lad whose life was spent behind the counter of the shop or in a backroom, washing bottles and making up the stocks of medicine, working late into the night” because his master was “selfish and negligent in the performance” of his responsibilities; Loudon, GP, 44. 53. For a contemporary view of what a progressive master would teach his charges, see T. Turner, Outlines of Medico-Chirurgical Science, 4, 10. See also Reader, Professional Men, 119. In 1815 there were no authorized provincial medical schools in England; in 1832 there were eight. See UK House of Commons, SCME (1834) 602-III, appendixes 27 and 23, and Anning, “Provincial medical schools,” in Poynter, Evolution of Medical Education, 124. 54. Turner and Arnison, Newcastle School, 13–20; SCME (1834) 602-III, appendix 27. In 1834 the medical college secured better quarters and officially inaugurated itself as a teaching institution, enrolling twenty-six students and adding lectures in midwifery, medical jurisprudence, and botany. The school continued to flourish, survived a schism among its faculty between 1851 and 1857 (when there were two rival medical schools in town), and affiliated with the University of Durham, after which it could bestow the degree of MD. Quotation about Anatomy Act from Porter, Greatest Benefit, 318. Thomas Wright attended a series of lectures at Surgeons’ Hall in March 1829 when John Fife was demonstrating “on the brain of the criminal” hung after being found guilty of murder; Wright, Diary of a Doctor, 69–70. 55. Richardson, L, vii. 56. Greenhow did not join the faculty of the new medical school in Newcastle until after its merger with Durham University in 1852, when the institution could confer the MD

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degree. On Greenhow’s futile attempts to set up a university in Newcastle, see Turner and Arnison, Newcastle School, 14–16. 57. Galbraith, WH, 161; memberships in Literature and Philosophical Society confirmed by Zuck. Thomas Wright was also a member of the Literary and Philosophical Society, so medical apprentices and assistants could join; Wright, Diary of a Doctor, 84–86. According to Kay Easson, librarian to the society, Snow does not appear among the new members added between 1827 and 1833; electronic communication to David Zuck, 20 May 2002. 58. Zuck, “Charles Empson”, and Galbraith, WH, 161. 59. Zuck discusses Robert Stephenson and Empson’s fascinating voyage to Colombia in “Charles Empson.” George Stephenson had also served as the railway engineer during construction of the Stockton–Darlington Railway while his son and Empson were in South America. 60. R. W. Heatherington, “Newcastle fifty years ago,” Newcastle Weekly Chronicle (17 November 1883), reprinted in Galbraith, JS-EY, 62–63; quotation from 62. See also WH, 162. The most complete scholarly study of Empson is Zuck, “Charles Empson.” See also Empson, Narratives, 1836 and the accompanying Portfolio. Empson was and remained a bachelor. Stephenson married after his return from South America. In 1830 Hardcastle married Ann Philipson; Empson appears to have been one of the witnesses.

Chapter 2

Senior Apprentice and Assistant, 1830-1836

S

NOW WAS SEVENTEEN WHEN he read John Frank Newton’s essay The Return to Nature: A Defence of the Vegetable Regimen. The argument convinced him that a vegetarian diet would reduce irritation of the intestines and promote personal health. Newton’s form of vegetarianism included a fastidious attention to drinking water, purifying it by distillation and testing its purity chemically. Newton’s essay convinced Snow that diet, pure water, and a healthy colon were essential to one’s well-being.1 Newton wrote Return to Nature to popularize an “important discovery” by the physician William Lambe. Newton, a lawyer, believed that Lambe had shown that all medical and social problems result from “the dire effects on the human frame of animal food, cooperating with that baneful habit, the use of water, or of something more pernicious [fermented drinks], to allay the thirst which that food occasions.” When Newton shifted to a “regimen of distilled water and vegetable diet,” his chronic intestinal distress disappeared within two years. In gratitude he wrote Return to Nature to make Lambe’s hypothesis known to a wide audience.2 The unifying assumption in Newton’s essay is that an Edenic fare of fruits and vegetables was created for human consumption and is essential for a full and healthy life span. After the Fall and the discovery of fire, however, humans increasingly partook of cooked meat. The die was cast: “Thirst, the necessary concomitant of a flesh diet, ensued; water [often polluted] was resorted to, and man forfeited the inestimable

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gift of health which he had received from heaven: he became diseased, the partaker of a precarious existence, and no longer descended slowly to the grave.” Newton then offered additional evidence to substantiate his scriptural premise that vegetables (as he called all plant products) are our only natural food, whereas animal flesh is unnatural and unhealthy.3 One who consumes a healthy plant diet needs only an occasional drink of water, but if the water is impure the vegetable diet is undermined. Modern humans had fouled the natural world to such a degree that “common water” near large settlements was invariably impure. In large metropolises like London and Paris, only distillation was foolproof. “Our own Thames water,” said Newton (who lived in Chester Street, Belgravia, London), was so polluted by “animal oil” and “septic matter” that every household should use a distillation apparatus such as he had constructed and placed in his own kitchen. Newton discarded the first three gallons of distillate, kept the next ten to twelve gallons of “almost imputrescible” water, and stopped the process when three or four gallons remained at the bottom of the still because of the “residuary filth” it contained. Before drinking he undertook “a test of the purity of water, familiar to every chymist. Drop into a glass of water a few drops of nitrate of lead.”4 If properly distilled, the fluid should remain clear; if it turned cloudy, he repeated the distillation. The recommended breakfast consisted of “dried fruits, whether raisins, figs, or plums, with toasted bread or biscuits [preferably without butter], and weak tea, always made of distilled water, with a moderate portion of milk in it.”5 For children the tea was replaced by diluted milk. A typical dinner was “potatoes, with some other vegetables, according as they happen to be in season [in a sauce of Portuguese onions and walnut pickle]; macaroni; a tart, or a pudding, with as few eggs in it as possible: to this is sometimes added a dessert. . . . As to drinking,” Newton cautioned that “we are scarcely inclined on this cooling regimen to drink at all; but when it so happens, we take distilled water.”6 At the time (1811) twenty-five people were actively practicing this regimen, including seven in Newton’s own household. The results were promising: All were in good health, use of medicines was rare, and indispositions, if any, were trifling. Because he had tested the vegetable and distilled water regimen on himself, his family, and several friends, he claimed that it “rests on the only firm basis of philosophical conclusions, on Experiment.”7 It took Snow several years to find a situation in which he could fully implement Newton’s regimen, but then he adhered to it rigidly for nearly a decade and in a modified form for the rest of his life. Obtaining pure water became a dominant element in his personal life and affected his view of public water supplies. Perhaps the prevalence of impure drinking water in his childhood town primed him as a teenager for Newton’s alternative. Certainly, when in 1848 he altered his views on the pathology of cholera, he was intellectually predisposed by Newton’s ideas to consider the intestines a primary site of infection and impure water a potential source of morbid poisons. Nevertheless, when epidemic cholera first

Senior Apprentice and Assistant, 1830–1836

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reached England in 1831, he assumed, like everyone else, that it was contracted by inhalation or contact.

Snow and Cholera, 1831–32 As the familiar adage emphasizes, Newcastle was a coal town. Hardcastle’s practice included people whose livelihood depended on the extraction, transport, and trade of this fuel, essential for the industrial revolution that had been changing the landscape and social structure in Northumberland county for half a century. He was the mine doctor at Killingworth, a company village owned by the “Grand Allies”—three wealthy families who also had extensive mineral holdings in County Durham south of the River Tyne. When Snow moved to Newcastle in 1827, the coalfield close to town was largely depleted, but it was still in full production beyond a three-mile arc north of the Tyne, including the mines near Killingworth, which lay five miles north of central Newcastle. Except for those who had had military or administrative service in India and those who had recently traveled to eastern Europe or Scandinavia, no English medical man had seen a case of Asiatic cholera until 1831. When several people became ill in the port of Sunderland early that fall, observers from the local board of health were unsure whether the disease was the endemic English, bilious, or summer cholera (interchangeable names for common diarrheal diseases) or the feared Asiatic cholera from abroad. However, as a precautionary measure against noxious vapors, or miasmas, lime was spread on the streets. When a Newcastle man died early in November 1831, three surgeons, including Mr. Greenhow of the infirmary, assured the mayor that there was no cause for alarm, because the “efficient cause” of cholera (presumed to be a miasma in the atmosphere) settled only in low-lying areas and was not contagious. Most of Newcastle was situated at an altitude considered safe. Consequently, Greenhow assumed the man who died must have contracted cholera elsewhere and would remain an isolated case.8 However, on 7 December 1831 Newcastle’s medical men officially confirmed that Asiatic cholera was indeed present in the town. Thereafter, the disease appeared in villages and towns throughout Northumberland and the adjacent county of Durham. The colliery villages were especially hard hit: “The majority of the houses were two or three roomed, terraced and built in rows. They were cluttered with sheds for pigs and poultry.” It was generally thought that overcrowding and manure produced an unwholesome air that facilitated the transport of the morbid poison of cholera, as well as other epidemic diseases, to its victims. Newburn, a mining village of 131 houses with 550 inhabitants, was decimated by fifty-five deaths among 320 cholera cases in the middle of January 1832. On Christmas day in Gateshead, across the Tyne bridge from Newcastle, “nearly fifty different cases occurred almost at the same instant.” When word of outbreaks in the collieries, river ports, and Gateshead reached

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London, the Central Board of Health sent medical agents to the Tyne region. They found walls placarded with a variety of handbills. Some implored people to report all suspicious illnesses; others suggested preventive potions and measures, sounded alarms, or appealed for calm in the midst of chaos. The medical men from London had no authority to intervene in local affairs, so they left the town to its own devices. Those who believed a mild winter had caused such a rapid diffusion of the disease felt vindicated when, early in February, the temperature dropped and the epidemic seemed to be over.9 Even so, new cases popped up early in the summer, and it was soon apparent that the epidemic had temporarily abated rather than ended. According to the Poor Law in place since the sixteenth century, parish authorities were responsible for sanitary measures related to the epidemic and for medical treatment for the destitute. On 7 August 1832 the vestry of St. John’s appointed Hardcastle and another surgeon as Poor Law medical officers for the duration of the crisis. Shortly thereafter, cholera was reported in another part of Hardcastle’s bailiwick, the mining village of Killingworth, which had been spared a “visitation of cholera” in 1831. Because he could not be in two places at once, he sent Snow to Killingworth as his unsupervised assistant.10 Snow was responsible for medical treatment for everyone in the village, but he appears to have remained on the surface and never ventured below ground.11

Burnop Field Crossing the bridge over the River Tyne between Newcastle and Gateshead, Snow turned southwest into the road to Stanhope in County Durham. After seven miles he reached Burnop Field, a village of about 100 houses. It was early April 1833 and Snow was about to become the assistant to a rural apothecary.12 A few years as an assistant would permit him to save money toward the two years of schooling in London he needed to become a licensed practitioner in his own right.13 He could probably have found a position in Newcastle, but the town may have held little attraction for him once his uncle moved to Bath early in 1833.14 Snow’s new employer was John Watson, a “pre-1815 medical man” without formal training who had established his practice before the Apothecaries’ Act became law. He lived in Burnopfield Hall, a spacious house on Front Street in the center of the village. Snow’s position included a room in the house and board. Mr. Watson and his wife, Jane (Toward) Watson, had five children ranging in age from one to thirteen.15 Watson was in his mid-forties, and Snow now probably met him for the first time. It was not uncommon for rural practitioners in Northumberland and Durham to advertise for an assistant in Newcastle newspaper, after which an agreement could be reached by post. Watson had very different attitudes about managing a practice than Hardcastle. Snow was in for a shock:


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I found his surgery in a very disorderly state, and thinking on my first day with him that I would enhance myself in his opinion by my industry, I set to work, as soon as his back was turned, to cleanse the Augean stable. I took off my coat, cleared out every drawer, relieved the counter of its unnecessary covering, relabelled the bottles, and got everything as clean as a new pin. When the doctor returned, he was quite taken by storm with the change, and commenced to prescribe in his day book. There was a patient who required a blister, and the worthy doctor, to make dispensing short, put his hand into a drawer to produce one. To his horror, the drawer was cleansed. Goodness! cried he, why where are all the blisters? The blisters, I replied, the blisters in that drawer? I burnt them all; they were old ones. Nay, my good fellow, was the answer, that is the most extravagant act I ever heard of; such proceedings would ruin a parish doctor. Why, I make all my parochial people return their blisters when they have done with them. One good blister is enough for at least half a dozen patients. You must never do such a thing again, indeed you must not. L, xxxiv This anecdote shows that Snow was organized, energetic, and impetuous. His desire to bring order to a chaotic shop obscured the diplomatic nicety that it would have been appropriate to consult his principal first and to follow his instructions.16 The purpose of counterirritation, whether via blistering, cupping, or the insertion of setons (usually threads or horse hairs placed under the skin) was to concentrate whatever irritation was causing a local inflammation or mild fever, then draw it from the body.17 When the blister had accomplished its intended purpose, the doctor lanced the swollen skin and judged by the appearance of the discharge whether the application had diverted the humor from the worrisome inflammation.18 In short, Snow as an assistant seems to have considered blisters an acceptable therapy under certain circumstances. His Case Books show he prescribed blisters, liniments, and setons in the 1850s.19 The blister anecdote reveals that Watson was a “parish doctor,” which in 1833 meant that a significant percentage of his practice included people too poor to pay him directly for treatment. The Parish of Tanfield paid him a retainer to care for “parochial people”—“the destitute, aged, infirm or sick . . . supported by a poor rate levied on householders in each parish.”20 Like most general practitioners at the time, Watson probably counted on trade in drugs for much of his income. It was usual to send fee-paying patients itemized bills of attendances and therapeutics every quarter, and Watson must have had a substantial number because the nearby Burnopfield Colliery employed many of the men in the village. Receiving no compensation for medications prescribed and prepared for patients covered by the poor rate, Watson cut his losses on the parish poor by demanding that they return the gauze so he could reuse it, but only on other parochial patients. He probably expected Snow to do the same, although Snow noted only that he never burned used blisters there-

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after. He had no choice. Being in “charge of a gentleman’s practice” meant following orders and doing most of the work.21 Two decades after his first day in Watson’s practice, Snow recalled that he and “the worthy doctor . . . never had any more serious misunderstanding” (L, xxxiv–xxxv). Watson soon summoned Snow from the erstwhile Augean stable to help him treat an unusual influx of patients with influenza. Years later Snow’s recollection was that the epidemic commenced shortly after a “sudden and considerable increase of temperature” in the region. After an extended period of “cold wet weather” earlier in April 1833, it had suddenly turned “warm and dry,” followed by the outbreak of influenza. “The complaint appeared to attack the coalminers in greater numbers than the agricultural and other people; now the coalminers . . . often had to work at night, and they were always deprived of day-light whilst at their work.” Night workers seemed predisposed to other epidemic diseases as well, such as erysipelas, which he characterized as “an asthenic inflammation, in some respects resembling influenza; so that it seemed probable that night occupations rendered persons more liable to diseases of this class.”22 These remarks contain parallel terminology to that used by three British medical theorists commonly cited in the 1830s and 1840s. The first was Thomas Sydenham (1624–1689), an English physician whose ideas were still influential in the nineteenth century. His concept of the “epidemic constitution” had become generic. “The core of this theory was the conviction that the seasons of the year and the atmosphere were the main determinants of the nature of a disease. While these determinants caused a particular atmospheric condition suitable to the spread of a particular disease,” whether an individual was susceptible depended on various predisposing factors such as humoral imbalance.23 Sydenham’s approach to “bedside medicine” was also widespread in Snow’s day. According to Sydenham, all diseases had distinguishing symptoms to the observant physician, so he recommended observation at the bedside with explicit purposes: to establish what disease the patient presented, determine the species of disease by association with the parts of the body it affected, decide whether to let nature take its course or administer therapeutics, and monitor the patient’s progress for the duration of the disease.24 Snow’s expression “diseases of this class” may signify familiarity with the nosology devised by William Cullen (1710–1790), a celebrated Scottish physician and teacher, but Cullen’s disease classification was so commonplace as to render a search for influence superfluous. A medical naturalist like Sydenham, Cullen also believed that a proper classification of diseases was essential to appropriate and standardized treatment.25 He reduced all diseases to four kinds, or classes, of physiological disruption, all caused by nervous dysfunction. The most inclusive of Cullen’s classes were the pyrexia, or febrile diseases.26 He considered most epidemic diseases to be fevers in which “some matter floating in the atmosphere, and applied to the bodies of men, ought to be considered as the remote cause. . . .”27 Many fevers were of uncertain origin, although he believed that there was probably a common origin that


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manifested itself differently, depending on predisposing factors such as vocation and the state of the nervous system.28 Snow’s suggestion that “night occupations” might predispose such workers to influenza and erysipelas more so than people on a “natural” diurnal schedule could be considered a susceptibility to a first-stage fever in Cullen’s system of classification. Snow’s comment that erysipelas was “an asthenic inflammation” could be interpreted as Brunonian. John Brown (1735–1788) diverged from the theory of his teacher, William Cullen, by asserting that all human diseases are reducible to insufficient or excessive “excitability.” Too little excitement produced “asthenia” (equivalent to Cullen’s stage of debility). Too much excitement, and the bodily reaction was “sthenic.” The appropriate medical response in the Brunonian system was countertreatment: stimulants (such as alcohol) to raise the level of excitability, sedatives (opium, for example) to reduce excitability to the desired midpoint, or health. Brown quantified the range between mortal asthenia (zero) and mortal sthenia (eighty). Brunonian practitioners prescribed therapeutics that were supposed to return the patient to the desirable midpoint of excitability—forty on Brown’s health and illness scheme,29 but we do not know what medical texts Snow was exposed to under Hardcastle’s tutelage or during his year of formal training in Newcastle. He may have read Sydenham, Cullen, and Brown, or he may have indirectly absorbed conventional medical theories at his master’s elbow in the early years of his apprenticeship and via lectures in his last year. Clinical experience was desirable in an assistant, not book learning.

Pateley Bridge Snow left Burnop Field in April 1834. Besides having little in common with Watson, Snow felt he had to “work too hard for his money.”30 He was now twenty-one and apparently still short of the funds required to complete his medical training. Uncertain about what to do next, he visited his family in York. A few things had changed, but much remained the same as it was when he had left York for Newcastle in June 1827. His parents were still alive, as were the seven siblings he had known before his departure. His three sisters were still living at home: Mary was eleven, Hannah nine, and Sarah seven. Of his brothers, William at nineteen was training to be a tailor, Charles at seventeen was helping his father with farm work, and Robert at fifteen and Thomas at thirteen were in school and still living at home. However, George, born in 1828, had died in infancy; it is unclear if Snow ever saw him. The family home was still on Queen Street, but in a different house. The move had been unexpectedly propitious: there had been many cases of cholera in North Street in 1832, but none in Queen Street.31 In compliance with the First Reform Bill, William Snow was registered in the York Poll as a property-owning farmer, and he had begun to purchase additional properties on Queen Street that he rented out.32

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After a short stay in York, John Snow traveled to Pateley Bridge, a small market town on the River Nidd in one of the dales of West Yorkshire. He signed on as assistant to Joseph Warburton, a licensed apothecary with an extensive practice in the town and the four rural parishes of upper Nidderdale. Warburton was nearing fifty and had lived in Pateley Bridge since 1807, apart from a six-month interlude at the London Hospital in 1816 while qualifying for the LSA. By one estimate, seventy-eight percent of general practitioners (GPs) who set up a practice in the north of England between 1820 and 1879 did so near their birthplaces. Warburton fit this pattern, even though he was only an apothecary and settled in Pateley Bridge a few years before the GPs covered in this sample.33 He married Harriet Thackery of Pateley Bridge, and by 1822 was the father of three children and had purchased Fog Close House, which served as home and practice premises.34 Snow joined the household on his arrival in 1834 and immediately became part of the medical team that sallied into the surrounding parishes. Warburton took charge of patients in town and supervised Joseph, Jr., his son and apprentice. Snow was responsible for patients in the rural parishes. As in Burnop Field, medical care during his second assistantship involved “many rough rides, [and] a fair share of night work”—but now in terrain that was stunningly beautiful and dangerously rough rather than dingy with mining hamlets. He continued to accumulate experience in bedside medicine as a provincial GP: diagnosing and prescribing for internal complaints, treating external lesions, setting fractures, performing minor surgery, and compounding his own prescriptions. Contrary to his experiences with Watson, Snow thought he was fairly treated during his eighteen months in Pateley Bridge. Afterward, he “spoke of Mr. Warburton, his ‘old master,’ in terms of sincere respect, and depicted his own life there with great liveliness.”35 The Warburtons also tolerated his “culinary peculiarities” as a vegetarian and shared his commitment to temperance reform. According to Richardson,“At or about the same time that he [Snow] adopted his vegetarian views, he also took the extremity of view and of action, in reference to the temperance cause.”36 Temperance was central to John Newton’s belief in a natural regimen: in his words, “the tutelar goddess of health and universal medicine of life.”37 It could be coincidental that Snow’s conversion to Newton’s vegetarianism and interest in immoderate alcohol consumption as a health problem occurred the same year, 1830, that a temperance society was founded in Newcastle. It is possible that Snow was introduced to Newton’s ideas at this society and then read his essay, but it is unlikely that we will ever know for sure how it came about. However, it is certain that near the end of his stay in Pateley Bridge he publically advocated vegetarianism and had moved beyond Newton in his opposition to alcohol. In 1836 he justified vegetarianism on medical grounds: “That diet is most conducive to strength which keeps the body in the most healthy and natural state, that food and drink which affords the necessary quantity of nutrition, and is at the same time least heating and stimulating.”38 He borrowed the words “heating and stimu-


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lating” from Newton, but the context suggests Snow believed that a vegetarian diet was as close as humans could come to a natural regimen. In addition, he followed Newton’s recommendation to avoid alcoholic beverages because they, too, are heating and stimulating. Snow preferred “cold water . . . I can drink it [in] moderation when I am thirsty, and I never tire of it.” This “limpid element” had great health benefits, but the drinking water available where humans lived often contained “impurities.” Because Snow considered pure water an ideal beverage, “The way to get water pure is to distil [sic] it. Those huge stills in different parts of the country that pour forth evils amongst mankind in greater proportion than the fabled Pandora’s box, may, by distilling water instead of spirit, be made to be the fountains of health; and wherever there is a steam engine, a very trifling expense in a few additional pipes would condense the steam that now flies away into the air, or is otherwise wasted, and supply plenty of the purest water to the whole neighbourhood.”39 Thus, pure water joined nonstimulating, vegetarian food in Snow’s ideal regimen for health. His third prescription was “exercise”; like his uncle, he had become an inveterate walker. With the Warburtons he was able to actualize his ideals. They permitted him to construct a simple still for producing pure water, and the cook provided him with vegetarian meals: fruits and vegetables but no butter, milk, or eggs. Warburton was active in local temperance activities and established a cocoa house as an alternative to the ubiquitous public houses (pubs).40 Toward the end of his contract as Warburton’s assistant, Snow converted from temperance to teetotalism—the latter distinctly more secular and radical–democratic compared to the evangelical and republican-minded moderationists.41 This shift occurred late in 1835 or early in 1836, after he met John Andrew, Jr. Andrew was the son of a corn-miller and maltster who forsook the latter after signing a “moderation pledge.” Young Andrew spent little time in the family business after he took a total abstinence pledge in 1834. Using Leeds as base, Andrew and a small band of campaigners visited villages and market towns throughout Yorkshire where like-minded persons had arranged meetings.42 After speeches extolling the benefits of abstinence, he would urge his listeners to show their commitment to “the teetotal principle” by signing a pledge book. Snow attended one such meeting and “became an abstainer.” The pledge he took was probably similar to the one adopted at Preston in 1832: “We agree to abstain from all liquors of an intoxicating quality, whether ale, porter, wine, or ardent spirits, except as medicine.”43 Andrew and his colleague, W. A. Pallister, visited Pateley Bridge in the spring of 1836. They contacted Snow, who assisted them in organizing a public meeting. “In addition to the stirring addresses of the zealous young advocates from Leeds, Mr. Snow read a paper on the physiological action of alcohol.”44 The next morning Andrew returned to Leeds, but Pallister “remained to the end of the week, holding meetings at some of the neighbouring villages, with enduring results.”45 When he had time, Snow participated with these itinerant abstinence missionaries at public debates and meetings.46

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In the summer of 1836 he returned to York for an extended visit with his family. By then temperance had become a family affair. Thomas Snow had joined the York Moderation Society in 1835 at the age of fifteen. Another brother, William, two years younger than Snow, was also a temperance advocate in York.47 On Snow’s “first walk into the heart of the city” in almost two years, he was struck by the conjunction of poverty and intemperance all around him. As he considered possible “means of introducing teetotalism” to the residents of York, someone told him about “another young man who was on a visit to his friends, and was also bent on the same errand” —William Laycock, a schoolteacher. Snow sought him out, and the two then met a teetotaling Methodist minister, who assisted them in organizing a meeting at the Methodist chapel on the last day of June 1836. Snow and Laycock spoke convincingly enough to garner seven pledges. “Several of the members of Mr. Snow’s family were present at this meeting, his mother taking an active interest in the arrangements for the comfort of those present.” Fanny Snow apparently served tea and a nonmalt beverage at the first meeting of what soon became the York Temperance Society (of the teetotal faction). Pleased with their success, Snow and Laycock advertised a public meeting for 6 July in Merchants’ Hall, at which John Andrew was the principal speaker. “Fifteen pledges were taken, making a total membership of twenty-two,” including, apparently, Thomas Snow, who could not attend the first meeting. Laycock had to leave town, “but Mr. Snow remained until September, continuing his efforts for the promotion of the cause” in weekly meetings in York and reform crusades into neighboring villages. He “secured the use of the Bilton Street schoolroom, Layerthrope, where a meeting was held, and another at Acomb [Empson’s native village], under the presidency of the clergyman. . . .”48

Snow’s Teetotal Address Like J. F. Newton, Snow made temperance a corollary of vegetarianism and pure water. In June 1836 he delivered a “teetotal address” in Pateley Bridge, which shows him to have been psychologically astute in assessing his audience, judgmental and decisive in his opinions, yet tolerant of people whose habits he might abhor.49 The address is the only direct source of Snow’s medical worldview after nine years as an apprentice and assistant. He objective was to give a medical explanation of the deleterious effects of alcohol. Physiologically, he asserted that the consumption of alcohol resulted in overheating and overexcitement, both of which caused “serious derangement in the [bodily] economy.” There were instances when alcohol had medicinal value, such as in “some case[s] of spasmodic pain,” but these were uncommon. The terminology may reflect Cullen’s influence, but it was in generic use by the 1830s.50 With respect to cholera, Snow believed the reliance on “the brandy treatment” early in the 1831–1832 epidemic tailed off as practitioners realized that administration of the liquor only “hurries on and makes more violent that reaction,


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that secondary fever which is most to be dreaded, and increases the tendency which there is to inflammation in the head and elsewhere.” Once again, Snow employed language that originated with Cullen and Brown but was so common by the 1830s that one should not connect him to them specifically.51 Nevertheless, Snow’s teetotal address is unambiguous in one respect: In the wake of the first cholera epidemic, he was (theoretically, at least) a therapeutic skeptic like many other medical men.52 “Medicines,” he told his audience in 1836, “are indeed a great blessing, but at the same time, their use is generally the substitution of a lesser evil for a greater”—death. Snow believed “the unassisted powers of nature inherent in the body” were usually superior to what medicines could accomplish.53 This perspective associates him with therapeutic skepticism, a notion that the healing power of nature (vis medicatrix naturae) rarely needed a helping hand. The skeptical medical man patiently monitored the patient’s struggle with disease, trusting in the inner strength of the mysterious life force and administering medicines only if the disease appeared to gain an edge. Despite “all our progress in natural history and the physical sciences,” he asserted, “we are far behind some of the civilized nations of antiquity in knowledge of the things most nearly connected with our health and well-being.”54 His admonitions against overdependence on medicines in combination with his preference for doctrines from antiquity that stressed diet and exercise echo John Newton and are remindful of Sydenham’s revival of the Hippocratic regimen. So while therapeutic skepticism likened him to Newton and Sydenham, it distanced him from Cullen and Brown.55 His early obsessions with pure drinking water and the diseases carried by impure water were unusual and indicative of an early interest in public health that he maintained when he moved to London for the rest of his life.

Notes 1. Newton, Return to Nature. When Richardson composed his biographical sketch of Snow’s life in 1858, he discovered a copy of Return to Nature in Snow’s personal library. It appeared to him that annotations in it had been made in 1833, but Snow told him that he had “formed an idea that the vegetarian body-feeding faith was the true and the old” as early as 1830 (L, ii). 2. Newton, Return to Nature, 2, 66. He based his argument for a natural diet on passages extracted from literature, examples from comparative anatomy, analogical reasoning, and what he termed “experiment.” Newton cites two works by Lambe: “Reports on Cancer” and “Constitutional Diseases.” The former is either Lambe, Reports on the Effects of a Peculiar Regimen, or Additional Reports; the latter is A Medical and Experimental Inquiry into Constitutional Diseases. Newton may also have consulted Lambe, Researches into the Properties of Spring Water. 3. Newton, Return to Nature, 9. Newton’s assumption about the basics of a healthy diet is based on Genesis: “Man is created and placed in a garden abounding with fruits and vegetables, with which he is commanded to sustain himself ” (4). Newton used fables and recent studies in comparative anatomy to construct physiognomic and anatomical descriptions of

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ideal humans. Again, he drew on Lambe: There are remarkable parallels in “the form and disposition of the intestines” in humans and orangutans. So, Newton reasoned syllogistically, because the orangutan “lives on fruits and vegetable in so vigorous [a] state” [and] the intestines are similar in both “tribes” of animals, that “man is wholly adapted to vegetable sustenance is evident from his anatomy” (17–19). 4. Ibid., 43. Newton entreated “earnestly that those who may be influenced by our reasoning, will not adopt this system by halves, since a small portion of fish or meat, taken daily, will maintain irritation [of the bowels], and vegetable diet, without quitting the use of common water, whether drank alone, or in tea, coffee, beer, &c will by no means insure health” (37–38). 5. Ibid., 113–14. 6. Ibid., 114–15. 7. Ibid., 71. Newton’s medical framework was humoral. Health existed when the body’s internal secretions were in balance, illness when the balance was disturbed. He assumed health was the natural order of things: “If we reason analogously, and consider how measured, how definitive nature is in her operations, . . . [then the only reasonable explanation] for the astonishing deviation from such laws of which human diseases are an instance, must be attributed to some extraneous cause, acting powerfully in contravention of the order of nature” (116–17). Although we do not have an “exact description of that morbid humour” that produces disease, “the investigation of the chymist or the physician” will discover it eventually. Regardless of what they find, we should immediately adopt the “regimen of distilled water and vegetable diet” (66) because it has indisputable benefits. Those who do will find “the stomach is so fortified by the general increase of health, that a person thus nourished is enabled to bear what one whose humours are less pure may sink under” (80). Distilled water and vegetables is the only diet “that secures and perfects digestion, and therefore avoids the fumes and winds to which we owe the cholic and the spleen; those crudities and sharp humours that feed the scurvy and the gout, and those slimy dregs out of which the gravel and stone are formed within us” (105). Everyone who has followed it to date reports “the secretions duly regulated, and the strength and health completely re-established” (70). 8. For a map of the first European pandemic, see Bonderup, “Cholera- Morbro’er”, 17, and Morris, Cholera 1832, 60–61. For Greenhow’s explanation of the lessons from the 1831–32 epidemic, see Lancet 2 (1848): 452. Durey, Return of the Plague, 101–18, discusses contemporary views of the cause of cholera; we defer an extensive discussion of this topic to later chapters. 9. Descriptions of housing in the colliery villages and the action of the board of health is from Morris, Cholera 1832, 61–63, and Creighton, Epidemics in Britain, 2: 802–05; on the Christmas day outbreak, see Greenhow, Cholera as It Has Recently Appeared, cited in Creighton, 803. 10. Morris, Cholera 1832, 59; Creighton, Epidemics in Britain, 803. 11. More than twenty years later Snow recalled “having seen [miners] brought up from some of the coal-pits in Northumberland, in the winter of 1831–32, after having had profuse discharges from the stomach and bowels, and when fast approaching to a state of collapse”; MCC2, 20. His use of plurals—“coal-pits in Northumberland” and “1831–32”—suggests that he may have observed cholera victims at collieries during the initial Tyne outbreak in the fall of 1831 as well as at Killingworth in 1832. Snow had no personal knowledge of conditions in the pits because later references are to published reports and information derived from a brother. Richardson did not explain why he thought Snow’s “exertions [at Killingworth] were crowned with great success”; L, iv. 12. We date Snow’s arrival in Burnop Field from remarks he made at a meeting of the Westminster Medical Society, Lancet 1 (1841–42): 598.


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13. Medical assistants in provincial towns earned £80–90 per year, the equivalent of a curate at a parish church. The salary in rural areas was usually less; see Loudon, GP, 258–60. The data base of GPs used by Digby generated few patterns about assistants in the early part of the nineteenth century, but it was apparently common after mid-century to interrupt one’s training with assistantships if one needed the funds; British General Practice, 46–47. In 1833 it cost £150–200 for two years of medical training in London; see Loudon, GP, 230, and S. Snow, JS-EMP, 146–48. Ellis suggested additional considerations behind Snow’s decision to delay schooling, including a realization that his grasp of Latin and Greek was inadequate for formal training; CB, xvi. 14. Empson “became the victim of a cruel, malicious, and slanderous report” by a former employee; see R. W. Heatherington, Newcastle Weekly Chronicle, 17 November 1883, quoted in Galbraith, WH, 162; Galbraith has reproduced the entire newspaper article; JS-EY, 62–63. We agree with Zuck that Empson probably left Newcastle in the spring of 1833, shortly after he auctioned “a large collection of Pictures and Prints, some of them well-known originals . . .”; Newcastle Chronicle, 23 March 1833, quoted in “Charles Empson,” 24. Robert Stephenson moved to London in 1833; see Galbraith, WH, 161. Galbraith found the following entry under the “Newcastle Police” column of the Newcastle Courant of 15 January 1831: “On Monday last, John Snow, an apprentice to a surgeon in the town, was brought before the Mayor, charged with having on the Sunday evening preceding, wilfully disturbed the congregation in the meeting house of the Rev. Mr. Syme . . . while they were assembled for religious worship, by letting off a [fire]cracker within the porch.” “Two friends” posted bail of £50 to assure “his appearance at the next sessions to answer the charge. . . .” The punishment for this misdemeanor was £60 or imprisonment in default of payment; JS-EY, 32. We do not know the outcome of this case, but lingering repercussions from this bit of mischief-making may have contributed to Snow’s decision to leave Newcastle as soon as he had fulfilled his contractual obligation as an apprentice. 15. The description of Burnop Field is from Surtees, History and Antiquities of Durham, 2: 219. The population was about 500. It is unlikely that Snow had visited the village while an apprentice. Hardcastle’s practice area did not include Burnop Field in County Durham. Also living at Burnopfield Hall were the house servants, including the family cook and her illegitimate infant son, reputedly fathered by Watson. For a description and illustration of the house, as well as particulars on the Watson family, see Galbraith, BF, 33–35. According to Galbraith, John Watson (1790/91–1847) was a practicing apothecary before the 1815 act and exempted from the licentiate examination; BF, 32. 16. The anecdote also gives us some hint of Snow’s medical philosophy at what would prove to be roughly the midpoint of his training. He did not dismiss Watson’s assessment that the “patient required a blister.” A blister was an irritating medicament applied to the skin on a piece of muslin or gauze with the object of raising a pustule that could be lanced to draw off the accumulated fluid. The standard application for nearly two centuries had been a paste or ointment containing powdered cantharides, derived from the green blister beetle, Spanish fly. But cantharides had an unpleasant side effect—irritation of the urinary tract and bladder. By the 1820s it was common for medical practitioners to use active ingredients that did not cause this complication, such as savine cerate (mixed with lard and wax), mustard, or capsicum; David Zuck, mail message, 4 July 2000. Blisters, including cantharides, continued as a standard method of treatment for various inflammatory and painful conditions until the end of the nineteenth century. 17. Some healers still believed that the offending irritation was cause by humoral imbalance. Three of the primary humors (black bile, yellow bile, and blood) were associated with dry and hot qualities that, in combination, produced the greatest amount of “sharpness” and consequent irritation in the body. The signature diagnostic signs were bitter taste and odor.

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The sharpness in yellow bile was particularly irritating, although the liver was less susceptible to surpluses because it was the source of that humor. Individuals whose normal constitution included a predominance of yellow bile were prone to overheating—their temperament was choleric, their physical disposition bilious—without, however, becoming ill, but if predisposing factors such as aging, improper diet, debilitating habits, or unusually hot weather generated too much yellow bile in the liver, a fluxion (flow) of irritating sharpness could cause local sites or the entire body to become overheated. See Porter, Greatest Benefit, 55–61; and King, Medical Thinking, 21–23. 18. Caustic blisters were sometimes applied to unaffected parts of the body “on the assumption that the excoriation of one area and consequent suppuration could ‘attract’ the morbid excitement from another site to the newly excoriated one, while the exudate was significant in possibly allowing the body an opportunity to rid itself of morbid matter, of righting the disease-producing internal imbalance”; see Rosenberg, “Therapeutic revolution,” 23 (endnote 8). On counterirritation as treatment until well into the twentieth century, see Brockbank, Ancient Therapeutic Arts, 105–34. 19. Snow prescribed “a large blister” (Ellis, CB, 107) in 1850 for a patient with pleurisy, followed a week later by cupping six ounces from “the right suprascapular space” (109). The next day, he wrote, the patient’s “pains removed by cupping” (109). Eventually the consulting surgeon tapped large quantities of fluid from the chest cavity and the patient recovered fully. Snow visited this patient on sixteen different days, often several times a day. In general, he employed cantharides such as plaster of lyttae and plaster of antimony potassium tartrate in his practice well into the 1850s; Earles, “Glossary of Latin abbreviations,” in CB, liii–lvii. 20. Porter, Greatest Benefit, 239. “Out-door” relief based on the English Poor Law of 1601 (sometimes referred to as the Elizabethan Poor Law) was still in effect in 1833. The New Poor Law, which consolidated 15,000 parishes into less than 600 Poor Law Unions and recommended institutional (“in-door”) relief in the form of workhouses, was enacted in 1834; see Webster, Caring for Health, 31, 41. Implementation varied by regions, with some parishes in London, for example, not incorporated into Poor Law Unions until well after midcentury. 21. “Westminster Medical Society,” Lancet 1 (1841–42): 598. 22. Ibid. 23. Durey, Return of the Plague, 105. See also Roy Porter, Greatest Benefit, 230, and Seale and Pattison, Medical Knowledge, 41, 33. 24. Sydenham classified diseases by analogy with current naturalistic approaches to plants: “It is necessary that all diseases be reduced to definite and certain species, and that, with the same care which we see exhibited by botanists in their phytologies; since it happens, at present [1676], that many diseases, although included in the same genus, mentioned with a common nomenclature, and resembling one another in several symptoms, are, notwithstanding, different in their natures, and require a different medical treatment”; Sydenham, Works, 1: 13. See also King, Medical Thinking, 112. Although Sydenham’s goal was to find a specific remedy for every specific disease, he was able to “reduce” only smallpox and ague (intermittent fever) to specific entities. The popular use of cinchona bark for the treatment of ague is attributable to him; see Porter, Greatest Benefit, 229–30. 25. “In the English-speaking world, the most influential attempt to set disease in a coherent framework lay in the teachings of William Cullen”; Porter, Greatest Benefit, 260. Cullen’s recommended therapeutics differed little from those advocated by humoral doctors—blisters to counter local irritations and venesection to reduce fever and an overly rapid pulse; see King, Medical Thinking, 197–98, 229–31. 26. Specific fevers were distinguished by variations in local inflammation and by which stage predominated: atony, an excessive relaxation of arterial walls that produced debility; irritation, caused by a buildup of acrimonious elements in the blood if the atony stage were


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not corrected; if irritation was unrelieved, arterial spasms set in, followed by heat and endstage fever. The three other classes of disease in Cullen’s nosology were neuroses (affections of sense and motion, without fever, caused by external stimuli); cachexia (wasting diseases such as consumption or the results of malnourishment); and local diseases (diseases that could not be classified in the other three classes, attributed to local conditions and not discussed in First Lines); see King, Medical World, 215–18; and Porter, Greatest Benefit, 261–62. 27. Cullen, First Lines, 1: 133–34, quoted in King, Medical World, 141. 28. Porter, Greatest Benefit, 261–62. 29. Porter, Greatest Benefit, 262; King, Medical Thinking, 232–33, and Medical World, 143–47; Risse, “Brownian system.” 30. Richardson, L, xxxiv. 31. Barnet, “1832 cholera epidemic in York,” 30. 32. S. Snow, JS-EMP, 37, 45. On Snow’s siblings, see Galbraith, JS-EY, 14–16. 33. Digby, British General Practice, 72, 74. 34. It was thirty-two miles from York to Pateley Bridge, a collection of houses along two roads meeting at a T-junction. A Black Swan coach to Harrogate departed York every Tuesday, Thursday, and Saturday at 7:00 in in the morning. Snow could have taken it as far as Knaresbrough, then walked fourteen miles to Pateley Bridge. Hargrove, York, 1: 410–11, 2: 674. 35. Joseph Warburton, Jr., was indentured from 1831 to 1836, took lecture courses in 1833 (probably in Leeds), served fifteen months at Leeds General Infirmary, and qualified for the LSA in December 1837; Galbraith, PB, 229, 233–34. On the multifarious activities of the rural general practitioner, see Loudon, GP, 54–99, 257–58. Snow’s comments about Warburton and life in Pateley Bridge were made to Richardson in the 1850s; L, iv. When Snow noted some years afterward that his work in Pateley Bridge had involved negotiating difficult terrain, often at night, he may have had the senior Warburton’s fate in mind: he died in 1841 after being thrown from his horse outside Pateley Bridge. 36. Richardson, L, iii. Richardson was also a temperance reformer, eventually president of the British Medical Temperance Association; Winskill, Temperance Movement, 1: v; 4: 241. On the first temperance society in Newcastle, see Galbraith, WH, 162. The Newcastle-upon-Tyne Total Abstinence Society was founded on 3 December 1835; Winskill, Temperance Movement, 1: 138. 37. Newton, Return to Nature, 105. Dietary autoexperiments in connection to temperance and teetotalism had been conducted since the seventeenth century; see Harrison, Drink and the Victorians, 111–12, although he does not discuss Lambe or Newton. 38. Snow, “Teetotal address,” (1836), 20. 39. Ibid. 40. Galbraith, BP, 231–32. 41. Harrison, Drink and the Victorians, 127–30. 42. Of the 261 teetotal leaders identified by Harrison, Yorkshire contributed thirty-five, just behind Lancashire (with forty); Ibid., 140. Other leaders beside Andrew abandoned the trade of a corn-dealer; Ibid., 147. 43. Winskill, Temperance Movement, 1: 89, 168. The abstinence pledge that Andrew used was “similar to the Preston one” (1: 164). Both distinguished teetotalers from the temperance advocates, who took a “great moderation” pledge such as the following: “We, the undersigned, believe that the prevailing practice of using intoxicating liquors is most injurious both to the temporal and spiritual interest of the people, by producing crime, poverty, and distress. We believe, also, that decisive means of reformation, including example as well as precept, are imperatively called for. We do, therefore, voluntarily agree that we will abstain from the use of ardent spirits ourselves, and will not give nor offer them to others, except as medicine. And if we use any other liquors, it shall at all times be with great moderation, and we will, to the

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utmost of our power, discountenance all the causes and practices of intemperance” (1: 87; pledge of the Preston Temperance Society, adopted 22 March 1832). It is possible that the abstinence pledge Snow signed in Yorkshire replaced a “great moderation” pledge that he had signed earlier in Newcastle. The origins of “teetotal” are unclear. Winskill attributes it to Richard (“Dickie”) Turner, who in a speech at a temperance meeting in Preston in September 1833 allegedly said, “I’ll have nowt to do wi’ this moderation, botheration pledge; I’ll be reet down and out and out tee-te-total for ever and ever” (1: 103). For a slightly different version of Turner’s assertion, see Harrison, Drink and the Victorians, 120. 44. Winskill, Temperance Movement, 1: 168. No copy of this paper is extant. Speeches on the physiological dangers of drink, especially on nutritional grounds, were common features of teetotal meetings; Harrison, Drink and the Victorians, 115–19, which includes an analysis of Joseph Livesey’s Malt Lecture, first delivered in Preston in 1833. 45. Winskill, Temperance Movement, 1: 168, 176–77. W. A. Pallister of Leeds was the same age as Snow; both were slightly younger than John Andrew, Jr. Pallister founded the Yorkshire Pioneer; Andrew eventually became secretary of the British Temperance League; Ibid., 1: v. 46. Galbraith, PB, 231; Winskill, Temperance Movement, 1: 165, 168. 47. William Snow eventually managed the City Temperance Hotel in York. 48. British Temperance Advocate (December 1886), 196–97, in Winskill, Temperance Movement, 1: 177–79. Winskill considered Snow “one of the pioneers of temperance in the Yorkshire districts” (Ibid., 2:174). In Harrison’s “occupational analysis of prominent teetotalers: 1833–1872,” there are nine doctors (sixth on the list); Drink and the Victorians, 144. He does not discuss Snow as a teetotaler, however. 49. Snow, “Teetotal address” (1836). After delivering the address, he read it to his brother Thomas, who said it converted him “to teetotalism from that day”; Winskill, Temperance Movement, 1: 179. In the 1880s Thomas Snow found a copy of the address “in some papers sent to him by his sisters from York,” and he published it in a temperance journal; British Temperance Advocate (1888): 182. 50. Snow, “Teetotal address” (1836), 182, 20. According to Cullen, the essence of this life force was nervous excitement, which produced sensation (irritation) in the body. A healthy state required a moderate amount of irritation, but normal organ functioning was disrupted by environmental stimuli that produced “spasms” in the nervous system. The exciting stimulus could be any external substance with an irritating “acrimony”: excessive heat or cold, trauma, or even the force of the circulating blood itself. Such nervous spasms could result in “increased action of the [blood] vessels,” reduced blood flow, spastic capillaries, and excessive fluid accumulation; Cullen, First Lines, 1: 276, cited by King, Medical Thinking, 231. See also King, Medical World, 139–43, and Porter, Greatest Benefit, 260. 51. Snow, “Teetotal address” (1836), 20. Thomas Snow believed his brother’s opposition to brandy treatment was connected to his temperance beliefs: “Having for two years been an earnest abstainer from alcoholics on hygienic grounds, and having no faith in the curative properties of brandy in cases of cholera, [Snow] objected to take it [to Killingworth], but was overruled. . . . On his return to Newcastle Mr. Hardcastle said: “Well, Snow, you’ve done exceedingly well.” And he promptly replied: “No thanks to the brandy, for the bottles were never uncorked” ”; cited in Winskill, Temperance Movement, 1: 176. By then temperance as an antidote to cholera was not limited to some medical men. For example, Directions to Plain People recommended that everyone during the epidemic “use wine in moderation, but drink no spirituous liquors, and indulge in no irregular and vicious habits, for these materially increase the virulence of cholera”; cited in Morris, Cholera 1832, 137. For additional discussion of teetotal opposition to alcohol as a medicinal restorative, see Harrison, Drink and the Victorians, 298–99. Such opposition could also be mounted on purely therapeutic grounds.


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52. On the conceptual basis for therapeutic skepticism, see Rosenberg, “Therapeutic revolution,” 14–21. Snow’s skepticism may antedate the cholera epidemic. According to a family story, Hardcastle had “complained he lost good patients because he [Snow] told them they had no illness”; Andrew L. Simpson, Snow Collection, VIII.3.iii. 53. Snow, “Teetotal address” (1836), 20. 54. Ibid. 55. On the concept of the healing power of nature and Sydenham, see Porter, Greatest Benefit, 58–59, 229–31. On the continuing influence of Sydenham into the 1840s, see Gavin Milroy, “On the writings of Sydenham,” Lancet 1 (1847): 60–65; 375–78, 400–03, and Lancet 2 (1847): 152–56, 673–77.

Chapter 3

London Medical and Surgical Training, 1836–1838

N AUGUST 1836 Snow left behind his family and his temperance activities in York to continue his medical training in London. He took a circuitous route, however, traveling first to Liverpool, perhaps to visit teetotal acquaintances. Thereafter, according to Richardson, he “trudg[ed] it afoot from Liverpool through the whole of North and South Wales, turned London-ward, calling at Bath on the way, on a visit to his uncle, Mr. Empson.” Like his uncle, who had hiked from New York to Montreal and back a few years earlier, Snow enjoyed walking. This tour from Liverpool to London covered almost 400 miles and probably took four or five weeks (Fig. 3.1).1 It is likely that Snow’s visit with Uncle Charles had a purpose beyond familial duty and personal friendship. Snow intended to be a full-time student, and it is improbable that he could have saved enough during his three years as an apothecary assistant to cover fees, books, and room and board for as much as two years of medical training. He probably received financial help from Uncle Charles and perhaps from his parents as well.2

I

Requirements for Certification Dual qualification necessitated that candidates complete the requirements of both the Royal College of Surgeons in London and the Worshipful Society of Apothe-

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57

Figure 3.1. Place-names, towns, and cities of significance to Snow.

caries. The Lancet, a London medical journal published every Saturday, listed current requirements in an issue each fall before the beginning of the academic year. There were two sessions for lectures—a winter session from 1 October to mid-April, with a two-week break around Christmas, and a session from 1 May to the end of July. Hospital attendance was available the entire year. The examiners in Apothecaries’ Hall specified the lectures they expected students to take in each session and when to begin and end medical practice. The Royal College of Surgeons, however, listed only the numbers of courses and length of surgical practice expected of students who wanted to take the qualifying examination. Some lecture courses and hospital rotations satisfied both college and hall (the monikers for these two medical corporations). Table 3.1 suggests how medical students might have planned their semes-

Table 3.1. Schedule of lecture courses and hospital attendance for dual qualification for students in London beginning in October 1835 1st Winter Session (Oct. ‘36–Apr ‘37)

1st Summer Session (May ‘37–July ‘37)

2nd Winter Session (Oct. ‘37–Apr ‘38)

2nd Summer Session (May ‘38–July ‘38)

3rd Winter Session (Oct. ‘38–Apr ‘39)

Chemistry

Botany

Anatomy and Physiology

Forensic Medicine

Dissections

Anatomy and Physiology

Electives

Anatomical Demonstrations

Midwifery and Diseases of Women and Children

Midwifery with attendance on cases

Anatomical Demonstrations

Dissections

Dissections

Midwifery (lectures)

Materia Medica and Therapeuticsa

Medicine (physic, lectures)

Surgery (lectures)

Medicine (physic)

Surgery (lectures) Hospital attendance

Hospital attendanceb (through September)

Hospital attendance c

Key: Italics—Required by Apothecaries Hall (AH) only. Bold—Required by College of Surgeons (CoS) only. Normal—Required by both college and hall. a

Pharmacology, including identification and compounding, preservation, and administration of mineral and vegetable drugs. The CoS required only a three month session. b CoS required twelve months of surgical attendance at an approved hospital in London, Dublin, Edinburgh, Glasgow, or Aberdeen; or six months in one such hospital plus twelve months in an approved provincial hospital (such as the Newcastle Infirmary). c

AH required a total of eighteen months of medical practice, which could overlap with surgical practice, at a recognized hospital or dispensary. Source: Lancet 1 (1836–37): 6–7.


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ters if they hoped to qualify in the shortest time: twenty-two months to become a Member of the Royal College of Surgeons (MRCS) in London, thirty-one months for a prospective Licentiate of the Society of Apothecaries (LSA).3 Snow took his surgical examination in May 1838 after eighteen months of training in London and the apothecary examination the following October. Therefore, both college and hall must have accepted some of his certificates of attendance from lecture courses at the uncertified medical school in Newcastle.4 In addition, the Royal College of Surgeons in London credited him with the full twelve months he had spent at the Newcastle Infirmary; to fulfill the remainder of its hospital requirement he needed only six months at a London hospital, but the examiners at Apothecaries’ Hall would only accept half of Snow’s clinical training at the Newcastle Infirmary. They insisted he spend a full year in hospital practice before qualifying.5

The London Medical Schools When Snow arrived in metropolitan London twenty-one schools of varying size and curricular range competed for students of medicine and surgery, who had to amass the required certificates of attendance at lectures, anatomical demonstrations, and dissecting (Fig. 3.2). Some of these schools were attached to hospitals where a student could also satisfy clinical requirements. Most were proprietary schools that offered a full complement of lecture courses, although a few advertised only a limited number of subjects. Two institutions of higher learning—King’s College and the new London University—had affiliated medical schools that offered all the required lecture courses, demonstrations, and dissecting opportunities. London proprietary schools of anatomy, medicine, and surgery traced their origins to the mid-eighteenth century and emerging doubts about the value of individual apprenticeships. It was more efficient for a few surgeons and apothecaries to offer formal instruction to a large assemblage of apprentices than for each master to teach his own. A number of committed and enterprising practitioners had renovated and extended buildings in the metropolis to provide amphitheaters for lectures, rooms for anatomical demonstrations and dissecting, surgical museums, and occasionally herb gardens and garrets for the study of botany and materia medica. When the London Corporation of Surgeons was reconstituted as the Royal College of Surgeons, the availability of institutional training was so extensive that the new medical corporation eliminated the apprenticeship as a requirement for membership. That meant a loss of income for hospital surgeons in the metropolis, but some soon offered lecture courses, students paid for tickets to attend, and hospital-based medical schools were in competition with the proprietary schools.6 There were advantages in attending an institution where lecture halls and wards were in close proximity, especially because after the first winter session theoretical and clinical instruction became more integrated.

Figure 3.2. Hospitals and medical schools of London, 1836–1837 (adapted from Lancet, 24 September 1836).


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When Snow reached London in 1836, medical education was still part of a bourgeoning market economy. Every school distributed a prospectus of the courses it intended to mount in the coming session, the names of the lecturers it had retained, the facilities it provided, and the perquisites that students received if they purchased “perpetual” tickets of admission, that is, took all courses at one school for a reduced fee compared to purchasing tickets for individual courses at several.7 Newspaper advertisements trumpeted the star quality of a school’s faculty and the success rate of its students in qualifying examinations. However, the editorial staff at the Lancet was generally unimpressed with what the schools actually delivered: The puffs and pretensions are innumerable, whereas the claims of the different teachers and establishments to distinction, where, indeed, any exist, are easily enumerated. The whole system . . . is the prolific source of extortion and fraud. . . . [It requires] from the students the outlay of such enormous sums of money in the purchase of “tickets” [of admission] and “certificates” [of having attended the expected number], under the colour of enforcing attendance on lectures not one-fourth of which, from their multiplicity, can ever be heard. . . .8 Nevertheless, if one hoped to practice general medicine in England and Wales, there was really no alternative to accumulating all the certificates expected by the examiners at college and hall. Snow, like hundreds of other incoming medical students in London in October 1836, had to decide where to take courses in the forthcoming session. Lectures during the first ten days were open to the public free of charge, with the expectation that students would shop for bargains (Table 3.2).9 Snow became a perpetual student at the Hunterian School of Medicine at 16 Great Windmill Street, near Haymarket in Westminster (an incorporated city in West London). The Hunterian, a continuation of the first school of anatomy in London, was renowned for having dedicated instructors. Among them in the fall of 1836 was John Epps—physician, phrenologist, medical radical, and temperance reformer.10 With so many schools to choose from, it is possible that Snow gravitated to a school that had at least one faculty member who shared his antispirit views, but the Hunterian also offered students excellent facilities, including an extensive pathological museum and a large dissecting room. The perpetual fee at the school was £34, which included access to the reading room and library, and it was the lowest priced among schools that offered a full complement of courses for dual qualification. Although not attached to a hospital, it was located near several of them.11 Snow found affordable lodgings near Soho Square, a short walk from the Hunterian School of Medicine. He rented a room at 11 Bateman’s Buildings, a terrace of row houses along an alley that connected Soho Square to Queen Street (now Bateman Street). Each house in this eighteenth-century speculative development had

Table 3.2. London medical schools, amenities, and “perpetual” fees as of October 1836 Private schools and colleges with a full complement of lecture courses and dissecting Aldersgate School of Medicine (library & medical society; £36 15s) Blenheim Street School of Medicine (£36 15s.) Hunterian School of Medicine (library, reading room, museum; £34) Mr. Grainger’s School, Webb Street (museum; medical society; practice privileges at Surrey Dispensary and the London Fever Hospital; £48 6s.) King’s College Medical School (£63) London University College Medical School (£70 10s.) St. George’s Hospital School of Anatomy and Medicine (£46 4s; including anatomy and demonstrations, £16 16s.) Westminster School of Medicine (£45) Source: Lancet 1 (1836–37): 7–15.

Private schools with limited offerings

Hospital-based schools with various offerings

Mr. Dermott’s Theatre of Anatomy (anatomy, including demonstrations and dissecting, physiology, surgery; £10 10s.)

Charing Cross Hospital Medical School (only medicine, midwifery, anatomy, and surgery; £19 19s.)

Dr. Robert’s Lecture Room (Theory and practice of medicine; £5 5s.)

Free Hospital Medical School (no chemistry or botany; no fees listed)

Mr. Smith’s Theatre of Anatomy (anatomy, including demonstrations and dissecting, physiology, surgery; £10 10s. Midwifery, including hospital practice; £5 5s.)

Guy’s Hospital Medical School (full complement; £69 6s.)

Dr. Waller’s Lectures on Midwifery (cases from the London Midwifery Institution; £5 5s.) St. George’s Hospital Theatre of Anatomy (anatomy, physiology, demonstrations, dissecting; £16 16s.)

London Hospital Medical School (full complement; £61 19s.) Middlesex Hospital Medical School (full complement; £45) St. Bartholomew’s Hospital Medical School (full complement; £66 4s., plus £1 10s. for use of library) St. George’s Hospital Medical School (£39 18s., no anatomy) St. Thomas’s Hospital Medical School (full complement; £55 13s.)


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three storeys above ground, as well as rooms in the cellar. Number 11 was one of the smaller houses, containing approximately 250 square feet of living space per floor,12 but it would have been sufficient as a place to read and sleep. Most of a first-year medical student’s time was spent at school, either in a lecture hall or in the dissecting room.

Snow the Medical Student Whether to enhance his qualifications or to establish close relationships with senior London doctors, Snow decided to repeat several courses he had already taken in Newcastle. During the winter session of 1836–1837 at the Hunterian School of Medicine, he attended Mr. P. Bennett-Lucas’s lecture course on anatomy and physiology, the associated anatomical demonstrations, plus dissecting on his own; chemistry with Dr. Hunter Lane; and the principles and practice of medicine, still termed physic by the Royal College of Surgeons, with Dr. Michael Ryan, an Irish physician with particular interests in obstetrics and a medical radical.13 Snow decided to attend Dr. Jewell’s lectures on midwifery and diseases of women and children at the Hunterian Theatre of Anatomy, perhaps because the course fee included attendance on cases at the Royal Lying-in Hospital on Queen Street, near both the Hunterian School and Theatre. This facility was listed as a Hospital for Clinical Midwifery in the Hunterian Theatre’s schedule of courses, indicating that students who walked its wards with Dr. Jewell would be taught obstetrics, an emerging specialty within general practice also pursued by Hardcastle and, a few years hence, by Snow himself14 (Table 3.3). Apothecaries’ Hall expected students to take botany and electives during their first three-month summer session in London. John Epps lectured in botany at the Hunterian School of Medicine, and Snow completed that course with him, probably during the 1837 summer session. When he was not in the lecture hall or the physic garden, he was probably dissecting in the “dead room.” In all, Snow would take four courses from Epps—two in materia medica, one in forensic medicine, as well as botany.15 During his first year in London, Snow developed a close friendship with a classmate, Joshua Parsons. “It happened,” recalled Parsons, “that we usually overstayed our fellows [in the dissecting room], and often worked far on into the evening. The acquaintance thus grew into intimacy, which ended by our lodging and reading together.”16 Each day was built around the lecture courses. The instructors arrived at the appointed hour, expounded information and opinion (sometimes reading verbatim material previously published in a medical journal), and then rushed off to resume private practice or do their hospital rounds, but outside the prescribed lectures medical education was largely self-directed. It was left to the students to supplement lecture notes with textbooks, to observe symptoms on the wards, to note the appearance of diseases in the glass jars on display in the anatomical museum, to

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Table 3.3. Snow’s likely schedule of lecture courses during the winter session of 1836–1837 Monday 9:00

Tuesday

|←

Wednesday

Thursday

Friday

Saturday

→|

Chemistry

10:00 |←

Practical anatomy and demonstrations

→|

3:00

|←

Anatomy and physiology

→|

4:00

|←

11:00 Noon 1:00 2:00

→|

Principles and practice of medicine (physic)

5:00 6:00 7:00

Surgery a

Midwifery b

Surgery

Midwifery

Surgery

Midwifery

a

We assume he attended these lectures; surgery was not a required course for apothecary candidates and therefore not listed by Snow’s examiner.

b

Taken at the Hunterian Theatre of Anatomy, not the Hunterian School of Medicine. Source: Lancet 1 (1836–37): 12; Society of Apothecaries, “Court of examiners entrance books,” MS 8241/10, 61 (“John Snow”).

correlate structures they could dissect with the demonstrator’s cadaver (or, if available, a wax model), to conduct experiments in the chemistry laboratory, and to study medicinal plants in the physic garden.17 The goal was to amass sufficient information to pass one comprehensive certifying examination at the very end of formal training. Snow left no diary of his experiences as a medical student, but those who did may be instructive. For example, James Paget entered the medical school attached to St. Bartholomew’s Hospital two years before Snow began at the Hunterian. “For the great majority of students, and for myself at first,” wrote Paget in his memoirs, “work at that time had to be self-determined and nearly all self-guided: it was very little helped by either the teachers or the means of study.” For most students “there was very little, or no, personal guidance; the demonstrators had some private pupils, whom they ‘ground’ for the College [of Surgeons] examinations, but these were only a small portion of the school.” The situation was somewhat better, he thought, at the nearby “Aldersgate Street school, where were . . . some active demonstrators, and where more ‘grinding’ was done.”18 It appears that Snow and Parsons had neither the need nor the resources to hire a grinder. Both were older and more experienced than the typical medical student: Snow was twenty-three with almost nine years of


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medical experience, while Parsons, although a year younger, had served a five-year apprenticeship and had already completed twelve months at the North London Hospital. The two friends probably drilled each other until Parsons became dually qualified in October and left London to set up a general practice in Somerset.19 Snow, on the other hand, had to take another series of lectures and fulfill the requirements for hospital attendance. During the winter session of 1837–1838 he took second courses in materia medica, chemistry, and midwifery with the same instructors as the year before, but in the new academic year Dr. Robert Venables offered physic, Mr. G. Jones delivered the lectures in anatomy and physiology, and Mr. Savage gave the anatomical demonstrations (Table 3.4).20 In addition, Snow attended medical and surgical practices at the Westminster Hospital. It lay relatively far from his lodgings, nearly a mile to the south, beyond St. James Park on Broad Sanctuary by Westminster Abbey and the Houses of Parliament. Although a mile meant little to an enthusiastic walker like Snow, it seems odd that he avoided University College Hospital on Gower Street, St. Pancras, only a third of a mile from his lodgings. University College Hospital offered case-study clinical instruction by, among others, the respected surgeons Astley Cooper and Robert Liston. Parsons had attended this institution when it was called the North London Hospital; perhaps he was dissatisfied with his training there and had urged his roommate to go elsewhere, or Snow may have been dissuaded by a change in the University College fee schedule that penalized students who attended practices at the hospital but were not enrolled for lectures.21 For the next twelve months Snow was expected to be at the Westminster Hospital shortly after noon six days a week. Most of the time, apparently, he shadowed the

Table 3.4. Snow’s likely schedule of lecture courses during the winter session of 1837–1838 Monday 9:00 10:00 11:00 Noon 1:00 2:00 3:00 4:00 5:00 6:00 7:00

Tuesday

Wednesday

Thursday

Friday

|← |← |←

Materia medica and therapeutics Practical anatomy and demonstrations Chemistry

→| →| →|

|← |←

Anatomy and physiology Principles and practice of medicine (physic)

→| →|

Midwifery

Midwifery

Saturday

Midwifery

Source: Lancet 1 (1837–38): 14–15; Society of Apothecaries, “Court of examiners entrance books,” MS 8241/10, 61 (“John Snow”).

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resident medical officers. One physician staffed the out-patient clinic each day. For example, Dr. John Bright came on Tuesdays and Fridays; Drs. George Roe and John Burne covered the other weekdays.22 In clinics physicians diagnosed and prescribed for patients, most of whom were accident victims, members of the laboring classes who paid subscriptions to friendly societies and provident funds to cover hospital care. After seeing the resident physician the patients waited at the dispensary for the hospital apothecary to compound and distribute medicines. If their complaints were unrelieved, patients could return the following day and repeat the procedure with a different physician. Only nonchronic cases were considered for admission to the hospital. Many of those cases required the attention of the house surgeons, of which there were four when Snow “walked the wards” at the Westminster: Sir Anthony Carlisle, Anthony White, George Gurthrie, and B. Lyon.23 These physicians and surgeons were proponents of what came to be called hospital medicine. This approach sought to develop the same habits of mind characteristic of accomplished practitioners at the bedside, but to do so in metropolitan clinical settings where students had two advantages not available to most apprentices. First, one could observe many more patients and a broader array of diseases in urban hospitals than in individual practices. Second, hospitals with morgues in which demonstrators could teach dissecting (or even a simple “dead room” in which students were left to their own, often notorious, devices) offered the opportunity to compare one’s clinical observations and diagnoses with anatomical structures and pathological lesions post mortem. Hospital medicine was touted as the preferred venue for the clinical–pathological method. Next to anatomy, the Lancet considered “Clinical Medicine—the study of disease, by the bedside of the patient, in the wards of an hospital, and of manual surgery, in the operation theatres of those institutions—” the most important subject for the aspiring surgeon.24 Snow may already have been introduced to this relatively recent medical perspective while attending practices at the Newcastle Infirmary, but he most assuredly experienced it at the Westminster Hospital. The Lancet was typical of advanced British medical thinking in its advocacy of hospital medicine, although not everyone agreed that experiential empiricism was its proper foundation. According to this journal, “medicine is, above all other sciences, a science of observation,—to be successfully studied only by careful and longcontinued watching of the symptoms of disorder, the phenomena of health, and the results of employing remedial agents for the cure of disease.”25 Methodical observation was often difficult to carry out in the out-patient clinic because there was such a high turnover of patients. Students could follow the medical staff on the wards for “fever patients” who could not be treated in their own homes, but such admissions depended on seasonal fluctuations in infectious diseases. The surgical wards, however, offered numerous learning opportunities during the academic sessions when house surgeons could be assured that the operating theaters were filled with gawking medical students and a few senior students were available (often paying a hefty


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fee for the privilege) to assist as dressers and clinical clerks. However, for the majority of students, attending a hospital practice was their best chance to observe a greater variety of diseases than they could possibly have confronted as an apprentice to a solo practitioner. The Lancet recommended a system for making the most of this opportunity: “The moment . . . a student enters an hospital he should commence making an accurate record of a certain number of cases in the wards. . . . He should . . . make a selection of the most common diseases, or accidents, and this limitation of his labour will enable him to follow a certain number of cases to their termination. . . ,” whether to cure or death of the patient. One advantage of attending hospital practices was that in the event a “case terminate[d] unfavourably, the post-mortem appearances of the subject” should be examined in the dead room.26 The object was to develop a personal collection of case notes that could be consulted for years thereafter. Snow’s extant casebooks and his remarkable facility at recalling specific cases during medical society meetings indicate that he mastered this objective, probably a result of a combination of his own initiative, Hardcastle’s tutelage, and training in London.27 Whether a particular student’s experience corresponded to the ideal posed by the Lancet depended largely on the views of the hospital staff where one received practical training unless, like Snow, the student had learned to keep case notes at the bedside during an apprenticeship. Again, James Paget’s recollections of his student years at Bart’s are instructive, whether or not they are representative. “In the second winter” session of 1835–1836, he wrote in his memoirs, “I gave myself to Hospital practice more than in the first. . . . In the first year, I had not neglected Hospital practice; but I had done little more than go round the surgical wards, . . . seeing what was rare, talking about cases, sometimes hearing a very few words of teaching. Besides, I had often sat . . . in the outpatients’ room.” Like Snow at the Westminster Hospital, Paget was not a surgeon’s assistant responsible for dressing wounds, “partly because the dresserships were expensive (10 guineas at least), partly because they seemed to offer scarcely more opportunities of studying surgery than I had had in my apprenticeship.”28 He found the instruction in the medical wards more congenial and spent most of his time there, serving several months as a clinical clerk for one of the house physicians. He thought the “teaching was admirable . . . and their expectation of what might be learned by continued research” set a standard for the remainder of his career.29 One physician stood out because “he would make those who went round with him examine for themselves, and would tell and show them how to learn, and have his case-books well kept. . . . This precision, and the early hours, were too much for the great majority of students,” but the baker’s dozen who attended the morning rounds “imitate[d] him in his mode of study. . . .”30 According to Paget, “I worked steadily all through the winter, still dissecting as much as I could, and helping in the post-mortem examinations whenever I had a chance.”31 That is, he took full advantage of the learning opportunities the new hospital medicine had to offer, even at an institution he considered in decline compared to the

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teaching available at University College Hospital—and, perhaps, at another relative newcomer in medical education, the Westminster Hospital. Several events punctuated the weekly routines during Snow’s twelve-month rotation at the Westminster Hospital. At the end of April 1838, he completed the six months on the wards of a London hospital required by the Royal College of Surgeons. He took the qualifying examination on 2 May. It is likely that his experience was similar to Paget’s two years earlier: The examination was very simple. The ten examiners sat at the outer side of a long curved table. Each in turn, I think, took a candidate; and, when he had finished, others could ask questions. My examiner-in-chief was Mr. Anthony White, of the Westminster Hospital [one of Snow’s teachers]: his questions were not difficult, and I believed that I brought them to a close by giving an account of the otic ganglion and its nerve-communications, in reply to some enquiry about branches of the fifth nerve. That ganglion was then known to few; and he who knew about it seemed to be thought sure to know all common things. After Mr. White, Sir Astley Cooper asked me some questions, and seemed satisfied. . . ; and then I was courteously dismissed.32 Groups of candidates—those who had completed all required lecture courses and months of hospital attendance—entered a room at the Royal College of Surgeons in Lincoln’s Inn Fields and were examined orally, one after the other. The examiners were particularly interested in the candidates’ knowledge of anatomy. Snow must have satisfactorily answered whatever questions they put to him. Subsequently, the London Medical Gazette published a notification: “College of Surgeons. List of Gentlemen who have received diplomas. May 1838.” Of 114 successful candidates, “J. Snow, York” ranked seventh. He had become a Member of the Royal College of Surgeons in London.33 Shortly before Snow earned his first medical title, the apothecary at the Westminster Hospital had resigned his post, and Snow began the process of submitting a full application, including eight references, as his replacement. The work of a hospital apothecary was wide-ranging, and, according to the Lancet, the Westminster’s had been extraordinarily effective: “(owing to the exertions of the apothecary and the matron) the diets are as wholesome and plentiful, the clothing is of as good a quality, and is as clean, and, in short, the whole working machinery is as efficient, as in any hospital in London.”34 Snow was aware that the hospital charter would engage only a Licentiate of the Society of Apothecaries, but he assumed that the examiners would permit him, as they occasionally had allowed others, to take the qualifying examination several months early, but they refused his request to be examined at the end of the summer session in July. When he appealed, they reminded him that his practice obligation would not be met until the end of September and again refused to grant him an exception. He was forced to withdraw his application.35 At the


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time it was a setback. Instead of building a practice from a base at a major teaching hospital with an annual salary to tide him over, Snow would have to scratch out a living in an open market glutted with general practitioners. One might wonder whether he did not later come to consider the legalistic intransigence of Apothecaries’ Hall a bit of good fortune, for in the same editorial in which the Lancet applauded the Westminster Hospital for the conditions it had established for ward patients, it castigated the house committee for its “mal-treatment of the apothecary by the imposition on him of unprofessional duties, in addition to those of his own department . . .” such as filling out forms, which was the proper job of a secretary. “What wonder, then, is it that no man of competent ability can be found long to fill this degraded medical office?”36 Over the years taking the apothecary post at the Westminster Hospital would have resulted in a considerable loss of time and energy for activities that Snow valued more than financial security—research and medical society meetings.

Snow the Public Health Investigator In November 1836, during Snow’s second month at the Hunterian School, Dr. Lane lectured on arsenic and its chemical properties. Snow took a special interest in the subject, so he lingered a bit after the lecture. Dr. Lane called his attention to an article in a foreign medical journal that described a new method of preparing cadavers for dissecting: injecting a saturated solution of arsenite of potash (potassium carbonate) into the blood vessels to eliminate most of the dried blood, followed by red ink into the arteries to highlight them. At Lane’s suggestion Snow replicated this procedure in the cadaver he was dissecting and later in several others at the request of some classmates. However, Snow had inadvertently introduced a public health problem at the medical school. While dissecting one of the prepared cadavers, a student became ill with severe abdominal cramps, vomiting, and diarrhea. Snow does not appear to have considered arsenic poisoning the cause until “the summer of 1837, [when] I injected another body, and dissected it, with five of my fellow students, during the very hot weather of, I think, August. Decomposition was retarded considerably [by the arsenic solution], but there was only one of us who did not suffer more or less indisposition, principally bowel complaints: and the subject gave out a peculiar odour, which I suspected arose from the arsenic rising in combination with the volatile products of decomposition.”37 He did not have time to test his suspicion until the Christmas recess, when he cut out a few portions of the cadaver for examination. He found no evidence of arsenic in the tissue, which supported his notion that the solution had turned gaseous and disappeared from the tissue. Again his studies took precedence, and it was not until “some time afterwards” that he devised “an experimentum crucis” to determine if the indispositions he and his fellows had experienced

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was due to inhaling arsenic vapors or individual constitutional factors (since not everyone was identically affected). The phrase that Snow employed in his first known publication, a letter to the editor of the Lancet, was defined in a popular contemporary text, A Preliminary Discourse on the Study of Natural Philosophy: “If more than one cause should appear, we must then endeavour to find, or, if we cannot find, to produce, new facts. . . . Here we find the use of what Bacon terms ‘crucial instances,’ which are phenomena brought forward to decide between two causes, each having the same analogies in its favour. And here, too, we perceive the utility of experiment as distinguished from mere passive observation.”38 Snow’s notion of a crucial experiment in this instance involved placing “some animal substances, in a state of decomposition, on a dish, along with solution of arsenite of potash, and also powdered arsenious acid. . . .” He covered the dish with “a bell-glass receiver to collect the gases given off, and, at the end of two or three weeks, . . . added the air contained in the glass to a sufficient quantity of pure hydrogen to make an inflammable mixture, and burnt this as it proceeded from a small jet. . . .” The result was “a small quantity of metallic arsenic”—in short, the arsenic was in the vapor. He informed the school authorities, who accepted his recommendation to discontinue the “mode of injection” he had introduced at the Hunterian.39 Snow’s investigations of poisonous cadavers coincided with his participation in a study of poisonous candles undertaken by the Westminster Medical Society. The society was founded in 1809 by Mansfield Clarke and Benjamin Brodie, the latter a lecturer in surgery at the Hunterian School of Medicine in Great Windmill Street, which is why meetings were initially held in the school’s museum. “For some years the Society seemed almost to be an appendage of the school, every student who attended the lectures becoming also a member. . . .”40 However, the rules were changed the year before Snow reached London to include a formal proposal and approval process. Weekly meetings were held every Saturday evening from October through April, with a pause for the summer months. Snow did not attend a meeting until 8 April 1837, when he was a guest of Dr. John Epps, who was scheduled to comment on the therapeutic administration of strychnine, bismuth, and arsenic.41 When the 1837–1838 session of meetings resumed in October, Snow was proposed as an ordinary member and approved.42 The society had taken a distinctly radical turn a few years earlier, when five months of debate about medical reform “culminat[ed] in motions calling for the merger of the three estates into one democratic faculty. These motions were passed by massive majorities, despite stonewalling tactics by the diehards.”43 Eventually, members who sought a compromise prevailed, although at the expense of defections by extremists at both ends of the political spectrum. The Westminster Medical Society had a reputation for debating matters relating to public health such as the cholera epidemic of 1832, and the members decided to investigate “arsenical candles” during Snow’s first year as a member.44 On 28 October 1837 Dr. James Scott reminded the membership of potential risks from inhaling


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the fumes of stearin candles infused with white arsenic, which were considerably cheaper and burned brighter than candles manufactured from pure wax or spermaceti. Earlier in the year a Mr. Everitt had demonstrated at a meeting of the MedicoBotanical Society in London that such candles produced vapors containing arsenic; he had boiled candles in water and reduced the precipitate with sulfurized hydrogen gas to several grains of arsenic per candle. Whereas some medical men did not believe a moderate amount of arsenic was harmful, Dr. Scott had recently received reliable information that at least two manufacturers had dramatically increased the proportion of arsenic to stearin in response to public demand. “Now, as these candles were not only much in use in private families, but had lately been introduced into some of the churches, and were likely to find their way into the theatres,” Dr. Scott “thought it would come within the province of the objects of the Society, to state its opinion respecting the safety of such a quantity of a poisonous mineral burnt, and its vapour inhaled.”45 In the ensuing week Mr. Richard Phillips and “Mr. Snow had succeeded in detecting arsenious acid in these lights,” thereby confirming Everitt’s findings. Everitt, in attendance as a guest at the meeting on 4 November, offered to give a public demonstration for the society later in the month. A committee was formed “to communicate with Mr. Everitt and Mr. Phillips,” who had agreed “to carry on the investigation.”46 Poisonous candles reappeared episodically on the society’s agenda in the ensuing weeks, but a select committee carried out investigations behind the scenes throughout. As promised, Mr. Everitt repeated several chemical analyses on arsenic–stearin candles before the membership in mid-November. Mr. Golding Bird, a recent graduate of Guy’s Hospital Medical School, extended the chemical investigation by burning candles in conditions with varying amounts of oxygen present; he detected various arsenic compounds under all conditions.47 The second set of experiments were physiological in nature. “A lofty and spacious apartment of Dr. Scott’s house in the Strand” was converted into a laboratory in which members of the select committee constructed four boxes with ventilation holes and glass fronts for viewing the responses of linnets, green finches, guinea pigs, and rabbits. They burned arsenic–stearin candles in two boxes and spermaceti candles in the other two over a seventy-two-hour period (in six twelve-hour blocks). Hourly observations were recorded in a register. Although the guinea pigs and rabbits were unaffected, most of the birds in boxes exposed to the vapors of arsenic candles died, whereas those “in the boxes with pure lights were as gay at the end of the experiments as before they commenced.” The select committee detailed these investigations at a meeting on 9 December and concluded “that the vapour given off . . . during combustion is likely to be prejudicial. In closing their Report, the Committee express their wish to be of service to the public in a matter of so much importance, in the absence of all medical police in this kingdom, the only country in Europe where the public health is so little regarded by the governing powers.” Before the society could vote on whether to accept the committee’s report, however, the bylaws required it to

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be printed, distributed to the full membership, and, if approved, made available to the public. After considerable discussion the society deferred a decision on whether to pay the printing costs and refund the expenses incurred in conducting the investigations.48 During the week of 10–16 December 1837, three members of the society undertook additional but ex-officio investigations. Mr. Golding Bird made post-mortem examinations of five birds exposed to arsenic vapors by the select committee. He detected minute amounts of arsenic in the body of one bird but nothing on any feathers. The drinking water was heavily contaminated, and “he thought it probable they had been poisoned in this manner,” perhaps because the deleterious effects of ingested arsenic was common knowledge. After he reported his findings at the 16 December meeting, Joshua Toynbee and Snow reported that they had “conducted a series of experiments on these candles, to ascertain the effects of their combustion on animal life.” First, they had experimented on guinea pigs, but Snow and Toynbee’s animals, like their counterparts in Dr. Scott’s experiments, presented no symptoms of illness, regardless of the length of exposure or the level of arsenic in the candles. Similar experiments on some birds, however, were inconclusive because the apparatus ignited during the investigation. The report of the meeting does not mention any discussion of the select committee’s report.49 Then the medical media became involved. The Lancet’s leading editorial on 23 December reminded its readers of the coverage it had already given to the Westminster Medical Society’s investigation of “Arsenical Candles.” The editorial gave additional information on the subject, including a history of their discovery by a French chemist in the 1820s, but thanks to “the vigilance of the French Government,” the candles were tested, found to be deleterious to health, and their manufacture banned in that country. “‘Cheap wax lights,’“ as they came to be called, made a commercial jump over the channel, and their investors made a hefty profit “at the expense of the wellbeing of the English community,” claimed the Lancet.50 The editorial then summarized the “variety of experiments” conducted by the select committee from the Westminster society and used the results to condemn the secretary of state for the Home Department of England for permitting the sale of candles that expose “the animal economy . . . to the action of five times a greater quantity of arsenic than any prudent physician would venture to administer internally. . . .”51 Whereas the Lancet referred to summations of society meetings by one of its reporters, the London Medical Gazette printed actual extracts from the committee’s report, accompanied by an editorial early in January 1838. At a special meeting early in February, a majority of the Westminster Medical Society soundly condemned this caper by a disgruntled member and decided to spend no more time or money on the topic. The society had not repudiated its own committee’s findings, it had acted on procedural grounds because premature publication of significant passages from the report interrupted the deliberative process called for in its bylaws. 52


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A New Scientific–Medical Perspective While the poison candle caper prevented the Westminster Medical Society from taking an unambiguous position on a public health matter, Snow’s involvement in the investigative process is suggestive of the training he was receiving in London. In his first year as a member of the Westminster Medical Society, he aligned himself with those who considered medicine a science rather than just an art practiced at the bedside. Like his concurrent investigation of arsenic vapors in the cadavers prepared at the Hunterian School of Medicine, his chemical analyses and physiological experiments conducted for the society were pragmatic investigations designed to address potential health hazards, not pure science. The only remarkable aspect of Snow’s investigative method in both instances was its typicality for his cohort. He considered chemistry one of the collateral sciences of medicine, a common view in the 1830s. For example, the subtitle of the London Medical Gazette at the time was “A Weekly Journal of Medicine and the Collateral Sciences.” He was part of a cadre of young medical practitioners whose training included an emerging laboratory complement to clinicopathological dimensions of hospital medicine.53 The arsenic candles investigations show Snow as a collateral scientist in keeping with the new scientific approaches to medicine that were part and parcel of his training. His approach to these investigations also reveals a model that would recur in his anesthesia and cholera research. At an early stage in his career he demonstrated an ability to set up a series of experiments that traced an agent as it circulated in a medical school dissection room, in rooms where arsenic candles were burned, and in the bodies of everyone who entered them. That is, he was already concerned with chemical analysis, employing animal experimentation, and asking questions about what he would later term modes of communication—the pathways by which a specific poison was introduced into a community and where and how it lodged in the body. Must arsenic be ingested to be poisonous (the common assumption at the time), or could it also be poisonous if inhaled (an unusual assumption)? A decade later he would articulate the principles of how ether and chloroform circulate in the body and cause their specific effects; shortly thereafter he would hypothesize how cholera could circulate through the water supplies of a neighborhood, a town, and a metropolis. This facility in imagining systems circulation and transmission in terms of patterns and pathways was the unifying conceptual orientation in Snow’s work. The hospital medicine to which Snow was exposed was an English variant of developments in western Europe associated with the Enlightenment. In mideighteenth-century London several surgeons believed that students should base their knowledge of medicine on anatomy rather than observations accumulated at the bedside as apprentices learning a craft. William Hunter established a private anatomy school in Covent Garden in 1746. His brother, John Hunter, joined him two years later, and the school prospered for more than a decade. In 1766 William Hunter

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on his own purchased and renovated a house at 16 Great Windmill Street as a combined residence and school, the forerunner of the Hunterian School of Medicine. Although its successful run was nearly over when Snow arrived, anatomy schools such as the Hunterian that emphasized morbid anatomy had set the stage for the incorporation by English hospital-based medical schools of the more expansive curriculum pioneered in France.54 In Paris between 1790 and 1830, a group of medical reformers, the Idéologues, augmented the provision of care and surgery in Parisian hospitals by the introduction of teaching and research. They believed that conventional Hippocratic–Galenic notions of humoral imbalance needed to be replaced by a scientific form of medicine within an Enlightenment worldview: modeled on the natural sciences, founded on the principles of Lockean empiricism, and pragmatic in the sense of understanding the “human economy”—how individual and social systems functioned.55 Their covering law, the medical equivalent to Newton’s theory of gravity, was that specific diseases were connected to particular organs or tissues in the body. They believed enlightened medical thinking should correlate empirical observation of individual patients at the bedside, statistical manipulation of multiple observations in clinical settings, and pathological findings from postmortem dissecting. Supporters of the Idéologue orientation gained control of several hospitals in Paris, where they reconfigured medical education to include training in sciences collateral to their vision of enlightened medicine, especially anatomy, physiology, mathematics, and chemistry.56 A leading figure was Pierre Louis (1787–1872), who devised the “numerical method,” involving statistical analysis of many cases in the Paris clinics to show that venesection was only minimally effective in the treatment of pneumonia.57 Statisticians like Louis were among the adherents of the new scientific–medical perspective in England during the middle third of the nineteenth century, but the general tendency was to think of hospital medicine as a branch of natural philosophy. Natural philosophy was the inquiry into the principles and laws underlying phenomena in nature, and in 1830 John Herschel had published a primer for actualizing it that was still popular reading during Snow’s training period.58 According to Herschel, natural philosophers should limit their searches to verifiable proximal causes; they should seek to trace, in whatever discipline they investigated, “the operation of general causes, and the exemplification of general laws. . . . Every object which falls in his way elucidates some principle, affords some instruction, and . . . [gives] a sense of harmony and order.”59 Experience acquired by observation and experiment (what Bacon termed active observation) was the foundation of natural philosophy. Herschel’s “perfect observer” was acquainted “not only with the particular science to which his observations relate, but with every branch of knowledge which may enable him to appreciate and neutralize the effect of extraneous disturbing causes.” We should observe until we are in a position to deduce general conclusions that encompass more than our experience, then test the validity our deductions by experimentation and further observation. That is, “the


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successful process of scientific enquiry demands continually the alternate use of both the inductive and deductive method”—or, in our term, hypothetico-deductive reasoning.60 The view that corollary sciences and analogical reasoning were central to the study of medicine lay at the core of natural philosophy. According to Herschel, “there is scarcely any natural phenomenon which can be fully and completely explained in all its circumstances, without a union of several, perhaps of all, the sciences. . . . Hence, it is hardly possible to arrive at the knowledge of a law of any degree of generality in any branch of science, but it immediately furnishes us with a means of extending our knowledge of innumerable others. . . .”61 For example, Herschel’s justification for analogical reasoning and horizontal moves among collateral sciences parallels Snow’s decision to use chemistry when investigating two medical problems associated with potential arsenic poisoning. Only in his mid-twenties, Snow was already the “perfect observer” and keen experimenter that Herschel considered central to scientific progress.

* * * Snow qualified as an apothecary in October 1838.62 He had already decided to remain in London, having moved the month before to lodgings in Frith Street, only a few blocks from Bateman’s Buildings. Here, in the heart of Soho, he set up a surgery in his apartment and hoped to establish himself as a general practitioner and accoucheur. Starting his own practice in central London “seems crazy.”63 There was a surfeit of surgeon–apothecaries in the metropolis as a whole, a half-dozen within a few blocks of where Snow hung his shingle. None of the conventional routes must have been available or seemed sufficiently attractive. Most medical students from the provinces returned to their home districts after qualifying, often relying on medical relatives to help them become established or joining an existing practice as a junior partner.64 Snow had burned his bridges to Yorkshire and Northumberland several years before. He does not appear to have had substantial medical connections in York, a city also suffused with medical men. If he had chosen not to continue as Hardcastle’s assistant (or never been asked) in 1833, there seems little reason to think he would return five years later to the city where his former master still maintained an active practice. In addition, Warburton’s oldest son was already a partner and due to inherit his father’s practice, which ruled out any temptation Snow may have had to renew his temperance activities from a base in Pateley Bridge. Opening a practice in London had certain advantages that must have outweighed the risks. The Westminster Medical Society offered a scientific community and the kind of comradeship that might equal the friendships he had made in the Yorkshire temperance movement. He lacked the connections, the affluence, and the patronage usually required to secure a hospital appointment in the metropolis, but he could hope to become a lecturer in one of the medical schools. What is more, London now

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had a university that would grant a doctor of medicine to someone who had not attended Oxford or Cambridge, which meant that Snow could aspire to become a physician and, perhaps, shatter the glass ceiling of social advancement that kept medical men of his background from attending patients in the upper classes.

Notes 1. Richardson, L, v. Galbraith suggested the motive for the stopover in Liverpool; personal communication, 4 October 2000. For the probable daily pace of a long-distance walker in the 1830s, see Galbraith, JS-EY, 49. 2. He may have spent as much as £170 on his London training, of which it seems unlikely that he could have saved more than half as an assistant apothecary from 1833 to 1836; S. Snow, JS-EMP, 147–48. By 1836 William Snow was an established farmer, perhaps with an annual income around £120; Ibid., 46. 3. “Regulations of Apothecaries’ Hall and College of Surgeons,” Lancet 1 (1836–37): 6–7. Apothecaries’ Hall required a five-year apprenticeship in addition to lectures and hospital rounds and set the minimum age for qualification at twenty-one. The Royal College of Surgeons expected at least five years devoted to acquiring professional knowledge, which could include a short apprenticeship; candidates for qualification had to be at least twenty-two years of age. 4. In chemistry, medicine, materia medica, therapeutics, surgery, anatomy, and physiology; G. G. Turner and Arnison, Newcastle upon Tyne School, 17–20. See also Richardson, L, vii–viii. 5. Society of Apothecaries, “Court of examiners entrance books,” MS 8241/10, 61 (“John Snow”). 6. Bailey, “The medical institutions of London,” British Medical Journal 1 (1895): 1289; Clark-Kennedy, “London Hospitals,” 111–12; Peterson, Medical Profession, 15, 71. 7. It was not until the 1850s that “private education in the anatomy schools was co-opted or destroyed by the hospital medical schools”; Peterson, Medical Profession, 64–65, 72. See also Desmond, Politics of Evolution, 12–13. 8. “Advertisement,” Lancet 1 (1836–37): 5. See also Peterson, Medical Profession, 66. For the editorial policy of the Lancet and the medical radicalism of its founding editor, Thomas Wakley, see Desmond, Politics of Evolution, 14–15, and passim. 9. Peterson termed it a “supermarket approach to medical education” (66). 10. John Epps, MD, was from Edinburgh and in 1826 a member of the Phrenological Society there. He was editor for the London Medical and Surgical Journal, author of a book on homeopathy and dropsy, and contributor to the Lancet and M-CR; Medical Directory, 1845. See also Desmond, Politics of Evolution, 166, 421. 11. Richardson, L, v–vi. See also Snow, “Arsenic as a preservative of dead bodies” (1838), 264, where he mentioned taking chemistry and performing dissections “at the school in Great Windmill-street.” Mr. Smith, who examined Snow for the LSA, noted the number of lecture courses completed between October 1836 and October 1838 and the names of the instructors; Society of Apothecaries, “Court of Examiners entrance books,” MS 8241/10, 61 (“John Snow”). All but one of the instructors were on the faculty of the Hunterian School of Medicine; “Hunterian School of Medicine,” Lancet 1 (1836–37): 12. In the previously cited letter to the Lancet, Snow described dissecting in August 1837—between sessions, when only perpetual students had access to the school’s facilities. See also Cope,“Private medical schools,” 91–92, and Peterson, Medical Profession, 72.


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12. Monmouth House and various ancillary buildings occupied an entire city block south of Soho Square until demolished in 1773. Two large houses facing the square were subsequently erected and leased by Lord Bateman, along with a collection of houses created for the artisans involved in the construction. Part of their pay included grants of subleases to the houses in which they lived, which came to be called Bateman’s Buildings; see Sheppard, Parish of St. Anne Soho, 113–14. Stephanie Snow estimates rent for a room was 13–18 shillings per week; JS-EMP, 147–48. In 1841 (three years after Snow moved out) a census enumerator listed 17 persons at 11 Bateman’s Buildings, among the most crowded of the sixteen houses in the terrace; UK, Home Office, 1841 Census, H.O. 107/730/2A, 1–8. 13. P. Bennet Lucas became a member of the Royal College of Surgeons of Edinburgh in 1833. In London, besides his appointment at the Hunterian School of Medicine, he was a surgeon at the Metropolitan Free Hospital. Among his writings is a text entitled Anatomy and Surgery of the Arteries and an article on asphyxia in the Cyclopaedia of Practical Surgery. He was a contributor to the Lancet and the Provincial Medical and Surgical Journal. John Hunter Lane was from Surrey but qualified as a surgeon (1829) and received the MD (1830) from Edinburgh. He lectured on chemistry and forensic medicine in the Liverpool School of Medicine before coming to the Hunterian. He was a regular contributor to the London medical journals; Medical Directory, 1845. Michael Ryan read medicine in Ireland, received the MD from Edinburgh, and focused his practice on obstetrics. He was for a time editor of the London Medical and Surgical Journal; see Desmond, Politics of Evolution, 171, 427. According to the Apothecaries’ Act of 1815, Scottish graduates could not practice in England unless they received an English qualification, whether the LSA, the MRCS of London, or an MD from Oxford, Cambridge, or (eventually) University College London. Apparently, few bothered to add English credentials and practiced without them. 14. We have not found biographical information on Jewell. The weekly schedule we constructed from the course descriptions in Lancet 1 (1836–37): 12 is the most likely scenario for fulfilling the courses noted in Society of Apothecaries, “Court of Examiners entrance books,” MS 8241/10, 61 (“John Snow”). It is possible that he attended lectures in surgery offered by James Wardrop (1782–1869), MRCS of Edinburgh, and highly recommended in Lancet 1 (1836–37): 20. The Society of Apothecaries did not require comparative anatomy, which was taught at the Hunterian during the 1836–1837 session by Robert Grant, a surgeon and physician educated in Edinburgh, Lamarckian evolutionist, lecturer in comparative anatomy at University College London, and fiery agitator for radical medical reforms; Medical Directory, 1845; see also Desmond, Politics of Evolution, 422. We do not know if Snow attended Grant’s lectures in 1836–1837. 15. Society of Apothecaries, “Court of examiners entrance books,” MS 8241/10, 61 (“John Snow”). 16. Quoted in Richardson, L, v. 17. Although the Anatomy Act of 1832 made it easier for medical schools to obtain cadavers legally, wax models were still used for demonstration purposes; see LMG 19 (1836–37): 32. A collection of wax models from the early nineteenth century is on display at the Gordon Pathological Museum of Guy’s Hospital, London. 18. S. Paget, Memoirs of Sir James Paget, 40–41. 19. Galbraith, “Joshua Parsons,” 108. 20. Lancet 1 (1837–38): 14–15; Society of Apothecaries, “Court of examiners entrance books,” MS 8241/10, 61 (“John Snow”). Robert Venables, MA and MB (1823) from Oxford, published his “Lectures on clinical history, pathology, and treatment of urinary disease” in LMG (1837–38); Medical Directory, 1845. 21. “Advice to students,” Lancet 1 (1837–38): 20; see also 11, 15. The North London Hospital in Gower Street was opened in 1834, replacing the University Dispensary in Euston Square

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that had provided practical training for medical students of the newly founded University of London between 1828 and 1833. In 1838 the name was changed to University College Hospital; Newman, Medical Education, 113–14. 22. Snow was not trained by Richard Bright, a physician at Guy’s Hospital, a respected clinical researcher on kidney diseases, and the developer of a chemical test for the kidney disease later named for him. 23. Lancet 1 (1837–38): 15. Westminster Hospital had been a dispensary in James Street until 1834, when it moved to a new location and added a medical school; Newman, Medical Education, 113. For the reputation of the medical officers and the method of teaching at Westminster Hospital, see S. Snow, JS-EMP, 135–37. 24. “Advice to students,” Lancet 1 (1837–38): 20. For the significance of the shift from the “history taking” in conventional bedside medicine to the study of physical signs in hospital settings, see Peterson, Medical Profession, 14–15, and her citations of studies by Figlio and Waddington. 25. “Advice to students,” Lancet 1 (1837–38): 20. 26. Ibid., 21. 27. There are parallels between the Lancet’s ideal case report and Snow’s format set forth in the extant casebooks (CB) from the last decade of his life, although the latter contains idiosyncrasies evolved over many years by a skilled experienced practitioner. Moreover, a number of his publications include statements such as the following: “The following case from my note-book”; in “Case of malignant hæmorrhagic small-pox” (1845), 585–86. 28. S. Paget, Memoirs and Letters, 59–60. 29. Ibid., 60. 30. Ibid., 61. 31. Ibid., 63. 32. Ibid., 64–65; Newman, Medical Education, 20, appears to be based on Paget’s account. 33. According to the Charter of 1822, examiners had to be selected from the twenty-one members of the council, and examinations were held in the college building; see Bailey, “Medical institutions of London,” British Medical Journal 2 (1895): 1291. “College of Surgeons,” LMG 22 (21 July 1838): 688. 34. “Editorial—1 April 1837,” Lancet 2 (1836–37): 60. The hospital apothecary, Mr. Thurman, also retired as secretary of the Westminster Medical Society in October 1837; Lancet 1 (1836–37): 177. 35. Richardson, L, vi–viii; S. Snow, JS-EMP, 140–43. 36. Lancet 2 (1836–37): 59–60. 37. Snow, “Arsenic as a preservative of dead bodies” (1838), 264. 38. Ibid.; Herschel, Preliminary Discourse, 150–51. John Herschel (1792–1871), a mathematician, chemist, researcher in optics, astronomer, and translator of various literary works, was the son of William Herschel (1738–1822), also an astronomer. 39. Snow, “Arsenic as a preservative.” 40. Bailey,“Medical Institutions of London,” British Medical Journal 2 (1895): 26, and British Medical Journal 1 (1895): 1389. See also Hunt, Medical Society of London, 16–17; S. Snow, JS-EMP, 170. 41. S. Snow, JS-EMP, 172; see also “Westminster Medical Society,” Lancet 2 (1836–37): 123, where Epps is recorded as warning that even “small doses of liquor arsenicals . . . in delicate females, soon brought on uterine hæmorrhage, though he had never witnessed a case in which it had gone to an alarming extent.” Official minutes or reporters’ abstracts of meetings were regularly published in the London medical journals. 42. Galbraith, JS-EY, 54. “Westminster Medical Society. To the Editor. . . ,” Lancet 1 (1836–37): 232. According to the new bylaws, three members had to propose a candidate for


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membership, and a majority of the society had to approve. Successful candidates had to pay an introductory fee of one guinea, which also covered annual dues for three years. 43. Desmond, Politics of Evolution, 105. 44. “Westminster Medical Society,” Lancet 2 (1831–32): 21–24, 51–54, 85–88, 146–50; discussions of cholera occurred on 31 March , 7 April, 14 April, and 28 April 1832. 45. “Westminster Medical Society,” Lancet 1 (1837–38): 212. It is possible that Everitt was a misspelling of David Everett, LSA (1839). 46. Ibid., 243. There were several medical men named Phillips, of which the most likely in this instance was Richard Phillips, LSA (1836), MRCS (1837). 47. Ibid., 425. While still apprenticed, Golding Bird became a student at Guy’s, where he soon developed a reputation as an accomplished chemist. He received the LSA in 1836 and earned an MD from St. Andrews in 1838; see Coley, “The collateral sciences in the work of Golding Bird.” 48. “Westminster Medical Society,” Lancet 1 (1837–38): 425–27. 49. Ibid., 463. 50. Editorial, Lancet 1 (1837–38): 457. 51. Ibid., 458. 52. “Poisonous Candles,” LMG 21 (1837–38): 577–80; “Westminster Medical Society,” LMG 21 (1837–38): 585–88; “Westminster Medical Society,” Lancet 1 (1837–38): 722. 53. However, the institutional approach to laboratory medicine did not develop as early in England as it did in France and the German states. See also Seale and Pattison, Medical Knowledge, 33–35. 54. See Cope, “Private medical schools,” 90–93; the Hunterian School of Medicine was sometimes called The Great Windmill Street School. See also Hays, “The London lecturing empire”; S. Lawrence, “Entrepreneurs and private enterprise”; Long, History of Pathology, 95; and Newman, Medical Education, 82–111. 55. Holloway, “Medical education,” 303–04. The Idéologues sought to emulate Giovanni Morgagni (1682–1771), whose essay De sedibus (1761; The Seat and Causes of Disease, 1769) argued for the correlation of clinical symptoms with pathological manifestations discovered during autopsies—which made morbid anatomy central in a medical student’s education. Leading figures among the Idéologues included Pierre Cabanis (1757–1808), physician–philosophe, and Marie F. X. Bichat (1771–1802), who substituted tissues for humors as basic units of health and disease; see Porter, Greatest Benefit, 306–07. 56. Teaching was integrated with research as hospital clinicians devised nosological systems for classifying diseases as distinct entities, either by “distinguishing separate diseases that had previously been believed to be the same, or . . . unifying as a single disease category a disparate collection of manifestations previously thought to be separate diseases” as in the research showing that different types of consumption were one disease, tuberculosis; Seale and Pattison, Medical Knowledge, 33. 57. See Porter, Greatest Benefit, 316–18, on the influence of the Paris “school” of hospital medicine in London. The Paris school of medicine included, besides Louis, René T. H. Laennec (1781–1826), a physician at two large Paris infirmaries, the Salpêtrière and Hôpital Necker, and developer of the stethoscope; Jean N. Corvisart (1755–1821), physician to Emperor Napoleon, proponent of morbid anatomy and the clinicopathological approach to understanding internal diseases; and Gaspard L. Bayle (1774–1816), physician at the Charité hospital and researcher on phthisis (tuberculosis) and cancer pathology. See Porter, Greatest Benefit, 312–13. Contemporary validation that the ideas from the Paris school were debated during Snow’s medical training is found in Edwin Lankester’s “Essay on the uncertainty of medical science, and the numerical method of M. Louis,” London Medical and Surgical Journal 10 (1836–37):

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468–76, read at a meeting of the Medical Society of London in November 1836. Lankester (with whom Snow would later work very closely) argues that Louis’s method is not just a mechanical collection of facts. Instead, a judicious use of the method would assist those who wished to move medicine from an art to a science. Some critics “will feel disposed to say, that, from the very nature of medicine, it is impossible to reduce it to the rank of a true science. To this I would answer,” wrote Lankester, “that it is as possible for the mind of man to have the relation of cause and effect in one series of actions as in another. . . . If the astronomer has thus succeeded, surely it is not too much to suppose that the medical philosopher may equally give laws to the relations of bodies infinitely more accessible to the apprehension of the sense” (476). However, the manner in which Lankester presented the numerical method indicates that its use in England was not the norm. 58. In an 1831 letter to W. D. Fox, Charles Darwin wrote, “If you have not read Herschel in Lardners Cyclo—read it directly”; Darwin, Correspondence, 1: 118. Herschel’s Preliminary Discourse (1830) was republished in Dionysius Lardner’s Cabinet cyclopædia in 1831. 59. Herschel, Preliminary Discourse, 87; quotation from 15. 60. Ibid., 132; 174–75. 61. Ibid., 174. 62. “Apothecaries’ Hall. List of gentlemen who have received certificates. Thursday, October 4,” LMG 23 (1838–39): 144; “John Snow, York,” was eighth on a list of ten. 63. Christopher Hamlin’s phrase, taken from his review of an early draft of the manuscript. 64. In the sample used by Digby, seventy-eight per cent of GPs in the north of England had their “main place of practice in [the] area of birth”; British General Practice, 74.

Chapter 4

Forging a London Career, 1838–1846

I

N OCTOBER 1838 John Snow “nailed up his colours” as a surgeon at 54 Frith Street, part of the parish of St. Anne-Soho, one of Victorian London’s most densely populated areas.1 A jumble of trades, shops, markets, offices, and residences, Snow’s new neighborhood was a mixture of the genteel and the humble, of family and industry. Once home to foreign aristocrats and Huguenot immigrants, this part of Soho was by the 1830s an area in flux. At its northern end was Soho Square, built around a central garden, with houses occupied by lawyers, dentists, architects, the publisher Routledge, and Crosse and Blackwell’s manufactory of condiments. At the northwestern edge of the square was the Soho Bazaar, a closed market originally established at the end of the Napoleonic Wars as a venue where the widows and daughters of army officers could rent stalls cheaply by the day to sell their handicraft, mainly jewelry, millinery, gloves, lace, and potted plants. 2 Snow lived at the opposite end, near where Frith dead-ends into King Street.3 According to the 1841 census, 540 people resided in the 600 feet that constituted Frith Street.4 It was a densely packed thoroughfare; on average, each house had nine residents, and many exceeded the average by a considerable margin. Twenty-nine people were listed in the five flats at number 19. William Searle, a fifty-five-year-old bookbinder and his wife, Lucretia, aged forty-five, headed one household containing two adult sons and three more children ranging in ages from nine to thirteen. Nine people shared another flat, and in yet another lived a forty-year-old woman of

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independent means, a boy of twelve, a painter’s apprentice, and a female servant. In the fourth flat lived a painter with his wife and their four children. The fifth contained a sixty-five-year-old gold-laceman, his wife, and an unmarried daughter of twenty-five.5 Londoners lived cheek by jowl with recent immigrants and migrants from the country. Apprentices lived next to picture dealers and solicitors. Tailors, embroiderers, music sellers, bookbinders, engravers, bakers, iron- and cheesemongers, tea merchants, and stay makers all made their home and living here. There was also a violin and guitar maker, a language teacher, a glass enameler, a coffee house, and a public house, the “Coach and Horses.” Young and old, day laborers and artists, dentists and doctors all crowded into the street, but 54 Frith Street was something of a refuge from the hubbub. The 1841 census indicated that just four people lived there: Sarah Williams[on], fifty-five and independent; her thirty-year-old daughter, Harriet; Jane Weatherburn, a female servant, aged thirty, born outside the county; and John Snow, surgeon, twenty-five years of age.6 Four other surgeons were located within a few doors of him—August Sannier at 56 Frith Street, George and Joseph Toynbee at 58 Frith Street, and Alexander Angus at number 66. Peter Marshall, with whom Snow would work regularly, had premises in Greek Street, which ran parallel to Frith. Like Snow, these were all men hustling to make a career for themselves in the great emerging medical middle class of London. The nearest physicians lived in Golden Square, a quarter-mile to the southwest.7 Snow’s practice for the first eight or nine years largely depended on patients from the area in which he lived. It would not be surprising if he often questioned his decision to start from scratch in a metropolis oversupplied with GPs, many of whom were having great difficulty attracting patients.8 Consequently, there was considerable turnover in general, and Snow’s part of Soho was no exception. For example, by 1841 J. L. Curtis and Co., surgeons, had set up shop at 7 Frith Street, the Toynbees and Sannier were no longer listed in the city directory, and Hugh W. Diamond, another surgeon who would go on to pioneer psychiatric photography, had moved into number 59.9 Curtis headed a group practice, Diamond brought an apprentice with him, Alexander Angus had an assistant, and Snow remained at 54 Frith Street until 1852. For those who could make a go of it, there was obviously demand in this district for general practitioners.10 Initially, at least, Snow followed custom in securing appointments as surgeon to four friendly societies, or sick clubs; 64 percent of GPs in a sample covering the years 1820–1879 had at least one nonhospital appointment such as a friendly society.11 These voluntary associations, forerunners of the capitation schemes of the next century, collected a few pence per week from every laborer and paid practitioners an annual lump sum—often quite small—for treatment of the workers and, sometimes, their families.12 Snow had an intense bent toward research, but there were no paid positions as a medical scientist in London until after midcentury. Not until the Public Health Act was passed in 1859 was there any provision for the paid employment of “investigatory” medical staff, and even then there were very few such positions and only on a temporary basis.13


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Before the advent of anesthesia, John Snow was largely able to make a living as a GP in London and still have time for research and medical society meetings because of his thrift and his energy. His modest means never exceeded his expectations. Richardson remarks that Snow “managed by his frugality to lay in store for a rainy day for himself, and to help such friends as needed.” A teetotaling vegan during his first five years as a London GP and a temperate vegetarian thereafter, he was a health enthusiast his entire adult life. He dressed plainly and remained a bachelor.14

Finding His Way, 1838–1839 Snow’s marginal success in general practice was all the more remarkable because he evidently did not possess an easy bedside manner. The word on John Snow was: “A quiet man, very reserved . . . not easily to be understood and very peculiar.” He habitually spoke in a husky voice, which “rendered first hearings from him painful,” and he sometimes had trouble making himself heard in meetings.15 When Snow did meet with success from using anesthesia, it was widely assumed that he got rich from milking this practice. While an obvious research talent, he was in some ways lacking in humanity. In his memoir Richardson felt compelled to defend Snow from these criticisms but readily conceded that “He did not become the idol of the people in common practice, far from it.”16 Richardson felt that Snow’s lack of popularity was a sign of his medical integrity. Richardson relates that in Snow there was too much of the skeptic to be popular and none of the quackery or “routine malpractice which the people love,” and as a poor boy from York he had no entrée to “the bedsides of dowagers of the pill-mania dynasty.”17 Such skeptics did not become rich by writing prescriptions or compounding medicines. Undoubtedly, he was never one to tell people what they wanted to hear for the sake of popularity. Nonetheless, his anesthesia casebooks indicate that he was very capable of putting nervous patients at ease. Additional factors not addressed by Richardson include Snow’s temperance, which likely alienated him from the heavy-drinking working clientele in his neighborhood. The casebooks occasionally reveal his impatience, sometimes downright irritability, with what he perceived as general ineptitude among his neighbors. In an example from April 1850 that ties together his antipathy toward alcohol and his skeptical attitude toward the locals, Snow consulted on a case of delirium tremens. His friend and colleague Peter Marshall asked for his assistance with a long-time alcoholic who had been unable to sleep for two days. The man was shrieking, shaking violently, and hallucinating when Snow was called in. His course of treatment was basically to sedate the patient with opium and to induce ordinary sleep by way of chloroform. The strategy seemed to be working but was undermined because the man was, as Snow complained in his notes, “surrounded by a lot of ignorant people who made him more excited by boisterous attempts to keep him quiet.”18 Eventually the patient was removed to St. George’s Hospital for further treatment in a more

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stable setting, but Snow’s remark does suggest the distance between him and the general public on how to behave when a medical man was in attendance. His candor about the deleterious effects of alcohol also came between him and his patients. On the other hand, he was immensely respected by his colleagues, and not just the research oriented. He was an acute diagnostician in regular practice, and his colleagues in Soho regularly consulted him about difficult cases. Marshall was in awe of Snow’s practical knowledge and encyclopedic knowledge. One area in which Snow excelled was in the care and delivery of babies. His interest in midwifery, which in his day included the study of diseases of women and children, probably began during his apprenticeship experiences at the lying-in hospital in Newcastle and was nurtured during his London training by Drs. Ryan and Jewell. When Snow began presenting case reports in journal articles and at medical society meetings, he often drew on his practical expertise in obstetric, gynecological, and pediatric practice.19 Obstetric work helped build up a practice, although it was time consuming, and the regular fee for a delivery in the poorer practices was only ten shillings and sixpence or even less,20 but it was a way in which a doctor might become the family physician. Having assured himself of at least a modest practice and the attendant income, Snow proceeded to solidify and deepen his relationship with the Westminster Medical Society, which he had first joined as a student.21 His career as a medical scientist and his involvement with the Westminster Medical Society were closely intertwined. Richardson stated, “I have often heard him say, both privately and publicly, that, upon this early connexion with the ‘Westminster Medical,’ his continuance in London depended, and all his succeeding scientific success.”22 The Westminster Medical Society had once had 1,000 members, but by the time Snow joined its fortunes were sinking. Soon after Snow completed his studies, the Hunterian Medical School in Great Windmill Street closed down. This was a double calamity for the Westminster. Most of its membership had been drawn from the student body of the school, and it had enjoyed rent-free use of the school’s facilities for meetings for many years. It suffered a dramatic decline in membership and depleted its financial reserves as it had to rent temporary quarters. In 1843 it reached low ebb, with only a dozen members remaining. Snow stuck with the Westminster during its dark days and was a faithful participant. In the first five years of his membership, he attended more than 90 percent of the weekly meetings on Saturday evenings, taking a guest more than a third of the time.23 Over time he was elected to various offices. For example, he was on the advisory committee for the 1842–1843 and the 1846–1847 sessions and vice-president in 1848–1849.24 Meanwhile, the society added new members, eventually reaching 275. It continued to be dogged by financial concerns, so in 1849 the officers sought amalgamation with the like-minded Medical Society of London, in part because the two societies had a large number of members in common. The Medical Society of London had been founded in 1773 by Dr. John Lettsom, a forerunner of the medical radicals who came into prominence in the 1830s. Sixty


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years earlier he perceived the need for a society that would admit physicians, surgeons, and apothecaries on an equal footing and that would allow Quakers and Dissenters to be members, but after thriving for a long period, the Medical Society of London had, like the Westminster, fallen upon hard times. An amalgamation of the two was a natural solution, but the joint society had to take the name of the former organization because of a technicality in the Medical Society of London’s lease on its property.25 In the early days of Snow’s career, however, the Westminster retained a distinct identity, and it provided him with a comfortable environment to meet most of his professional and social needs.26 While Snow’s fondness for the Westminster was deep and abiding, it was not exclusive. In 1843 he was elected a fellow of the Royal Medical and Chirurgical Society, but, according to the society’s Transactions, he gave few papers at this staid society of medical conservatives, and the medical press recorded few comments by him.27 The more bellicose side of Snow, who had argued with Hardcastle over the brandy treatment for cholera and who set out to clean up Watson’s surgery without first consulting his principal, was reserved for the Westminster, where he could participate in the rough-and-ready debates without making enemies. Generational differences in the membership brought stark disagreements. The older generation at the Westminster consisted mostly of men whose formal London training involved far fewer courses than Snow was required to take, occurred at a time when Cullen and Brown were considered “modern” theorists, and preceded the wave of Continental ideas and foreign influences that transformed medical schooling in the 1830s.28 The newer generation, by contrast, either had the social advantages necessary to travel to the Continent for additional training or became aware of the newer work in hospital and laboratory medicine through journals.29 Snow shaped his nascent career by allying himself with the new generation and (as politely as possible) lecturing to the older generation to insist that the hospital and laboratory approaches received a fair hearing. Because the norm for research, especially laboratory research, at that time was still solo investigation, Snow indicated his allegiance to the new generation primarily by citing the same authorities and referring to the same published works. This generational divide and Snow’s position in it was evident in the early papers he delivered at the Westminster. On Saturday, 7 December 1839, he read a lengthy account of twelve cases of scarlet fever that had been followed by severe edema, with four deaths. His conclusion was that “disorganization of the kidney might be occasioned by scarlet fever.”30 The context for his discussion of these cases was recent medical research, not empirical medicine. His review of the literature featured the discovery by Dr. Richard Bright of the relationship between albumin in the urine and certain diseases of the kidney.31 Then he showed how Bright’s findings could explain the cases he had treated. The first was a girl aged twelve whose severe form of scarlet fever was followed by a generalized swelling involving the chest and abdomen, eventually leading to death. His postmortem examination—Snow laid the specimens

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before the society—showed that her kidneys were grossly enlarged. In two of the other deaths the kidneys were found to be much congested postmortem, the lungs were edematous, and there was pericarditis (inflammation of the membrane surrounding the heart). In ten of the twelve cases albumin had been found in the urine and was probably present in the other two, but the tests had been inadequate.32 He added that generally the urine was dilute and low in urea content; these findings indicated that urea was accumulating in the blood. It had often been detected by others in such cases, and Snow suggested that a rise in circulating urea might be the cause of some of the problems, including disease of the heart itself. In terms of treatment he recommended, in view of the congestion, that blood-letting at the commencement of the disorder should be beneficial, together with free purgation. Snow was immediately challenged by William Addison.33 Dr. Addison was unconvinced by Bright’s researches that the kidney was the source of the problem in dropsy. Instead he attributed all the symptoms described by Snow, including the disease of the kidney, to a peculiar state of the system that might be induced by intemperance and a variety of other causes. He thought it more likely that the entire human “economy” had been disrupted, and the cause could not properly be localized to a single organ. He was ready to dismiss a laboratory discovery—albumin in the urine—as a mere epiphenomenon providing no basic insight into the disease process. However, Dr. Golding Bird, recently appointed an assistant physician at Guy’s Hospital, took up the torch for the new generation while still disagreeing with Snow’s interpretation. He doubted whether increased urea in the blood contributed to the symptoms. He noted that François Magendie (1783–1855) had injected urea into the blood, and no bad effects had resulted. Bird’s citation of data from the laboratory of Magendie, a skilled neurophysiologist and experimental pharmacologist, positioned him with Snow as an advocate of a new approach to clinical medicine in which theory and laboratory research structured one’s interpretation of diseases.34 This relatively early case report and discussion provides a glimpse of the young Snow’s progress. He enjoyed an advanced grasp of basic concepts of pathophysiology, especially when understanding a disease process required seeing the relationships among various organ systems and tracing fluids from one body compartment to another. He also demonstrated facility in performing postmortem examinations, but his suggestion that blood-letting and purgatives could be the treatment of choice shows that current options in therapeutics differed little from Watson’s and his drawer of used blisters.35

Snow’s Early Publications The free debate tradition in the Westminster shaped Snow’s earliest attempts at scientific publication. From the outset he structured his written arguments as if he were


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presenting a lecture: identifying a clinical or public health problem, surveying the most recent medical literature on the topic, and dealing in advance with anticipated objections—in short, using the medical journal as a forum to deliver the same messages he articulated in person at society meetings. He also floated trial balloons before his colleagues. Reading a paper allowed him to weigh criticism from his peers and to decide whether the material was worth sending to a journal, having it published as a pamphlet at his own expense (or both), or leaving it as a presentation. The latter approach had some payoff, too, because reporters for the Lancet and LMG generated detailed summations of papers. Because the reports of what transpired at the medical societies usually included the reactions of each commentator, Snow could also make his mark by responding to papers presented by his colleagues and the occasional guest lecturer. Snow was no exception to the generalization that, for London medical men in the nineteenth century, participation in medical society affairs brought professional recognition, and regular publication was a critical aspect of career advancement.36 His first four publications were letters to the editor written in response to articles published in the Lancet and LMG. These letters were not, however, purely ad hoc rejoinders. His reply to a Professor Goodeve on the use of arsenic to preserve cadavers included a description and analysis of the experimental inquiry he had undertaken during his student days. Thomas Wakley, editor of the Lancet, added a sentence to the effect that Goodeve had reported no ill effects from his arsenic-treated cadavers. Wakley’s comment was as revealing as it was gratuitous. He was an old-school surgeon who considered medicine solely an inductive science and appeals to experimental medicine either faddish or harmful,37 but Snow was undeterred. In January 1839 he sent another letter to the Lancet because a recent article by John Goodman on the “Physiology of the mechanical action of the heart” was “open to some objections.”38 Mr. Goodman had proposed that the auricles (atria) of the heart, being less muscular than the ventricles, had no need for muscle fibers in their walls. He argued that when the ventricles contracted, the diminution in their volume produced a vacuum in the pericardium; atmospheric pressure acting on this vacuum squeezed the auricles, emptying them into the ventricles without the need for them to contract. He reasoned that the rib cage and the diaphragm were of such construction as to be able to withstand “the pressure of the atmosphere, generally understood to be 15lbs. on every square inch of surface. . . . The bony arch, by its unyielding structure, presents itself to the oppressing forces with the firmness of the oak, in an arched and resisting form, while the more yielding diaphragm, like the willow before the wind, bending beneath the atmospheric pressure, presents a concave, but still resisting and equally protecting surface.”39 Snow began his rejoinder with the above quote, minus the sylvan flourish. He agreed with Goodman that “the most delicate structures on the earth bear the pressure of the atmosphere without detriment, so long as it is equal in all directions; a distended bladder, and bubbles blown in soap and water, bear it because it is equal

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inside and out; but this is not what Mr. G. means. . . .”40 The anatomy and physiology of the thorax, according to Snow, did not support Goodman’s conclusions: “A thorax 10 inches deep and 30 inches in circumference (not a very large one), has 300 square inches of surface, and would, in this case, have to resist a force of 4500 pounds, or more than two tons; and, in addition, the diaphragm and the parts closing the top of the thorax, would have to resist half as much; this would require thick walls of cast iron, instead of mere flesh and bone. The truth is, that with very slight variations the pressure on every part of the thoracic viscera is exactly the same as on the exterior of the chest.”41 The walls of the thorax are movable and elastic, and atmospheric pressure on them and inside the lungs keeps the surfaces of the lungs in close contact with the inside walls of the chest. The only variations in pressure between inside and outside occur during inspiration and expiration. These are slight, Snow explained, having quantified them by measuring his own intranasal pressure while breathing with both a mercury and a water manometer. The rest of the letter proceeded in like manner, with quotes from Goodman followed by correctives drawn from current medical authorities and his own clinical experience. He cited a recent paper by Magendie on blood pressure in dogs and suggested that Goodman’s confusion stemmed from a misreading of Johannes Müller’s Physiology, a textbook that served as the most advanced European treatise on the subject during the 1830s and 1840s (Snow quoted from the English translation).42 Müller (1801–1858) belonged to a generation of natural historians who believed scientific truth lay somewhere between the warring perspectives of their elders. For Müller, Enlightenment physiology was too mechanistic and reductionist to account for life forces, whereas the archetypal forms and Platonic ideas in Romantic Naturphilosophie struck him as “fables.” His alternative, a “rational creative force,” was akin to vitalism and served as the organizing principle in his discussion of embryology,43 but Snow used Müller’s principles of physiology to expose fallacies in Goodman’s reasoning. As such, Snow was not out to score debating points at an opponent’s expense.44 His agenda was to advance the cause of a new scientific generation. Although he lacked the resources to travel to France or Germany to study under such teachers, he could read their works and position himself within the larger movement of experimental physiology and chemistry that was transforming laboratory medicine. Goodman could have done likewise and would not have gone astray had he fully understood the contributions of Müller and Magendie.45 A few months later another opportunity arose for Snow to enter the lists as an advocate of the new medical science. Someone who identified himself as “M.H.” submitted a brief note to the Lancet on “Respiration and asphyxia.” After commenting on the various nerves responsible for stimulating respiration, “M.H.” argued that what incites the first breath in the newborn cannot be the same mechanism that incites breathing in the mature animal, because the latter depends on “evolved carbonic acid” produced by the animal after it has begun to breathe oxygen.46 The author went on to claim that asphyxia was closely allied to epilepsy because of the


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convulsive nature of the attempts of the asphyxiated animal to breathe. Snow, in reply, would very likely have alluded to the fact that the fetus in utero produces carbon dioxide that is chemically indistinguishable from that produced by the organism after birth. As he would write later, there was no reason in his mind to argue that whatever causes the newborn to take its first breath is different from what causes it to take its second or third breath.47 We will never know what Snow’s letter to the editor contained because Wakley chose not to print it. Instead, the 25 May 1839 issue of the Lancet included the following notice: “The remarks of Mr. John Snow on a recent communication from M.H., on the physiology of respiration, have been received. We cannot help thinking that Mr. Snow might better employ himself in producing something, than to criticising the productions of others.”48 Wakley’s statement can be read as a snub: Snow was an upstart trying to make a name for himself by finding fault with his elders. It can also be read as the reaction of a prickly editor who thought Snow was criticizing him for including flawed articles in his journal, and it can be read as a gentle, if ham-fisted, warning by a senior colleague that Snow should temper himself at so early a stage of his career. Whatever Wakley’s intent, his comment was patently unfair to Snow. His first letter to the editor had detailed arsenic experiments, and the Lancet had reported on Westminster Society meetings at which Snow had read several papers on his research activities. He appears to have taken offense, for he found a friendlier reception in LMG.49

Setting His Own Agenda, 1839–1843 Snow took Wakley’s comment to heart in that he refrained from sending further letters to editors for the next few years and used this period to stake his own claim to experimental territory and to establish areas of special interest. The territory he laid claim to included the physiology of respiration and the chemistry and physics of inhaled gases, with special attention to their implications for midwifery. Although at first glance Snow’s early research and scholarship might seem eclectic in subject matter, his persistent interest was the physiology and pathology of respiration. He investigated the mechanics of breathing and ways to restore vitality when respiration was interrupted. He studied the properties of inhaled toxins and gas exchange at the tissue level. His understanding of factors that stimulated or depressed respiration, or that supported or interfered with gas exchange, would prove enormously useful when his major professional challenge became finding the middle ground between preventing pain and suppressing breathing when administering anesthetic gases. In addition, his deep understanding of the inhalational route of toxins led in a direct path to his skepticism of the miasmatic origin of cholera. One should not read Snow’s articles and presentations during the next half-dozen years as anticipations of William T. G. Morton’s discovery of ether or of the return of cholera to England, but it is highly unlikely that without the insights Snow derived from these forays into

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medical science, he could have so successfully addressed the twin problems of anesthesia and cholera. Snow’s emerging focus was in evidence at the Westminster Medical Society in March 1839, when Dr. Golding Bird read a paper on how carbonic acid gas produced death in animals. Snow thought the paper so interesting that he requested a continuation of the discussion. At the next meeting he began by noting that Bird’s paper had “induced him to modify his opinion as to the modus operandi of charcoal fumes. He had formerly entertained the idea that carbonic acid [carbon dioxide], like hydrogen and nitrogen, produced death simply by the exclusion of oxygen; but the experiments of Dr. Bird and Collard de Martine had convinced him of the contrary . . .”—that carbon dioxide was deleterious, although he was not ready to accept Bird’s view that it was an active poison.50 During the week after this presentation Snow had undertaken several experiments on small birds and white mice using various mixtures of atmospheric air, carbon dioxide, and oxygen. He described his results in detail and concluded that oxygen could act, to some degree, as an antidote to carbon dioxide, and that while the physiological action of carbon dioxide was unclear, its destructive powers might arise from constant stimulation of “the mucous membrane of the air-cells.”51 This extended comment indicates Snow’s facility in planning and conducting a set of experiments designed to answer a specific question. The chemical procedures he described required a considerable amount of apparatus and of skill, and his comments reveal an understanding of the physical and physiological principles involved. He was particularly interested in the public health implications of these investigations. He cited a recent study that “death might be produced in an atmosphere which supported the flame of a candle.” Because such a flame went out in an experimental atmosphere containing four percent carbon dioxide, “a fortiori, such an atmosphere could not support life.”52 This conclusion was at odds with the reassurances of chemists that charcoal-burning stoves lacking a chimney were safe for domestic use. When Snow published his next paper in 1841, he provided further evidence that he was carefully focusing his investigations (Table 4.1).53 From a general interest in the chemistry and physics of inhaled gases, he began to turn his attention increasingly to aspects of asphyxia, notably the increased resistance to blood flow through the lungs and the site of the metabolic processes.54 He also showed a predilection for inquiring into instances and mechanisms of poisoning, particularly if the poisonous substance were inhaled. He demonstrated both an interest and a facility in the invention and design of apparatus. Snow resumed his publications with an article on deformities of the chest and spine in children.55 While he focused on how abdominal enlargement might prove to be the basic cause of chest deformities in the growing child, he was especially concerned about the impact the deformities had on respiratory function and lung development. About six months later Snow published a paper initially read at the Westminster Medical Society on 16 October 1841.56 His explanation of the resuscitation

Table 4.1. Snow’s published research, 1836–1846 Datea

Experiment conducted

Arsenic as preservative of dead bodiesb

1836–1837

X

Action of recti musclesb

1838

Mechanism of respirationb

1839

Action of recti musclesb

1839

Distortions of chest in children with abdominal enlargement

1841

Resuscitation of stillborn infants

1841

Paracentesis of thorax

1841

Uterine hemorrhage with retention of placenta

1842

Circulation in capillaries

1843

Topic

Apparatus constructed

Involved respiration, gases

Involved poisons

X

X

Collateral sciences used Chemistry Anatomy, physiology, physics

X

Physiology, Physics Anatomy, Physiology

X

X

Anatomy, pathology, physiology, clinical case report

X

X

Physiology, physics

X

X

Physiology, physics Physiology, clinical case report

X

X

Physiology, physics, microscopy

New kind of pessary

1843

Lead carbonate poisoning

1844

Hemorrhagic smallpox

1844

Pathology, clinical case report

Pericarditis after scarlet feverb

1845c

Pathology, clinical case report (continued)

X

Clinical case report X

Pathology, chemistry, clinical case report

Table 4.1. Snow’s published research, 1836–1846 (Continued) Datea

Experiment conducted

Atmospheres with reduced oxygen and normal carbon dioxide

1846d

X

Strangulation of ileum in mesentery

1846

Alkaline urine

1846e

Topic

aDate

Apparatus constructed

Involved respiration, gases

Involved poisons

X

X

Collateral sciences used Chemistry, physics, physiology Pathology, clinical case report

X

Chemistry, physiology, clinical case report

given is that of publication unless the article states specifically that the observation or experiment was carried out at an earlier time. to previous publication by another author. cReports case that occurred in 1844. bReply

dRefers

to research conducted in 1839.

eReports

case that occurred in 1842.


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of the stillborn infant draws on several of his research interests, including respiration and asphyxia, as well as a practical interest in designing apparatus. In a more general way, it illustrates important features of Snow’s thought and writing and the extent to which he had achieved a level of scientific competence at this relatively early stage of his career. The paper is dense in ideas and material, while the style is clear and brisk. Snow began this paper by reviewing a number of physiological and philosophical questions relating to asphyxia and marshaled experimental evidence to show that animals tolerate lack of oxygen much better at low temperatures than at high temperatures. He cited many physiological experiments performed by authorities he cited by name, the best known being Lorenzo Spallanzani (1729–1799) and Marie François Xavier Bichat (1771–1802). After explaining why many commonly used resuscitation methods were unsatisfactory because they were at odds with this large body of experimental data, Snow turned to the new device produced after his own plans by Mr. John Read of Regent Circus and described its use and advantages.57 The apparatus consisted of two syringes placed side by side, one to withdraw air from the lungs via the mouth and the other to push fresh air into the lungs via the nostrils. Atmospheric air, provided by an efficient device such as Read’s, ought to be sufficient by itself to restore respiration if the asphyxia were reversible at all. Snow added that should the physician desire to add oxygen, “oxygen gas can be generated in great purity, in a few minutes, from chlorate of potash, by means of a spirit-lamp and a small retort.”58 After a few comments on possible uses of mild electric shocks in stimulating respiration, Snow mentioned the experiment he had performed on a guinea pig to show that he could restore some heart action an hour after death by artificial respiration. He concluded his paper with some observations on the mechanism that causes the newborn to take its first breath—perhaps held in reserve from his neverpublished reply to M.H. in the Lancet—and how long after cessation of placental circulation fetuses of various ages would survive. This paper seemed to stimulate the Westminster Medical Society almost as much as Read’s apparatus was said to stimulate newborn respiration. The society took the unusual step of extending discussion of the paper into the next two meeting sessions, 23 and 30 October. For the most part, the many comments and criticisms from the other members reflected the tradition of bedside medicine, although Mr. William D. Chowne added a statistical dimension: He reviewed his records and found only sixteen stillborns among his last 500 obstetrical cases, leading him to dispute Snow’s one-in-twenty figure as grossly inflated. Mr. Forbes Winslow attacked Snow for not distinguishing between two causes of asphyxia, plethora and collapse, and argued that only blood-letting would help in cases of plethora. Many shifted the course of discussion to the question of resuscitating nearly drowned adults and debated how many minutes without breathing might pass before it became impossible to restore respiration. Each speaker had a case report to prove the point he was making, often flatly contradicting the lesson of someone else’s case report. Only Sir Benjamin Brodie

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offered a comment that seemed on the same plane as Snow’s discussion of experimental physiology, claiming that artificial respiration could not be effective if the heart had stopped.59 When Snow was granted time to reply to these objections on 30 October, he had obviously used the intervening period to prepare his remarks carefully. He turned aside the plethora/collapse distinction by carefully defining his terms, arguing that the correct current usage restricted the term asphyxia to “the pathological state occasioned by the stoppage of the respiration.”60 He considered asphyxia a unitary phenomenon, physiologically, and therefore the experimental data he had originally cited were applicable. He also took up the question of the resuscitation of nearly drowned adults. Many of the cases cited by the members at the previous meeting had occurred in the Serpentine pond at Hyde Park, and the Royal Humane Society had erected a receiving-house specifically for the purposes of treating such victims. Snow expressed dismay that the society recommended immersion in a warm bath (always at the ready) before attempting to restore respiration. Instead, the authorities should have an apparatus like Read’s (adult-sized) in the boat that was sent out to pull the victim from the water and work to restore respiration before reaching the receivinghouse. These remarks of Snow’s were only the lead-up to what he considered his conclusive rejoinder. Since delivering his own paper, he had located one in the Philosophical Transactions of the Royal Society written by John Hunter, the eighteenthcentury surgeon and founder of the school of anatomy in Windmill Street. Hunter had recommended a bellows for artificial respiration, designed on a principle almost identical to Read’s two-syringe device. He had performed some experiments with his bellows on a dog whose heart had been exposed and showed that the heart action would flag soon after artificial respiration ceased and pick up again after artificial respiration was resumed. He was able to restart the dog’s heart ten times using his bellows, even after the heart had ceased to beat for as long as ten minutes. If Sir Benjamin Brodie doubted the evidence of Snow’s own guinea pig experiment, he could hardly maintain his objection in the face of this experiment by Hunter, whom Snow considered “one of the greatest physiologists that ever lived.”61

Snow’s Evolving Scientific Thought The paper on newborn resuscitation illustrates a complex method of attacking a problem in medical science. Snow had found a comfortable balance among newer perspectives in hospital and laboratory medicine and an updated version of bedside medicine. For him the ideal form of clinical observation, whether conducted personally at the bedside or in hospital wards and supplemented by reports from medical journals, consisted of a long series of cases that had been carefully recorded and could be statistically analyzed, but conclusions were tentative unless confirmed by


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laboratory findings. In this instance he had to resolve an apparent dichotomy between laboratory experiments showing that cold was desirable and accumulated bedside experience suggesting that heat was desirable. He rejected neither out of hand, however. Instead, he offered a distinction to try to reconcile the laboratory and the bedside findings—warmth might be preferable if the infant were to begin spontaneous breathing soon; cold might be preferable if attempts at resuscitation were going to last indefinitely. Snow also demonstrated ease in moving among different scientific disciplines. His resuscitation paper was based largely on applied physiology, but he also made detours into chemistry, anatomy, and physics just as readily as he moved between laboratory and bedside. It was a pattern he followed his entire career, specifying the precise relationship between medicine and its collateral sciences.62 Snow was a systems–network type of reasoner. He seldom dealt with linear chains of cause and effect but rather with interacting networks of causes and effects. He viewed the human organism, and the world it inhabits, as a complex system of interacting variables, any one of which, isolated temporarily for careful study, might provide a useful clue to the clinical–scientific problem—but only when seen in its proper context, and only when the variable, having once been isolated for study, was then put back into its place in the system and restudied in its natural environment. The heat–cold discussion in the stillborn-resuscitation paper provides a limited example of this mode of thought. At the chemical level, the temperature controls the rate at which reactions occur. If a chemical reaction consumes oxygen, it will consume it faster if the temperature is increased. At the physiological level, changes in temperature will affect the animal’s nervous system and occasionally stimulate a nervous reaction, including a reflex inspiratory effort. Snow was equally comfortable isolating these variables for study at one level of biological organization or seeing their interactions at the multiple levels that make up the intact organism within its environment. In some clinical circumstances the positive effects of heat in stimulating the nervous system compensate for any negative effects heat might have in causing increased consumption of the limited oxygen that is available. In other circumstances the opposite would hold true. Snow showed further evidence of his understanding of the physics and physiology of respiration, as well as his ability to put that knowledge to clinical use, when he discussed a new apparatus for paracentesis of the thorax at the Westminster two months after delivering the paper on stillborn resuscitation.63 Paracentesis is the withdrawal of fluid from the pleural space (the space surrounding the lungs) to allow the lungs to expand fully and relieve labored respiration. Conventional methods of draining fluid from the pleural cavity allowed air to flow in as the fluid was withdrawn. Snow’s explanation of why this was undesirable began with a brief review of the mechanics of respiration. “In the normal condition there is no vacant space within the thorax. The pleura on each side of the chest is a vacant bag, merely lubricated on the inner surface with serum; and the pulmonary and costal portions

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glide gently over each other during respiration. Whenever any fluid, whether a liquid or a gas, accumulates within the pleura, it is desirable that we should get rid of it.” When the diaphragm is depressed during normal inspiration, the pressure in the lungs becomes slightly less than the pressure of the atmosphere, and air comes in through the trachea, expanding the lungs to fill the space made available. “But so soon as an artificial opening is made into the pleura, the atmospheric pressure is at once equal on the inner and outer surfaces of the lung on that side; it collapses in accordance with its own elasticity, and remains unaffected by the motions of the ribs and diaphragm.” When the diaphragm is depressed under these circumstances, it sucks in air through the opening in the pleura, which compresses the lung and does not allow it to expand. “It follows from this that at the completion of paracentesis, performed in the usual way, the lung must be collapsed, and the space between it and the ribs occupied by air, provided all the liquid has been removed. And, in fact, with the stethoscope applied to the chest during the operation, the air can be heard passing in by bubbles as the liquid flows out.” By replacing one fluid in the pleural space (pus or serum, depending on the underlying disease process) with another fluid (air), one has done nothing to relieve the basic problem.64 Snow then outlined an ingenious procedure that would work. He believed that, “provided the serum can be removed without making a communication between the external air and the pleura, I do not see why tapping may not be performed on the thorax with . . . safety and success. . . .” A Glasgow physician, Dr. Davidson, had tried but failed to prevent the ingress of air by applying a cupping glass over the canula. Snow showed his colleagues an instrument manufactured for him with great accuracy, again by Mr. Read of Regent Circus. It consisted mainly of an outer hollow tube (canula) and an inner solid tube (trocar). Both trocar and canula had beveled ends so that when one was placed within the other, the entire apparatus formed a thick, solid needle suitable for puncturing the pleural cavity. The trocar could then be withdrawn, leaving the canula as a hollow tube connecting the pleural cavity with the outside, suitable for sucking out fluid. The novel feature was a stopcock near the outer end of the canula. This had been extended so that the accurately machined trocar, which bore a mark, could be withdrawn beyond the stopcock while maintaining an airtight fit. The stopcock would then be closed, the trocar removed, and an elastic tube connected at one end to a double-action valved syringe like a stomach pump. Fluid could thus be removed without allowing air to enter, and “the integrity of the chest as a pneumatic apparatus is not impaired during the operation.”65 With characteristic generosity, driven by the belief that the practice of medicine should be a public service, he laid before the society a drawing of the instrument that any member could have devised by his own instrument maker. Snow had provided both a clear physiologic rationale and a practical way to bring that wisdom to the bedside for the relief of the patient.66


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Deeper Into Asphyxia Snow’s interest in the mechanisms of asphyxia was again evident two years later in a published paper on circulation in the capillary vessels.67 Again, he reasoned back and forth between the realms of physiologic theory and practical therapeutics. The medical question at issue was whether the pumping force generated by the heart fully accounted for the circulation of blood in the capillaries. A number of experimental findings suggested that it did not, and he reviewed the relevant literature. He then proposed a unifying explanation: Capillary flow was assisted by the “attractions and repulsions” caused by the “mutual changes which take place at the capillaries, between and blood and the tissues.”68 As some substances move out of the bloodstream to nourish the surrounding tissues, and as other substances move into the bloodstream to be carried away from the tissues, all these processes of exchange create and impart a motive force to the flow of blood in the capillaries.69 One piece of evidence he offered in support of his hypothesis was the arrest of the pulmonary circulation in a state of asphyxia. Once the exchange of gases has ceased to occur within the pulmonary capillaries, the motive action of the heart is insufficient to propel the blood through the pulmonary circulation. He argued similarly that camphor and other volatile medicines were capable of assisting difficult and impeded respiration. By virtue of the fact that they were exhaled with the breath in chemically unchanged form, these medications exerted an increased attractive force upon the pulmonary circulation that could help to remedy the effects of certain lung diseases. Snow suggested that this group of medicines might be called “diapnetics,” based on their analogy of function with diuretics—the former enhanced excretion through the lung, the latter through the kidney.70 His reason for claiming the privilege of naming this group of medicines was a peculiar one. He did not claim to have discovered any of the medications. He claimed, instead, to have discovered the fact that their common medicinal and chemical properties allowed them to be classified as a family of agents. The family resemblance lay both in the chemical fact that they underwent no alteration in the body before they were exhaled and in the (purported) therapeutic fact that they could assist impeded respiration. While the individual drugs had been known previously, Snow now suggested that the profession had failed to appreciate the family resemblance and its underlying chemical mechanism. He was tentatively exploring the notion that a hypothesized family resemblance among a class of drugs could henceforth guide his research into the properties and mechanisms of these and related drugs, both in the laboratory and at the bedside, and his attempts to better integrate laboratory findings with bedside observations. Chemistry was the laboratory science Snow was most likely to employ. If microscopic examination was of value, however, he referred to what others described. He may have considered this collateral science insufficiently developed to be helpful in many instances.71

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Although his research focus was on respiration, Snow remained engaged in the full range of topics discussed at the Westminster Medical Society.72 When commenting he occasionally referred to experimental work of his own, such as the use of dogs and cats as subjects, differences between ordinary respiration and cough, chemical studies of the absorptive actions of the gut, experiments relating to diabetes, and the effects of woorara poison on guinea pigs.73 In February 1839 he commented about malformations in birds and reptiles, and in April he discussed appropriate treatment of mental diseases. Some years later he discussed mind–body interdependence, the relationship between plague and outside temperature, and how he had counted an adult lion’s heart rate at sixty by observing the pulsations of the radial artery.74 Snow’s may have been a shy man who either kept to himself or kept his colleagues at a polite social distance, but he did have some close friendships. One was surely Peter Marshall, the surgeon in Greek Street who lived near him. In three publications, Snow referred to Marshall as “my friend.”75 Marshall was also Snow’s general practitioner. In the summer of 1845, when he developed a protracted illness suggesting a kidney disease, Marshall undertook his medical care, eventually consulting Drs. Richard Bright and William Prout, both notable authorities on kidney disorders.76 They persuaded him to take a vacation, an unusual practice for him. He visited his friend and one-time roommate, Joshua Parsons, in Somerset. Parsons was surprised to find that Snow was now taking a little wine and eating some meat. The physicians must have convinced him that teetotalism and a strict vegetarian regimen were unsuited to his delicate state of health. He ended his summer vacation with a short visit to the Isle of Wight and then returned to London and resumed his normal schedule.77

Seeking an Academic Position The dual qualification MRCS and LSA that Snow obtained in 1838 was the basic legal requirement for general practice, but Snow wanted more than what the life of a typical GP had to offer. In addition to involvement in medical societies and experimental research in his home laboratory, he wanted an academic post and certification as a physician. Two pathways to an academic post in medicine existed at the time. Each hospital appointed two or three surgical and medical “visitors.” These were unsalaried posts, but they brought their occupants many referrals and prestige. Well-heeled patients expected their surgeon or physician to be experienced, and where better to gain it than on the bodies of those who had no choice but to go to a hospital? In London the most sought-after visitor posts were at the hospital-based medical schools, which gave one an academic appointment and often first chance at the second pathway, a lectureship in surgery, medicine, or obstetrics. There were, of course, other subjects


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to teach and therefore other posts available. Qualification as a surgeon made “Mr. Snow,” as he was referred to in the medical journals, eligible for an appointment as surgical visitor, and Richardson states that he found a vacancy in the outpatient department at the Charing Cross Hospital. However, he is not listed as such on any records housed in the hospital archives, so at best he had an informal arrangement that never eventuated in a formal position.78 Only physicians were eligible to be medical visitors, and many medical school lectureships also fell to doctors of medicine; whatever his ultimate goal, Snow decided he wanted to attain the triple crown in his field. The bachelor of medicine (MB) was a prerequisite, and only Oxford and Cambridge had offered these degrees in England for several centuries, but since 1828 the University of London in Gower Street, within walking distance of Snow’s flat, had offered both degrees. Table 4.2 lists the requirements for the MB, along with remarks on Snow’s ability to meet each of them. The Hunterian School of Medicine was a “recognized” institution, which permitted Snow to bypass the required lecture courses and proceed directly to the examination when he felt Table 4.2. Prerequisites for a bachelor of medicine (MB) degree examination at the University of London in 1844 Prerequisites

Snow’s Status

At least 19 years old

Age 30 in 1843

Degree in arts from recognized university, or passed University of London matriculation examination

No degree in arts; exempted from matriculation examination after translating a portion of Celsus’s De Re Medica

At least 2 years’ attendance at recognized medical school

Completed full curriculum, Hunterian School of Medicine; one year of courses in Newcastle

Attended course of lectures in four of the following subjects: descriptive and surgical anatomy, general anatomy and physiology, comparative anatomy, pathological anatomy, chemistry, botany, materia medica and pharmacy, general pathology, general therapeutics, forensic medicine, hygiene, midwifery, surgery, medicine

Attended ten of these courses, either at the Hunterian or in Newcastle

Nine months of dissection

Completed at the Hunterian

Course in practical chemistry and ability to carry out common laboratory procedures

Satisfied at the Hunterian; publications demonstrated this facility as well

Practical knowledge of preparation of medicines

Qualified as LSA

Source: University of London Calendar, 1844, 44–45; Alun Ford to David Zuck, 27 February 2001; Julia Walworth, University of London Library, to David Zuck, 4 August 1989.

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he was prepared.79 He took the examinations given on 23 November 1843. To pass he had to demonstrate both theoretical and practical knowledge, answering, among others, questions on how to tell blood spots from rust spots, the poisonous dose of laudanum in an infant and the symptoms it would produce, the determination of pregnancy in a variety of cases, the anatomy of the portal system, the nature of ciliary motion, and the auditory apparatus of the cuttlefish, a fish, and a reptile. He passed, placing in the second division.80 Upon gaining this degree, custom permitted him to replace his surgeon’s designation with the physician’s title, Dr. Snow, although it was increasingly expected that “Dr.” should be reserved for recipients of the MD.81 A year later he was among the candidates at the University of London who hoped to pass the arduous oral and written examinations for the MD degree. All had to show proficiency in philosophy and logic in the form of written commentary on excerpts from Locke, Berkeley, and Leibnitz. All had to translate passages from French and Latin. They had to discuss a case of rheumatism accompanied by chest pain and a heart murmur, a surgical case involving management of bladder stones, and a midwifery case with secondary arrest of labor followed by spontaneous delivery. Finally, they were asked questions on displacement of the heart, scarlet fever, pneumonia, pleurisy, diarrhea, and delirium tremens.82 This time Snow was placed in the first division. Passing this academic milestone also provided a suitable occasion for having his portrait painted for the first and only time (Fig. 4.1).83 Snow now possessed the credentials required for a medical school post. The medical schools of London were in considerable flux at this time; those of the large teaching hospitals, with their attached clinical facilities, were growing in stature and influence and displacing the private ones, a number of which, like the Hunterian, had closed. In the eastern part of London, however, the private medical school in Aldersgate Street had for some time provided stiff competition for the nearby St. Bartholomew’s Hospital Medical School. For many years the Aldersgate school had boasted a string of popular lecturers that the hospital school could not match and for some time brought St. Bartholomew’s (“Bart’s”) to the brink of closure.84 Alfred Baring Garrod, a friend of Snow’s through the Westminster Medical Society, had joined the Aldersgate Street School in 1844 as a lecturer in materia medica. Two years later the lectureship in forensic medicine became vacant, and Snow was appointed. His work on poisons and his knowledge of obstetrics would have been applicable to the subject.85 His first lectures on forensic medicine were duly advertised in the fall issue of the Lancet: one course to be offered in the summer session of 1847. Enrollment required a ticket costing two pounds, two shillings.86 Snow thought highly enough of his academic appointment to add his description as “lecturer in Forensic Medicine at the Medical School, Aldersgate Street” to several papers published in 1846 and 1847.87 However, the school’s fortunes soon fell as its rivalry with Bart’s took a dramatically different turn. Some five years earlier, Bart’s had scored a double victory over its rival by attracting Mr. James Skey, a well-respected lecturer in anatomy, away from the Aldersgate and by appointing the extremely popular James Paget as its new lecturer in physiology. As the years went by it became clear that the Aldersgate School


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Figure 4.1. John Snow, age about 33 (portrait by Thomas Jones Barker, courtesy of Geoffrey Snow; black-and-white reproduction supplied by David Zuck).

could not offer a staff of lecturers in the most basic subjects to rival the reputation of the new Bart’s faculty.88 It was in disarray by the fall of 1848; it was late in publishing a prospectus for the coming session, and when it did the lecturer in forensic medicine was not mentioned. In all likelihood, however, Snow offered the course. The school closed completely at the end of the 1848–1849 session, and the final reward from his short association with it was the privilege of helping pay off its debts.89 Alfred Baring Garrod transferred to University College Hospital, but Snow apparently made no move to seek another academic post.

Snow in 1846: The Mind Prepared—For What? In his first ten years out of medical school, Snow was able to make a living as an urban general practitioner. He attained considerable scientific skill, some degree of professional recognition, and a level of education and certification that took him near the top of his profession. In some other ways he seemed hardly to have left the rural north. He cared daily for the same class of working poor among whom he had

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grown up in York, reinforcing his generally egalitarian outlook. His austere lifestyle fit well with his habitual moral rectitude. He had personally investigated a wide range of medical problems, many of them suggested by his experiences as a practitioner. He had identified with and learned from a group of authorities who represented the most advanced thinking in physiology and chemistry. He had developed rare skills that allowed his mind to flow easily among the three realms of bedside, hospital, and laboratory medicine. Given any medical issue, Snow could readily imagine what would be seen when one examined a patient at the bedside, what sorts of statistical regularities one might uncover by considering a series of cases, how one might elucidate basic mechanisms through laboratory experiments—and, finally, how one could take back to the bedside the fruits of one’s research to improve the care of the patient and the general public health. Snow’s research skills were widely applicable, but he tended to focus rather than scatter his research efforts. From the beginning he had identified respiration and asphyxia as his special province. He devoted special attention to the effect of respiration on the circulation and the chemistry and physics of inhaled gases. He was proving adept at designing apparatuses based on a clear understanding of underlying scientific mechanisms and well adapted to practical needs. He had illustrated his skills and interests in his entire series of scientific publications, perhaps none more striking than the 1841 paper on the resuscitation of the stillborn infant. It was informed by major philosophical questions: What exactly was the dividing line between life and death, living and nonliving? What was the basic difference between an infant born apparently dead but destined to live, and one who would remain dead? What made states of near-death reversible or irreversible? What was the relationship between the oxygenation of the organism and its state of sensibility or insensibility to stimuli such as pain? How could asphyxia be distinguished from other states that resembled it but that had fundamentally different properties? What role did temperature play in all of these processes? All of these questions provided a framework for the scientific investigation of related puzzles that might present themselves to Snow in the future. As 1847 approached Snow had much to be thankful for. Nonetheless, he remained a relatively obscure general practitioner, little known outside two London medical societies and a small private medical school whose best years were behind it. He still had a flat in Frith Street, and he still worked long hours serving working-class patients for the most part. The time and energy available for medical research were limited. No change for the better was on his horizon. Then came news about ether anesthesia.

Notes 1. Richardson, L, ix. 2. Mozart had lodged in Frith Street, Constable had lived there, and Hazlitt had died there. Hare, Walks in London, 126–132; Weinreb and Hibbert, London Encyclopaedia, 295, 779; Cunningham, Hand-Book of London, 193, 445–46.


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3. Robson, Royal Court Guide, 29. We are grateful to Agnes H. Widder of the Michigan State University Library for providing research assistance with the city directories and 1841 census reports. 4. UK Home Office, 1841 Census, H.O. 107/730/3, 10–32 (County of Middlesex, Liberty of Westminster, parish of St. Anne-Soho; Registrars’ districts, Strand/St. Anne Westminster/3). The population may be somewhat inflated because enumerators included overnight visitors. 5. Ibid., 15–16; Pigot and Co., Royal Street Directory of London for 1840, 122. 6. Pigot and Co., Royal Street Directory of London for 1840, 122; Robson, London Directory for 1840, 132. The first city directory listing for Snow that we have found was in 1840. In 1841 the enumerator wrote Williams; UK Home Office, 1841 Census, H.O. 107/730/3, 27. Ten years later, the spelling changed to Williamson, the same used by Richardson; 1851 Census, H.O. 107/1510/82; and Richardson, L, ix. 7. Robson, London Directory for 1838, 163; for 1839, 129; for 1840, 132; for 1841, 136–37; for 1843, 121. “Physicians,” Pigot & Co., Directory of London, 1839, 180–81. 8. S. Snow, JS-EMP, 331–32. For a discussion of the travails of the fledgling Victorian physician trying to set up practice in a town where he has no social relations and connections, see Peterson, Medical Profession, 90–135. Peterson relies heavily on the fictional Dr. Stark Munro, a character created by Arthur Conan Doyle in his semiautobiographical novel The Stark Munro Letters (1895). Peterson argues that the problems faced by Stark Munro were typical of the entire Victorian period. Doyle provided a condensed portrayal of Dr. Stark Munro, with “more in his brains than in his pocket,” in the better-known character of Dr. Percy Trevelyan in the Sherlock Holmes story “The Resident Patient”; Doyle, Memoirs of Sherlock Holmes, 177–78. We are grateful to Christopher Hamlin for pointing out that contemporary medical autobiographies, such as that of Thomas Watson, confirm these points; private communication. 9. On Diamond see Gilman, The Face of Madness. 10. Robson, London Directory for 1841, 136–37; UK Home Office, 1841 Census, H.O. 107/730/3, 11. 11. Richardson, L, xii; Digby, British General Practice, 79. 12. In the 1830s some medical men were paid as little as 2 shillings per person per year; Peterson, Medical Profession, 114–15. 13. John Simon, as head of the medical department of the Privy Council, created a Laboratory Investigation Division in 1865 that employed several physicians on a part-time basis and whose employees eventually became leading medical scientists; Lambert, Sir John Simon, 279–84. Full-time positions attached to medical schools employing physician–scientists remained the vision of reformers rather than an accomplished reality; Worboys, Spreading Germs, 27. 14. Richardson, L, ix–x, xl. He also stated that Snow in later life regretted not having married and had children, noting vaguely, “the fates had been against him permanently on that score”; Ibid., xxxviii. 15. Ibid., x, xxxiii. A reporter at a December 1838 meeting of the Westminster Medical Society noted that “Mr. Snow now made some observations in a very low tone, and consequently his meaning could not be very well caught”; LMG 23 (1838–39): 426. The reporter for the Lancet at the same meeting apparently was sitting closer to Snow and was able to report his statement, which had to do with chemical affinity between gases and the role that played in the amount of oxygen the lungs could extract from the air; “Westminster Medical Society,” Lancet 1 (1838–39): 419. Similar remarks about Snow’s lowness of voice may be found in “Westminster Medical Society,” LMG 23 (1838–39): 954. 16. Richardson, L, xxxix. 17. Ibid., xii. 18. Ellis, CB, 121.

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19. Snow listed himself as a general practitioner in the 1845 London Medical Directory but by 1847 had changed his designation to “physician and accoucheur,” indicating the significance he attached to obstetric work in his evolving career; S. Snow, JS-EMP, 209. Between October 1849 and September 1850, fully half the new patients Snow added to his practice were obstetrical cases; Ibid., 286. By then he was also increasingly restricting himself to administering anesthesia. 20. Peterson, Medical Profession, 99–100. 21. We might wonder how Snow was regarded as a practitioner by his peers. At least some colleagues viewed Snow as a shrewd clinician who could be a valuable ally when faced with a puzzling case. Richardson described Snow’s talents: “He had great tact in diagnosis; an observant eye, a ready ear, a sound judgment; a memory admirably stored with the recollection of cases bearing on the one in point, and a faculty of grouping together symptoms and foreshadowing results, which very few men possess.” Richardson, L, xxxix. Richardson stated that another close associate of Snow’s who had in fact consulted with him on a number of difficult cases, Mr. Peter Marshall, would concur item by item with this description. Richardson’s praise was part of a eulogistic memoriam, and Richardson did not meet Snow until fifteen years after these events. Nevertheless, Snow’s published case reports and commentaries seem to lend some support to Richardson’s opinion. 22. Richardson, L, viii–ix. The importance of medical societies for the development of nineteenth-century medicine, of which Snow’s experience might be seen as a microcosm, is stressed by S. Snow; JS-EMP, 173. 23. S. Snow, JS-EMP, 172. The annual sessions of the medical societies generally ran from early October to early May. 24. Lancet 1 (1842–43): 327; Lancet 1 (1843–44): 163. Snow’s election as vice-president was noticed in AMJ 1 (1853): 218; he added “Vice-President of the Westminster Medical Society” to his by-line in the fourth paper of an eight-part series, “On narcotism by the inhalation of vapours,” LMG 41 (1848): 330–35. 25. “The Westminster Medical Society,” BMJ 2 (1896): 26; Hunt, Medical Society of London, 3–5, 15–18, 73–74. We are grateful to Roy Porter and Caroline Overy for aiding us in identifying these sources. Richardson apparently was still grieving the old Westminster name when he reported in 1858 that the venerable organization had “sunken into” the Medical Society of London; L, viii. However, it was very important that the Medical Society of London’s title to its property not be jeopardized, because it was precisely as a result of owning its own meeting house that the new amalgamated society could be financially secure. 26. Snow’s election as fellow of the Royal Medical and Chirurgical Society was announced in M-CT 26 (1843): xxii. 27. On the social and political orientations of the society, see Desmond, Politics of Evolution, 223–25. 28. See Hardcastle’s requirements for certification as an apothecary; Society of Apothecaries, “Court of Examiners entrance books,” MS 8241/1, 213. 29. A reflection of the new interest in medical affairs outside Britain was the inauguration of the British and Foreign Medical Review in 1836. 30. “Westminster Medical Society,” Lancet 1 (1839–40): 441–44. Snow’s paper was “The anasarca which follows scarlatina”; only the reporter’s summation exists. Scarlet fever was a dreaded disease right up to the introduction of sulphonamide drugs in the mid-1930s; valvular disease of the heart resulted from the associated rheumatic fever. Bright himself was aware of the causative association between kidney disease and an earlier attack of scarlet fever; Peitzman, “From Bright’s disease to end-stage renal disease.” We are grateful to Dr. Peitzman for the further information that William Charles Wells and John Blackall, between 1810 and 1820, had described the relationship between scarlet fever and dropsy, although they did not view


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the dropsy as representing renal disease. While Snow’s observations were thus not original, the recognition of the relationship between scarlet fever, dropsy or anasarca, kidney disease, and albumin in the urine was still fresh in 1839, thereby justifying the reporting of a series of cases; e-mail message; Peitzman to Brody, 27 February 2002. See also Maher, “Origins of American nephrology.” 31. R. Bright, Reports of Medical Cases and “Cases and observations.” See also P. Bright, Dr. Richard Bright, 131–42. 32. The test most commonly used for albumin in the urine at that date was gross and qualitative—heating a teaspoon of urine over a candle flame to see whether coagulation occurred; Peitzman, “Bright’s disease.” 33. No first name is given, but the content of the remarks make it unlikely to have been Thomas Addison of Guy’s Hospital. 34. Golding Bird, it appears, by this time accepted the basic fact that urea accumulated in the blood in Bright’s disease of the kidney. In 1833, as a young student at Guy’s, he had made himself somewhat notorious by engaging in a running debate (in the pages of the LMG) with another student of Bright’s, George Owen Rees, in which Bird had taken the losing side on the question of whether urea was increased in the blood; Peitzman, “Bright’s disease,” 316. See also Coley, “The collateral sciences in the work of Golding Bird.” 35. Snow’s prescribing habits and general mode of practice were not noticeably different than those of the usual general practitioner of his time; see Earles, “Prescription records,” CB, xliv–l. The new discoveries resulting from hospital and laboratory medicine were only slowly applied to therapeutics and did not affect daily practice until very late in the nineteenth century; see Warner, The Therapeutic Perspective, and Durey, The Return of the Plague, 133. 36. S. Snow notes the importance of journal publication in advancing the careers of physicians; JS-EMP, 184. She also notes that when Snow listed his name in the 1845 London Medical Directory, he mentioned five papers he had published and also noted that he was inventor of a new instrument for paracentesis of the thorax and of a sponge pessary; Ibid., 209. 37. Snow, “Arsenic as a preservative” (1838). Wakley’s comment seems gratuitous because Snow had himself admitted that not all dissectors fell ill and that illness might depend on variables such as room temperature. Wakley was an advocate of the clinical–pathological method introduced to London medical schools by Scottish trained surgeons; see editorials about the need for ready access to autopsies and complete case notes for students walking the wards in Lancet 1 (1836–37): 16–17. For his view of scientific medicine, see the book review that “wisely advises” that “the progress of medicine, as an inductive science, is retarded by the construction of hypothetical theories . . . and by the deduction of general principles or conclusions, from a limited number of facts”; Lancet 2 (1831–32): 153. 38. Snow, “Mechanism of respiration,” (1839). Goodman’s paper, read to the Manchester Medical Society, had appeared in Lancet 1 (1838–39): 515–19. 39. Goodman, Lancet 1 (1838–39): 515. 40. Snow, “Mechanism of respiration,” 653. 41. Ibid. 42. In Goodman’s defense, Magendie and investigators following the line of Lavoisier’s investigations of the chemistry of respiration were proposing new concepts in physiology so rapidly that one medical man complained, “How often does it fall to the lot of the student of physiology to unlearn what he has been at pains to acquire!” See Williams, Observations, 7. 43. Desmond, Politics of Evolution, 342, 346–47. 44. For a contrary interpretation, see P. E. Brown, “Autumn loiterer” and “Another look.” Snow’s harshest critic, Brown considered him an upstart who sought instant visibility by attacking an older, established medical man. 45. For brief synopses of the work and influence of these two figures in nineteenth-

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century medical science, see Porter, Greatest Benefit, 327–29, 333–34, 337–38. Müller and Magendie were perhaps less influential than the students they trained—Hermann von Helmholz (1821–1894) and Karl Ludwig (1816–1895) in Müller’s case, Claude Bernard (1813–1878) in Magendie’s. Snow lacked the expanded laboratory facilities those investigators enjoyed some years later on the Continent. Snow remained in the generation of experimental physiologists who mostly studied intact animals and who had limited abilities to derive quantitative data. The capability of isolating specific organs and tissues for physiological experiments and deriving precise measurements of their functions was beyond Snow’s facility at that time. 46. “M.H.,” “Note on respiration and asphyxia,” Lancet 2 (1838–39): 240. 47. Snow, “On asphyxia, and the resuscitation of still-born children” (1841–42), 227. 48. Lancet 2 (1838–39): 352. 49. Snow did not publish in the Lancet again until 1846, when he sent a brief epistle attacking homeopathy, with which he believed Wakley would sympathize; Lancet 1 (1846): 229. Indeed, Wakley appended a favorable comment. 50. “Westminster Medical Society,” LMG 24 (1838–39): 60, 62. 51. Ibid., 61. Snow published these results several years later; see “On the pathological effects of atmospheres vitiated by carbonic acid gas, and by a diminution of the due proportion of oxygen” (1846). Because it is difficult in this article to separate the experiments he undertook in 1838 from those that came later, we have relied on the synopses reported in the medical journals. 52. Ibid. 53. We have omitted from Table 4.1 Snow’s letter “On the use of the term ‘allopathy’“(1846), in which he dismissed homeopathy as an unscientific fad. The letter is not properly a scientific report but rather an expression of political opinion. 54. S. Snow agrees that the contents of these early papers show Snow concentrating on respiration, but she also claims that he indicated an equal interest in “epidemic disease”; JS-EMP, 203. We have found no evidence of the latter. 55. “On distortions of the chest and spine in children” (1841). 56. Snow, “On asphyxia, and on the resuscitation of still-born children” (1842); “Westminster Medical Society,” Lancet 1 (1841–42): 132–34. Shephard considers this paper particularly significant for Snow’s later anesthesia research; JS, 45. 57. Owen, “A man called Read.” Read (1760–1847) was born in Sussex and trained as a horticulturalist. He invented a brass syringe for spraying plants and, having read reports of deaths from poisoning, modified it for use as a stomach pump. He was taken up by Sir Astley Cooper and opened a workshop in Southwark, near Guy’s Hospital, moving later to Oxford Circus. Versions of his pump, which was used also as an enema syringe, are illustrated in Brockbank, Ancient Therapeutic Arts, 53–56. 58. Snow, “On asphyxia,” 226. 59. “Westminster Medical Society,” Lancet 1 (1841–42): 149–51. 60. “Westminster Medical Society,” Lancet 1 (1841–42): 212. 61. Ibid., 213; Hunter, “Proposals for the recovery of persons apparently drowned,” discussed by Zuck, “Diagnosis of death.” 62. The remarks in which Snow most fully developed his vision of medicine and the collateral sciences came later, when he assumed the presidency of the Medical Society of London; “Medical Society of London,” Lancet 1 (1855): 292. 63. Snow, “On the paracentesis of the thorax” (1841). 64. Ibid., 705–06. 65. Ibid., 707. In a footnote the editor of LMG added that although Snow had provided a drawing of the instrument, the description in his text was so clear that it was not thought necessary


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to have an engraving made. According to Zuck the innovative nature of Snow’s apparatus had not been fully appreciated; “John Snow on paracentesis of the thorax.” His invention was the precursor of all trocars and canulas and all exploring and spinal needles fitted with a stopcock, of which there are many to be found in instrument catalogues. Until 1920 the routine treatment for empyema was still rib resection and open drainage, and many died as a result. Matters came to a head during the 1918–1919 influenza epidemic, when a large number of victims suffered from the complication of streptococcal empyema. The death rate among American servicemen as a result of open drainage was so appalling, seventy percent in some centers, that an Empyema Commission was set up to find the cause. Its report pointed out the fatal error of the neglect of the physiology of the open chest wound; Coope, Diseases of the Chest, 376–77. 66. After Snow presented his new instrument for paracentesis, he had to defend the proposition that it was bad for air to be admitted into the pleural space as the pathologic fluid was withdrawn. Dr. William Addison, Dr. Frederick Bird, and Dr. Golding Bird all defended the view that air in the pleural space was harmless—or at any rate, that as air was much more easily compressible than a liquid, replacing the pathologic fluid with air would be a therapeutic advantage. Snow had to go back and restate the basics of the physics and physiology of respiration, adding that while air was an elastic and compressible fluid, in the pleural cavity it would expand during inspiration and be compressed during expiration, thereby impeding lung movement. In this instance, at least, resistance to Snow’s ideas crossed the “generation gap” within the society; “Westminster Medical Society,” Lancet 1 (1841–42): 484–86. 67. Snow, “Circulation in the capillary blood-vessels” (1843). Snow had mentioned his preferred theory of capillary circulation in “On asphyxia” (1841), 224. 68. Snow, “Circulation in the capillary blood-vessels” (1843), 810. 69. Snow was at his most preliminary and least speculative mood in this paper: “I have nothing to advance respecting the intimate nature of the attractions and repulsions which accompany the changes of composition at the capillaries, and which tend to move the blood in a definite direction. I have carefully avoided such terms as chemical, electrical, and vital, both in order that I might not be misunderstood, and because I look upon chemical affinity, electricity, and vitality, rather as expressions which are useful to us in the infancy of science than as forces which have a separate and defined existence”; Snow, “Circulation in the capillary blood-vessels” (1843), 813. By contrast, in CMC ten years later Snow would speculate more fully on the (chemical) nature of these forces and processes. 70. “Circulation in the capillary blood-vessels” (1843), 813. Snow’s proposal to classify a series of medications as belonging to a single family might at first glance appear to be a standard move of his time, following in the Linnaean tradition made popular in English medicine by Sydenham and Cullen. What seems to us distinctive is Snow’s use of underlying chemical properties and mechanisms, and not merely similarities in clinical effects, as part of the rationale for creating the “family.” 71. Porter, Greatest Benefit, 320–21. In the 1840s and 1850s microscopes had relatively poor resolution, and no chemical stains were available. Snow’s avoidance of microscopy ran counter to the recommendations of one of his virtual teachers, the physiologist Müller, who particularly emphasized that branch of science; Ibid., 327. 72. Richardson provides a picturesque account of the timid young Snow being largely ignored when he ventured his first comments at the meetings of the Westminster and only very slowly winning the respect of his elders; L, ix. The records of the meetings as published in the Lancet and LMG suggest otherwise. Snow seems to have been an active discussant almost from the beginning of his involvement with the Westminster, at least following his role in the investigation of the arsenical candles. If anything, he spoke with greater frequency during his early years in the society than later.

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73. For these meeting reports see the notices for “Westminster Medical Society”respectively in LMG 24 (1838–39): 255–56; Lancet 1 (1842–43): 184; MTG 4 (1852): 22–24; MTG 10 (1855): 167–68; and Lancet 1 (1855): 242–43. 74. “Westminster Medical Society,” Lancet 1 (1838–39): 771–73; “Westminster Medical Society,” Lancet 2 (1838–39): 200; “Psychotherapeia,” MTG 6 (1853): 331–33; “The Indian plague and the Black Death,” MTG 7 (1853): 614–15; “Physiological meeting,” MTG 7 (1853): 541–42. 75. Richardson, L, xiii. One would guess that any friend of Snow’s from those days would probably be active in the Westminster Medical Society. Peter Marshall served as president of the Medical Society of London in 1869, the year following Richardson’s term in office. On at least one occasion Snow returned the favor and assisted Marshall in some research. On 14 September 1846 Marshall read a paper on sudden death before the Westminster and acknowledged that Snow assisted him in the autopsy; Lancet 2 (1846): 586. 76. Snow’s health appears to have been indifferent from his student days. Parsons recalled that Snow periodically suffered from fever and rapid pulse after minor injuries and often experienced fatigue, even though Snow was able to complete all but the last mile of a fifty-mile, one-day walk on Easter Monday, 1837; Richardson L, vi. Sometime before 1845 he also developed symptoms suggestive of incipient pulmonary tuberculosis but “took plenty of fresh air, and recovered”; L, xiii. 77. The modern view is that Snow suffered from longstanding hypertension that caused his premature death by stroke; Shephard, JS, 70. Hypertension could result from kidney disease or could itself be a cause of kidney disease. 78. Richardson, L, x. An exhibit about Snow at the London School of Hygiene and Tropical Medicine in May 1855 included a poster that stated, “In 1838 he became a visitor to the Out-patient Department at Charing Cross Hospital”; Clover/Snow Collection, VIII.2. He is not listed as such in the hospital minute books between 1834 and 1845, although an informal appointment is a possibility because Charing Cross Hospital was affiliated at that time with Westminster Hospital, where Snow trained in 1837–1838; search undertaken by Howard Hague (assistant librarian, Charing Cross Hospital), electronic communications to Brody, 27 March 2002 and 21 June 2002. Although Snow never included an affiliation with Charing Cross as a by-line in his early articles, he began a late paper as follows: “On commencing, in the year 1839, to see a considerable amount of practice amongst the poor of London, chiefly the out-patients of a public hospital, I was very much struck with the great number of cases of rickets”; “Adulteration of bread as a cause of rickets” (1857), 4. 79. For a contrary but undocumented view that Snow had to complete additional lecture courses, see Shephard, JS, 38. 80. These questions, mostly from the forensic medicine portion of the exam, were reprinted in Lancet 1 (1843): 195–96. Julia Walworthy (University of London Library, Paleography Room) in a letter of 4 August 1989 to Zuck confirmed Snow’s position among the successful candidates. 81. Richardson, L, xii. The reported minutes of the meetings of the Westminster Medical Society reflect this change in Snow’s title. 82. Shephard, JS, 39–40. Copy of the original MD examination from the University of London Library provided by Zuck, who believes that some of Snow’s research papers in 1843 and 1844 may have been by-products of preparations for the MB and MD examinations. 83. For specific questions, Walworthy to Zuck, 4 August 1989. The name of the portraitist and the year it was painted remained unknown until Zuck, “Snow, Empson and the Barkers of Bath.” 84. In 1829 the Lancet advised St. Bartholomew’s prospective students to divide their attention: “Follow the teaching of Lawrence, Stanley and Earle at Bart’s, and go to the Alders-


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gate Street School to learn from Clutterbuck in medicine, Cooper in chemistry and pharmacy, Waller in midwifery, King and Evans for demonstrations in anatomy”; Lancet 1 (1829–30): 47, quoted in Cope, “The private medical schools of London,” 101. Dr. Henry Clutterbuck (1767–1856), besides being a distinguished lecturer on medicine, was an early president of the Westminster Medical Society; Story, “Henry Clutterbuck.” 85. “Gossip of the week,” MT 14 (1846): 68. A number of legal issues in medicine related to paternity and determining whether a woman was pregnant and the date at which she became pregnant. Other legal issues related to determining cause of death, including cases of poisoning. One of the few publications in which Snow assumed the role of a forensic specialist was ON, Part 14 (1850), in which he addressed the question of detecting chloroform administered antemortem in dead bodies. He mentioned several times having consulted with Dr. Alfred Swaine Taylor, author of a popular textbook of medical jurisprudence and perhaps the foremost forensic expert of the day, and he described his own investigation of tissues taken from “a woman who was found dead, under mysterious circumstances, in the Wandsworth Road” (327), which turned out to be negative for chloroform. 86. Lancet 2 (1846): 345. A similar notice appeared the next year: Lancet 2 (1847): after 362. 87. The first such paper was “Some remarks on alkalescent urine and phosphatic calculi” (1846). This paper, incidentally, earned Snow praise from another quarter. Golding Bird wrote a treatise on urinary deposits that went through four editions. In the last he praised Snow’s experiment on urine alkalinity for its elegance and conclusiveness. Snow’s experiment involved keeping newly voided urine in an upper vessel at a temperature of 100⬚F and dripping it into a lower one at about the rate at which it enters the bladder. The upper vessel was emptied completely and washed every six to eight hours, while the lower one always had a few drops of the stale urine left in it. The result was that the urine in the lower vessel was always alkaline, while that in the upper was constantly acid; summation by Zuck. Bird concluded that “These researches afford a strong argument in favour of the practice of frequently washing out the bladder, in cases of alkaline urine”; Urinary Deposits, 280. The problem of alkaline urine, as both Bird and Snow explained, was that it predisposed to the precipitation of phosphates and the formation of encrustation and stones. 88. Cope, “Private medical schools of London,” 103–04. 89. Lancet 2 (1848): 376, 412. For Snow’s sense of irony about paying the debts, see Richardson, L, xiii.

Chapter 5

Ether

N SATURDAY, 19 December 1846, a London dentist, James Robinson, demonstrated the use of ether for the first time on his side of the Atlantic. The demonstration occurred in the study of Dr. Francis Boott, an American living in London, who had learned of the new drug from friends in Boston.1 Sponges saturated with ether were placed in a glass vessel attached to an elastic tube and a mouthpiece. Robinson held this apparatus while Miss Lonsdale inhaled the gas and was rendered unconscious. Robinson quickly extracted a firmly fixed molar from her mouth and just as quickly she regained consciousness. The procedure had taken a scant three minutes. The patient had felt no pain and had not even moved a muscle.2 On receiving his letters from America, Boott had also notified Robert Liston, professor of surgery at University College Hospital.3 Liston and his medical student assistant, William Squire, arrived after the dental surgery performed on Miss Lonsdale, and they observed Robinson administer ether with considerably less success to three or four other patients.4 Liston then consulted Peter Squire, William’s uncle, the queen’s pharmacist, at his shop in Oxford Street. After another unsuccessful trial of ether (from a cloth), Liston had Squire construct an inhaler from part of a Nooth’s apparatus, a device for carbonating water. This apparatus worked better.5 On Monday afternoon, 21 December, with many influential people in attendance, Liston prepared to perform two operations, an amputation at the thigh and removal of a

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toenail, at University College Hospital. He was uncertain if ether would make patients insensible during major surgical operations. Some practitioners of animal magnetism claimed that they could induce insensibility in test subjects, but mesmeric demonstrations to date were more entertaining than medical. Would William Mortonís claims prove more conclusive? The benches in the operating theater were packed, apparently with medical men and lay folk who were curious about the new agent and its first use in a London hospital.6 Liston is reported to have announced, “We are going to try a Yankee dodge today, gentlemen, for making men insensible,” but when the operation concluded successfully, he exclaimed, “This Yankee dodge, gentlemen, beats mesmerism hollow.”7 Robinson was still worried about the unpredictability of ether when given with the modified Nooth apparatus. He developed alternative specifications for a new inhaler and mouthpiece.8 After several successful dental operations a week later, Robinson was emboldened to give Boott another demonstration, which was successful. Then on Monday, 28 December, Robinson performed a dental operation with ether anesthesia “with the most perfect success in the presence of my friends—Mr. Stocks, Mr. Snow, and Mr. Fenney.”9 In this way John Snow saw with his own eyes what ether could do.

Medical and Public Reaction News of ether as an anesthetic agent had begun to swirl about London even before Robinson’s first demonstration. A day earlier LMG trumpeted, “animal magnetism superceded—discovery of a new hypnopoietic.” The editor noted that the writer claimed “the process simply consists in causing the patient to inhale the vapour of ether for a short period, and the effect is to produce complete insensibility, —or . . . intoxication.”10 But LMG’s endorsement was conditional: “Ether is a strong narcotic, and its vapour speedily produces complete lethargy and coma. . . . It must be regarded as producing a state of temporary poisoning in which the nervous system is most powerfully affected.”11 By equating the drug’s power to induce sleep with its ability to kill pain, the editor had begun to ponder the mystery of this new condition. Within a week of the announcement in LMG, Liston hailed anesthesia as successful based on his two cases of 21 December,12 but he was soon disappointed when other patients could not be put under at all, or insufficiently so to prevent pain.13 Most medical professionals, however, immediately endorsed ether as one of the important discoveries of the age. In a time when medicine could deliver to the patient precious little in the way of effective treatment and surgery was usually a last resort—a risky and excruciating ordeal—ether seemed to promise a new era in the alleviation of pain and suffering. Despite difficulties in administration and even some deaths attributed to the agent, a general consensus soon emerged that William Morton had

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introduced “a radically new remedy to a profession undergoing massive changes” that orthodox practitioners could use to restore public trust after decades of increasing disillusionment with their heroic therapeutics.14 For example, Robinson described Morton’s discovery fancifully, calling the vapor of ether a form of “steam.”15 Just as steam engines were revolutionizing industrial production and transportation, Robinson believed ether would revolutionize the practice of medicine. The lay press was not far behind the medical journals in addressing the new phenomenon. On 9 January 1847 the Illustrated London News, a popular magazine, carried an illustration of an ether inhaler. The Times blew hot and cold, and the humor magazine Punch greeted ether as a cure for scolding wives.16 If the public thought that the world of medical practice had been turned upside down by this new discovery, they were not far off the mark. Ether brought the lower echelons of medical practice into contact with the elite. It brought dentists into the surgical theaters of teaching hospitals and, in a short while, into the accoucheurs’ chambers as well.17 It permitted medically untrained entrepreneurs to engage in broad and sometimes risky medical practice. Many of the important early discoveries and innovations with ether reflected this confluence of the different social strata of medicine. In the United States dentists like Morton and Horace Wells argued from the outset over patents and priority, while Harvard medical men authorized the validity of their claims. Indeed, ether precipitated great activity along the entire spectrum of medical practice, from storefronts to hospital operating theaters. In 1847 most practitioners were content to enjoy whatever financial benefits ether might bring or, like James Young Simpson in Edinburgh, to flamboyantly champion a powerful drug that magically took away people’s pain. An English physician publicly commenting on ether during the first few weeks of 1847—as Snow did—would initially have been seen as merely one of a number of practitioners jostling for attention.

Snow’s Initial Approach to Ether A variety of English medical opportunists were quickly off the mark and “getting quite into an ether practice” within a fortnight of hearing about its new use as a pain blocker.18 Richardson wrote that Snow encountered “a druggist . . . [who] without the remotest chemical or physiological idea on the subject,” was bustling about town with an apparatus under his arm and evidently doing a brisk business. “If he can get an ether practice,” Snow told Richardson, “perchance some scraps of the same thing might fall to a scientific unfortunate.”19 In 1847 Snow was, in his own words, a “scientific unfortunate”—a telling phrase about the nature of London medical society at midcentury. Nearly ten years of dedication to medical science, including active participation in the Westminster Medical Society and frequent contributions to major medical journals, had brought Snow little recognition as a medical man. The ether phenomenon, however, permitted him

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to bring his laboratory experience and work at the bedside and in hospitals to bear on a number of problems with a chemical agent that was as potent as it was mysterious. He realized straight away that the mixed reviews of the drug’s efficacy were due not merely to technical problems with the apparatus. The problems revealed a basic ignorance about the quantity of the drug to administer and its precise actions within the body. Bedside medical experience was effective in deciding how much powder or solution to measure out for particular patients with certain symptoms, but only laboratory medicine could offer clues to the precise doses of a vapor to administer and for how long.20 In this setting his approach took the form of combining more than a decade of experience with the chemistry and physics of gases, as well as clinical knowledge and experimental interest in respiration and asphyxia, into a scientific understanding of anesthesia with lucrative practical applications. However, for Snow personal gain from the practice of anesthesia was a by-product of his commitment to science and public health. While in America Morton struggled to patent his discovery, Snow never patented any apparatus he designed. On the contrary, he published clear descriptions, including engraved figures, so that others could copy them if they chose. There were problems in the administration of ether, as Liston had quickly realized. Some patients went under peacefully, while others resisted mightily, sometimes spewing vulgarisms that upset the ladies on the observation benches at the operating theater. Robinson tinkered with the inhalation apparatus, especially the mouthpiece, and endorsed his own model. Within a month of the announcement in LMG, there seemed to be as many different inhalers on the market as there were people who called themselves anesthetists.21 Robinson and others were interested in creating a device that was easy to use, but the principles of design were not based to any great extent on the chemistry of ether or the physiology of inhalation. When Snow first witnessed the administration of ether as an anesthetic, he was already familiar with many of its properties. He had experimented several years earlier with “æther and . . . other volatile medicines” while studying the capillary circulation. He had found that ether “separated from the blood in the lungs and escape[d] with the breath . . . in the gaseous form with the carbonic acid gas and watery vapour, . . . in this way lessening congestion and relieving its attendant distressing symptoms.”22 While experimenting in 1843 with ether as a “diapnetic” for promoting respiration, Snow concluded (hastily) that it could be used to promote normal mechanisms of respiration.23 In other words, he had already considered ether as an inhaled medicine that had a discrete impact on the circulatory system. Soon after he saw ether administered, a research agenda took shape in his mind that would occupy him for the next few months. Animal experiments led him to believe that all sentient creatures were susceptible to the effects of ether. Consequently, the inconsistencies Robinson and other pioneers in ether inhalation were encountering could not be due to constitutional variations among the patients; the cause must be that the patients were not receiving as much ether as the administrators

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thought. It was common knowledge among chemists and chemically inclined medical men like Snow that the amount of ether in saturated air depended on temperature, so he decided to determine the concentration of ether vapor in a standard amount of air at different temperatures. The second part of his research agenda was to design an inhaler that would allow control of the amount of ether administered. When Snow began this enterprise he did so working largely at home on his own.24 The medical community began to describe the process of etherization as anesthesia, an eighteenth-century coinage meaning insensibility or the suspension of sensation (its most useful and astonishing effect), but a new science was required to make sense of it.25 In the United States ether was promoted as Letheon—in classical Greek mythology the river in Hades that rendered drinkers oblivious to their past.26 While others may have let this new powerful gas go to their heads, Snow managed to bring an analytic perspective to the mystery of ether. He sought not only to identify its problems but to solve them on all levels, clinical and theoretical, physiological and chemical, individual and collective. His success would transform him from an obscure, struggling Soho GP into a doctor who “was in constant requisition by all the principal London surgeons at their operations, and . . . devoted himself to it as his chief branch of practice.”27 By September 1847 Snow had published On the Inhalation of Ether, a practical and comprehensive guide to the clinical use of ether anesthesia. This book shows that he accomplished four major goals in nine months. First, he had addressed the matter of temperature and determined the precise dose of ether to be given under various conditions. Second, he had designed an inhaler that took advantage of the chemical and physical properties of ether to control the dose in a reliable fashion. Third, he had conducted animal experiments, for which he was sometimes one of the experimental animals, to begin to demonstrate the basic mechanisms by which inhalation anesthesia worked. Fourth, he developed an active ether practice, bringing him a wealth of clinical experience and observations as well as needed financial resources. All four accomplishments occurred simultaneously in the first half of 1847 (Table 5.1).

Controlling the Dosage Two and a half weeks after he had seen his first ether demonstration, Snow attended a meeting of the Westminster Medical Society, where members commented on the inhalation of ether. Most offered case descriptions relating the outcome of attempts to render patients insensible prior to operations—sometimes successful, sometimes not, but, Dr. Snow said that the great effect of temperature over the relations of atmospheric air with the vapour of ether, had apparently been overlooked in the construction and application of the instruments hitherto used. This circum-

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Table 5.1. Snow’s anesthesia research and practice from December 1846 to September 1847 16 October 1846

Morton administers ether for an operation in Boston

19 December 1846

First use of ether for anesthesia in London by James Robinson

28 December 1846

Snow witnesses ether administered by Robinson for dental extraction

16 January 1847

Preliminary table for calculating the strength of ether vapor by temperature

23 January 1847

Displays ether apparatus he designed to control temperature

28 January 1847

First administers ether with new apparatus at St. George’s Hospital

29 January 1847

Revised table for calculating the strength of ether vapor by temperature

4 February 1847

Administers ether with modified apparatus at St. George’s Hospital

13 February 1847

Reads paper at WMS, “Observations on the vapour of ether, and its application to prevent pain in surgical operations”

20 February 1847

Discusses new experiments showing that ether is exhaled unchanged and that production of carbon dioxide is reduced during anesthesia

18 March 1847

Administers ether using apparatus with wider (3/4 inch) tubing

19, 26 March 1847

“On the Inhalation of the vapour of ether”

3 April 1847

Demonstrates a portable apparatus for ether inhalation

6 May 1847

Uses Sibson’s facepiece on his own apparatus at St. George’s Hospital

12 May 1847

“Lecture on the inhalation of vapour of ether in surgical operations”

10 June 1847

Modifies Sibson’s facepiece, adding two swing valves to admit air

September 1847

On the Inhalation of the Vapour of Ether in Surgical Operations

12 November 1847

“Dr. Snow on the effects of ether vapour”—letter to editor of LMG

28 January–2 September Administers ether in fifty-two cases at St. George’s Hospital 3 May–8 September

Administers ether in twenty-three cases at University College Hospital

Source: Lancet 1 (1847); LMG 39 (1847); Lancet 2 (1847); LMG 40 (1847).

stance would explain, in some measure, the variety of the results, and account for some of the failures. The operators did not at present know the quantity of vapour they were exhibiting with the air; it would vary immensely according to the temperature of the apartment, as would be seen by some calculations he had made, and suspended in the room.28

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Snow’s previous work with ether and his extensive experience with the chemistry and physics of gases and the physiology of respiration had obviously allowed him to hit the ground running. He was beginning work on the science of inhalation anesthesia while most of his fellows reported only anecdotal cases in the London medical journals. Snow realized that the volatile nature of ether was the source of the speed with which it acted and subsided and the source of its many difficulties. The colorless, highly flammable anesthetic liquid we know as diethyl ether was commonly prepared by the reaction of sulphuric acid and ethyl alcohol. Chemists had readily synthesized it for many years before its anesthetic properties were discovered. Snow was fortunate that the first anesthetic had been so widely studied from a chemical point of view. In 1802 both Joseph-Louis Gay-Lussac and John Dalton had used it in studies of the rates of expansion of gases.29 Dalton had also investigated ether’s elastic force, its ability to change states easily at room temperature from liquid to gas, as had the chemist Andrew Ure, a member of the Royal Medical and Chirurgical Society. Snow was familiar with Ure’s extensive 1818 paper on “The leading doctrines of caloric,” in which he reviewed Dalton’s findings and produced a table showing the variations in the elastic force of ether, among other vapors, by temperature.30 Snow was also familiar with Dalton’s work showing that “all vapours in contact with the liquid which gives them off ” saturate the air in a proportional manner, depending on the “elastic force,” or what would be known today as its saturated vapor-pressure.31 “It occurred to my mind,” Snow wrote after the fact, “that by regulating the temperature of the air whilst it is exposed to the ether, we should have the means of ascertaining and adjusting the quantity of vapour that will be contained in it.” Several experiments on “the quantity of ether vapour taken up at various temperatures corresponded with calculations” of elastic force in Ure’s table.32 Hence, Snow felt comfortable using Ure’s formula and table in developing the “Table for calculating the strength of ether vapour” (Fig. 5.1) he presented at the 16 January meeting of the Westminster Medical Society.33 He soon realized, however, that while his numbers matched Ure’s, they had both tested ether that was not altogether free from alcohol. He fashioned “a graduated tube, bent in the form of Dr. Ure’s eudiometer” with one leg blocked with mercury and introduced a few drops of ether through the mercury and up the tube. Then he plunged the device into a temperature-controlled water bath, took a reading, repeated at another temperature, and in this way collected his data. He found that saturation ratios were the same, but there were four-degree differences in temperature; at constant barometric pressure, what occurred at 40°F with unwashed ether occurred at 36°F for washed ether (ether from which the alcohol has been replaced by water). By March Snow had constructed a revised table using washed ether, which he considered the most suitable form for inhalation, and presented the results in a way that reflected more closely what takes place physiologically during inhalation.34

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Figure 5.1. Table “suspended in the room” at the 16 January 1847 meeting of WMS and published on 29 January (Lancet 1 [1847]: 99; LMG 39 [1847]: 219).

Designing an Inhaler When Snow published (in two parts, on 12 and 19 March) his first survey “On the inhalation of the vapour of ether,” he immediately hammered out the clinical implications of his laboratory researches: “It will be at once admitted that the medical practitioner ought to be acquainted with the strength of the various compounds which he applies as remedial agents, and that he ought, if possible, to be able to regulate their potency. The compound of ether vapour and air is no exception to this rule. . . .”35 Regulation meant being aware of the concentration–temperature problem with ether and then designing an apparatus that could administer precise

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amounts of the agent. At the time of his first communication to the Westminster Medical Society (16 January 1847), after describing his findings on “air, saturated with the vapour of ether” at various temperatures, he announced that he would soon be able to demonstrate a “cheap and portable” instrument, currently being contrived “on the plan of the inhaler of Mr. Jeffreys. . . .”36 Even the first, imperfect table for determining the amount of ether in air at various temperatures was sufficient for Snow to design an ether inhaler quite different from others on the market. The inhaler used in Liston’s operations, “contrived by Mr. Squires [sic], of Oxford-street,” was mentioned often in January 1847.37 The Lancet published illustrations and descriptions of various apparatuses for administering ether. On 13 January the Pharmaceutical Society exhibited a variety of inhaling devices.38 Many of the early inhalers were made of glass and contained a sponge onto which liquid ether was poured. A chemist, Jacob Bell, had devised a new simplified glass flask inhaler that was used in a normally excruciatingly painful lithotomy; the patient felt no pain “after blowing the horn,” and remained in a “dreamy and ‘very comfortable state’” during the evening following the operation,”39 but, in general, the results of administering ether with these inhalers were inconsistent. Snow reasoned that as the ether changed state from liquid to gas, it absorbed heat from the surrounding atmosphere. Because glass is a singularly poor conductor of heat, the air temperature inside the inhaler dropped, reducing the quantity of ether vapor at full saturation. Patients as a result inhaled insufficient amounts to render them insensible. Snow, therefore, designed an inhaler in which the administrator could control the air temperature by “placing it in a bason [basin] of water, warmed or cooled to a given temperature. . . .”40 On Saturday, 23 January at the meeting of the Westminster Society following his first communication on ether, he demonstrated the apparatus constructed on the basis of his design by Mr. Daniel Ferguson, surgeon’s instrument maker and cutler in Giltspur Street. It consisted of a round tin box four or five inches in diameter and two inches deep (Fig. 5.2). There was an opening at the edge through which the air entered a metal tube coiled around the outside of the box, which led to the inside. The idea was to warm the inhaled air before it entered the vaporizer. Internally the vaporizer had been designed to maximize ether uptake. It contained a metal spiral, or volute, which directed the inhaled air over a much longer ether surface than its area would otherwise have allowed. The spiral plate had been soldered internally to the top surface and almost reached the bottom, and the air had to circle over the surface of the ether three or four times. Snow chose a diameter (6˝) and depth (1.25˝) of the chamber and size of the coils (5/8˝ between coils) that maximized the surface area contact between air and ether and that could contain enough ether, without sloshing, as the patient breathed. From the center of the top of the box a removable flexible tube led the saturated vapour mixture to a mouthpiece, which contained valves to prevent the return of expired air into the apparatus. There was no sponge to create an obstruction, and the box was made of metal, which was a good

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Figure 5.2. Snow’s first inhaler, demonstrated at the WMS on 23 January 1847. “It consisted of a round tin box, two inches deep, and four or five inches in diameter, with a tube of flexible white metal, half an inch in diameter, and about a foot and a half long, coiled round and soldered to it. There was an opening in the top of the vessel, at its centre, for putting in the ether, and afterwards attaching the flexible tube belonging to the mouth-piece. In the interior was a spiral plate of tin, soldered to the top, and reaching almost to touch the bottom” (Lancet 1 [1847]: 120–21).

conductor of heat. The apparatus was portable and cheap. In use it was placed in a basin of water at a temperature that corresponded to the proportion of vapour that the operator wished to give.41 The metallic chamber easily conducted heat from the water bath to the air–ether mixture passing through it, preventing the ether from cooling for the relatively brief duration of most operations. Snow based the shape of the coils in the spiral chamber of his inhaler on the design of Julius Jeffreys’s volute humidifier published in LMG in 1842.42 This is another instance of the way Snow retained a ready acquaintance with nearly everything published in the London medical journals in his lifetime. Jeffreys’ device was an apparatus designed for the amelioration of chronic bronchitis by the humidification of air. Snow had consulted Jeffreys’s 1842 article describing the humidifier when writing his capillary circulation paper. He had used the humidifier in his clinical practice, and in 1846 he immediately saw its potential for modification into an ether inhaler. Because ether was more volatile than water, Snow’s spiral did not require the degree of involution that Jeffreys had given his. Snow’s inhaler was subsequently modified several times. For example, a tap was introduced to allow air to be drawn in to dilute the ether mixture (Fig. 5.3) Snow also removed the external tube for warming the air. Possibly he came to realize that the very low specific heat of air would hardly influence the uptake of ether, so this added complication of construction was not worthwhile, but his methodology for

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Figure 5.3. Snow’s first modification of his inhaler. Snow first administered ether to surgical patients on 28 January 1847. Because “the sudden access of air highly charged with ether produces irritation and cough in some persons, I was desirous of having the means of diluting the vapour to any extent, and Mr. Ferguson, of Giltspur Street, who has taken great pains to carry my wishes into effect, got a tap cast of wide calibre, opening two ways, by means of which the patient can begin by breathing unmedicated air, and have this gradually turned off as the etherized air is admitted in its place. This tap offers the further advantage of enableing the medical attendant to keep up the state of insensibility during an operation by a more diluted vapour than that which was necessary to produce that state” (LMG 39 [19 March 1847]: 500–01).

knowing and controlling the strength of vapor was very simple and immediately clear. The operator should read from the table the temperature corresponding to the vapor concentration required and adjust the temperature of the water bath accordingly. The specific heat of water being so much greater than that of ether, the temperature of the water bath would remain relatively constant for the short duration of the majority of operations then being performed. Snow mentioned that in one case, with the water at a temperature of 70°F, anesthesia had been induced in half a minute. Soldering the spiral volute to the top plate rather than the bottom made it much easier to pour the ether in and out, and it was also easier to construct. Early in April in response to a request for a portable inhaler, he “laid before the [Westminster Medical] Society a small and very neat apparatus for the inhalation of

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ether.”43 Also made by Mr. Daniel Ferguson, this inhaler was small enough to be carried in the pocket of a coat, yet affixed with wider tubes for the admission of more air than the earlier model. Snow had provided a pocket-sized inhaler, although “he did not intend it to supersede the [larger model], which was better adapted for exact observations.”44 He had also increased the width of the tubing on the large inhaler, and both models employed “a ferule to admit external air into the tube, near the mouth-piece, when required” instead of a “two-way stop-cock” in the tube as it emerged from the inhaler.45 The two versions of the inhaler Snow described in April were little changed in the final model (Fig. 5.4) he described and illustrated in the clinical manual published early in the fall. In this definitive version of the inhaler, a portable “box of japanned tin or plated copper, of the size and form of a thick octavo volume,” functioned as the housing for the spiral chamber and water bath when the apparatus was in use.46 Between operations the box could be emptied of water and used as a storage space for the tubes and face masks. In 1846 the idea of compelling patients to get their air through tubes and valves was, as Snow remarked, “perfectly new” (E, 21). All early inhalers, even Snow’s, obstructed the patients’ breathing to some degree.47 Valves were frequently too small. In some cases the inhaler was placed above the patient’s head so that the heavier

Figure 5.4. Snow’s ether inhaler, used exclusively from June 1847. His description: “A. Box of japanned tin or plated copper, of the size and form of a thick octavo volume, serving as a water-bath when the apparatus is in use, and at other times containing the elastic tube and facepieces. Attached to this by clasps, and moveable at pleasure, is B. The spiral ether chamber, of thin tinned brass, or copper plated with silver. C. Opening in ditto for putting in and pouring out ether, and for screwing on, D. Brass tube, by which the air enters which the patient inhales. E. Another opening in ether chamber for screwing on F. Elastic tube about three feet in length. G. Face-piece. H. Inspiratory valve of ditto. I. The same face-piece compressed, to fit it to a smaller face. S. Section of spiral ether chamber, B” (Snow, E, 16–17).

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ether flowed into the patient’s lungs while the lighter air sat on top, unmixed and uninhaled. Often in these cases anesthesia failed, or worse, insensibility was induced by way of partial asphyxiation. After administering ether for several weeks, Snow decided that the primary cause of most failures was the use of “tubes of too narrow calibre” (E, 21).48 The apparatus he demonstrated in April was fitted with a tube three feet long with an internal diameter of 3/4˝ (after a 5/8˝ tube had proved inadequate). He reasoned that the tube “must be wider than the trachea, to compensate for the resistance arising from friction of the air against the interior” (E, 21). Finding a satisfactory mouthpiece was considerably more troublesome than the modifications required to perfect the basic apparatus. Snow’s first mouthpieces did not cover the nostrils (see Fig. 5.3), so the patient had to breathe through the mouth while the nostrils were pinched shut. Although this method often functioned quite well, it caused trouble for those patients who tried to breathe through their blocked noses—they drew air through their tear ducts, turned blue, or both. In such instances Snow had to free the nose and let them breathe air, delaying the whole process. He tried and discarded several mouthpieces before settling in early May on a face mask “invented by Mr. [Francis] Sibson, of the Nottingham General Hospital. It was made of metal and covered with silk, in the form of a partial mask, and admitted of respiration both by the mouth and nostrils, the border of it contained pliable sheet lead, which could be moulded to the peculiarities of the features, and retained the form given to it.”49 After a month, however, he “introduced two swing valves into it, to supersede the spherical valves he had previously used. The expiratory valve is made to be moved gradually at will from the opening it covers, so as to admit external air and supersede the two-way tap.”50 So, by late spring of 1847 Snow had a complete apparatus with which he could control the dosage of ether. With its constancy of temperature and the anesthetist’s ability to control the concentration of vapor, it became popular, was manufactured by four instrument makers, and was often recommended in the medical journals. Unlike Morton, Snow made no attempt to secure a monopoly on the use of his ideas. He wrote and lectured on his experience and gave freely of his knowledge. His reward was the recognition of his ability by the leading surgeons of his time, which assured an increasing number of consultations and a growing and lucrative anesthesia practice.

Basic Research into Anesthesia While Snow was determining the dosage and concentration of ether at various temperatures and designing his initial apparatus, he was also beginning basic research into the mechanisms of anesthesia. He set out to answer several questions. How uniform was the effect of ether on different species and on individuals within the same species? How did ether render the animal unconscious and free from pain? What

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observable signs and symptoms correlated with different levels or degrees of anesthesia? Snow was so successful at this research program that in a few months he elucidated and formulated most of the basic principles that anesthesiologists use today to design anesthetic vaporizers. At the Westminster Medical Society on 13 February, Snow delivered his first formal paper on ether. He outlined what was known about the compound’s properties, including the fact that in the gaseous state it occupies space when mixed with air. However, he had found by experiments on mice that ether did not produce insensibility by excluding oxygen from the air—that is, cause asphyxia—because “supplying the displaced oxygen did not counteract the effects of the vapour.”51 The distinction between etherization and asphyxia was critically important and poorly appreciated by many at the time because the forms of primitive apparatus then in use commonly interrupted breathing and caused a degree of asphyxia of which the operator was unaware. Asphyxia, while it produced insensibility to pain, was a great danger to life and ended in death. Ether, Snow determined, worked by a very different route. Although its precise physiological mechanism was uncertain, animal experiments suggested to him that ether “allowed the blood to be changed from venous to arterial in the lungs, but probably interfered with the changes which take place in the capillaries of the system. He had ascertained that a little vapour of ether mixed with air would prevent the oxidation of phosphorus placed in it, and considered that it had a similar effect over the oxygen in the blood, and reduced to a minimum the oxidation of nervous and other tissues.”52 This paper shows the range of Snow’s thinking and his creative linking of inorganic chemistry with biology.53 At the society meeting on the following Saturday, on 20 February, Snow brought his earlier experiments to their logical conclusion. Reduction of the metabolic process implied reduced carbon dioxide production, and this he had now demonstrated. Since the last meeting “he had completed some experiments, by which he had ascertained that the vapour of ether was given out again from the lungs unchanged, and that the amount of carbonic acid gas produced during the inhalation of ether was less than at other times: these circumstances he considered confirmed the explanation of the modus operandi of ether which he had previously given.”54 If, as previously, he had been working with mice, the accuracy of his measurements was impressive. There were many reports in 1847 of outright failures to induce insensibility by the inhalation of ether as well as of patients crying out and struggling to varying degrees. When employed in some operations, Snow wrote in his clinical manual, “the ether has often been left off, and given up as a failure, on account of the excitement produced by it, under an impression that it was producing an opposite effect to its usual one, and acting as a stimulant instead of sedative” (E, 33). Such responses were usually attributed to individual susceptibility. Snow disagreed. He thought that every sentient being was susceptible to ether. He had commented early in 1846 on results from experiments conducted on various

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animals seven years earlier: “We find that the birds were uniformly sooner distressed and killed than the mice by corresponding atmospheres [containing different amounts of oxygen, carbon dioxide, etc.]. The human being, as regards his respiratory function, is placed between the bird and the rodent, and we may therefore conclude that the fatal effects of vitiated atmospheres on him will likewise be intermediate.”55 It appears that in his apartment Snow kept a large supply of laboratory equipment (graduated cylinders, pneumatic troughs, etc.), chemicals, and a menagerie of thrushes, linnets, rodents, frogs, and fish upon which to experiment. When he began investigating the physiological responses to the inhalation of ether, his home laboratory was as prepared as was his mind. In January 1847 he made “a few experiments on small animals” (E, 33). In one he placed a bird inside a jar filled with known proportions of ether and air for very specific periods of time, generally one to fifteen minutes. He carefully monitored the effect of the gas on the subject, noting how quickly the bird went under and how quickly it recovered, pricking it to check for a reaction to pain. He repeated these experiments with small rodents and soon reached the conclusion that “ether acts in a very uniform manner on the various classes of animals. The difference in the time they take to become affected and to recover, depends on the difference in the activity of the respiratory and circulatory functions.”56 He found that birds reacted most quickly, rodents less so, frogs slower than rodents, and fish, breathing air via water, slower still. The respiratory law was the same as in his earlier experiments on vitiated atmospheres. “There may be persons,” Snow asserted, “on whom [ether] does not act favorably, but I believe that no sentient being is proof against its influence.”57 He undoubtedly confirmed the “principle that there is no person who cannot be rendered insensible by ether” (E, 33) on his own thirty-three-year-old body, using a timepiece to determine rates of induction, unconsciousness, and recovery. Variations in human reactions depended mostly on size and respiratory and circulatory factors, not a vague and unprovable constitutional disposition. Children and youths were like linnets, with rapid breathing and small bodies and therefore easier to anesthetize than adults. If some adults became excited when administered ether or some alcoholics seemed impervious to its influence, the explanation was simple: the quantity of ether had been insufficient to suspend their “cerebral functions . . . altogether” (E, 33). In very short order Snow had established two basic principles that would inform much of his research: (1) There is a universal susceptibility to ether, and (2) the rate at which a regular dose of ether affected a body was dependent upon the rate and efficiency of breathing and blood circulation.

Five Degrees of Etherization In early May 1847 Snow’s portrait was on display in the National Gallery in Trafalgar Square in the rooms occupied by the Royal Academy of Arts. In addition, he had

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been invited to present a lecture–demonstration at the United Service Institution for its medical members, including physicians in the army and the Royal Navy.58 Snow used this lecture to cover many aspects of ether anesthesia. Early in the lecture, he suffered a mishap. He placed a thrush in a jar containing one-third ether vapor and two-thirds air. He turned to his audience and summarized the two principles of etherization he had formulated—that while all animals are susceptible, differences in the time it takes to render a particular animal insensible and to recover depend on “differences in the activity of the respiratory and circulating functions.”59 When he next looked at the jar the bird was dead. Snow was embarrassed and immediately admitted, “It is a result I did not intend, and it has arisen from my going on with the lecture, and looking at my notes, instead of directing my whole attention to the animal.” Snow recovered quickly even if the thrush did not. He immediately emphasized the object lesson: “This accident shows the power of the agent.”60 Ether required the administrator’s undivided attention. Such an accident should never happen to human patients as long as they were carefully monitored by trained and observant medical men. Snow thus had an opportunity to emphasize another of his basic themes—anesthesia is a medical procedure and should not be left to dentists, druggists, or the unskilled people who were then often employed to administer ether. Ether is dangerous and requires conservative dosages. He had determined that an upper limit of fifty percent ether to air was required to induce insensibility, but only ten to fifteen percent to maintain it. Snow went on to describe his anesthesia technique in great detail and to suggest its various military applications. On the battlefield ether would reduce mortality by saving wound victims from a second shock, the shock of an operation without anesthesia, which often compounded the damage done by the initial shock of the wound itself.61 Off the battlefield, where malingering was a common problem in military medicine, he suggested ways in which anesthesia might be used to help distinguish between feigned and real disability or deformity. On this occasion he emphasized the way he had combined his experiences in the laboratory and at the bedsides of patients to determine the precise symptoms and signs that allowed him to gauge the depth of anesthesia: I let the patient begin by inhaling only air, and then turn the two-way tap a little at each inspiration, till the etherized air is admitted, to the exclusion of the other. This prevents the coughing which the sudden access of the vapour occasions in some persons. . . . I usually get the tap quite turned on in a quarter of a minute. I find that consciousness and the power of voluntary motion are soon lost, generally in the first minute, and for some time before a surgical operation could be commenced without causing pain, and awakening the patient. . . . As the patient gets under the influence of ether, the limbs become relaxed, and drop down, if not supported, but the eyelids still retain their sensibility, and close again on being opened by the finger, but in a little

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time they cease to do so, or close feebly; the breathing becomes deep, regular, and, as it were, mechanical; and the eyes generally turn upwards, as in sleep. When these phenomena take place, an operation may be commenced, without fear of its causing cries or struggles, or being felt by the patient.62 Snow added that “an observant medical man will have no difficulty” determining when patients are sufficiently insensible for a painless operation. “I have not once been mistaken,” he said, “with respect to the time when the operation might be commenced.”63 By the time that Snow condensed his clinical observations into his eighty-sevenpage monograph, On the Inhalation of the Vapour of Ether in Surgical Operations, he had organized the important signs into five degrees of etherization.64 The degrees were, “in some measure, arbitrary” because they gradually ran into one another and were not always clearly distinguishable (E, 1). Nonetheless, Snow considered them near-infallible guides to monitoring patients undergoing anesthesia (Table 5.2).65 Snow was not the only researcher in 1847 to divide etherization, a continuum, into discrete degrees. In England Plomley had suggested three broad stages early in 1847; Snow’s five degrees parsed the same effects differently (E, 13). In France Longet undertook animal experiments on how the inhalation of ether affected nervous systems and proposed two stages.66 M. Flourens, experimenting on dogs, determined

Table 5.2. Snow’s five degrees of narcotism Degree

Symptoms

First

Patients know where they are and what is happening to them, can direct voluntary movement, and experience tingling in limbs, singing in ears, and dizziness. Some absence of sensation when returning to this stage after insensibility.

Second

Mental functions and voluntary actions may be performed, but in a disordered manner. Patients appear asleep, but groaning, talking, dreaming, and struggle may occur.

Third

Mental functions and voluntary motions cease, eyes no longer react and tend to incline upward; muscle contractions and respiratory contractions may occur, as well as rigidity and spasms. Unintelligible muttering or crying out may occur as patients are being subdued. Conjunctiva does not respond to touch.

Fourth

Breathing stertorous, pupils dilated, no movements except respiration. This degree is seldom necessary for complete insensibility.

Fifth

Respiration becomes difficult, then feeble and irregular. Respiration eventually reaches paralysis or ceases while heart continues beating for a short time.

Source: Snow, E, 3–13.

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the sequence in which ether shut down the brain and nerve centers; Snow used Flourens’s study as a physiological basis for the signs he described.67 Snow’s refined formulation suggests that he was concerned with degrees of narcotism as distinct from simple etherization. That is, he was interested in the total effect of the agent on the body, not just the the elimination of pain. His scheme enabled the anesthetist to read the signs of an etherized body. Snow remained committed to the general principle that all humans, like all animals, were subject to the influence of ether, but he had seen in the laboratory how some factors, such as body size and respiratory rate, could predictably alter the response. As he gained increased clinical experience and as he organized his anesthesia experiences into a formal case series, he realized that individual differences reflecting class, age, body type, and health might also affect response to anesthesia in understandable and predictable ways.68 For example, the effects of ether might be different in patients suffering from diseases of the lungs or heart. He could also be quite precise in predicting how long each degree might endure. For example, he wrote: “If etherization is carried to the fourth degree, complete insensibility usually continues for three minutes after the inhalation is discontinued . . . A state of unconsciousness usually lasts five minutes longer, a period during which any pain there might be would not be remembered afterwards” (E, 42). Snow’s specific concerns with degree and duration of anesthesia reveal a broad and abiding commitment as a clinician. In the previous example he was informing surgeons how much time they should expect to have for a particular operation on a patient in a given state (in this case a harelip, which would necessitate removal of the face piece).69 He was also suggesting that conservative approaches to anesthesia were highly desirable for patient welfare: Use as little as possible to keep the patient as deep as necessary, but no more. In his elaboration of five degrees of narcotism, Snow continued an intellectual process from his student days. His fundamental premise, that susceptibility to narcotism is a universal phenomenon affecting all classes of animals, challenged a central tenet of traditional bedside medicine—that the unique constitution of each patient always trumps what physicians know about human physiology in general, whether conceptualized as humoral fluids, inflammation, nervous irritation, etc., but instead of rejecting the bedside medical perspective outright, Snow reconfigured it as a practical extension of hospital and laboratory contributions to a new medical specialty. He made careful observations of patient reactions during etherization, and these observations constituted case studies of the sort urged by practitioners of hospital–clinical medicine. Because the variables Snow observed were qualitative and did not vary in kind among the patients in the case series, there was no need for a statistical analysis, and there was always the laboratory in which to deepen his understanding. As he wrote a year after his first presentation on ether inhalation at the WMS, “There can be no doubt that these degrees of narcotism correspond with different proportions of vapour which are dissolved in the blood at the time— proportions which I hope to be able to determine.”70

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Snow’s Anesthesia Practice Snow’s anesthesia practice—in the operating theaters of hospitals for the lower classes of patient and in the private quarters of surgeons and dentists for the upper classes— came to serve two major purposes. It brought him increasing financial security and valuable contacts within the social world of London medicine, and it served as a vital extension of his home laboratory. His success as a skilled administrator with a reliable inhaler gave him entrée to the surgical theaters in a number of London hospitals, especially St. George’s and University College Hospital.71 By the time he addressed the military surgeons and physicians at the United Service Institution on 12 May 1847, he could state that he had “given the ether for a great number of operations in private practice, in addition to twenty-eight operations, most of them serious ones, in St. George’s Hospital.”72 When he published On the Inhalation of the Vapour of Ether in September, he could include detailed reports of seventy-five operations (E, 56–76). Snow first administered ether publicly during three operations at St. George’s Hospital on 28 January. He did so “by means of the inhaler described and depicted in [the] last number” of the Lancet. He was then still trying to refine his apparatus and his technique and experimented with water-bath temperatures of 65°, 70°, and 75°F.73 On 4 February three operations at St. George’s were carried out “in which the vapour of ether was exhibited again by Dr. Snow, in the presence of Sir B. C. Brodie, Mr. Keate, and a numerous assembly of spectators.”74 Two of the patients, a man being operated on for fistula and a woman having a mastectomy, “began by inhaling merely atmospheric air, and when a little initiated to the process, etherized air from the apparatus was gradually let on, by means of a tap, opening two ways, which had been added since the previous week, and which Dr. Snow said Mr. Ferguson, the instrument maker, had contrived” (Fig. 5.3). One of the two surgeons, Mr. Caesar Hawkins, addressed the audience on the benches of the operating theater afterwards: “he wished publicly to express the thanks of himself and colleagues to Dr. Snow” for inventing an apparatus “he considered . . . very much superior to those they had previously used; and it had the great advantage of enabling us to regulate the proportion of vapour administered.” 75 In May, when Snow was the anesthetist for Liston, the surgeon was so impressed that he changed from skeptic to cautious advocate of ether inhalation when administered according to Snow’s guidelines: “Dr. Snow managed the ether better than he had previously seen it given.”76 At this early stage in his practice, Snow made a few mistakes, even if he did not readily admit to them. During his eighth operation as anesthetist at St. George’s Hospital, a woman about to undergo a mastectomy inhaled for four minutes, when it was ascertained by Dr. Snow that the cap which admits air to the ether was not removed, and, consequently, she got no ether, and but little air. This was remedied, and she had the disadvantage of

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beginning the inhalation of ether rather out of breath. It excited some coughing, and in three or four minutes the face was becoming purple, and the pulse feeble and quick, and the features rather distorted. The inhalation was accordingly discontinued, and the operation commenced. She struggled and moaned during the operation; but at the termination of it, having recovered her faculties, she said that she had felt no pain whatever, and seemed in very high spirits.77 His own case report published several months later tells a rather different story: “This patient was suffering from bronchitis at the time of the operation, and the ether caused a good deal of coughing, and was left off somewhat prematurely on this account, and the operation performed” (E, 58). Although the surgeon had mentioned the bronchitis at the time to explain the coughing, Snow omitted his own error noted by the Lancet reporter.78 On another occasion Liston stood ready to excise a diseased elbow joint as Dr. Snow, who administered the ether, placed his apparatus in the cold water of the operating theater, which was 65°[F], and put into it two ounces of ether which was there [sic], a quantity which generally suffices for an operation. The patient inhaled quietly, and the operation was commenced at the end of five minutes. . . . It was found soon after, that the ether was finished, and some one went to another part of the hospital for more; in the meantime, the incisions and directions preparatory to sawing the bones having been completed, the man began to complain, and Mr. Liston waited till he was rendered again insensible, which was in about a minute after the inhalation was resumed . . . . A couple of days later, Snow again administered ether for one of Lister’s patients, “This patient found the ether disagreeable, and wished to leave it off when partly under its influence, but with a little trouble she was partly persuaded and partly compelled to persevere, and soon became quite insensible, and had her finger removed without feeling it.”79 In his own case report, Snow just noted that the elbow excision “went on favourably” (E, 72) and that Mary Mills was “discharged, cured,” thirteen days after her finger amputation (E, 73). Snow’s mistakes were minor and did not affect the outcome of any operation. From his point of view, perhaps, there was no point in reciting them later in a clinical manual intended to show that ether was safe if administered as he described. Certainly the surgeons whom he assisted had great respect from the outset for his facility as an anesthetist. Besides regular work in the operating theaters of St. George’s and University College Hospitals, Snow very quickly developed a thriving private practice in administering ether, particularly in dental operations. He was renowned for his skill in controlling the dosage emitted from an inhaler that was easy to

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use and designed to adapt ether’s physical properties to the alleviation of human suffering. Between mid-May and early September Snow was the anesthetist for twenty-four more operations at St. George’s Hospital, for a total of fifty-two, all of which he described in the clinical manual published shortly thereafter (E, 56–71). In four cases which could not wait for the weekly operating day (Thursdays), another surgeon gave ether using Snow’s inhaler. He also administered ether for twenty-one operations at University College Hospital during this period, for a total of twenty-three at this institution (E, 72–76). Of these operations, twenty-six were amputations of limbs, five lithotomies, six radical mastectomies, and there were a number of operations for hemorrhoids, polyps, diseased testicles, and scirrhous and encysted tumors. Six patients died, five of them from complications after amputation. Snow noted that such mortality rates were superior to those of other hospitals and suggestive that the inhalation of ether augmented the surgeons’ success rate—and certainly did not reduce it. Snow’s purpose in reviewing these cases was to show that “in none of the six cases that ended fatally . . . can the event have been caused, or in any degree promoted, by the inhalation of ether, since there are very sufficient and well-recognized [other] causes to account for the result” (E, 76). He also hoped to demonstrate his own success as an anesthetist: “in no case in which I have given ether did the patient know anything of the operation, except, two or three times, some trivial part of it, such as the tying an additional small artery after the inhalation had been discontinued” (E, 55). The patients Snow anesthetized in hospital settings ranged in age from four years old to seventy-six and were, more often than not, working class. They included William Cowen, a twenty-three-year-old groom thrown from a horse, with a mangled and infected leg, and Samuel Richards, “aged 9, a boy of colour,” with a diseased ankle. Anne Atkinson, an extremely feeble eleven-year-old girl with a badly infected and abscessed leg, survived her surgery but never regained strength and died. While operations on more affluent patients were typically conducted in the patient’s home or the surgeon’s personal premises rather than a publicly accessible operating theater, some hospitals had private wards for people like “A.H., a woman aged 27,” operated on for hemorrhoids; and an unnamed female, from whose nose “Mr. Liston extracted a polypus” (E, 74). Working in hospitals and in private homes as a professional anesthetist must have given Snow a certain epidemiological perspective. Watching all walks of life come under the surgeon’s knife and the controlled doses of his own gas mask gave him ample opportunity to judge the aggregate effects of ether. If his first thought had been to convince himself of the universal power of ether, his hospital work gave him the opportunity to assess its powers on the broadest array of individuals in an extraordinary number of medical, dental, and surgical situations. In short, this experience allowed Snow to generalize about the varied states of anesthesia and to establish norms. He had realized from the outset that when administering ether “to

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determine when it has been carried far enough” was the “point requiring most skill and care” (E, 1). Consequently, he had refrained from administering ether in surgical settings until he had developed a method to deliver precise dosages in a uniform manner. Once he had developed accurate saturation tables and a suitable inhaler, he kept meticulous clinical records on his patients’ responses to different concentrations and undertook parallel laboratory investigations on animals. His knowledge of the chemistry of gases and respiration, skill in designing apparatuses, and attention to the nuances of symptomatology all contributed to an approach to the difficulties of etherization that differed from the ways most of his colleagues responded. Snow’s apparatus was critical to his contributions to anesthesia in its early months, but while his apparatus reflected a physiologically precise, constantly testable, and increasingly sophisticated concept of narcotism, other apparatuses only yielded gradually improved techniques for delivering unregulated amounts of ether to patients. The advances in the latter were technical; the advances in Snow’s were both technical and scientific. Even as Snow’s achievements as an anesthetist were greeted with applause, the medical community of the day often failed to distinguish between Snow’s in-depth, comprehensive approach and the unscientific tinkering of other operators. Even before Snow’s monograph on ether garnered praise in a three-column review in the Lancet, that periodical had given considerable attention to an approach far different from Snow’s.80 In a letter to the Lancet in July, William Morton had announced an improvement he had made in the mode of administering ether. Despite the various modifications he had made to his original glass globe and its valves, he had never been satisfied with any apparatus for the purpose of inhalation. Further experiments had resulted in his abandoning his old inhaler and replacing it by a sponge. This was about the size of the open hand or a little larger and concave, to fit over the nose and mouth. It was thoroughly saturated with ether, applied to the nose and mouth, and the patient directed to inhale as fully and freely as possible. Morton had found the result more sure and satisfactory and the difficulty of inhalation very much reduced or entirely removed. “The beauty and importance of this means is its perfect simplicity.”81 Thus, for some, convenience counted for more than science, but even if Snow might privately have decried these developments, the popularity of Morton’s sponge and similar throwbacks did nothing to reduce the size of his growing practice in London.

The Vicissitudes of Ether As Snow increasingly focused his practice on administration of anesthesia, it became evident that the benefits of ether were growing more complex, as well. It not only prevented pain and shock, it kept patients still. With ether dislocations could be relaxed and treated in minutes, whereas in the past gradual applications of warm baths and emetics were typical and marginally effective treatments. Snow’s comments to

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the military physicians on the use of ether to detect some cases of malingering, revealing as it is of Snow’s willingness to apply ether to all sorts of practical situations, is equally suggestive of the heady power with which ether seemed to render the body open for medical inspection and medical operation. For good or for ill, ether could inspire “a devotion to technological evidence,” could become a means of bypassing the patient’s words, an agent by which the sick person was silenced and converted into an object, a disease entity.82 Ether also seemed to offer new access to the recesses of the mind. In his first formal publications on ether in March, Snow offered some observations about the effects of anaesthesia on the mental processes that were involved in the perception of pain. “Metaphysicians [like Descartes, Locke, and Hume] have distinguished between sensibility and perception—between mere sensation and the consciousness or knowledge of that sensation, though these two functions have, as they supposed, always been combined.” However, he had observed something different. “Ether seems to decompose mental phenomena as galvanism decomposes chemical compounds, allowing us to analyse them. . . . During the recovery of the patient, consciousness, which first departed, generally returns first, and the curious phenomenon is witnessed of a patient talking, often quite rationally, about the most indifferent matters, whilst his body is being cut or stitched by the surgeon.”83 Snow observed that many patients dreamed of early periods of life or “that they are travelling” (E, 11). By the end of his life he would elaborate on this phenomenon, attributing this feeling to a particular set of symptoms. When anesthetics take effect, he explained, patients would frequently experience singing in the ears, dizziness, tingling limbs, darkening vision, and a loud noise; “it not unfrequently happens that a person feels as if he were entering a railway tunnel, just when he is becoming unconscious.”84 For Bernard and Flourens the power of ether to close down the body’s systems in a particular sequence helped to reveal physiological principles. Similarly, for Snow the shutting down of consciousness gave a glimpse into the mechanisms of consciousness. He observed that dreaming took place only in the lighter phases of anesthesia, despite the testimony of patients who recalled having lengthy dreams. He argued that “impression of the length of dreams can of course be no argument as to how long the person was dreaming, and that the impression is often of a longer time than the whole period of insensibility” (E, 11). In one case Snow recorded an example of “the smallest amount of etherization with which an operation can be satisfactorily performed” (E, 49). A knighted gentleman underwent an operation for “two sinuses by the side of the rectum” (E, 50). Toward the end of the operation, which lasted a total of three or four minutes, as the surgeon was thrusting lint into the wound, “the patient flinched and uttered an angry expression; and directly afterwards tried to raise himself up from the sofa, but was easily prevented. In less than a minute, he said he had been in Lancashire disputing with some people” (E, 50). Only eight and a half drams of ether were used. Upon learning that the operation was over he was

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surprised and satisfied. Snow concluded that the “dream about the conversation probably occurred at the moment when he first spoke” (E, 51). Because he was deeply interested in determining whether a given patient experienced pain, he used his degrees of anesthesia to pinpoint the instant of the dream within the hypnagogic flow of ether. He recognized that dream states were dependent on basic mental functions. “I think that there is every reason to presume, that there can be no dreams or ideas of any kind in [deep anesthesia], and that for a short time there is not only, as in a sound sleep, the absence of mental functions, but also the impossibility of their performance” (E, 11). Snow was beginning to explore the possibility that a chemical agent, which temporarily suspended certain molecular processes in human tissues, could affect in a basic way the stuff that dreams and ideas are made on. On the Inhalation of Ether was Snow’s attempt to present the gist of his research in a way that was readily useful for the surgeon and anesthetist alike. It promoted his inhaler and the beneficent and effective use of ether. The reviewer for the Lancet thought Snow had accomplished his purpose and recommended it,85 but the reviewer for LMG resisted the entire spirit of Snow’s work and challenged most of his central assertions.86 While Snow’s apparatus was ingenious, the sponge appeared to have superceded “more elaborate contrivances.”87 Snow was insistent that ether could provide pain-free surgery in a safe manner to virtually anyone, but the reviewer was not so sure. Snow considered children to be favorable candidates for ether, yet the reviewer worried whether children with “latent tubercular disease of the brain,” acute hydrocephalus, or meningeal lesion might prove exceptions.88 Where Snow found ether to increase heart rate, the reviewer feared that it might stop the heart. Where Snow defined the five stages of etherization and advocated a reliable method of distinguishing among them, the reviewer emphasized their arbitrariness and the fluidity with which patients slipped in and out of them. Where Snow claimed that patients feel no pain, the reviewer asked “who shall say through what vicissitudes of varied, and perhaps, fearfully exalted, though afterwards unremembered suffering, the apparently passive wretch is exposed while his stupefied faculties are gradually becoming roused from the state of absolute insensibility?”89 But the LMG reviewer misread and misrepresented Snow’s book. Where Snow wrote, “It is not possible always to avoid having the breathing somewhat stertorous” (E, 39), the reviewer misquoted him as stating, “It is not possible to avoid. . . .”90 Both reviewers failed to mention the bench chemistry that formed the basis for Snow’s assertions, and the error in the LMG review tellingly reveals the kinds of skepticism that Snow’s certainty and precision about ether engendered. Snow saw a consistent pattern where others saw vicissitudes. He thought surgical procedures performed with ether tended to induce favorable terminations from hospital care, whereas others thought this questionable. He viewed the impact of ether as discrete whereas others were concerned about predisposing conditions. In November 1847, not quite a year after Snow first learned of ether as an inhalation agent, news of chloroform as an anesthetic reached London. The emergence

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of this new agent confirmed Snow’s intuition that ether and, before that, nitrous oxide (whose anesthetic properties had been discovered in 1802) were part of a family of inhalants. He would continue the research project he had begun, extending it beyond ether to a more general class of “narcotic” agents. He would soon come to believe “that other agents would be met with more eligible for causing anæsthesia by inhalation.”91

Notes 1. On 16 October 1846 the Boston dentist William Thomas Green Morton gave a successful ether demonstration at Massachusetts General Hospital. Several letters arrived in England between mid-November and mid-December 1846 communicating news of ether inhalation. The first was from a Boston lawyer who was assisting Morton in securing a patent; Ellis, “Early ether anaesthesia,” 69–76. A letter describing Morton’s demonstration from Edward Everett, president of Harvard, to Henry Holland, a London physician, arrived on 2 December. Boott received a letter from Jacob Bigelow, professor of medicine at Harvard and also a witness of Morton’s exhibition, with details and an article on experiments with ether on animals by Bigelow’s son, Henry; see “Surgical operations performed during insensibility,” Lancet 1 (1847): 5–9. On the dispute whether inhalation anesthesia began with Morton or his former partner, Horace Wells, who used nitrous oxide successfully in his dental practice as early as December 1844, see Wolfe and Menczer, I awaken to glory. 2. James Robinson, letter to MT 15 (1847): 273–74. Surgeon–Dentist to the Metropolitan Hospital, Robinson claimed to have been “the first in this country to employ the inhalation of ether as a means of rendering surgical operations painless.” 3. An alternative version is that Liston was present at the 11 November 1846 meeting of the Medical–Chirurgical Society where one of Morton’s assistants, on a visit to London, “demonstrated the anaesthetic properties of ether”; Merrington, University College Hospital, 31. 4. Lancet 1 (1847): 9, reprinted in J. Robinson, Treatise on Ether, 6. 5. Zuck, “Dr. Nooth and his apparatus”; see also Merrington, University College Hospital, 31–33. 6. Woolley, Bride of Science, 226–30, and Winter, Mesmerized, 165–74. For the argument that opponents of mesmerism, including Wakley and Liston, hoped inhalation ether would scuttle what they considered a medical fad, see Winter, 172–83. 7. Merrington University College Hospital, 32–33; Cock, “First major operation”; and Reynolds, Essays and Addresses, 273–74. A description written shortly after the operation by Liston’s assistant (“dresser”), Edward Palmer, makes no mention of Liston’s reaction to the successful outcome; Liston, Casebooks, 11: 221, accurately transcribed by Merrington, University College Hospital, 33. Winter reproduced the painting of Liston’s operation (181) commissioned by Henry Wellcome in 1910, but Merrington says the Wellcome Foundation destroyed it in 1946 because they considered it inaccurate (33). 8. Nooth’s apparatus “had originally been designed for the domestic production of sodawater”; Zuck, “Physics of heat,” 88. 9. Robinson signed his letter “7 Gower Street, 28 December [1846]”; MT 15 (1847): 274. 10. “Medical intelligence,” LMG 38 (1846): 1085; issue of 18 December. 11. Ibid., 1089. A month later, LMG summarized a French editorial that warned unknowledgeable practitioners undertaking surgery by candlelight that ether was not only inflamma-

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ble but explosive. In addition, “operators should bear in mind that ether vapour is very heavy . . . compared with air. . . . Hence it follows, that, when the apparatus is above the level of the patient’s mouth, the respiration of the vapour is much facilitated by its density and its tendency to flow at once into the lungs”; LMG 39 (1847): 219. 12. “Surgical operations performed during insensibility,” Lancet 1 (1847): 5–9. 13. For example, on 1 January 1847 Joseph Clover recorded in his diary that Mr. Squire was unable to fully anesthetize two of Liston’s patients; K. Thomas, “Clover/Snow Collection,” 437. On skepticism among other London surgeons, see Ellis, CB, xviii. Another early skeptic was Nikolai Ivanovitch Pirogoff, professor of surgery at St. Petersburg, who noted that generations of surgeons had learned to steel themselves to the patients’ screams; Researches on Etherization, 3. He changed his views after performing animal experiments designed to show the effects of ether on nerves. He described four degrees of etherization and concluded that the best route to administer ether was via the rectum. 14. Pernick, Calculus of Suffering, 30; Rosenberg, “Therapeutic revolution,” 14–25. Gotfredsen summarized the period from discovery in the United States to its European introduction in John Snow, 13–16. 15. “This new application of steam will be, indeed, a wide blessing; and . . . may lead to results as new, whether in surgery, physiology, or psychology, as the steam of water and its application has been in the physical, domestic, and social existence of mankind”; “Letter from Mr. J. Robinson,” MT 15 (1847): 274, dated 28 December 1846. 16. Adams, “Scolding wives.” 17. In the 29 January issue LMG believed “that Professor Simpson has the credit of having first employed ether vapour in the practice of midwifery” in England. The journal then published an extract that noted that “whilst breathing the ether, the labour pains or throes continued, and yet the mother (to speak paradoxically) felt no pains”; 39 (1847): 218. 18. Richardson, L, xiv. See also Ellis, CB, xviii–xix. 19. Richardson, L, xiv. 20. Pharmacology was still in a rudimentary state; see Caton, What a Blessing She Had Chloroform, 59. 21. Duncum discussed sixteen different inhalers produced in 1846 and 1847; Inhalation Anesthesia, 130–57. 22. Snow, “Circulation in the capillary blood-vessels” (1843), 813. 23. Ibid. He refused to speculate about the forces involved: “I have nothing to advance respecting the intimate nature of the attractions and repulsions which accompany the changes of composition at the capillaries, and which tend to move the blood in a definite direction. I have carefully avoided such terms as chemical, electrical, and vital . . . . Our ignorance, however, of the ultimate cause of these attractions is no argument against their existence; since we admit many laws in science of the causes of which we are ignorant” (813). 24. While there is some question as to where Snow conducted the bulk of his experiments, in “On narcotism,” which ran serially in LMG between 1848–1851, Snow makes several explicit references to work done at home. It was common at this time to set up home laboratories for chemical research. It is possible that Snow conducted some ether experiments at the Aldersgate School of Medicine, where he was an instructor in forensic medicine during summer sessions, but when the school dissolved in 1849, Snow’s pace of experimentation accelerated, an unlikely outcome if the school’s chemistry laboratory had been his primary workspace. 25. Oliver Wendell Holmes is credited with the new usage (letter to Morton November 18, 1846), although the word was used in a similar way by John B. Quistorp, De Anaesthesia in 1718; see also E. Warren, Letheon, 79.

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26. In November 1846 Morton filed for U.S. patent a preparation of ether under the name of Letheon in an attempt to control its commercial exploitation. This effort ultimately failed. 27. Charles Locock, Presidential address, Proceedings, RM-CS 3 (1858–61): 47. 28. “Westminster Medical Society,” Lancet 1 (1847): 99. 29. Gay-Lussac, “The expansion of gases by heat”; Dalton, “Experimental enquiry into the proportion of the several gases or elastic fluids, constituting the atmosphere.” 30. Snow, “Inhalation of the vapour of ether” (1847), 498; Ure, “New experimental researches,” 359 (table 3). See Zuck, “Physics of heat,” on the English context for Snow’s researches, including Cullen, Robert Hooke, Ure, and a reproduction of Dalton’s table of saturated vapor pressures. 31. Snow, “Inhalation of the vapour of ether” (1847), 498. 32. Ibid. 33. Lancet 1 (1847): 99, containing an abstract of the table. The table was published in full on 29 January; LMG 39 (1847): 219–20. See also Zuck, “Physics of heat,” 91–92. 34. For the eudiometer-like instrument, see “Inhalation of the vapour of Ether” (1847), 498–99. “A table formed in this manner is the most correct way of exhibiting the subject, because, since the vapour of ether is absorbed as fast as it arrives at the pulmonary cells, the quantity inhaled will be influenced rather by the volume of the air, than by that of the mixture of air and vapour, provided the patient’s respiration is not obstructed, and it never should be, by the apparatus”; Ibid., 499. 35. Ibid., 498. These were the statements by Snow about ether printed in his own words, rather than as the transcript of a reporter at a society meeting. 36. Lancet 1 (1847): 99. The editor of PharJ missed Snow’s explicit mention of his indebtedness to Jeffreys’ humidifier: “By a remarkable coincidence we find that an instrument identical in principle with that invented by Dr. Snow, was invented some years ago by Mr. Jefferey [sic] as an inhaler”; “Apparatus for inhaling ether,” PharJ 6 (1846–47): 425. Snow clarified the misunderstanding in the following issue: “To the Editor . . . ,” PharJ 6 (1846–47): 474–75. 37. Lancet 1 (1847): 17. 38. “Pharmaceutical Society—13 January 1847,” Lancet 1 (1847): 73. 39. “Correspondence,” LMG 39 (1847): 218–19. Anticipating a modern phenomenon, “Mr. Bell, the Chemist [and inventor of the inhaler] . . . was present, and assisted Mr. Tomes in its application”; Ibid., 219. 40. Lancet 1 (1847): 99. 41. “Westminster Medical Society,” Lancet 1 (1847): 120–21. 42. Jeffreys, “Artificial climates,” LMG 29 (1841–42): 821–22. According to Zuck, Jeffreys considered this humidifier “virtually a throwaway” in the mid-1830s on his path to devising a respirator that would constantly warm and humidify inspired air. Jeffreys patented the design of a respirator in 1836, then demonstrated it at the WMS in January 1837, three months before Snow first attended a meeting as a guest. See Zuck, “Jeffreys—Pioneer of humidification,” 4–6. 43. “Westminster Medical Society,” Lancet 1 (3 April 1847): 388. 44. Ibid., 389. 45. Ibid., 388. 46. Snow, Inhalation of the Vapour of Ether in Surgical Operations, 16; hereafter cited parenthetically in the text as E. 47. In all likelihood many unsatisfactory outcomes could be attributed to “cyanosis resulting from respiratory obstruction,” although most contemporaries did not recognize it as such; Zuck, “Cyanosis,” 1–2. 48. On 18 March Snow used an apparatus with wider tubes than before; “Operations without pain. St. George’s Hospital,” Lancet 1 (1847): 368.

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49. “Operations without pain. University College Hospital,” Lancet 1 (1847): 546. 50. “Hospital reports. St. George’s Hospital,” Lancet 2 (1847): 35. 51. “Westminster Medical Society,” Lancet 1 (13 February 1847): 227. The paper was “Some observations on the vapour of ether, and its application to prevent pain in surgical operations.” 52. Ibid. 53. In mentioning phosphorus Snow was referring to an observation made by Thomas Graham in 1829 that the presence of certain vapors (including sulfuric ether) would inhibit the slow oxidation of phosphorus in air. For a full discussion, see Zuck, “Thomas Graham,” 40. That Snow knew of this observation argues a close acquaintance with the literature of experimental chemistry. The reference to capillary action confirms that Snow’s mindset in approaching ether inhalation involved the application of earlier research interests and experimentation. His reference to the “changes which take place in the capillaries” was to the metabolic processes, chemical reactions that involve the removal of oxygen from the blood and the production of carbon dioxide, and were at that time thought to take place in the terminal capillaries, not, as was thought earlier, in the lungs. According to a contemporary textbook, “As it is now generally believed that the oxygen which enters into the blood combines with the carbon, not in the lungs, but in all the extreme vessels, and in them forms carbonic acid, the evolution of heat throughout the body is thus at once explained—it is a mere instance of combustion in the extreme vessels, the union of carbon and oxygen being always attended by an increase in temperature.” Elliotson, Human Physiology, 238. It was demonstrated some thirty years later that the site of this reaction was in the cells. 54. “Westminster Medical Society,” Lancet 1 (1847): 228. At this same meeting members commented on the effectiveness of different inhalers including Snow’s, which one member “had seen . . . used on many occasions . . . [to] great advantage . . . .” 55. Snow, “Pathological effects of atmospheres” (1846), 54. 56. Snow, “Lecture on inhalation of vapour of ether” (1847), 551. Snow was not unusual in experimenting with ether on animals. Early in 1847 a veterinarian did so on sheep and horses; “Medical intelligence: Painless operations on the lower animals,” LMG 39 (1847): 260–61. A Dr. Gull read a paper at the South London Medical Society; “On the Effects of ether on the different classes of animals,” LMG 39 (1847): 777–78. In Russia Pirogof introduced ether into the bowels of various animals; “New method of etherization.” LMG 39 (1847): 950–51. 57. Snow, “Inhalation of the vapour of ether” (1847), 498. 58. The United Service Institution had been founded in 1830 as a repository for objects, books, and documents connected with the professional arts, science, and natural history and for the delivery of lectures on appropriate subjects. Its premises were in Whitehall Yard, and it had on display, among many other things, such military relics as the swords of Oliver Cromwell and General Wolfe, part of the deck of the Victory, and the skeleton of the horse ridden by Napoleon at Waterloo; Cunningham, Hand-Book of London, 517. 59. Snow, “Lecture on the inhalation of vapour of ether in surgical operations,” 551. 60. Ibid. 61. Snow the teetotler could not resist adding here that the ether and apparatus would not add anything to the necessary baggage, for it would take the place of a far greater amount of brandy. He also avoided mention of a point that had been mentioned in some early French reports: that ether poses an explosive risk; “Westminster Medical Society,” LMG 39 (1847): 219. 62. Snow, “Lecture on the inhalation of vapour of ether in surgical operations,” 552. 63. Ibid. 64. Snow, E. Snow’s publisher, Churchill, still survives as a constituent of the medical publishing house Churchill-Livingstone.

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65. Gotfredsen succinctly summarized Snow’s five stages in John Snow, 22–25. 66. Longet, “Experiments on the effect of inhalation of ether on the nervous system of animals,” Archives de Médecine (March 1847), cited by Snow, E., 13. A translation of an extract appeared in British and Foreign Medical Review 23 (April 1847), 570–72. Longet concluded that narcotism was a form of asphyxia. Snow was unconvinced based on his own earlier studies of asphyxia. In a hypotheticodeductive manner, he devised an experiment on mice to disprove Longet. Snow found that the effects of ether were not dependent on the amount of oxygen in the inspired air, that ether was unchanged when exhaled, and that it was possible that the amount of expired CO2 lessened during narcosis. His conclusion was that insensibility resulted from reduced tissue oxidation, especially in the nerves. See Snow, “Lecture on inhalation of vapour of ether” (1847), 553; and Gotfredsen, John Snow, 20–21. 67. Flourens, “On the effects of inhalation of ether on the nervous centres,” cited in Snow (E, 13). This extract was translated in British and Foreign Medical Review 23 (April 1847), 572–73—the same number that carried extracts from the second of his LMG articles “On the inhalation of the vapour of ether” (March 1847). Gotfredsen noted that Snow’s early animal experimentation with ether was undertaken partially to confirm Flourens’s results; John Snow, 21. 68. Clinical classification, as well as case series development and monitoring, is considered central to the practice of clinical epidemiology. It can therefore be argued that Snow’s ether anesthesia researches in 1847 laid some methodological groundwork for his later investigations into the mode of transmission of cholera, now considered to be pioneering work in the field of epidemiology. 69. Shephard, commenting on Snow’s work from the perspective of a modern anesthesiologist, noted how Snow anesthetized a number of difficult patients, such as those with compromised breathing, and stated that even today with modern equipment Snow’s safety record would be enviable; JS, 271. 70. Snow, “On the inhalation of chloroform and ether” (1848), 178. 71. The attending surgeons whom Snow assisted included Richard Quain, Henry Charles Johnson, Caesar Hawkins, Sir William Fergusson, Robert Liston, and Edward Cutler. 72. Snow, “Lecture on inhalation of vapour of ether” (1847), 553. He did not mention two operations at University Hospital on 3 May. 73. “Operations without pain,” Lancet 1 (1847): 158. 74. “Operations without pain. St. George’s Hospital,” Lancet 1 (1847): 184. 75. Ibid. The apparatus was illustrated the next month in Snow, “Inhalation of the vapour of ether” (1847), 501. 76. “Operations without pain. University College Hospital,” Lancet 1 (1847): 546. 77. “Operations without pain. St. George’s Hospital,” Lancet 1 (1847): 210. 78. Zuck noted Snow’s silence about such mistakes in “Cyanosis.” 79. “Hospital reports. University College Hospital,” Lancet 1 (1847): 639. 80. “Reviews,” Lancet 2 (1847): 410–11. The five stages of etherization, the inhaler, and the case reports were discussed at some length, and the reviewer concluded that “Dr. Snow’s little work . . . will prove valuable to all who undertake to administer the ether-vapour, by giving them very useful rules for their guidance. . . . Some have rejected the employment of etherization in surgery, because it annuls pain, which they deem necessary to success in operating, but we have seen no want of success where it has been resorted to, and if there had been . . . we should be much rather disposed to attribute it to . . . bad surgery, than to the want of pain”, Ibid., 411. 81. “Letter from Dr. Morton, of Boston, U.S.” Lancet 2 (1847): 81. Wakley added a footnote—”the inhalation, by means of a sponge, had been recommended and practiced for some

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time, in this country, by Dr. Smith, of Cheltenham.” The ether sponge replaced all apparatuses, certainly in America, and was the method observed and described so vividly by Charles Tomes during his visit to the Massachusetts General Hospital in 1873. In Great Britain events took a different turn, but when ether was reintroduced at the end of the 1860s, administration was by a sponge also, usually contained in a leather or even cardboard cone. Snow had pioneered the first dosimetric technique for the administration of an anesthetic; the second dosimetric movement, under the influence of the physiologist A. D. Waller, did not begin until the 1890s. 82. Reiser, Medicine and the Reign of Technology, 38–43. Anesthesia can be seen as one element in a line of historical argument that traces the depersonalization of medicine in the nineteenth century as clinical approaches and medical science developed. For analogous arguments, see Foucault, Birth of the Clinic; Jewson, “Disappearance of the sick-man from medical cosmology.” 83. Snow, “Inhalation of the vapour of ether” (1847), 541. Here Snow gives the first description of the state of general analgesia, and this observation was the basis of the ether analgesia technique introduced by Artusio for cardiac surgery a century later; Artusio, “Ether analgesia.” 84. Snow, On Chloroform (1858), 36. 85. Lancet 2 (16 October 1847): 410–11. 86. LMG 40 (5 November 1847): 812–14. 87. Ibid., 814. 88. Ibid. 89. Ibid., 813. 90. Ibid. Snow called attention to this misstatement and its consequences for an understanding of his argument: “Dr. Snow on the effects of ether vapour,” LMG 40 (1847): 859. 91. Snow, “On the vapour of amylene” (1857), 61.

Chapter 6

Chloroform

W

HEN ANESTHESIOLOGISTS WITH A TASTE FOR the history of their specialty read John Snow, they generally turn to On the Inhalation of Ether or On Chloroform and discover comprehensive, albeit dated, accounts of these subjects, but reading Snow’s work from the white-hot years 1847 to 1851 is a very different experience. He conducted research on the installment plan, and he was a serial and accumulative thinker in the golden age of serialization. As the novel-reading public eagerly awaited the latest installment of David Copperfield in Household Words, the British medical world followed the latest developments chiefly via Lancet and LMG. London had learned of ether through articles, bulletins, letters, and journals. Definitive reference works or compendiums were few and far between. Most of the real action was taking place in lectures, medical societies, and journals, and it is in the latter that one finds evidence of Snow’s furiously productive months of research in 1847 on the properties of ether and the risks of administering it, within the context of contemporary debates. Often writing in installments, repeating himself to get new readers up to speed, and modifying as he went, he gradually developed his views on the subject. Then, as the workaholic Snow raced to keep pace with and ahead of developments, the ground shifted unexpectedly. Just as a serial novel might have it, an Edinburgh professor of obstetrics, James Young Simpson, directed the attention of the Medico–Chirurgical Society of Edinburgh to a new agent termed, with all the chemical nicety of the day, perchloride of formyle, or chloroform.

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Pharmaceutical Profiling Ten days after Simpson’s announcement, Snow was at the Westminster Medical Society comparing “the new letheon agent” (as the Lancet described it) to the old one, ether. It was 20 November 1847, only a year since ether’s discovery, but it seemed like an eternity had passed.1 The early storm of excitement surrounding ether had lulled to a calm. Now the Scottish announcement created another storm. A local chemist had given Snow a quantity of chloroform rectified from calcium chloride (expense and ease of production were important factors that Snow never failed to consider). Snow placed this sample on the table for the edification of his colleagues and gave them a favorable report. He had tried chloroform himself and found that it made him no more wretched than ether did. In advance of his comments at the Westminster, he had placed his watch on a table, sat down, and begun to inhale. He felt a pleasant inebriation and thought nothing was out of the ordinary until he noticed that the second hand had disappeared. He found it again only by pressing his nose up to the face of the watch (ON, 4: 334).2 He told the society that chloroform was preferable to ether in some respects. Chloroform affected the nervous system in the same way that ether did; animal experiments had confirmed this. Less pungent than ether, it was more easily inhaled, producing its effects “with great rapidity.” He also noted that it was more economical. “The quantity of it consumed was curiously small when compared with ether.”2a Preliminary surgical trials indicated superior efficiency. A few days before his presentation, using his ether inhaler (water bath at 55°F.) he had administered chloroform for a mastectomy at St. George’s Hospital. The third or fourth degree of “etherization” was induced in less than a minute, and the whole operation used one tenth of what would have been necessary with ether. Snow felt that the speed of its action might even help to bypass the “preliminary excitement” (hysteria, spasms, or convulsions) commonly encountered in the first stages of ether inhalation. He then presented a table, just as he had done with ether, that showed the quantity of chloroform gas that air would hold in solution at various temperatures (Table 6.1). Table 6.1. Quantity of chloroform that 100 cubic inches of air will take up Temperature ⬚ F.

Cubic inches

50 55 60 65 70 75 80 85 90

9 11 14 19 24 29 36 44 55

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Chloroform was almost twice as heavy as ether but took up one fourth the volume, and for this reason it neither excluded as much air nor impeded respiration to the extent that ether did. Simpson administered it by way of a sponge or handkerchief, but Snow preferred the precision and efficiency of his apparatus. With quiet confidence Snow proffered his judgment that chloroform, while not without danger, was faster acting than ether and easier to use. Discussion followed. Dr. E. W. Murphy (professor of midwifery, University College, with whom Snow would work on a number of deliveries in 1848–1849) remained unconvinced. He avoided using ether in labor whenever possible because of the nervous reactions it seemed to cause “both before and after insensibility,” including spasms that resembled “puerperal convulsions.” Murphy feared that the use of ether in labor might cause hemorrhaging. Did Snow think chloroform caused similar excitement? No, he replied, this kind of nervous excitement was caused by the slowness with which it was necessary to give ether. The fast action of chloroform should mitigate this problem during induction, but the nervous reactions would likely occur as the patient recovered. He also suggested that patients do not die from convulsions while inhaling but from continuing to inhale after collapse had appeared and recommended that two practitioners be present for labor and delivery, one dedicated to anesthesia. In other words, Snow admitted that chloroform did cause spasms similar to those seen with ether, but these were neither to be understood as convulsions nor to be dreaded. His recommendation was not to avoid using these drugs but to bring in a specialist. Snow was quick to appreciate chloroform’s properties. It seemed to behave like a concentrated form of ether, generally acting like ether only faster. It fit what was to Snow’s mind an emerging pharmaceutical profile. Simpson had been empirically searching for other anesthetics when he hit upon chloroform, but Snow recognized ether and chloroform as constituting a family of anesthetic agents in which similar chemical composition and properties indicated similar physiological action. It was a matter of calibrating safe dosages for the new drug. There were differences, but chloroform conformed to the pharmacokinetic model (how drugs are absorbed, distributed, metabolized and excreted) that Snow had developed for ether. There were undoubtedly other agents with similar properties waiting to be tested. As early as February of 1847 Jacob Bell, editor of Pharmaceutical Journal, had tested chloric ether (which consists of chloroform in wine spirits) with some success.3 Snow and others returned with fresh eyes to Robert M. Glover’s Harvean Prize essay for 1842 that described bromoform, chloroform, and iodoform. According to Glover, “Great resemblance exists among the properties of this class of bodies, which appear to form a new order of poisonous substances, uniting in themselves physiological properties which are not found united in any other known class of poisons.”4 Snow realized that the medical miracle of ether and chloroform was made possible by a beneficial side effect of a family of toxins.

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In a scant ten days chloroform had moved to the center of Snow’s research, which meant to the center of his life. The extant Case Books of his practice begin in July 1848 (CB, 3), and they chart a widening circle of anesthesia from teaching hospitals and Soho environs to virtually every quarter of London and beyond. Chloroform moved to the center of his thoughts about anesthesia, as he proceeded to make it the basis of his pharmaceutical profile and to build a family of agents around it (as the title of his last work, On Chloroform and Other Anesthetics, indicates). Whatever risks chloroform presented were clearly outweighed, in Snow’s mind, by its benefits. He believed that anyone who followed his methods could work with it safely. Although he would greatly amplify, complicate, and qualify his understanding of chloroform in the ensuing decade, he remained within the paradigm created in 1848. According to Richardson, Snow recalled a talk in which he stated that “in his opinion sulphuric ether was a safer narcotic than chloroform. Why, then, said a listener, do you not use ether? I use chloroform, he resumed, for the same reason that you use phosphorous matches instead of the tinder box. An occasional risk never stands in the way of ready applicability.”5 Snow’s attitude was representative of British medical opinion at the time; according to Richardson, chloroform “was immediately used everywhere to a greater extent than ether had been,” rapidly becoming the anesthetic of choice (OC, 22).6 In 1848 Snow would follow Glover’s lead and expand the range of his investigations beyond one or two specific agents toward a larger concept of a family of drugs that fit the same pharmaceutical profile. His approach was both bold and prudent—bold in its confidence, prudent in the way it controlled the dosage. Chloroform’s very virtues, its power and convenience, made it dangerous, even though many doctors had the impression (largely thanks to Simpson) that chloroform was safer than ether (OC, 22). Within months of its discovery its risks would become all too real; the euphoria of national pride at the Scottish breakthrough that rivaled, perhaps even surpassed American self-satisfaction at having “discovered” ether, gave way, like a serial novel, to death and doubt.

Hannah Greener On 22 October 1847 a fifteen-year-old girl named Hannah Greener was admitted to the Newcastle Infirmary suffering from an ingrown toenail on the big toe of her left foot. The big toe on her right foot was also affected, but less so. She had not had much of an appetite lately but was otherwise healthy. A few days later the surgeon to the infirmary, H. G. Potter, operated to remove the left toenail. Ether was to be used, but the first two inhalers failed to produce the desired effect. A third inhaler (designed by Hooper) did the trick. According to Potter, the patient “screamed during the operation but did not feel any pain.” She had not cried or laughed or exhibited any “hysterical symptoms.” She never paled. Her pulse did weaken but then

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regained strength. Thirty minutes afterward, sans toenail, she was fine, said that she felt no pain, and “was asleep the whole time.”7 On 28 January 1848 Greener’s feet were still giving her trouble, and her family decided to have another surgeon pay a visit to their home in Winlaton (near Newcastle) to have the other nail removed. Thomas Meggison and his assistant, Mr. Lloyd, arrived and found the girl in a fairly agitated state. She began crying from the moment that they walked in and continued to weep as they seated her in a chair and began to administer chloroform.8 Meggison poured about a teaspoonful of chloroform on a “tablecloth” and held it to her nose. After drawing two breaths she pulled his hand down. He told her to keep her hands on her knees and breathe quietly. The girl complied, and in about thirty seconds he observed rigidity in her arm. Her breathing quickened but was not stertorous. Her pulse was fainter than normal but steady. Lloyd began the operation making a semicircular incision in the toe, and Greener’s leg gave a sudden jerk. Meggison thought she might need more chloroform and was about to give her the cloth again when he lifted her eyelids and they stayed open. Then the patient’s face and lips turned white, and she moaned or spluttered. The sound, he later explained, was “similar to the expiration in epilepsy or hysteria.” He dropped the cloth and dashed water in her face. It was no use. He gave her some brandy, laid her down, and tried to bleed her. He opened a vein in her arm but nothing flowed. He tried her jugular with the same result. In total, about a fluid drachm, or three and a half milliliters, of chloroform was used. The elapsed time of the entire process of inhalation, operation, venesection, and death: two to three minutes.9 The next day Sir John Fife and Dr. R. M. Glover conducted a postmortem examination. They attributed the cause of death to “congestion in the lungs” caused by the inhalation of chloroform in combination with the idiosyncrasy of the patient. Meggison and Lloyd were not held responsible for Greener’s death. Dr. Fife argued that “no human foresight, no human knowledge, no degree of science, could have forewarned any man against the use of chloroform in this case.” The jury convened at the coroner’s inquest unanimously agreed,10 but would juries continue to agree if more cases of sudden death occurred? This was both a crisis of medical knowledge and a public relations nightmare for chloroform and doctors, like Snow, who promoted its use. Pain relief was a blessing, but it had its limits. Whatever went wrong had yet to be determined, but it was clear that a procedure to remove an ingrown toenail should not result in the death of a fifteen-year-old girl. In the months that followed the press was full of analyses of the case and soul-searching about the benefits and dangers of chloroform. The same page of the Lancet that carried a report of the inquest into Greener’s death contained an account of Professor William Brande’s lecture on the chemical properties of ether and chloroform. It ended, the report tells us, with a demonstration of Snow’s inhaler and Brande’s endorsement of these chemicals as “of the greatest benefit to the medical profession and to humanity.” Following the account of this well-attended lecture, the Lancet chose to run

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an editorial that scolded Brande for killing a guinea pig during his demonstration of the effects of chloroform. The performance seemed to confirm chloroform’s dangers rather than to highlight its beneficent powers, and this was the last thing the general public needed to see. There were ladies in the audience.11 Reports of other deaths from chloroform began to proliferate.12 In the general press there were calls for abandoning its use. In its “Medical News” column the Lancet reprinted an account from the Scotsman dated 12 February of a young man in his late teens from Aberdeen who had been given to joy-popping chloroform and had been found dead.13 A letter to the Lancet from a Robert Selby musing on the benefits and dangers of chloroform admitted to nearly killing a nine-year-old boy.13a In February in a dental parlor in Cincinnati, Ohio, a thirty-five-year-old mother of six died under chloroform. A Boston man died in March. In May a thirty-year-old woman in Boulogne, France, succumbed. Snow, who assiduously collected and scrutinized every case of death involving the medical use of chloroform, counted thirteen fatal or allegedly fatal cases for 1848. By the end of his career in 1858, these would number more than fifty (OC, 120–222). Doctors using ether and chloroform generally reacted defensively to these adverse reactions and suggested that the proper stewardship of these drugs was the most pressing issue. It was most commonly argued that the agents could be used safely but must be administered by informed, competent professionals. The letters in the Lancet were quick to remind readers that toenail surgery is intensely painful, fully mandating the use of anesthetics despite the fatality that occurred. Simpson led the way with a defense of chloroform. Two weeks after Greener’s death he reviewed the facts of the case and the autopsy as reported in the Lancet, concluding that she must have died of asphyxia; he believed the dose was “so small as to render it exceedingly improbable that it could have been the essential cause of the death of the patient.”14 She appeared to have fainted (syncope) at a critical moment. The water and the brandy used to restore her, Simpson argued, inadvertently caused her to choke and cut off her air, but he did not blame Dr. Meggison for using these techniques, because he had no way of knowing their dangers in the treatment of chloroformed patients.15 Reactions to Simpson’s analysis were generally sympathetic, with important distinctions that reveal the uncertainty surrounding the chloroform-related emergencies. One correspondent agreed that the cause of death could not have been chloroform but believed “that the girl Greener died from the shock of the surgical operation,” not efforts to revive her.16 David Davies, the house surgeon at Loughborough Dispensary, disagreed with Simpson’s analysis. Simpson’s account did not jibe with his or Marshall Hall’s understanding of how anesthetic agents paralyze the nerves. “Would it not have been more physiological to have said,” he wondered, “that this poor woman’s death was owing to the power which anæsthetic agents have, in some very rare instances, of destroying the functions of the spinal and ganglionic systems of nerves.”17 Davies felt that Simpson needed to be more critical of the agent he had discovered.

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Like Davies, Snow disagreed with Simpson as to the cause of death, and he also disagreed with the coroner’s conclusion. Snow sent a letter to the Lancet, stating that the evidence did not support the thesis of syncope followed by asphyxia. While he agreed with Simpson that brandy and water were not wise in this case, he could not agree that they had asphyxiated the girl. Congestion of the lungs and heart, as was found with Greener, was not compatible with fainting prior to asphyxiation. Snow, who was lecturer on forensic medicine at Aldersgate School of Medicine, pointed out that “a certain number of those who are drowned” do not have congestion in the heart and lungs, and it is believed that “those persons have fainted on falling into the water.” The autopsy did not support Simpson’s account and pointed back toward the chloroform and, to Snow’s thinking, toward Simpson’s preferred way of giving it, the hanky. There is a note of accusation in Snow’s critique. “For if anyone could prevent his patient from getting into a state which cannot be looked on otherwise than as one of imminent peril, it would be the authority who introduced that agent, and recommended this method of its administration.”18 Snow wrote Meggison seeking clarification on a number of points and then published his opinion in the LMG. He reasoned that if chloroform had caused death in the manner concluded at the inquest, it “would necessarily invest the inhalation with some degree of danger, however small, and would entail some anxiety on both the operator and the patient. My view of the matter holds out more hope for the future. I look on the result as only what was to be apprehended from the over-rapid action of chloroform when administered on a handkerchief.”19 He believed that the handkerchief had induced a much deeper degree of anesthesia than had been supposed, and the rapid action of the chloroform was carried too far too fast, to the point that it put a stop to Greener’s respiration. Snow had found that the effects of chloroform, unlike ether, seemed to increase for twenty seconds or so after leaving off inhalation, and this would account for the acceleration into a lethal degree. He argued that experiments had shown that a teaspoonful of chloroform was sufficient to induce dangerous levels of anesthesia in a large man, and this would therefore also be possible in a smaller, younger female, even if given in the inefficient handkerchief. In his letter to Meggison Snow asked for details about time and Greener’s symptoms in order to correlate them with the degrees of “etherization” he had established the year before. What was “the nature of the breathing after the inhalation was stopped?” “How long did the patient breathe after the removal of the cloth?” What was the exact nature of the moan? From Meggison’s reply Snow reasoned that the rigidity of the patient’s arm placed her in the third degree. From that position he interpreted all subsequent symptoms as acceleration to the fifth degree. He argued that the overdose stopped respiration and then the circulation, and this was the fundamental cause of death. This was a key moment in the development of Snow’s thought. He noted that some of his more recent animal experiments indicated that in some cases “the respiration and circulation seem to cease together.”20 By October 1848 he would go even further and claim that chloroform at this strength “paralyzes the

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action of the heart at the same time as the respiratory movements.”21 In the ten years of using chloroform that followed this investigation, Snow would elaborate on his theory, especially in response to the commentary of Francis Sibson, who pointed to the heart as the key to the trouble and also mentioned fear as a factor.22 Snow would discuss more cases and complications, but he would never essentially depart from his conclusions in the Greener case.

Concerns: On Narcotism As he had done with ether, Snow looked to the mode of administration as the source of the problem. He concluded that with ether problems typically eventuated in an underdose; with chloroform, however, the danger was an inadvertent overdose. This assessment would turn out to be only part of the story, but in 1848 there were too many other basic questions that needed answering before subtler complications could be pinpointed. He needed to find a way to explain the effects of chloroform and ether in general, and he needed to detail the emerging pharmaceutical profile. What was the appropriate name for it? His former term, etherization, was obsolete. Anesthesia was useful, but it placed the emphasis on the absence of sensation and distracted attention from other phenomena associated with these agents that should be scrutinized. He settled on narcotism, because ether and chloroform closely resembled narcotico-irritants (the Greek narco encompassed both stupor and numbness). Strange as it may sound to modern ears, narcotism in the mid-nineteenth century referred exclusively to narcotic vapors. In an era before the availability of nerveblocking local anesthetics, anesthetists were using gases that produced unconsciousness or stupor. Today, we tend to keep the pain relief derived from anesthetics separate from that produced by narcotics like morphine and heroin, which carry an association with addiction. We also tend to distinguish the main property of a drug from its side effects, which frequently suggest more about a drug’s common application than its properties. For Snow, however, narcotism seemed the most comprehensive term for the entire range of phenomena, and his usage resonates with the term narcosis. In February 1848, with the notes to fifty chloroform cases carefully logged, he announced the next plank in his research agenda. Having established to his own satisfaction that chloroform conformed to the five degrees of etherization, he concluded that there “can be no doubt that these degrees of narcotism correspond with different proportions of vapour which are dissolved in the blood at the time—proportions which I hope to be able to determine.”23 Narcotism was the total effect of the drug on the system, and anesthesia was just one consequence. These drugs could be measured against each other with respect to blood saturation levels, anesthetic and narcotic power, and various other effects. Snow used Flourens’s theory of the cessation of neurological function as a working model of

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narcotism. “A certain quantity of vapour disturbs the functions of the cerebral hemispheres; an additional quantity appears altogether to suspend these functions, and to impair those of the spinal cord, and probably of the cerebellum; a still larger quantity to suspend their latter functions, but to leave the medulla oblongata more or less unaffected.”24 As the gas escapes the lungs, the sequence is reversed. With this model in mind, Snow began his pioneering study, “On narcotism by the inhalation of vapours,” published in eighteen installments by LMG between May 1848 and December 1851. He completed twelve installments by August 1849, when he interrupted his research to develop his theory of cholera. He completed four more installments between the spring of 1850 and the spring of 1851 and finished his serialization that December, just before LMG amalgamated with MT to become MTG. “On narcotism” (ON) placed his earlier work on ether in a broader context of narcotic and anesthetic phenomena. It is studded with examples of outstanding scientific observation and problem solving. Snow laid out the significance of saturated vapor pressure. He expressed his rule of thumb that the amount of an agent needed to produce anesthesia was inversely related to its solubility in blood. He identified a family of agents that worked in this way, gauging their potencies relative to one another. He added further considerations to his ether study on the mechanics of inhalation. He discussed oxidation, closed-circuit techniques, and tests to detect chloroform in air, blood, and tissues.25 It was an evolving study, written in periods of great activity and energy and responsive to emerging controversies about deaths while patients were under chloroform. In sum, the installments of ON reveal the reach of Snow’s mind, the patterns of his thinking, and his ability to incorporate developments on practical, experimental, and theoretical levels. His basic goal in ON was to determine the exact correspondence among precise doses of ether or chloroform, degrees of narcotism, and quantity in the bloodstream, but first Snow needed to show experimentally what was already plain: ether and chloroform enter the blood via respiration. To show this he “passed a tame mouse” through a mercury trough and into a graduated jar containing a mixture of ether and air. After a short while he removed the mouse from the first jar and placed it in a second graduated container containing only air. He then removed the mouse from the second jar, let both jars return to the starting temperature, and observed that in the first jar the mercury rose a good deal while in the second it fell somewhat (ON, 1: 850). With relatively simple techniques of chemical analysis he had demonstrated that the mouse had inhaled ether from the first jar and exhaled it into the second. Even so, how could he determine the precise amount the mouse had inhaled and the minimum required to induce the five degrees of narcotism? In 1847 Jean-Louis Lassaigne and Andrew Buchanan had made crude estimates of how much ether was required to fully anesthetize an adult. Snow was prepared to offer a more accurate method. Rehearsing the laws of proportion for gas mixtures and liquids that he had confirmed in 1847, he explained that when gases like ether or chloroform come in contact with a liquid like blood or water, the gas is absorbed into the liquid until

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equilibrium is established. At a given temperature and pressure, equilibrium occurs when both the gas and the liquid contain “the same relative proportion to the quantity which would be required to saturate them” (ON, 1: 850). If one knows the concentration of the gas, the concentration at which that gas saturates air (at the temperature of the air in the alveoli), and the concentration at which that gas saturates blood (at the same temperature), then one can calculate the concentration of the gas in the blood. He expected to find that, if one started with a three percent concentration of gas to air at equilibrium, the blood would contain a one percent concentration of the gas (assuming thirty percent was required for air saturation and ten percent for blood saturation). That is, the ratio of anesthetic gas to air would be proportionate to the ratio of gas to blood. In Snow’s words, “As the proportion of vapour in the air breathed is to the proportion that the air, or the space occupied by it, would contain if saturated at the temperature of the blood, so is the proportion of vapour absorbed into the blood to the proportion the blood would dissolve” (ON, 1: 850). For the sake of clarity, this rule was perhaps best not condensed into one sentence, but Snow’s formulation gives us a sense of how he saw the problem. To regulate the dosage, he created an inhaler, which was a temperatureand volume-controlled environment for gas–air mixtures. To calculate the quantity absorbed in the blood, the dosage had to be adjusted for alveolar temperature. Once saturation levels were established and concentrations known, determining the amount of the drug absorbed in the blood became a matter of solving for X. Snow had come to see temperature, volume, and saturation as the keys to controlling concentration and concentration as the key to understanding the physiology of narcotism and the process of anesthesia. The first series of experiments described in ON dealt with chloroform; he had decided to use the new drug, not ether, to build the database of narcotism. Using minimal doses and allowing enough time to see that the drug’s effect no longer increased, Snow combined his acute powers of clinical observation with the numerical precision of chemistry to determine the quantity of chloroform necessary to induce a particular degree of narcotism. Working from a chemical and physiological perspective, Snow was practicing modern scientific medicine. He placed guinea pigs, mice, chaffinches, green linnets, and frogs in jars with different quantities of chloroform, allowed the effects to run their course, and monitored the animals for symptoms. In the course of the first sixteen experiments, Snow pinched the guinea pigs and chaffinches to see if they would flinch and made his notes. Table 6.2 summarizes his findings. The medical model enabled a new kind accuracy in his estimates. The selection of rodents, birds, and frogs afforded a variety of sizes and respiratory rates, allowing for a range of differences in reactions while supporting the general validity of the blood concentration model. To prove this last point, Snow concluded the first installment by recounting the experiments he was invited to perform at the Royal College of Physicians for James Arthur Wilson’s Lumleian Lectures (29 March 1848). In a very large jar (almost 1000

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Table 6.2. Snow’s early experiments with chloroform Degree of narcotism

Quantity of chloroform/air

Chloroform/ blood concentration

2nd

1 grain (64.8 mg)/100 cubic inches air

1/16,285

3rd

1.5 grains (97.2 mg)/100 cubic inches air

1/10,857

4th

2 grains (129.6 mg) /100 cubic inches air

1/28

5th

2.5 grains (162 mg) /100 cubic inches air

1/22

cubic inches) Snow had placed a frog and a chaffinch (in a small cage) and then introduced five grains of chloroform. In less than ten minutes the frog was insensible whereas the bird was perfectly conscious. He inserted another frog and chaffinch in a much smaller jar (200 cubic inches) and added five grains of chloroform. In ninety seconds the bird was insensible, but the frog was still very conscious (ON, 1: 854). These demonstrations showed how crucial dilution, respiration rate, and blood temperature were in the process of narcotism. In the first case the dilution was too great for the small, warm-blooded chaffinch to be affected despite its quick respiration, but the cold-blooded, slowly respiring frog was affected because the lower temperature of its blood meant that it did not require as high a concentration to achieve saturation. In the second case the greater concentration worked quickly on the bird, but ninety seconds was not long enough for the slow-breathing frog. Snow added further confirmation by demonstrating that a warmed frog ceased to be affected by diluted gases that would narcotize it at low temperatures. The second installment of ON analyzed ether, using the same approach as he had done with chloroform, and then compared the two agents. Snow found that the second degree of narcotism corresponded to .000875, or 1/1,142 proportion of ether in the blood at 100° F., and that the fourth degree corresponded to .00175 or 1/572. He compared these results to his experience with human subjects. Working from Gabriel Valentin’s calculations of the weight of the blood in the adult human (about thirty pounds, equivalent to 410 fluid ounces), Snow calculated that the total quantity of chloroform in the blood was 12 minims (.71 ml) for the second degree and 24 minims (1.42 ml) for the fourth. For ether, the corresponding numbers were 171.84 minims (10.17 ml) and 340.8 minims (20.17 ml). He found these to correspond very nearly with his experiences when administering both agents: “a considerable portion is not absorbed, being thrown out again when it has proceeded no further than the trachea, the mouth and nostrils, or even the face-piece” (ON, 2: 895). He confirmed this hypothesis by breathing chloroform over and over again from a balloon (as with nitrous oxide). Using this recycling technique, he found twelve minims sufficient to induce the second degree. He was particularly sensitive to the role temperature played in the administration of vapors, both in the apparatus and the alveoli. He noted that birds “were found to

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require nearly twice as much” ether as were mice to render them insensible, while this was not the case with chloroform. Because these birds generally maintained a temperature of 110° F., he reasoned that the blood serum at that temperature would dissolve much less ether than at 100° (the temperature of Snow’s mice), and therefore the birds would require greater concentrations to achieve the same degree of saturation. Snow also began to consider the impact of ether and chloroform on animal temperature, not merely noting the difference between warm-blooded and coldblooded creatures but as a physiological process. Snow came across Jean Nicholas Demarquay and Auguste Dumeril’s statements that these agents lower body temperature during inhalation. Several ether experiments on linnets confirmed this, registering drops of as much as eight degrees in fifteen minutes (ON, 2: 893–94). This was John Snow in early 1848—poking guinea pigs, pinching chaffinches, passing mice through quicksilver, and warming frogs near the fire in the name of medical science. His medical model focused on narcotic symptoms, concentration, volatility, respiration, time, and temperature. Differences in species and individuals now came down to measurable differences of minutes, minims, cubic inches, degrees Fahrenheit, degrees of saturation, and degrees of narcotism. Through the alembic of this medical model, he transformed a narcotized menagerie of experimental animals into reliable data on blood concentrations. To our knowledge no one else took such a comprehensive numerical approach to these drugs, nor did anyone else wed chemical analysis to a physiological progression with such consistency. After establishing a baseline with chloroform and ether, Snow concerned himself with broadening the spectrum of vapors that might have narcotic properties and might be inhaled for anesthetic purposes. Through the spring and summer of 1848, when he published the third and fourth installments, he investigated six other agents: nitric ether (ethyl nitrate, C2H5ONO2), bisulphuret of carbon (carbon disulphide CS2), benzin (benzene C6H6 [Snow gives it as C12H6]), bromoform (HCBr3) ethyl bromide (C2H5Br), and Dutch liquid (1,2-dichloroethane C2H4Cl2). He had begun to compile a systematic pharmacology of inhaled anesthetics. Whereas many were engaged in the search for better anesthetic agents (Simpson and Thomas Nunnely from Leeds, for example, experimented with many of the same agents), and medical journals were filled with suggestions for new agents, Snow established a method of comparison based on general principles of anesthetic and narcotic action. “His grand search,” according to Richardson, “was for a narcotic vapour which, having the physical properties and practicability of chloroform, should, in its physiological effects, resemble ether in not producing, by any accident of administration, paralysis of the heart.”26 No doubt that would have been a desirable practical outcome from Snow’s research, but this was actually Richardson’s project. For Snow, the grand search was for “the ‘perfect’ anaesthetic” as well as a general theory of narcotism itself.27 That was why he went to the trouble of calculating the blood saturation levels for substances like bisulphuret of carbon, when all of his evidence showed that it was too powerful, noxious, and dangerous; it caused convul-

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sive tremors in mice (ON, 3: 1076–77). He never really considered this agent a viable substitute for ether or chloroform, but he studied it because he wished to place it on a continuum of inhaled agents that induced narcotism in the same way as did ether and chloroform. In particular, he was looking for extremes to set the endpoints on this continuum. He was careful to point out that not all narcotics functioned like ether and chloroform, and he mentioned hydrocyanic acid (prussic acid) as an example of one that did not. He was only interested in those narcotics “producing effects analogous to what are produced by ether,” “and having . . . a similar mode of action.” However, he regretted that he was not “able at present to define them better than by calling them, that group of narcotics whose strength is inversely as their solubility in water (and consequently in the blood)” (ON, 4: 333). The analogical, deductive pattern of his thought is evident; similar substances producing analogous effects implied similar pharmacodynamic mechanisms. In this manner he invented a family of volatile liquids where formerly there had been only individual agents. He linked blood solubility with the narcotic power, rated by the minimum concentration in the blood, necessary to induce the second degree. He considered nitric ether a promising candidate, and he asked one of his regular chemists to make him a sample. When he tried it on himself (“on two or three occasions”), a small amount “caused a disagreeable feeling of sickness each time” (ON, 3: 1075). In May 1848 he used it with encouraging results in a tooth extraction at St.George’s Hospital, but he never used it again, clinically, despite evidence that it was an effective painkiller. He was also interested in benzene, despite its tendency to cause convulsive tremors. Trials showed it to be nearly as efficient as chloroform, but its effects “are not so rapidly produced as the effects of chloroform, on account of its lesser volatility.” He tried benzene on human subjects at St. George’s Hospital, with success in minor operations, but in an “amputation, where its effects were carried further, the patient had violent convulsive tremors for about a minute, which, although not followed by any ill consequences, were sufficiently disagreeable to deter me from using it again, or recommending it in the larger operations” (ON, 3: 1078). Snow was a cautious practitioner, and it is admirable that he stopped using benzene. At the same time, given his reaction to the carbon compound, which also caused convulsions, one may wonder why he bothered to put benzene to clinical trial at all, or, for that matter, why he never pursued nitric ether, despite its promise. Convulsions alone would not have dissuaded him; both ether and chloroform could produce spasms. He was deeply invested in the model of narcotism he had constructed around chloroform, and it shaped his theoretical and practical considerations of related agents. He probably did not pursue nitric ether because it was a weaker and more expensive agent than was chloroform.28 In the case of benzene, the potential of having a drug as economical and efficient as chloroform that acted less quickly (Snow considered gradual induction desirable) made it worth trying until convulsions proved too violent. The sulfur–carbon compound was too fast acting to control effectively, so it held no clinical interest for him. Snow synthesized his own bromo-

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form, a substance with a molecular formula similar to chloroform and now known to cause kidney and liver damage in animals. He found it “very pleasant to inhale” but too costly to produce (ON, 4: 330). He found ethyl bromide to be too volatile, requiring very high concentrations to be effective, so he never bothered to get an experimental reading of its blood solubility. Dutch liquid tasted “at once sweet and hot,” and Simpson considered it too caustic to be inhaled by most patients (ON, 4: 331). Snow determined that it required 46 minims (2.7 ml) of Dutch liquid to create 1/50th relative saturation of the blood to induce the second degree of narcotism. He was not particularly sanguine on its prospects as an anesthetic agent for additional reasons: Two mice died after trials, and postmortem examinations revealed that their lungs were congested, their hearts swollen, and the blood coagulated and dark. Snow would continue for the rest of his life making trials of all kinds of hydrocarbon inhalants, but his main concern in 1848 was to confirm and reconfirm that degrees of narcotism corresponded to the quantity of the substance in the blood. He believed that this quantity was a proportion of “what the blood would dissolve—a proportion that is almost exactly the same for all of ” these substances. The actual differences in quantity were accounted for by differences in solubility: “When the amount of saturation of the blood is the same, then it follows that the quantity of vapour required to produce the effect must increase with the solubility, and the effect produced by a given quantity must be in the inverse ratio of the solubility” (ON, 4: 332). Snow included acetone, pyroxilic spirit, and alcohol on his list, even though they are infinitely soluble in blood, because they shared properties with the other volatile liquids and were proportionately less potent, which seemed to prove his rule. In this fourth installment of ON, he again described the degrees of narcotism, using chloroform as his model, began to make observations about chloroform and midwifery (a subject that would increasingly preoccupy him), and put forward an idea that he had not previously mentioned: “The division into degrees is made according to symptoms, which, I believe, depend entirely on the state of the nervous centres, and not according to the amount of anesthæsia, which I shall give good reason for believing depends very much on local narcotism of the nerves” (ON, 4: 334). It turns out that Snow’s last opinion was incorrect, but it reveals the general pattern of his thought. Painlessness was, for Snow, a local epiphenomenon of narcotism.

Narcotism’s Reach In these early installments Snow established the pharmacology of narcotism and a model of how the body responds to relative quantities of narcotics. The fifth and sixth installments addressed the general physiological effects of chloroform, how the nerves were affected, how death could occur, and what autopsies on animals revealed. After reviewing the dangers of chloroform in part seven, he made a case for its safe

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use with a slightly modified version of the temperature-controlled chloroform inhaler (Fig. 6.1). In part eight he described the various conditions that influence the action of chloroform such as age, strength, debility, disease, diet, hysteria, epilepsy, renal convulsions, and diseases of the heart, lungs, and brain. In parts nine and ten he analyzed the data for amputation and other procedures under chloroform. Next (parts eleven and twelve), he considered various mixtures of chloroform and ether, and described an alternative mode of administration via a balloon and a valved face piece. He made a few more trials of Dutch liquid and in 1849, as cholera raged in London, Snow evaluated it as a potential treatment. A seven-year-old girl was in the throes of the disease, constantly vomiting and evacuating and in jactitation from horrific cramps. He had used chloroform in a number of cholera cases that year, and he found that it offered some relief by inducing sleep free “from sickness and spasm.” For this girl, however, he administered Dutch liquid, which gave her only a few minutes’ respite, although she did recover (ON, 12: 277). In June 1849 Snow continued to experiment with his growing armamentarium of pain relievers in the face of

Figure 6.1. The modified chloroform inhaler and mouthpiece from November 1848 (Adapted from ON, 7: 843).

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cholera. Sometimes he was able to give patients enough rest to make a recovery, sometimes he simply eased the suffering of the dying. In the process it must have become clear to him that giving chloroform and Dutch liquid to cholera victims was only a stop-gap measure.

Chlorophobia On a night in early January 1850, a Lime Street solicitor named Frederick Hardy Jewett was walking along the bustling Whitechapel Road in the East End. Suddenly, someone put a felt rag or handkerchief over his mouth. The next thing he remembered was waking up the next morning in the filthy bed of a lodging house in Thrawl Street, Spitalfields. When he attempted to leave, he found the door locked from the outside. He was naked, covered with rags, and most of his valuables had been stolen. Two young women, Margaret Higgins and Elizabeth Smith, were arrested, tried, convicted, and sentenced to fifteen years. At one of their hearings Catherine Donovan, the wife of a local grocer, testified that Higgins had confessed to the crime and told her that the man with whom she lived had been operated on at a London hospital. They gave him “some stuff to send him to sleep,” and afterwards he had managed to steal some of it. Higgins had used this “stuff ” in the Whitechapel Road mugging. About the same time, a man was walking along the Borough Road, south of the Thames, toward London Bridge when a woman passed a handkerchief across his face. He immediately felt indisposed, and the woman helped him into a nearby pub for a tumbler of brandy. Her name was Charlotte Wilson. Ten minutes later the man was unconscious, and she left the pub with his hat and scarf in hand. Wilson was soon apprehended. In the opinion of the court, she had used “some deleterious article such as chloroform,” and she received ten years for robbery.29 It was not just a problem of women attacking men. In April 1850 a young man named Charles Jopling and his girlfriend walked home from a pub dance near Marylebone. He beckoned her to follow him into a mews, where he poured the contents of a vial on a hanky and tried to smother her. Repulsed by the wet hanky and the pungent odor, she cried out for help. A policeman on his beat heard the screams and took the man into custody. Jopling paid bail and married his girlfriend, and she dropped the charges against him.30 This was not exactly news. As early as November 1847, when Simpson’s new agent was first publicized, there had been reports of chloroform described as a rape drug.31 There were a few reports of street robberies in 1849, but in the aftermath of Hannah Greener’s death the medical risks of chloroform received more press than its criminal potential.32 In 1850 and 1851, however, chlorophobia swept the country, as the agent intended for medical purposes was increasingly perceived as an alleged agent of crime, robbery, rape, and murder. An old man asleep in a hotel room was attacked with chloroform by a man hiding under his bed. Prostitutes were charged with hocussing by

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way of chloroform, using it to lace the drinks of unsuspecting johns and then robbing them. In France a dentist raped a female patient while she was under its influence.33 Chloroform’s fast action, incompletely reported in the press and experienced by growing numbers of patients, led to a sensational misunderstanding of its powers in the public and popular imagination. Long before the chloroformed handkerchief became a staple of fictional abductions—the kidnapper’s method of choice for surreptitiously overpowering victims—the powers of chloroform were mythologized on the streets and in the criminal courts. Things came to a head in February 1851, when Lord Campbell, the recently appointed chief justice of the Court of Queen’s Bench, proposed An Act for the Better Prevention of Offences that called special attention to the use of chloroform for criminal purposes. Lord Campbell believed that British criminal law was too liberal and that too many criminals were able to skirt whatever law did exist. He lobbied for stricter sentences as a deterrent. He wanted to make possession of tools of criminal trades (e.g., picklocks) an offence for which the punishment was deportation. A clause in Lord Campbell’s bill depicted chloroform as a potential tool in the criminal’s trade: “And whereas it is expedient to make further provision for the punishment of persons using Chloroform, or other stupefying things, in order the better to enable them to commit felonies: be it enacted, that if any person shall unlawfully apply or administer, to any other person, any Chloroform, Laudanum, or other stupefying or overpowering drug . . . every such offender shall be guilty of felony, and being convicted thereof shall be liable, at the discretion of the Court, to be transported [to Australia] for life, or for any term not less than seven years.”34 Snow believed Lord Campbell’s bill was unnecessary and unfairly targeted chloroform. In his opinion, “It ill becomes the gravity of the law, and is, I feel assured, far from your Lordship’s intention, that a legal enactment should be made on a false alarm, or to meet a trivial and unsuccessful innovation in the mode of attempting a crime: to legislate on this matter would revive the groundless fears of the public.”35 Snow was skeptical of public reporting on the purported uses of chloroform to commit crimes. Most descriptions did not conform to the known properties of the agent. The drug was far too pungent to be inhaled unawares. To force it upon someone required smothering, or “burking”—a felony for which the law already provided. Perhaps Lord Campbell was cracking down in advance of the Great Exhibition of 1851, when tourists were expected in London. The bill had a distinct animus against the working class, especially with its stiff sentencing. Snow thought social hypocrisy explained much of the chlorophobia: “Persons who have been dead drunk are very unwilling to admit, even to themselves, that the result was the consequence of their own voluntary potations, and still less willing to admit it to the world, when they have to complain of having been robbed whilst in bad company.”36 The editorial staff of the Pharmaceutical Journal concurred, stating that, “It may be a convenient subterfuge for a man who finds himself in a scrape . . . to conjure up a mysterious and exciting story about chloroform and a handkerchief, for the purpose of throw-

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ing dust in the eyes of the magistrate, and working upon the prejudices of the jury. [This act] may be the means of entailing an unjustly severe punishment for a comparatively trifling offence.”37 Snow’s letter was discussed in the House of Lords. The Times reported that “a most respectable physician” had done Lord Campbell the honor of writing him a letter, stating that the fear of using chloroform in this way was “altogether imaginary.” Nonetheless, Campbell kept the provision and hoped that anyone convicted would “be guilty of a felony, and liable to be transported beyond the seas.” To which his fellow lords replied, “Hear! Hear!”38 The act passed in June 1851.

Narcotism’s MO When Snow resumed publication of ON in April of 1850, he apologized for the interruption. He justified it on the grounds that he needed to “repeat many experiments and institute fresh ones,” but his study of cholera in 1849 may have been an additional factor (ON, 13: 622). The new installments reflect a shift in thinking. Earlier, his goal was to establish a pharmaceutical profile of narcotism, to measure inverse ratios of solubility, and to describe the benefits of various agents in amputation and dentistry. Now, in 1850, he concerned himself with the underlying physiological mechanisms, or, as he called it, “the modus operandi of ether and chloroform” (ON, 13: 622). He began to tackle complex questions involving the biotransformation of these drugs as they circulated in the body.39 This approach would push him beyond the pharmacokinetics of narcotic agents into thornier issues of pharmacodynamics (how drugs interact at cellular and molecular levels). It was terra incognita. Where to begin? His cholera research had led him deeper into pathophysiology to Liebig’s Animal Chemistry, especially Liebig’s descriptions of how carbon and hydrogen in fat, starch, sugar and gum “combine with oxygen in the blood, and are given off as carbonic acid gas and water” (ON, 13: 627). Based on this general model, Liebig also offered an “explanation of the physiological action of alcohol,” that is, how it was metabolized in the system (ON, 13: 626). When ether came along, Snow observed, “many persons were inclined to extend” Liebig’s alcohol thesis to ether (because of its chemical similarity to alcohol). Snow would begin by testing the validity of Liebig’s theory of the physiology of alcohol to see what he might learn about the physiology of narcotism. Snow began by reconfirming what his blood solubility table had shown: a family relation between alcohol, chloroform, and ether.40 He showed that alcohol did, indeed, correspond to the pharmaceutical profile he had set up for narcotism. It obeyed the inverse ratio rule of blood solubility. He also extended his analysis by confirming that its clinical effects corresponded to his model of degrees. This was not easy to do because the effects of alcohol last so much longer than those of chloroform or ether. He concluded that “ordinary drunkenness does not exceed the second degree

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of narcotism; the popular term of dead drunk being often applied to a state of sleep from which an individual is still capable of being roused to a state of incoherent consciousness.” He calculated the blood-alcohol level for this condition (fifteen ounces of proof spirit) and asserted that less than twice this amount taken all at once on an empty stomach ought “to prove fatal” (ON, 13: 625). The result corresponded well with common experience and his established degrees of narcotism (and today’s blood-alcohol standards). Snow concluded that the “amount of anesthesia from alcohol is apparently as great, in proportion to the narcotism, of the nervous centres attending it, as from chloroform and ether,” but it does not yield enough vapor at room temperature to cause insensibility in a reasonable amount of time (ON, 13: 626). Were it a more practical anesthetic, the teetotaler Snow mused, alcohol would be in public opinion “as praiseworthy as it is disgraceful when resorted to for the purpose of supposed enjoyment, or to satisfy a craving which has resulted from a pernicious habit” (ON, 13: 626). Alcohol, a substance he had opposed his entire adult life, was actually a cousin to ether and chloroform, substances he championed and sources of his livelihood. Snow concluded that alcohol was a narcotic, for which Liebig had supplied a thick description of its physiological action. According to Snow, Liebig argued that observation had led him to conclude that “neither the expired air, nor the perspiration, nor the urine, contains any trace of alcohol after indulgence in spiritous liquors . . . ; that the elements of alcohol combine with oxygen in the body, and that its carbon and hydrogen are given off as carbonic acid and water; that the elements of alcohol appropriate the oxygen of the arterial blood, which would otherwise have combined with the matter of the tissues, or with that formed by the metamorphosis of the tissues: and that thus the change of the tissues . . . are diminished” (ON, 13: 626). Snow believed this description was largely incorrect and, as any Breathalyzer will reveal, he was right, and Liebig was wrong. Whereas Snow concurred that alcohol and other narcotic vapors diminish or suspend “molecular change” (Liebig’s catchall for chemical and biochemical interactions) of the affected tissues, it was not the result of “appropriating the oxygen in the blood” (ON, 13: 626–27). While oxygen may combine with hydrocarbons in fat, starch, sugar, and gum, yielding carbon dioxide and water, none of these substances were in any degree narcotic. Second, the amount of carbon and hydrogen present in enough chloroform to render someone completely insensible was “totally insignificant” compared to the amount of oxygen absorbed in the lungs (ON, 13: 627). Alcohol has a very similar action to chloroform and therefore could not, as Liebig argues, appropriate very much oxygen in the bloodstream. Third, if alcohol did indeed create its narcotic effect by appropriating oxygen, then supplying more oxygen should prevent or diminish the narcotic effect, but this was not the case. Snow had observed patients in states of complete insensibility whose skin turned “bright vermillion” with excess oxygen coursing through their arteries. Through the summer of 1850 Snow demonstrated how to detect the presence of chloroform, ether, and alcohol excreted in the breath. Consulting with Dr. Alfred

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Taylor of Guy’s Hospital, he refined a test for the presence of chloroform in the blood in the Journal de Chemie Medicale (March 1849). By inhaling chloroform and breathing into a heated tube lined with silver nitrate, Snow obtained precipitates of silver chloride crystals that corresponded to the amount of chloroform taken. He showed how this method could detect chlorine in urine and tissue samples as well. Snow was careful to qualify his analysis, reminding his readers that the process did not “prove the presence of chloroform itself, but only that of a volatile [at the heat of boiling water] compound containing chlorine” (ON, 14: 326).41 This meant that only the compounds in the family he had been studying were likely candidates, of which only chloroform was commonly used. Snow devised a parallel series of experiments to detect traces of ether and alcohol in the breath. He had smelled ether on the breath of patients in the same way one smells alcohol on the breath, but, as with chloroform, he sought quantitative chemical confirmation. In both cases he took the drugs himself, trapped his respiration in a balloon, and was able to rectify pure ether and alcohol from the breath. Braving the perils of intoxication in the name of science, the temperance advocate manfully took his measured dose of spirits with bread and butter, became mildly intoxicated, and breathed into a spiral tube connected to a small bath of sulfuric acid. Trapping the alcohol vapor in the acid, he developed a process of heating the mixture to obtain alcohol in a pure state (ON, 15: 751–53). This was classic Snow. The implications of his research spun off, like a serial novel, in social and medical directions. He wished to demonstrate that Liebig was wrong about alcohol. He had also devised tests for detecting both alcohol and ether that were more conclusive than was the test he devised for chloroform, yet he began the discussion with chloroform because it had become the baseline for all his research on narcotism. He was also highly sensitive to the social uproar surrounding chloroform in 1850. Snow’s test would be very useful in forensic investigations in which chloroform was suspected. There was no pressing social need to detect alcohol or ether on the breath, so he did not bother to develop a socially useful test for them. He continued to investigate alcohol and ether in order to solidify his claim of the family relations of narcotic agents, to further his physiological theory, and to prove Liebig wrong. The detection of chloroform, ether, and alcohol yielded a key physiological insight rather than the modus operandi of narcotism per se. “I have assumed from the first,” he explained, “that the speedy subsidence of chloroform and ether, in comparison with that from alcohol and other narcotics, depends on the volatility of the former substances, which allows of their ready exit by the expired air. Indeed, the effects of these medicines usually subside in the period which a calculation founded on this view would assign to them” (ON, 15: 753). Snow preferred the term degrees of narcotism to stages because degrees suggested the passage of time on the face of a clock. The duration of the effects of narcotism were determined by solubility and volatility: how much of the narcotic gas was absorbed by the blood, how fast the blood

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circulated, and, once the narcotic gas was left off, how quickly the air removed the gas from the blood. With their quicker circulation and respiration, children went under and came out more quickly than did the slow-breathing elderly. He suggested that diffusion of the agent to smaller vessels and tissues could play an ancillary role in “allowing the brain to resume its functions” (ON, 15: 753). Ether was more volatile than was chloroform but much more soluble, so the quantity absorbed by the blood was much greater. Greater solubility compensated for the lesser volatility, Snow reasoned, and therefore ether wore off more slowly than did chloroform. It followed that alcohol, with even greater solubility and less volatility than ether, lasted even longer. It also followed that one could prolong the effects of a narcotic by recirculating the expired breath. Snow devised an autoexperiment, based on an attempt to relieve the sufferings of a cholera victim in 1849, in which he first filled a balloon with pure oxygen. Using a glass condensing coil, he connected the balloon to his ether inhaler, which was filled with a “solution of potassa” (potassium monoxide) and attached this setup to a valveless mouthpiece.42 After inhaling as much chloroform as possible without passing out, he breathed and rebreathed from the balloon–inhaler device; the oxygen he inhaled became mixed with the air already present in the inhaler, while the potassium solution absorbed his CO2. He reported that the narcotism, which ordinarily would have passed off in three to four minutes, lasted a full ten minutes, with feelings persisting for approximately thirty minutes afterwards. It worked for ether as well (ON, 15: 754). The potassium solution permitted him to quantify the amount of CO2 produced while he was under the influence of narcotic gasses.43

Oxidation–Asphyxia Theory In April 1851 Snow presented a theory that explained how narcotic vapors worked. It was based on two fundamental observations: The inhalation of narcotic gases reduces “the amount of carbonic acid formed in the system,” and “chloroform and ether are exhaled unchanged from the blood” (ON, 16: 626). These agents, defined as “the volatile narcotic substances not containing nitrogen, or those subsances whose power was found to be in the inverse ratio of their solubility in water and the serum of the blood,” have “the effect of limiting those combinations between the oxygen of the arterial blood and the tissues of the body which are essential to sensation, volition, and, in short, all the animal functions” (ON, 16: 626). They “modify, and in larger quantities arrest, the animal functions, in the same way, and by the same power, that they modify and arrest combustion, the slow oxidation of phosphorous, and other kinds of oxidation unconnected with the living body” (ON, 16: 626). He articulated his theory of narcotism in the form of twelve propositions. The first was an assumption that the life force is a variation of basic laws of physics: “Sensation,

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motion, thought, and indeed all the strictly animal functions, are as closely connected with certain processes of oxidation going on in the body, as the light and heat of flame are connected with the oxidation of the burning materials” (ON, 16: 626). Propositions two through six summarized the clinical and experimental findings detailed in earlier installments. The seventh was a conclusion drawn from his longstanding research into respiration: “The different parts of the nervous system lose their power under the influence of the narcotics we are considering, in the same order as in asphyxia—the privation of oxygen, as was observed by M. Flourens with respect to ether, in 1847” (ON, 16: 627). The last five propositions summarized earlier comments on the effects of narcotic vapors on muscular irritability, ordinary combustion and oxidation, and putrefaction, as well as the narcotic parallel produced by a reduction in body temperature. In Snow’s theory narcotic gases were an unusual kind of antioxidant that slowed down the body’s oxidizing processes without combining with the blood’s oxygen. In other words, the narcotized body behaved as if it were being asphyxiated; the body could not make use of the oxygen present. Asphyxia and narcotism enjoyed a parallel relationship with respect to the molecular action of oxygen: “The relation between asphyxia and narcotism is this—that in asphyxia there is an absence of oxygen, whilst in narcotism the oxygen is present, but is prevented from acting by the influence of the narcotic” (ON, 17: 1053). In both conditions body temperature dropped, nervous centers lost power in the same sequence, and the heart continued to beat after breathing had stopped. When robust athletic individuals were narcotized or asphyxiated suddenly, convulsions or rigidity frequently occurred. When either occurred gradually, convulsions tended not to take place. Both states were accompanied by delirium and languor. He noted that acute bronchitis, in which the patient could not breathe, often produced delirium, strange visions, and dreams. He speculated that the languid movement of the fetus in utero was due to the reduced level of oxygen available via the placenta. And, as Snow had long known from his efforts to resuscitate guinea pigs, muscular irritability was reduced by asphyxia and suspended by narcotics. In the final part of ON, he suggested that the antiseptic power of chloroform, ether, and alcohol could result from their antioxidant properties. In those pre–germ theory days, Snow reasoned that preventing oxidation functioned to prevent, or at least inhibit, putrefaction. Essential oils, like lemon and peppermint oil, that possessed narcotic properties might be used to preserve meat. A dead rabbit that he injected with lemon oil “kept very well for seventeen days” (ON, 18: 1091). Oxidation was the key for Snow, and he considered biochemical oxidation similar to what took place outside the body. According to Richardson, Snow believed he “could illustrate all the meaning of this great practical discovery of narcotism on a farthing candle” by showing the flame subdued but glowing under the influence of chloroform.44 In Snow’s metaphor, narcotic vapors did not only inhibit combustion (oxidation) of a candle flame, they inhibited the oxidation of bodily tissues. It was an analogy born

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of experience and theory. In his 1841 paper “On asphyxia and the resuscitation of still-born children” he had compared respiration with combustion and the lungs to a furnace: “The whole body ought to be compared to the furnace, and the lungs to the draught and chimney department—a view which better explains the uniform diffusion of warmth throughout the body.”45 Respiration was combustion fueled by oxygen, whereas asphyxia was deoxygenation of the blood. Years before he ever learned of the properties of ether or chloroform, he had formulated the basics of oxidation and asphyxia that would inform the physiological model in his theory of narcotism. He had witnessed, time and again, the incandescence of respiration under chloroform. He had seen his patients’ breathing grow stertorous and sputter. He had seen their skin glow red with unignited oxygen. Small wonder that most of the agents he experimented with were potential fuels or coolants. Keeping someone under during anesthesia was like knowing how to stoke a fire or run a combustion engine.

Chemical Affinity/A Balance of Forces After four years of research, Snow had found the handle to a complex process, but a fundamental question remained unsolved. “Having traced the narcotic action of ether and other bodies to the more general law of their power of preventing oxidation under a great variety of circumstances,” his “mind naturally inquire[d] by what kind of power oxidation is thus prevented” (ON, 18: 1092). His hypothesis, offered with “considerable diffidence,” was that chemical attraction or affinity is a constantly acting force, by which each atom of matter exerts an influence on all other atoms within the sphere of its attraction, . . . varying with the respective nature of the substances, and the physical conditions in which they are placed. In this point of view, it will be seen that any two substances in a condition to unite together might be prevented from doing so by the intervention of a third body possessing a sufficient attraction for either of the others; and it would not be necessary that this third body should enter into chemical combination; for a balance of forces might be established, so that the three substances would remain exerting reciprocal attractions for each other, but unable to enter into more intimate union. ON, 18: 1092 Snow reasoned that narcotic gases entered into the bloodstream and attracted the oxygen with a force insufficient to bond with it. Even so, the force was strong enough to counter the attraction between oxygen and “certain constituents of the blood and tissues of the organs,” thereby inhibiting or preventing (depending on the dosage) “those changes which are, in a manner, the essence of all the animal functions” (ON, 18: 1093). Although this hypothesis did not pan out, Snow proposed that chemical affinity explained the stalemate he considered characteristic of narcotism: oxygen,

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chloroform (or any other narcotic gas), and the materials of the body were coursing through the bloodstream in a state of suspended molecular animation. He considered it possible that counteraffinity was a form of molecular anesthesia in which the forces that explain normal oxygenation were neutralized. He was pushing his theory of narcotism into a speculative realm well beyond what anyone at the time could demonstrate in the laboratory. The Medical Society of London (successor to the Westminster) would select him as their orator for 1853. The address he delivered, entitled On Continuous Molecular Changes, contained a grand theory of biochemistry that included speculations on the basic mechanisms of narcotic vapors and the nature of epidemic diseases, chiefly cholera. Since the fall of 1848, an understanding of that dreaded disease and how to prevent its communication had rivaled inhalation anesthesia as major medical concerns in London.

Notes 1. Simpson’s announcement took place at a meeting on 10 November 1847; LMG 40 (19 November 1847): 906 contained a brief notice, but Snow already knew about it. During a mastectomy at St. George’s Hospital on November 18, “The chloroform was administered by Dr. Snow with his ether apparatus”; “Operations without Pain,” Lancet 2 (1847): 661. For Snow’s remarks at the Westminster Medical Society on 20 November 1847, see LMG 40 (1847): 1030–31; and Lancet 2 (1847): 575–76. 2. Snow, “On narcotism by the inhalation of vapours,” 4: 334. Citations to the original series in LMG are placed parenthetically in the text as ON, indicating part number and pages. 2a. Lancet 2 (1847): 575. Subsequent quotations from this meeting taken from Ibid., 575–76. 3. PharJ 6 (1847): 357. Snow contributed a version of his ether saturation table to this issue and made mention of Bell’s experimentation in OC, 20. 4. R. M. Glover, “On the properties of bromide and chloride of olefiant gas of bromoform, chloroform, iodoform,” Edinburgh Medical and Surgical Journal 58 (1842). The essay was excerpted in PharJ 7 (1848): 348–49. For Snow’s citation, see OC, 112. 5. Richardson, L, xxxv. 6. For support of Snow’s observation, see Duncum, Inhalation Anesthesia, 178–81; Davison, Evolution of Anesthesia, 137. 7. Potter, “Late fatal case at Newcastle,” Lancet 1 (1848): 214. 8. Although this detail does not appear in the inquest, it does appear in Snow’s definitive account; see OC, 124. 9. This account is drawn from several sources: “Fatal application of chloroform,” Lancet 1 (1848): 161–62; J. Y. Simpson, “Remarks on the alleged case of death from the action of chloroform,” Lancet 1 (1848): 175–76; “Fatal case of inhalation of chloroform,” LMG 41 (1848): 255. Snow, “Fatal chloroform case at Newcastle”(1848); “Remarks on the fatal case of inhalation of chloroform (1848); and OC, 124. 10. “Fatal application of chloroform,” Lancet 1 (1848): 161–62. 11. “Royal Institution,” and “Experiment with chloroform at the Royal Institution,” Lancet 1 (1848): 162–63. Quotation from 163. 12. Times (3 February 1848) reprinted the report from the inquest. 13. “Medical news—another death from chloroform,” Lancet 1 (1848): 218–19. See also “Fatal effects of chloroform,” Times (14 February 1848), 6. 13a. “Chloroform—its benefits and its dangers,” Lancet 1 (1848): 190.

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14. “Remarks on the alleged case of death from the action of chloroform,” Lancet 1 (12 February 1848): 176. 15. Ibid., 175–76. 16. “The alleged death from chloroform at Newcastle,” Lancet 1 (1848): 240. 17. “The Fatal Chloroform Case at Newcastle,” Lancet 1 (1848): 296. 18. Snow, “Fatal chloroform case at Newcastle” (1848). 19. Snow, “Remarks on the fatal case of inhalation of chloroform” (1848), 277. See also “Westminster Medical Society,” Lancet 1 (1848): 312. 20. Ibid., 277–78. 21. Snow, “On the discussion respecting chloroform in the Académie de Médecine of Paris” (1849), 324. See also Snow, ON, 6: 614–19. 22. For example, see OC, 120–27. 23. Snow, “On the inhalation of chloroform and ether, with description of an apparatus” (1848), 178. 24. Ibid. 25. For a longer summary and interpetation, see Ellis, introduction to reprint of ON. 26. Richardson, L, xxviii. 27. Duncum, Inhalation Anesthesia, 208. 28. Nitric ether was apparently difficult to obtain and required 1.5 drachms (5.3 ml) to reach the second degree, whereas chloroform required only .71 ml to reach the same state. Snow was quick to suggest that the anesthetic power of nitric ether was not unique: “I do not look on [it] as a peculiarity of nitric ether, for I have met with it occasionally from chloroform and sulphuric ether when the vapour was introduced slowly” (ON, 3: 1076). 29. For accounts of the case, see “Police—Higgins, Margaret, and another, for stealing,” Times (25 January 1850); Times (1 February 1850); and “Criminal trials—Higgins, Margaret, and another, for robbery,” Times (9 February 1850). 30. “Police—Jopling, Chas., for attempted rape,” Times (1 May 1850). 31. “New crime, rape on young girls under chloroform,” Times (5 November 1847). 32. “Chloroform, use of, by thieves,” Times (5 October 1849). 33. Snow, “A letter to Lord Campbell” (1851), 13. 34. Quoted in Ibid., 14. 35. Ibid., 4. 36. Ibid., 14–15. 37. “The use of chloroform for criminal purposes,” PharJ 10 (1851): 488–89. 38. “Parliamentary proceedings—Prevention of Offences Bill,” Times (15 March 1851). 39. Shephard, JS, 136. 40. Snow included the other two agents from his table in this series of experiments, pyroxilic spirit (methyl, or wood, alcohol) and acetone, but his main focus was on ethyl alcohol (ON, 13). 41. See also the description in A. Taylor, Medical Jurisprudence, 320. 42. ON, 15: 753–54. In a footnote Snow wrote, “I used the same arrangement in giving oxygen gas last year, at the request of Dr. Wilson, to a cholera patient in St.George’s Hospital. The patient, who was in a state of collapse, was not saved or relieved by it.” 43. In 1851, using an apparatus devised by Regnault and Reiset described in the Annales de Chemie et de Physique (1849), he confirmed his findings from autoexperiments on chloroform, ether, and alcohol with extensive animal experimentation; ON, 16: 622–26. 44. Richardson, L, xvii. 45. Snow, “On asphyxia and the resuscitation of still-born children,”(1841), 223–24.

Chapter 7

Cholera Theories: Controversy and Confusion

A

S LATE SUMMER TURNED TO AUTUMN in the year 1848, Snow occupied himself with narcotism research and his growing anesthesia practice. No other British physician or scientist was engaged in the project he had undertaken: to study ether and chloroform as members of a family of volatile narcotic agents related by common chemical and physical properties and to determine the physiological mechanisms by which members of the family exerted their effects. In addition, following the initial reports from Flourens’s laboratory, no work on the basic physiology of anesthesia was underway in France. Occasional reports of deaths under chloroform continued to appear in the medical literature. These deaths demanded Snow’s analysis because, as an advocate of inhalation anesthesia, he needed to determine whether they were due to the chloroform itself or (as he had stated on many occasions) defects in the apparatus and improper administration. In October 1848, however, articles advocating chloroform as a treatment for cholera began appearing in the medical journals. Henry Clutterbuck, former president of the Westminster Medical Society and Snow’s superior at the Aldersgate Street School, endorsed such treatment at a meeting of the Medical Society of London. A visiting physician to a poorhouse, he had observed the resident surgeon including chloroform in a new method of treating cholera victims. The treatment involved putting the patient to bed wrapped in warm blankets, followed by “a glass of brandy

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in hot water, with sugar, and spice”; briskly rubbing the body and applying a heating liniment; and placing “the patient under the influence of chloroform by inhalation” for as long as “the bad symptoms recur.” Discussion of this procedure, as well as other ways of administering inhaled chloroform for cholera, continued at the weekly meetings of the Medical Society of London into December.1 Snow was not a member of this society, but he could have read summaries of the meetings in the journals he regularly consulted. These journals also carried articles and letters in November and December 1848 from medical men who had found that chloroform worked best when given internally or who preferred other anesthetic agents as treatments for cholera.2 Epidemic cholera, after dying away in England in 1832, soon after Snow had attended to the Killingworth miners, had been mercifully absent for sixteen years. It returned to England in the summer of 1848, with the first cases appearing in London in October. In the interim no consensus had been reached about efficacious therapeutics. Virtually every known treatment had been tried during the first epidemic. The three medical corporations had not agreed on what to recommend, and guidance received from the Board of Health was too inclusive to be useful. The range of disagreement was even broader in 1848, because anesthetics could be added to the mix,3 and the situation remained unchanged when the third major epidemic came to England in the mid-1850s. Just as no consensus existed about how to cure cholera, there were continuing disagreements about its pathology and cause; between 1845 and 1856 some 700 works on cholera were published in London alone.4 The Medical Times noted in an editorial at the end of 1847, “It must be acknowledged that scientific investigations have done but little in advancing sound knowledge upon some most important points connected with the disease.”5 Six years later, at the onset of the third epidemic, an editorial in the Lancet emphasized continuing uncertainties: “The question, What is cholera? is left unsolved. Concerning this, the fundamental point, all is darkness and confusion, vague theory, and a vain speculation. Is it a fungus, an insect, a miasm, an electrical disturbance, a deficiency of ozone, a morbid offscouring from the intestinal canal? We know nothing; we are at sea, in a whirlpool of conjecture.”6 Controversy was endemic in the midst of so much confusion.7 But the disputants had coalesced into several camps depending on whether they believed the “exciting cause” was a contagious “virus” generated in the bodies of the sick, a noncontagious atmospheric principle, or some amalgam of the two. Pure contagionist opinion was dominant early in the 1831–1832 epidemic but lost ground to modified versions and noncontagion by the second and third epidemics. To acquire cholera the purely contagionist perspective required contact either with a sick person’s body or with the fomites from infected bedding and clothing; smallpox was often cited as a model. A third variation of contagion, the idea of infection, became increasingly prevalent among medical men in the 1840s: according to this notion, the bodies of cholera victims produced an infectious “virus” that, in vola-


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tized form, emanated into the immediate atmosphere and was inhaled by the healthy. A few contagionists believed that a person must swallow the cholera matter or its germs.8 Adherents of pure noncontagiousness believed that epidemic cholera was better explained by Sydenham’s theory of the epidemic constitution, in which general atmospheric changes occasioned by seasonal fluctuations produced diseases in susceptible individuals.9 Each disease was associated with a particular seasonal–atmospheric condition, but only people with physiological predispositions unfavorable to the condition actually became ill. Once cholera had spread westward from the Indian subcontinent during the first pandemic, climatologists thereafter looked for patterns in temperature, humidity, barometric pressure, wind, and so on that would permit prediction about the extent and duration of the next one. However, some critics of atmospheric causation believed the evidence about cholera transmission pointed to local circumstances, in which “a poison formed by the decomposition of organic matter [miasma] . . . , when applied to the human body, produces the phenomenon constituting fever.”10 For some local miasmatists what appeared to be distinct diseases were variations of one pathological state, fever. Others believed in specific diseases associated with particular conditions, so that ague was common near malarial marshes, whereas cholera was prevalent in areas of concentrated animal putrefaction. Most miasmatists (whether general or local) believed that the primary cause of epidemic disease was inhaling poisons generated by a chemical reaction during putrefaction; this view was so pervasive that the name epidemic was often associated with it. Some local miasmatists, however, grudgingly acknowledged that person-to-person transmission of cholera by infection did occur in rare circumstances of unusual overcrowding and filth. That is, particular environmental “contingencies” could predispose people to become ill.11 This contingent contagion perspective offered a congenial middle ground for miasmatists who considered individual predisposition an outmoded explanation, and for contagionists who could not find evidence of cholera’s progress in every local outbreak. Unsanitary environments could transform a normally noncontagious disease into a contagious one, or vice versa. By the mid1840s local miasmatists, infection contagionists, and contingent contagionists increasingly downplayed theoretical disputes in order to unite behind practical sanitary reform measures directed at eliminating nests of cholera fever. Snow appears to have been an interested listener rather than an active participant in professional debates about the nature of cholera during this period.

The Horror from the East Concern about epidemic cholera began appearing in the London medical press in 1817, when British physicians in India reported that an endemic native disease was

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spreading widely and with great virulence.12 The symptoms of this disease were striking. In the first, or premonitory, stage the sufferer might experience nothing but a vague unease and perhaps a mild diarrhea, as if having eaten spoiled food. The second stage was characterized by vomiting, muscular spasms, and pains in the lower chest and upper abdomen, accompanied by a profuse diarrhea. The diarrhea, widely accepted as the signature symptom of the disease, was of a peculiar type—there was virtually no fecal color or smell to the stool, which instead appeared watery with small white particles suspended in it. Because it looked like water in which rice had been boiled, it was dubbed “rice-water stool” and considered a hallmark indication of second-stage cholera.13 The third stage was one of profound collapse. Victims retained mental function until near the end, but the body became cold, a pulse could scarcely be felt, and the face and extremities often turned dusky.14 Blue, corrugated skin made even young patients seem aged (Fig. 7.1).15 The conceptual and therapeutic confusion regarding cholera was reflected in its name. Searching about for something to call this epidemic disease, surgeons and physicians with the East India Company chose cholera, a name already in use for quite a different condition. “Cholera,” or “cholera morbus,” was well known in England as an endemic diarrheal disease most common during the summer months. It got its name from the yellow–brown color of the diarrhea and vomit, suggesting that it was caused by an excess of “choler” (the humor yellow bile).16 Relatively few

Figure 7.1. “Blue Stage of the Spasmodic Cholera,” showing blue coloration of face, neck, hands, and feet as well as the abnormally aged appearance of cholera victims (Lancet 1 [1831–32]: between 538 and 539).


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died of English cholera, and those that did tended to be infants or the debilitated. By contrast, the disease spreading out of India was marked by an absence of yellow bile and often struck those in the prime of life with a mortality rate of up to fifty percent.17 To avoid confusing this emerging epidemic disease with English cholera, authors often added a qualifying term such as malignant, Asiatica, or Indica (Table 7.1), but the profusion of terms impeded medical and popular understanding of the new disease.18 The language dispute suggests some of the conceptual issues—a person who elected to use the term spasmodic cholera probably favored a view of the disease as essentially involving the nervous system, for example. A disease that could seize a British soldier in perfect health, reduce him six hours later to a whimpering infant unable to control the discharge from his bowels, and lay him out a corpse six hours after that inspired horror even in supposedly objective medical observers.19 One account from an official Indian report seemed to depict cholera as a man-eating tiger: “It was [in an army camp near the banks of the Sinde in Bundlekund] that the disease put forth all its strength, and assumed its most deadly and appalling form. . . . After creeping about . . . in its wonted insidious manner, for several days among the lower classes of camp followers; it, as it were in an instant, gained fresh vigor, and at once burst forth with irresistible violence in every direction.”20 British medical practitioners became more anxious over the next fourteen years as the tiger progressed westward. In 1821 the disease spread northwest from India into Persia and the Middle East, eventually reaching the city of Astrakhan on the Caspian Sea in 1823. It then died out but retraced these same steps in 1829–1830, this time continuing northward through Russia. It had spread westward to the Baltic ports in the spring of 1831 and from there hopped to Sunderland, a British port just south of Newcastle, that fall before petering out by the turn of the year.21 It reappeared the following summer, spread north to Edinburgh and south to London. Newcastle was hard hit once again, including outlying mining villages like Killingworth, where Snow was sent to treat its victims. Table 7.1. Alternative terms for cholera morbus, 1831–1855a Algideb Asiatic Asphyxial Epidemic a

Indian Malignant Pestilential Spasmodic

Only one term is shown when the term was often used in either an English or a Latin variant, e.g., “Asiatic cholera” and “cholera Asiatica.” b From Latin algor, “cold.”

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With cholera on their very doorstep, British physicians felt called upon to take decisive action—but what should one do? It was difficult to make any sense of the accumulating literature. Regarding the spread of cholera, for example, E. O. Spooner stated that from 1817 cholera had followed well-established trade and travel routes, always attacking a port city, for example, before spreading inland and never moving from one location to another faster than human beings traveled,22 but G. H. Bell offered contrary evidence that the disease usually moved about in ways totally unconnected to human trade and travel.23

Social Upheaval and Sanitary Reform Cholera arrived in England at a time of social upheaval as well as medical controversy. The first epidemic struck shortly after the opening of the first steam-powered public railway in 1830. Manufacturing interests began to flex their political muscles while many workers, especially in the new industrial towns, lived in horribly crowded, unsanitary, and dangerous housing. The Reform Bill of 1832 shifted the power structure within Parliament by expanding the franchise to include small property owners, but radical democrats considered these measures incomplete because the working classes were still excluded. Unemployment, poverty, hunger, and unmet expectations spawned the Chartist Movement, riots, and unrest of the mid-1830’s. Cholera seemingly took advantage of the new conditions of industrialized England—entering through the seaports, traveling inland along the new highways and railroads, and attacking first the most densely populated and unsanitary abodes of the desperately poor. To many contemporaries epidemic cholera was just another symptom of the social unrest and upheavals that plagued Great Britain. Radical democrats among medical men, such as the physician James Phillips Kay-Shuttleworth, thought the epidemic was an opportunity to “follow the footsteps of this messenger of death” into “the abodes of poverty . . . the close alleys, the crowded courts, the overpeopled habitations of wretchedness, where pauperism and disease congregate round the source of social discontent and political disorder in the centre of our large towns, and behold with alarm, in the hot-bed of pestilence, ills that fester in secret, at the very heart of society.”24 Radical reform meant the expansion of liberal values to the entire population. Everyone should share the new wealth generated by industrial and commercial capitalism. Epidemics were just proof of this for medical radicals: Eliminate the environmental conditions that permit these diseases to “fester . . . at the very heart of society,” or they will soon spread to the middling and upper classes. Just as an expansion of the franchise was fair in a democratic society, medical radicals argued that good public policy required the state to undertake positive (in the sense of legislative) sanitary measures. Yet another divide had emerged in the medical profession; many medical men believed reform was uncalled for or too incendiary.


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Not everyone shared Kay-Shuttleworth’s view that disease and social conditions were intimately connected. Edwin Chadwick, a barrister who had been secretary to the utilitarian philosopher Jeremy Bentham, was instrumental in designing the New Poor Law of 1834. His initial goal was efficiency, seeking both to centralize the response to poverty and to create systems that discouraged pauperism and reduced total state expenditures. The previous system had focused on “out-door relief ”— assistance provided to the poor mostly in their own homes—and was administered by 15,000 individual parishes. The New Poor Law shifted some responsibilities to Boards of Guardians of about 600 unions, thereby creating another administrative level of geographical units with the financial base to construct and maintain large workhouses. Workhouses were supposed to provide “in-door relief ” for paupers only; “least eligibility” requirements were restrictive by design and conditions within the workhouses repellent to encourage the population to seek gainful employment rather than welfare. The New Poor Law was an example of the intent of liberal social engineering. Benthamites believed that effective government should actively promote the work ethic necessary for capitalism to function and promote the wealth of nations. In addition to deciding who was eligible for admission, Boards of Guardians appointed surgeons to attend sick inmates in the infirmaries attached to the workhouses; managed paving, sewer construction, and local water pumps; and supervised all sanitary and medical measures undertaken during epidemics. Only after the new system began to operate did Chadwick realize that the incentives were not working as he had planned and that many of the poor became paupers not because they were lazy, but because they were often too sick to be employable. With workhouses choked by the sick poor, the infirmaries turned out to be the most rapidly expanding and expensive part of the entire system.25 By 1837 Chadwick shifted direction and began to focus more on the goal of preventing disease as a means to reduce the burden of poverty on the nation. He sought the help of medical advisers, most notably Thomas Southwood Smith, another close associate of Bentham’s.26 In the Benthamite spirit they believed a compilation of statistics on a national scale would illuminate the precise relationship between poverty and illness, after which Parliament could design sound public policy. A General Register Office was formed in 1837, and the Report on the Sanitary Condition of the Labouring Population followed in 1842, based in part on the reports submitted by the New Poor Law medical officers.27 A Royal Commission on the Health of Towns was established in 1843, and various items of sanitary reform legislation followed.28 Chadwick’s and Southwood Smith’s efforts culminated in the Public Health Act of 1848, the year the second great cholera epidemic reached England. A threemember General Board of Health was created as a strong central authority. Medical Officers of Health were appointed to oversee local sanitary conditions in each district, regulate offensive trades such as slaughterhouses and tanneries, condemn houses unfit for human habitation, and supervise burial grounds, sewers, water supplies, and waste disposal. In short, this new medical arm of the state was given

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primary responsibility for ensuring a healthy population and a productive workforce. By 1853 103 towns had come under the Public Health Act.29 Champions of local control, however, mounted considerable opposition to the national sanitary policy advocated by Chadwick and his allies. According to Baldwin the Benthamite version of sanitary reform was “a totalizing worldview resting on certain presuppositions concerning the balance of nature and the role of illness and disease in the divine harmony of the universe. . . . Sanitationism was a remarkably consistent and unified vision that combined social reform and public hygiene in a seamless whole. All epidemic diseases were to be prevented, or at least ameliorated, in one fell swoop while at the same time social problems were addressed. . . . Housing reform and disease prevention, for example, went hand in hand, part and parcel of the same grand vision of a society that through its concern with public health also improved the lives of its poorest.”30 Baldwin has contrasted sanitarianism with the “quarantinist” posture, which was narrowly concerned with preventing the spread of disease. Advocates of quarantine saw no link between preventing disease and bettering the lives of the potential disease sufferers.31 Comprehensive sanitarianism, on the other hand, was a central plank in the radical reform agenda and suited the meliorist attitudes of those in the middle and upper classes, both moderate Whigs and Tory Democrats, whose social conscience was piqued by altruism, worry about epidemic diseases, or fear of social revolution.

Sanitary Reform and Anticontagion As disciples of Bentham, the sanitarians embraced the most up-to-date methods of statistical analysis, which they believed would identify the environmental sources considered predispositions to constitutional or epidemic diseases. The common view among sanitarians was that epidemics were caused by inhalation of agents in the atmosphere. Once inhaled, the causative agent acted upon the blood to disrupt the body’s internal balance, resulting in fever and other symptoms of each epidemic disease. The lineage of atmospheric causation was ancient, with origins in the Hippocratic corpus that was updated in England by Thomas Sydenham. He attributed the “exciting cause” of each epidemic disease to particular atmospheric conditions affecting large areas. The required elements for disease were peculiar vagaries of climate and season—the “epidemic constitutions.” Whether one became depended ill on the situation of one’s “internal constitution.” People in whom seasonal changes produced significant humoral imbalances were particularly susceptible to epidemic diseases; those whose humors remained in balance were not normally afflicted. No personto-person transmission was invoked. Sydenham’s followers retained the notion of “epidemic constitution” but replaced the humoral framework with chemical imbalances. For example, a correspondent to the Lancet in 1837 compared influenza and


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cholera: “both are of an epidemic nature, arising, passing over the face of the earth, and disappearing, in a mysterious manner. Both seem to be influenced by the season of the year, or by the state of the atmosphere as regards heat and moisture. The course of both is, mostly, from east to west. . . .”32 John Snow himself seemed to employ this line of thinking in 1842, when he commented to the Westminster Medical Society about an outbreak of influenza he had seen during his first year as an assistant: “The epidemic in April, 1833, occurred immediately after a continuance of cold wet weather had been succeeded by that which was warm and dry; and the epidemic in the winter of 1837 took place after a frost had yielded to weather considerably warmer.”33 By Snow’s day, however, the appearance of Asiatic cholera had sharpened disagreements about the causes of epidemic disease, and Sydenham’s theory had been relabeled as general anticontagionism.34 The appearance of cholera in the west also resurrected an eighteenth-century variant of the theory of “epidemic constitution,” atmospheric corruption by local miasmatic sources.35 Thomas Southwood Smith, a visiting physician to the London Fever Hospital, advocated this version of anticontagionism, which explained why epidemic disease appeared in one locality while leaving nearby areas untouched. No longer was it sufficient to state, for instance, that a spell of cold weather had been superseded by a period of warm weather. To local anticontagionists concentrated amounts of rotting vegetable matter generated “a principal, or give origin to a new compound,” that was emitted into the surrounding atmosphere by gaslike miasmas that were poisonous to humans.36 Southwood Smith’s theory of local miasmas adopted Sydenham’s assumption that disease took its character, in part, from the geography, climate, and the individual histories of the people in the places where it occurred: “The fever of one country is not the same as the fever of any other country; in the same country, the fever of one season is not the same as the fever of any other season; and even the fever of the same season is not the same in any two individuals.”37 Many local miasmatists believed that diseases such as typhoid fever, dysentery, and cholera were variants of one basic form of fever and that local changes in atmospheric conditions would determine which variant one might contract. It was also taught that when a particular epidemic disease (such as influenza) was raging in an area, other diseases that happened to occur there (such as diarrhea) would be modified by the prevailing epidemic influence and bear the “impress” of the epidemic disease.38 Local miasmatists assumed that putrefying animal matter produced the most lethal concentrations of poisonous agents, sometimes distinguished as effluvia. Southwood Smith regarded the noxious effluvia given off by fever sufferers in closely confined spaces as “by far the most potent febrile poison.”39 He cited a case report that suggested how locally generated miasmas could be transformed into effluvial poisons: The suddenness with which a fever sometimes attacks individuals on board a ship, or even an entire ship’s crew, on the approach of a vessel to a shore where the poison is generated in large quantity, and in a high state of concentration,

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illustrates its operation, perhaps, in a still more striking manner. Dr. Maculloch . . . relates an instance of some men on board a ship, who were seized, while the vessel was five miles from shore with fatal cholera, the very instant the landsmell first became perceptible. Several of these men, who were unavoidably employed on deck, died of the disease in a few hours. The armourer of the ship, who, before he could protect himself from the noxious blast, was accidentally delayed on deck a few minutes, to clear an obstruction in the chain cable, was seized with the malady while in that act, and was dead in a few hours.40 Unlike the weaker miasmas, to which only predisposed individuals were susceptible, some effluvia killed everyone who inhaled them. Like Sydenham, local miasmatists resorted to the long-standing doctrine of constitutional predisposition to explain why, although many people breathed the air containing a miasma, only some became sick. This is what Southwood Smith meant when he wrote, “even the fever of the same season is not the same in any two individuals.” Unlike Sydenham, nineteenth-century local miasmatists generally cited personal characteristics and environmental conditions rather than humors as predisposing factors. For example, W. Lauder Lindsay of Edinburgh argued in the 1850s that strong emotions, especially fear, rendered one susceptible to epidemic diseases like cholera. He had “full faith in the Board of Health views on the noncontagiousness of the disease,” so he felt no fear when he attended its victims at the Surgeon’s Square Cholera Hospital in Edinburgh and did not render himself susceptible.41 Immorality (specifically, overindulgence in alcohol and sex) also predisposed people to contracting cholera, especially when the “epidemic constitution” was most conducive: “The probability of an outburst or increase during [calm, mild] weather, I believed to be heightened on holidays, Saturdays, Sundays, and any other occasions where opportunities were afforded the lower classes for dissipation and debauchery.”42 Improper nutrition, overcrowding, and inadequate ventilation could also make one unusually susceptible to cholera. The inclusion of certain environmental circumstances among the predisposing factors for epidemic diseases allied local miasmatists with Benthamite sanitary reformers, who believed only a governmental agency could undertake the sophisticated statistical analyses necessary to prevent the spread of disease in the first place (Fig. 7.2). In general, the sanitarians believed that many diseases were caused by “filth.” Filth could be detected by the unaided senses, and the major way to prevent disease in urban settings was to clean up accumulations of garbage and sewage or whatever else produced foul odors.43 Careful statistical studies could identify where concentrated pockets of disease existed and then trace the hoped-for decline in disease rates as the filth was cleaned up. By this reasoning one should focus on removing fever nests within one’s own land rather than worry about threats from without. Sanitarians and local miasmatists, therefore, opposed quarantine measures during pandemics. In an island nation that depended heavily on trade, this position won


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Anticontagionist (Miasma) Theory decomposing organic matter

miasma atmospheric influences ?(mild) lungs

IMPORTANT: humoral/ constitutional predisposition

under certain conditions

humoral disruption

noxious effluvia exhaled (via skin, sweat)

disease state lungs

new cases of disease

Figure 7.2. Anticontagionist theory according to sanitarians such as Southwood Smith.

them support among the mercantile and manufacturing classes, who wished to avoid any major impediment to the flow of ships and goods.44 Miasmatists also argued that their position was good public policy because it would not result in public panic or abandonment of the sick, as a belief in contagious properties of cholera might.45 The General Board of Health (GBH), established by Parliament during the second cholera epidemic and in place until 1853, was sanitarian and local miasmatic in orientation. Chaired by Chadwick, its only medical member was Southwood Smith. Its reincarnation during the third cholera epidemic of 1854–1855 maintained this double orientation, albeit even more aggressively critical of contagionism than was its predecessor.46 In retrospect, the advice given by the sanitary reform movement could hardly fail to be helpful. In a day when one could hardly walk the streets of the working-class section of any English city without tripping over piles of decaying garbage and landing in pools of human excrement, cleaning up whatever smelled bad seemed certain to improve the overall public health.47

Contagion Although official pronouncements during the second and third cholera epidemics leaned toward local miasmatic and sanitarian views, most government officials at the

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time of the 1831–1832 epidemic believed cholera was a contagious disease.48 The contagionist position had been little modified since propounded by Fracastorius in 1546.49 In essence, contagionists viewed the causative agent of epidemic diseases as a particle, often described as a “virus”; Fracastorius’s phraseology suggested an analogy to a seed.50 In the following century Athanasius Kircher (1602–1680) proposed that animalculae (microscopic animals) might be the causative agents of infectious diseases,51 but like the undetectable “principal” or “compound” of the local miasmatists, the structure of the contagious particle remained unknown during Snow’s lifetime, so contagionists were primarily concerned with the effects that could be attributed to it. Significant subdivisions existed within the contagionist camp (Fig. 7.3), but all were in agreement that in some diseases the bodies of sick persons produced “viruses,” or seeds, that could cause the same disease in a previously healthy person. The contagious particles could be transmitted in several ways. In smallpox, for instance, there was general consensus that spread could occur by simple touch. Fol-

ANTICONTAGIONISM

CONTAGIONISM

Disease-causing matter in atmosphere and physical environment, inhaled through lungs, enters blood and disrupts physiological balance

Disease-causing matter (virus) produced in bodies of sick persons and transmitted by:

General

Infection

Local

Widespread atmospheric conditions, etc. (Sydenham: epidemic constitution)

Miasma due to putrefaction of vegetable or animal material

Anomalous facts unexplained by theory

Fomites

Touch

Virus given off by sick in exhalations; inhaled by healthy

In closely confined spaces, effluvia from sick may infect the healthy via lungs

Anomalous facts unexplained by theory

CONTINGENT CONTAGIONISM Disease may be contagious or not depending on factors such as: individual susceptibility, filth/poverty, diet, habits, elevation, virus dosage, weather.

Figure 7.3. Three theories of cholera transmission, 1830–1850.


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lowing the development of smallpox inoculation (and later vaccination), inoculation directly into the body or the blood became recognized as a mode of transmission under the general category of contagion. A form of indirect contact was through fomites—articles such as clothing and bedding used by the sick that harbored the shed “virus” and preserved its capacity to transmit disease for some period of time.52 Another route was “infection,” in which healthy people inhaled the “virus” after it was given off in the exhaled breath or from the skin pores of the sick person.53 Some medical men distinguished infection from “true” contagion, which they limited to transmission by touch.54 James Copland, a physician colleague of Snow’s, was representative of those who believed in “the infectious nature of pestilential cholera” rather than contact contagion: “It was not caused or propagated by immediate or mediate contact—by a consistent, manifest, or palpable virus or matter; but by an effluvium, or miasm, which, emanating from the body of the affected, and contaminating the air more immediately surrounding the affected person, infected the healthy who inspired the air thus contaminated. . . .” He believed that “this morbid effluvium or seminium of the distemper—this animal poison emanating from the infected—was often made manifest to the senses of smell and even of taste; it attached itself to the body and bed-clothes; . . . and reproduced the disease when the air respired by predisposed persons was contaminated or infected by the clothes imbued by the effluvium or poison.”55 Whether Snow accepted Copland’s notion of an infectious effluvium is unclear. He may have, because according to the minutes from an 1838 meeting of the Westminster Medical Society, “Mr. Snow believed that typhus fever was contagious, and related a case in which a servant girl was attacked with the disease, and sent home, a distance of many miles; there had been no typhus fever in the place; the whole of her family suffered from the complaint, and several of the members died.”56 One cannot determine from such a cryptic synopsis if he believed the contagion had occurred by touch, fomites, or infection.

Contingent Contagion Occasionally the dispute between contagionists and anticontagionists could be decisively settled by the characteristics of the disease itself. Very few British physicians in the nineteenth century denied the contagiousness of smallpox. It seemed obvious to all that susceptible people coming into close contact with a smallpox sufferer frequently contracted the disease and that smallpox cases occurred sequentially in a manner consistent with person-to-person spread.57 Influenza, on the other hand, was most often thought to be an exemplary miasmatic epidemic, appearing to break out within a local region with numerous cases simultaneously. After the clear-cut diseases were addressed, medical men were left with a number of diseases, including plague, cholera, typhus, and yellow fever, for which the facts were less decisive.58

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When it came to cholera, the problem was that while some outbreaks and individual cases of cholera followed anticontagionist criteria, others seemed to fit contagion (Table 7.2). Observers in India reported that surgeons and others caring for the sick seldom if ever contracted cholera, but reports from Russia indicated that physicians fell ill in substantial numbers.59 Each camp put forth explanations designed to cover the anomalous cases. Fomites (infected articles such as clothing) helped the contagionists to explain an outbreak of cholera in a vicinity as yet unvisited by any known cholera sufferer, while anticontagionists appealed to individual predisposition to explain why some who inhaled noxious miasmas and effluvia nevertheless failed to develop the disease. Autoexperiments in which researchers ingested fluid from cholera victims without contracting cholera themselves seemed to disprove the contagionist claim that the stomach could be a portal of entry for the “virus.”60 In general, each side of the dispute was more skilled at pointing out the anomalies left unexplained by their opponents than at repairing the chinks in their own arguments,61 but contagionist ranks suffered the greatest number of defections after the 1831–32 epidemic. “As it became increasingly clear that cholera was not as directly contagious as the plague, as experience showed that the medical personnel in closest contact were not necessarily more afflicted than others, that its incidence varied by class, season, region, neighborhood and person, the evidence seemed to mount that something other than a contagion was at work. . . .”62 Although theoretical purists reviled it, contingent contagionism became increasingly popular with the accumulation of anecdotal evidence about cholera outbreaks that could not be explained by either of the extreme perspectives. Its initial London proponent was James Johnson, former naval surgeon and editor of the Medico–Chirurgical Review.63 During the Napoleonic Wars he had observed a cholera epidemic in India. About a quarter century later, during the first “visitation” of Asiatic cholera to England, he offered readers of his journal a definition that spanned the contagionist–miasmatic divide: “In epidemic cholera, as in most other epidemics,

Table 7.2. Characteristics of outbreak favoring competing theories Anticontagionism

Contagionism

Instantaneous; greatest number of victims in first few days

Propagates gradually; number of cases builds

Not traceable to human contact

Traceable to human contact

Medical attendants spared

Medical attendants often contract disease

Apparent spontaneous initiation in locations without obvious contact among sick individuals

Often brought to a previously unaffected place from an affected locality by a sick visitor Previous case of disease creates immunity (follows smallpox inoculation model)


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a poison or sedative principle, whether emanating from the earth, from animal or vegetable bodies on the earth, or engendered in the air, strikes a predisposing individual, and after an uncertain period of incubation, . . .” produces the visible symptoms of the disease.64 Local miasmatists could agree with Johnson’s assumption that the causative agent was a chemical produced by decomposing vegetable and animal matter, and Johnson’s multicausal definition could satisfy moderate contagionists, who accepted transmission by an infectious “virus” produced in the bodies of the sick. However, his qualification that the predisposing factors (“contingencies”) were environmental rather than constitutional ruled out an alliance with general miasmatists. In his view most diseases required particular contingencies to render them epidemic: “diseases arising from aerial or terrestrial influences, far beyond our control, have, in the hovels of the indigent, in crowded populations, in concentrated filth, and in the absence of ventilation, taken on a character of infection or communicability which they did not originally possess, and of which they are quickly deprived under opposite and favourable circumstances.”65 For example, filth and overcrowding were essential for typhus.66 Johnson considered cholera analogous to typhus; both were contingent–contagious diseases and easily controlled by removing filth and improving ventilation (Fig. 7.4). Smallpox was the exception that proved the rule. Unlike the majority of epidemic diseases, it was a purely contagious disease because it could develop and be transmitted in all environmental circumstances. Thus, contingent contagionists could actively join local miasmatists in recommending sanitary reform as the most effective preventive against Asiatic cholera. By and large, Johnson’s theory became the refuge of perplexed miasmatists: “we are infinitely more favourable to the views of the exclusive anti-contagionists than to those of their opponents . . . because we are convinced that their [sanitary] doctrines, on the whole, are infinitely more beneficial to society and to the sick, even if they are wrong, than are those of the opposite sect.”67 Filth should be removed, regardless of whether one believed it was a necessary environmental contingency or just a predisposing factor for cholera.68 Their preference for anticontagionist allies notwithstanding, Johnson and his followers had staked out the basis for theoretical overlap with moderate contagionists, who admitted cholera could be transmitted by the inhalation of bodily effluvia generated in its victims (“infection” in contagionist parlance). By the mid-1830s most local miasmatists were prepared to admit disease causation by bodily effluvia in rare circumstances such as close confinement with poor ventilation. Their concession that cholera was occasionally contagious reduced the controversy considerably thereafter.69 Consensus was emerging on one key point: The agent that caused cholera was inhaled. Miasmatists felt vindicated. Most contagionists by the mid-1830s, with the exception of a minority who cited etymology (con + tangere, “to touch”), believed that infection (inhalation) was as likely a mode of transmission as contact for a disease like cholera.70 An example of a contagionist strongly committed to the infection theory was E. O. Spooner of Blandford.71 In 1849 he ridiculed the local miasmatic stance of the

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Contingent Contagionism J. Johnson, 1831 (per Durey) decomposing organic matter

miasma

"contingencies" environmental factors: filth & overcrowding

lungs

lungs

humoral disruption

humoral disruption

effluvia

individual disease state

individual disease state

X no spread to others

spread to other persons

Figure 7.4. Contingent contagionism theory according to James Johnson.

GBH. There had been rotting garbage and other evil smells in the streets for decades, but cholera epidemics occurred only in 1831–1832 and 1848–1849. He claimed that miasmatists had gained unwarranted support by demanding unrealistic standards of proof: “The difficulty sometimes found in tracing an infectious disease up to its true source, does no more invalidate the doctrine of contagionism than would a hundred undetected larcenies lead us to suppose that they could be committed without the thief.”72 Contagionists had identified three different routes of possible transmission: touch (whether direct or via fomites), infection (inhalation), and deliberate inoculation. Spooner believed the presence of a specific rash or exanthem suggested infection as the most likely route: The substance causing smallpox was inhaled into the lungs, transmitted to the blood, and from there caused an eruption of the skin


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that eventually caused the skin to peel. The same model applied to scarlatina.73 By analogy, the substance that caused cholera should be inhaled, transmitted to the blood, and cause similar changes—only to the inner lining of the bowel instead of the skin.74 Spooner relied heavily on the pathological investigations of Ludvik Böhm of Berlin, who had claimed that the desquamation of the inner lining of the mucous membrane of the intestinal canal was a hallmark of cholera.75 Spooner assumed that this peeling away of the intestinal mucous membrane was, in effect, the “rash” of cholera, making the analogy with smallpox complete. Perhaps Snow had a similar model in mind when discussing a case of smallpox he had treated: “The row of small dwellings, in one of which this boy lived, are damp and ill ventilated, and all the illness I have seen in them has been more severe and intractable than in the rest of the neighbourhood. I have treated two cases of sporadic cholera [English cholera, or cholera morbus] there, as bad as any cases of the epidemic disease [Asiatic cholera] which I have known to end in recovery. . . .”76 The reference to local circumstances (dampness and poor ventilation) producing diseases equivalent in severity to epidemic cholera parallels the reasoning of contingent contagionists.

Farr and Zymotic Disease While some sanitary reformers seemed wedded to the older bedside medicine with vestiges of the humoral paradigm, others incorporated new ideas from hospital and laboratory medicine that accommodated the infection model with its emphasis on spread by the respiratory route. William Farr (1807–1883), Benthamite radical and sanitary reformer, regular contributor to the Lancet, and compiler of health and mortality reports at the General Register Office, was a master disease statistician (Fig. 7.5).77 When Farr began classifying diseases for statistical purposes in 1837, he employed the categories “endemic, epidemic, and contagious diseases.” His scheme’s inclusiveness appealed to contingent contagionists, and Farr’s weekly disease reports were reprinted in medical journals and the lay press. In the early 1840s he replaced the tripartite categories with “zymotic diseases,” by which he meant diseases caused by a chemical process similar to, if not identical to, fermentation.78 Farr adopted his ideas on fermentation and allied processes from the work of the German chemist Justus Liebig (1803–1873).79 Liebig argued that yeast was an “exciter,” a nonliving organic material that, when in a state of decomposition and placed in a fluid with the proper chemical constituents, was capable of reproducing itself within the fluid. He rejected the notion that yeast was a living organism that lived on sugar and excreted alcohol and carbon dioxide. The blood, which Liebig considered one of the most dynamic and unstable components of the body, was a prime target for an externally introduced exciter capable of reproducing in the blood. When this happened the outcome was an internal state of decomposition because the exciter, in order to reproduce itself, absorbed the chemical constituents normally used

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Figure 7.5. William Farr (1807–1883).

to maintain the blood in a healthy state. Liebig thought that two distinct types of exciters caused the blood decomposition symptomatic of all diseases. In smallpox, syphilis, and plague the exciters initiated a process of decomposition in the blood of the victim that both reproduced (“propagated”) the exciter substance and also produced the disease symptoms. The new generation of exciter particles produced by internal propagation explained the disease’s capacity to spread from person to person. Miasmata, by contrast, caused blood to decompose and produced disease, but these exciters could not reproduce within the body and, therefore, could not be transmitted to another person.80 Besides borrowing Liebig’s notion of fermentation, Farr relied on an analogy between the exciters and chemical poisons in classifying zymotic diseases. If one saw in the body the specific set of symptoms and signs that were consistent with arsenic poisoning, one was entitled to infer that arsenic had been taken into the body and was the exciting cause. Similarly, zymotic diseases arose when a poison specific for that disease entered the body and became seated in the blood. Like chemical

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poisons, zymotic poisons affected some organs more than others, and such local pathological changes accounted for the specific characteristics of different diseases. Farr assigned names for the unseen but hypothesized exciting causes, so that smallpox (variola) was caused by the poison “varioline,” cholera by “cholerine,” and so on. These names were placeholders until investigations in the collateral sciences could uncover the specific nature of the causative agents.81 Although Farr was unsure about the precise features of the agents that produced zymotic diseases, the data he collected suggested that they were small particles of nonliving organic matter rather than gases. The spread of contagious diseases did not match the predicted pattern for the diffusion of gaseous vapors alone (Fig. 7.6).

Farr circa 1840s—1850s cholerine (specific organic nonliving particle)

decomposing organic matter atmospheric conditions, altitude, etc.

usually

occasionally

lungs

lungs

excites chemical reaction in blood akin to fermentation

reproduction of cholerine particle

excites chemical reaction in blood akin to fermentation

disease symptoms

person-to-person spread

Figure 7.6. Farr’s contingent contagionism theory.

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By 1852 his analysis of two cholera epidemics in England suggested that the primary factor was elevation above sea level; the lower the elevation, the higher the mortality (Fig. 7.7). It made sense to him that cholerine, the particulate matter that caused cholera, would be concentrated in the air at lower elevations and that cholera would therefore be more prevalent along the seacoasts and tidal rivers than in the interior.

Figure 7.7. Farr’s graph of cholera incidence related to elevation ([Farr], Cholera in England, 1848–1849, lxv).


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Farr remained uncommitted at this point on whether cholerine was also produced inside the human body and propagated by infection, ingestion of impure water, or by multiple channels.82 His “zymes,” like Liebig’s exciters, spanned the contagionist and anticontagionist divide. No matter how the disease might be spread, one could still claim that its underlying process was explainable in chemical terms as a sort of ferment.83 By 1854 Farr had extended his theory to embrace four subcategories of disease—the miasmatic (which included smallpox as an infectious disease); the enthetic or contagious (limited to those spread only by direct contact, such as syphilis), the dietetic (such as scurvy), and the parasitic.84

Infection, Pathology, and Treatment In the London-based medical journals at midcentury, disagreement about the cause and mode of transmission of cholera was often overshadowed by uncertainty about its pathology and the continuing controversy over how to treat it. Theories of cholera pathology sought to incorporate information taken from research in the collateral sciences, which proved frustrating. Autopsy was the dominant tool of the day in applying hospital medicine to the problems of epidemic disease, and most experts reported that autopsies of cholera patients revealed few consistent or characteristic findings.85 Those who thought that massive diarrhea was the cardinal symptom of the disease developed pathological theories that implicated the intestines. Spooner assumed that Böhm’s idea of desquamation of the intestinal lining effectively linked the theoretical model to the final result, diarrhea. Others were more impressed with the spasms and the symptoms during the third stage (collapse), which seemed to predict a fatal outcome, and postulated the nervous system as the “seat” of cholera.86 The local miasmatist Southwood Smith believed putrefactive poisons first attacked the central nervous system. The fevers characteristic of epidemic diseases were merely symptomatic of the body’s loss of regulatory control, after which the other organ systems fell like a row of dominoes—first circulation, then respiration, and finally the organs of secretion and excretion.87 Some medical men hoped chemistry would solve the cholera puzzle. Virtually all observers agreed that the rice-water stools contained a large amount of water, a little bit of protein and various salts, almost no bile or other recognizable components of normal feces, and some cellular components that were probably shed epithelial cells from the inner lining of the gut.88 William Brooke O’Shaughnessy (1809–1902) performed some pioneering experiments on the chemistry of the blood in cholera during the 1831–32 epidemic. He reported that the blood retained its normal anatomical structures but had lost much of its water and neutral salts; and that elements deficient in the blood were found in excess in the stools.89 In the 1840s Alfred Baring Garrod, Snow’s Westminster and Aldersgate colleague, confirmed these findings.90 The chemical analyses by O’Shaughnessy and Garrod would explain why the blood of cholera victims appeared unusually viscid at autopsy.

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Even so, other medical men, including Edmund Parkes and Lauder Lindsay, denied that the postmortem appearance of cholera blood differed materially from the findings in other diseases. Parkes argued that the blood was indeed affected in cholera, secondarily to changes that occurred in the heart and lungs, but that it was the fibrin in the blood rather than the fluid and salt content that was altered.91 George Johnson of King’s College Hospital agreed that the blood was altered in appearance but denied that the amount of fluid lost via the bowels could account for the changes in the blood. Johnson agreed with Parkes that death occurred in cholera because the cholera poison impeded the circulation of the blood through the right side of the heart and the pulmonary vessels. That is, death by cholera resembled death by asphyxia: The blood was unable to circulate through the lungs and so could carry no oxygen to the rest of the body. Johnson insisted that no matter how the poison might enter the system, its final point of action was the bloodstream. In this regard, Johnson added, the cholera poison acted in a manner analogous to an inorganic poison like arsenic.92 When it came to treatment of cholera, traditional bedside remedies remained largely unchanged; the new laboratory medicine had yet to eventuate in a therapeutic revolution.93 The efficacy of every treatment was still judged in terms of whether it helped restore the body’s internal balance. Sydenham’s theory of “epidemic constitutions” might have lost most of its currency in the debate about cause and transmission, but it was largely undisputed among clinicians. They selected therapeutics based on their assessment of the interaction of external environmental factors (such as the season), constitutional peculiarities of individual patients, and the natural history and progression of disease. For example, in slower-progressing cases of cholera, the earliest phase of diarrhea resembled the stool in typical mild gastrointestinal illnesses, and it should be treated as such. Early implementation of an aggressive regimen of therapeutics, such as one should use in later stages, might push a relatively innocuous case of premonitory choleraic diarrhea into full-blown cholera.94 The range of contradictory therapeutic approaches was huge and ultimately confusing.95 A reporter for the Lancet noted, “The drinking of water ad libitum, the employment of sulphur, of calomel and opium, of sulphuric and tannic acids, of nitrate of silver, of large quantities of whey, of saline injections, of creosote, of charcoal and lime water, had each its advocates” among members of the Medical Society of London in 1854.96 The contradictory recommendations of calomel and opium are exemplary: If one assumed (as did George Johnson) that vomiting and diarrhea were natural efforts by the body to rid itself of the cholera poison, then calomel was an ideal remedy because it promoted these processes. However, if one considered the diarrhea in cholera an excessive reaction indicative of a severely imbalanced system, opium should be administered to bind the stools.97 Drinking huge quantities of water containing neutral salts was called the “saline treatment,” an adaptation of a popular hydropathic method to the results of chemical researches on choleraic evacuations.98 Also reflective of these results was the recommendation to employ “saline


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injections” into the veins to restore the fluid lost via the bowels and to replace the missing elements in the blood. Saline injection, which today is considered the most rational therapy for cholera, was proposed by O’Shaughnessy in 1832 as a way to restore the salts his experiments had shown to be depleted in the blood. Dr. Thomas Latta of Leith, near Edinburgh, decided to try O’Shaugnessy’s proposal on patients in the last stage of cholera after finding that fluid replacement by rectum only aggravated their symptoms.99 After initial failures he was able to report several successful outcomes. Perhaps the most remarkable case was that of a fiftyyear-old woman in far advanced collapse. He administered two prolonged fluid injections, but each time the cholera symptoms returned a few hours later. However, the third injection resulted in complete recovery. More than twenty pints had been injected in all.100 Wakley in the Lancet praised Latta and his treatment,101 but others were very critical. The air fizzled from Latta’s balloon as he spent more time rebutting charges that his method was unsafe than he did in trying to save patients.102 By the 1848–1849 epidemic there was so little interest in this mode of therapy that the GBH did not bother to mention it in its official report.103 The results were decidedly inconclusive. George Johnson, reviewing the total body of evidence from the 1832 experiments, noted that of 156 patients injected, only twenty-five recovered, “a result which can scarcely be considered satisfactory.”104 Moreover, with the social prestige of the profession at relatively low ebb during this period, physicians could not afford to put their reputations further in jeopardy by therapeutic experiments likely to be regarded as rash by the laity.105 Practitioners who experimented on patients with newfangled measures risked being labeled “empirics,” viewed as only one step (if at all) removed from quackery. Government authorities produced a fairly standard list of recommended treatments whenever cholera broke out. When cholera struck Exeter in 1832, the local health board posted handbills that repeated information distributed by the GBH in London. Therapeutics, whether self-administered or prescribed, were considered most effective during the premonitory diarrheal phase and less likely to work in the rice-water stool and collapse phases. When the symptoms of cholera first appeared, health officials recommended external warmth and stimulants, including hot blankets and frictions, hot poultices, perhaps with oil of turpentine, and hot water bottles applied to the stomach. Brandy and laudanum were recommended as internal stimulants. Treatment should be geared from the outset to prevent the extreme coldness of the body surface and extremities characteristic of the collapse stage.106 Two epidemics later, little had changed. Cholera victims in 1854 who were transported to the Middlesex Hospital received the same stimulant regimen under the nursing care of Florence Nightingale.107 Because of the prevalent view that cholera was caused by a blood-borne poison, bleeding to remove as much of the poison as possible was frequently recommended during the 1831–1832 epidemic. G. H. Bell’s Indian experience had convinced him of the special value of bloodletting. Bell, following his teacher Annesley, argued that

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the nervous derangement of cholera led to marked venous congestion, preventing healthy arterial blood from flowing to the lungs. Drawing off venous blood could reverse the disease process; by contrast, bleeding from an artery only worsened the patient’s condition.108 Bell was extremely optimistic that cholera patients could be cured if medical men employed the correct treatment.109 By midcentury medical men were less sanguine about the benefits of bleeding: “It is sufficiently notorious that in severe visitations of the disease in different localities in Scotland in former years, when many cases were totally left to themselves in consequence of desertion by friends, or the inability of the medical officers to pay them any attention, these constituted the first and most favourable recoveries; and the mortality was seldom or never found greater in cases thus abandoned than in those subjected to the most active and careful treatment by the most experienced members of the profession.”110 Lauder Lindsay’s views were representative of the therapeutic nihilism that emerged when all the touted remedies failed to bring the promised results.

* * * Snow’s writings and public comments between 1836 and 1848 suggest that his views on epidemic diseases and their treatment followed conventional lines, although he generally opposed the use of alcohol. The terms Snow used in his teetotal address suggest that his general theory of diseases contained key features from Cullen (“debility,” “reaction,” “secondary fever,” and “inflammation in the head and elsewhere”) and Brown (“reaction” and “aesthenic”) and shared by all medical men who believed that cholera was a febrile, infectious disease. His scattered comments suggest he believed typhus, influenza, and smallpox were contagious diseases. The analogy he cited between smallpox and cholera in particular environmental circumstances suggests he was a contingent contagionist with respect to that disease, but something happened in the fall of 1848 that changed his mind.

Notes 1. Clutterbuck’s comments were published in “Cholera at Peckham.—Use of chloroform,” LMG 42 (1848): 767–68; and “Treatment of cholera by chloroform,” LMG 42 (1848): 988. The surgeon who devised the treatment was James Hill, and the particulars were described in “Treatment of the cholera by chloroform &c. in Peckham House (Poor) Asylum,” Lancet 2 (1848): 514, a reprint of Hill’s letter to the Times, 30 October 1848. Two weeks later he sent a brief notice to LMG that was published in the correspondence section as “The cholera—Results of treatment by chloroform,” LMG 42 (1848): 902–03; and a longer report that the Lancet summarized under “Cholera and its treatment by chloroform,” Lancet 2 (1848): 694–95. 2. See, for example, “Research,” “Suggestions for the treatment of cholera by anæsthetic agents” (Letter), Lancet 2 (1848): 82–83; P. Brady, “Asiatic cholera successfully treated by chloroform given internally,” MT 18 (1848): 237–38; and James Moffat, “On chloroform in cholera,” Lancet 2 (1848): 551–52.


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3. See Jones Lamprey, “Chloroform as a remedy for cholera,” MT 19 (1848–49): 286–87, for the view against giving chloroform to cholera victims. 4. Wohl, Endangered Lives, 121, in turn citing Pelling, Cholera, 60. Baldwin notes that some German wags diagnosed a new epidemic they called “bibliocholera,” which was clearly contagious even if its subject matter was not; Baldwin, Contagion and the State, 38. 5. “Cholera and quarantine,” MT 17 (1847–48): 198. 6. Editorial, Lancet 1(1853): 393. Because disagreements about the pathology and transmission of cholera continued throughout Snow’s lifetime, our discussion of this context does not discriminate between ideas proposed before or after Snow first published his hypothesis in 1849. 7. Shephard uses the phrase “confusion and controversy” to describe English responses to cholera epidemics; JS, 151. 8. “Medium of contagion,” Lancet 1 (1842—43): 111. At the time, infection meant disease acquisition by the inhaled route only. 9. Durey, Return of the Plague, 105–06. 10. Southwood Smith, in Examiner (1 March 1832), quoted in Ibid., 107. 11. Durey, Return of the Plague, 115. 12. Today authorities tend to suspect both a change in the biotype of the cholera organism around 1817 plus the enhanced prospects for wide transmission provided by increased global commerce; Colwell, “Global climate and infectious disease,” 2025–26; Crowcroft, “Cholera: Current epidemiology,” R158–59. A detailed account with statistical tables of the progress of cholera from India to the West until 1844 can be found in William J. Merriman, “Some statistical records of the progress of the Asiatic cholera over the globe,” M-CT 27 (1844): 404–31. 13. While most authors regarded rice-water diarrhea as the hallmark of cholera, some insisted that severe muscle spasms and cramps were more distinctive features, as indicated in the choice of the descriptive term spasmodic cholera. In “Account of the epidemic spasmodic cholera, which has lately prevailed in India,” M-CT 11 (1821): 110–56, Frederick Corbyn recounted, “then followed spasms so violent as sometimes to require six men to hold the patient” (113). 14. Samuel Jackson of Philadelphia said of the typical patient in the collapse stage, “The appearance he exhibits is frequently that we may conceive of a corpse, inhumed some days, suddenly reanimated”; “Personal observations and experience of epidemic or malignant cholera in the city of Philadelphia,” American Journal of Medical Sciences 12 (1833): 88. 15. For a detailed and representative catalog of cholera symptoms, see Greenhow, Cholera, As It Recently Appeared, 11–12. Contemporaries often stressed the peculiar facial expression (described as anxious and as having an “earthy” quality) that might precede the development of other symptoms; see Bell, Cholera Asphyxia, 10. A similar description occurs in Shapter, Cholera in Exeter, 211. 16. Cholera was the name given to any enteric disease, reflecting the humoral doctrine that such illnesses were caused by an excess of choler (yellow bile). Cholera morbus was a later refinement designating a particular diarrheal disease; OED. By the nineteenth century the two terms were often used synonymously. See also Thomas Laycock, “Summer diarrhœa, cholera, and typhus fever,” LMG 38 (1846): 227–28; and Thomas Watson, “Lectures on the principles and practice of physic,” LMG 30 (1841–42): 114. 17. Relatively few works on cholera of that era provided mortality statistics. Merriman, in his extensive statistical analysis of the epidemic of 1831–1832, calculated mortality rates of thirty percent in England, fifty-three percent in Scotland, thirty-five percent in Wales, and thirty-nine percent in Ireland; M-CT 27 (1844): 404–31. Jacob Bell, editor of the Pharmaceutical Journal, declared that the case–mortality rate during the height of the 1848–1849 epidemic was between twenty-five and sixty percent; “The cholera,” PharJ 9 (1849– 50): 53–54.

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A survey of legally qualified practitioners in 1855 produced a mortality rate of 45.6% in 4,271 cases; UK GBH, Supplement 1 to Report of CSI, 87. 18. Some believed that the Asiatic cholera reported in India after 1817 was a variant of English cholera, or cholera morbus, and that both were first described by the ancient Greeks; see W. F. Chambers, “Three lectures on cholera,” Lancet 1 (1849): 37–39. Others argued that Asiatic cholera was a different disease and was never seen in England before 1831; see Thomas Watson, “Lectures on the principles and practice of physic: Epidemic cholera,” LMG 30 (1841–42): 117. The etymology of cholera was in dispute from the outset. G. H. Bell, an early British authority, dismissed two possible Greek derivations: ␹␱␭␩ (bile) and ␹␱␭␣␵ (intestine); Cholera Asphyxia, 8. Robley Dunglison, the American (but British-born and -trained) medical lexicographer, suggested ␹␱␭ε␳␣ (the rain-gutter of a house), which many contemporaries accepted; see Dunglison, Dictionary of Medical Science, 199; and Raufman, “Cholera,” 386. The evolution of terms from cholera morbus to Asiatic cholera is summarized in Jackson, Spasmodic Cholera, 3–4. 19. W. F. Chambers described Asiatic cholera as “the most formidable epidemic by which the human race has ever been scourged”; “Three lectures on cholera,” Lancet 1 (1849): 137. Thomas Watson noted that “the cadaverous aspect that sometimes precedes death in longstanding diseases, would come on in the course of an hour or two in [cholera]”; “Lectures on the principles and practice of physic: Epidemic cholera,” LMG 30 (1841–42): 116. Dr. Thomas Addis Emmet, attached to the Emigrant Refuge Hospital in New York City (later a pioneer gynecological surgeon), included in his memoirs a description of an incident that occurred twice during the 1854 cholera epidemic. Newly afflicted cholera patients were brought into a ward to join patients already receiving care. The ward, including night attendants, was locked each evening. When physicians and day attendants opened the ward the following morning, everyone in the ward—patients and attendants alike—had died during the night; Walsh, Medicine in New York, 110, citing Emmet, Incidents of My Life. Emmet’s successor lasted less than a week before dying of cholera, although Emmet, like many English writers, noted that such deaths among physicians were unusual. 20. From the 1820 report of assistant surgeon James Johnson for the medical board of Bengal, quoted in [Jackson], Spasmodic Cholera, 8. 21. “In Asia, the fiend was contemplated by us with curiosity—in the wilds of Russia, with suspicion—in Germany, with alarm—but on English soil, with TERROR!” [James Johnson], “Epidemic cholera,” M-CJ 16 (1832): 163. 22. E. O. Spooner, “The contagion of Asiatic cholera,” PMSJ 13 (1849): 34–37, 62–66, 91–97, esp. 65–66. 23. Bell, Cholera Asphyxia, 79–80. W. F. Chambers also argued that the trade route hypothesis was based on inaccurate or selective observations; “Three lectures on cholera,” Lancet 1 (1849): 222–23. 24. Kay-Shuttleworth, Moral and Physical Condition, 8. 25. For professional medical dissatisfaction with the effects of the New Poor Law on the poor themselves, the medical officers who worked for the unions, and the emergence of the radical British Medical Association in 1836, see Desmond, Politics of Evolution, 31, 124–29. 26. Porter, Greatest Benefit, 409–10. Bentham, in his will, had left his body to be dissected for the benefit of medical science and appointed Southwood Smith to carry out the dissection, which he did; Webster, Caring for Health, 45–46. 27. Chadwick, Report into the Sanitary Condition of the Labouring Population. In the Lancet, Wakley argued that medical men should lead efforts at sanitary reform because they understood best what was needed to improve health; Lancet 1 (1847): 101; Lancet 2 (1847): 578. Snow echoed this view in his inaugural address when he assumed the presidency of the Med-


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ical Society of London in 1855. For a comprehensive study of Chadwick and the sanitary movement, see Hamlin, Age of Chadwick. See also Halliday, The Great Stink of London, 35–42. 28. LMG endorsed the Health of Towns Bill then before the House of Commons, highlighting the statistical analysis of “wasted lives,” that is, the calculated number of lives unnecessarily lost to filth-induced diseases in large cities compared to the death rates in the countryside; “Editorial,” LMG 39 (1847): 634–39. The same editorial quoted Southwood Smith testifying before the Health of Towns Commission that filth from sewer gases produced fevers (635). 29. Porter, Greatest Benefit, 411–12; Webster, Caring for Health, 46, 55, 69–71. 30. Baldwin, Contagion and the State, 127–29. 31. Ibid. 32. “Influenza and cholera,” Lancet 2 (1836–37): 115. See also Thomas Laycock, “Atmospheric changes as causes of disease,” LMG 38 (1846): 1043, in which he noted that “changes in temperature have a considerable influence on the health of man, but not always directly. The problem is one of considerable complexity, because the changes in temperature are complicated with tidal changes in the atmosphere, and with disturbance of the magnetism of the earth and of the electricity of the air.” 33. “Westminster Medical Society,” Lancet 1 (1841–42): 598. 34. See examples in Ackerknecht, “Anti-contagionism,” although his generalizations have been superseded by Durey, Return of the Plague; Delaporte, Disease and Civilization; and Baldwin, Contagion and the State. 35. Durey, Return of the Plague, 105–06. 36. Ibid., 107. Edmund Parkes believed cholera was caused by a “specific morbid agent or virus” that was presumably one “of the more subtle gases” undetectable by the chemical means then available; Parkes, Researches, 156. 37. Southwood Smith, Treatise on Fever, 41–42. 38. “Cholera and quarantine,” MT 17 (1847–48): 198–99; see also Southwood Smith, Treatise on Fever, 66. Greenhow accepted Sydenham’s “epidemic constitution” with a local miasmatic twist: “That the atmospheric condition, be it what it may, on which depends the efficient cause of Cholera, has been gradually forming itself in the course of the summer, is rendered yet more probable, when we review the character of the diseases which have principally prevailed, in the neighbourhood, during that period. . . . It has been a general remark, amongst medical men, that the ordinary complaints of the season all tended to resolve themselves into the prevalent febrile affection. Throughout the epidemic, a marked determination has been observed in the mucous membrane of the intestines, showing the irritable condition of that tissue . . .”; Cholera, As It Recently Appeared, 100. 39. Southwood Smith, Treatise on Fever, 364. However, a few pages earlier he wrote, “Without doubt, a febrile poison, purely of animal origin, in a high degree of concentration, would kill instantaneously” (360). 40. Southwood Smith, Treatise on Fever, 354–55. 41. Lindsay, “Clinical notes on cholera,” AMJ 2 (1854): 1116. G. H. Bell, in fact, argued that one reason physicians who had seen service in India were so strongly anticontagionist was because so few physicians had been struck down, whereas because “fatigue of mind and body is a powerfully predisposing cause” of cholera, “every medical man, who has done his duty to Cholera patients, must feel, that had the disease been communicable from one individual to another, he could scarcely by possibility have escaped”; see Bell, Cholera Asphyxia, 86–87. 42. Lindsay, “Clinical notes on cholera,” AMJ 2 (1854): 840. Farr showed that cholera deaths were more common on Saturdays, as well as Mondays through Wednesdays, which he attributed to the payment of weekly wages on Saturdays and the heavy drinking that typically occurred thereafter; Farr, Cholera in England, 1848–49, xlix.

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43. Florence Nightingale may have held similar views to the very end of the nineteenth century; Rosenberg, Explaining Epidemics, 93–107. Rosenberg believes that Nightingale never accepted the germ theory of disease, although this is currently a matter of dispute. 44. Durey states that the only point on which all contagionists could agree was approval of quarantine, and anticontagionists were in agreement only that quarantine was unworkable; Return of the Plague, 107. Similarly, Baldwin found a division between quarantinist and environmentalist views; Baldwin, Contagion and the State, 4–5. See also Worboys, Spreading Germs, 39–40. However, some contagionists offered only conditional support for quarantine; see “Contagion and quarantine,” LMG 30 (1841–42): 262–64. Ackerknecht argued that anticontagionism during this period tended to be associated with political liberalism and contagionism with defenders of the status quo and bureaucracy; “Anti-contagionism,” 567. Delaporte considers this generalization overly simplistic; Disease and Civilization, 145–49. While Britain generally had trading interests that made quarantine an unpopular measure, forces within the country did not necessarily line up for or against quarantine solely because of their own pecuniary interests; Baldwin, Contagion and the State, 97. Baldwin adds that traditional quarantine fell out of favor as the century wore on less because of a shift in the basic understanding of disease and more because it proved practically impossible and inordinately expensive; Baldwin, Contagion and the State, 79, 120, 123–89. 45. “Asiatic cholera,” MT 19 (1848–49): 11–12. 46. William Budd wrote of the GBH of the era from 1848 to 1855, “To make unceasing and implacable war against contagion and contagionists seemed with the [GBH], indeed, to be, for some years, the chief purpose of its existence”; “On intestinal fever: its mode of propagation,” Lancet 2 (1856): 694. On the GBH’s reaction to Snow’s theories in 1855, see Paneth et al., “A rivalry of foulness.” 47. On why sanitarianism led to practical accomplishments despite its theoretical limitations when viewed from today’s perspective, see Winslow, Epidemic Disease, 244–49. 48. Baldwin, Contagion and the State, 101. 49. Baldwin, Contagion and the State, 7. M-CR attributed the theory that “contagious or infectious matters enter the body . . . by . . . the skin” to “Fracastor, and [the theory] has had but few advocates since his time”; Lancet 1 (1842–43): 111. However, an editor at LMG thought the dispute was long-standing, and a century hence anticontagionists would still regard contagionists as “men lagging behind in the march of intellectual improvement, as followers of an idle fantasy of the brain, incapable of proof; as well-meaning, but weak-minded and prejudiced”; “Contagion and quarantine,” LMG 30 (1841–42): 262. 50. Porter argues that Fracostorius imagined his “seeds” as spores, not microorganisms; Porter, Greatest Benefit, 174–75. 51. Morton, Medical Bibliography, 447. 52. For a detailed discussion of ways to disinfect clothing and bedding as a preventive for cholera, see LMG 43 (1849): 199–202. 53. “Diseases are propagated either by inoculation and contact (contagion) or by inhalation (infection) . . .”; [Farr], Cholera in England, 1848–1849, lxxx. However, infection was often used in contradictory ways; for usage during the 1831–1832 epidemic, see Durey, Return of the Plague, 112–14; more generally, see Hudson, Disease and Its Control, 142. 54. “[Cholera] does not appear to be in the least degree contagious, and scarcely, if at all, infectious, unless, perhaps, where many sick are congregated together, as in the wards of a hospital; in fact, I should consider it as an almost true epidemic, such as the influenza which has prevailed here since the last cholera disappeared”; report of Vice-Consul Bassam of Mossul, quoted in E. O. Spooner, “The contagion of asiatic cholera,” PMSJ 13 (1849): 63. Anticontagionists frequently used epidemic as a synonym for miasmatic.


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55. “The infectious nature of pestilential cholera,” LMG 38 (1846): 520, excerpted from Copland, Dictionary of Practical Medicine, part 10. 56. “Westminster Medical Society,” Lancet 1 (1837–38): 868. It is unclear from this example whether Snow distinguished typhus from typhoid fever. 57. An editor at LMG listed smallpox, measles, scarlet fever, and whooping-cough as undeniably contagious diseases; “Contagion and quarantine,” LMG 30 (1841–42): 263. 58. Indeed, it seems safe to say that, on balance, there existed more data favoring anticontagionism than contagionism in the first half of the nineteenth century. The eventual supremacy of contagionism depended on an understanding of factors (largely unknown during the period we are studying) such as animal vectors and asymptomatic carriers, without which contagionist theory could not fully explain data presented by typical epidemic diseases; Winslow, Conquest of Epidemic Disease, 182. Thomas Watson, however, hypothesized that an asymptomatic carrier could explain the (occasional) contagiousness of cholera; “Lectures,” LMG 30 (1841–42): 118. See also Daniel Noble, “On the question of contagion in cholera,” LMG 43 (1847): 141–49, esp. 146. 59. Ackerknecht states that Anglo–Indian surgeons and physicians were “uniformly” anticontagionist; “Anti-contagionism,” 575, but Durey states that a number of Anglo–Indian physicians supported contagionism; The Return of the Plague, 110. The committee of the Massachusetts Medical Society, reviewing the extant European literature in 1832, reported that opinion among the Indian physicians was “divided” but that “a decided majority” embraced anticontagionism; [Jackson], Spasmodic Cholera, 40–41. Thomas Wakley, editor of the Lancet, was strongly contagionist in the 1830s but moderated his stance thereafter as sentiment went against him; see Lancet 1 (1831–32): 669–84, esp. 674–79. 60. The stomach route was “an ancient notion, . . . advocated recently by Lind, Darwin, and Jackson”; “Medium of contagion,” Lancet 1 (1842–43): 111. The reference to James Lind (1716–1794), discoverer of the lemon juice cure for scurvy, is perplexing. He claimed that the seeds of infections like yellow fever, plague, and jail distemper were suspended in the air and inhaled and added simply that the stomach and intestines were often the first organ systems to be affected by them; Lind, An Essay on Health of Seamen, 236–41, 256–57, 316. The other references are to Erasmus Darwin and Robert Jackson. Autoexperiments with plague and yellow fever had produced negative results as well; Ackerknecht, “Anticontagionism,” 567–68. Edmund A. Parkes, who converted to a contagionist position in the 1860s, mentioned these autoexperiments as one of the main reasons he had initially rejected contagionism; Practical Hygiene, 74–75. A 1971 study on prisoner volunteers in the United States in which varying doses of cholera vibrios were administered orally produced some evidence of cholera in only twenty-six percent. When the volunteers were also given sodium bicarbonate to neutralize the stomach acid, the response rate rose to eighty-five percent; Hornick et al., “The Broad Street pump revisited.” However, it has more recently been discovered that the cholera vibrio undergoes changes in gene expression upon passage through the human gut that make the bacteria acquired in epidemic situations more virulent than bacteria grown under laboratory conditions; Merrell et al., “Host-induced epidemic spread of the cholera bacterium.” 61. Worboys suggests that it is anachronistic to imagine that an inability to reach consensus about the cause of cholera posed a serious problem for the medical profession of that day: “Traditional physic and modern medical science had not constituted disease in causal terms, where treatment would focus on removing causes. Disease involved structural or functional perturbations, and hence treatment was in large part about positive interventions to promote repair, to restore function or to aid in the regeneration of damaged structures”; Worboys, Spreading Germs, 33. He also cautions against overcharacterizing British medical thinking in the 1830s and 1840s about the cause and spread of cholera, because “one of the few things

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doctors did agree on was to avoid ‘theory’ and to try to be empiricists who did not have overarching principles” (28). At the time the pejorative use of theorist referred to an adherent of an outmoded medical “system” from the eighteenth century. 62. Baldwin, Contagion and the State, 123. 63. He twitted the GBH for making an abrupt shift from a strongly contagionist view of cholera to contingent contagionism, indicated by a fall in temperature from 120° to 92° in only three weeks. The highest degrees on this “loimometer,” or “pestgage,” for “measuring the temperature” of disputants about the causes of cholera indicated ultra-contagionism. The middle range was indicative of contingent contagionism, while the lowest was ultra noncontagionism; J. Johnson, “Cholera in England,” M-CR 16 (1832): 267, who credited an “ingenious friend” with constructing this cholera thermometer. 64. J. Johnson, M-CR. (1832), cited in Durey, Return of the Plague, 115. 65. J. Johnson, “Epidemic cholera,” M-CR 16 (1832): 163. Watson, a contingent contagionist, thought the most common predisposing influences were poverty, poor ventilation, and abuse of alcohol; “Lectures on the principles and practice of physic: Epidemic cholera,” LMG 30 (1841–42): 118–19. 66. “Derobe a typhous patient of filth and foul air . . . and you take away from the fever the power of propagation. You may then feel his pulse, examine his tongue, analyse his evacuations, press his abdomen—and, when he dies, dissect his body, with about as much chance of catching the fever, as of learning from him the secret of alchemy”; J. Johnson, “Cholera in England,” M-CR 16 (1832): 268. 67. J. Johnson, “Epidemic cholera,” M-CR 16 (1832): 163. See also Durey, Return of the Plague, 114–17. 68. Edmund Parkes became a contingent contagionist based on observations in India during two epidemics between 1843 and 1845. He had seen no evidence of contagion from person to person, but insisted, “I by no means wish to generalize this observation, and to conclude that the poison of Cholera is never reproduced by the human body”; Researches, 192. E. O. Spooner had Parkes in mind when he stated, “A disease cannot be contingently contagious, though it may spread or not according to certain contingencies. The theory of a disease being sometimes contagious and sometimes not, is self-contradictory and absurd. Similar kinds of matter always possess similar properties, and the specific virus of the choleric pestilence forms no exception to the general rule”; E. O. Spooner, “The contagion of Asiatic cholera,” PMSJ 13 (1849): 36. 69. In the previous century Cullen had suggested such a category of “doubtful” fevers, sometimes contagious and sometimes not, thereby giving the notion of contingent contagionism a respectable pedigree; Porter, Greatest Benefit, 261. Watson adopted a contingent contagionist position because neither the contagionist nor the anticontagionist hypothesis alone could “reconcile the phenomena of the appearance and extension of the malady”; “Lectures,” LMG 30 (1841–42): 117. 70. An excerpt from an article in M-CR from October 1842 listed three routes by which “contagious or infectious matters enter the body”—the lungs, the stomach, and the skin. The author endorsed the lung route, “the most ancient conjecture . . . advocated by Lucretius; it has been supported also in recent times by Sir A. Cooper”; “Medium of contagion,” Lancet 1 (1842–43): 111. 71. Delaporte found a rural–urban theoretical division in France during the 1831–1832 epidemic. Rural physicians were likely to see relatively small epidemics up close and often had contact with each person afflicted. They could readily trace any pattern of spread from one person to another and could obtain detailed information as to the circumstances and timing of each illness. By contrast, no single urban physician was likely to see every cholera sufferer


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within a circumscribed area. By the time urban health authorities and medical men realized a cholera outbreak had occurred, scores of cases had already occurred, creating the impression that the disease had broken out everywhere at once. After the fact the victims were often unable or unwilling to provide details about their contacts and previous habits. Therefore, a rural practitioner’s experience generally conformed to contagionist doctrine, whereas their urban counterparts tended to think that cholera was not contagious; Disease and Civilization, 171–72. 72. E. O. Spooner, “The contagion of Asiatic cholera,” PMSJ 13 (1849): 35. When J. G. Swayne, Budd’s Bristol colleague, sought confirmation for his fungus cell theory in 1849, he sent samples to E. O. Spooner as well as to Edwin Lankester and Arthur Hassall in London; Pelling, Cholera, 175. Hence, Spooner must have been a respected microscopist. 73. For the reliance of both contagionists and anticontagionists on “model” diseases, see Delaporte, Disease and Civilization, 163-70. 74. Frederick Corbyn disagreed, citing the instance of three natives in a general hospital in Seroor who had not contracted cholera despite being surrounded by cholera victims and “inhaling by day and night at every inspiration, mouthfuls of the infection.” Thus, cholera could not be contagious, even contingently; “Account of the epidemic spasmodic cholera, which has lately prevailed in India,” M-CT 11 (1821): 143. Other contagion theories of cholera very similar to Spooner’s were J. H. James’s, “Some remarks on the nature and probable causes of the propagation of cholera maligna,” LMG 42 (1848): 929–34; and Ogier Ward’s, “Contagion of cholera,” LMG 41 (1848): 559–62. 75. See Dr. Bushnan, “Progress of German medical science,” MT 18 (1848): 120 (where the pathologist’s name is given as “Boehm”). 76. Snow, “Case of malignant hæmorrhagic smallpox,” LMG 35 (1844–45): 586. By “sporadic cholera” Snow meant summer, or English, cholera—various intestinal complaints with attendant diarrhea. The cases of epidemic Asiatic cholera he refers to were presumably those he had treated at Killingworth in 1832. 77. See Eyler, “William Farr on the cholera”; and Desmond, Politics of Evolution, 28, 31. 78. “A single word, such as Zymotic, is required to replace in composition the long periphrasis ‘epidemic, endemic and contagious “diseases,” [sic] with a new name and a definition of the kind of pathological process which the name is intended to indicate”; Farr, 4th Annual Report of the Registrar-General (1842), in Vital Statistics, 246. Farr’s new term took a while to catch on. A few years later, “A reader” sent a letter to the editor of the Lancet: “Sir: will you be so good as to give a definition of the word ‘Zymotic,’ which occurs in the RegistrarGeneral’s “Return,” and say from whence the word is derived?” The reply offered several derivations, and noted that ferment “may also be employed in English . . . as general designation of the morbid processes and their exciters”; Lancet 1 (1848): 55. 79. Farr was also familiar with the work of Jacob Henle (1809–1885), who assembled and analyzed a mass of evidence accumulated by other investigators and drew the conclusion that contagious diseases were caused by microscopic living organisms, probably of a plant variety. He was influenced by the fact that these diseases displayed an incubation period (evidence that the causative agent must be capable of multiplying within the body), as well as the pattern of specific symptoms and a specific time course whenever the disease appeared. Henle was known only second-hand by most English authorities, as his works had not been translated from German at this time; Pelling, Cholera, 193–94. Henle’s research was summarized in M-CR. of October 1842, but the excerpt in Lancet stated (contra Pelling) that Henle believed contagious diseases “depend for their existence and propagation on certain parasitical organised beings, or their germs. . .”; Lancet 1 (1842–43): 111. Henle’s Miasma and Contagions (1840) was admittedly more the framework for a set of future scientific investigations

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than a fully developed scientific theory. Robert Koch, Henle’s pupil, eventually carried out much of the envisioned research program; Rosen, “Jacob Henle’s medical thought.” Winslow credits L.-B. Guyton-Morveau (1737–1816) as perhaps the first nineteenth-century thinker to posit specific living particles capable of reproducing themselves as the causative agents of contagious diseases; Guyton-Morveau was also a godfather to the sanitary movement, arguing that chemicals that eliminated the smell of putrefaction should for that reason be useful agents in preventing this class of diseases; Winslow, Conquest of Epidemic Disease, 239–42. Perhaps Henle influenced Farr’s postulate that each “zymotic” disease was caused by its own specific and discrete particle. 80. Liebig, Chemistry and its Application, 121–27. 81. Farr, Cholera in England, 1848–1849, lxxx–lxxxiii (footnote). See also Eyler, “William Farr on the cholera,” 84–85. 82. Pelling, Cholera, 100–12; Eyler describes how Farr gradually modified his views as new bacteriological evidence became available and made a smooth transition to a germ theory; “William Farr on the cholera,” 94–95. Around 1850 Farr was unwilling to state exactly what sort of material or particle cholerine was. By that date the collateral sciences had shown that fungi could cause plant diseases and at least one human disease (favus, a skin disorder). This discovery led Charles Cowdell (1815–1871) to argue that the specific causative agent of cholera was a type of fungus that developed morbid properties under certain atmospheric conditions, was inhaled, and infected the blood; Cowdell, Pestilential Cholera, 198–210. With respect to transmission, however, he seems to have been a contingent contagionist. He believed Copland’s notion of infection had merit in some situations, when “germs given off by exhalations from the bodies of the sick” seemed to enter the local atmosphere and infect others (201). 83. Worboys, Spreading Germs, 34–41. 84. Farr, Sixteenth Annual Report of the Registrar General, in Vital Statistics, 250–53. 85. “The examination of the dead bodies threw no light, that I know of, upon the nature of this frightful disease”; Watson, “Lectures,” LMG 30 (1841–42): 116. The clinical approach included reliance on medical statistics as well as on autopsy findings. 86. David M. Morens read an early draft of this chapter and suggested that French physicians, too, could not agree on the pathological lesion that typified cholera. Morens’s view is confirmed by Delaporte, who categorized the major pathophysiological theories during the 1831–1832 epidemic as physiological, with inflammation of the gastrointestinal tract the defining feature (Broussais); experimental, with depleted cardiac function as primary (Magendie); nervous, with the nervous system as the seat (various authors); and humoral, with chemical changes in the blood the basic problem (Bonnet); Delaporte, Disease and Civilization, 115–30. Broussais believed cholera was noncontagious, and his recommended treatment was extensive bleeding. 87. Southwood Smith, Treatise on Fever, 346–47. Many other authors during the 1830s and 1840s adopted the nervous-system explanation of the pathology of cholera. See Annesley (G. H. Bell’s teacher in India), Most Prevalent Diseases of India, 147; and Shapter, Cholera in Exeter in 1832, 226. Indirect evidence for a nervous “seat” was deduced from a report of the therapeutic success of cannabis tincture in eleven cases of cholera in Cairo; “On the employment of cannabis indica in cholera,” LMG 43 (1849): 217. 88. See a report of experiments by Robert Dundas Thomson of Glasgow, “Royal Medical and Chirurgical Society,” Lancet 2 (1850): 154–55. 89. William B. O’Shaughnessy, “Experiments on the blood in cholera,” Lancet 1 (1831–32): 490, a summary of his Report on the Chemical Pathology of the Malignant Cholera. In 1830 a Professor Hermann of Moscow had reported roughly similar findings. O’Shaughnessy drew therapeutic conclusions from his experiments, advocating intravenous injection of saline flu-


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ids in severe cases but did not conduct clinical trials of this mode of therapy. Later he was a medical officer in India and helped establish the Indian telegraph system; Moon, “Sir William Brooke O’Shaughnessy.” Snow was aware of O’Shaughnessy’s 1832 researches (some of which were conducted in Newcastle while Snow was an apprentice there); “Principles on which the treatment of cholera should be based” (1854). 90. Alfred B. Garrod, “On the pathological condition of the blood in cholera,” LJM 1 (1849): 409–37. 91. Parkes, Researches, 103–13. Parkes thought that “fibrin” was deposited in the smaller vessels and that this obstructed the flow of blood to various organs. See also Lindsay, “Clinical notes on cholera,” AMJ 2 (1854): 412. 92. G. Johnson, Epidemic Diarrhœa and Cholera, 123–24. Thomas Watson agreed that the blood in cholera victims was invariably black and tarry; “Lectures,” LMG 30 (1841–42): 116–17. 93. Rosenberg, “The therapeutic revolution,” in Vogel and Rosenberg, Therapeutic Revolution, 3–25; Warner, Therapeutic Perspective. 94. Shapter’s suspicion of specific remedies reflected a humoral therapeutic perspective: “Is there no cure for Cholera? I would make this reply: There is no specific cure for Cholera; but, as in fever and other diseases, its various stages require management and treatment according to the phenomena that are developed, and the individual constitutions in which they arise, and that a wise conduct and judicious management of these are likely, under God’s blessing, to be attended with benefit; while a wild and indiscriminate resort to specifics must inevitably be injurious”; Cholera in Exeter in 1832, x–xi. The Lancet remained a staunch defender of holistic, bedside medicine until well after midcentury: “Physicians who have learned their lesson at the bedside, and who know that the object of the healing art is not to cure a disease, but to treat a patient, will not waste their labour in the vain search for specific methods”; Lancet 1 (1869): 164; quoted in Worboys, Spreading Germs, 31. In this mind-set, the use of “specifics” was equivalent to crude empiricism and quackery. 95. Following the 1853–1854 epidemic the Scientific Committee of the GBH undertook a crude nonrandom statistical analysis of various treatments grouped under four classes: alteratives (of which calomel was the most commonly employed), astringents (chalk, or chalk and opium, or sulphuric acid), stimulants (ether and brandy), and eliminants (castor oil). The overall death rate across Britain based on surveys of local practitioners ranged from twentyseven percent when astringents were used to seventy-six percent when eliminants were employed. For patients in the collapse stage, the range was fifty-seven percent with alteratives to seventy-eight percent with eliminants; UK GBH, Report on Different Methods of Treatment. 96. “Medical Society of London,” MTG 8 (1854): 98–99. Discussion occurred after Snow delivered a paper,“Principles on which the treatment of cholera should be based.”“Saline injections,” we should note, do not refer to intravenous saline injections, but rather to the much more common rectal route. For an overview of treatments used in the 1832 epidemic, see P. Smith, Cholera: An Inquiry, 26–29. N. Howard-Jones dismissed most treatments as ineffective; “Cholera therapy in the nineteenth century.” Baldwin adds that the failure of medical opinion to agree on an optimal treatment approach and the associated diminution in the public respect for physicians created a marvelous opportunity for quackery; Baldwin, Contagion and the State, 38. 97. Parkes considered excessive diarrhea one of the major components of cholera and important to treat. But he did not consider arrest of the diarrhea as synonymous with cure of cholera; Researches, 202. 98. Many were dismissive of this treatment: “However it might be with pigs or herrings, salting a patient in cholera was not the same as curing him”; Thomas Watson, “Lectures,” LMG 30 (1841–42): 119. 99. “Letter from Dr. Latta to the secretary of the Central Board of Health, London, af-

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fording a view of the rationale and results of his practice in the treatment of cholera by aqueous and saline injections,” Lancet 2 (1831–32): 274–77. 100. Ibid., 275. 101. Lancet 2 (1831–32): 284–86. 102. Thomas Latta, “Reply to some objections offered to the practice of venous injections in cholera,” Lancet 2 (1831–32): 428–30. Latta died in 1833, after which fluid injections fell out of favor until the 1890s; Dhiman Barua, “History of cholera,” in Barua and Greenough, Cholera, 1–36. 103. UK, GBH, Report on Epidemic Cholera of 1848 & 1849. 104. G. Johnson, Epidemic Diarrhœa and Cholera, 112. Johnson was unconvinced that virtually all would have died had the injections not been given, because experimenters generally selected only the sickest patients. He concluded in 1855, “There are probably few practitioners who now expect any practical benefit from saline injections in cholera” (114). Cowdell had drawn similar conclusions in 1848; Pestilential Cholera, 98. Parkes also mentioned in passing that intravenous saline injections had been tried by some Indian practitioners with notable lack of success; Parkes, Researches, 219–39. Merriman quoted a Canadian report from 1832 in which saline transfusion was attempted in twenty “hopeless” cases with no cures, although one patient survived for seven days as a result of the treatment; “Some statistical records of the progress of the Asiatic cholera over the globe,” M-CT 27 (1844): 429. Samuel Jackson of Philadelphia adopted a view similar to O’Shaughnessy’s in 1832 to 1833 regarding the central role played by dehydration of the blood and had good success at his cholera hospital by giving patients copious amounts of oral fluids; Samuel Jackson, “Personal observations and experience of epidemic or malignant cholera in the city of Philadelphia,”American Journal of Medical Sciences 12 (1833): 76–121. 105. Durey, Return of the Plague, 133. 106. Shapter, Cholera in Exeter in 1832, 18–20. 107. Winterton, “Soho cholera epidemic 1854,” is based on a contemporary report from the apothecary to the hospital. Florence Nightingale, according to one of her correspondents of that time, was “ ‘up day and night, undressing them . . . putting on turpentine stupes, etc. herself to as many as she could manage.’ . . . From Friday afternoon until Sunday afternoon she was never off her feet”; quoted in Woodham-Smith, Florence Nightingale, 80. Nightingale had at this time in her career not yet traveled to the Crimea, where she achieved fame for her wartime nursing efforts. 108. Bell, Cholera Asphyxia, 25–26, 104. See also Annesley, Most Prevalent Diseases of India, 166. Greenhow, who also held miasmatist views and attributed the pathology of cholera to nervous derangement, opposed bleeding in part because freely flowing blood was so hard to obtain in advanced cases; Cholera, As It Recently Appeared, 22–32. 109. Bell, Cholera Asphyxia, 3. George Johnson favored bleeding because he thought cholera was caused by a specific poison in the bloodstream that produced right-sided heart congestion, which venesection could relieve; Epidemic Diarrhoea and Cholera 2: Section 10. For similar views, see review of G. Calvert Holland, Nature and Treatment of Cholera in Lancet 2 (1837–38): 488. 110. Lindsay, “Clinical notes on cholera,” AMJ 2 (1854): 1118. Consider also T. M. Greenhow: “When patients rally from collapse, it is often most difficult to ascertain on what causes their emergence from it has depended. I fear various remedies have often obtained the credit which has been due to the spontaneous efforts of nature”; “Treatment of malignant cholera at Newcastle,” Lancet 1 (1832–33): 52.

Chapter 8

Snow’s Cholera Theory

A

FTER NOTING WITH INCREASING ANXIETY that cholera was spreading across Russia and into western Europe in the summer of 1848, the Lancet reported several confirmed cases of cholera in the London metropolis early in October.1 However, Dr. John Webster, the incoming president of the Westminster Medical Society, stated at the opening meeting of the session on 21 October that it had not “made much progress in the metropolis” since then despite the attention given to its advance, whereas influenza and scarlatina received little press but were no less dangerous. The minutes reveal that the society was prospering: “the rooms in Saville-row were completely crowded, reminding us of the society in its most palmy days. About sixty fellows and visitors were present.”2 After the president concluded his remarks and a fellow presented a case report on removal of a placenta while the patient was under the influence of chloroform, Mr. Francis Hird read a paper on “The pathology and treatment of cholera.” “After giving an account of the disease, and describing the symptoms in a highly graphic manner” (perhaps for the benefit of members who were not in the profession during the 1831–1832 epidemic), he reviewed “post-mortem appearances he had observed in twelve cases of the disease.”3 In his mind “no known remedies have any specific power of counteracting the peculiar agency of the poison,” so it was imperative that medical men choose remedies likely to counter the known pathological effects of the disease at each stage. Among others, he recommended chalk powder, opium, calomel,

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cayenne, sugar, spirits of cinnamon, mustard emetic, and an enema of starch. If these did not check the symptoms, “a mustard poultice, or a flannel wrung out of hot water, and saturated in a mixture of equal parts of liquor ammoniæ and turpentine, and frictions to the chest, abdomen, and extremities” should be used to maintain circulatory function and prevent “internal congestions.”4 In the ensuing discussion, Dr. Thomas Peregrine seconded the use of chalk powder and opium in the early stages of cholera as well as friction and hot applications to the chest and abdomen in its advanced stages, but “Dr. Snow objected to the application of warmth in cases of cholera and founded his objection to its employment on the fact that in cases of asphyxia such application was injurious. Cholera was not asphyxia, but in some points resembling it, so far as the internal congestion was concerned.”5 His thinking about the pathology of cholera appears unchanged from that of 1836—that it is a febrile disease.6 Even so, ten months later, at the end of August 1849, he wrote and paid to have published an essay, On the Mode of Communication of Cholera, in which he argued that “the disease is communicated by something that acts directly on the alimentary canal,” analogous to intestinal worms (MCC, 8–9).7 He claimed in this essay that “it has always appeared, from what the writer could observe, that in cholera the alimentary canal is first affected” (MCC, 7). Something had raised doubts in his mind about the theory of cholera asphyxia, for he had come to believe that “the thickened state of the blood, which will scarcely allow it to pass through the capillaries,” characteristic of late-stage cholera, was a consequence of the “fluid lost by purging and vomiting” in the early stages (MCC, 8, 7). Moreover, it seemed logical to Snow that the mucous membrane of the alimentary canal was irritated by a local rather than “an inhaled poison” (MCC, 6). Based on his understanding of gas laws, the physiology of respiration, and the action of intestinal parasites, he now dismissed the conventional notion that cholera was propagated as an effluvium by the respiratory route.8 It is unclear why Snow became so interested in the communication of cholera late in the fall of 1848. Perhaps he was intrigued by claims that chloroform was proving effective in treating symptoms as the number of reported cholera cases rose dramatically. Dr. Webster was wrong about the mildness of this epidemic. Snow discussed his views with several colleagues, including two researchers on the chemistry of cholera evacuations, mailed written inquiries about sewage and water conditions in areas that were experiencing unusually high mortality, and began a systematic search of medical journals and government reports on the subject. When two outbreaks in metropolitan London seemed to offer sufficient evidence to make his case plausible, he finished a sketch of his hypothesis (MCC) that the cholera poison was transmitted in the evacuations of its victims and then inadvertently ingested by others. Within two months he presented a complete theory of the pathology and mode of communication of cholera (PMCC), with substantiating evidence about the association of the incidence of cholera mortality, water supply, and sewage disposal throughout England. Because PMCC was produced within two months of MCC and


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yet has so much additional confirmatory evidence, one wonders if PMCC was really Snow’s intended work all along. If so, MCC was, in effect, forced out of him early by a sense of public health urgency in the late summer of 1849, when cholera deaths were still mounting during the second year of the epidemic. The change in his thinking from infection via the lungs to oral–fecal transmission required only a lateral move among contemporary contagionist perspectives. In the opening paragraph of MCC, Snow stated that “an examination of the history of that malady, from its first appearance, or at least recognition, in India in 1817, has convinced him, in common with a great portion of the medical profession, that it is propagated by human intercourse” (5). While he could have come to this conclusion in 1848 or 1849, his known views on typhus, smallpox, and cholera prior to that date suggest that he was a modified contagionist (perhaps contingently so in certain circumstances) about epidemic diseases. He thought the morbid matter could be produced in the bodies of the sick and in an effluvial form be inhaled by others; that is, he accepted infection as a mode of transmission as late as his comments about cholera asphyxia at the Westminster in October 1848. The shift from lungs to stomach as the portal of entry required no conversion to a new doctrine. The ingestion route had already been proposed by some contagionists as an alternative to contact and inhalation, but it would have required him to assume that the negative results of autoexperimental ingestion of cholera matter during the 1831–1832 epidemic were inconclusive and to find an analogous disease in which a known agent was not destroyed by stomach acid.9 Snow brought to cholera his personal biases as well as his knowledge and scientific skill. He had long been committed to John F. Newton’s philosophy of vegetarianism, including the value of pure drinking water. Newton’s theory may have prepared Snow for the idea that epidemic diseases could be caused by material taken orally into the body at a time when most believed that causative agents were inhaled.

Out with the Old After the opening endorsement of the communication of cholera by humans, Snow used the next three paragraphs of MCC to refute the notion that the disease could be transmitted only in the form of effluvial infection. He defined the term precisely: “emanations from the sick person into the surrounding air, which enter the system of others by being inhaled, and absorbed by the blood passing through the lungs” (MCC, 6). As such, he rejected the modified contagionist perspective he seems to have held until then, as well as the view of local miasmatists who were willing to consider contingent contagionism in specific circumstances. Snow found it particularly “difficult to imagine that there can be such a difference in the predisposition to be affected or not by an inhaled poison, as would enable a great number to breathe it without injury in a pretty concentrated form . . . , whilst others should be killed by it when millions of times diluted” (MCC, 6).

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While his reasoning about the improbability of effluvial infection was respectful, he was downright dismissive of those who supported “the hypothesis of a cholera poison generally diffused in the air, and not emanating from the sick” (MCC, 6)— that is, general miasmatists of the “epidemic constitutions” persuasion. Perhaps his research into the nature and mechanisms of anesthesia by inhaled gases made him certain that gaseous vapors alone, whether general or local, could not cause specific epidemic diseases, as miasmatic theory posited. Moreover, his investigation of arsenical candles had suggested that when a body inhaled a specific poison, it showed the specific effects of that poison, not the generalized fevers typically claimed for miasmatic and local effluvial poisoning. Contrary to the older generation of medical men, who dismissed the law of the diffusion of gases as armchair theorizing, Snow’s training and daily experience administering anesthesia made him believe that careful attention to the chemistry and physics of gases could have practical benefits. It was precisely that which permitted him to use otherwise dangerous medicinal agents with safety and with exact application to the peculiar needs of each patient and each surgical operation. Neither miasmatic nor effluvial notions that cholera was primarily a blood-borne disease squared with the clinical and pathological evidence of which Snow was aware. Diseases in which the blood is poisoned at the earliest stages due to an inhaled causative agent show general symptoms such as headache, chills, and rapid pulse before any localized symptoms appear (MCC, 6–7). In cholera, however, all the constitutional symptoms occur later and can be better accounted for by the amount of fluid lost from the gut as the result of the massive vomiting and diarrhea and the consequent state of dehydration (MCC, 7–8). He reasoned, moreover, that the fluid losses were most likely due to “some local irritant of the mucous membrane” of the gut, rather than to some generally circulating poison, “no instance suggesting itself to the writer in which a [blood-borne] poison causes irritation of, and exudation from, a single surface” (MCC, 8).

In with the New The argument in MCC is a complex blend of epidemiological evidence, pathological observations, and bold analogies (Fig. 8.1). Snow needed to formulate some basic assumptions in order to launch his theory. He had to assume that cholera was a specific disease attributable to a specific exciting cause. He also had to assume that the cause of cholera did not act like a typical mineral poison—it caused the disease in a statistically significant portion of those exposed to it, but not in all of them. That is, “proof ” would be a matter of statistical probability and not certainty.10 First, he emphasized humans were central to the spread of cholera. There was simply too much positive evidence to doubt “its communicability” (MCC, 5). He pointed to the many known incidents “in which cholera dates its commencement in a town or

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Snow’s Cholera Theory Snow’s Theory Hand-to-mouth spread

Transmission within a household Causative agent

Transmission over large distances and areas

Orally ingested Enters intestine

Drinking water contaminated with cholera evacuations

Multiplies

Attaches to mucous membrane

Local irritation, intense exosmosis of fluids & salts

Constitutional symptoms of cholera

Rice-water stools (+ vomit)

Figure 8.1. Snow’s 1849 theory of cholera.

village previously free from it to the arrival and illness of a person coming from a place in which the disease was prevalent . . .” (MCC, 5). The first two cases of cholera in London in 1848 proved his point: “Who can doubt that the case of John Harnold, the seaman from Hamburgh . . . was the true cause of the malady in Blenkinsopp [the second victim], who came, and lodged, and slept, in the only room in all London in which there had been a case of true Asiatic cholera for a number of years? And if cholera be communicated in some instances, is there not the strongest probability that it is so in the others—in short, that similar effects depend on similar causes?” (MCC, 29–30).

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However, the undeniableness of person-to-person spread still left open the specific mode of communication. Having dispensed with the idea that transmission must necessarily be by inhalation, he reasoned “by analogy from what is known of other diseases . . . that in cholera the alimentary canal is first affected” (MCC, 6–7). The primary intestinal symptoms characteristic of cholera suggested that the morbid poison had to be ingested. If one looked for an agent that would cause local irritation of the alimentary mucous membrane, the most likely hypothesis was that “the excretions of the sick . . . [contain] some material which, being accidentally swallowed, might attach itself to the mucous membrane of the small intestines, and there multiply itself by the appropriation of surrounding matter, in virtue of molecular changes going on within it, or capable of going on, as soon as it is placed in congenial circumstances” (MCC, 8–9). The capacity to undergo “molecular changes” meant that the morbid “material” causing cholera was “organized,” whether living or not, and obeyed chemical laws. The German researcher Henle argued that some contagious diseases were caused and propagated by “certain parasitical organised beings, or their germs,” and Snow’s analogical argument parallels Henle’s.11 Snow thought it possible that the unknown causative material in cholera behaved like the ova of intestinal worms. Extremely small and undetectable by the unaided senses, they reproduce and multiply in the gut. As in cholera, in many cases one cannot trace a case of worm infestation to a known carrier or discover the exact means by which the second victim swallowed the ova, but one would not thereby conclude in the second case that the disorder arose spontaneously (MCC, 9). There were problematic aspects to this analogy. With respect to differences in disease manifestation, worms produce indolent, chronic, seldom fatal diseases, whereas cholera is a severe, acute, and often rapidly fatal condition. In addition, Snow had not identified the microscopic morbid matter or particles that caused cholera, but neither had anyone else. Still, because the ova of intestinal parasites possessed some of the same properties, he proposed that such a particle was sufficiently within the realm of possibility for him to proceed with a discussion of its likely modes of communication. A fecal–oral transmission explained the most likely means by which cholera spreads within a limited area, such as a household. The copious diarrhea of cholera victims makes it certain that clothes and bedding become saturated, and because rice-water stools lack the usual feculent color and odor, members of the house may unknowingly soil their hands with cholera evacuations and transfer the morbid material to their mouths while eating. If the caregivers also prepared food, others would probably ingest the morbid material as well. In any case, the likelihood of such ingestion increased in the absence of hand-washing facilities and habits of cleanliness (MCC, 9–10). By contrast, when cholera spread rapidly over wide areas, the most likely explanation was contamination of drinking water by sewage containing the evacuations from cholera victims (MCC, 11–12). The potential for spread via a contaminated drinking water supply suggested, in turn, that cholera particles were capable of being infective despite great dilution (MCC, 27).12 In keeping with Snow’s


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general scientific approach, his reasoning on the modes by which cholera could spread were subject to empirical disproof. He realized that his theory would become suspect if one were to find that cholera spread within a household in which very careful hand washing was practiced or throughout a town with an undoubtedly pure source of drinking water.

Elements of Snow’s Hypothesis In MCC Snow was a pathologist first, a clinician second, and an epidemiologist third. His reasoning proceeded from pathological hypothesis to clinical effects to mode of transmission, followed by an epidemiological method by which the transmission hypothesis could be empirically tested.13 He reinterpreted a point of general agreement—what caused the “exudation of the watery part of the blood” into the intestines and subsequent discharge by “purging” (MCC, 7). Recent chemical analyses of the blood of cholera victims had shown dramatic increases in the proportion of blood solids to water: “The valuable analyses of Dr. Garrod have recently confirmed what had been stated in the former visitation of Europe by the cholera, viz., that the solid contents of the blood of patients labouring under this disease are greatly increased in proportion to the water—a state of the blood that is not met with in any other malady” (MCC, 7–8). However, the thickened consistency of the blood was compatible with either of two explanations: A poison in the blood pushed water and salts into the intestines, or a poison in the intestines irritated the mucous lining and pulled serum from the blood. Snow’s hypothesis required the latter explanation, whereas it turns out that Garrod assumed the cause was blood poisoning: “It would appear that the cholera poison, when introduced into the blood in sufficient quantities, causes an intense exosmotic action of the mucous membrane of the alimentary canal, at the same time destroying its endosmotic power. The blood therefore being deprived of a certain amount of water and salts, by the intestinal evacuations, and not possessing the power of regaining these by absorption from the stomach, becomes altered in the manner we have seen. . . .”14 Garrod’s interpretation of his own analyses did not trouble Snow because the evidence supported his own hypothesis. He conducted no chemical analyses of his own. It is unclear why at that time he did not cite evidence from the 1831–1832 epidemic, which unequivocally favored his view: that the injection of saline into the circulatory system temporarily restored bodily functioning in cholera victims. Instead, he offered only personal observations and his experience as a clinician in support of intestinal transmission (MCC, 7–8).15 He postulated the existence of an unknown agent or particle that, upon being ingested, would irritate the mucous membranes of the intestines and eventuate in the fluid losses detailed by Garrod. For his purposes it was sufficient for the cholera agent to be external, capable of being ingested by humans, and then multiplying within

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the gut. The agent’s action, not its structure, was critical to Snow’s hypothesis about cholera pathology and transmission. Hence, he “appeal[ed] to that general tendency to the continuity of molecular changes, by which combustion, putrefaction, fermentation, and the various processes in organized beings, are kept up” (MCC, 9). As long as the agent behaved as required, Snow could be circumspect about the agent’s nature without affecting his argument: “The writer . . . does not wish to be misunderstood as making this comparison [to ova of intestinal worms] so closely as to imply that cholera depends on veritable animals, or even animalcules [microscopic organisms]” (MCC, 9).16 It did not matter whether the agent was living or nonliving as long as it obeyed universal physical and chemical laws and was capable of the action and transmission that Snow hypothesized. Snow’s analogy between an unknown causative agent of cholera and the betterknown ova of intestinal worms was critical to establishing ingestion as the mode of entry. His mode of transmission required that the particle could multiply, for which there existed an analogy in the reproduction of animal parasites. Snow was a rarity among midcentury contagionists in thinking that parasitic worms could illuminate the problem of contagious diseases generally.17 Many of his contemporaries believed that parasitic worms were spontaneously generated within the human gut rather than arising from ingested ova.18 The most extensive work on parasitic worms during the period 1780 to 1840 was conducted in Germany by scientists who tended to support a theory of spontaneous generation. According to Farley, “the more expert one was on parasitic worms, the more likely one was to embrace the doctrine of spontaneous generation” (106). V. L. Brera, however, had proposed in 1798 that one could become infested with worms by ingesting their eggs as part of a diet of animal food. His Treatise on Verminous Disease was translated into English. Although most English writers on worms opposed spontaneous generation, usually on philosophical grounds, Snow the vegetarian would have found Brera’s argument congenial long before writing MCC.19 Also available to him was an English translation of J. J. S. Steenstrup’s On the Alternation of Generations (1845). Steenstrup described the life cycle of the liver fluke, showing that the source of the egg might be an animal superficially quite different in appearance from the generation that hatches from it. His research eliminated a major barrier to a contagionist view of parasitic infections, showed that intestinal worms issued from the ova of worms, and generally undermined the doctrine of spontaneous generation shortly before Snow used the worm analogy for cholera.20

Supporting Evidence in MCC Snow formulated his new hypothesis of cholera pathology and transmission during the last few months of 1848. At the time “he hesitated to publish them, thinking the evidence in their favour of so scattered and general a nature as not to be likely to


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make a ready and easy impression. Within the last few days [of August 1849], however, some occurrences have come within his knowledge which seem to offer more direct proof . . .” (MCC, 12). The bulk of his essay is a description and analysis of two local outbreaks south of the River Thames, followed by some suggestive remarks on cholera mortality in relation to metropolitan water supply. He intended to present more evidence but was content with the proviso that, “These opinions respecting the cause of cholera are brought forward, not as matters of certainty, but as containing a greater amount of probability in their favour than any other, in the present state of our knowledge” (MCC, 29). The “occurrences” that tipped the balance toward premature publication were two reports by John Grant, an assistant surveyor for the Commission of Sewers. On 9 August 1849 Grant had written up the results of his investigation into “The Condition of Surrey Court, Horsleydown,” in which there had “been an excessive mortality from cholera—nine or ten deaths in five days”: There are thirteen houses in the court, which is built up at both ends, and badly ventilated; there is an open ditch at the end, and the house-drainage is into cesspools, with common privies in small back areas. The houses in this court and those in Truscott’s buildings (another court) have a double set of small privies, cesspools, and small areas between the backs of them. Although there has been such mortality in Surrey court, there has been but one case (that of an infant) of cholera in Truscott’s buildings. The only apparent cause to which this difference can be attributed is, that in Surrey court the inhabitants used the water of a well in the court, the mouth of which was on a level with the paving and a gutter or side channel by which foul water was admitted into the well. This well the parish authorities have had cleaned out, and the mouth of it raised. Despite the renovations to the well, however, Grant recommended that the inhabitants be temporarily relocated until the open ditch was replaced by sewer pipes. In his mind escaping sewer gases during drainage repairs could produce more cholera cases.21 Two aspects of this report would have caused Snow to think that the Horsleydown outbreak could provide empirical evidence for his new notion that the morbid matter of cholera was ingested rather than inhaled. First, drinking water had been contaminated by sewage. Second, the contamination had occurred only in one of two neighboring courts—that is, the outbreak had a control sample, or, in the terminology of the time, it constituted a “natural experiment.” Grant’s report was insufficient to establish that the well had been contaminated by excrement from cholera patients, so Snow spoke with the attending practitioners to determine the chronological order of attacks and details about their disposition (MCC, 12–15).

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The second local outbreak of cholera that Snow believed offered support for his hypothesis had occurred in late July and early August 1849 in Albion Terrace, Wandsworth Road. Again, a report by Grant on sewage overflow into drinking water caught his attention (MCC, 16). As with Surrey Court, Snow described the layout in great detail for readers of MCC, drawing upon Grant’s investigation.22 We constructed diagrams of the drains and water supply at Albion Terrace based on Snow’s description in MCC (Fig. 8.2 and Fig. 8.3). Snow was thinking in spatial and topographic terms, although he made no diagrams himself.23 Snow’s investigative technique for the two cholera outbreaks described in MCC conformed to that of a “village epidemiologist” who attempts to establish the source of an outbreak of infectious disease within an area no greater than several city blocks.24 He established that the two outbreaks shared a number of defining features. One or two cases of cholera appeared in the neighborhood, probably contracted elsewhere, which was no greater than the general incidence of cholera in that part of metropolitan London. In Snow’s view these cases of cholera could not have produced a sudden epidemic outbreak unless the means existed by which water contaminated with the evacuations from resident cholera victims could become mixed with the drinking water supplied to nearby houses. In Horsleydown the means for contami-

Brick drain (to sewer to Battersea Fields) Brick drain

Water storage tank (brick & cement)

6" stoneware pipe (from spring)

48"

Cesspool (beneath privy)

Lead pipe to pump in kitchen

HOUSE

Figure 8.2. Diagram of house drainage at Albion Terrace. Drains, water pipes, and tanks were found to have leaky joints. Water levels in the cesspools and drains were higher than the levels in the water tanks (adapted from Snow, MCC).


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To sewer, Battersea Fields Drinking water in all houses found to be impure after 26 July

Drains

1

2

3

4

5

Cesspools full; apparently over-flowing into drinking water tanks

6

8

7

Spring

9

10

11

12

Drain burst during heavy rain on 26 July; lower level flooded with fetid water

13

14

15

16

17

First cholera case (28 July)

Figure 8.3. Diagram of Albion Terrace showing main events suggesting sewage contamination of drinking water at a time when cholera evacuations were present in the sewage (adapted from Snow, MCC).

nation were ongoing, whereas in Albion Terrace contamination had occurred only once, during a severe rainstorm. Consequently, after several days many cases broke out almost simultaneously in other houses using the common water supply. Snow believed he detected organic impurities when making visual examinations of the drinking water supply that he considered suggestive of sewage contamination. The fact that no similar outbreaks occurred in nearby houses with different sources of drinking water but exposed to similar local atmospheric conditions meant that the cause in both locations was communicability of a specific cholera poison via ingestion, not inhalation of miasmas. In addition to the two outbreaks traceable to local contamination of drinking water, Snow hypothesized that river water contaminated by cholera evacuations explained variations in cholera mortality throughout metropolitan London. The determining factor was the source of the drinking water supplied by various water companies. From the Weekly Returns of Births and Deaths published during the current cholera epidemic, Snow devised a table that listed the number of deaths by regional districts. The west, north, and central districts had the smallest percentage of deaths, and many residents there received piped drinking water from commercial companies whose sources were upstream of any major contamination by sewage. The greatest percentage of deaths—seven times higher than in north London—occurred in south London, where the water companies supplying those districts drew from the tidal zone of the River Thames, near the outlets of large municipal sewers. The east district had four times the average mortality, which was surprising to Snow because the East London Water Company had shifted its source to a point above tidal reach of the River Lea. He suspected the company still drew some water from

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reservoirs at Old Ford that were filled from a portion of the Lea heavily contaminated by sewage outflows. He had been unable, however, to obtain the “exact information” he desired on water supply for each part of London (MCC, 25). His table could show only a rough association among the rate of cholera deaths in each of five broad districts and what he could preliminarily determine about the sources of drinking water used by the commercial water companies. That is, his argument that cholera was transmitted in metropolitan London via contaminated river water was very inconclusive, but he did note that population concentrations and associated effluvia in South London would not favor local miasmatic or contingent contagionist explanations of high cholera mortality in that region: Central London is “quite on a par with the worst parts on the south of the Thames as regards overcrowding and bad smells” (MCC, 25).25

Anticipating Criticism Snow anticipated possible objections to his hypothesis, especially from sanitary authorities who reasoned that general impurities either contained the cholera poison or predisposed individuals to fall victim to it. He was aware that Dr. Gavin Milroy, who was associated with the GBH, had investigated the outbreak in Albion Terrace and attributed the high mortality to a combination of factors: In Snow’s words, “firstly, to an open sewer in Battersea Fields, which is 400 feet to the north of the terrace, and from which the inhabitants perceived a disagreeable odour when the wind was in certain directions; secondly, to a disagreeable odour from the sinks in the back kitchens of the houses, which was worse after the storm of July 26; and lastly, to the accumulation [of offensive rubbish] in the [cellar of] house No. 13 . . .” (MCC, 21–22). Snow countered each of Milroy’s explanations with several of his own: With respect to the open sewer, there are several streets and lines of houses as much exposed to any emanations there might be from it, as those in which the cholera prevailed, and yet they were quite free from the malady, as were also nineteen houses situated between the sewer and Albion Terrace. As regards the bad smells from the sinks in the kitchen, their existence is of such every-day, and almost universal prevalence, that they do not help to explain an irruption of cholera, like that under consideration; indeed, offensive odours were created in the thousands of houses, in London, by the same storm of rain on July 26th; and the two houses in which the offensive smell was greatest, viz. Nos. 8 and 9,—those which were flooded with the contents of the drain,—were less severely visited with cholera than the rest; the inhabitants having only had diarrhœ a or mild attacks of cholera. The accumulation in the house No. 13 could not affect the houses at a distance from it. MCC, 22


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Because local spread of effluvial vapors could not explain why some residents in adjoining houses did not contract cholera or why vapors generally present should suddenly become poisonous, Snow concluded “that the only special and peculiar cause connected with the great calamity which befel the inhabitants of these houses, was the state of the water, which was followed by the cholera in almost every house to which it extended, whilst all the surrounding houses were quite free from it” (MCC, 22–23).26 Snow also anticipated a possible objection to the contaminated river water portion of his hypothesis. To those who assumed that the immense quantity of water in rivers as large as the Thames would sufficiently dilute the cholera poison to render it harmless, he proposed that “the poison consists probably of organized particles, extremely small no doubt, but not capable of indefinite division, so long as they retain their properties” (MCC, 26). Although cholera evacuations diluted in the Thames lessened the chances that a given glassful of Thames water contained poisonous particles, every particle retained the power of reproducing within the gut and doing its mischief. He anticipated criticism of his hypothesis on two other counts. Some might object that stomach acid would destroy the ingested cholera poison, whatever its form or source. Snow admitted the possibility, noting that it might explain why some people were able to resist “its effects,” whereas those whose “digestive powers have been weakened by a fit of drunkenness” could not (MCC, 26). In this instance he referred to a common belief that excessive drink increased one’s susceptibility to cholera. For some reason he decided not to anticipate a reasonable anticontagionist rebuttal: several autoexperiments in the 1830s in which those who had swallowed cholera excretions or vomitus generally failed to contract the disease.27 He admitted the possibility of airborne transmissions from victims to healthy persons, but not as understood by the theory of infection. In his view airborne cholera particles had to be ingested to cause the disease: “the organic part of the fæces, when dry, might be wafted as a fine dust, in the same way as the spores of cryptogamic plants, or the germs of animalcules, and entering the mouth, might be swallowed” (MCC, 27).28

Prevention of Cholera In the penultimate paragraph of MCC, Snow outlined a few socially practical and commercially unintrusive measures by which “cholera might be checked and kept at bay” (MCC, 30). He considered it prudent for “all persons attending or waiting on the patient to wash their hands carefully and frequently, never omitting to do so before touching food, and for everybody to avoid drinking, or using for culinary purposes, water into which drains and sewers empty themselves; or, if that cannot be accomplished, to have the water filtered and well boiled before it is used” (MCC, 30).29 These recommendations would deter the ingestion of cholera particles,

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whether dissolved in drinking water or invisibly saturated in the victim’s linens. They also reflect his extension of Newton’s distilled water regimen into the public health arena, as he had advocated years earlier in his teetotal address. Whereas simple cleanliness in the household could prevent incidental transmission of cholera, Snow believed “the sanitary measure most required in the metropolis is a supply of water for the south and east districts of it from some source quite removed from the sewers” (MCC, 30). That would prove to be a more contentious and expensive proposal. Snow’s simple measures for preventing cholera were significant at the time for what they did not include. He did not advocate quarantine. Much of the anticontagionist sentiment, especially in maritime nations, was a reaction to quarantine. Snow made it clear that the preventative measures his hypothesis called for “would not interfere with social or commercial intercourse” (MCC, 30).30 In his view cholera was communicable in only very limited circumstances and in very specific ways. If one linked quarantine with “contagion” theory and equated “contagion” with transmission either by touch or by (inhaled) infection, then cholera was not contagious by those criteria. His hypothesis suggested that focused reforms in behavior would keep cholera at bay. He supported cleanliness in general, but only certain practical measures would prevent the spread of cholera—hand washing by caregivers and food handlers who were likely to encounter cholera patients and assuring that drinking water was not contaminated with sewage that might contain cholera evacuations.

Initial Elaborations of MCC After MCC appeared Snow became preoccupied with additional on-the-spot research at Albion Terrace. Later published reports had differed from his own account, portraying events in such a way that a local miasmatic explanation of the outbreak seemed more probable.31 Snow reinterviewed one of the local surgeons and interviewed a gardener who had helped clean up debris from a burst drain after a second thunderstorm in August. The gardener had subsequently fallen ill of cholera but recovered. Snow recounted for the medical audience the facts that confirmed his own explanation of contaminated water as the source of the outbreak and that rendered a miasmatic account unlikely. He concluded the letter with a remark that he had nearly finished a more extended paper containing “a variety of details, collected from different parts of the country, which show the connection between tainted water and the extension of cholera, and also the great freedom from cholera, both now and in 1832, enjoyed by certain large towns . . . that have a plentiful supply of water that is totally unmixed with the contents of sewers.”32 Snow kept his promise, delivering the paper “On the pathology and mode of communication of cholera” in mid-October at the Westminster Medical Society, which was published shortly thereafter under the same title (hereafter PMCC). Although he reused passages (some verbatim) from MCC and preserved its organizational


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structure, PMCC provided the additional substantiation necessary to transform a suggestive hypothesis into a theory that could be falsified by evidence at variance with its conclusions (PMCC, 746–47).33 Snow slightly expanded the discussion of the pathological process found in MCC. He noted that the difficulty in breathing experienced by cholera victims in advanced stages was caused by the thickened state of the blood obstructing pulmonary circulation. Such capillary congestion also explained reduced urinary output, accumulation of urea in the blood, and the albumen present in whatever urine was produced (PMCC, 745). The other significant difference in the pathology section was his replacement of the phrase “general tendency to the continuity of molecular changes” with a vaguer reference to “a kind of growth . . . like any other morbid poison” (PMCC, 746). Near the end of the essay, he stated that “a poison capable of multiplying in the body must, one would conclude, be organized, and therefore consist of particles, however minute . . .” (PMCC, 928). He admitted the possibility that the poison might be a chemical compound capable of being imbibed by epithelial tissue.34 Even so, he considered its nature relatively unimportant because its action, mode of propagation, and the measures necessary to prevent it from spreading were clear if one accepted his theory. Snow devoted the bulk of the two-part article to substantiating his theory by presenting “instances of severe [cholera] visitation, or of exemption from its ravages” (PMCC, 747) (Table 8.1). By what means did Snow accumulate such a rich set of examples to support his theory in October, when in August he had almost withheld publication because he had so little evidence? His footnotes (much more numerous in PMCC than in MCC) show that he had consulted published literature, including reports by parliamentary committees and case reports in medical journals. In other instances he made use of personal contacts and correspondents. For example, he cited excess fatality in the village of Newburn, near Newcastle. He learned of it by writing a general letter of inquiry to a friend in Newcastle, Dr. Dennis Embleton, who procured information from a Rev. John Reed and put Snow in touch with a local surgeon, Mr. Robert Davison. Examples from York and Bath indicate he relied on personal and family acquaintances. In other cases it appears that fellow members of the Westminster Medical Society provided information or names of potential informants. Perhaps, as Snow’s theory matured in the summer of 1849, he had begun to initiate these inquiries by post but had not received enough complete answers in time to include the data in MCC. After his water-borne theory of cholera transmission was printed in early September, correspondents submitted unsolicited examples and counterexamples in letters to the editors of the medical journals. He limited evidence from the London metropolis to “instances of severe visitation, or exemption from its ravages”(PMCC, 747), beginning with a summary of his findings in Horsleydown and Albion Terrace. He noted similar point-source outbreaks where well or Thames-ditch water, contaminated by evacuations from cholera victims, had caused the epidemic outbreaks regardless of the level of the ground, the state of the air, the classes of the inhabitants, or the type of housing. He also noted

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Cholera, Chloroform, and the Science of Medicine Table 8.1. Substantiating evidence in PMCC

London

Provincial towns: Affected

Provincial towns: Exempted

(Study of south London water supply: deferred) 1. Horsleydown: Surrey Bldgs. affected; Truscott’s Court exempt 2. Albion Terrace: affected; nearby houses exempt 3. Silver Street, Rotherhithe 4. Charlotte Place, Rotherhithe 5. Specific examples: (a) Contaminated wells and ditches (b) Bethlem Hospital, Queen’s Prison: exempt with uncontaminated wells despite nearby neighborhoods affected c) Millbank Prison: water drawn from Thames, affected although nearby neighborhood exempt 6. Westminster districts overcrowded and lowlying, but little cholera because water pure 7. Brixton: open streets, rising ground, middle class, but high mortality because water sewagecontaminated

1. Bath (one neighborhood only): local well contaminated by cesspools

1. Birmingham: river polluted by sewers but drinking water obtained elsewhere

2. York: mortality depended on whether water drawn from river above or below sewers

2. Bath: piped water from surrounding hills

3. Exeter: water works repositioned upstream, reduced mortality 4. Hull: New water works but drew water from tidal river, mortality increased 5. Dumfries: water from tidal river, high mortality 6. Newburn (near Newcastle): well water contaminated by sewer drain 7. Bilston: water contaminated by mine pits, high mortality 8–10. Metthyr, Tydvil, Kendal: sewage seeped into wells

3. Cheltenham: drinking water free of sewage 4. Leicester: river polluted with sewage, low-lying, but drinking water from springs 5–7. Preston, Oldham, Paisley: drinking water from surface drainage of nearby hills 8. Nottingham: filtered river water upstream from sewers 9. Stafford: water contaminated with sewage, but individual wells with no central supply, so any outbreaks confined to only a few houses (i.e. impure water itself did not cause cholera)

places where cholera should have occurred, according to a rival theory, but had not because the water was uncontaminated by sewage. He noted that districts south of the Thames had suffered the greatest mortality in both epidemics, indicated that he was “endeavouring to compile a full account of the recent epidemic in London, in its relation to the water,” but that he would say no more about it until he had completed his investigations (PMCC, 747).


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Snow discussed several provincial towns visited by cholera in the epidemics of 1831–1832 and 1848–1849 where the water could be blamed. Some outbreaks could be attributed to water drawn from wells, springs, and mine pits contaminated by feces from cholera initially transmitted interpersonally. In others the attributed cause was a river that served both as a source of water and a receptacle for the town’s sewage. In two towns Snow associated mortality differences in the two epidemics with the water supply. The water works in Exeter had been repositioned upstream of sewer outlets after 1832, and mortality was reduced in the current epidemic. In Hull, however, the water works built after 1832 drew river water from a tidal zone containing intermittent sewage, and the mortality rate increased dramatically during the second epidemic. Snow considered negative evidence equally significant for his theory, and he described nine towns he believed were exempt from cholera because their water was uncontaminated by sewage. It did not matter whether drinking water came from wells, rivers, springs, or surface run-off as long as it was pure. He cited Stafford to show that impure water would not cause cholera unless the impurities included evacuations from cholera victims. According to a resident physician, water in the town’s many wells often contained sewage sediments, but each well was used only by a small cluster of houses. There were no epidemic outbreaks of cholera in Stafford because the water sources were separate from one another, not interconnected as in many large cities. Cholera outbreaks were thus limited to one household, or a few at most. Snow explained how his theory of the pathology of cholera explained the differences in epidemic duration exhibited in villages, towns, and cities. Population size determined when the disease ran out of fresh victims in which to multiply, and contrary to “the usual theory of contagion or infection . . . all the members of the community are not liable to be reached by a poison which must be swallowed, as they would be by one in the form of an effluvium” (PMCC, 928). As in MCC, he presented a list of preventive measures, adding recommendations to avoid “the fruit that is hawked about the streets” during an epidemic (it was often stored at night under beds and was liable to become contaminated) and altering the shifts in mines so workers did not have to eat in the pits (PMCC, 929).

Snow and the Bristol Cholera Fungus Theory Snow was not the only English investigator to be alert to the intestinal worm analogy and thereby to decide that fecal–oral transmission would explain cholera data better than any inhalation theory. MCC appeared less than a month before a pamphlet on the cause and transmission of cholera by William Budd of Bristol. The dismissal of the Bristol fungus theory by the London medical establishment suggested the barriers Snow had to overcome before his theory would be accepted.

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William Budd (1811–1880) is best known today for his discovery that typhoid fever is a water-borne contagion. In 1828 he visited Paris to study under François J. V. Broussais and other figures in the development of hospital medicine. Broussais believed that all fevers were caused by local inflammations seated in the gastrointestinal tract, which may account for Budd’s inclination toward a localized gastrointestinal pathology in cholera as well as in typhoid.35 In late September 1849 Budd presented a theory of cholera in the form of five propositions: 1. That the cause of Malignant Cholera is a living organism of a distinct species. 2. That the organism . . . is taken . . . into the intestinal canal, and there becomes infinitely multiplied by self-propagation. . . . 3. That . . . the action that [the organisms exert in the intestine is] the cause of the peculiar flux which is characteristic of malignant cholera. . . . 5. That these organisms are disseminated . . . in the air, . . . in contact with articles of food; and . . . principally, in the drinking water of infected places.36 Budd had timed publication of his theory to coincide with reports from two fellow investigators in Bristol, Frederick Brittan and Joseph Swayne, who claimed to have discovered the fungus particle that was the causative agent of cholera,37 but microscopists in London were unconvinced. On 17 October 1849 George Busk demonstrated to the Microscopical Society of London the presence of the same fungus particles in a loaf of bread; the suspected cholera cells were simply spores of the uredo similar to that that causes smut in grain.38 Three days later Edwin Lankester affirmed Busk’s findings at a meeting of the Westminster Medical Society.39 Other researchers wondered if the particles were even fungoid. Regardless of the precise identification of the particles, professional opinion expressed in the London medical journals was soon virtually unanimous that the Bristoleans’ claim to have discovered the causative agent of cholera was premature.40 Although Budd’s theory could stand independently of his colleagues’ identification of a specific fungus or causative organism (Fig. 8.4), his later willingness to accept inhalation for the transmission of cholera under certain circumstances raised doubts about the consistency of his theory. In 1854 he described a cluster of cases arising in a hospital ward among patients who shared the use of a privy and blamed the spread on inhalation of “effluvia” arising from cholera evacuations.41 This modification put him in the position of claiming, on the one hand, that cholera was closely analogous to intestinal diseases caused by animal parasites, which presumably spread only when one ingested the parasitic eggs orally, and on the other, that cholera could be spread just as readily by inhalation as by fecal–oral transmission. If one postulated the latter, it was easy to see why cholera should be first and foremost a disease of the alimentary canal, but if the cholera agent could also be taken into the body via the lungs, it becomes more difficult to understand why only the


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Budd Cholera fungus

oral ingestion

inhaled in lungs not explained reproduces in gut

symptoms of cholera cholera fungus evacuated in stool

spread over distances by water supply

household spread by contact

Figure 8.4. Budd’s contagion theory.

gastrointestinal tract should be affected—or why cholera transmitted via the lungs should show the same signs and symptoms as cholera transmitted by a fecal–oral mode. Snow agreed with Budd that cholera was a gastrointestinal disease, that its nongastrointestinal features arose from dehydration, and that water contaminated with cholera evacuations was a major source of spread, but they disagreed on two key points: that inhalation was a feasible mode of transmission under some circumstances and that the actual causative agent of cholera was the “fungus” identified by Brittan and Swayne. Budd’s reasoning on the inhalation issue was similar to that of the contingent contagionists, who argued that if two cholera outbreaks seemed to

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follow two different patterns, it must mean that the cholera poison acts differently under different circumstances (“contingencies”). Snow, by contrast, considered his view of cholera pathology the foundation of his theoretical edifice and refused to alter it in order to explain apparently anomalous outbreaks. Given the mind-set of most of his colleagues, Snow’s decision guaranteed that he would be viewed as a radical, inflexible thinker compared to someone like Budd, whose willingness to consider multiple routes was mainstream at the time.42 Apparently, Budd considered it premature to suggest that cholera could spread via water contaminated by the excrement of its victims unless he could point to a specific cholera-causing agent in the water. Hence he joined his Bristol associates in identifying a fungus as that agent. Snow at first suggested that the Bristol fungus discovery lent credence to his own theory, but he soon drew back and then dissociated himself completely from the fungus claim.43 In so doing he continued a policy of theoretical parsimony that played to his strengths as a medical researcher. He had two pathways to follow in building evidence for his hypothesis: the microscopic route of identifying and investigating the particle, or the epidemiological–statistical route of tracing the consequences of his theory over large areas and among large populations. He was not a microscopist, but his understanding of the collateral medical sciences of statistics and epidemiology was sophisticated. Detailed suggestions about the specific nature of the cholera agent would have been distracting and potentially counterproductive to his purpose: to prevent the transmission of cholera within households and through contaminated drinking water. In taking this approach Snow revealed a singular sense of focus. He realized that he had to ground his theory of cholera transmission in the pathology of cholera in order to make it plausible. The spread of cholera by oral ingestion and the nature of cholera as a localized disease of the alimentary canal were two sides of the same coin. The pathological account forced him to propose the existence of a particle with the capacity to multiply and produce the characteristic symptoms of the disease. He needed to say no more about the cholera agent to propose a testable hypothesis,44 but this line of reasoning made Snow vulnerable to criticism from infection contagionists and local miasmatists, who assumed the morbid material was transmitted through the air and then inhaled. The poisonous agent for their mode of transmission was as mysterious as Snow’s, but why reject clinical wisdom accumulated over two millennia on hypothetical grounds alone? Perhaps that was why Budd and his Bristol colleagues believed they could proceed no further with their line of investigation unless they could demonstrate the existence of the infectious agent. In fact, Budd’s endorsement of Snow’s 1849 hypothesis was conditional precisely because Snow did not specify the nature of the infectious particle: “Of being the first to develop and to publish this very important conclusion”—that cholera is transmitted by contaminated water—Snow “must, therefore, have the whole merit. To no part of this merit do I lay the slightest claim. . . . The detection of the actual cause of the disease, and the determination of its nature, were all that was wanting to convert


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[Snow’s] views into a real discovery.”45 Presenting a plausible mode of transmission without identifying the “actual” particle fell short of the ideal for some who otherwise agreed with Snow.

The Structure of Snow’s Thought Snow’s early writing on cholera displayed the patterns of scientific inquiry that he developed during his early research work between 1838 and 1846 and then consolidated in his work on ether and chloroform. Table 8.2 shows how the multilevel systemspattern of his thinking came to full fruition in the study of cholera transmission. Snow considered the human organism a complex system in interactions with other complex systems. For him the “person” was a hierarchy of systems that could be studied at many different levels of organization, from molecules at the lowest and smallest end to nations and continents at the highest and largest end. Each level of organization was associated with a collateral scientific discipline that was suited for the study of the natural phenomena that tended to occur at that level.46 This hierarchy of systems provided the medical scientist with alternative ways of investigating health and disease. Sometimes one could observe the phenomenon directly. At other times the phenomenon could best be understood by observing its ripple effects at other organizational levels. For example, one could understand something about the ova of parasitic worms by direct microscopic inspection, whereas one could understand the contagious poison of smallpox only by seeing how it affected the body and its component organs and tissues. He was (in today’s terms) an interdisciplinary thinker. He appreciated not only the horizontal levels of the hierarchy but also the vertical channels of communication that linked the levels. He saw causal linkages at a single level, where one could understand cause–effect chains within one science, and between levels, when one needed to integrate the methods of different sciences to capture the phenomenon under study. His use of the term “mode of communication” broadly suggests how he envisioned the cycling of matter both within and among levels.47 Snow’s systems thinking required a sequence of steps. First, he reviewed the vast scientific literature on cholera and selected the key facts that seemed least open to dispute. He laid out in the opening pages of MCC what he took to be the leading facts: how cholera followed trade routes across continents; how early symptoms affect the gut and how constitutional symptoms arise only after dehydration; and how the blood is thickened and lacking in water and salts. As such, he was thinking at multiple levels by collating geographic and epidemiologic data with clinical, pathological, and chemical data. In somewhat similar fashion Snow took as his point of departure in ether anesthesia the realization that the inconsistent clinical effects of ether might be explained by the quantity inhaled, which depended largely on concentration of the vapor at different air temperatures. For a coherent theory of

Table 8.2. Snow as a systems thinker on cholera transmission Hierarchical level

Collateral science

Reasoning

Cholera findings or implications

Nation or continent

Geography

Induction

Appeared to follow trade and travel routes

Large town or city

Vital statistics, descriptive sociologya

Deduction

Cases increased in areas where populace used sewage contaminated water (especially river)

Neighborhood

Vital statistics, numerical method (of Louis), descriptive sociology

Deduction

Cases increased where point source of drinking water (pump, cistern, etc.) contaminated with cholera feces, or where person-to-person communication occurred (due to, e.g., occupational patterns such as in coal mines)

Household

Vital statistics, numerical method (of Louis), descriptive sociology

Deduction

Cases increased where food preparer or eater had hands soiled with cholera feces, or where drinking water was contaminated with feces

Person

Clinical medicine

Induction

Constitutional symptoms arose only after dehydration

Organ systems

Physiology, pathology

Induction

Early symptoms confined to gut

Deduction

Other organ systems affected late by thickened blood and decreased circulation

Tissues

Pathology

Induction

Minimal autopsy findings overall; sometimes bowels filled with fluid even when there had been no cholera evacuations during life

Deduction

Causative agent or particle must be local irritant to gut membrane causing massive fluid loss

Microscopic particles

Microscopy

Deduction

Causative agent not yet seen but has functional attributes: swallowed; excreted via feces; capable of multiplication within gut; in process of multiplication causes gut irritation that leads to diarrhea, partial analogy to ova of intestinal worms

Molecules

Chemistry, Physics

Assumption

Continuous molecular changes: complex particles capable of maintaining structure and multiplying by assimilating surrounding material; follow laws of chemistry and physics; no clear line between vital and nonvital processes; analogies to putrefaction and combustion

Induction

Blood lacks elements (water, salts) that are found in increased quantity in stools

a

This term was not in use in Snow’s day. We mean by it a qualitative understanding of the habits and practices of the population in question.

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cholera to emerge from the disparate facts he gathered in the fall of 1848 and early winter of 1849, he needed the insight that the dominant view, (contingent) contagion equals infection, was an unwarranted and unproven assumption. Thereafter, he needed the analogy between the postulated cholera particle and the ova of intestinal worms to link his pathological hypothesis (cholera as confined to the gut), his chemical hypothesis (cholera poison as a sort of organized particle capable of multiplication in a suitable environment), and his transmission hypothesis (fecal–oral spread). Once he had a unified hypothesis, he could deduce expected phenomena at other levels of the systems hierarchy.48 At this step he used a hypotheticodeductive model of science similar to Herschel’s formulation, including the insight that advances often come from collating information among several scientific disciplines rather than from pursuing research solely within a single discipline.49 He then surveyed various deductions and asked which occurred at levels of the hierarchy where the relevant collateral science had developed the most useful tools of observation and inquiry. Snow began with a suspicion that microscopy was the thinnest reed upon which to lean his inquiries. Therefore, he made deductive leaps to adjacent organizational levels, the tissue and the molecular levels. From observations at those adjacent levels, he could in turn deduce the functional properties of the purported cholera particle, such as its irritation of the mucous membrane resulting in exudation of fluid. When Snow heard about the Bristol fungus, he realized that Budd and colleagues claimed to have discovered a structure without discerning anything useful about its function. Until he had some reason to believe that the fungus particle shared important functional characteristics with the cholera agent that he had deduced, Snow felt little temptation to pursue that line of inquiry.50 Finally, Snow adopted the scientific tools of the relevant collateral sciences to determine if cholera behaved as his theory predicted. He found empirical evidence to support his theory. The evidence would be stronger to the extent that it could be found at multiple levels of the systems hierarchy and discovered by the techniques of different collateral sciences. Snow reported the results of his initial inquiries regarding the household and the neighborhood levels of organization in MCC. In PMCC he was able to add evidence drawn from larger geographic regions thanks to his correspondence and more extensive review of the literature. Snow believed that a more detailed inquiry into the water supply of the different districts of London— especially south of the Thames, where cholera mortality was highest—would provide even more telling evidence, but he decided to publish PMCC without substantiating his theory at the metropolitan level of population density.51 Snow approached the highest level of sophistication in systems thinking when he proposed in PMCC that one could use his theory of the mode of transmission of cholera to explain the difference among villages, towns, and cities in the duration of epidemic outbreaks. To a modern epidemiologist he was beginning to explore the idea of the “epidemic curve,” the mathematical laws that epidemics must follow. He appreciated the fact


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that if one took the same mode of communication, fecal–oral spread, and applied it to populations of different sizes, the disease should behave in different ways. He was able to reason directly from disease pathology in the individual patient to population-level manifestations. That is, he reasoned from micro- to macro-level phenomena. Snow addressed the cholera problem from this intellectual platform in 1848 and 1849 in full confidence. He had, after all, used this same approach to ether anesthesia during the first half of 1847, placing both the science and the practice of etherization on a firm footing in short order. Snow saw no reason why cholera transmission should not be amenable to the same strategy, but he miscalculated his intended audience. When Snow administered ether to a patient, he had a known agent, and the results of the intervention could be directly observed by any witness. With respect to cholera, however, he posed an unknown agent and argued for a mode of communication that was essentially invisible. Although he believed in the late summer and fall of 1849 that the available evidence satisfied his personal threshold for publishing a new cholera theory, he would soon find that his medical colleagues and the public health bureaucracy considered it inadequate and unpersuasive.

Notes 1. “Medical news,” Lancet 2 (12 August 1848): 195–96; Lancet 2 (9 September 1848): 303–04; Lancet 2 (16 September 1848): 331–32; and Lancet 2 (14 October 1848): 436. For a progress map, see Bonderup, “Cholera-Morbro’er” og Danmark, 20. 2. “Westminster Medical Society,” LMG 42 (1848): 768. 3. LMG 42 (1848): 769. 4. Ibid., 769–70. 5. Ibid., 770. Copland classified both “asphyxy” and “cholera” as “nervous diseases”; Dictionary, 1: 128, 318. Cholera asphyxia was a commonly used term at the time; see J. G. French, “Observations on cholera.” LMG 38 (1846): 328, in which he wrote, “Dr. Copland states that paralysis of the lungs is essentially the disease, and proposes the name of Pestilential Asphyxy for it.” Copland’s definition of asphyxy was “suspended animation proceeding from a primary arrest of the respiratory actions, the other functions being thereby abolished”; Dictionary 1: 128. Snow may have had this parallel in mind when he compared cholera and asphyxia. 6. “The brandy treatment has been extensively tried in Cholera, but it is now abandoned in all parts of the world. If the debility is not so great that life is not destroyed by [brandy], still it hurries on and makes more violent that reaction, that secondary fever which is most to be dreaded, and increases the tendency which there is to inflammation in the head and elsewhere”; Snow, “Teetotal address” (1836). 7. Snow, On the Mode of Communication of Cholera (August/September 1849), 8. Hereafter, citations to this pamphlet are made parenthetically using the abbreviation MCC. 8. “At a time when the chemistry of gaseous substances did not exist, and when certain diseases were attributed to a putrefaction of the fluids of the living body, these diseases were supposed to be occasioned by the effluvia given off during ordinary putrefaction”; Snow, “On the chief cause of the recent sickness and mortality in the Crimea” (1855). 9. P. E. Brown suggests that the idea that cholera was a local affection of the intestines was an “old-standing foible” of Protheroe Smith; “Another look at John Snow,” 650. While Smith

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did state that “the peculiar action of the inciting cause [of cholera] is clearly that of morbid impression on the follicular apparatus of the intestines,” he thought the pathological process was triggered by the body’s nervous system to “resist the assailant” by “an abnormal and inordinate increase of action . . . in the functions of the alimentary canal”; Cholera: An Inquiry, 14–15. For the contagionist opinion closer to Snow’s thinking, given his interest in Liebig’s work and parasites, see “Medium of contagion,” Lancet 1 (1842–43): 111. 10. We are grateful to Christopher Hamlin for pointing out the need for these assumptions. Snow did not articulate these assumptions in MCC. He did, however, come much closer to both explicating and justifying these assumptions in his oration CMC (1853). 11. “Medium of contagion,” Lancet 1 (1842–43): 111. 12. P. E. Brown claimed, “Snow had hit on an idea which he had not the means nor the abilities to put to the test,” in part because “his original inspiration was the result of a haphazard process of reasoning which no later rationalisation could ever turn into a convincing argument”; “Autumn loiterer,” 527. 13. Margaret Pelling wrote that Snow’s theory rested on twin pillars: “a consideration of the pathology of the disease and from a conviction, based on cholera’s predilection for lines of human intercourse and on consecutive cases in the one household, that the disease was communicable person to person”; see Cholera, 204. Similarly, Shephard argues that Snow the epidemiologist should not distract us from his clinical and pathological perceptions; JS, 163. 14. Alfred B. Garrod, “On the pathological condition of the blood in cholera,” LJM 1 (1849): 409–37; the quotation is from 436. Garrod’s article was a companion piece to Edmund A. Parkes, “On the intestinal discharges in cholera,” LJM 1 (1849): 134–52, published two months earlier. Parkes and Garrod were then assistant physicians to University College Hospital and had collaborated in their respective chemical analyses of the blood and stool of cholera patients. Both believed the cholera poison entered the bloodstream first, the alimentary canal secondarily, if it at all. Although Snow did not cite Parkes’s article, he had broached his hypothesis with him and Garrod before writing MCC. 15. Snow strengthened his pathology argument after MCC. In 1855, for example, he cited Garrod’s article at length and added other references: “The analyses of Dr. O’Shaughnessy and others, during the cholera of 1831–32, showed that the amount of water in the blood was very much diminished in proportion to the solid constituents, and that the salts of the blood were also diminished. The analyses of Dr. Garrod and Dr. Parkes, in the spring of 1849, were more numerous and exact. The amount of water in the blood of healthy persons is on the average 785 parts in 1000; whereas, in the average of the analyses performed by Drs. Garrod and Parkes, it was only 733 parts, while the amount of solid constituents of the blood, relatively to the water, was increased from 215—the healthy standard—to 267. . . . Dr. Garrod is of the opinion that a chemical analysis will determine whether or not a specimen of blood has been derived from a cholera patient”; MCC2, 11–12. For the 1855 edition of his essay, Snow also calculated that one would have to replace 5 pints of water to restore the blood of a cholera victim in the state of collapse to normal health, which showed that the amount of fluid lost was well within the estimates of the total amount of fluid evacuated through the intestinal tract; MCC2, 14. Snow added that the dramatic reversal of cholera symptoms by intravenous saline injections was strongly in favor of the dehydration hypothesis and went against the theory that the symptoms of cholera were caused by a blood-borne poison; MCC2, 13. 16. We have found no evidence that Snow had “proof ” before 1853 that cholera was caused by a “microorganism,” as asserted by Shephard, JS, 152–53. 17. As early as 1843 Snow was aware of entozoa from the perspective of comparative anatomy: “In many species of the lowest tribes of animals, the circulation of the blood which takes place in capillary tubes is independent of contractions and all mechanical forces, and must


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arise from the functions taking place in the vessels: for instance, the trematoda, an order of intestinal worms, possess two vessels on each side of the body, in which the blood moves in opposite directions; and, according to the observations of Ehrenberg and Von Nordman, these vessels do not contract in the least”; Snow, “On the circulation of the capillary blood-vessels, and some of its connections with pathology and therapeutics,” (1843), 811. Thereafter, Snow did not discuss intestinal worms until he decided the analogy was apt in his first essay on cholera. Surely he had read the reference to Henle’s “parasitical organised beings” as “the exciting cause” of contagious diseases in “Medium of contagion,” Lancet 1 (1842–43): 111. Perhaps he had also read the article about Henle’s researches in the October 1842 issue of M-CR abstracted under the title, “Medium of Contagion,” by the Lancet, and Henle’s writings as well. 18. Pelling’s interpretation of the pathology in Snow’s theory stresses an analogy between smallpox and cholera, although Snow barely alludes to it in MCC. She does not consider the intestinal worm analogy significant; Cholera, 206–08. According to John Farley, “few contagionists believed that living organisms caused infections”; “Parasites and the germ theory of disease,” 37. See also Farley, “Spontaneous generation controversy”, and Foster, History of Parasitology, 6–27. 19. Farley, “Spontaneous generation controversy,”106. On Brera, see Ibid., 111, and Foster, History of Parasitology, 8. It is possible that Snow was aware of a series of lectures that T. B. Curling delivered at the London Hospital, which were serialized as “Lectures on the entozoa, or internal parasites of the human body,” LMG 1 (1837–38): 518–23 ff. Curling argued that worms derived solely from the eggs of worms, citing well-studied species such as the tapeworm. If only a tiny percentage of eggs found environments suitable for hatching and development, the species could be maintained. He was troubled, however, by several experiments that had failed to produce infestations in animals fed large quantities of ova. Also available to Snow was J. L. Drummond’s article in which he argued against spontaneous generation of entozoa on the grounds that they were structurally too complicated; “Thoughts on the equivocal generation of entozoa,” Annals and Magazine of Natural History, Botany, and Geology 6 (1841): 101–08. 20. On Steenstrup’s research around midcentury, see Farley, “Spontaneous generation controversy,” 117–19, and Farley, “Parasites and the germ theory,” 36–37. Steenstrup described an “alternation of generations” whereby the larval stage of the liver fluke developed within the bodies of snails before emerging to infect a mammalian host; his analysis did not include a discussion of intermediate hosts, however. 21. “Report on the condition of Surrey Court, Horsleydown, by Mr. John Grant, assistantsurveyor,” MCS/477/61, London Metropolitan Archives. Surrey Court, Thomas Street, Horsleydown, is shown on Reynolds’s 1859 map of London, and the 1870–1872 ordnance survey map of that area specifically shows a row of buildings marked “Surrey Buildings.” For detailed views of the 1859 map as well as details regarding Surrey Buildings, see www.ph.ucla.edu/epi, organized and maintained by Dr. Ralph R. Frerichs, University of California-Los Angeles, School of Public Health. In a “Report on two cases of cholera in Mount Place, St. George’s Road,” dated 6 August, Grant implied that cholera was transmitted by morbid effluvia: these “deaths immediately following the emptying of cesspools by hand, without using the hose or any deodorising agent, struck me so forcibly as bearing the relation of cause and effect . . .” that if such cleansing must be done during a cholera epidemic, it should be “done with caution, and the use of the best means at their disposal of preventing smell during and after the operation . . .”; MCS/477/56, London Metropolitan Archives. 22. We have been unable to locate Grant’s report of his excavations at Albion Terrace. The location of Albion Terrace was tracked down with the assistance of Dr. Ralph R. Frerichs, University of California-Los Angeles, School of Public Health; see Dr. Frerichs’s website,

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www.ph.ucla.edu/epi, for details and maps. Albion Terrace and several streets in the immediate vicinity were renamed soon after the outbreak. It appears, however, that Albion Terrace referred to a row of houses on the north side of Wandsworth Road, about two blocks to the northeast of the street now called Albion Avenue (and named Albion Road in the nineteenth century). For another contemporary account see “The cholera,” PharJ 9 (1849–50): 113. 23. Snow did not construct a map to illustrate the results of any of his investigations until December 1854, and he never used a disease spot map as an actual tool during an investigation in progress; see Brody et al., “Map-making and myth-making in Broad Street.” Earlier, McLeod had argued that Snow never intended his Broad Street map as an investigative tool; “Our sense of Snow,” 930–31. 24. Pelling used the term village epidemiologist to describe Budd’s penchant for looking at isolated outbreaks; Cholera, 275–79. The term is apt for Snow’s investigative method in this section of MCC. 25. Jacob Bell found Snow’s evidence inconclusive. Bell quoted from the Registrar-General’s returns of 5 January 1850, identifying some of the same patterns observed earlier by Snow, but complained that there were too many confusing variables to conclude that the quality of the water was causally associated with cholera. Bell thought it likely that elevation above sea level and density of population were more important; “On the nature and effects of the organic matter in drinking-water,” PharJ 9 (1849–50): 416–17; “Extract from the RegistrarGeneral’s return,” PharJ 9 (1849–50): 481. 26. Excerpts from Milroy’s report appeared in UK GBH, Cholera of 1848 & 1849, 25–28. 27. Ackerknecht, “Anticontagionism,” 567–68. Snow was forced to take up this issue again in MCC2 after the publication of a case report from the Newcastle Infirmary of a dispenser who “drank (by mistake) some rice-water evacuations, without any injurious effect whatever”; J. S. Pearse and Jeffrey A. Marston, “Statistics of the cases of the cholera epidemic, 1853, treated at the Newcastle Dispensary,” MTG 8 (1854): 106–08, 129–31, 182–83; quote from 182. Pearse and Marston specifically allude to Snow’s theory and offer the case of the dispenser as a refutation. 28. Later, some critics overlooked this proviso, claiming that Snow’s theory made contaminated drinking water the only possible mode for the transmission of cholera. He was adamant, however, that cholera must enter the alimentary canal—the only environment favorable for its multiplication—for the pathological process of cholera to become established. 29. Snow later reinforced this theme: “If the view I am explaining be correct, we have, therefore, the power of avoiding cholera as easily as one may avoid the itch. Every man may be his own quarantine officer, and go about during an epidemic among the sick almost as safely as if no epidemic were present”; “Further remarks on the mode of communication of cholera” (1855), 84. There is no discussion of the treatment of cholera victims in MCC, perhaps because his emphasis was that the disease was easily prevented. Snow focused on the treatment of cholera that was naturally suggested by his pathological and transmission theories in only one later work, “Principles on which the treatment of cholera should be based” (1854). 30. The anticontagionist rejection of quarantine has been interpreted as indicative of a de facto alliance of interests between general practitioners and merchants; for example, see Ackerknecht, “Anticontagionism,” 567. Snow may have equated commerce with jobs and so have seen himself as supporting the laboring classes. 31. Snow complained in his letter to the editor of LMG dated 15 September 1849 that others had “contradict[ed], in some points, the particulars which I collected with great pains and trouble. . . .” He was also upset that the journal had published what he considered a “very brief and scarcely correct abstract” of Grant’s survey report that gave no indication of the careful investigation that had been undertaken. To top it off, the anecdotal opinion of a res-


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ident of Albion Terrace was given equal weight with Grant’s report and his pamphlet; Snow, “The cholera at Albion Terrace” (1849). 32. Snow, “The cholera at Albion Terrace” (1849). 33. Shephard noted that in the ordinary course of events, PMCC, being published in two parts in a major journal, probably reached a far wider audience than MCC, published as a separate pamphlet. We agree with Shephard that in PMCC the central element of Snow’s theory is fecal–oral transmission, with transmission by water being an important but still secondary issue. However, we have found no evidence that Snow’s theory of the nature of cholera underwent a major revision between the two publications, as Shephard claims; JS, 173–77. 34. The phrase dropped from MCC reappeared once thereafter in the expansive and speculative address entitled On Continuous Molecular Changes (1853). Later, Snow considered it likely that the cholera agent was “like a cell”; MCC2, 15. He first used the word cell in relation to the cholera particle in a letter dated 5 August 1854 (“Cholera in the Baltic fleet”). Worboys warns against the mistake of viewing Snow as a “proto-germ theorist” (Spreading Germs, 117), but he provides no clear explanation of why he regards such a view as mistaken or, indeed, of exactly what he means by “proto-germ theorist.” 35. Dale C. Smith, introduction to Budd, On the Causes of Fevers, 9. See also Budd, Typhoid Fever, although his papers on the disease began in the 1850s. Budd was in Paris during the time that Louis, using a numerical method, conducted the study distinguishing typhus from typhoid. 36. Budd, Malignant Cholera, 5–6 (dated 27 September 1849). Budd had been looking into the nature of intestinal parasites from about 1841 and had argued that aspects of parasitic diseases could explain some features of cholera; Pelling, Cholera, 253–54. Superficially resembling Budd’s (and Snow’s) views of water as the main vehicle for transmission of cholera was the theory presented by John Parkin in 1832. Parkin thought that the cholera poison was taken into the stomach from polluted water, but he also thought that the poison was generated in the earth and from there infected various springs, so that his theory was not contagionist at all; John Parkin, “Suggestions respecting the cause, nature, and treatment of cholera,” LMSJ 2 (1832): 151–53. 37. J. G. Swayne, “An account of certain organic cells peculiar to the evacuations of cholera,” Lancet 2 (1849): 368–71, 398–99. 38. Pelling, Cholera, 170–77. At least one anonymous member of the Bristol Microscopical Society suspected that the London rejection of their findings was based on metropolitan arrogance and an assumption that provincial physicians did not know how properly to look through a microscope; “A member of the Bristol Microscopical Society,” “The Bristol Microscopical Society, versus the president of the Microscopical Society of London,” Lancet 2 (1849): 450. 39. The main agenda item at this meeting of the Westminster was Snow’s long paper on the pathology and mode of communication of cholera, later published as PMCC. Lankester made his announcement about the fungus particle during the discussion that followed Snow’s paper. Edwin Lankester (1814–1874), like Snow, grew up in a poor provincial household, was apprenticed to a provincial surgeon, and later tried to make his career as a London physician. He served many years an editor of the Quarterly Journal of Microscopical Science, where he focused on natural history and popular science. He was also an active medical and public health reformer; see English, Victorian Values. One London editor who was immediately skeptical of the fungus claim was Jacob Bell of the Pharmaceutical Journal. At the first announcement from Swayne and Brittain, he trotted out several reasons to regard their theory as preposterous and was happy to report confirmation later from the London microscopists; “Hypotheses of the cause of cholera,” PharJ 9 (1849–50): 223–24; “Fungus hypothesis of cholera,” PharJ 9 (1849–50): 266–67.

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40. Pelling argues that the 1849 cholera fungus controversy at least temporarily raised the bar for would-be germ theorists by setting stringent standards for “proof,” which for practical purposes could not be met with the technology available at that time; Cholera, 189–201. This is a puzzling interpretation because fungi and some bacteria could be seen easily with contemporary microscopes, and favus (a skin condition) was generally thought to be fungal in origin. The cholera bacillus was visible with contemporary microscopes. Hassall drew particles that, in retrospect, he recognized as identical to Koch’s Vibrio cholerae. Filippo Pacini, working in Florence in 1854, detected microscopic particles in the evacuations of cholera victims similar to those Koch discovered and named thirty years later. See Paneth et al., “A rivalry of foulness,” 1547; Hassall, Memoirs, 76; Filippo Pacini, “Osservazioni microscopiche e deduzioni patologiche sul cholera asiatico,” Gazetta Medica Italiana Toscana 6 (1854): 1; Bentivoglio and Pacini, “Filippo Pacini.” 41. Pelling, Cholera, 276. Snow was one of those to raise the question of logical consistency: “Dr. Budd entirely agrees with me that the cholera poison is produced only in the alimentary canal and acts only on that canal, which it reaches by being swallowed. . . . [T]here is no difference between us respecting the essential mode of communication of the disease, but only as to the extent to which it is communicated through the air. . . . In my opinion the cholera poison only produces its effects through the air when carried by insects or when the evacuations become dry, and are wafted as a fine dust”; Snow, “On the mode of communication of cholera,” Edinburgh Medical Journal (1855–56): 669. 42. Pelling believes that Budd’s willingness to consider multiple causes made his theory palatable to most medical men at the time. She compares the “inclusive” nature of Budd’s theory with the “exclusive” nature of Snow’s, to the latter’s detriment; Pelling, Cholera, 275–81. Pelling’s view of Snow parallels to some extent P. E. Brown, “Autumn loiterer.” Benjamin W. Richardson, despite his idolization of Snow, agreed with Budd on multiple causation, noting that poisons often produced identical effects whether swallowed, inhaled, or rubbed onto the skin and that the symptoms of malaria (which Snow suggested was a water-borne infection) were not confined to the gastrointestinal tract; Richardson, “Water supply in relation to health and disease,” JPH&SR 1 (1855): 133–35. 43. The reporter for the LMG quoted Snow as saying before the Westminster on 13 October 1849, when presenting part one of the papers later published as PMCC, that the “recent discovery of peculiar microscopic cells, believed to be of a vegetable character, in great abundance, in the cholera discharges, tends to confirm [his] view of the nature of cholera”; “Westminster Medical Society,” LMG 44 (1849): 731. When, a short time later, Snow wrote up PMCC for publication, he omitted any mention of the Bristol “discoveries.” P. E. Brown thought Snow shied away from the cholera fungus group in Bristol to avoid granting them priority in the discovery of a causative agent; “Autumn loiterer,” 522–23. See also Pelling, Cholera, 169–70. 44. S. Snow agrees that Snow accepted the limitations of his day’s medical science regarding the identification of the cholera agent, whereas its mode of transmission could be established with the tools then at hand; JS-EMP, 235. Christopher Hamlin, on the other hand, in commenting on an earlier draft of this chapter, noted that Snow assumed a major logical risk by failing to identify the causal agent. Without an independent measure of whether any individual had been exposed to the causal agent, Snow could always be accused of reasoning in a tautological mode: People who get cholera are people who have been exposed to the causal agent; people who do not get cholera are people who have not been exposed. This, in a sense, would put Snow in precisely the same position as the miasmatists, who invoked “predispositions” whenever their theory failed to predict who fell ill and who did not. We believe that Snow was aware of this difficulty and that it was precisely for this reason that he spent so much effort later in showing via statistical “proofs” that people probably exposed to the causal


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agent (via drinking water contaminated with cholera ejections) contracted the disease much more often than people not so exposed. That is, Snow realized, as do epidemiologists today, that identifying the causal agent was not synonymous with demonstrating the transmission of a disease. 45. Budd, Malignant Cholera, 19. Several years later, when Budd posed the possibility that the cholera poison could spread through the air, Snow remarked: “if [Budd] can establish this point, the credit of it will be due to him”; Snow, “On the mode of communication of cholera,” Edinburgh Medical Journal (1856), 669. 46. Snow’s manner of thinking shares many features with the systems-hierarchical perspective proposed in 1977 by George Engel as the “biopsychosocial model” of medicine; Engel, “New medical model.” Although Table 8.2 closely resembles Engel’s model of the hierarchy of natural systems, we have modified it to conform to the levels of organization and the collateral sciences known in Snow’s time. We claim that Snow’s pattern of thought resembles this modern systems-hierarchical model in terms of understanding how biological phenomena lead to networks of “ripple effects” at other levels of organization, requiring the methods of different scientific disciplines. That is, no study at only one level of organization using the tools of only one scientific discipline can ever provide a full and complete picture of human health or disease. We do not claim that Snow had any understanding of twentieth-century systems, cybernetic, and information theories, which Engel drew upon in constructing his model in the 1970s. 47. An example of Snow’s interdisciplinary systems thinking is provided by his later comment on the transmission of influenza: The fact that many people seem to come down with influenza almost simultaneously is not an argument against its contagion by inhalation, since bad news seems to travel every bit as fast as an influenza outbreak; “Chemical researches on the nature and cause of cholera,” Lancet 1 (1850): 155. The remark illustrates a systems mode of thinking by being figurative and literal at the same time. Figuratively speaking, Snow saw the possibility of a functional analogy between processes that occurred at widely separated levels of organization—disease spread and human speech. Literally, Snow was arguing for an analogy in the timing of transmission of verbal information and of influenza, assuming that both were spread by the physical medium of the human breath. 48. Although Shephard states that “Snow’s view of communicable disease was an ecological one” (JS, 265), he contrasts Liebig’s focus on chemical processes with Snow’s on pathological processes, as if they were somehow mutually exclusive; JS, 187. In our view, Snow reasoned back and forth between his understanding of underlying chemical mechanisms and their pathological manifestations; theories and observations at the chemical and pathological levels were complementary, not competing. 49. Although Snow’s approach to science was not unique in his generation of medical scientists, an address by Sir Benjamin Brodie suggests the persistence of an older notion. In his remarks to a group of medical students, Brodie equated scientific medicine with precise observation and with careful use of an inductive method, not the use of a hypotheticodeductive method or a multilevel approach coordinating disparate phenomena; “Introductory discourse on the mode of investigating the sciences belonging to the medical profession,” LMG 38 (1846): 603–13. 50. Besides making sense from a systems perspective, Snow’s strategic move with regard to the fungus particle marked him as a pioneering epidemiologist because the essential feature of epidemiology is gathering scientific information about the occurrence and spread of disease through a population when the causal agent is unknown. A modern example is establishing the causal linkage between cigarette smoking and lung cancer, even if one does not know at a biochemical and cellular level what it is about cigarette smoke that causes cancer

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cells to form. The London Epidemiological Society, and the first developments of epidemiology as a discipline, were founded in the wake of the cholera epidemic of 1848–1849 by Snow and like-minded colleagues. 51. The occupational level, which Snow also addressed, is difficult to display as a separate line on Table 8.2. Snow’s deductions of how cholera might spread in coal mines, as well as his recommendation that a quick and cheap preventive might be splitting shifts into four-hour blocks so the miners could wash and eat above ground, shows that he took occupational patterns of human behavior into account. He showed a similar sensitivity to occupational concerns in his later work on “nuisance” trades, “On the supposed influence of offensive trades on mortality” (1856).

Chapter 9

Professional Success

HE ROOMS OF THE SOCIETY, this evening, were crowded to excess,” noted the Lancet’s reporter at the meeting of the Westminster Medical Society on Saturday, 13 October 1849. “Dr. Swayne, of Bristol, was among the visitors” who, along with the regular membership, had gathered to hear Snow read a paper, “On the pathology and mode of communication of cholera.” At the end of his presentation, after outlining preventive measures, Snow mentioned that the visitor from Bristol was a colleague of “Dr. Brittan [who] had found microscopic bodies in the atmosphere, which he considered to be the same as those existing in the alimentary canal.” Snow was skeptical, however. Other investigators had been unable to replicate Brittan’s findings, and “all the evidence he had collected was opposed to the idea that the cause of cholera existed in the air.”1 Swayne took the cue. Their microscopical examinations of about sixty samples of cholera evacuations yielded ninety percent evidence of “the bodies in question.” He had found none in diarrheal evacuations that resulted from causes other than cholera. In fact, he had brought a “diagram he had made, which exhibited their peculiar structure.” He “felt quite disposed to agree with the remarks which had been made by Dr. Snow in his paper respecting the probability of cholera being primarily a disease of the alimentary canal and not of the blood.” Swayne also offered additional evidence that cholera could be transmitted via soiled linen, noting “the frequency with which the disease attacked washerwomen and others who had had much to do with the

“T

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discharges of cholera patients.” On the other hand, he did not believe one should rule out airborne transmission. He had developed a headache and experienced nausea while simply emptying bottles of cholera evacuations, followed by fever and violent diarrhea that night and the next morning.2 Subsequent discussion was equally spirited and wide-ranging. In opposition to Snow’s theory, medical men recounted symptoms they had observed that suggested that “local affection” of the alimentary canal was secondary rather than primary; evidence that impure water “bore a mere contingent relation to the disease, nothing more,” which could be eliminated by general sanitary improvements; and the “experiment performed by some French physicians, at Warsaw, in 1831, of swallowing some portion of the cholera stools . . . [with] no ill effects, . . . [contrary] to the opinion of Dr. Snow.” Dr. James Copland, author of the Dictionary of Practical Medicine, which was in common use at the time, was “greatly interested in the discovery of the microscopic bodies. He had long been of the opinion that the decomposing effluvia given off in infectious diseases might take on special organized forms peculiar to each disease,” a contingent contagionist view that Dr. Snow’s remarks had not dissuaded him from holding. Time ran out, so the debate was adjourned until the next meeting.3 The discussion was resumed the following Saturday after two papers were presented, one of them on muscular contractions found in some cholera victims after death. Dr. Francis Sibson, one of the senior members of the society, reviewed Snow’s argument as well as Dr. John Webster’s earlier paper on general atmospheric causes of cholera. He thought neither author had sufficiently accounted for contrary evidence and that air and water might both be vehicles for propagation. “He did not agree with Dr. Snow, that the primary seat of the disease was in the mucous membrane of the intestines” because he had treated cholera patients in whom diarrhea first occurred in the latter stages, if at all, but he did agree, citing Garrod and O’Shaughnessy, that if the blood was not the first affected, it became so as the disease progressed. Their researches confirmed his own practice of using saline injections to rally patients in the state of collapse, who uniformly recovered if the urinary secretions could be restored. Overall, however, Sibson was not ready to reject William Cullen’s long-standing doctrine of nervous irritability as the primary cause. Other members shared Sibson’s view that water could not have “more than partial effect in spreading cholera,” argued that “the atmosphere is the principal channel by which cholera is disseminated, though the human recipient of the morbific miasm occasionally becomes, as in yellow fever and influenza, a secondary agent in propagating it” under favorable conditions, and amplified Copland’s remarks from the previous meeting by pointing to their medical experience that intestinal affection was secondary to “the lost vitality of the blood” and capillary congestion. Someone asserted that even if “the cholera depended, as some supposed, on the presence of organized bodies in a state of putrefaction in the water,” existing filtration capacities were sufficient to render the poison innocuous.


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Dr. Edwin Lankester reasoned that if the skin could produce a poison in cases of smallpox, it was also possible for the mucous membrane of the intestines to do so in cholera. “No such poison had, however, yet been demonstrated to exist. . . .” A friend of his, Mr. Busk, had not found “the presence of fungi in the evacuations and vomited matters of cholera patients,” as mentioned by Dr. Joseph Griffiths Swayne at the last meeting. Instead, he had found the usual variety of “organic and inorganic matters,” spores of a fungus often found in bread, husks of wheat, and “bodies [that] resembled starch granules.” Lankester had “examined Mr. Busk’s preparations, and compared them with those of Dr. [Frederick] Brittan and Dr. Swayne,” and he agreed with Busk that “we must look in some other direction for the poison of cholera.” “Dr. Webster and Dr. Snow having replied, the society adjourned.”4 Although the essay the LMG published in two installments as PMCC was essentially the paper Snow delivered to the Westminster Medical Society, a few differences are suggestive of a pattern that he followed for several years while awaiting an opportunity to complete the study of cholera in south London that he believed would convince all his critics. He never wavered on the accuracy of his fundamental conclusions about pathology and mode of transmission, but he took seriously all objections to his theory, undertaking literature searches and gathering information to counter them. Snow was also acutely sensitive to any incident that might support his 1849 theory. The tone in his publications and commentary at medical society meetings was usually respectful of those who disagreed with him.

On the Mode of Communication of Snow Snow was in rarified circles on an April afternoon in 1850, applying chloroform directly to the stump of the elderly Marquis of Anglesey, an old, distinguished officer from the Napoleonic era revered more for his bravery than his tactical skill.5 Lord Anglesey’s stump and the right side of his face had been giving him intense pain, and Snow attempted to alleviate it by using chloroform as a topical anesthetic, applying it with “bibulous paper, and on lint, and covered up closely with oilsilk” (CB, 122). After two and a half hours this had had no effect, and Snow suggested that the patient might inhale. At this moment Anglesey, as master of the ordnance, received a dispatch from Woolwich “containing” (as Snow noted in his Case Book) “an account of the death of an artillery man (gunner and driver) on board ship in the Mauritius in Feb. last from chloroform given on a handkerchief.” Snow and Lord Anglesey discussed the particulars of the case. Although Anglesey was hearing of it for the first time, Snow had actually known of it for two weeks because he had been informed by “the Secretary of Sir William Bennet, on whose son Mr. Fergusson operated at Camberwell” (CB, 123; OC, 147–48). The courageous and agonized Anglesey inhaled, undeterred by the implied risk in the report, just to the point of unconsciousness, suspending the waves of pain and the accompanying spasms.

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After repeated inhalation, the marquis was feeling better, drifting momentarily out of consciousness. Each time he came to he made a speech: “On recovering his consciousness, the patient talked for a minute or two as if addressing the Board of Ordnance.” Snow gave him chloroform on and off for the rest of the night and again several weeks later, and each time the marquis gave an imaginary speech (CB, 127–28). Chloroform seemed to possess an uncanny power to reveal underlying conditions. If a patient (generally female, but in some cases male) suffered from hysteria, Snow found that the drug induced hysterical symptoms (OC, 104–05). If a patient were anemic and weak, this tended to appear under chloroform. If a patient were physically active and robust, this might come out as a struggle or rigors. Patients who could be violent in daily life might become violent under the anesthetic. In the case of Lord Anglesey, it revealed his lifelong propensity to make speeches “as if addressing a meeting or a dinner party” (CB, 127). In a different but related way, chloroform revealed the increasing momentum of Snow’s career, his widening circle of acquaintance, and the degree to which his expertise had plugged him into the nerve centers of London as they touched upon his research. If anything happened connected with chloroform, he would know about it before almost anyone. While his old Soho general practice, which had never been very large, languished, Snow was tending to the illustrious and the wealthy and using these connections to gain more and more information.6 As with his cholera research, Snow readily exchanged information about chloroform and had a network of informants that was intimate and far-flung. By the late 1840s and early 1850s, chloroform allowed Snow to circulate almost as widely as had cholera when it visited the metropolis; it afforded him new modes of communication. He was privy to military dispatches and the phantom speeches of an old marquis. Snow was the first to assiduously track and analyze case reports of anesthetic fatalities longitudinally. He left an assembled record in On Chloroform of his researches from 1847 until 1858, but it was his ability to gather information—through correspondence, medical society meetings, and the social nexus of his anesthesia practice—that enabled him to become a leading authority.7 This facility led to moderate degrees of financial and social success. In 1851 he was appointed a physician to the Hospital for Consumption and Diseases of the Chest in Brompton, south of London. At the end of 1852 he moved from the apartment in Frith Street to a house of his own at 18 Sackville Street (Fig. 9.1). This new location, a fifteen-minute walk from his old premises, was just northwest of Piccadilly Circus, a fairly posh neighborhood. Snow convinced his former landlady’s servant, Jane Wetherburn, to move with him as his housekeeper.8 In terms of research, Snow was in a confirmatory mode rather than one of fresh discovery. The long series of articles “On narcotism” in LMG had been something of a dissertation for Snow in which he had laid out all his basic principles and methods. Toward the end of that study in the early 1850s, delayed as it was by the need “to repeat many experiments and institute fresh ones,” his ideas about the cellular


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Figure 9.1. John Snow’s house at 18 Sackville Street.

mechanisms of anesthesia were having an impact on his notions of cholera, and vice versa.9 He was beginning to formulate a full answer to the many questions that chloroform raised. Snow, ever the advocate of chloroform, was continually aware of the controversy, fear, and public outcry that dogged the drug. For the rest of his life he sought to debunk and demythologize the chlorophobia that circulated throughout the general populace and, often as not, “informed” medical opinion. This was the impetus behind his public letter to Lord Campbell in 1851 arguing against any special legislation punishing those who used chloroform in the commission of a felony. Snow considered the bill unnecessary and misguided and marshaled his clinical knowledge of chloroform to criticize apparent inconsistencies and fallacies in the reports of crimes involving chloroform, even though he was perfectly aware of the usefulness of chloroform in subduing violent patients in what he deemed legitimate medical contexts.10 He wished to calm the public about chloroform, and this desire seemed to spring

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from his own sober, cool temperament and a deep understanding of the nature of the drug and its effects. He always brought a sense of tranquility to the use of chloroform. When patients were recovering from its effects, he advised that it was best not to speak to them but to leave them to collect themselves and wait until they were conscious enough to make a remark or initiate a conversation (OC, 99). In this era in which surgery might very well take place in a home surrounded by friends and family, when medical practice and procedure was not quite so removed from everyday life, and when operating theaters were commonly visited by the general public, medicine was subject to a kind of interference we seldom see today. By the 1850s in Britain, chloroform anesthesia was becoming a mass phenomenon, available to virtually everyone, yet its effects made it nearly impossible for lay people to understand what they were observing when it was used in controlled medical situations. If they were actually coming under its effects, the disorientation and loss of consciousness equally obscured their understanding of the degrees of narcotism involved. Snow, a medical man arguing for medical control over the use of anesthetics, always had a mixture of solicitude and skepticism when it came to the public. He observed, If not prevented by the medical attendant, the friends of the patient often address him the moment he opens his eyes; and the words they generally use are of a very equivocal meaning to one who cannot understand their application. They usually say “It’s all over,” which very often has the effect of raising an indefinite feeling of alarm in the patient; for, until he has time to recover his memory, the operation he was to undergo is generally the farthest thing from his mind. When left to himself the patient usually recovers from the insensibility in a very tranquil manner . . . and in a great number of instances will contend . . . very stoutly, even after a protracted operation . . . that the chloroform has not taken effect. It is well to let him remain in this conceit for a while, or even till he finds out the mistake himself; for, if reminded of the pain they have been spared, just on waking after an operation, persons are liable to be excited by emotions of pleasure and gratitude; but a few minutes later . . . they are better able to control their emotions. OC, 99 This passage contains Snow’s ethics for the administration of chloroform: promote neither dread nor excessive gratitude, and keep the family and friends from meddling. Excitement and emotion needed to be controlled for good medical reasons but also to avoid as much as possible the embarrassment of Victorian propriety that surgery and anesthesia necessarily entailed. The two subjects for which John Snow is remembered, chloroform and cholera, both produced a host of symptoms seemingly calculated to embarrass the Victorian sensibility. Cholera produced uncontrollable diarrhea, and chloroform produced a general lack of control, not to mention that its chief drawback was that it frequently


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made people vomit. It was Snow’s contribution to see that one could control many unpleasant manifestations by controlling, in some measure, what people put in their mouths. With chloroform and ether, nausea and vomiting seemed to be an inevitable side effect, and one reason for Snow’s search for better anesthetics was to find one that did not make the patient sick. By the 1850s he had seen enough cases to lay out the basic guidelines to reduce the chances of vomiting during inhalation: avoid meals before surgery; do not move the patient after inhalation; and do not give the patient anything to eat or drink for about an hour after inhalation. These rules still basically apply today and have become routine parts of surgical protocol. Snow had little sympathy for the naysayers who believed that chloroform could make people permanently ill. In 1852 he saw a clergyman who was convinced that he had been unwell ever since he inhaled chloroform. After the patient laid out a host of symptoms and a list of eminent physicians who had failed to make him well, Snow dismissed him. “It was my opinion,” he later wrote “that the complaint of this gentleman was coming on long before he inhaled the chloroform, and that it depended on a much less transient cause. I have not heard from him since” (OC, 107).

Professional Enhancement and Recognition In the 1850s Snow completed his credentialing as a medical man. He became a Licentiate of the Royal College of Physicians, the penultimate hierarchical status within the medical corporations of the day. This was as far as a working-class lad from Yorkshire could go. Whether or not he aspired to the higher status of fellow, Snow’s medical degree from the University of London prevented him from becoming a candidate, which was still limited to graduates of Oxford and Cambridge. However, he was elected to membership in another prestigious medical society and became president of two societies of which he was a long-standing member. He also helped found the Epidemiological Society of London in order to further research into the causes and treatment of epidemic diseases. The examination to become a Licentiate of the Royal College of Physicians of London (LRCP) was an oral examination like those he had taken in 1838 to qualify as a surgeon and an apothecary. Until 1830 the examination was a viva voce in Latin of classical medical texts lasting an hour or so. In June 1850 the viva was conducted in English, although Latin could enter the conversation at the examiner’s discretion. There were neither practical dimensions nor written preliminaries. The licenciateship augmented Snow’s professional status, but it did not gain him access as a GP to fashionable society in the metropolis. Fellows, not licentiates, dominated that realm, and Snow was an outsider. As a student he had not become the protégé of an established surgeon or physician. After 1850 his Case Books show that although he became the anaesthetist of the upper classes in the London metropolis, he never became their physician.11 Even so, this social limitation mattered little, because by the

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early 1850s his practice was almost exclusively anesthetic, and he made a comfortable living from it.12 One benefit from the LRCP was election to the Pathological Society of London in the fall of 1850. This prestigious group acknowledged Snow’s accomplishments by an offer of membership after he received his license as a London physician.13 Soon there were further indications of his growing reputation among professional colleagues. The Medical Society of London (which had amalgamated with the Westminster Medical Society in 1850) elected Snow to the coveted role of orator for the 1852–1853 session, vice-president for the following session, and president in 1855. In 1854–1855 he was also president of the Physiological Society, a specialty group within the Medical Society of London that met once or twice a month on Monday evenings. In addition, he maintained his membership in the Royal Medical and Chirurgical Society and the Provincial Medical and Surgical Association (forerunner of the British Medical Association), as well as attending meetings of other societies (including the Royal Medico-Botanical) as a visitor when the topic interested him.14 As president of the Medical Society of London, Snow was responsible for chairing weekly meetings on Saturday evenings, conferring with members of the council who set the agenda, controlling the society’s finances, and supervising a small staff at the building in George Street, Hanover Square, where the society met from its amalgamation with the Westminster in the fall of 1850. The society had disposition over an assembly room and a large room that had been outfitted as a library. At the head of the assembly room was a seat for the president behind which hung a large painting of “the members of the Society at the close of the last century,” including Edward Jenner. On one side of the room was a large portrait of Dr. Henry Clutterbuck, considered “the Father of the Society” (its oldest member) but a rare visitor in recent years,15 but one Saturday evening when Snow was presiding Dr. Clutterbuck did enter the room. Before he could seat himself Snow “rose, and in a way that was irresistible in its simple courtesy resigned his chair to the veteran Esculapian” for the duration of the meeting. In this manner Snow recognized the senior physician’s preeminence in the society, as well as acknowledged an indebtedness for hiring him years before as a lecturer at the Aldersgate School of Medicine.16 In addition to achieving a leading position in several of the London medical societies, Snow helped J. H. Tucker, a surgeon, found a society “to one special end— the investigation of epidemic or spreading diseases.”17 Tucker had first proposed a society with a much narrower mandate: surveying medical men about treatments for epidemic diseases, particularly cholera, in advance of developing “some systematic plan” of the most successful methods to date.18 The organizing meeting of the Epidemiological Society of London occurred at the end of July 1850. It was held in the meeting room of the Medical Society of London and presided over by a nonmedical man, Lord Ashley, who indicated his sanitarian leanings when he stated that the “object of the Society is to exalt the poor, to raise them out of the mire. . . . A


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very large proportion of the pauperism of these realms tended to result from deficient sanitary arrangements. Bad drainage, bad ventilation, bad water, over-crowding, and filth, tended to propagate disease. . . .” Several resolutions then carried unanimously, including the formal creation of a society “for the investigation of epidemic diseases” to which “all gentlemen interested in its objects shall be eligible as members” and the selection of Benjamin Babington as president.19 The inaugural public meeting was held the following December, at which Dr. Babington set forth the society’s specific objectives. The Epidemiological Society should “endeavor, by the light of modern science, to review all those causes which result in the manifestation and spread of epidemic diseases, . . . to collect together facts, on which scientific researches may be securely based, to remove errors which impede their progress, . . . to suggest those means by which their invasion may either be prevented, or . . . combated and expelled.”20 Thereafter, the Society met on the first Monday of each month except in the summer; papers, letters from corresponding members, and subcommittee reports were read and commented upon. The Epidemiological Society began publishing the Journal of Public Health and Sanitary Review in 1855, which included Transactions of selected papers delivered at its meetings or sent by corresponding members. In the opening volume of its new journal, the Society justified its existence by referring to a recent “philosophical yearning after fixed principles as to the nature of disease. . . . If the elements of diseased action are few and simple, the principles of prevention or cure are, it is thought, few and simple also. The materia medica is thus undergoing a thorough revision and curtailment. . . . Its principles are preventive, its objects wide, and its elements— some seven only, and the world’s general property—are no more than—Pure air— Proper nourishment—A regulated temperature—Bodily exercise—Cleanliness—Mental education—Good morals.” The editors wanted a journal “of free opinion and liberal sentiments; but encumbered by nothing approaching to personality, venality, unfair criticism, or angry disputations with other journals and publications.” They were open to contributions of “all men of science . . . [and] public writers” who wished to promote “hygiene as a branch of medical education,” elucidate “those great laws, under the influence of which diseases are produced and fostered,” and bring the attention of the wider public to “the principles of preventive medicine.”21 Although few of the founding members appear to have supported his cholera theory, Snow found the goals of the new society appealing on many counts. He was active from the outset. In January 1851 he commented on Alexander Bryson’s paper on cholera; at the May and June meetings in 1851 Snow read a paper of his own, “On the mode of propagation of cholera.” In 1852 and 1853 he participated in discussions of several papers on vaccination to prevent the spread of smallpox, emphasizing its utility because the disease was “invariably communicated by contagion.” In May 1853 he delivered another paper, comparing mortality in large towns with rural districts.22 Over the years the Epidemiological Society became a forum in which Snow refined his cholera theory in response to objections from opponents. For

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example, in December 1853 his comments on a paper comparing “the Indian plague [Asiatic cholera] with the black death of the fourteenth century” included a reminder “that, in a paper read some time ago [May and June 1851], he had come to the conclusion, from the similarity between the course and localities of the two diseases, that they were propagated in the same manner, probably by the swallowing of infectious matter with the food; and he mentioned that the natives of India believe that the infection may be conveyed from place to place in provisions, as in a pot of ghee.” Balderdash, replied Dr. Gavin Milroy (whose views Snow had first criticized in MCC): “the true plague of the Levant had appeared in India, and that spontaneously. . . . Probably, at certain times, a malarious influence spreads over the whole globe, and causes different forms of disease in different parts of the world.” The next speaker agreed with Milroy, noting that plague disappeared in Egypt “when the weather became dryer; but he was not aware that any similar law was known to hold in India.” Snow replied that plague cases appeared in all kinds of weather, and so the repartee proceeded until the meeting was adjourned, after which members and visitors chatted amiably.23 Snow met Benjamin Ward Richardson (1828–1896) at meetings of the Epidemiological Society and the Medical Society of London in 1850. They soon found that they had other interests in common, including medical research and anesthesia. Richardson considered Snow a model GP and medical scientist: “When I was living at Mortlake, he would run down, on request, after his day’s duties were over, to a post-mortem, to see a poor patient, or to take part in an experiment, returning as cheerily as if he had been to receive the heaviest fee.”24 In their anesthesia researches they functioned more as friendly critics than as collaborators. At a meeting of the Medical Society of London in 1853, Richardson read a paper on “The anæsthetic properties of the lycoperdon proteus—Common puff ball,” after which “the President asked, if Dr. Snow had any remarks to make. Dr. Snow corroborated Mr. Richardson’s observations, having witnessed several of his experiments.”25

Midwifery When James Young Simpson introduced the use of chloroform in labor in 1847, the outcry of the clergy could be heard far and wide that this went against biblical precepts that women should endure pain in childbirth. This concern never bothered John Snow. His medical interests in childbirth were long-standing, and he adopted a liberal attitude to the use of chloroform in midwifery: “With regard to the cases of labour in which chloroform may be employed, it will be readily conceded that, in cases where the pain is not greater than the patient is willing to bear cheerfully, there is no occasion to use chloroform; but when the patient is anxious to be spared pain, I can see no valid objection to the use of this agent, even in the most favourable cases


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. . . and the patient may be fairly allowed to have a voice in this, as in other matters of detail which do not involve the chief results of the case” (OC, 319). The issue that concerned him was how chloroform should be given in labor, not whether to give it. Simpson’s application of chloroform in midwifery took place a year after the introduction of ether anesthesia, at a point when the norms of etherization consisted of a light state for dental procedures and a heavy one for surgery. Simpson, who was always heavy on the handkerchief when it came to chloroform, opted for keeping the mother completely unconscious through the labor and delivery, but Snow, taking a cue from some of his London colleagues, found that it was unnecessary in many cases to put the mother completely under in order to remove the pain of labor.26 A debate arose between some doctors who asserted that pain could always be removed without the mother losing consciousness and others who believed (equally mistakenly, according to Snow) that “no relief can be afforded unless unconsciousness be induced” (OC, 318–19). In his experience labor was highly variable from stage to stage and patient to patient, and all of them may or may not have called for chloroform. Therefore, he believed that the object of chloroform in labor should be to “relieve the patient without diminishing the strength of the uterine contractions and the auxiliary action of the respiratory muscles” (OC, 321). Complete anesthesia was never used unless “in cases of operative delivery.” His technique was to give the chloroform at the beginning of a labor pain and leave off “when the uterine contraction subsides, or sooner, if the patient is relieved of her suffering” (OC, 320). Snow would, if necessary, use a handkerchief in parturition but preferred to use his inhaler in these cases; it saved on chloroform, especially over the course of a protracted labor. It also gave him more precise control of the small doses used. He was of the opinion that chloroform seemed to speed up some labors and retard others. He found that it tended to diminish the strength and duration of uterine contractions but promoted dilation. It was, of course, of great use in forceps deliveries and when it was necessary to turn the child. Snow attended nine forceps deliveries, and in six it was necessary to turn the child. The use of chloroform in midwifery fell somewhere in between that of operations and dentistry. It frequently required small doses to maintain light anesthesia for long periods of time, with the anesthetist responding to and adjusting to the rhythm of the contractions. Although in his publications on such matters Snow tended to present himself exclusively as an anesthetist, his casenotes reveal that he frequently helped with deliveries and other problems. The day after Christmas 1850 he was called “by Mr. Cooper of Moor Street, Soho, to assist him in a case of retention of the placenta” (OC, 326). In his published account of the case, Snow explained that the mother had given birth two hours before he arrived: “Mr. Cooper had introduced his hand, but had been unable to bring away the placenta, on account of firm contraction of the uterus in a sort of hour-glass form. On the chloroform being administered, the hand was easily introduced, and the placenta detached, and extracted. There was very little hæmorrhage” (OC, 326). Snow’s casenotes clarify that the introduced hand was

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his, not Cooper’s (CB, 157–58). By obscuring the active role he played in many cases and representing himself as the anesthetist, Snow reinforced the role that chloroform played rather than his own. As with all other aspects of chloroform, Snow felt embattled because people constantly mistook its effects. In the late 1840s Snow was requested to give chloroform to the wife of a medical man during her labor. “I was sent for late one evening, but as there were no pains at the time when I arrived, I was requested to go to bed in the house. After a time, I was called by a servant, who told me the baby was born” and the doctor had been sent for (OC, 329). The birth had happened so quickly that the husband, who had been in the room, could not get to the bedside before the baby was born. After the birth the patient seemed well enough and Snow went home, but when the doctor arrived shortly thereafter, the patient passed out and the doctor thought she might die. This went on for hours, and although she ultimately recovered, it was quite puzzling because there had been no hemorrhage or any other obvious cause of her syncope. Snow understood the doctor to say “that if the patient had inhaled chloroform, he should have blamed it for the condition into which she lapsed” (OC, 329). In Snow’s view chloroform remained suspect, even among doctors and especially in labor, when the lives of loved ones, mothers, and children were at stake.

Queen Victoria For much of the English-speaking world in the early 1850s, the question was whether chloroform should be given at all in childbirth. When Queen Victoria neared the completion of her eighth pregnancy in March 1853, the possibility of her receiving pain relief was quietly being floated, and Snow was advised that he might be called in.27 Asked to administer chloroform for a patient in labor residing at 18 James Street, Buckingham Gate, on 24 March, Snow mistakenly wrote the address as “Buckingham Palace” in his Case Book, suggesting that he had royal affairs on his mind at the time (CB, xxx). Two weeks later Snow was, in fact, called to the palace and the queen took chloroform during the delivery of Prince Leopold. Snow recorded the event: Thursday 7 April: Administered Chloroform to the Queen in her confinement. Slight pains had been experienced since Sunday. Dr. Locock was sent for about nine o’clock this morning, stronger pains having commenced, and he found the os uteri had commenced to dilate a very little. I received a note from Sir James Clark a little after ten asking me to go to the Palace. I remained in an apartment near that of the Queen, along with Sir J. Clark, Dr. Ferguson and (for the most part of the time) Dr. Locock till a little a [sic] twelve. At a twenty minutes past twelve by a clock in the Queen’s apartment I commenced to give a little chloroform with each pain, by pouring about 15 minims [0.9 ml] by


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measure on a folded handkerchief. The first stage of labour was nearly over when the chloroform was commenced. Her Majesty expressed great relief from the application, the pains being very trifling during the uterine contractions, and whilst between the periods of contraction there was complete ease. The effect of the chloroform was not at any time carried to the extent of quite removing consciousness. Dr. Locock thought that the chloroform prolonged the intervals between the pains, and retarded the labour somewhat. The infant was born at 13 minutes past one by the clock in the room (which was 3 minutes before the right time); consequently the chloroform was inhaled for 53 minutes. The placenta was expelled in a very few minutes, and the Queen appeared very cheerful and well, expressing herself much gratified with the effect of the chloroform. CB, 27128 For this event Snow used the hanky instead of the trusty inhaler.29 It was no doubt more decorous than placing a face mask over the royal nose, and because it was a short labor he used very little chloroform. He likely considered the amount necessary to induce analgesia negligible and more in keeping with the periodic nature of labor pain.30 The inhaler might have appeared too controlling to the royal physicians and perhaps overly invasive to the general public.31 His attendance on the Queen was momentous for Snow’s reputation, and the fact that he was increasingly called on to administer anesthetics during childbirth reflected a change in attitude about biblical injunctions that women should bear children in sorrow. Giving the queen “that blessed chloroform” set a positive precedent for some: An editorial in the AMJ noted that the excellent reports on the queen’s health after her delivery indicated the “responsible position, and the acknowledged skill” of all the physicians involved. These “circumstances . . . will probably remove much of the lingering professional and popular prejudices against the use of anesthesia in midwifery.”32 The physicians attending the daughter of the archbishop of Canterbury during her delivery had no hesitation in calling Snow to Lambeth Palace to administer chloroform in October 1853.33 Whereas the main point of public controversy was whether obstetric analgesia was consistent with biblical teaching, the issue for some medical men was the wisdom of administering to the queen a medicinal agent that had been held responsible for a number of anesthetic-related deaths.34 In May 1853 a Lancet editorial expressed “astonishment” at the “rumour” that the Queen had received chloroform. Because chloroform in surgical anesthesia “unquestionably caused instantaneous death in a considerable number of cases,” the editorialist (presumably Thomas Wakley) expressed his confidence that “the obstetric physicians to whose ability the safety of our illustrious Queen is confided do not sanction the use of chloroform in natural labour.”35 The AMJ leapt to the defense of Snow and the Queen’s obstetricians, pointing out that sufficient chloroform to produce unconsciousness was

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neither contemplated nor used and that experience had shown that cautious inhalation of small amounts of chloroform during labor was safe.36 The example of the queen would compel the medical world to catch up with the arguments Snow had been making for several years.

Elaborations of Cholera Theory from 1849 During the early 1850s Snow made little progress in substantiating his cholera theory. In his mind the theory still lacked a compelling correlation at the metropolitan level between high mortality and a water supply contaminated by cholera evacuations. London seemed a promising test case because Southwark had nearly three times more deaths than the average in London and was supplied by the Southwark Water Works with unsettled, unfiltered, sewage-contaminated Thames water. Between 1832 and 1848 the water company had moved its source of supply upstream to Battersea, which was still within the tidal zone. Snow had published his 1849 theory without “a full account of the recent epidemic in London, in its relation to the water,” hoping that vital statistics prepared thereafter by the GBH and the RegistrarGeneral’s office would contain the information he needed to determine if the Southwark water company’s move away from the major sewer outlets had reduced mortality from cholera in the borough it supplied (PMCC, 747). Neither report must have entirely suited Snow’s purposes, for his promised comprehensive study of the 1848–1849 epidemic in south London did not appear. While awaiting the next major visitation of cholera in London, Snow used medical society meetings and the medical journals to restate his 1849 thesis, with an occasional elaboration on a portion of it. An early opportunity occurred at a January 1850 meeting of the Royal Medical and Chirurgical Society. Sir Benjamin Brodie read a paper sent by Dr. Robert D. Thomson from Glasgow detailing his “chemical researches on the nature and cause of cholera.” The author’s conclusion was that “the cause of cholera is not a specific, tangible poison, introduced into the body from without, but rather a vicarious transference of the cutaneous excretion to the intestinal mucous membrane, dependent partly on an atmospheric influence, and partly on a predisposing state of the system, in those who are affected with the disease.”37 Dr. Thomas Addison, the president, acknowledged Snow as first respondent. Snow began by noting that Thomson’s analyses of the state of the blood “confirmed those previously made by Drs. Garrod and Parkes in almost every particular,” thereby supporting his own theory of the pathology of cholera that was based in part on Garrod’s and Parkes’ papers. Nevertheless, Snow found it curious that while Thomson’s carefully conducted experiments proved “cholera did not depend on a poison diffused in the atmosphere . . . [and had] given an account of the fanciful reasons which had led medical men to attribute cholera to the presence of a poison diffused in the atmosphere . . . he did not seem to have emancipated his own mind from


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the atmosphere as a cause of the disease.” Snow dismissed both general and local miasmatic explanations with an off-hand remark that cholera appeared in “cold and foggy” Glasgow as easily as it did in warmer London. He returned to the pathological element in his theory by noting that congestion in capillary circulation was brought about by a prior withdrawal of water from the system and was therefore secondary to the intestinal affection. He supported Thomson’s “parallel between cholera and influenza” and posited that “both these epidemics were propagated by a poison generated in the human body”—that is, carried in the evacuations or exhalations, respectively, of the sick to the healthy—and “the poison was in each case applied to that mucous membrane which was the chief seat of the disease.” Those who dismissed the contagiousness of influenza on the grounds that it spread too rapidly were laboring under an outmoded notion of contagion, whereby transmission must occur by direct contact or infection by inhaling morbid matter volatilized from the skin of the sick. “But if it was communicated by the breath, from one person to others, this difficulty disappeared, for influenza did not spread so swiftly as a piece of bad news, also communicated by the breath.” Because the cholera poison had to be swallowed, according to his theory, cholera spread more slowly than did influenza but usually “most extensively where there were the greatest facilities for the swallowing of excretions” such as “want of personal cleanliness” and contaminated drinking water. Statistical tables recently published by the Registrar-General clearly showed that “the epidemic [of 1848–1849] had been most fatal in those districts of London supplied with water obtained from the Thames in the neighbourhood of the chief sewers, and which must, when cholera is prevalent, contain the evacuations of the patients.” He also pointed to a contamination of local water that paralleled the incidents he had recounted in MCC and PMCC: The cholera had been particularly fatal in the Bridge Street neighborhood of Blackfriars, London, “around which spot the inhabitants used to send to St. Bride’s pump for their drinking water; and this pump had since been closed, at the instance of Mr. Hutchinson, surgeon, it having been ascertained that the well was contaminated, by a sewer running into the Fleet ditch”—not, in a final jab, by the atmosphere.38 Snow must have talked for many minutes, because the reporter’s account of his comments exceeds the space allotted to Thomson’s paper. Snow’s enthusiasm for his theory that the cholera poison must be ingested may explain why he proposed a parallel with the pathology and transmission of influenza. His dismissal of miasmatic explanations as “fanciful” shows that there were limits to his patience with opponents from this camp. His disagreement with contagionists and contingent contagionists was temperate and respectful. He essentially asked them to substitute “method of communication” for contagion and local affection of the alimentary canal for systemic blood infection. The reference to the Registrar-General’s tables indicates that Snow found enough information in them to support his theory of local, neighborhood differences in cholera mortality in London, but insufficient information for a full-scale confirmation. The story of the surgeon who identified the

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St. Bride’s pump as the source of a neighborhood outbreak was tucked away in Snow’s memory for a later occasion. We do not know what Snow said a year later at a January meeting of the Epidemiology Society when commenting on a paper “On the infectious origin and propagation of cholera.” The reporter noted only that Snow and a few other members made “some remarks,”39 but it seems likely that he would have supported Dr. Alexander Bryson’s dismissal of “a general aërial cause—an epidemic constitution of the atmosphere,” and Bryson’s conclusion that “we have no reasonable proof that there ever did exist a specific condition of the atmosphere capable of producing cholera, or that there ever was evolved from the earth, or engendered in the air, a cause capable of producing it.” Bryson saw no merit in anticontagionist reasoning, whether of the general atmospheric and seasonal variety (epidemic constitutions) or the production of local miasmas view. With respect to Snow’s cholera agenda at the time—refining his 1849 theory and seeking more confirmatory evidence—Bryson listed many instances of “the propagation of cholera from one or more cases transported from an infected locality into a healthy ship, which can only be explained by the reproduction of an infectious virus through a series of consecutive cases.”40 Snow had already pointed out such a progress of cholera in PMCC, and it would become increasingly prominent in future writings. However, he no longer shared Bryson’s view that “an infectious virus” developed in the bodies of cholera victims could be inhaled by others in overcrowded, poorly ventilated spaces and then produce a systemic fever. Snow did focus on points of agreement with Bryson in the opening paragraph of a paper he read at meetings of the Epidemiological Society in May and June of 1851, the first formal elaboration of his 1849 essays on cholera. This time he chose a slightly different title, “On the mode of propagation of cholera,” and returned to the opening used in MCC on the communicability of the disease from person to person, “being probably the real feature of distinction between epidemic and other diseases.”41 He cited the table in PMCC in which he had used Merriman’s figures on “the direct relation which exists between the number of the population and the duration of the disease” in the 1832 epidemic to make the case that personal intercommunicability characterized cholera. He thought it likely that “the same rule has obtained during the recent epidemic, but I have no precise information on this point”(559). The expected statistical information was not forthcoming from governmental reports, so Snow had continued his literature searches and extensive correspondence in hope of building a support for his theory by an enumeration of instances. He had recently received a letter recounting the spread of cholera from a “want of personal cleanliness” (560), another detailing cases produced by eating contaminated cow heels (560), and personal observations by himself and Mr. Peter Marshall, his friend and medical colleague, of cholera spread through furnishings contaminated by cholera evacuations (560). The paragraph on cholera pathology was essentially a reprise of what he had written in MCC and PMCC, with the exception of a statement that “it appears, indeed, that the cholera poison never enters the circulation . . .” (559).


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Then Snow shifted to “another very important medium for transmitting the cholera poison from the sick to the healthy” not covered by traditional concepts of contagion—“the water which people drink” (560). Dr. Lloyd had articulated the same principle when he presented his findings on Rotherhite (described in PMCC) at a medical society meeting at the same time MCC appeared. Snow rounded out the first part of his paper by quoting extensively from MCC on the outbreaks in Albion Terrace and Horsleydown, as well as repeating the gist of Lloyd’s study and summarizing remarks sent him by a physician from Essex. He concluded part one with a critique of the GBH’s notification that “vitiated water acts as a poison on the stomach and the bowels . . .” (562). Not so, said Snow: “However repulsive to the feelings the swallowing of human excrement may be, it does not appear to be very injurious so long as it comes from healthy persons, but when it proceeds from cholera patients, and probably patients with some other maladies, it is a means of communicating disease” (562). He finished reading this paper at the June meeting of the Epidemiological Society. Whereas part one had enumerated local outbreaks of cholera, part two detailed the current state of his research on cholera outbreaks “on a more extensive scale, [communicated] by means of the sewers which empty themselves into various rivers, from which the population of many towns derive their supply of water” (610). First summarizing the findings outlined in PMCC, he then turned to his still incomplete study of mortality in relation to the water supply in London during the 1848–1849 epidemic. He confirmed the results listed in the table in MCC showing that mortality was lower in districts supplied by some water companies than others. There were few deaths from cholera where Chelsea Company water was distributed, except for one location, where it turned out that “many of the people obtained water by dipping a pail into the Thames” (610). Dr. Arthur Hill Hassall’s report on London water confirmed that filtered water from this company was “free from the hairs of the down of wheat, yellow ochreous substance, (believed to be partially-digested muscular fibre,) and other substances which had passed through the alimentary canal, and were found in the Vauxhall and Lambeth Companies’ water” supplied to districts south of the Thames (610). Snow also mentioned another report by John Grant, the surveyor who had brought the outbreak in Horsleydown to his attention, of a “house to house visitation” that connected unusually high mortality to the consumption of water from ditches connected to the Thames. Snow presented a table copied from a Weekly Return that showed “the mortality from cholera in the different districts of London supplied by the various Water Companies” (611). This table further confirmed what he had suggested about London in MCC: “the mortality will be found to bear a very close relation to the absence or presence of connexion between the sewers and the water supplied. It also appears from the same table that the average mortality from all causes in a series of years bears a relation to the quality of the drinking water. There is great reason to believe that typhoid fever and some other epidemic diseases are communicated occasionally through the drinking water;

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and . . . [that plague] is communicated exactly the same way as cholera,” and perhaps ague in some situations as well (611). He had sympathetic words for the dismal fate of the Bristol fungi researchers. The “supposed fungus” had not withstood microscopic scrutiny, but “it was, perhaps, too much to expect that we should obtain a knowledge of cholera more exact than that which we possess of syphilis, smallpox, and other better known diseases” (612). Nevertheless, “the labours of these gentlemen” were not in vain, at least from Snow’s perspective, for they “confirm the fact of the water in various places being a medium of communication between the alimentary canals of cholera patients and those of other people” (612). In addition to collecting new evidence in support of his theory, Snow elaborated on the preventive measures he had outlined in 1849. In the paper read at the Epidemiological Society he listed five: avoid water that might be contaminated by sewers, drains, cesspools, and “persons living in boats”; extend availability of wash basins among the poor; urge everyone who came in contact with cholera patients, especially food preparers, to be especially attentive to cleanliness; immerse linen soiled by cholera evacuations in water until it can be boiled; and separate cholera patients from the healthy, even placing them in “another abode” if necessary (612). Although most sanitation conscious medical men would have agreed with the first four measures, the fifth was at odds with the views of those who thought cholera was not contagious. Separation of the sick from the healthy would also be expensive to carry out, which did not incline public authorities toward Snow’s views. In a separate article published in MTG two years later, he reiterated the five measures he believed should be taken when cholera was present, and added a sixth—washing “all the provisions which are brought into the house” with clean or boiled water. In addition, he suggested that improvements in drainage, water supply, and lodging houses, as well as the cultivation of “habits of personal and domestic cleanliness among the people everywhere,” should be undertaken to avoid future epidemics of cholera.41a Snow’s article on prevention, written late in September 1853, when the third cholera epidemic had just begun, contained two additional elaborations of the 1849 theory. First, he strengthened his argument about the person-to-person transmission of the disease in coal mines by quoting from a letter sent by his brother, Robert Snow, a colliery agent near Leeds.” The pit is one huge privy, and of course the men always take their victuals with unwashed hands” (368). Second, “a medical friend in Newcastle” had sent him a report on how that town and Gateshead, immediately across from it on the River Tyne, had fared in the last three epidemics. The 1832 epidemic had been severe, as Snow knew well enough from his own experience there as an apprentice: “There were no waterworks in Newcastle” at the time, but the spring water used for drinking—stored in cisterns and public fountains—was probably contaminated. In 1849 the new waterworks drew its supply from distant springs, and there was little cholera. In the most recent visitation the water company supplemented its regular supply with water from the Tyne a mile upstream. “The tide, however, flows for several miles further, and, consequently, carries the sewage past the


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place where the water is obtained. When the cholera became established in Newcastle” early in September, the sewers carried evacuations into the river, which were sucked into the water pipes. As had happened earlier in Bermondsey, the cholera soon “became generally diffused among all classes of the community” until complaints about water quality caused the company to discontinue drawing river water (368). In Snow’s mind this incident was “a fresh illustration” of how “whole towns were, more or less, affected by drinking the water of rivers into which the sewers discharged their contents” (368). The problem was that he needed precise figures and a controlled experiment, not more illustrations, to convince the skeptics.42

Treatment of Cholera Until the third epidemic reached England in 1853, Snow seems to have focused on prevention rather than treatment of cholera, but government authorities had not, generally, adopted the simple sanitary measures he advocated to keep the inevitable cases of cholera that reached port cities from spreading. In January 1854 he turned to the subject of treatment in a paper read at the Medical Society of London.43 He reasoned directly from pathology to therapy, noting that one should only employ remedies that would coat the intestines and perhaps reduce the loss of fluid and salts from the blood or replace lost fluids. The therapeutic regimen he proposed, therefore, was considerably more restrained than the heroic measures advocated by many of his colleagues. Snow’s therapeutic frame of reference was conventionally humoral. He believed that the premonitory phase of cholera, resembling an ordinary case of diarrhea in most features, was part of the overall choleraic disease process, so that successful treatment of that phase might abort the entire attack. Accordingly, he recommended a mild antidiarrheal treatment then in common use (such as pulvis cretae compositus cum opio, powder of chalk combined with opium), adding that its efficacy provided indirect proof of his hypothesis, because antidiarrheals could act only within the gut and could not possibly affect any blood-borne poison (181). His therapeutic practice was based on the view that the cholera material was ingested and reproduced in the gut; in this respect, Snow was anything but conventional. He assumed (drawing on the researches of Liebig) that a process of continuous molecular change analogous to fermentation or putrefaction was going on along the mucous membrane of the alimentary tract, so that the best medicine to administer early in the course of cholera would be a substance that would (a) “come in contact, if possible, with every part of the mucous membrane of the whole alimentary canal” and (b) “have the property of destroying low forms of organized beings, and of arresting fermentation [and] putrefaction” (181). Because the cholera particle had not been identified, he reasoned by analogy. He did not claim that the cholera particle multiplied or did its damage specifically by means of the processes

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of fermentation or putrefaction. Instead, he proposed that as some sort of “low form of organized being” with a cellular structure, the cholera particle was susceptible to being killed or inactivated by the same chemical substances that were known to be effective against processes caused by other low forms of life. Such chemical substances included olive oil, animal charcoal, sulphur, oil of cajeput, camphor, and creosote, all of which had been reported by other physicians to have some efficacy in cholera treatment. Chloroform taken orally exhibited similar “antiseptic and medical properties; and it has gained some reputation as a remedy for cholera, when introduced into the stomach. Administered in the way of inhalation, it is merely useful in relieving the cramps, and has no effect on the progress of the malady; while, if cholera were a blood disease, it would be by inhalation that this and every other volatile medicine ought to be exhibited” (181)—a succinct defense of his new cholera theory, based on his expertise as an anesthetist. For victims who entered the collapse stage Snow recommended saline injections into the veins. He noted that “the results obtained, by injecting the blood-vessels in 1832, were so far encouraging, that it is somewhat surprising that this practice was hardly resorted to in 1849” (182). Despite mortality data that others interpreted as highly unfavorable to this procedure, Snow refused to abandon a treatment option that fit so well with his theory of cholera pathology. Snow even mentioned that Mr. Henry Lee had suggested injecting a weak saline solution into the arteries instead of the veins. Snow calculated the fluid loss necessary to produce the amount of hemoconcentration noted in the 1849 experiments of Garrod and Parkes as approximately 100 ounces in a healthy adult. “This calculation may be useful as indicating the amount of fluid, which ought not to be exceeded in the injection of the bloodvessels” (181). He also attributed to Garrod a suggestion that phosphate of soda be used rather than carbonate of soda as a component of the saline solution, so as better to replace the electrolytes that had been lost from the bowels. On the other hand, Snow thought there were other effective ways to replace lost fluid volume: “To allow the drinking of cold water, for which there is a great desire, is in accordance both with reason and experience” (182), but “reason and experience are just as much opposed to hot air-baths and other attempts to raise the heat of the surface, which can only have the effect of increasing the symptoms of asphyxia, so long as the blood remains so thick and tenacious.” On this point we find Snow reaffirming one of his earliest statements about cholera, but on a very different theoretical basis. Whereas in the fall of 1848 he assumed (like most of his colleagues) that cholera “in some ways resembled” asphyxia, when new cholera cases appeared five years later he could offer a coherent account of precisely how the pathology of cholera could eventually produce secondary, asphyxialike symptoms. The year 1853 was a banner year for Snow. He continued to advance his understanding of inhalation anesthesia, and his recognized skill in that field had taken him directly to Buckingham Palace. He became even more convinced that his theory of cholera transmission was correct, and he had continued to accumulate examples of


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person-to-person and water-borne transmission. When it became clear late in the fall that a third cholera epidemic was underway in London, Snow began collecting data from the Weekly Returns to use for the oft-postponed study of cholera mortality in relation to metropolitan water supply.

Notes 1. “Westminster Medical Society,” Lancet 2 (1849): 431–32. Snow had presented a “Lecture on the causes and prevention of cholera” at the Western Literary Institution on Thursday, 4 October, which may have been an excerpt of the paper he delivered nine days later; Lancet 2 (1849): 413. 2. “Westminster Medical Society,” Lancet 2 (1849): 432. 3. “Westminster Medical Society,” Lancet 2 (1849): 431–32. The society’s procedure required that Snow wait until everyone who wished to comment had done so before he could reply to any comments, so the proceedings of this meeting do not include any of Snow’s reactions to criticisms. Dr. Stewart’s comment about the autoingestion experiment suggests that Snow added the reference to a similar Berlin experiment in PMCC subsequent to delivering the paper because the Lancet report did not mention it. Stewart also thought “that Dr. Snow’s hypothesis did not explain certain great and sudden outbreaks of cholera that had happened in India”; PMCC contains a paragraph on that, as well. 4. “Westminster Medical Society,” Lancet 2 (1849): 459–60, meeting of 20 October. 5. “Death of the Marquis of Anglesey,” Times (1 May 1854), 8. The implicit point of Snow’s lengthy first entry in his casebooks also reinforces his sense of the old soldier’s bravery (CB, 122–23). 6. Snow continued to provide anesthesia services gratis in three workhouse infirmaries, in addition to continuing to attend to some of his old general practice patients; S. Snow, JS-EMP, 296. John French, the surgeon that Snow assisted at the Poland Street Workhouse, later acknowledged his colleague’s commitment to aiding the poor; Lancet 2 (1858): 103. 7. Sykes, “Anaesthetic deaths,” 26–43. 8. The enumerator for the 1851 census listed two households at 54 Frith Street: John Snow, born in the city of York, unmarried, aged 38, physician, MD, University of London, LRCP. The other consisted of Mrs. Sarah Williamson, widow, aged 70, on an annuity; her daughter Eleanor, aged 48, fancy needle and bead worker; Marion Watkin, aged 19, crochet worker; and Jane Wetherburn, aged 39, general servant; UK Home Office, 1851 Census, H.O. 107/1510/82. According to Richardson, Snow rented his flat from Mrs. Williamson; L, ix. 9. Snow, “On narcotism” LMG 45 (1850): 622. 10. Snow, Letter to the Right Honourable Lord Campbell (1851). The casebooks reveal many examples of situations in which chloroform was forced on an unwilling patient. 11. David Zuck constructed a map of all the general practice (i.e., nonanesthesia) domiciliary visits recorded by Snow in CB from 1848 to 1858. The map shows Snow’s failure, by and large, to expand his general practice beyond its initial base in Soho. A notable exception are two visits paid by Snow to 40 Ampthill Square and 37 Gloucester Road in 1849 and 1851, respectively. Both visits were to the home of the same person—Thomas Jones Barker (1815–1882), a historical painter and member of the Royal Academy. Charles Empson knew the painter’s father, Thomas Barker, in Bath, so it may have been via his uncle that Snow made the family’s acquaintance. Barker, best known for his battle scenes of the Napoleonic and Crimean Wars, exhibited his portrait of “Dr. Snow” (see Fig. 4.1) at the Royal Academy in 1847; see Zuck, “Snow, Empson, and the Barkers of Bath.”

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12. Newman, Medical Education, 8–9; G. Clark, Royal College of Physicians, 2: 518, 686–87; Peterson, Medical Profession, 6–7; Shephard, JS, 63–64; and Ellis, CB, xviii. Zuck supplied the data on Snow’s practice in the 1850s. Snow was probably not disappointed that he would never be able to join the elite “club” of fellows among physicians. He was eligible to become a fellow of the Royal College of Surgeons when that honorific title was established in the 1840s, but had not done so. His view of professional involvement seems to have been egalitarian, not hierarchical. Snow continued to serve as GP to predominantly poorer patients in the Soho area until 1849; Shephard, JS, 59. 13. Snow’s name first appears for the 1850–1851 session; Pathological Society of London, Transactions 3 (1850–52): 14. 14. Shephard, JS, 62–64. 15.“Medical Society of London,” Lancet 2 (1850): 456–57. See also Storey,“Henry Clutterbuck.” 16. Richardson, L, xxiii. 17. Richardson, L, xxiv; quotation from JPH&SR 1 (1855): 3. 18. “Proposed new society for the investigation of cholera and other epidemic diseases,” Lancet 2 (1849): 301, issue of 15 September; “Further remarks on the proposed new society for the investigation of cholera and other epidemic diseases,” Lancet 2 (1849): 592, issue of 17 November. 19. “Epidemiological Society,” MT 22 (1850): 132–33. Benjamin Guy Babington (1794–1866), a physician at Guy’s Hospital, was interested in organic chemistry and is credited with the invention of the laryngoscope in 1830. He shared with Snow an interest in a broad array of sciences and a willingness to draw useful analogies from nonmedical scientific fields; A. Evans, “Let’s not forget B G Babington”; Wilson, “Benjamin Guy Babington.” 20. “Epidemiological Society,” Lancet 2 (1850): 640. 21. JPH&SR 1 (1855): 2, 3, 5–6. 22. “Epidemiological Society,” MT 2 (1851): 54; “On the mode of propagation of cholera,” MT 3 (1851): 559–62, 610–12; “Epidemiological Society,” MT 3 (1851): 522–24; “Epidemiological Society,” MTG 5 (1852): 177 (papers on “Failure of vaccination in Bengal” and the “Success of vaccination in Bombay”); “On the relations of vaccination and inoculation to SmallPox,” MTG 6 (1853): 74–76 (from which the quote is taken); Snow, “On the comparative mortality of large towns and rural districts, and the causes by which it is influenced,” reported in MTG 6 (1853): 561, and AMJ 1 (1853): 404, published in full in Transactions, JPH&SR 1 (1855). 23. “He used often to meet with opponents to his peculiar opinions at the meetings of this Society, but he always retained friendships”; Richardson, L, xxiv. For Snow’s comments on the ostensible similarity in mode of propagation of cholera and black death, see “Epidemiological Society,” MTG 7 (1853): 615. 24. Richardson, L, xxxii–xxxiii. 25. “Medical Society of London,” MTG 6 (1853): 610. The president at the time was Forbes Winslow. 26. Snow, “On the use of chloroform in surgical operations and midwifery,” LJM 1 (1849): 54. 27. Before being asked to treat the queen in 1853, Snow had worked with two of the royal physicians, Drs. Clark and Locock, on other cases since 1849 and had administered anesthesia to two palace servants and a lady-in-waiting; S. Snow, JS-EMP, 306. 28. About two weeks after administering chloroform to the queen, Snow altered the way he entered notes in his Case Books. Previously, he had entered all his cases, whether general practice or anesthesia, in chronological order. Shortly after the Buckingham Palace experience he separated the two, placing anesthesia case notes at the front of his book and general practice notes at the back. S. Snow believes that this change in note taking marks Snow’s sense of himself as a specialist anesthetist; JS-EMP, 303.


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29. For example, within a month of the queen’s delivery, on 23 April 1853, Snow reported that he used the inhaler for the last forty-five minutes while Dr. Reid delivered the Honorable Mrs. Proctor Beauchamp’s first child; Ellis, CB, xxx. 30. Shephard, JS, 117. 31. The general public came only belatedly to know about the use of chloroform and Snow’s role in administering it. The initial court statements to the press mentioned neither Snow nor chloroform. It was not until 23 May that the Times gave an account of Snow’s administration of the chloroform, after the medical press had already “broken” the story. 32. “Her Majesty’s accouchement: Chloroform,” AMJ 1 (1853): 318. 33. Ellis, CB, 300–01. 34. Caton, What a Blessing; Pernick, Calculus of Suffering. 35. Lancet 1 (1853): 453. The Lancet was careful not to impugn the value of chloroform in surgical anesthesia and noted with satisfaction that reportedly the queen had never lost consciousness. By the time the editorial appeared the fact that chloroform had been administered to the queen had been authoritatively reported in several places, so Wakley was presumably being coy by referring to the fact as a “rumour.”As we have seen (Introduction and Chapter 4), this was neither Snow’s first nor last run-in with Wakley’s journal. Snow published approximately 89 separate papers (depending on how one counts multipart articles) in medical journals, of which fifteen appeared in Lancet. Eight of the fifteen papers were published after 1853, so the flap over giving chloroform to the queen did not discourage Snow from submitting. 36. “Her Majesty’s accouchement: Chloroform,” AMJ 1 (1853): 450. The AMJ editors noted in passing a similarly approving statement that had appeared in MTG. 37. “Royal Medical and Chirurgical Society,” Lancet 1 (1850): 154–55. Thomson was the chief chemical consultant to the Committee on Scientific Inquiries of the GBH in 1854 and 1855. Subsequent citations to the report of Snow’s comments at this meeting are not individually cited. 38. Lancet 1 (1850): 155. 39. “Epidemiological Society,” MT 2 (1851): 54. 40. “On the infectious origin and propagation of cholera,” MT 2 (1851): 669, 666. The entire paper was published in three installments; MT 2 (1851): 506–10, 648–51, and 666–71. 41. Snow, “On the mode of propagation of cholera” (1851), 559. 41a. Snow, “On the prevention of cholera” (1853), 369. 42. See also Snow, “The water supply at Newcastle,” Times, 11 November 1853. 43. Snow, “Principles on which the treatment of cholera should be based” (1854).

Chapter 10

Cholera and Metropolitan Water Supply

O

F ALL THE CONVENIENCES that the modern industrialized world takes for granted, the availability of free-flowing water in every kitchen and bathroom is surely one of the foremost. During Snow’s lifetime few in London were so fortunate. Many continued to haul water from a neighborhood pump, and those who had water piped to their residence frequently received it, albeit with intermittent flow, in cisterns or butts in a courtyard rather than inside. Nevertheless, a water supply directly to one’s house was a much desired commodity in London, and private companies had competed for the opportunity to provide it since the previous century.1 In 1817, however, this open market was replaced by a regional patchwork of monopolies within which a single company laid pipes. When water rates under this cartel system rose considerably, limited competition was reintroduced in the mid-1830s. In north London the Hampstead and New River water companies were permitted to lay pipes in the same streets and solicit customers. In south London the Lambeth and Kent water companies were given similar access to neighborhoods previously reserved for the South London Water Works. Elsewhere, the monopoly system remained in force. Piped drinking water was often foul and became increasingly more so in the first half of the nineteenth century, particularly when the source of supply was the Thames or the Lea, which flowed into the Thames opposite Greenwich. These rivers served as the final destination of many sewers constructed as part of the sanitary reform

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campaign to reduce urban effluvial vapors from human wastes, husbandry barns, slaughterhouses, and other so-called nuisance trades. Public clamor at the growing filth of river water led to the appointment in 1828 of a royal commission to investigate London water quality and supply. Although several medical men testified that drinking water contaminated with raw sewage was a likely cause of ill health, the commission did not recommend significant parliamentary intervention. On their own volition, however, some water companies established filtration mechanisms and settling reservoirs, and a few shifted their supply to purer sources after the cholera epidemic of 1831–1832. For example, the East London Water Company added an intake pipe on the Lea River above the tidal reach of the Thames, and the Grand Junction Company (supplying west London) shifted its supply source from Chelsea to Brentford, several miles above London on the Thames (Fig. 10.1).2 However, sanitary reformers, led by Edwin Chadwick, were less concerned about water for human consumption than about its potential for flushing dirt and sewage from homes and streets. Every town and city, they thought, should have a highvolume water supply and a well-engineered sewage disposal system that, together, would carry the contamination of urban life back into rivers and eventually to the sea. In London the general increase in the volume and pressure of water supplies in the first half of the nineteenth century did, indeed, lead to more efficient flushing

Figure 10.1. Map of metropolitan London showing Rivers Thames and Lea, as well as the metropolitan districts served by various water companies.

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of sewage into the Thames, but because the Thames also served as London’s principal water source, improvement in sanitation actually increased the admixture of sewage in drinking water, especially as the sanitary reformers were successful in convincing people to replace cesspools with water closets. When objections were raised, sanitary reformers assured the public that all contaminants were harmlessly diffused in the large volumes of river water.3 After the second cholera epidemic of 1848–1849, public pressure to improve the quality of London water rose steadily. In 1852 Parliament approved a bill that required private water companies in London to filter all water, cover all reservoirs, and move their sources of supply above the tidal flow of the Thames and the Lea. They were given until the end of August 1855 to comply.4 Snow, who distilled his own drinking water, agreed that London water should be improved, but he considered the abolition of cesspools and the increasing preference for water closets a sanitary disaster. Cesspools were odoriferous, but they did contain and prevent the transmission of the morbid agents of cholera until they could be disposed of safely. By contrast, water closets connected to sewer lines that emptied into rivers also used for metropolitan drinking water were, in his mind, primarily an efficient means of recycling the cholera agent through the intestines of victims as rapidly as possible. Sanitary reforms were needed, but flushing the waste of a town into the same river by which one quenched one’s thirst seemed sheer stupidity. The agent that made cholera lethal to humans had not been isolated, but Snow was convinced that it retained its constituent form regardless of how much water was added to it. If he was right, any change in water supply, whether local or municipal, that lessened the chances of people ingesting sewage from cholera victims should be reflected in reduced cholera mortality.

Linking Water Supply to Cholera Snow’s thinking about cholera and the water supply reflected the extension of a physiological hypothesis across a hierarchy of levels of organization (see Table 8.2). He took a disease hypothesis, formulated fundamentally from clinical observations in sick patients and built on a foundation of insight into likely mechanisms and observations about pathophysiology and clinical symptomatology, and used it to explain the geographic and temporal patterns created by tens of thousands of cases of disease occurring in populations of millions. His first principles were physiological and clinical; the observations that he predicted (and confirmed) at the population level were experimental evidence for the correctness of the underlying hypothesis about the way in which cholera is transmitted. He sought evidence for his transmission hypothesis at a variety of ecological levels, each of which received different prominence in his writings. His cholera transmission hypothesis, and its extensions to different ecological levels, is expressed formally in Table 10.1.


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Table 10.1. Ecological levels in Snow’s theory about cholera transmission Hypothesis

The morbid agent of cholera is found in the evacuations of cholera patients and must be ingested to cause disease.

Corollary at level A— individuals

Circumstances that promote contact with the evacuations of cholera patients (lack of light, lack of washing facilities, mines, overcrowding, food at wakes) promote person-to-person transmission and the clustering of cholera in families, households, lodging houses, mines, ships, and similar circumscribed areas.

Corollary at level B— neighborhoods

Brief localized epidemics of cholera in which many individuals are simultaneously affected are likely due to a local water supply contaminated with the evacuations of one or more cholera patients.

Corollary at level C— large populations

The general pattern of epidemic cholera in large populations such as cities and towns over the entire duration of an epidemic is strongly related to the extent to which its municipal water supplies are fecally contaminated.

The escalation of Snow’s hypothesis from individual to city is a distinctive feature of his thought. Until that time no hypothesis of disease etiology had successfully explained any pattern of disease occurrence simultaneously at several individual and ecological levels. During the fall of 1848, his clinical experience with cholera victims and his reading in medical journals substantiated the corollary at level A, person-toperson transmission in mines and households, but he had hesitated to publish his hypothesis until he could cite examples of transmission at the next two ecological levels. The initial breakthrough came the following August, when Snow learned of John Grant’s engineering reports describing the drainage and water supply in Surrey Court, Horsleydown, and Albion Terrace. Snow devoted most of MCC to a minute reconstruction of events that could have produced sewage contamination of a local water source, followed by water-borne transmission of cholera from the initial victims to their neighbors—exactly as predicted by his corollary at level B. In MCC he also presented evidence that indicated an association between degrees of cholera mortality in towns and the nature of their water supplies (level C). The Rivers Nith and Clyde, like the Thames, functioned simultaneously as recipients of human waste and as sources of municipal water. The information available to him was incomplete, particularly about mortality in the current epidemic, but it appeared that the three major cities served by these rivers—Dumfries, Glasgow, and London—suffered more severely in 1832–1832 and 1848–1849 than did towns with purer sources of drinking water.

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The principal difference between MCC and PMCC (published two months later) was an increase in the number of instances of urban water-borne transmission that Snow could document, particularly outside of London. He had carefully searched the literature, had investigated water supply patterns in some localities, and had enlisted the help of physicians, ministers, and friends in assembling such evidence from towns throughout England. The most persuasive new evidence supporting his hypothesis of level C transmission came from Exeter and Hull, each of which had changed its water supply between the 1832 and 1849 epidemics. Exeter had repositioned its waterworks upstream of the main sewer outlets after the first epidemic, and cholera mortality was less in 1849. In Hull new waterworks were also constructed between epidemics, but they were positioned within the tidal reach of the Humber estuary. The result was the opposite of that in Exeter: Whereas cholera mortality in Hull was low during the 1832 epidemic, when the drinking water came from springs outside of town, it increased in 1849, when the water was drawn from a polluted tidal river.5 The situation in Snow’s hometown offered confirming evidence within the same epidemic: “When the cholera made its appearance at York, about the middle of July last [1848], it was at first chiefly prevalent in some narrow streets near the river, called the Water Lanes. The inhabitants of this spot had been in the habit from time immemorial of fetching their water from the river at a place near which one of the chief sewers of the town empties itself; and recently a public necessity had been built, the contents of which were washed every morning into the river just above the spot at which they got the water” (PMCC, 750). Local authorities eliminated access to the River Ouse and opened the taps to drinking water supplied from pure sources outside the city; cholera mortality soon decreased in the area. The taps were closed, and the people drew water from the river and began to die again. When the taps were reopened and remained so, “the cholera again ceased, and has not recurred” (PMCC, 750). Nevertheless, these examples from Exeter, Hull, and York were only suggestive. London was the major metropolis in Great Britain, yet the “want of exact information” about its water supply noted in MCC (25) continued to stymie Snow’s effort in PMCC to prove his hypothesis about level C transmission. Equally troublesome were skeptical reviews of MCC, particularly one in LMG that challenged his analysis of Albion Terrace as an example of local level B transmission.6 In essence, that reviewer did not consider Snow’s reasoning more persuasive than Milroy’s. Gavin Milroy, the physician associated with the sanitarian oriented GBH, had investigated the outbreak in Albion Terrace and turned in a report before Snow finished writing MCC. Snow believed he had effectively countered Milroy’s local miasmatic interpretation that effluvia wafting from nearby sewers and ditches could have swept across the row of houses in Albion Terrace and caused the outbreak. If he did not realize it before, there was no denying after the reviews of MCC that the editors of two major London medical journals thought he had not answered the “Milroy objection” to his theory. In each instance in which cholera was associated with impure water, it was possible for a miasmatist to argue that dirty water


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was not the determining factor. Snow had not excluded the possibility that the quality or nature of the local atmosphere could account for the patterns of the disease. The papers he published on cholera in 1851 and 1853 continued to adduce the importance of water supplies, but he found no examples at the metropolitan level that unambiguously answered the Milroy objection to his hypothesis.7 The opportunity he sought occurred in London when epidemic cholera returned before all the private water companies had shifted their sources of supply in compliance with the new law. He documented his findings in a book published early in January 1855 as the second edition of MCC. At 137 pages MCC2 was “much enlarged” from the thirty-one-page pamphlet published five and a half years earlier.8 While MCC2 replicated much of the evidence first presented in MCC, it contained even more from PMCC; in fact, MCC2 is better described as a second edition of PMCC. The critical evidence presented in MCC2 was the association between differential water supplies and cholera mortality in south London that Snow discovered in the fall of 1853, began investigating the following summer, and finished analyzing in 1856.

The Weekly Returns of November 1853 Absent since 1849, cholera returned in the summer of 1853. As autumn came and temperatures dropped, Londoners hoped that the cholera epidemic would abate, but it was still in the grip of the epidemic in the middle of November. At the main General Register Office (GRO) in Somerset House, William Farr’s staff published each Saturday a new edition of the Weekly Return of Births and Deaths in London.9 The issues of 19 and 26 November contained new information that Snow found very compelling. For the previous thirteen weeks Farr’s staff had been retabulating cholera deaths by district in relation to the nine different metropolitan water companies that provided piped water to each district. The issue of 19 November included a special supplement on “Cholera and the London water supply.” In it Farr reminded the public (and the water companies) of the 1852 act, which required that by the end of August 1855 no company could supply water obtained from the lower, tidal portions of the Thames.10 Farr was as sympathetic to Snow’s 1849 theory as any medical man in London, but he believed it remained unsubstantiated. In his analysis of the GRO data for the 1848–1849 epidemic, Farr thought the association between cholera mortality and the elevation at which people resided was greater than the relationship of cholera to the purity of their drinking water. His zymotic theory could explain this association: In the London metropolis evaporation rising from certain stretches of the Thames contained cholera “matter” that, when combined with smog (“London fog”), settled in higher concentrations at lower elevations.11 In his mind impure drinking water probably predisposed susceptible individuals living at lower elevations to cholera

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(and other diseases), but it was not the cause of them. Farr was, therefore, less concerned with the water Londoners ingested than with the water vapors they inhaled. As such, his thinking was closer to that of sanitarians who shared Milroy’s local miasmatic concerns about effluvia than to Snow’s. Farr acknowledged that Snow might be correct, but he thought the requisite threshold of proof was very high and ultimately unattainable: “To measure the effects of good or bad water supply, it is requisite to find two classes of inhabitants living at the same level [elevation], moving in equal space, enjoying an equal share of the means of subsistence, engaged in the same pursuits, but differing in this respect,—that one drinks water from Battersea, the other from Kew. . . . But of such experimenta crucis the circumstances of London do not admit. . . .”12 Farr’s usage of the same Baconian term that Snow had employed in his first publication indicates the importance of the hypotheticodeductive method to some medical men of this generation. In the laboratory one can conduct a “crucial experiment” in which two samples are treated in identical fashion except for the factor in dispute. The results of the experiment then tell one with certainty whether the underlying theory is correct, but London was not a laboratory, so Snow could never satisfactorily disprove Farr’s elevation theory or counter the sanitarians’s argument that other factors—overcrowding, poor ventilation, local sources of effluvia—made the real difference in epidemic cholera, whereas impure water played only contributing or “predisposing” roles. While Farr in his comments on 19 November underlined the difficulty of sorting out the contribution of water supply to cholera, Snow drew quite opposite conclusions when he read the Weekly Return published the following week (Fig. 10.2).13 The issue of 26 November contained a table describing water supplies and cholera mortality that appeared identical to a table in the 19 November issue except for the number of deaths, but Snow noticed a critical difference. The new table contained a footnote that “in three cases (marked with an asterisk), the same districts are supplied by two companies.” A week after Farr had set the bar at a seemingly impossible height, he had given Snow hope that London could be the setting for a crucial experiment that would substantiate his cholera hypothesis at the metropolitan level. The makings of this “natural experiment” took place in 1852, when one of the water companies supplying south London moved its supply above the tidal reach of the Thames, whereas its competitor, serving customers in the same districts, had decided to defer its transfer closer to the August 1855 deadline.14 There seemed no need to hurry matters; sixteen years had elapsed between the first two cholera epidemics in England, but by returning well ahead of schedule, so to speak, in 1853, the third cholera epidemic slipped through an open window when the Lambeth Company provided pure water, while the Southwark and Vauxhall Company (S&V) still supplied sewage-contaminated water. This window for a natural experiment had not existed in 1848–1849 because both companies drew water from polluted points on the Thames. It would disappear as soon as the S&V moved its intake source to comply with the law. It existed only because these districts had been opened to competition

Figure 10.2. Weekly Return of Births and Deaths ( 26 November 1853).

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in the 1830s, and different water companies had laid pipes and solicited customers in the same streets.

The Crucial Experiment The third cholera epidemic in London began in September 1853, died down the following winter, and resumed its deadly work in the first week of July 1854.15 It raged for fourteen weeks in 1854, but a few cases were still appearing when MCC2 went to press in December of that year. Snow focused most of his attention on the second phase of the epidemic in London that began in July of 1854, when he had more time to undertake house-to-house investigations than in the waning weeks of the 1853 epidemic.16 Of course, he did not know in November 1853 that the epidemic would resume the following year, so he began what has since been termed the South London study by analyzing the data on the 1853 epidemic compiled by Farr and his staff at the GRO. For the thirteen weeks from 21 August through 19 November 1853, mortality in all districts supplied by S&V alone was 94 per 10,000, whereas for the districts supplied by both Lambeth and S&V, mortality was 61 per 10,000. Snow dug deeper into the Weekly Returns, examining cholera rates by district in south London for the first seventeen weeks of the epidemic (through 17 December). He noted that the registration district of Lambeth, mainly supplied by the Lambeth Company, had improved with respect to cholera mortality in London, from the seventh-worst in 1849 to thirteenth-worst in 1853. Snow then undertook what Farr had not—to compare cholera mortality by water supply at the subdistrict level. He reorganized all cholera deaths reported in the Weekly Returns through the end of December 1853 by addresses and placed them in three groups: twelve subdistricts exclusively supplied by S&V, three subdistricts supplied only by Lambeth, and sixteen supplied by both companies (Fig. 10.3).16a Not a single person had died of cholera among the 14,632 residents of Norwood, Streatham, and Dulwich, whose water came from the Lambeth Water Company. The mortality rate in the subdistricts served only by S&V was 114 per 10,000; in the subdistricts with overlapping supply the rate was 60 per 10,000 (MCC2, 72–74). While suggestive, the absence of cholera in the three subdistricts served only by Lambeth compared to the high mortality in subdistricts served only by S&V did not greatly advance Snow’s argument. Other factors could be cited by his opponents. Norwood, Streatham, and Dulwich were pleasant residential suburbs. The areas served only by S&V were tainted by poverty, overcrowding, and the noxious fumes characteristic of inner London,17 but environmental conditions in the sixteen subdistricts served by both companies were similar and therefore met the criteria Farr had set for a crucial experiment: The intermixing of the water supply of the Southwark and Vauxhall Company with that of the Lambeth company, over an extensive part of London,

Figure 10.3. Cholera deaths in 1853 in south London organized by subdistricts (Snow, MCC2, 73, Table 6).

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admitted of the subject being sifted in such a way as to yield the most incontrovertible proof on one side or the other. In the sub-districts . . . supplied by both Companies, the mixing of the supply is of the most intimate kind. The pipes of each Company go down all the streets, and into nearly all the courts and alleys. A few houses are supplied by one Company and a few by the other, according to the decision of the owner or occupier at that time when the Water Companies were in active competition. In many cases a single house has a supply different from that on either side. Each Company supplies both rich and poor, both large houses and small; there is no difference either in the condition or occupation of the persons receiving the water of the different Companies. Now it must be evident that, if the diminution of cholera, in the districts partly supplied with the improved water, depended on this supply, the houses receiving it would be the houses enjoying the whole benefit of the diminution of the malady, whilst the houses supplied with the [S&V] water from Battersea Fields would suffer the same mortality as they would if the improved supply did not exist at all. As there is no difference whatever, either in the houses or the people receiving the supply of the two Water Companies, or in any part of the physical conditions with which they are surrounded, it is obvious that no experiment could have been devised which would more thoroughly test the effect of the water supply on the progress of cholera than this, which circumstances placed ready made before the observer. The experiment, too, was on the grandest scale. No fewer than three hundred thousand people of both sexes, of every age and occupation, and of every rank and station, from gentlefolks down to the very poor, were divided into two groups without their choice, and, in most cases, without their knowledge; one group being supplied with water containing the sewage of London, and, amongst it, whatever might have come from the cholera patients, the other group having water quite free from such impurity. To turn this grand experiment to account, all that was required was to learn the supply of water to each individual house where a fatal attack of cholera might occur. MCC2, 74–7518 Snow positioned these paragraphs between discussion of the Weekly Returns that gave him the idea for such a “grand experiment” and his description of the subsequent investigations of the 1854 epidemic. A possible interpretation is that Snow actually envisioned in November 1853 the procedure he used when conducting this experiment the following late summer and fall: attempting to visit every house where a person had died of cholera in the sixteen subdistricts with intermingled water supply and determining in each instance which water company supplied that house. However, important facts remain unexplained by such a reading of MCC2. Why did he not begin the investigation in December 1853? He says the days were too short


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and he could not spare the time, but neither should have stopped him from solving a problem that had eluded him for nearly five years (MCC2, 75–76). There was no assurance that cholera would return to London before S&V changed its supply, so would he let this opportunity slip away in December had he already decided to undertake the extensive investigations detailed in MCC2? Moreover, why did he not begin house-to-house surveys as soon as cholera reappeared the first week of July rather than wait until mid-August if he knew from the outset that he would have to investigate all sixteen subdistricts where there was overlapping supply? Snow’s conception of the “grand experiment” likely evolved as he carried it out.19 In our view the experiment he anticipated in the fall of 1853 may have been “grand” in the number of people living in the affected portions of London, but not “grand” in the demands he thought it would place on his own time and labor. His reformulation of Farr’s data in the winter of 1853–1854 and again in July and early August of 1854 suggests that he initially believed he could do most of the required work by careful sifting of information published in the Weekly Returns, supplemented by house-to-house inquiries in selected subdistricts. Snow’s decision to focus exclusively on deaths from cholera was itself a simplification with important pragmatic consequences. In a disease with a mortality of fifty percent, counting only deaths excluded half the cases. Moreover, if, as Snow suspected, some asymptomatic or mildly symptomatic individuals failed to receive “cholera” as a clinical diagnosis, the undercount would have been even more severe; many such cases were diagnosed as “diarrhœa.” On the other hand, attribution of a death to cholera was relatively easy to establish because cholera symptoms are very distinctive, and death is rapid. Snow made use of a case definition that, while incomplete, was reasonably accurate. In so doing he anticipated modern epidemic investigations in recognizing that the scientific ideal of a perfect all-inclusive case definition must be abandoned if progress in identifying the cause of a disease is to take place. Lists of cholera deaths were readily available from Farr or district offices of the GRO, so Snow took advantage of a system for reporting deaths that had been in place in England and Wales since 1837.20 At the time, however, there was no way to obtain a list of cholera cases for an area as large as south London.

August 1854: The Investigation Begins When cholera returned to south London early in July 1854, Snow responded at first in leisurely fashion, consistent with his activities of the previous winter. He waited for several weeks to see if the Weekly Returns would show the same pattern Farr had noted for the 1853 epidemic. They did: The intermingled subdistricts had notably less mortality than did areas supplied only by S&V. Apparently, this was the information Snow wanted before choosing an area in which to check on the water supply at every house where cholera deaths had occurred.21 He elected to begin

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on-the-spot inquiries in two subdistricts of Kennington, probably because they had been in the middle range of cholera mortality in 1853 and were so again in 1854. He learned two things of significance when he began shoe-leather inquiries in Kennington. First, his theory appeared to hold up very well. Of the forty-four deaths that had occurred in the two subdistricts by 12 August (the first five weeks of the epidemic), no fewer than thirty-eight were in houses supplied by S&V water (Table 10.2). Snow’s second discovery altered the strategy of his entire investigation. He became aware that the intermingling of the water supply was much greater than he had imagined: “After commencing the inquiry I found that the circumstances were calculated for affording even more conclusive evidence than I had anticipated. The Table 10.2. Preliminary results from Snow’s investigation of four subdistricts Kennington, first part Supply Southwark and Vauxhall Lambeth Pump wells on premises Total

No. of houses 27 2 2 31

Kennington, second part Southwark and Vauxhall Lambeth Total

11 2 13

Waterloo, first part Southwark and Vauxhall Lambeth Not yet ascertained Total

7 1 1 9

In Waterloo, second part, 27 deaths have occurred in 24 houses, which are supplied as follow Southwark and Vauxhall Lambeth Pump well close to the Thames; water dirty Wells at the Lion brewery Not yet ascertained Total

No. of houses 17 3 1 1 2 24

If the cases are enumerated instead of the houses in this last subdistrict, the return is as follows Supply Southwark and Vauxhall Lambeth Pump wells Not yet ascertained Total

Cases 19 3 3 2 27

Source: Snow, “Communication of cholera by Thames water” (2 September 1854), 247.


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pipes of the two water companies not only passed down all the streets, but into nearly all the courts and alleys. A single house often had a different supply from that on either side.”22 If it was not clear to him in November 1853 that this “grand experiment” was also a “crucial experiment,” it was now. If every other house received S&V water and the intervening houses had Lambeth water, ardent local miasmatists and contingent contagionists could hardly claim that noxious effluvia skipped over every other house to afflict the nearest neighbor. Snow was energized, and it seems more likely it was in mid-August, and not a month earlier, that he “resolved to spare no exertion” to complete the necessary inquiries in all sixteen of the intermingled subdistricts (MCC2, 76). Although Snow wrote, “I was desirous of making the investigation myself, in order that I might have the most satisfactory proof of the truth or fallacy of the doctrine which I had been advocating for five years,” he soon realized that would be impossible (Ibid.). The weekly death toll was rising, and the epidemic had yet to peak. At this point he showed Farr the preliminary data he had gathered from the two Kennington subdistricts. Farr agreed that the ratio of deaths between the two companies was worth pursuing. Farr therefore ordered his registrars to gather information on the water supply of houses each time they recorded a death from cholera in every subdistrict supplied by either S&V or Lambeth. The employees of the Registrar-General could not begin this task until 26 August, however.23 That meant Snow himself would have to investigate all deaths that had occurred in the overlapping subdistricts through the Weekly Return of 25 August—that is, the first seven weeks of the current epidemic.

More Problems, Some Solutions Snow understated matters when he wrote that the “inquiry was necessarily attended with a good deal of trouble” (MCC2, 77). He soon discovered that finding out whether the water to a given house was supplied by Lambeth or S&V was not as simple as he had anticipated, for “there were very few instances in which I could at once get the information I required. Even when the water-rates are paid by the residents, they can seldom remember the name of the Water Company till they have looked for the receipt. In the case of working people who pay the weekly rents, the rates are invariably paid by the landlord or his agent, who often lives at a distance, and the residents know nothing about the matter” (MCC2, 77). But Snow’s ingenuity as a chemist, combined with a hefty dose of good luck, provided a solution: the water provided by Lambeth and S&V during his inquiry contained consistently different amounts of salt. On adding solution of nitrate of silver to a gallon of the water of the Lambeth company, obtained at Thames Ditton, beyond the reach of the sewage of London, only 2.28 grains of chloride of silver were obtained, indicating the

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presence of .95 grains of chloride of sodium in the water. On treating the water of the Southwark and Vauxhall Company in the same manner, 91 grains of chloride of silver were obtained, showing the presence of 37.9 grains of common salt per gallon. Indeed, the difference in appearance on adding nitrate of silver to the two kinds of water was so great, that they could be at once distinguished without any further trouble. Therefore when the resident could not give clear and conclusive evidence about the Water Company, I obtained some of the water in a small phial, and wrote the address on the cover, when I could examine it after coming home. MCC2, 7824 Finding a way to track the source of the water, however, turned out to be simpler than calculating death rates from cholera in the intermingled subdistricts. The number of deaths per water company in each subdistrict served as the numerator in this fraction. This information was readily available from the Weekly Returns during the height of the epidemic, which listed each death from cholera by residence in the metropolis. The ideal denominator for Snow’s natural experiment would be the total number of people living in houses supplied by each water company. Such information was unavailable, but Snow reasoned that the total number of houses supplied by each company in each subdistrict would yield a satisfactory approximation, and he knew that such records had been submitted to parliament.25 Without such denominator figures for each subdistrict, cholera death rates by subdistrict could not be calculated. Five times as many deaths in S&V-supplied houses than in Lambethsupplied houses would not indicate a higher risk if S&V supplied water to five times as many houses. But neither Farr nor anyone at the GBH would or could provide him the data he needed. The best information he could locate in the public domain was a return to the GBH from 1850, which gave “the entire number of houses” that each water company supplied: 34,217 for S&V, 23,396 for Lambeth.26 In short, he had denominator data only for each company’s total supply. Snow faced a major dilemma: either abandon this highly promising crucial experiment or extend the inquiry to include all the subdistricts supplied by both water companies.26a Because his denominator data extended across the entire area supplied by each of the water companies, he could calculate death rates only if he obtained numerator data over the same area. That meant that instead of just studying sixteen co-mingled subdistricts, he would have to investigate cholera deaths in thirty-two subdistricts.26b Such a task would require personal inquiries from Putney in the west to Rotherhithe in the east, from the banks of the Thames as far south as Streatham Common—an area of nearly fifteen square miles. Farr’s stable of registrars were prepared to cover this area for all deaths that occurred after 26 August, but if Snow was to have a meaningful analysis of the first seven weeks of the current epidemic, someone would have to help him cover the additional territory. He enlisted the assistance of “a medical man, John Joseph Whiting, L.A.C.”27


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The two investigated 334 cholera deaths, with Snow covering the entire Lambeth territory and Whiting primarily the S&V area. They found that twenty times as many deaths occurred in S&V-supplied homes. Where S&V supplied the water 286 deaths took place, but only fourteen where they could trace the supply to the Lambeth Company. Twenty-two deaths were associated with dipping pails into the Thames for water, four with pump wells, and four with ditches. The final four deaths were in individuals away traveling at the times of their deaths. During the first four weeks of the epidemic, the 286 cholera deaths they could connect to S&V-supplied houses accounted for more than half of the metropolitan total of 563. Snow thought the oneby-one investigation of these 334 cholera deaths sufficiently important to list them each individually in an appendix to MCC2 “as a guarantee that the water supply was looked into, and to afford any person who wishes it an opportunity of verifying the result” (80). In the meantime he had discovered another return to Parliament, according to which the “Southwark and Vauxhall Company supplied 40,046 houses from January 1st to December 31st, 1853, and the Lambeth Company supplied 26,107 houses during the same period” (MCC2, 80). Consequently, the death rate from cholera in S&V-supplied houses was 71 per 10,000 houses, while in Lambethsupplied houses it was 5 per 10,000, a fourteen-fold in risk when S&V supplied the water. Modern epidemiologists distinguish between a point source (also known as a common source) and a propagated epidemic. When many people drink from a contaminated water source such as a pump well, a sharp increase in cholera mortality follows, but only in those who drank from the pump well (level B transmission). The suddenness of the increase is due to the simultaneous exposure to the cholera agent of a large number of people. Propagated epidemics, on the other hand, build up gradually, because they are composed not just of individuals exposed to a point source, if there is one, but of secondary cases resulting from contact with those initially infected—person-to-person (level A) transmission. Snow understood that in the initial stages of a large urban epidemic transmitted by the water supply, cases would first appear almost exclusively in populations directly exposed to contaminated water. Inevitably, however, individuals not directly exposed to contaminated water would also contract the disease by virtue of person-to-person contact, thereby diluting the difference in risk between those exposed and unexposed to contaminated water. That is, level A and B transmission would gradually augment level C transmission. Snow predicted that the huge difference in initial risks between recipients of the two water supplies would diminish as the epidemic progressed, and so it did. Snow continued to investigate household water sources of cholera victims who had died during the fifth through seventh weeks of the epidemic in the Lambeth and comingled subdistricts, but Whiting for unknown reasons was unable to do likewise for subdistricts where S&V was the sole supplier of water. Snow overcame this obstacle by estimating the distribution of cholera cases in relation to water sources for the last three weeks in these S&V subdistricts. He based this estimation on the

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distribution of deaths by water supply in the first four weeks, although he admitted that the dynamics in the transition to a propagated epidemic might lead to an overestimate by this method.28 After seven weeks the resulting S&V-to-Lambeth cholera death ratio, although not as high as during the first four weeks of the epidemic, was still between eight and nine to one. For the seven weeks of the epidemic through 25 August, Snow’s personal inquiry involved the investigation of 658 deaths. In addition to all subdistricts served exclusively by the Lambeth company, Snow covered two subdistricts (Wandsworth and Putney) in the S&V area. Whiting worked only S&V subdistricts, with the exception of Clapham, where both companies had water customers. It must have been an arduous undertaking, even allowing for the clustering of deaths within families, houses, and streets in a London in which, as Snow tells us, “in many streets there are several houses having the same number,” while other house numbers were painted over or missing altogether (MCC2, 80).29 In fact, many residents did not know their own addresses. Consequently, Snow often visited two or three houses before finding the one in which a cholera death had actually occurred. It is unclear if he walked from street to street or hired a hansom cab and asked the driver to wait as he made his inquiries, but we do know that he reduced his anesthesia practice substantially from the middle of August through September to accomplish this time-consuming inquiry. According to his Case Books, he averaged 1.58 cases per day between 1 July and 10 August, whereas the case load drops to an average of 0.57 cases a day between 11 August and 30 September.30 Snow and Whiting had together tracked down the water supply to the houses of 860 cholera victims (Whiting’s 202, plus Snow’s 658), but investigating the water supply where cholera deaths occurred after 26 August became the responsibility of Farr’s registrars. Snow was indeed fortunate he had secured Farr’s assistance, for he would have had to investigate at least 3,000 deaths reported in the area supplied by the two water companies through 14 October. The information procured by Farr’s registrars was less reliable than that collected by Snow and Whiting, but, as Snow put it, they “could not be expected to seek out the landlord or his agent, or to apply chemical tests to the water as I had done” (MCC2, 86). In fully twenty percent of reported deaths, the registrars could not ascertain the precise water supply, but for the remainder Snow’s hypothesis held: 2,353 deaths took place in the 40,046 S&V houses, 302 in the 26,107 Lambeth houses, a risk ratio that Snow described as “nearly five” but which in fact is 5.1 (MCC2, 88). By combining the results of his own investigations with those of Whiting and Farr’s registrars, Snow could tabulate the rate of cholera deaths by water supply over the entire fourteenweek period of the epidemic. He apportioned the deaths where water sources were unknown between the two companies in proportion to those whose supply had been ascertained, yielding 4,093 deaths in S&V-supplied houses and just 461 in Lambeth houses. The overall risk ratio for cholera deaths over the fourteen weeks of the epidemic was 5.8 to one.31


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More Evidence Although the natural experiment in south London takes up only twenty-one pages in the middle of MCC2 (Table 10.3), Snow included evidence in the rest of the essay that complemented the centerpiece in substantiating of his cholera theory. He set up a discussion of the crucial experiment with a comparative analysis of cholera mortality in London during the 1831 to 1832 and 1848 to 1849 epidemics. In his mind the conclusion was inescapable: Sanitary reforms had contributed to an increase in deaths, not reduced them. In 1832 London’s population of almost 1.4 million people experienced 4,736 cholera deaths, a mortality rate of 34.1 per 10,000.32 Metropolitan London of 1849 was larger in area (it had incorporated nine new districts), and the population had increased by more than sixty percent, to almost 2.3 Table 10.3. Contents of MCC2 (1855), by topic Topic

Number of pages

Pathology and mode of communication (review of material presented in 1849, with minor revisions; includes Albion Terrace and Horsleydown)

32

Other water-borne outbreaks over relatively small areas (level B) Broad Street outbreak Transmission by sewage-contaminated river water (level C)—introduction Effect of water supply on mortality in London, 1831–1832 and 1848–1839 Crucial experiment—Lambeth Company’s intake site moved; opportunity to test hypothesis conclusively; data obtained

6 16 2 12

21

Comparison of Lambeth and Southwark and Vauxhall death rates, 1849 vs. 1854

2

Other examples of water-borne transmission in London, 1853–1854

6

Reply to Farr’s elevation hypothesis

2

Level C examples: other cities in Britain

11

Replies to objections and alternative theories

16

Other diseases possibly spread by water

8

Preventive measures suggested

5

Appendix: list of all cases in first four weeks of epidemic of 1854 personally investigated by Snow

24

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million. Even so, there were more than three times the number of deaths (14,137), and the mortality rate doubled to 62.0 per 10,000 (MCC2, 62–63). Despite the construction of new drains to empty ever more water closets and reduce the presence of ostensibly pestilential effluvia in the metropolis, Londoners had fared worse the second time cholera came to town. Comparative data from south London confirmed Snow’s assessment that water quality had deteriorated despite the changes in the sources of supply. The three districts supplied by the Southwark Water Works lost more than one percent of their population to cholera in 1832. In 1849, however, eight districts supplied by its successor, S&V, and the Lambeth Water Company suffered just as high a mortality rate. One of the districts, Rotherhithe, lost more than two percent of its population to cholera. By contrast, districts north of the Thames had lower cholera mortality than in 1832, which Snow attributed to improvements in water quality such as shifting to upriver sources well above the major sewer outlets and the wider use of settling reservoirs and effective filtering. The conclusion was inescapable: In the 1849 epidemic, “in every district to which the supply of the Southwark and Vauxhall, or the Lambeth Water Company extends, the cholera was more fatal than in any other district whatever . . . [because they were] deriving a supply from the Thames, in a situation where it is much contaminated with the contents of the sewers . . .” (MCC2, 64).33 Snow’s argument was especially forceful when he compared mortality in districts supplied by S&V and Lambeth in the two epidemics preceding and following the Lambeth change of water source. Cholera deaths in districts supplied by S&V increased by nine percent between 1849 and 1854, while in Lambeth-supplied districts they declined by seventy-five percent (MCC2, 90). Similar parishes with different water supplies, such as the adjoining Southwark parishes of St. Saviour’s and Christchurch, illustrated Snow’s thesis particularly well. In 1849 their cholera mortalities, like most of the parishes in Southwark, were exceptionally high. However, in 1853, S&V-supplied St. Saviour’s lost 2.3 percent of its population to cholera—almost one in forty, while Christchurch mortality, with Lambeth as its water source, lost just 0.43 percent. Waterloo Road (part one), the parish immediately east of Christchurch, was a region of high mortality in 1849, but it experienced just a single cholera death in 1853. It, too, took Lambeth water (MCC2, 72–74). Snow reasoned that if the S&V mortality was the same or had actually increased from 1849 to 1854 while Lambeth mortality dropped significantly between 1849 and 1854, the most plausible explanation would be that the change in the Lambeth water intake accounted for the whole of the difference. If Lambeth deaths were less in 1854 because of some improvement in the atmosphere, one would assume the same would be true in contiguous areas served by S&V (MCC2, 89–91). The comparison across time was not as definitive a reply to the Milroy objection as was the crucial experiment of 1854, but it nevertheless showed that all the evidence was lining up in Snow’s favor, no matter how one parsed the data.


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The roles of settling and filtering in purifying sewage-contaminated water also came under Snow’s scrutiny. He suggested that “detention of the water in the [Chelsea] company’s reservoirs permitted the decomposition of the cholera poison” (MCC2, 94). Again, a comparison lay at the heart of his reasoning. He had observed that carefully filtered Thames water, such as that supplied to Millbank prison, did not prevent cholera from killing 4.3 percent of the inmates in 1849, whereas the Chelsea Company, although drawing water from virtually the same spot as did the S&V Company, allowed to it to settle in reservoirs before distributing it. While residents in the districts supplied by Chelsea water experienced mortality higher than was the average in the whole metropolis in the 1853–1854 epidemic—there was a limit to the benefits of settling reservoirs if the water was very polluted—it was still half the rate of that among S&V customers (MCC2, 93–94). In MCC2 Snow gave examples of provincial towns where the water supply affected cholera mortality rates. He summarized evidence already presented in PMCC as well as in the papers and articles prepared since 1849. Most of this evidence came from the northern towns with which he was most familiar. The essence of Snow’s argument was that the experience of urban northern England showed that water from tidal rivers was generally bad, while surface water, especially from hills, was usually good. Like the Thames, the Humber, and the Tyne, the Nith, the Trent, and the Clyde all served as vehicles of cholera dissemination during the epidemic of 1854. Some improvement was possible if the river water was permitted to settle and was then filtered. Only towns that depended on surface water from rural hills or rural springs were spared water-borne epidemic outbreaks (MCC2, 98–104). Snow recycled his discussion of the Newcastle experience in July 1853, which documented both the reliability of rural water and the dangers of using tidal rivers simultaneously for sewage disposal and drinking water (MCC2, 104–07).34

Completing South London—A Predictive Model By the beginning of October 1854, Snow had completed his personal investigation (aided by Whiting) of all deaths attributed to cholera through 25 August for all subdistricts served by the S&V and Lambeth water companies. Farr’s registrars were collecting similar data for deaths that occurred thereafter, until the cholera epidemic ended after a run of fourteen weeks. Snow prepared an interim communication to MTG and then set out to write the manuscript that would be published as MCC2.35 He had now seen his inquiry through several stages, each designed to take advantage of an opportunity or to respond to a problem that he had not anticipated earlier, but Snow was not satisfied that he had fully completed his analysis of the “grand experiment” in south London. He still lacked the denominator data on the number of houses supplied by both water companies at the subdistrict level, which was necessary to calculate comparative death rates. In early October he had thought the

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information was forthcoming: “I hope shortly to learn the number of houses in each sub-district supplied by each of the water companies respectively. . . .”36 He did not receive it in time, however, to include the promised analysis in MCC2. In what way did he imagine that a detailed subdistrict analysis would add to the conclusiveness of an already extensive presentation of differential mortality associated with the two companies? First, he believed in October that a comparison of the comingled subdistricts would constitute the clearest, most unambiguous support for his theory and falsify both the Milroy objection (local effluvia) and Farr’s elevation theory. The entire sentence quoted in the previous paragraph shows why he thought it was so important to have subdistrict data: “I hope shortly to learn the number of houses in each subdistrict supplied by each of the water companies respectively, when the effect of the impure water in propagating cholera will be shown in a very striking manner, and with great detail.”37 It would provide the long-sought parallel to Horsleydown at the metropolitan level of ecological analysis: indisputable evidence that atmospheric effluvia did not explain what was known about the communication of cholera. It would also refute the elevation hypothesis. In August he had written that based on the data collected “in the [four] sub-districts to which the inquiry has extended, the people having the improved water supply enjoy as much immunity from cholera as if they were living at a higher level, on the north side of the Thames.”38 The expansion of the investigation he undertook as an expedient in the absence of the desired data about water supply turned out to have an unexpected benefit. He had already taken into account the relative effects on the mortality rate of the three ecological levels over time. He hypothesized that level C (metropolitan area) mortality would dominate early in the epidemic but eventually would be diluted by spread at levels A (person-to-person and households) and B (neighborhoods), and so it had, as the difference in the ratio of deaths in S&V-supplied houses compared to houses receiving Lambeth water dropped from fourteen in the early weeks to five during the last half of the epidemic. Statistically speaking, however, Snow came to believe that if one considered the epidemic as a whole, it was likely that level C spread would still dominate level A and B transmission. To confirm this belief, he devised a statistical model in which cholera was presumed to have spread over south London only by means of piped water. The closer his model came to predicting the actual number of cholera deaths in south London, the stronger would be his evidence that the metropolitan water supply was the major means by which cholera was transmitted. However, constructing a model of this sort was impossible with the numbers Snow had available when he wrote MCC2. He lacked the number of houses supplied by each company in every subdistrict needed to calculate, by subdistrict, the cholera mortality rate that should have occurred on the assumption that the numbers of deaths precisely paralleled the numbers of houses supplied with impure water. With these data he intended to compare for every subdistrict his calculated number to the


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actual number, a total of thirty-two paired data comparisons. A reasonable match between predicted and actual deaths in only a handful of subdistricts could be explained by chance, but a reasonable match across all thirty-two subdistricts would strongly support the soundness of the underlying theory that gave rise to the prediction. Snow finally obtained the desired subdistrict data in 1856 from an unexpected and disturbing source: the “Report on the last two cholera-epidemics of London as affected by the consumption of impure water” by John Simon, medical officer of the Board of Health. Simon essentially duplicated Snow’s south London water analysis, making the same observations about the high cholera mortality in those districts and also noting the significance of the movement of Lambeth’s water supply to Thames Ditton during the interepidemic interval while the S&V supply remained unchanged. Like Snow had done in MCC2, Simon showed a double contrast between cholera mortality rates in the areas supplied by the Lambeth Company in 1848 and in 1854, and between Lambeth and S&V consumers in 1854. Not a mention of Snow’s work can be found in this report, even though Simon used words similar to Snow’s in stating that the differences in the purity of water of the two companies had created a massive human experiment.38a While Simon had access to the data that provided the number of houses supplied by each company within each subdistrict, he used it only to calculate cholera mortality rates by water supply in each subdistrict; he did not propose the kind of predictive model that Snow envisioned. Nevertheless, now Snow had the numbers he needed to do that himself. Snow immediately prepared a paper for the JPH&SR that served as a rebuttal to what he took to be errors in Simon’s report and as an expansion of his MCC2 inquiry. The centerpiece of this paper was his analysis of the predictive model. After recapitulating for the reader how he came to design the methods for his inquiry and the data he had previously presented in MCC2, he presented a table for cholera mortality over the entire epidemic in thirty-one subdistricts in relation to water supply.39 He found it to be 160 deaths per 10,000 in S&V supplied houses and 27 per 10,000 in Lambeth houses.39a Snow then applied these overall death rates to the number of houses supplied by each company in each subdistrict and compared these “expected rates” to the deaths actually enumerated.40 For example, Lambeth Church, part two, had 7,868 houses supplied by S&V and 16,023 by Lambeth. Snow calculated that this ratio would yield a death rate of 71 per 10,000 inhabitants. The actual death rate in that subdistrict was 73 per 10,000. Snow was similarly on target in the Leather Market and Rotherhithe subdistricts, predicting death rates of 150 and 160, respectively, while the actual rates were 155 and 159. As expected in light of the problems encountered by himself, Whiting, and the registrars in gathering water supply information to houses in which a cholera deaths occurred, Snow’s predictions were less exact in many subdistricts. A more typical example was Christchurch, with an expected rate of 57 and an actual rate of 71. In five subdistricts he was off the mark. For example, he estimated the death rate in

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Putney should have been 160, whereas the actual number was 17. But while Putney lay in the S&V area, only thirteen of its 918 houses were actually served by that company. On the other hand, he underestimated the rate in Borough Road as 104, when the actual number was 171 (Fig. 10.4). Taking the entire series of thirty-one subdistricts, Snow was content with what he called “a very close relation to the real mortality” that “proves the overwhelming influence which the nature of the water supply exerted over the mortality, overbearing every other circumstance which could be expected to affect the progress of the epidemic.”41 Snow demonstrated in his analysis of the London water supply in relation to cholera that the entire phenomenon of a huge cholera epidemic could be explained.

Figure 10.4. Deaths from cholera in 1854 compared with calculated mortality (Snow, “Cholera and the water supply in the south districts of London,” Table 6).


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Every facet of the epidemic—its origin in water-borne traffic from infected regions, its distribution through the pipes of London, its transmission within households, its exacerbation in subsidiary outbreaks resulting from a contaminated point source such as a well pump—were unified by a common theory that found its proof not in any laboratory experiment, but in the record of cholera deaths collected by civil authorities. Snow had now pushed his cholera thesis as far as any predictive hypothesis about human disease can be pushed. Not only was the water supply a major determinant of the differences in mortality among subdistricts, it was the dominant determinant, in effect a proxy for cholera mortality. He anticipated modern epidemiological methods by using indirect standardization and modern scientific practice by creating a quantitative predictive model. Snow now finally proclaimed that he had finished his south London study and immodestly but accurately noted that his overall analysis of cholera mortality in London “probably supplies a greater amount of statistical evidence than was ever brought to bear on a medical subject.”42 This chapter has focused on Snow’s assessment of the relationship of London cholera to municipal water supplies, but MCC2 also contains an extended description of a level B incident that has become much more celebrated than the south London study: an outbreak of cholera in Golden Square that killed 500 people living within 250 yards of a single pump, doubling the number of deaths in the entire metropolis during the first days of September 1854.

Notes 1. Halliday, The Great Stink of London, 18–24. 2. Trench and Hillman, London under London, 83–90. 3. Halliday, The Great Stink of London, 34–38; Luckin, Pollution and Control, 11–20. 4. “After 31st August 1855, it shall not be lawful for any company to supply London with water from any part of the Thames below Teddington Lock, or from any part of its tributary streams below the highest tidal point”; Act, 15 & 16 Vict. cap 84, quoted in UK GRO, Weekly Return (19 November 1853). A special one-year extension was granted to one water company, the Chelsea Company; UK GRO, Weekly Return (3 December 1853). 5. Snow, “Cholera and the water supply” (1856), 240. 6. Anonymous review of MCC, in LMG 44 (1849): 466–70; anonymous review in Lancet 2 (1849): 318. 7. Snow, “Mode of propagation of cholera” (1851); “Prevention of cholera” (1853). Only the Newcastle experience in 1853 offered support for his hypothesis at the metropolitan level. When, during that epidemic, the local authorities began to use water directly from the sewagecontaminated River Tyne, mortality rose; when that practice ceased, mortality fell as had happened in York during the 1848 epidemic. 8. Snow, On the Mode of Communication of Cholera, 2nd ed., cited parenthetically in the text as MCC2. In addition Snow added a twenty-four page appendix containing information about cholera deaths and water supply to the houses where the deaths occurred during the first four weeks of the epidemic.

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9. UK GRO, Weekly Return. The data reflected death certificates compiled by registrars through the week ending the Saturday prior to the date of publication; thus the Weekly Return of 19 November contained information gathered through the week ending 12 November. 10. UK GRO, Weekly Return 14 (26 November 1853). 11. Farr, Report on the Mortality from Cholera in England, 1848–1849, lix, lxi–lxvi. 12. UK GRO, Weekly Return 14 (19 November 1853), supplement. 13. UK GRO, Weekly Return 14 (26 November 1853), cited by Snow, MCC2, 68. 14. It is traditional in epidemiology to refer to opportunities to study the influence on disease of large changes in the environment as “natural” experiments, but Snow does not use this term, although he does speak of the study of contrast in water supplies as a “grand experiment” (MCC2, 75). Simon was later to refer to such phenomena as “popular experiments”; “Experiments as a basis of preventive medicine,” Public Health Reports 2: 589–614. 15. On 5 August 1854 Snow submitted a letter to the editor of MTG which suggested a source for the 1854 London epidemic. Responding to a notice about cholera on British ships in the Baltic fleet, he deduced, with Sherlock Holmes-like finesse, that the outbreak must have been communicated from drinking water in the Baltic, which, he claimed, was fresh in early summer and preferred by sailors to water stored on shipboard in casks. Because the British ships had no communication with the shore, the only other source of cholera would have been from captured vessels from the cholera-infected towns of Cronstadt or St. Petersburg. Because the Lancet had reported that cholera was restricted to the larger vessels that proceeded up to Cronstadt, whereas the capture of prizes was engaged in only by the smaller steamers, Snow identified Baltic water as the most likely source. He also thought that cholera was imported to London in July 1854 by mariners returning from the Baltic. As in 1849, Snow reminds his readers, cases early in the epidemic were noted in individuals living on the Thames or linked to shipping, a sure sign that water was a key mode of transmission; Snow, “Cholera in the Baltic fleet,” (12 August 1854). 16. A paired set of letters from Snow, published in MTG in September and October 1854, offer preliminary analyses of the epidemic, but virtually the entire content of these letters is reproduced in MCC2; See “Communication of cholera by Thames water”; and “On the communication of cholera by impure Thames water.” 16a. Snow soon included another subdistrict, Sydenham, in the Lambeth Company watershed for a total of thirty-two. 17. Snow admitted that the absence of cholera from these rather favored suburban locations was not a very strong test of his hypothesis, as their “freedom from the epidemic might be attributed to other causes than the mere absence of the polluted water”; “Communication of cholera by Thames water,” 247. Snow anticipated at least one of his critics. In a review of MCC2, E. A. Parkes pointed to what could be considered favorable social and geographical factors in parts of the Lambeth area compared to that of S&V in general; British and Foreign Medico-Chirurgical Review 15 (1855): 449–63. 18. In the late months of 1853, Farr continued to come close to Snow’s theory without ever accepting it fully. Farr concluded that after adjusting for his favorite influence, elevation, “a large residual mortality remains, which is fairly referable to the impurity of the water.” For Farr, water remained just one influence. “Its fatality bears a certain relationship to the impurity of the soil, the water, and the air”; UK GRO, Weekly Return 14 (3 December 1853). 19. According to Christopher Hamlin, no textbook of clinical epidemiology existed at the time; private communication. 20. “Just as Snow’s ability to posit an appropriate etiological agent was a product of changes both scientific and technological, so equally was his epidemiological reasoning a product of


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the multiple aspects of change which had taken place in the first half of the nineteenth century . . . [including the creation of the Registrar-General’s Office]. It would be hard to imagine a mid-eighteenth-century student of epidemic disease determining individual cases and then plotting them on street maps. By the mid-nineteenth century, Snow was only one among a number of physicians who carefully mapped individual cholera cases in recording and analyzing the history of local epidemics”; Rosenberg, Explaining Epidemics, 119. However, Snow was particularly interested in statistical analyses of deaths rather than cases. 21. “Observing, therefore when the cholera returned in 1854, that there was the same advantage in favor of the districts partly supplied with water from Thames Ditton, I determined to make an inquiry, the idea of which I had previously entertained”; Snow, “Cholera and the water supply,” (1856), 241. His pause in July and early August is not explained in MCC2: “When cholera returned to London in July of the present year, however, I resolved to spare no exertion which might be necessary to ascertain the exact effect of the water supply” (76). Only a few lines later he noted, “I commenced my inquiry about the middle of August” (76). This date is confirmed by Snow’s first report of his investigation, in which he stated that he had been undertaking house-to-house inquiries for ten days. The report was a letter to the editor without a precise date. Because it was published in the issue of 2 September, he probably penned it on 26 or 27 August; see Snow, “Communication of cholera by Thames water.” His “exertions” from mid-July to mid-August appear to have been solely of a statistical nature. Perhaps Snow was not yet aware of the great dangers of delaying such an inquiry, as many prospective informants often fled soon after an area was afflicted. 22. Snow, “Cholera and the water supply” (1856), 241. The first published report of Snow’s awareness of the intimate intermingling of the pipes and supply was in September; Snow, “Communication of cholera by Thames water” (1854). See also MCC2, 76. 23. According to our reconstruction of the chronology, Snow could hardly have compiled his data and spoken with Farr until approximately 19 August 1854. 24. At the time Snow was unaware that this large and easily demonstrable difference in salinity between the two water sources depended on weather conditions. He originally supposed that the high salt content of S&V water came from sewage but later learned from Mr. Quick, an engineer at S&V, of the tidal backflow from the North Sea into the Thames, which was exaggerated under the hot and dry conditions that characterized the first months of the epidemic; MCC2, 95–96. Snow himself tested water from the Thames at Hungerford on three dates in November 1854, two months after his investigations, and found that the sodium chloride concentration varied from 5.8 grains to 63.3 grains per gallon. He also noted that S&V water tested in 1851 had been found to have only 1.99 grains per gallon. Had that salt concentration been obtained during the epidemic, Snow’s chemical test might not have reliably distinguished the two water sources. In short, Snow was lucky and acknowledged as much: “for throughout all the dry weather, which lasted whilst my inquiries were being made, a mixture of the sea water extended farther up the Thames than usual”; “Cholera and the water supply” (1856), 242. 25. Snow, “Communication of cholera by Thames water” (1854), 247. He noted in this preliminary statement (written at the end of August) of his findings in four subdistricts that the companies had sent returns to Parliament and the Board of Health that included the total number of houses they supplied by district, at a minimum. Early in October he thought he would soon have data on houses supplied for each subdistrict; Snow, “On the communication of cholera by impure Thames water” (1854), 365. 26. Snow, “On the communication of cholera by impure Thames water” (1854), 366. 26a. “But as the number of houses which they supplied in particular districts was not stated, I found that it would be necessary to carry my inquiry into all the districts to which the supply of either Company extends . . .” (MCC2, 78–79).

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26b. Davey Smith reminds us that E. A. Parkes noted in 1855 that Snow diluted the significance of the “grand experiment” when he expanded the inquiry beyond the sixteen subdistricts in which both companies supplied water: “on first reading . . . we thought that the deaths referred to took place only in the district with the intermingled supply. . . . But on reperusing the passage, we found that these deaths had taken place in all districts supplied by the two companies, separately or conjointly”; British and Foreign Medical Review 15 (1855): 461, and Davey Smith, “Behind the Broad Street pump,” 925. But neither Parkes nor Davey Smith comment on Snow’s reason for expanding his south London study to thirty-two subdistricts—he lacked the required denominator data (the precise numbers of houses supplied in each subdistrict by each company) to analyze the co-mingled subdistricts alone. 27. John Joseph Whiting was born in 1827, the son of an apothecary–surgeon, in King’s Lynn, Norfolk. After apprenticing with his father, he took the required lecture courses in London and completed eighteen months of hospital experience at St. Bart’s. He failed in his first attempt at the LSA in 1850, passed the following year, but his license did not permit him to practice within ten miles of London; Dee Cook, e-mail to David Zuck, 12 April 2002. Zuck has discovered that Whiting lived in Cambridge in 1856 and in King’s Lynn in 1860. However, he apparently never registered with the General Medical Council set up under the Medical Act of 1858, although he may have practiced anyway; Medical Directories for 1856, 1860, 1861. LAC, or Licentiate of the Apothecaries’ Company, was a variant of LAS. 28. Snow made minor errors that assigned S&V five more cases in those three weeks than a more precise calculation would have produced. In Table 8 of MCC2, he applied the same percentage of cholera deaths in each S&V neighborhood associated with S&V water as he found during the first four weeks of the epidemic (given in Table 7 of MCC2). His calculation was exact for eight of the ten neighborhoods for which data were unavailable during the following three weeks, but using this algorithm, our computation yields one case less to S&V water in St. Olave and four fewer cases in St. James. 29. We use the figure, 658 deaths, given by Snow in 1856; “Cholera and the water supply in the south districts of London, in 1854” (1856), 251 (Table 1). This is twelve fewer than suggested by Table 8 in MCC2, 85. The slight variation is explained if in the latter table one subtracts Clapham from Snow’s count (it has an asterisk indicating that Whiting investigated there) and adds Wandsworth and Putney (both in the S&V-only watershed, and lacking asterisks) to Snow’s workload. The resulting figures match the number of deaths that Snow attributes to each of them in Tables 1 and 2 in 1856. 30. Ellis, CB, 335–44. During what was likely his busiest period of house-to-house investigations, Snow traveled to Manchester on Sunday, 17 September, to administer chloroform to the sister of a physician. However, he did not administer anesthesia at all from 22 September to 1 October. Snow does not tell us precisely when he conducted his investigation, but the report of the forty-four deaths to 12 August that he investigated in Kennington and thirty-six additional deaths to 19 August in Waterloo were reported on 2 September in MTG, while all of his personal investigations along with those of Whiting and Farr’s registrar’s of deaths to 26 August were reported in a letter sent on 2 October to MTG. It seems safe to conclude that Snow’s investigations took place from the middle of August until the end of September 1854. 31. Table 11 in MCC2 introduces as a denominator the population estimated to live in those houses instead of the number of houses supplied by the two companies, but the cholera death ratio is not altered by this change, as the GRO (the source of these population estimates according to Snow) appears to have multiplied the number of houses in both groups by 6.655 to obtain the population. 32. Snow states that he obtained these data from the First Report of the Metropolitan Sanitary Commission, 1847; MCC2, 57. 33. Only one other company, the Chelsea, drew water from that part of the Thames. “But


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this company, which supplies some of the most fashionable parts of London, took great pains to filter the water before its distribution, and in so doing no doubt separated, among other matters, the greater portion of that which causes cholera” (MCC2, 64). The S&V and Lambeth companies “professed to filter the water,” but Arthur Hill Hassall examined samples and identified “hairs of animals and numerous substances which had passed through the alimentary canal” in S&V water; Hassall, Food and Its Adulterations, 90. There was no reason to think it had been any better during the epidemic. 34. This episode was also detailed in Snow’s two cholera publications in the autumn of 1853. See “On the prevention of cholera” (1853) and “The water supply at Newcastle,” Times, 11 November 1853. See Luckin, Pollution and Control, 69–86, on additional context for Snow’s investigations. 35. Snow, “On the communication of cholera by impure Thames water” (1854). Advertisements that MCC2 was available for purchase from the publisher, Churchill, were printed early in January, 1855. A note in which George Budd thanks Snow for sending him a free copy is dated 3 January 1855; Clover/Snow Collection, VIII.4.i. 36. Snow, “On the communication of cholera by impure Thames water,” (1854), 365. 37. Ibid. 38. Snow, “Communication of cholera by Thames water” (1854), 247. 38a. In Simon’s formulation, “An experiment . . . has been conducted during two epidemics of cholera on 500,000 human beings. One half of this multitude was doomed in both epidemics to drink the same fecalized water, and on both occasions to illustrate its fatal results. While another section . . . was happily enabled to evince by a double contrast the comparative immunity which a cleanlier beverage could give”; Report of the Last Two Cholera Epidemics, 9. 39. Snow, “Cholera and the water supply in the south districts of London in 1854” (1856), 255. The first five tables in this paper show data for the thirty-two subdistricts included in MCC2. But he dropped Sydenham from his analysis in the sixth table, presumably because he found virtually no reliable data there. 39a. In Snow’s 1856 article, Table 1 includes the subdistricts personally investigated by Snow; he figured that the mortality rates were 47.2 per 10,000 for S&V subdistricts and 6.6 for Lambeth—a ratio of 6.94. Davey Smith argues that Snow reported a lower death ratio (6.9) for the sixteen co-mingled subdistricts than he had earlier reported in MCC2 for all thirty-two subdistricts during the same period (8.5), a difference that would confirm Parkes’ criticism that Snow confounded matters by enlarging the area to include all subdistricts served by the two companies; “Behind the Broad Street pump,” 925. But Davey Smith’s reasoning is suspect if he derived the 6.9 ratio from Table 1 of the 1856 article, since it does not include Clapham (a subdistrict with co-mingled pipes) and does include Wandsworth and Putney (both in the S&V watershed). Water-supply specific cholera death rates for the sixteen comingled districts during the first seven weeks of the epidemic, as calculated from Tables 1 and 2 of the 1856 article, are 49.4 and 6.7 respectively, yielding a mortality ratio of 7.3. In short, it appears that Snow did overestimate the difference in risk when he expanded his inquiry, but not as much as Davey Smith suggests. 40. The calculation of expected death rates based on a simple predictive model is a staple of analytic epidemiology, particularly for studies relying on population death rates from vital data. In this instance Snow is, in effect, performing an indirect standardization of cholera death rates by water supply. His thesis was that if one took account of water supply, little variance in death rates within subdistricts would remain. That variance was the difference between the expected rates calculated from Snow’s model and the actual rates. This may be the first use of indirect standardization in epidemiological research. 41. Snow, “Cholera and the water supply in the south districts of London in 1854” (1856),

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248. Snow compared actual rates of cholera in 1854 with rates predicted by assuming that the fraction of the population in each subdistrict exposed to Lambeth water will be 27 per 10,000 (the overall Lambeth rate) and the fraction exposed to S&V water will be 160 per 10,000 (the overall S&V rate). We calculate that the correlation between the predicted and actual rates in the thirty-one subdistricts is 0.745. Two subdistricts, Putney and Wandsworth, had death rates much lower than predicted, apparently because relatively few residents depended upon the piped water for drinking. If we remove these two outliers the correlation coefficient for the remaining twenty-nine subdistricts is 0.878, indicating that Snow’s water-supply based model explains 77% of the variance in cholera mortality. Snow was not unique in his statistical approach. In 1852 Farr used subdistrict analysis on cholera mortality during the 1848–49 epidemic and concluded that altitude was the single most critical variable in cholera mortality. Our analysis of thirty of the subdistricts analyzed by Snow in 1854 resulted in a correlation of 0.53 between altitude and cholera mortality, compared to 0.745 for water supply. In South London water supply and altitude were strongly correlated during this period, with S&V water supplying almost entirely low lying areas, while Lambeth water also went to relatively higher subdistricts. 42. Ibid.

Chapter 11

Broad Street

Monday, 28 August 1854 ARAH LEWIS’S FIVE-MONTH-OLD DAUGHTER had never been very healthy, nor had Mrs. Lewis herself, for that matter. Unable to suckle the child, she had to feed her from the bottle on boiled ground rice and milk. She had fed her son that way several years before, and he had been extremely sickly and had died at ten months. For a while it looked as if the little girl was going to do better, but then she had a bout of diarrhea in June. Dr. William R. Rogers of Berners Street treated her, and she was better after about five days. This morning Mrs. Lewis had to send for Dr. Rogers again. The same diarrhea was back, he said—pale or green, slimy, watery, offensive-smelling stools. Now the baby was also vomiting, unable to keep down food or medicine.1 The Lewis family lived in the back parlor at 40 Broad Street, an attached multistoried house of eleven rooms. They were relatively fortunate; nineteen or twenty people lived in the house, while elsewhere in the district four or five to a room was not uncommon. Even so, the back of the house was near the yard of the public house at 7 Cambridge Street, and the bad smells from the water closet there had been bothersome for a long time.2 A century earlier the streets around Golden Square, St. James’s, Westminster, were part of fashionable London, and the houses had originally been erected as single-

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family town dwellings.3 As people of fashion moved to the west and the north, Golden Square became the abode of the working poor; the houses were subdivided and rented out by the room (Fig. 11.1). “The families of labourers, mechanics, and journeymen” was how the majority of the residents of the area were later described (CIC, 51). Mrs. Lewis’s husband was a policeman. Other families in the remaining rooms at 40 Broad Street were headed by a carpenter and a tailor, among others.4 Poverty, hunger, and filth were everywhere in evidence, although the area was far from being the most squalid in London. There were also a number of cow yards, slaughterhouses, and similar animal enclosures in the neighborhood, adding to the offensive odors.5 Since the baby’s diarrhea had commenced at 6:00 that morning, Mrs. Lewis had been soaking the infant’s soiled diapers (napkins, or “nappies”) in buckets of cold water. Before washing the diapers she poured the water into the cesspool in the front area of the house (CIC, 159, 164). Above her, at street level and a few feet to the east, people gathered around the water pump or the pub next door. Strangely, Mr. Thomas Lewis absolutely refused to drink the pump water and would not have it in the house (CIC, 126). In general, the cold water from the pump near the corner of Broad and

Figure 11.1. 16-21 Broad Street, 1888; currently 48-58 Broadwick Street (adapted from Frederick Calvert’s watercolor, City of Westminster Archives, new house numbers from Sheppard, St. James Westminster, 2: 216).

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Cambridge Streets was held in high esteem by the residents of Golden Square. Some who lived a number of streets away, much nearer to another pump, still came to Broad Street for their water. No one, including Dr. Rogers, suspected that the infant’s diarrhea might be a premonition of cholera (CIC, 164). In London’s two earlier epidemics, Westminster and Golden Square had been largely spared. Now, as on those earlier occasions, the worst of the epidemic was raging south of the Thames, where John Snow was at work on a house-to-house study of cholera deaths. He had set aside an entire week for the survey. Since 24 August, when he had administered chloroform for Mr. Hewett at St. George’s Hospital while he removed a tumor from a woman’s breast, Snow had had no calls upon his anesthesia services (CB, 342). The date 26 August 1854 marked an important turning point in Snow’s south London study. Before that date Snow and his assistant, Mr. Whiting, had investigated all deaths. After that date the district registrars were instructed by William Farr to inquire into the water supply of each house where a cholera death was reported. Nevertheless, Snow still had a backlog of onsite inspections from deaths that had occurred before August 26, and he needed time to compile and analyze his data.6

Tuesday, 29 August 1854 Mrs. Lewis’s little girl continued to vomit and to pass copious stools (CIC, 164). The Eley brothers owned and managed the percussion cap factory two doors away at 38 Broad Street. Their father, who had founded the business, had long lived in Broad Street nearby. After his death their mother, Susannah, now aged fifty-nine, moved some miles north to rural Hampstead, but she remained partial to the water from the Broad Street pump. As a cart had to go every day from the factory up to Hampstead, the Eley brothers made sure that a bottle of water from the pump was carefully packed for delivery to their mother’s home. Out of respect for their parents’ preferences, the brothers also made sure that two tubs of the pump water were kept fresh inside the factory as drinking water for the 200 workers.7

Wednesday, 30 August 1854 Mrs. Lewis’s little daughter was worse. Early in the day the baby had rather abruptly stopped passing stools and vomiting. Dr. Rogers had noted no fever or cramps, nor did the infant seem blue or cold. Even so, she appeared thoroughly listless and exhausted, and overall the doctor was not at all optimistic (CIC, 164). Nearby, on Berwick Street, Rev. Henry Whitehead was returning to St. Luke’s Church after a series of visits and errands. To reach it he had to wend his way among stalls and barrows selling fish and eels, fruit, cat’s meat, old rags, and bones.

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The twenty-nine-year-old clergyman, son of a Kent schoolmaster, had taken his B.A. at Lincoln College, Oxford, in 1850 and the following year had been ordained a deacon. His first appointment as an assistant curate was at St. Luke’s, a post which, according to the vicar, Mr. Stooks, was “for such as care more for the approval than the applause of men.” Unmarried, Whitehead was sharing lodgings with his brother in nearby Soho Square.8 He was considered an intelligent and diligent young man, devoted to his clerical work, a good companion, and a lively storyteller.

Thursday, 31 August 1854 The atmosphere was unusually hazy, although the sky was clear. In the latter part of the day the wind shifted from southwest to northeast.9 The day was much the same as the previous one for Mrs. Lewis. Her little girl remained largely free of diarrhea and vomiting but would take no food. The day was quite different for Henry Whitehead. Early in the morning he had had an urgent call to one of the houses in his parish, where four people had been seized with an attack of cholera during the night. As he left the house he found similar scenes wherever he turned. By noon he had returned to the vestry hall of St. Luke’s and there learned from the other curate and the scripture-reader that each had spent the morning in a similar fashion. Whitehead hastened out in response to fresh calls, and it was evening before he had completed his round.10 One of the many residents of the neighborhood who fell ill was Mr. G., the tailor who lived on the first floor at 40 Broad Street. His economic situation was much like that of the Lewis family, although he and his wife did not share Mr. Lewis’s aversion to the water of the street pump.

Friday, 1 September 1854 Mrs. Lewis’s little girl continued to sink into lethargy, although her diapers were still stained with urine every so often (CIC, 164). Mr. G.’s illness progressed rapidly, and he died of cholera approximately twenty-four hours after he was first seized. This pattern of disease was being repeated throughout the neighborhood: The people in this district were, no doubt, reading in the newspapers, or learning from others, that cholera had reached London, but felt . . . that they were themselves safe. On Friday morning, however, . . . people might be seen before the break of day running in all directions for medical advice. “The angel of death had spread his wings over the place,” and by midday, groups were standing in the street, looking the picture of wonder and consternation.11

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Henry Whitehead spent another exhausting day rushing the length and breadth of his parish visiting the sick and dying. He was hardly less busy than the medical practitioners of the area, “whose labours day and night in behalf of the sufferers were beyond all praise,” he later wrote.12 As he went past the top of Berwick Street, where a yellow flag now hung to warn the populace of cholera, and observed the dead carts removing the bodies, Whitehead reflected that virtually all of those he had visited the previous day were now dead.13 Cholera was raging in Golden Square. Hampstead, by contrast, with its higher elevation and more spacious and well-ventilated homes, was free of the dread disease—almost, for Susannah Eley, alone among her neighbors, had been laid low with cholera.

Saturday, 2 September 1854 At 40 Broad Street at 11 A.M., the Lewis infant died (CIC, 164). Dr. Rogers filled out the death certificate: “Exhaustion, after an attack of Diarrhœa four days previous to death” (CIC, 159). There was also mourning in Hampstead. Susannah Eley died after a sixteen-hour illness. Quite a number of the workers at the percussion cap factory also were coming down with cholera (MCC2, 43). Whitehead and his fellow clergy had another hectic and depressing day as the disease seemed to be raging without letup. Even busier than Whitehead was Florence Nightingale. She had been at the Middlesex Hospital for about a month to superintend the nursing of the cholera patients there. “Patients [were] brought in every half hour from the Soho district, Broad Street, etc., . . . chiefly fallen women of the district. . . . The prostitutes came in perpetually—poor creatures staggering off their beat! It took worse hold of them than of any.” Miss Nightingale was “up day and night, undressing them . . . putting on [cloths soaked in] turpentine. . . .” She had reportedly not had any rest all night and was on her feet all day that day as well.14 John Snow had to put aside his south London work when he was called upon by Mr. Duffin to administer chloroform to a three-year-old girl from Blackheath for amputation of a toe (CB, 342).

Sunday, 3 September 1854 Snow had no anesthetics to administer, yet for the first time in weeks his attention was not focused on his south London study. There was much talk about the great outbreak of cholera in Golden Square, which seemed to have begun on Thursday or Friday. Snow knew the area well—it was immediately to the west of the Soho district where he had lived as a medical student and then practiced while living in Frith

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Street. It was a mere five minutes’ walk to Broad Street from his current home in Sackville Street. As he heard more details, Snow came to suspect that the pump in Broad Street, the most popular in Golden Square, was the culprit. A sudden, severe outbreak in a relatively localized area meant that a street pump, drawing water directly from the ground, had become contaminated. The two companies providing piped water to the houses in this region, the Grand Junction Company and the New River Company, supplied relatively clean water, and their customers had been almost entirely free of cholera. The current outbreak reminded him of several earlier incidents that he had carefully studied: “In the autumn of 1848, when cholera had just commenced in London, a number of cases occurred about Bridge Street, Blackfriars; and it was found by Mr. Hutchinson, Surgeon, of Farringdon Street, that the well of St. Bride’s pump had a communication with the Fleet ditch, up which the tide flows.”15 There were similar accounts of point-source outbreaks in the official government report on the 1848–1849 epidemic. A sudden, violent outbreak in a street in Manchester was attributed to a pump well into which a stopped-up sewer had leaked. In the thirty houses using the pump, twenty-five people had died, while in sixty nearby houses with another water source, there was no cholera at all.16 In Lambeth, in south London, an isolated court had several cases of disease, including two of cholera. The local surgeon had examined the court’s pump and found the water discolored and smelling like a cesspool. The enterprising surgeon removed the piston of the pump, and no further cholera occurred in the court.17 In the evening Snow went directly to the Broad Street pump (Fig. 11.2) and took water samples for visual inspection. The water was clear, which surprised him because he expected to find some cloudiness, evidence of organic impurities (CIC, 98–99). So he next inspected the water of four nearby street pumps, those in Warwick Street, Bridle Lane, Vigo Street, and Marlborough Street. He found some impurities, white flocculent particles evident to the naked eye, in each, the greatest quantity in the Marlborough Street pump, and passers-by told him that the neighborhood residents usually avoided that pump altogether and used the Broad Street pump instead. For Henry Whitehead this day went just like the preceding three. He was constantly on the move, going from house to house, everywhere finding scenes of dismay and devastation. When he ran into any of the local physicians, he heard the same general comments. The cholera was striking with few premonitory symptoms, the sufferer going from normal health to complete collapse in a matter of hours. Medicine’s usual remedies were proving to be singularly unavailing.18 It was not until eleven o’clock at night that Whitehead finally had time to relax. He took advantage by treating himself to a drop of brandy with some cold water drawn from the Broad Street pump (CIC, 156).

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Figure 11.2. Broad Street pump, modern replica; Broadwick Street, London (photograph by authors).

Monday, 4 September 1854 Mrs. G., the widow of the tailor at 40 Broad Street, developed symptoms of cholera (CIC, 161). The Times reported the happenings in Golden Square in the form of a notice from the General Board of Health. Henry Whitehead continued on his dismal rounds, but despite the grim scenes he witnessed, more hopeful thoughts occupied his mind. He was impressed with the calm among most residents in the neighborhood. He had heard of numerous acts of great generosity and courage as people tended to the sick, in some cases total strangers caring for others with complete disregard for their own safety.19 John Snow thought matters over and was not satisfied with the results of his pump water inspection of the previous evening: “Further inquiry . . . showed me that there was no other circumstance or thing common to the circumscribed locality in which this sudden increase in cholera occurred, and not extending beyond this

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locality, except the water of the [Broad Street] pump.”20 After administering chloroform for Mr. Cartwright while that dentist extracted two teeth (CB, 343), Snow went back and reexamined water from the Broad Street pump. Again he saw the white particles, and this time he did a chemical test and detected a large quantity of chlorides, which he took to be evidence of impurity. Not trusting his own microscopic skills, he took a sample of the water to the eminent microscopist Dr. Arthur Hill Hassall.21 Hassall reported that he saw a good deal of organic matter and some oval “animalcules” that seemed of no importance except to signal the presence of the organic matter on which they fed. Perhaps there were more organic impurities in the water than Snow had originally assumed. Snow returned to the Broad Street neighborhood and began to ask more questions of the inhabitants. No one had seen a change in the character of the water just before 31 August, when the outbreak had begun. One of the Eley brothers said he had noticed for quite a while that the water became offensive if it sat for about two days. Farther afield, on Poland Street, an informant claimed that the water would form a film if it remained motionless for a few hours (CIC, 99).

Tuesday, 5 September 1854 Mrs. G. died around 10 a.m. at 40 Broad Street having lasted only a little longer than her husband once her attack began (CIC, 161). The clergymen at St. Luke’s had much to talk about when they met for their regular noontime gathering. There had been a definite decrease in the number of deaths, and the new cases of cholera were both fewer and less severe.22 As Whitehead reflected on the cases of recovery he had seen in the past several days, he was struck by the victims’ intense thirst and how often some had sent to the Broad Street pump for fresh water. He had visited a servant woman daily who had had a severe attack on Friday, soon was in a state of near-total collapse, but had ultimately rallied, drinking great quantities of the pump water all through the illness. On Sunday one boy who recovered had drunk ten quarts, and a girl in similar straits drank seventeen (CIC, 136). The president of the General Board of Health, Sir Benjamin Hall, visited Broad Street that morning as part of a tour of the affected areas to inspect the “sanitary and preventive measures” that had been taken. The next day’s Times reported, “Groups of people formed themselves in the streets, and evinced much gratitude at his presence.”23 The Board of Health had just been through a serious shake-up. Edwin Chadwick, the main force behind the board since it had been formed in 1848, had stepped on too many toes in the business and medical communities in his zeal for sanitary reform. On 31 July Parliament had used the expiration date of the authority of the previous board as an opportunity to dismiss Chadwick and his allies. Hall, a member of Parliament, had been put in charge of the newly reorganized

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board, with a smaller staff and reduced authority to ensure that the board did not stray from its Parliamentary mandate.24 John Snow had no anesthesia work and went back to interviewing the residents of Broad Street. His patient inquiries turned up Mr. John Gould, “the eminent ornithologist,” who lived just up the street from the pump and routinely drank the water. He had been away from home, had returned on Saturday, and immediately sent for some of the water, but despite it being freshly drawn and perfectly transparent, he noticed an offensive smell. His assistant noticed it, too (CIC, 100). Despite the great amount of negative testimony, this one positive assertion from a scientific observer of a recent change in the water was enough to spur Snow forward. He decided that his inquiry now required statistical methods rather than chemistry or microscopy. He hastened to the General Register Office to ask for a list of cholera deaths in the districts of St. James’s and St. Anne’s, Soho. William Farr’s staff were then tabulating the week that ended on Saturday, 2 September, during which they had recorded eighty-nine deaths from cholera in that quarter of London. The daily distribution told the same story that Snow, Whitehead, and others had already observed—six deaths occurred during the first four days of the week, followed by four on Thursday, 31 August alone, and seventy-nine on Friday and Saturday. Snow decided to eliminate the first six deaths as not properly being part of the great outbreak and focused his attention on the remaining eighty-three. Armed with the list of cholera deaths showing the address of each victim, Snow returned to Broad Street. He did a mental calculation to determine the point on each street from which it would be closer to walk to another street pump than to the pump in Broad Street. He observed from the addresses that seventy-three of the eighty-three deaths had occurred in residents of houses closer to the Broad Street pump than to any other. Snow next made inquiries at the houses on his list located outside of the area of the Broad Street pump. He discovered that eight of these ten deaths occurred among people known or thought to have drunk the Broad Street water. Some went to that pump by preference, others were children who went to school near the pump. Snow then turned to the addresses located inside the pump’s area as he had calculated it. He found in sixty-one cases that the deceased person drank the pump water. In another six cases every possible informant had either died or fled. In only six cases was Snow informed that the victim was known not to have used the pump water. Snow concluded from his data that if he eliminated those known to have drunk the water from the pump, the number of cases of cholera could easily represent the background level of sporadic cases occurring elsewhere in the metropolis. It seemed clear to him that there had been “no particular outbreak or prevalence of Cholera in this part of London except among the persons who were in the habit of drinking the water of the above-mentioned pump well.”25

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Wednesday, 6 September 1854 The Times published the Weekly Return of the Registrar General, which included the eighty-nine deaths of which Snow had been informed the previous day. The summary noted, “On the north side of the Thames there has been a remarkable outbreak in the St. James’s district.”26 The staff at St. Luke’s held their customary daily meeting in the vestry at noon. There were still many visits to be made, even though the cholera thankfully seemed to be waning. Whitehead was concerned: the scripture-reader, James Richardson, a Scotsman and retired grenadier guard, was not there. He hastened to Richardson’s house and found the sergeant in bed with cholera. “I knew you would come,” said Richardson.“And I knew how I should find you when I did come,” Whitehead replied. The sergeant was calm in the face of the threat: “I shall look up to my God, and though he slay me, yet I will trust in him.”27 Whitehead learned that the sergeant had been suffering premonitory symptoms for the past day and a half, which he had not mentioned to anyone. The sergeant also recalled that on 2 September, quite contrary to his usual custom, he had drunk half a pint of water from the ladle at the Broad Street pump.28 Snow was busy with his practice, first administering chloroform to a linendraper in the Edgware Road for ligation of hemorrhoids. The man had lost a good deal of blood and had a bounding pulse. Nonetheless, Snow was relieved to report that the chloroform produced no faintness or depression. The next operation, a tooth extraction in Hanover Square, was much simpler (CB, 343). He then returned to his detailed inquiries near Golden Square. He visited one of the small coffeeshops near the pump, frequented by mechanics, where the pump water had been the main beverage supplied with dinner. The proprietor mentioned that she knew of nine of her regular customers who had so far died of cholera (Fig. 11.3) (CIC, 103–04).

Thursday, 7 September 1854 The General Register Office had not yet received the death returns for the week after 2 September, but local observers knew that the cholera around Golden Square, though now declining, had exacted a very high toll. The numbers meant little until one realized how very few city blocks made up the affected area. A walk of less than three minutes sufficed to take one from the epicenter of the outbreak to a region mostly free of cholera.29 Whitehead could stand at the front door of St. Luke’s and point to four houses, at an average distance of fifteen yards, that had collectively lost thirty-four inhabitants in four days.30 The official body most directly responsible for local health matters in St. James’s parish in 1854 was the Board of Governors and Directors of the Poor, rather than

MARSHALL STREET #28 Edw. Malton, Surgeon; Wm. Ridley, Furrier 5 residents, 0 deaths

12 residents, 3 deaths #29 Mary Hooper; Grocer 10 residents; 1 death #30

Patrick Quigley, Tailor; #27 Robert Bonner, Bootmaker 7 residents, 0 deaths

Henry Cooke; Straw bonnet maker #31 15 residents, 3 deaths

Robert White, Billiard table maker #26 18 residents, 2 deaths

Eliza Grimmond, Baker #32 14 residents, 2 deaths

Edward Brown, Blacking mfgr. #25 ? residents, 0 deaths

William Peel, Grocer 19 residents, 3 deaths #33

Ersser, Lapidary #24 Anne 14 residents, 1 death

Edmund Tisdall, Saddle tree mfr. #34 7 residents, 0 deaths Edwin Bell, Engraver 7 residents, 1 death #35

Thomas Bennett, Plumber & painter #23 18 residents, 1 death

Eliz. Main, Ironmonger #36 11 residents, 2 deaths

#22

William Pollit, Trimming seller 29 residents, 5 deaths #37

John Haws, Wardrobe dealer #39 19 residents, 3 deaths Theo. Hammond, Boot tree mfr. #40 20 residents, 5 deaths

CAMBRIDGE STREET Cambridge St. 23 residents, 2 deaths

#6

50 residents, 5 deaths #41 Engraver, carpenter, dyer 15 residents, 2 deaths #42 26 residents, 3 deaths #43 Alexander Jeffrey, Veterinarian #44 29 residents, 2 deaths Arthur Abbott & Sons, Builders #45 28 residents, 5 deaths

NEW STREET

#7

BROAD STREET

Cambridge St.; Newcastle-on-Tyne pub 6 residents, 1 death

DUFOURS PLACE Pump-well

Eley Brothers, Percussion cap mfrs. #38 150 workers, 16 deaths

Crown pub, J. F. Hallatt ? residents, 0 deaths

#21 Griffiths, Lodging House ? residents, 0 deaths John Gould, FRS #20 5 residents, 0 deaths #19 28 residents, 2 deaths William Stannard, carver/Gilder; #18 John Williams, Tailor 16 residents, 3 deaths Samuel Carlson, Jeweler #17 25 residents, 2 deaths Thomas Davis, Die sinker #16 20 residents, 6 deaths Angelo Pontecorboli, Warehouse #15 3 residents, 1 death #14 20 residents, 2 cholera cases, 0 deaths

POLAND STREET #13 Francis Stringer, Undertaker 0 residents, 0 deaths #12 McAuliffe & Ross, Leather case mfrs. 20+ residents, 5 deaths #11 William Beal, Timber dealer 11 residents, 1 death #10 John Greenfield & Son, Machinists 23 residents, 3 deaths

#8

C. Ash & Sons, Mineral teeth mfrs. 42 workers, 6 deaths

#7

James Smith, Umbrella maker 10 residents, 1 death

#6

William Dutton, French water gilder 20 residents, 1 death

N

➲

#9

⎧ ⎨ ⎩

Lion Brewery Edw. G. & John Huggins #50 80 workers, 0 deaths

Figure 11.3. Diagram of the western portion of Broad Street showing principal businesses at each address, number of residents, and cholera deaths (adapted from GBH, Appendix to CSI, 343–46; Watkin’s London Directory for 1855, 695).

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a Board of Guardians. The parish had been exempted from implementation of the New Poor Law. Instead of in-door relief provided in a union workhouse, St. James offered its poor a combination of out-door relief or admission to a small local workhouse. The Board of Governors handled day-to-day affairs and reported to the parish vestry. The governors and directors were concerned about the threat of cholera and on 14 August 1854 had voted to abandon their usual meeting protocol and form themselves into a special emergency response committee to deal with the it. It seemed during the past week as if their worst fears had been realized. As they considered at their weekly meeting what course of action to pursue next, they were notified that Dr. John Snow had respectfully requested an interview with them. He was admitted and presented an account of his investigation so far. As a result the committee issued an order that the handle be removed from the Broad Street pump.31

Friday, 8 September 1854 The order was carried out, and the pump handle was removed. The event passed totally unnoticed by the newspapers and journals of the day,32 but it was certainly noticed by the local populace, who were not pleased. The butts and cisterns in which piped drinking water was stored (because the water companies typically provided running water only a few hours each day) were coated with dirt, uncovered, and often located in “close, unwholesome, and disgusting propinquity” to the water closets and garbage cans.33 Small wonder that many supplied with piped water still preferred the Broad Street pump. Mr. Thomas Lewis, the policeman living at 40 Broad Street whose infant daughter had died on 2 September, developed unmistakable symptoms of cholera. His symptoms, however, did not seem to be progressing as fast as those of his late neighbors, the G. family (CIC, 161). The General Board of Health took the action promised earlier by Sir Benjamin Hall and issued instructions for a house-by-house medical inspection by Dr. David Fraser, Mr. Thomas Hughes, and Mr. J. M. Ludlow. The inspectors were instructed to focus on the areas of St. James where cholera was most prevalent. While Chadwick and his reformist allies on the old Board of Health had been dismissed, the further instructions to the inspectors showed that the new board was equally devoted to a miasmatic theory of cholera. The inspectors were told to investigate atmospheric conditions, the ventilation of streets and buildings, the presence of nuisances and noxious trades, bad smells in the streets (especially from sewers) and houses, privies and cesspools, the state of the basements, the floor of the house where each case had occurred, the condition and habits of the inhabitants, and the quantity and quality of water supply.34

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The General Board of Health was not alone in adopting a miasmatic view. The neighborhood was rife with rumors that recent sewer works had disturbed the soil of an ancient pit, just northwest of Broad Street, where bodies had been buried during the plague of 1665. As a local resident wrote to the Times, “Is it not therefore reasonable to suspect that . . . when the new sewer was constructed . . . , it must have most injuriously disturbed the soil, saturated with the remains of persons deposited here during the great plague . . . , and that a deadly miasmatic atmosphere has been for some months arising through the gully holes connected with this sewer, poisoning the surrounding atmosphere . . . ?”35 It was Rev. Whitehead’s turn to speak from the pulpit at St. Luke’s. There was no point in trying to talk about anything other than the cholera. Enumerating instances of God’s providence, Whitehead congratulated the poor old women, who made up a substantial proportion of the congregation, on their relative immunity from the great outbreak. Privately, he was puzzled by the disproportionate exemption of these elderly women.36

Saturday, 9 September 1854 Once again Mrs. Lewis was occupied emptying pails of water into the cesspool in the area at 40 Broad Street. Instead of her now-dead baby’s diapers, this time she was washing her husband’s soiled bedclothes. There was less noise outside her house with the handle of the pump removed.37

Tuesday, 11 September 1854 Dr. Fraser, Hughes, and Ludlow, the Board of Health inspectors, had located many sources of noxious odors. A charwoman had died of cholera at 44 Silver Street; she had kept a total of seventeen dogs, cats, and rabbits. The inspectors found most houses overcrowded, with people forced to wash, cook, and sleep in the same room. They were surprised to note that a number of deaths had occurred among temperate people of clean habits. They also found that they were not the only official inspectors in the neighborhood—they ran into Edmund Cooper, an engineer from the Commission of Sewers.38 Since the Golden Square outbreak began the commission had been besieged with criticism. As long as bad smells were held to be a cause of cholera, the sewer system was a natural suspect. Some residents, like the author of the letter to the Times on 8 September, blamed the disruption of the ancient plague pit. Others alleged that cholera deaths had been especially numerous in houses next to gully holes, the openings through which sewer gases were vented to the surface.39 Cooper had been dispatched to look into these allegations.

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Friday, 15 September 1854 Thomas Lewis still clung to life in the front kitchen at 40 Broad Street.40 Residents of the neighborhood read about themselves in the Times: The outbreak of cholera in the vicinity of Golden-square is now subsiding, but the passenger through the streets which compose that district will see many evidences of the alarming severity of the attack. Men and women in mourning are to be found in great numbers; and the chief topic of conversation is the recent epidemic. The shop windows are filled with placards relating to the all engrossing subject; and, if it be true that in a multitude of counsels there is wisdom, the good people of this parish ought to be so wise in the matter of cholera as to be quite beyond the chance of a second attack. At every turn the instructions of the new Board of Health stare you in the face. In shopwindows, on church and chapel doors, on dead walls, and at every available point appear the parochial handbills, directing the poor where to apply for gratuitous relief. The homoeopathists are not behindhand, but energetically assert their capability of putting a stop to the epidemic. An oil-shop puts forth a large cask at its door, labelled in gigantic capitals “Chloride of lime.” The most remarkable evidence of all, however, and the most important, consists in the continual presence of lime in the roadways. The puddles are white and milky with it, the stones are smeared with it; great splashes of it lie about in the gutters, and the air is redolent with its strong and not very agreeable odour. You might at first imagine that a vast amount of building was going on, but not so. The fact is that the parish authorities have very wisely determined to wash all the streets in the tainted district with this powerful disinfectant; and, accordingly, the purification takes place regularly every evening. The shopkeepers have dismal stories to tell—how they would hear in the evening that one of their neighbours whom they had been talking with in the morning had expired after a few hours of agony and terror. It has even been asserted that the number of corpses was so great that they were removed wholesale in dead-carts for want of sufficient hearses to convey them; but let us hope this is incorrect.41 The extensive use of lime in the streets (to eliminate bad smells from decaying organic matter) showed that the Board of Governors was adopting a local miasmatist position. They apparently saw no conflict between that theory of cholera spread and Snow’s hypothesis on the wisdom of removing the pump handle.

Tuesday, 19 September 1854 Thomas Lewis died of cholera after eleven days of illness (CIC, 161).

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Thursday, 21 September 1854 Snow’s letter to the Medical Times and Gazette summarizing his work on the Broad Street outbreak and the positive response he had received from the Board of Governors was in the hands of the editor awaiting publication.42 Perhaps Snow thought he was finished with Golden Square and could turn all his research attention to south London again, but he found himself back doing “shoe-leather epidemiology” in St. James. Snow now realized that the original figures he had obtained from the General Register Office on 5 September had seriously undercounted the deaths in Golden Square. He had thought that there had been seventy-nine deaths on the first two days of September, but a recount the following week, as well as information from surrounding hospitals to which Golden Square victims had been taken, raised the actual total to 197. This spurred Snow to return to do more detailed inquiries, but he immediately found himself stymied by the general flight of the population in the aftermath of the epidemic.43 Many of the houses and shops where he had hoped to ask questions were empty: “In less than six days from the commencement of the outbreak, the most afflicted streets were deserted by more than three-quarters of their inhabitants” (MCC2, 38). Nevertheless, the people he was able to interview provided much new information to support his original conclusion that the pump was the source of the outbreak. The new data took the form of both positive and negative evidence. On the positive side he found a number of ways in which residents of the area could have drunk the pump water without being aware of it. The local pubs used the water freely for mixing with spirits, and it was similarly served in coffee shops and restaurants. Several little shops put an effervescing powder in the water and sold it as “sherbet.”44 Eighteen of the 200 workers in the Eley percussion cap factory, where the pump water was made available in tubs for drinking, had died. Mr. Peter Marshall, Snow’s medical friend and associate who resided nearby on Greek Street, told Snow about seven workmen at Ash & Sons, a manufacturer of dentists’ materials located at 8–9 Broad Street. All of these men had died in their homes nearby. Marshall said that all of them had regularly drunk pump water, usually half a pint once or twice a day. Two others who worked at that factory but did not drink any pump water had only mild diarrhea. Marshall also passed along the case of an army officer who lived well outside the district but came to dine at a house in Wardour Street and had some pump water with his dinner. He developed cholera and died in a few hours. Marshall had some other interesting cases to recount, all implicating the pump, but Snow was especially fortunate to run into Dr. Fraser, one of the medical inspectors for the General Board of Health.45 Fraser told him about the case of Susannah Eley, the “Hampstead widow” who had the water from the pump brought to her every day (CIC, 102–107; MCC2, 40–45). On investigating that case further, Snow found that Mrs. Eley’s niece had been visiting her at the time of her attack and had

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also drunk some of the pump water. The niece went home to Islington, which was at that time free of cholera, developed the disease, and died. A servant in Mrs. Eley’s house drank a small quantity of the water, developed diarrhea (diagnosed by the physician as not being cholera), and lived. Snow was also indebted to Dr. Fraser for the report of the case of: a gentleman in delicate health [who] was sent for from Brighton to see his brother at No. 6, Poland Street, who was attacked with Cholera and died in twelve hours on the 1st of September. The gentleman arrived after his brother’s death and did not see the body. He only staid [sic] about twenty minutes in the house, where he took a hasty and scanty luncheon of rump steak, taking with it a small tumbler of cold brandy and water, the water being from the Broad Street pump. He went to Pentonville, and was attacked with Cholera the evening of the following day, September the 2nd, and died the next evening. CIC, 106 Snow was accumulating one case after another in which people whose only contact with the Golden Square neighborhood was the pump water and who had contracted cholera. The association seemed strong enough to postulate a cause-and-effect relationship. However, he was not content to accumulate only positive evidence in support of his hypothesis. He devoted particular effort to looking into negative evidence that at first glance appeared to discount it. In several instances further investigation of the negative evidence actually gave him additional support. For example, one unlikely sanctuary was the workhouse in Poland Street—only five of 535 inmates had died, while the houses on the adjacent streets had been hit severely. A miasmatist would have had a hard time explaining this, especially because the workhouse residents, being poorly nourished, sickly, and probably of indifferent morals, might be thought to be more predisposed to disease. Snow found that the workhouse had its own well and also took piped water from the Grand Junction company. He calculated that had the death rate at the workhouse been equal to that of the adjacent streets, there would have been more than fifty deaths.46 Another interesting sanctuary was the Lion Brewery in Broad Street. Miasmatists thought that alcohol increased susceptibility to cholera, yet none of the seventy-odd workers at the brewery was known to have died. The proprietors, Edward and John Huggins, told Snow that they supplied their workers with New River Company water and also had their own deep well on the premises. However, that hardly mattered; to their knowledge, because the men were allowed an allotment of malt liquor, they did not drink any water at all, in apparent defiance of the third precaution against cholera published by the General Board of Health on 4 September. Thus, in two important instances Snow found that the factors identified as important by miasmatists—breathing the supposedly contaminated epidemic atmosphere of the

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neighborhood and suffering from various predisposing factors—were much less important in explaining freedom from cholera than the fact of not drinking the pump water. Whitehead, for his part, was at work on a pamphlet about the outbreak, which he titled The Cholera in Berwick Street, perhaps not unnaturally concluding that his own church had been the true epicenter of the calamity. He described the reactions of the populace, especially the general lack of panic, in order to put an end to rumors from other quarters.47 He also indulged his mathematical bent by constructing a table to show the relationship between the day on which the victims contracted cholera and how fast that person’s disease progressed to document his assertion that it was much more virulent during the first days of the epidemic. He showed that people who contracted cholera in the earlier days of the outbreak were more likely to die even though the duration of their illness was shorter.48 Whitehead learned of Snow’s hypothesis that had led to the removal of the pump handle. Perhaps thinking back to his own drink of brandy and water on 3 September, but especially remembering the residents who had survived the cholera specifically by drinking huge quantities of the pump water, Whitehead rejected Snow’s theory. He told “a medical friend” that all it would take would be a careful investigation (as contrasted with Snow’s quick visits during the period 3 to 7 September) to conclusively disprove Snow’s idea. Moreover, Whitehead himself was the ideal person to do this study. With his intimate knowledge of the people of the district and the fact that his church work took him up and down Broad Street almost every day, he could track down all the information that was needed.49 No matter if much of the population had fled, he knew how to trace them much better than did Snow. Plus, he knew the friends and families of those who had died, who could give him accurate information on the habits of the deceased.

Monday, 25 September 1854 With the inspection of houses in Poland and Marshall Streets, David Fraser, T. Hughes, and J. M. Ludlow finished their investigations on behalf of the General Board of Health, so that in the preceeding two weeks there had been three independent but simultaneous inquiries (by Snow, the Commission of Sewers, and the board) in the neighborhood, with the investigators periodically running into one another as they made their rounds. Dr. Fraser and his colleagues had visited 800 houses and smelled and duly noted an incredible variety of bad odors. They had looked at the Broad Street pump to be sure that no drainage from the sewer had percolated into the water. They found no evidence of this when they inspected the brick lining of the well under the pump, and a local surveyor, Mr. York, informed them that the sewer ran ten feet away from the well anyway and was twenty-three feet below ground. They had found two cases (both of which Dr. Fraser had described to Snow) that

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implicated the pump; but they had found a greater number of cases in which those drinking the water had either never been attacked or had recovered. They completed their work by inquiring into the death at 37 Marshall Street, said to be due to cholera, but discovered that the victim was a drunkard who had been in a fight the day before and was just as likely to have died from his injuries.50

Tuesday, 26 September 1854 Edmund Cooper, engineer for the Commission of Sewers, had completed his investigation. To apprise the local populace of his findings, the commission held a special “court” in their offices in Greek Street, Soho. Cooper had prepared a detailed report accompanied by a map (see Fig. 12.4) that showed all details of the sewer system and the location of each house in which a death from cholera had occurred.51 He pointed out that the houses nearest the gully holes had no greater number of deaths than did houses farther away. He also drew attention to an old plague pit at a far corner of the cholera district. Very few deaths had occurred nearby. The sewers that drained the plague pit area flowed northward to Regent Street, where few, if any, cases of cholera had occurred. Cooper put forth a miasmatist account of the cause of the outbreak. The sewers of the area where most of the deaths had clustered were in quite good condition. The drains of the houses of the region were in generally bad condition, with many cesspools and deteriorating brickwork, and most of the owners had not taken advantage of the opportunity to connect their drains to the recently constructed sewers. Bad air was without doubt the cause of cholera, but it came from within the houses and not from the commission’s well-kept sewers.52 The chairman of the commission concluded accordingly that “the sewers were not the cause of the cholera; that they were not in any way connected with the disease; but that the real cause of the calamitous occurrences in the locality . . . was the filthy and undrained state of the houses.” The commissioners expressed their hopes that these facts would be widely circulated so as to allay public fears.53 Looking at a carefully and accurately drawn map showing the location of the deaths did nothing to dispel the power of miasma theory. Apparently, none of the many people who studied Cooper’s map that day thought to wonder about the concentration of deaths around the corner of Broad and Cambridge Streets—the approximate location of the pump.54

Wednesday, 25 October 1854 Snow administered anesthesia for the repair of an infant’s harelip and for the extraction of seventeen teeth and stumps. He was relieved that the dental anesthesia

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led to no ill effects despite the long duration of the procedure (CB, 347). This was an average day in his practice.55 He then returned to his cholera research. He was engaged in revising his monograph On the Mode of Communication of Cholera (MCC2). Since he had published the slim volume of thirty-one pages in 1849, he had amassed much additional data to support his theory of water-borne transmission. The centerpiece of the new edition would be the detailed statistical analysis of his south London study, but he also wanted to include a full account of the Broad Street outbreak. This would require further data on cholera deaths and the water drunk by each individual, especially those who had died at some distance from the pump. Some of those who had fled were now returning to the district, making it easier to pursue his inquiries.56

Thursday, 23 November 1854 The vestry of St. James’s was holding one of its regular meetings. On the table for final action was a motion by Dr. Edwin Lankester: “That a Committee of this Vestry be appointed for the purpose of investigating the causes arising out of the present sanitary conditions of the Parish of the late outbreak of cholera in the districts of Golden Square and Berwick Street.”57 After some discussion the motion was passed, and a committee of eight, Dr. Lankester included, was formed.58 Lankester thought at first that eight members would suffice. He imagined that most of the information needed could be secured from two sources: written questionnaires distributed throughout the parish and a review of the data laboriously gathered for the General Board of Health by Fraser, Hughes, and Ludlow. Lankester was soon disabused of his optimism. The first questionnaires distributed produced no useful returns. The approach to the president of the General Board of Health for copies of data resulted in a blunt refusal on the grounds that “investigations of this kind were more valuable when independent.”59 Perhaps this was a polite way of saying that the amateurs in St. James had better stand aside while government professionals did the work properly. Faced with the need to conduct its own personal interviews house by house, the committee added eight more members. Dr. Snow was now asked to join as well as that earnest young clergyman who had written a pamphlet.60

Monday, 27 November 1854 At the instigation of the parish authorities, the Paving Board (which had authority over the street pumps) conducted a survey of the interior of the well under the Broad Street pump. Snow wrote, “I was informed by Mr. Farrell, the superintendent of the works, that there was no hole or crevice in the brickwork of the well, by which any

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impurity might enter . . .” (MCC2, 52). This was something of a setback as he worked to complete the revision of his cholera monograph. He was pointing his finger at the pump as the source of the outbreak yet was unable to prove or even show how it could have become contaminated with cholera evacuations.

Monday, 4 December 1854 Snow produced an exhibit for the evening meeting of the Epidemiological Society of London, a cholera spot map of the Broad Street area.61 By now he had gathered data on 616 deaths and displayed these data in tabular form. Where he could discover the address, he showed these deaths as black bars on the map (see Fig. 12.5). He wanted to use his new map to illustrate the Golden Square outbreak in his revised monograph. Churchill, the publisher, needed a copy of the map immediately to prepare the plate, but it was still two weeks before Snow was to submit his report on the water supply of Golden Square to the St. James Cholera Inquiry Committee. Perhaps he could continue to tinker with the map in the meantime.

Tuesday, 12 December 1854 Snow had a light day—only a tooth extraction (CB, 353)—and so was able to complete his work for Dr. Lankester’s Cholera Inquiry Committee. He had been asked to report on the water supply to the affected district, but he used the report as a platform for his theory of the cause of the outbreak as supported by his investigations. After just a few paragraphs in which he generally described the water supply, he simply copied the relevant portions of the text of his cholera monograph. However, having sent that text off to Churchill a few weeks earlier, he was able to make some corrections and additions. In particular, he had continued to refine his map. He found that he had shown the Broad Street pump in the wrong place, at the corner by the public house instead of in front of the house at number 40. His new map relocated it correctly (see Fig. 12.7). His most important addition was a dotted line that graphically depicted the mental process Snow had carried out on site in September. It showed the points of equal walking distance between the Broad Street pump and all other street pumps. Snow wanted his readers to be struck visually by the fact he had deduced initially from inspecting the list of addresses of deaths from the Registrar-General—that the number of deaths fell off dramatically as soon as one reached the point where it was closer to walk to another street pump than to the pump in Broad Street. (Since 4 December Snow had gone back and carefully measured the distances along the streets [CIC, 109].) Moreover, he now had much more data on those who had died but whose residences lay outside the dotted line, showing that in most cases they were known to have used the Broad Street pump.

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He accompanied the map with a table accounting for all 616 deaths by date. He enumerated his data on how many of those who died were known to have drunk the water from the pump. He mentioned the workhouse, the brewery, and the percussion cap factory as well as a number of other instances. He also included the case of the “Hampstead widow.”62 Even so, Snow could hardly regard his case as open-and-shut. He had no direct evidence of any contamination of the Broad Street pump water with cholera evacuations. It was true that Dr. Hassall’s microscopic examination had shown organic impurities, but while the miasmatists might be satisfied with vague accounts of putrefying organic matter of any sort, Snow’s theory required that one specific sort of organic matter be present. In addition, lacking any knowledge of an “index case,” he had no explanation of how the cholera evacuations could have found their way into the pump well.63

Thursday, 14 December 1854 The St. James Cholera Inquiry Committee was in jeopardy. The vestry had weighed in and objected strongly to the creation of the committee, which would have to be paid for by the Poor Law funds for which it was responsible. The area was just starting to recover; people were moving back and customers could be seen in the shops. All that was needed to drive people away again was some sort of official reminder of recent calamities. The poor rates were already far below what was needed to meet the extra expenditures necessitated by the cholera. All the placards and the lime in the streets had cost a lot of money. Dr. Lankester, however, was not one to be put off easily.64 He offered a spirited defense, and after considerable discussion the vestry reluctantly allowed the committee to continue its work.65

Tuesday, 19 December 1854 The latest issue of Gazetta Medica Italiana Toscana, from Florence, featured a leading article by Filippo Pacini, a prominent microscopist and professor at the local medical school. Pacini reported on the results of his microscopic inspection of the mucous membranes of the intestines from postmortem exams of cholera patients. He called particular attention to a bacterium, which he called a “vibrio,” with a distinctive “comma” shape, and he postulated that this organism was the specific causative agent of cholera.66

Saturday, 27 January 1855 The Medical Times and Gazette published the notice on its front page that J. Churchill of New Burlington Street had released the revised and expanded edition of On the

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Mode of Communication of Cholera, by John Snow. It could be purchased for seven shillings. Among the complimentary copies Snow gave out was one to his new acquaintance on the Cholera Inquiry Committee, Henry Whitehead. Whitehead discovered on reading the book that he had originally misunderstood Snow’s theory regarding the pump: I found, moreover, that he attributed [the cholera-causing properties of the pump water] not to general impurity in the water, but to special contamination of it from the evacuations of cholera patients, which he conjectured must have reached the well from a sewer or cesspool. In thanking him for the book, whilst I could not help admitting the weight of many of his recorded facts, I still clung, as a last resource, to an a priori objection to his theory—urging that, if special contamination of the water in the way suggested had begun the mischief, the outbreak ought not so soon to have subsided, when much larger quantities of cholera excretions must have been continually pouring into the well through the same channel . . . of communication with the sewers. As for cesspools, I at that time supposed they had mostly been abolished.67

Tuesday, 20 February 1855 The previous September Henry Whitehead had told his medical friend that he could easily disprove Snow’s theory of the pump. The young clergyman reflected that he now knew a good deal more about the complexity of a thorough inquiry into a disease outbreak. The vestry’s Cholera Inquiry Committee had assigned to Whitehead the special task of reporting on Broad Street and its residents, and he wanted the report to be as complete as possible. A later acquaintance wrote that during this period Whitehead would combine his church duties with gathering evidence on the cholera and after a long day’s work would then sit up writing till 4:00 A.M. to record all of his data.68 While Whitehead had originally set out to disprove Snow, Snow had become his teacher. Three on the committee—Snow, Lankester, and Dr. King—had drawn up a list of questions for the house-to-house surveys, and Whitehead adopted their questionnaire. In effect, Whitehead found himself replicating more thoroughly Snow’s necessarily hasty investigation carried out during the first week of September 1854. That investigation had an important flaw. Snow studied the use of the pump only among those who had died and did not examine two other groups, those who had developed cholera but recovered and, most important, those who did not have cholera at all. If it had turned out, for example, that the same percentage of those who had no cholera had drunk the pump water as those who had died, then Snow’s case would have fallen to the ground.

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Whitehead had now set out to complete his appointed task properly, limiting himself to Broad Street in particular. The denominator would be the number of people living in the street, not those who had died of cholera. He soon discovered that the street had been decimated—of 896 residents, 90 had died. As Snow had found, a fair number of the living had moved away, and Whitehead patiently followed many of them to their new addresses, some far across town. He was able to accumulate detailed information on about 500 of them. Whitehead also discovered that repeated questioning was often needed to arrive at the facts he sought. Among the anecdotes he eventually included in his report was this illustration: I next went to the top of the house where lived a family consisting of father, mother, a little girl about ten years old, and an infant. They had moved out of the district September 4th, but had recently returned. I asked whether any of them had been attacked with Cholera or Diarrhœa? No. Were they in the habit of using the pump water? Yes. Who fetched it? The little girl. Was she not afraid (I then asked the child), going through the streets to see the shutters all up and so many hearses about? Didn’t go through the streets. Why not? Was ill in bed with a cold. I asked the mother whether that was the case. She called to mind that it was so. Who fetched the water when the child was unable to go for it? Why then they got it from the cistern. CIC, 146–147 Whitehead concluded that his predecessors, both Snow and the General Board of Health inspectors, probably received many unreliable answers because of their time constraints. Whitehead still had much to do to complete his study. So far, the numbers he had assembled seemed more likely to confirm Snow’s theory than to disprove it. He now understood the mystery that had perplexed him on 8 September. It was no wonder that the old women of the parish were often spared from the cholera. They were infirm, often lived alone, and most had no one to fetch water from the pump.

Tuesday, 27 March 1855 Whitehead had nearly completed his report. Far from rejecting Snow’s pump hypothesis, his data supported it in the most conclusive way possible. Of those who drank the pump water, 58 percent developed cholera while 42 percent escaped. Of those who did not drink the water, only 7 percent were attacked while 93 percent were unaffected. Or, to put the matter a different way, among those who developed cholera, 80 percent had drunk the water while 20 percent had not. Among those who were free of the disease, only 17 percent had drunk the water while 83 percent had not.69

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Whitehead had also narrowed down the window of infectivity of the pump water. The earliest cases he could attribute to the pump began on 31 August, and he could not implicate the pump in any deaths after 6 September. Indeed, the pump water seemed to have become considerably less infectious just about the time that he took some of it himself with his brandy on 3 September. His work, it seemed, was finally done. It was, he explained, “for a purpose unconnected with this matter” that he was studying the returns of the Registrar General when his eye fell upon an entry from the week ending 3 September 1854: “At 40, Broad Street, 2nd September, a daughter, aged five months, exhaustion, after an attack of Diarrhœa four days previous to death.” Whitehead continued: “I knew the case, and had recorded the date of death, but somehow had neglected to inquire about the date of attack, having passed it by lightly, I suppose, because it was the case of an infant. Neither had it occurred to me that the child might have been ill all the week” (CIC, 159). Whitehead immediately went to the address and spoke to Mrs. Lewis. As he heard her describe how she emptied the pails into the front area cesspool, he realized that he finally had what he and the rest of the committee had been searching for—a case of choleralike disease occurring close enough to the pump to point to a likely source of contamination and at precisely the time when the water must have acquired its infectious properties.70

Monday, 23 April 1855 With Whitehead’s discovery it seemed to the Cholera Inquiry Committee that the investigation of the pump well the previous November had been too superficial. Jehoshaphat York, a surveyor, was also the secretary to the committee, so it seemed natural to delegate the task to him. York superintended the excavations of the cesspool, drains, and pump well at 40 Broad Street and wrote up a formal report for the committee dated 1 May, with an accompanying plan (Fig. 11.4). York found that the cesspool in the area was “intended for a trap, but misconstructed” so as to create a dam across the drain, forcing sewage to back up rather than flow out. Both the cesspool and the drain into which it emptied were lined with decaying brickwork, the bricks being so loose as to be easily lifted out of their beds without applying any force (CIC, 171). A mere two feet and eight inches away from the house drain was the brick lining of the well under the Broad Street pump. The state of the surrounding soil and gravel made it clear that there had been a steady percolation of waste from the cesspool and drain into the well (CIC, 173–74). York’s excavation showed the great importance of Whitehead’s discovery of the case of the infant. Beginning with the cesspool and working toward the well, York found clear evidence of the route of contamination. The Paving Commission, looking only within the well itself in November, had thought that nothing was amiss.

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A B

A

C B

Figure 11.4. J. York’s plan of the drain from 40 Broad Street and its position relative to the well under the Broad Street pump. Left: plan view, from above. Right: side view. A: well under pump; B: main drain from house; C: sewer (adapted from CIC, 170–71).

Wednesday, 25 July 1855 The St. James Cholera Inquiry Committee had finally completed its general report, to which separate reports from Snow, Whitehead, and York were attached. The result was a partial victory for Snow. The committee commended Snow’s and Whitehead’s investigations and concluded, “The Committee is unanimously of the opinion that the striking disproportionate mortality in the ‘Cholera area,’ as compared with the immediately surrounding districts, which . . . constitutes ‘the sudden, severe and concentrated outbreak,’ beginning on August 31st and lasting for the few early days of September, was in some manner attributable to the use of the impure water of the well in Broad Street.”71 However, after reviewing Snow’s specific theory of the nature of the causative agent in cholera and alternative theories of what precise form the contamination of the pump water took, the committee expressed no opinion one way or the other.72 The committee had a problem with the case of baby girl Lewis at 40 Broad Street. On the one hand, Whitehead had received a detailed letter from Dr. William Rogers explaining why he thought the case was not one of cholera and emphasizing that the infant never had the typical rice-water stools, which Whitehead dutifully quoted in full in his own report (CIC, 163–65).73 He, for one, was loath to question the diagnosis of the medical attendant who had been personally involved in the case,74 yet neither Whitehead nor his fellow committee members could avoid the conclusion

10

July 20 30

10

August 20 30

September 10 20 30

October November 10 20 30 10 Mean daily air temperature Average air temperature

Golden Sq. outbreak

Mean daily wind direction

Max air pressure

Thames River: Mean daily water temperature Mean daily cloud

Daily rainfall

Diarrhoea deaths

Cholera deaths

Relative amounts of fog or mist

Figure 11.5. Cholera deaths per day in London, August–September 1854. The peak reflects a doubling of deaths during the ten-day outbreak in Golden Square. Meteorological data was entered on the graph for miasmatic analysis (adapted from GBH, Appendix to CSI, opposite 106).

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that the days during which the diaper water was emptied into the cesspool coupled with the results of York’s excavations provided a compelling reason for the contamination of the pump. Despite Sir Benjamin Hall’s earlier refusal to release the inspection data, the St. James Cholera Inquiry Committee eventually was given leave to use for its own report a copy of the Golden Square map prepared by the General Board of Health’s Committee on Scientific Inquiries, which was published in the official board report on the cholera epidemic.75 When they reprinted the board’s map,

Figure 11.6. Number of deaths at 40 Broad Street: (top) Snow’s MCC2 map, detail—number of bars identical in CIC map; (bottom) General Board of Health map, detail.

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however, the committee made one modification. The “official” theory remained firmly miasmatic, and the board saw no reason to focus attention on the Broad Street pump (Fig. 11.5). However, the St. James committee, at Whitehead’s instigation, drew a circle on its map with a radius of 210 yards, with the Broad Street pump at the center (see Fig. 12.8). Whitehead had noted to the committee that this circle included the “cholera area” in which almost all the deaths had occurred (CIC, 17–18). Ironically, while the General Board of Health dismissed Snow’s and Whitehead’s hypothesis completely, they concurred with one critical piece of confirmatory evidence. While Whitehead and the committee had hesitated to disagree with Dr. Rogers and declare that the little girl at 40 Broad Street had died of cholera, the government inspectors showed no such compunction. Their house-to-house survey listed five cases of cholera at that address, including “policeman and child,” and their map showed five black bars adjacent to number 40. Snow’s map, completed before Whitehead’s discovery, showed only four bars (Fig. 11.6).76

Wednesday, 26 September 1855 The commissioners of paving of St. James’s again received a petition from the inhabitants of Broad Street and environs. There was much complaint in the neighborhood that the Broad Street pump remained without its handle. Back in June the parish medical officer, John G. French (a friend of Snow’s since 1849 and a member of the Cholera Inquiry Committee), had warned of the increased threat of cholera with the warm weather and had advised strongly that all the street pumps be closed down.77 The pumps remained popular, however, compared to the filthy cisterns that normally held the piped water. Besides, it was now autumn, and the cholera seemed to be gone from London. On a 10–2 vote the commission decided to reopen the Broad Street pump.78

Notes 1. Dr. W. R. Rogers to Rev. H. Whitehead, 30 May 1855, reprinted in CIC, Report, 163–65. Hereafter, citations to CIC are given parenthetically when possible. Henry Whitehead referred to the family as “L.” in a table in his CIC report (161). The General Board of Health (hereafter GBH) house-by-house report did not use any names or initials, and the street and post office directories list only principal businesses at each address (see Figure 11.3). The 1851 Census enumerator, however, listed seven households at 40 Broad Street, only one beginning with “L”: Thomas Lewis, head, age 46, police constable; Sarah Lewis, wife, age 40; and two children, Thomas (age 13), and Anne (age 8). See UK HO 107/1485/232. Because the head’s vocation matches what was recorded by the GBH, we are confident that Whitehead’s “L” were the Lewis family.

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2. UK GBH, Report of CSI, appendix, 345. 3. On the history of Broad Street and its buildings, see Sheppard, St. James Westminster, 2: 221–23. The Survey of London is silent on the early history of the house at 40 Broad Street. The row of houses directly across Broad Street (north side) had been built originally in 1722–23. 4. The data on the house at 40 Broad Street and its inhabitants were later gathered during a house-to-house survey undertaken by the GBH; see UK GBH, Report of CSI, appendix, 345, reprinted in Paneth et al., “A rivalry of foulness,” 1551. 5. Years later a commentator recalled the local custom of keeping cows on the top story of these houses. The animals were hoisted up by windlass and remained shut up in the attics so long as they gave milk; Rawnsley, Henry Whitehead, 34. On the other hand, the inspectors for the GBH were most industrious in rooting out any possible source of bad smells in the region during their house-to-house visitations from 11 to 25 September. They reported no cows in any attics, although they did describe the noxious cow yards. According to the report of the medical officer of health, Edwin Lankester, a decade later there were eight cow houses in the parish with a total of 205 cows. “The nuisance of the cow house in Marshall Street is notorious throughout the whole parish. . . . The herding together of 25 or 30 cows in a room of a dwelling house, in a row of other houses. . . . These cow houses, though probably not more injurious to health than slaughter houses, are very great nuisances to the neighbourhood in which they are situated”; Saint James, Annual Reports, 1864–65, 24–25. 6. Snow, “Further remarks on the mode of communication of cholera” (1855). 7. On the “Hampstead widow,” see MCC2, 44–45, and Whitehead’s report, CIC, 139–40. The Eley’s percussion cap factory was apparently quite a successful concern. Years later the name was well known—Sherlock Holmes told Dr. Watson in “The Adventure of the Speckled Band,” “I should be very much obliged if you would slip your revolver into your pocket. An Eley’s No. 2 is an excellent argument with gentlemen who can twist steel pokers into knots”; Doyle, Adventures of Sherlock Holmes, 184. Doyle confused the name “Eley,” for the cartridge, with “Webley,” for the revolver. The firm survives today, although relocated to Birmingham. 8. Rawnsley, Henry Whitehead, 29, 32–33. 9. These atmospheric details were carefully noted later by the official inspectors for the UK GBH, Report of CSI, appendix, 139–40. 10. Whitehead, “Broad Street pump,” 113. 11. Editorial, “The life and death question. The outbreak in Berwick-Street—A word or two on protective measures,” Builder 12 (9 September 1854): 473. 12. Whitehead, “Broad Street pump,” 113. 13. Another local clergyman, Harry Jones, later recalled: “Whitehead fought like a hero night and day, with hand and lips and brain, helping to strengthen the living, heal the sick, and comfort the dying. . . . I can’t say I saw much of Whitehead then, for we both had our hands full; but one thought of the man in the thickest of the fight . . .”; Rawnsley, Henry Whitehead, 41–42. 14. Mrs. Gaskell to Emily Winkworth, recounting the story Mrs. Gaskell had heard from Miss Nightingale, in Woodham-Smith, Florence Nightingale, 79–80. The CIC took issue with accounts such as Nightingale’s: “It is remarked by Mr. Sibley, the registrar of the Middlesex Hospital, that a large number of the persons brought there for treatment presented a very uncleanly appearance. . . . This may doubtless be explained, partly by the circumstances that the patients so admitted were probably the most destitute of those who were attacked, and partly by the fact of their being suddenly seized by the disorder whilst engaged in the usual occupations of their trade”; CIC, 31–32. Both Snow and the CIC documented that cholera struck all occupations and social classes in the district with equal severity.

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15. Snow, “Cholera near Golden Square” (1854): 322. In addition to this letter to the editor, he wrote two more accounts of his Broad Street investigations: “Dr. Snow’s report” to the CIC (1854) and a segment of MCC2, 38–56. A detailed word analysis shows that MCC2 was submitted to the publisher before Snow wrote his report for the CIC. Copies of MCC2 were available in late December 1854 despite a date of publication of 1855; see G[eorge] Budd to Snow, 3 January 1855, Clover/Snow Collection, VIII.4.i, in which Budd acknowledges receipt of a copy. The three accounts agree on all major points and help to indicate the order in which Snow obtained new information as his investigations proceeded. When Snow revised material, he tended to add more text instead of altering the existing text. For example, in MCC2 and CIC he repeats almost verbatim from the MTG article the account of the first eightythree deaths he investigated and then adds later that the true number was 197, not eightythree, as he learned from the later returns (see below). 16. UK GBH, Cholera of 1848 & 1849, 62. 17. UK GBH, Cholera of 1848 & 1849, 61–62. We are indebted to Professor Pamela Gilbert for calling our attention to this incident. It is much less likely that Snow had seen a letter sent to the GBH to report a suspicious occurrence: “A few days ago some friends of mine residing in Regent St. (No. 181) wishing to take some brandy & water, sent the servant to a neighbouring pump in Warwick St. hoping to obtain water fresher and purer than that which the house furnishes, but, to their astonishment, when they came to mix it with the brandy it instantly turned black: a second experiment being made with the same result, it was [taken] to a chemist to be examined & his assertion was that the Sewer had entered the well and deteriorated the water which, in appearance, is perfectly lucid”; John Clarke Rowlatt (?) to GBH, 10 September 1849, “Metropolitan nuisances,” 1849, MH 13, 261, PRO, Kew. Rowlatt, a clergyman, resided at 32 Lower Belgrave Street, from which the letter was sent. 18. Whitehead, “Broad Street pump,” 113. 19. Rawnsley, Henry Whitehead, 203–04. 20. Snow, “Cholera near Golden Square” (1854), 322. 21. Hassall eventually was called upon by the GBH to conduct microscopic studies of this cholera outbreak. 22. Whitehead, “Broad Street pump,” 113. 23. “The Board of Health and the cholera,” Times (6 September 1854). Sir Benjamin Hall later became commissioner of works and in that capacity in 1859 superintended the installation of the great bell in the tower of the Houses of Parliament. Hence the bell, and eventually the clock, were called Big Ben. 24. The end of July and the beginning of August was a particularly inauspicious time for Parliament to be tinkering with the GBH, as the cholera epidemic was just then gaining momentum. During July cholera deaths in London had increased from one to 133 per week. The abolition and recreation of the GBH in July–August 1854 is recounted in more detail in Paneth et al., “A rivalry of foulness.” 25. Snow, “Cholera near Golden Square” (1854): 322. Nearly identical passages appeared in Snow’s report, CIC, 101–02, and MCC2, 39–40. Snow’s circumstantial account of his reasoning and investigation up to this point makes no mention of any map or graphical representation of the data. For the role that mapping did (and did not) play in Snow’s and other investigations, see Chapter 12 and Brody et al., “Map-making and myth-making in Broad Street.” 26. “The public health,” Times (6 September 1854). The public impact of such a news announcement can scarcely be appreciated by readers today. St. James and the neighboring parish to the east, St. Giles, had long been paired in the popular mind as the extremes of what was good and bad about London. While St. James had tenements, it also had St. James’s Palace,

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St. James’s Park, and Pall Mall. St. Giles, by contrast, was a particular haunt of poor Irish immigrants and had been the site of “The Rookery,” a particularly notorious slum and criminal den. For cholera to afflict St. James, while St. Giles was mostly spared was therefore to turn the natural order of the world on its head, much as if Dr. Jekyll had been caught stealing candy from tots while Mr. Hyde was canvassing for donations for the church bazaar; Gilbert, “‘Scarcely to be described.’” Gilbert goes on to speculate, “The outbreak in St. James’s [by dashing the existing folk theories of cholera causation] probably did far more to advance Snow’s credibility with the public than his meticulous research did” (161). 27. Whitehead, “The experience of a London curate,” 203. This anecdote was in his farewell address on leaving London in 1874. 28. Whitehead, “Remarks on the outbreak,” 102. 29. UK GBH, Report of CSI, appendix, 161. 30. Rawnsley, Henry Whitehead, 203. 31. We know little about what actually transpired at the meeting. On 14 August 1854 when, acting in response to “an apprehended visitation of Asiatic Cholera,” the Governors and Directors of the Poor again formed themselves into a “general Sanitary Committee,” they agreed to keep a separate minute book, which is no longer extant; St. James, Minutes of the Governors and Directors of the Poor (D2151), 455. They had formed a similar Sanitary Committee in April 1853 and submitted a report on 3 October 1853; Ibid., 151. Snow’s account of what happened is terse: “I had an interview with the Board of Guardians of St. James’s parish, on the evening of the 7th inst., and represented the above circumstances [i.e., the results of his investigation] to them. In consequence of what I said, the handle of the pump was removed on the following day”; “Cholera at Golden Square” (1854): 322. Identical language appeared in MCC2, 40, and “Dr. Snow’s report,” CIC, 102, except that “the 7th inst.” was changed to “Thursday, 7th September.” Snow’s confusion of Guardians for Governors may reflect unfamiliarity with Poor Law regulations in St. James, compared to most parts of the metropolis that were organized into unions. The vestry did not meet on 7 September; St. James, Vestry Minute Book (D1777), and Rough Minutes of the Vestry (D1810). 32. We have been unable to find any contemporary accounts. 33. UK GBH, Report of CSI, appendix, 151. 34. UK GBH, Report of CSI, appendix, 138. 35. “A Resident of Broad-street” (letter to the editor), Times (8 September 1854). The GBH inspectors scouted the plague pit theory and suspected that it had “been prominently put forth by interested persons, who were desirous of diverting the current of popular indignation from their own particular nuisances.” The owner of the “monster slaughter-house in Marshall Street,” they suggested, might have been one such interested party; see UK GBH, Report of CSI, appendix, 151. 36. Whitehead, “Broad Street pump,” 120. 37. Whitehead specifically called attention to the efficacy of removing the pump handle in possibly preventing a new outbreak of cholera, even if it were true, as he and Snow later wrote, that the original outbreak was already on the wane before 8 September. Whitehead suggested that the discharges from the infant’s father, thrown into the same cesspool, would surely have contaminated the well again on the days following 8 September. Henry Whitehead, “Remarks on the outbreak,” 99–104. 38. UK GBH, Report of CSI, appendix, 142, 145, 150–51, 336. 39. For example, “I was accidentally accosted by a friend in passing along the highway. . . . After a few minutes I was surprised and somewhat alarmed to find a feeling of great sickness and faintness suddenly coming over me. . . . [M]y friend called my attention to the fact that we were in close proximity to one of [the] untrapped gully-holes, from which, now that my

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attention was directed to the circumstances, I soon found that a most deadly effluvium was arising. I immediately moved from the vicinity of the grating and felt almost instantaneous relief ”; Times (15 September 1854). 40. When Whitehead interviewed Mrs. Lewis in the spring of 1855, she was living in the back parlor of 40 Broad Street; “Rev. Whitehead’s report,” CIC, 159. During the 1854 epidemic, however, her ill husband and infant had lain in the front kitchen, which was why it was easier for her to pour the dirty water from rinsing bedding and diapers into the cesspool in the front area rather than carry it to the privy at the back of the house; Whitehead, “Remarks on the Outbreak,” 104. The GBH only listed the two cholera cases as having occurred on the ground floor of 40 Broad Street; UK GBH, Report of CSI, appendix, 345. 41. “The cholera in Golden-square,” Times (15 September 1854). 42. Snow, “Cholera near Golden Square”(1854). This letter appeared on 23 September. 43. It is difficult to reconcile Snow’s account of the flight of the population with Whitehead’s assertion in the summer of 1854 that there was a notable calm and lack of panic. Later Whitehead admitted that a flight had occurred, and he had an advantage over other investigators because he knew the families better and so could more easily track them down in their new locations; “Broad Street pump,” 116. Perhaps Whitehead, in his earlier pamphlet, exaggerated the calm so as to defend what he took to be the reputation of his community (The Cholera in Berwick Street, 14–17), or perhaps the population fled calmly. 44. “Dr. Snow’s report,” CIC, 103–04. The popularity of the pump water was partly due to the fact that the chemical by-products of organic impurity, carbonic acid and nitrates, gave the water a sparkling quality, as was noted by many observers; see CIC, 72–74. 45. Snow refers to “Dr. Fraser, of Oakley Square” in his writings, but he does not mention Fraser’s official connection with the GBH; see CIC, 106; MCC2, 44. 46. “Dr. Snow’s report,” CIC, 104. Earlier Snow had written that 100 would have died, but this would have produced a mortality rate twice that of the one in ten that Whitehead later found in Broad Street; MCC2, 42. The corrected figure is further evidence that Snow’s CIC report was completed after MCC2. 47. Whitehead’s point was not whether people had fled the neighborhood, but that sick people were cared for compassionately by their relatives and neighbors rather than being ruthlessly abandoned out of fear of contracting the disease. 48. Whitehead, The Cholera in Berwick Street, 13. Whitehead reprinted this table in his report to the CIC, 155. Fraser, Hughes, and Ludlow of the GBH found it useful in their report to quote extensively from Whitehead’s pamphlet (by “the exemplary and indefatigable curate of St. Lukes’”), especially in regard to the floors of the houses on which the most deaths occurred, the ages and conditions of the victims, and the small area within which the cholera deaths were concentrated. UK GBH, Report of CSI, appendix, 158–60. 49. Whitehead, “Broad Street pump,” 116. The notion of conducting an investigation of his own to disprove Snow’s theory of the pump seems to have occurred to Whitehead after he had finished work on The Cholera in Berwick Street, which makes no mention of Snow’s theory or his own doubts about it. 50. UK GBH, Report of CSI, appendix, 139, 153–55, 351. 51. Cooper, “Report.” Whether Snow attended this meeting is not recorded. Between 22 September and 2 October his casebooks show no anesthesia work; CB, 344. During this period he was undertaking additional investigations in Golden Square. 52. “Since the outbreak, six men have been employed in these lines of sewers getting up information on this subject, all of whom, I am glad to state, are quite healthy, and entirely free from disease”; Cooper, “Report.” Consequently, he suggested that sewer gases per se were unlikely to spread cholera.

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53. Times (27 September 1854). While the GBH inspectors agreed with Cooper about the plague pit, they disagreed on the role of the gully holes. Their report eventually blamed the outbreak mainly on the “multitude of untrapped and imperfectly trapped gullies and ventilating shafts constantly emitting an immense amount of noxious, health-destroying, lifedestroying exhalations” made worse by a stagnant atmosphere; UK GBH, Report of CSI, appendix, 161. Dr. Fraser and his team claimed that many of the houses closest to the gully holes had been most severely hit by cholera (143), whereas the corner houses, being in the best ventilated positions, often escaped (161). Neither Cooper nor the board inspectors provided any statistical analysis to back up their respective (and contradictory) claims. 54. The point is worth noting because of some of the later inaccurate and mythical accounts of Snow and the pump. Many of today’s authors speak as if merely glancing at the map, with its distribution of bars (or dots, as most modern versions have it), would be sufficient to convince the most skeptical observer that the pump water was the source of the outbreak. Cooper noted that of all the local streets, Broad Street had been most heavily visited by the cholera, but he focused only on the sewers in his inquiry as to why this was so. Broad Street was served by two nonconnecting sewers, one of recent vintage and one rather old, but the numbers of deaths appeared equally divided between the portions of the street served by the two different sewers. 55. For most of October Snow attended one or two cases a day, with a high of five cases on 28 October; CB, 348. 56. The late October date for these inquiries is given in “Dr. Snow’s report,” CIC, 114. 57. Chave, “Henry Whitehead,” 94. 58. Chave, “Henry Whitehead,” 94. Chave states that the original committee had nine members, but CIC, iii, lists eight. 59. CIC, v. 60. Chave notes that this was probably the occasion for the first meeting between Snow and Whitehead; “Henry Whitehead,” 95. We do not know why Edwin Lankester, who had served as a fellow officer with Snow of the Westminster Medical Society and was a vestryman of St. James’s at the time when Snow made his appeal regarding the pump, delayed so long in asking Snow to join the committee. Perhaps ill will lingered over Snow’s association with A. B. Garrod, who had been selected over Lankester for a medical school professorship in 1846; see English, Victorian Values, 44–45. On the other hand, in 1849 Snow had credited Lankester with an idea regarding the transmission of cholera in bodies of water; PMCC, 928. 61. “Epidemiological Society,” Lancet 2 (1854): 531. 62. The “Hampstead widow” case was the one that even his severest critics later found most difficult of all his facts to dismiss. For example, Edmund Parkes, in a review of MCC2, rejected Snow’s views on cholera and dismissed the map as being precisely what one would expect to see in the case of a concentrated, noxious miasma causing an epidemic of disease. There were so many pumps in that neighborhood, he noted, that no matter where the epidemic had its center, there was sure to be one of them close by, yet he admitted that the case of the Hampstead widow was, “if there is not some fallacy, . . . certainly unanswerable”; Parkes,“Review: Mode of Communication of Cholera by John Snow,” British and Foreign MedicoChirurgical Review 15 (1855): 449–63; quotation from 456. 63. “Dr. Snow’s report,” CIC, 97–120. He revised his report to the CIC as late as 14 June 1855, but he did so in a footnote that was explicitly dated and kept separate from the main body of text (CIC, 116). The lack of firm data on the contamination of the pump did not stop Snow from speculating: “The reason why the water of this pump produced the great outbreak is, I feel confident, that the evacuations of one or more Cholera patients found their way, by some means, into the well. There were fatal cases of Cholera, a few days before the

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great outbreak, not far from the well, and there may have been other cases, not fatal, which are not recorded”; “Dr. Snow’s report,” CIC, 119. In MCC2 he noted that as the well water passed with almost all observers as being perfectly pure, “the quantity of morbid matter which is sufficient to produce cholera is inconceivably small” (54). 64. Chave, “Henry Whitehead,” 94. 65. Ibid. 66. Pacini, “Osservazioni microscopiche,” 1. This article remained unknown and unremarked upon by the vast majority of British physicians. See also Bentivoglio and P. Pacini, “Filippo Pacini.” By the time Robert Koch took credit for discovering the bacillus Vibrio cholerae in 1883, Pacini’s work had been forgotten, and it was many decades before Pacini’s priority in the discovery was officially recognized. 67. Whitehead, “Broad Street pump,” 116. 68. J. Netten Radcliffe, quoted in Rawnsley, Henry Whitehead, 40. 69. Whitehead expressed his numbers as more difficult to interpret ratios rather than percentages; “Rev. Whitehead’s report,” CIC, 132–33. 70. Whitehead dated this portion of his report “April 3rd” and stated that the event here described occurred “one day last week”; CIC, 159. We have arbitrarily chosen the date exactly one week before April 3. 71. “General report,” CIC, 83 (italics in original). 72. “General report,” CIC, 84–91. Lankester seems to have been closer to Budd’s position on cholera than to Snow’s, and while acknowledging the role played by contaminated water, was unwilling to deny a possible role for atmospheric spread; English, Victorian Values, 104. For the view that the CIC report “finally . . . substantiated” Snow’s theory, see S. Snow, JSEMP, 244. 73. Dr. Rogers even showed up personally at the meeting of the Epidemiological Society on 4 July 1855, when Snow was giving a paper on the Broad Street outbreak that included mention of Whitehead’s identification of the index case. Rogers objected that because Snow’s theory apparently hinged on cholera evacuations getting into the well and because his own case was being cited as the “cholera” case, he remained unconvinced by Snow’s presentation as he knew that his case was not one of cholera at all: “Epidemiological Society,” Lancet 2 (1855): 11–12. 74. Years later Whitehead expressed himself somewhat more forcefully on that issue: If the infant’s discharges, thrown into the cesspool that communicated with the pump well during those exact days, did not cause the outbreak, then it was “indeed a very remarkable coincidence”; Whitehead, “Broad Street pump,” 122. 75. UK GBH, Report of CSI, frontispiece. The GBH map (according to CIC) was based to some extent on Cooper’s earlier map and was similarly sophisticated from a cartographic standpoint. Thus, the CIC Report contained two maps—the GBH map (with the circle added) accompanying the general report and Snow’s revised map accompanying his own report. 76. Confirmation of Whitehead’s theory of how the pump came to be contaminated became generally known in the summer of 1855, when the GBH Report was published. The actual raw data from which the number of bars at each house were derived were gathered by Dr. Fraser’s team in September 1854, which means that the GBH inspectors (who knew of no connection between the drains at no. 40 and the well) believed that infant girl L[ewis] had died of cholera. They presumably arrived at this conclusion from the mother’s testimony because there is no record that they consulted the infant’s physician. 77. St. James, Board of Commissioners of Paving, Rough Minutes (D1941), 20 June 1855. 78. St. James, Board of Commissioners of Paving, Rough Minutes (D1941), 26 September 1855. A sanitarian minded local resident sarcastically described the scene when the pump was

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reopened: “High festival was held that day in Broad-street. . . . Full many a copious stream, arrears of libation to offended Cloacina, did the pump send forth. Loud and long the exulting shouts of children working the handle in wantonness of exuberant joy . . .”; Mens Sana in Corpore Sano [pseud.], “What has been done in St. James’s, Westminster?” Builder (27 October 1855): 510. By then repairs at 40 Broad Street were finished: “All [the] old drainage has been removed; the cesspool destroyed, and new tubular pipe drains with cemented joints, and a syphon trapped closet have been substituted”; “Mr. York’s report,” CIC, 172–73. However, the sievelike brickwork of the nearby pump well remained unchanged. The Broad Street pump was not permanently closed until the cholera epidemic of 1866, when Edwin Lankester was medical officer of health for the parish; see Chave, “John Snow, the Broad Street Pump, and after,” 349. In the 1864–1865 report he had noted, “The wells in this Parish are gradually being abandoned, as the longer they stand the more liable they are to impurities from the leakage of drains through rat-holes and the percolation of street gutters and cesspools”; Saint James, Annual Reports, 1864–65, 52. With respect to Thames water, he thought it had improved since the last epidemic, “and a supply is now afforded to London free from the injurious influence of organic contamination. It is to be regretted that this supply is still intermittent, and is stored in leaden cisterns and wooden butts, which when neglected to be cleansed, render the water impure”; Ibid., 51.

Chapter 12

Snow and the Mapping of Cholera Epidemics

O

N THE EVENING OF 3 June 1851 Snow delivered the second part of a paper on the propagation of cholera at the monthly meeting of the London Epidemiological Society. The society had again rented the library of the Royal Medical and Chirurgical Society in Berners Street. Snow began the paper by offering a general principle of “epidemic diseases, the whole of which I look upon as communicable from one patient to another, this communication being probably the real feature of distinction between epidemic and other diseases,” and he reviewed several local outbreaks that conformed to this principle.1 He proposed to show that “cholera was often communicated through the water, on a more extensive scale, by means of sewers which empty themselves into various rivers, from which the population of many towns derive their supply of water” (610). A map extracted from the second Report on the Health of Towns, suspended in the room, indicated which water companies supplied particular districts in London. Snow then pointed to another map (Fig. 12.1), produced by Mr. Richard Grainger from the Board of Health, that depicted the “relative prevalence of the late [1849] epidemic in different parts of London” in varying shades of blue.2 A comparison of the two maps showed that “cholera was most prevalent . . . in those districts supplied with water vitiated by the contents of sewers and cesspools” (610). This presentation is the first recorded instance of Snow using a disease map. In the past he had frequently used data tables when presenting papers at medical

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Figure 12.1. Mr. Grainger’s “Cholera Map of the Metropolis. 1849. Exhibited in the Registration Districts” (detail). There were four districts south of the River Thames that might have interested Snow—#25, St. Saviour, Southwark; #26, St. Olave, Southwark; #27, Bermondsey; #28, St. George, Southwark; and #29, Newington. The dotted lines indicated where crosssections were taken for showing elevation above the high-water mark on the River Thames. Places with “bad ventilation,” “no drainage,” “open sewer,” and “overcrowding” were also marked on the map (GBH, Report on Cholera, 1848–49, appendix B, opposite 200).

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society meetings and in his published writings.3 He had limited his other graphical devices to demonstrations and drawings of apparatus. Why, then, did he make use of two maps in this presentation? Perhaps it was because they were readily available, cost him nothing to display, and, in the case of the Board of Health map, carried a touch of irony by employing a device prepared by sanitarian opponents to support his contrary explanation of what had caused the 1848–1849 epidemic. Although many epidemiologists and public health figures today consider him a pioneer in disease mapping, Snow published only two disease maps, of which the spot map in MCC2 of the Golden Square outbreak in 1854 is the better known.4 It was an afterthought to the investigative process. That is, he had not used this map inductively, collecting data, putting a mark by the address of each case, and eventually developing a theory to explain the cluster of cases around the Broad Street pump, nor had he used the map deductively, hypothesizing at the outset that the cause was contamination of the Broad Street pump, then plotting cases to confirm his hypothesis or falsify an alternative. Instead, the spot map in MCC2 is an example of illustrative mapping, a visual enhancement of the descriptive narrative of his investigation in Golden Square. Snow wrote the passage on his Golden Square investigation for a revised edition of MCC a few weeks after the outbreak had ended, and textual analysis suggests that he had decided from the outset to include a map showing most of the cholera cases.5 At a meeting of the Epidemiological Society on 4 December 1854, he displayed an advance copy of this spot map that would be published in MCC2 in a few weeks time.6 Something must have happened that evening to make Snow believe the Golden Square spot map he had constructed to illustrate his theory would not have the intended effect. Until then, spot maps were generally the preserve of anticontagionists, and it is possible that a member of the Epidemiological Society interpreted Snow’s map as showing local miasmatic causes. It was too late for Snow to remove the spot map from MCC2, but there was time to alter it for a report on the outbreak he was preparing for the parish of St. James. In a matter of ten days he had collected new data and had expanded an aside in MCC2—“It may also be noticed that the deaths are most numerous near to the pump where the water could be more readily obtained” (47)—into an analytical exercise in disease mapping. Snow methodically plotted equidistant walking points between pumps for every street on his spot map in order to refute counterclaims that the geographical clustering of cases supported miasmatic explanations of the outbreak rather than his hypothesis of a water-borne source (CIC, 109). Nonetheless, the Golden Square map most frequently reproduced or redrawn to the present day is the illustrative one in MCC2, not the CIC map that reflects Snow’s deductive reasoning and innovative mapping. Besides Snow, other contemporary observers constructed three spot maps of the horrific cholera outbreak in Golden Square. One involved deductive reasoning, like Snow’s CIC map, although this author was testing a miasmatic hypothesis. Two others were illustrative accompaniments to committee reports on the outbreak.7


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Origins of Cholera Mapping Humoralism had stressed the role of “airs, waters, and places”—the title of an often referenced Hippocratic essay—in causing epidemics, and long after the heyday of humoral theory medical authorities continued to describe the topography and climate where epidemic diseases prevailed. They included no disease maps, however, as distinct from purely topographical maps, until the latter part of the eighteenth century.8 By the mid-nineteenth century, however, the German geographer Augustus Petermann (1822–1878) believed medical cartography had developed to the point that it could play a significant role in elucidating the “general laws” underlying the spread of cholera.9 He lived in London between 1847 and 1852, during which time he produced a map of the 1831–1833 cholera epidemic in the British Isles. In an accompanying text he trumpeted the importance of inductive and illustrative disease mapping. One prepares a map “to obtain a view of [that is, illustrate] the Geographical extent of the ravages of this disease, and to discover [that is, induce] the local conditions that might influence its progress and its degree of fatality.” Petermann argued that, For such a purpose, Geographical delineation is of the utmost value, and even indispensable; for while the symbols of the masses of statistical data in figures, however clearly they might be arranged in the Systematic Tables, present but a uniform appearance, the same data embodied in a Map, will convey at once, the relative bearing and proportion of the single data together with their position, extent, and distance, and thus, a Map will make visible to the eye the development and nature of any phenomenon in regard to its geographic distribution. In other words, Petermann considered disease maps both an essential part of the discovery process for the medical topographer and an illustrative enhancement of data and description for the reader.10 The first recorded instance of a spot, or dot, map being used to record the geographical distribution of individual cases of a disease was in 1798. Dr. Valentine Seaman (1770–1817), a surgeon at the New York Hospital, published a detailed paper about the 1796 yellow fever outbreak in New York City. His article was illustrated by two carefully drawn disease spot maps.11 Seaman mapped two areas along the harborfront, New Slip and Burling Slip, with a symbol to indicate the residence of each person who had suffered from yellow fever. Based on these maps he inferred that the disease was caused by putrefying substances in the nearby wetlands and stagnant water, factors he described in the article but did not indicate on the maps. While yellow fever remained a feared disease in the New World, it was soon overshadowed in Europe by the specter of epidemic cholera. To a large extent the

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history of disease cartography during the years 1820 to 1850 is the history of cholera maps. These fell into two general categories, progress maps and spot maps. Progress maps depicted the temporal spread of cholera across large areas such as nations or continents. A solid circle or similar symbol on a progress map represented a city or town, and the date adjacent to the dot indicated when the first cases of cholera had appeared in that place. Some progress maps used arrows or lines to show the sequence of towns in which cholera broke out. One example is the “Chart Shewing the Progress of the Spasmodic Cholera” that accompanied a report compiled by A. Brigham in 1832 (Fig. 12.2).12 Along with dated points, the solid reddish “flow” lines illustrate the diffusion of cholera from southeast Asia, through the Middle East and Europe, to England, and across the Atlantic Ocean to the eastern seaboard of Canada and the United States. The contagion–anticontagion debate was in full swing at the time of the 1831–1832 epidemic. Both camps often agreed that progress maps showed that cholera first appeared, for example, in town A in July, town B in August, and so on, but contagionists considered that such progress of cholera across a country was evidence of personto-person contact along established trade and travel routes, whereas anticontagionists interpreted the same data as disease being spread by the prevailing winds. Thus,

Figure 12.2. A portion of the “Chart Shewing the Progress of the Spasmodic Cholera.” Solid reddish lines (shaded in this figure) indicated the movement of cholera from southeast Asia to western Europe and England and then on to the eastern seaboard of Canada and the United States (Brigham, Treatise on Epidemic Cholera, frontispiece).


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progress maps were used by contagionists and anticontagionists alike to illustrate their own preconceived theories. James Jackson and his committee at the Massachusetts Medical Society prepared a progress map of the spread of “cholera morbus” from Hindustan to England based on the published literature, dispassionately listed the arguments for and against contagion and anticontagion, and concluded that insufficient evidence existed to come down definitely on one side or the other.13 The other category of cholera map was the spot map. Such a map typically covered a much smaller geographical area than the progress map, such as a village, a city, or a part thereof, and represented each case of cholera with a symbol such as a dot. In the accompanying texts medical cartographers generally associated clusters of dots with topographical or other physical features, including housing, regardless of whether such features were noted on the maps. Many early spot maps followed Seaman’s example, showing cases of cholera but not the purported causal factor, but dots without dates, whether of morbidity or mortality, conveyed an impression of simultaneity that favored anticontagious causal explanations, such as the rapid spread of a noxious miasma from a nearby marsh or effluvial emanations from an overcrowded and filthy district. Contagionists could have added specific dates to spot maps showing how an epidemic began in a particular location and spread in gradually widening ripples, but we have found none. Like Seaman, some cartographers used spot maps inductively, formulating hypotheses of probable causal factors while actually plotting the cases. For others the spot map was purely illustrative, playing no role in the investigative process. For example, Dr. Thomas Shapter (1808–1902) constructed a spot map purely to illustrate his narration of events during the cholera epidemic in Exeter during 1832–1834 (Fig. 12.3).14 In order to depict the geographical distribution of individual cholera deaths for each year, he employed a different red symbol of uniform size: a thick line, or bar, for 1832, a cross for 1833, and a solid dot for 1834. He published his book in the 1840s, after major renovation and sanitary projects had altered the town significantly from what it had been during the epidemic. Shapter did not believe that cholera was contagious and referred to his map to support his view that the disproportionate number of deaths that occurred in the low-lying southeastern quarter of the old walled city were primarily caused by stagnant river miasmas carrying “zymotic” particles.15 As an additional causal factor, Shapter pointed to “a few isolated spots in which a remarkable and undue amount of mortality took place, . . . the very places in which . . . a large amount of mortality had been anticipated, and of whose bad drainage and unwholesome state, complaints had been made” (224). The effects of low elevation and bad drainage could be mitigated by other factors. For example, St. Edmund’s parish was “situated at the bottom of the hill,” on low-lying ground, “densely people,” inhabited “chiefly by the poor,” and had “no particular sanitary arrangements”(224). But the death rate was only one-third that of the worst-affected parish because the area’s “sole peculiarity” was “being freely intersected by running streams of water”(224).16 That is, Shapter was a sanitarian

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Figure 12.3. Cholera mortality in Exeter between 1832 and 1834 (Shapter, Cholera in Exeter in 1832, frontispiece).

who believed his narrative vindicated the aggressive approach of the local Board of Health. In the words of one reviewer writing in 1849, “When cholera visited Exeter in 1832, it found a city close, confined, badly drained, and still worse supplied with water. . . . These things are different now, and so likewise . . . is the progress of the present epidemic.”17

Later Developments in Spot Mapping Techniques Cholera maps appeared during the first three major epidemics in Europe (Table 12.1). The later progress maps were not substantially different from the earliest. Spot mappers, by contrast, evolved new cartographic techniques and expanded the use of disease maps in investigating the causes of cholera outbreaks. A significant change in spot mapping came with the realization that the mere display of dots within a

Table 12.1. Examples of cholera maps published between 1832 and 1855. These examples are listed according to how they were used (denoted by a “✓”): (1) illustratively (without any analytic purpose), (2) inductively (seeking causative associations), and (3) deductively (whereby a hypothesis or theory was tested). Type of map analysis: Author(s)

Date published

Date constructed

Location of epidemic

Date of epidemic

Illustrative

Inductive

Deductive

1833 1849 1854 1850 1854 1855 1855 1855 1855 — 1857

1833? ? 1854? 1850? 1854 1854 1854 1855? 1855 1854 1854

Manchester, England Exeter, England Chorlton-Upon-Medlock, England Boston, Mass. Golden Square, London Golden Square, London Golden Square, London Golden Square, London Golden Square, London Kingdom of Bavaria Aubing, Germany

1833 1832–34 1853–54 1849 1854 1854 1854 1854 1854 1854 1854

✓ ✓ — ✓ — ✓ — ✓ ✓ ✓ —

— — ✓ — — — — — — — ✓

— — — — ✓ — ✓ — — — —

1833? ? ? 1848? 1849 1848 ? ?

Leeds, England Hamburg, Germany Leeds, England Bethnal Green, London Glasgow, Scotland England England Paris, France

1832 1832 1831–32 1848 1848–49 1848 1849 1852–54

✓ ✓ ✓ ✓ ✓ — ✓ ✓

— — — — — ✓ — —

— — — — — — — — (continued)

Spot maps Gaulter Shapter Hatton Shattuck Cooper Snow/MCC2 Snow/CIC Board of Health St. James CIC von Pettenkofer von Pettenkofer

Shaded and cross-hatched maps Baker Rothenburg Chadwick Gavin Sutherland Petermann Farr Administration Générale

1833 1836 1842 1848 1850 1852 1852 1855

Table 12.1. Examples of cholera maps published between 1832 and 1855. These examples are listed according to how they were used (denoted by a “✓”): (1) illustratively (without any analytic purpose), (2) inductively (seeking causative associations), and (3) deductively (whereby a hypothesis or theory was tested). (Continued) Type of map analysis: Author(s)

Date published

Date constructed

1832 1832 1850

1832? 1832? ?

Location of epidemic

Date of epidemic

Illustrative

Inductive

Deductive

1817–32 1831–32 1817–48

✓ ✓ ✓

— — —

— — —

Progress maps Brigham Jackson, et al. General Board of Health

India–North America India–England China, England, North America

Source: Gaulter, after 207; Shapter, Hatton; Shattuck; E. Cooper; Snow, MCC2, between 44 and 45; Snow, “Report,” CIC, between 107 and 08; GBH, Report, Committee for Scientific Inquiries, 1854; Pettenkofer (Bavaria) in Barrett, 501; Pettenkofer (Aubing) in Barrett, 501; Baker; Rothernburg; Chadwick; Gavin; Sutherland, in GBH, Report on Cholera, 1848–49, appendix A; Petermann; Farr; Administration Générale, in Kudlick, 16; Brigham, facing title page; J. Jackson, 170; GBH, Report on Cholera, 1848–49, facing title page.


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geographical area could be highly misleading unless the population density was relatively constant over the same area. Suppose that there are twice as many dots on the left-hand side of a spot map as on the right. It might be that some environmental factor that predisposes toward cholera exists on the left side. It might also be that twice as many people live in the left of the region than in the right, so that the actual rate of cholera cases per unit of population is identical. In a retrospective map of the 1831–1833 epidemic, Petermann accounted for variations in population density by adapting Quetelet’s method of continuous tonal shading to depict the differential rates of cholera mortality in various parts of Britain.18 This cartographic change was made possible when census authorities in 1841 distributed an official “household schedule” to every house, and enumerators transferred data from these schedules into books subsequently available from the Registrar-General’s Office.19 The concentrations of cholera deaths (shown by dots) “seemed to lie all in the lower ground and valleys,” which would confirm Farr’s theory that residing at low elevations increased the risk of cholera,20 but Petermann was not convinced. He engaged in a “minute investigation” of the relationships among terrain, demography, and cholera deaths, concluding from this inductive exercise that “of all of the local causes of the spread of the disease, altitude is one of little comparative influence . . . it is much more affected by the density of the population.”21 Because more large cities were located at lower than at higher altitudes, lower elevation was associated with both population density and various unsanitary features such as overcrowding, making it hard to blame elevation alone for increased cholera incidence. The Lancet acknowledged receipt of this “cholera map . . . the ingenious production of Mr. A. Petermann,” and suggested “that a map of a similar character, coloured weekly, agreeably to the report of the Registrar-General, so as to indicate the localities successively invaded by cholera at the present time, would not be destitute of public interest.”22 No such combination of spot and progress maps of cholera appeared during the 1848–1849 epidemic, however. Other cartographers also expanded the spot map’s potential for showing associations among variables. John Hatton, working contemporaneously with Snow in London, displayed a spot map in his lecture on the sanitary condition of Chorlton-UponMedlock, a district in the city of Manchester, in 1854.23 He incorporated shading and various circular symbols to show a broad array of data. He distinguished between “fevers” and actual cholera cases, mapped such cases and deaths, included details about local sewers, and indicated “unhealthy districts” as shaded areas. A sanitarian, Hatton constructed the map to feature a striking concordance between clusters of cholera cases and the “unhealthy districts.” A star denoting the first recorded case of cholera, which epidemiologists now term the “index case,” suggests that he may have been a contingent contagionist and that he added an inductive, discovery dimension to an otherwise illustrative map. Although Hatton assumed that the efficient cause of this epidemic disease was a local miasma, plotting the index case on the map was part of the investigative process he used to determine the spread of the

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epidemic through the inhalation by others of effluvial emanations from the earlier victims. Max von Pettenkofer (1818–1901) joined a commission investigating the lethal 1854 cholera epidemic in Bavaria. His reading of medical literature on cholera, including Snow’s MCC, left him unconvinced by any current theory. Each one, be it contagion, noncontagion, contingent contagion, or communication by water, could account for only some of the available evidence about the propagation of this disease; there had to be a causal factor that existing theories had not considered. During surveys in Bavaria he produced at least two spot maps that reflected his understanding of new cartographic techniques. One was a three-color map superimposed on a military map of the kingdom that showed various geographical features. The spatial distribution pattern of cholera deaths was depicted by three levels of intensity: epidemic (red), sporadic (green), and scattered (blue).24 This map appears to have been an inductive exercise, designed to help Pettenkofer develop a hypothesis about the causal factors producing cholera. The color shading of varying disease prevalence indicated that people residing in moist, low-lying areas were more often and more severely affected than those who lived on drier and more elevated terrain. He speculated that peculiar environmental features of the soil, groundwater, and organic pollution might explain this variation, but he still had no working hypothesis.25 Later in the summer of 1854 he studied cholera outbreaks in ten Bavarian cities, including Munich and outlying villages. For an outbreak in Aubing, west of the city, he plotted the location of cholera deaths by households on a topographical map and added numerical identifiers for each death. When analyzing the map he was struck by certain associations between deaths and high groundwater levels in partly saturated gravel soil at low elevations.26 The following year his inductive mapping experience in Aubing may have been critical in formulating the soil (Boden) theory of cholera he would articulate in a succession of papers thereafter.

Disease Mapping in Golden Square At least five spot maps were constructed of the most deadly, localized cholera outbreak in London during the epidemic of 1853–1854. The first was made by Edmund Cooper, an engineer at the Metropolitan Commission of Sewers. The commission sent him to Golden Square early in September 1854 to mollify vociferous residents of St. James Parish, who believed that new sewers, including one that ran through a seventeenth-century plague burial ground, vented cholera poison into their neighborhoods, which had experienced few cases in the two previous epidemics. Cooper thought otherwise. Although he shared the residents’ anticontagionist assumption that offensive odors could carry epidemic disease particles, it seemed highly unlikely that the corpses of plague victims buried almost two centuries earlier would still be decomposing. Moreover, any disease particles introduced into the sewer mains


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during construction would have been flushed into the Thames long before the current outbreak, which had commenced at the end of August. A sanitarian himself, like the commissioners for whom he worked, Cooper’s hypothesis was that the outbreak was caused by incomplete sanitary renovations in the parish—cesspits still collecting wastes from latrines—together with insufficient drainage in certain houses, overcrowded and filthy living conditions, and so on. The only way to exonerate the Sewer Commission from public accusations was to show, somehow, that cholera deaths in the parish were clustered in local effluvia hot spots rather than along the offending line through the plague pit or near grates and shafts to the connecting sewer lines. That is, Cooper had to devise a way to confirm his own hypothesis and refute the residents’ counterclaims. He decided to undertake a study that involved deductive mapping because the problem was inherently geographical. First, he consulted the Registrar-General’s Weekly Reports through 9 September, from which he compiled a table of 316 deaths at addresses for each street in the area. He then inspected every house in the table. On a detailed engineering map of the parish that showed all sewer lines, gratings, and gully holes, he drew a thick line along the street frontage at each address where at least one death was listed; behind the street numbers he drew individual bars representing each case listed at that address (Fig. 12.4). The thick lines are the map’s striking feature that Cooper used as scientific evidence to disprove the residents’ complaints: “It will be seen by the Plan [map], that the houses in which the great majority of deaths have taken place, are not situate opposite to gullies or ventilating shafts.”27 The map and sanitary details from the data table permitted him to prove his own hypothesis: Throughout the neighbourhood, it is important to observe, that the houses are, for the most part, let out in lodgings; a separate family, and in some cases even two, are living on one floor, whereas but one water-closet, or privy in the yard or area, exists for the use of the whole house; consequently, in the rooms above the ground floor, portable cesspools or slop pails are kept, into which night soil, dirty water, and all refuse are thrown, and these are emptied about once a day, either down a sink, or into the water-closet or privy; and not unfrequently into a gully in the street. On the top or attic floor, the occupants generally make use of the gutter for the emptying of these accumulations, which find their way down the rain water pipe on to the paving in the yard at the back of the house, and sometimes on to the footway in the street front.27a He concluded that local unsanitary conditions had caused the outbreak. Cooper was an engineer, not a medical cartographer. His map combined the traditional use of marks for each case—solid black bars like Shapter’s rather than dots— with the addition of thick black lines at street frontages for every house with at least one case of cholera. The combination of bars and lines indicate the deductive

Figure 12.4. Edmund Cooper’s map of the Broad Street cholera epidemic made for the Metropolitan Commission of Sewers, September 1854. Inset: the Broad Street pump and surrounding addresses. Cooper designated each affected house by a large solid bar, and the cholera deaths occurring in each house by thin lines.


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nature of this mapping enterprise. His goal was to disprove public criticism of the commission for which he worked, not to medically map the epidemic. Consequently, his map and report made no use of advanced cartographic features such as tonal shading to represent variations in mortality by population density or a symbol to note the index case. Snow prepared the second and third known maps of the Golden Square cholera outbreak several weeks after the brief investigation that eventuated in his recommendation that the Board of Governors remove the handle of the Broad Street pump. His investigative process involved spatial visualization rather than mapping: As soon as I became acquainted with the situation and extent of the late outbreak of cholera in Broad-street, Golden Square, and the adjoining street, I suspected some contamination of the water of the much frequented streetpump in Broad-street, near the end of Cambridge-street: but on examining the water, on the evening of the 3rd inst., I found so little impurity in it of an organic nature, that I hesitated to come to a conclusion. . . . I requested permission, therefore, to take a list at the General Register Office of the deaths from cholera registered during the week ending September 2, in the subdistricts of Golden-square, Berwick-street, and St. Ann’s, Soho. Eighty-nine deaths from cholera were registered during the week, in the three sub-districts. . . . On proceeding to the spot, I found that nearly all the deaths had taken place within a short distance of the pump. . . . I have not thought it necessary to inquire into the very large number of deaths that occurred in the week ending Sept. 9, as I deem the above inquiry sufficient to establish the cause of the outbreak.28 This is Snow’s first account of his investigation, published on 23 September 1854. He arrived on the scene with a hypothesis in mind and, based on anecdotal information about the outbreak, prior knowledge of sudden, violent local outbreaks, and personal understanding of neighborhood preferences for drinking water, intuited the cause as contamination of the pump in Broad Street by cholera dejecta from an unknown victim. He sought a list of addresses only after an inspection of the pump water showed no evidence of sewage. The subsequent investigation involved houseto-house questioning of residents, which revealed that seventy-seven of the victims had unquestionably taken water from that pump, only six probably had not, and for six others there was no information about their drinking habits. “The result of this inquiry, then, is, that there has been no particular outbreak or prevalence of cholera in this part of London except among the persons who were in the habit of drinking the water of the above-mentioned pump-well” (322). Later in September Snow realized that the GRO list he had used grossly under-reported the number of deaths. He conducted a second house-to-house investigation, received new data from the Registrar-General’s office, and expanded his letter to the editor of 23 September into

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a full descriptive section of the projected MCC2. For some reason he decided at that point to prepare an illustrative map of the Golden Square outbreak and made brief references to it in the manuscript. This disease map (Fig. 12.5), which Snow subsequently displayed at the Epidemiological Society early in December, is a modification of an existing street map. Snow’s template did not show the location of sewer lines, grates, or vent shafts. It lacked precise house boundaries and numbers, so that the addresses at which deaths occurred could only be approximated. Snow added symbols (circled dots) to locate street pumps, although he misplaced the pump in Broad Street, and used individual black bars to represent the 574 victims for whom his new investigation could establish an address.29 The text connected the onset of cholera in most of those victims to drinking Broad Street water. The bars clustered around the Broad Street pump on the accompanying map illustrated his argument; it played no part in his investigations either early in September or during the weeks after the outbreak was over.

Figure 12.5. Snow’s spot map of the Golden Square outbreak, 1854 (MCC2, between 44 and 45).


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The map (Fig. 12.6) he prepared for the St. James Cholera Inquiry Committee was only partly illustrative of the accompanying text. For the CIC report Snow imported as much as he could of the Golden Square section of MCC2, retaining many passages verbatim, correcting street names in the text to match those on the map, occasionally refining the language, and editing some examples, particularly the case of the Hampstead widow. There is no indication of a major departure in the argument until the opening reference to the spot map (Table 12.2). After making a few minor changes to clarify how he had obtained addresses where cholera deaths occurred and “the pump in Broad Street . . . indicated on the map” (correcting the location on the revised map as well), Snow introduced new wording that showed that he had

Figure 12.6. Detail from Snow’s spot map of the Golden Square outbreak showing area enclosed within the Voronoi network diagram. Snow’s original dotted line to denote equidistance between the Broad Street pump and the nearest alternative pump for procuring water has been replaced by a solid line for legibility. Fold lines and tear in original (adapted from CIC, between 106 and 07).

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Table 12.2. Snow’s text illustrates changes in the Golden Square spot mapa MCC2

CIC “Report”

The dotted line on the map surrounds the sub-districts of Golden Square. . . . All the deaths from cholera which were registered in the six weeks from 19th August to 30th September within this locality, as well as those of persons removed into Middlesex Hospital, are shown in the mapb by a black line in the situation of the house in which it occurred, or in which the fatal attack was contracted (46).

The outerdotted line on the map surrounds the sub-districts of Golden Square. . . . All the deaths from Cholera which were registered in the six weeks from August the 19th to September the 30th within this locality, as well as those of persons removed into Middlesex Hospital, are shown by black lines in the situation of the houses in which they occurred, or in which the fatal attacks were contracted (108).

a

We italicize every difference and boldface those significant to the maps.

b “The

particulars of each death connected with this outbreak were published in the “Weekly Returns” of the Registrar General to 16th September, and I procured the remainder through the kindness of the Registrar-General and the District Registrars”; MCC2, 46.

undertaken additional investigations involving deductive mapping to strengthen his hypothesis (Table 12.3).30 Details from the two maps (Fig. 12.7)31 indicate an illustrative revision (repositioning the Broad Street pump to its proper location) and the deductive addition of an “inner dotted line”—a line demarcating equal walking distance between the Broad Street pump and the nearest alternative pump.32 The new line meant that 380 of the 574 cases on the map lived closer in pedestrian terms to the Broad Street pump than to any of thirteen other pumps within the study area. Establishing such an irregular catchment area for the pump strengthened the probability that many victims whose drinking habits Snow could not determine by interrogating survivors may have taken Broad Street water. This new line also countered possible noncontagionist interpretations that the MCC2 spot map showed precisely the clustering of deaths that one would expect from effluvial vapors diffusing from the pump in an ever-widening circle.33 Snow could neither have added further confirmation to his original hypothesis nor falsified a noncontagionist reading of the MCC2 map without this exercise in deductive mapping.34 The fourth spot map of the Golden Square outbreak was produced under the auspices of the Committee for Scientific Inquiries of the General Board of Health (GBH). This illustrative map charted the locations of 697 deaths determined by an extensive house-to-house survey conducted by Fraser, Hughes, and Ludlow in September 1854.35 The cartographer consulted Cooper’s map and incorporated its engineering precision in the GBH map, but the committee did not agree with Cooper’s conclusion. The committee believed that the preponderance of evidence indicated that the outbreak was caused by an unknown atmospheric influence emanating from putrefying organic matter, and contrary to Cooper’s report and map, the Fraser team

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Table 12.3. Snow’s deductive addition to the CIC spot map.a MCC2

CIC “Report”

It requires to be stated that the water of the pump in Marlborough Street, at the end of Carnaby Street, was so impure that many people avoided using it. And I found that the persons who died near this pump in the beginning of September, had water from the Broad Street pump. With regard to the pump in Rupert Street, it will be noticed that some streets which are near to it on the map, are in fact a good way removed, on account of the circuitous road to it.

It requires to be stated that the water of the pump in Marlborough Street, at the end of Carnaby Street, was so impure that many people avoided using it; and I found that the persons who died near this pump, in the beginning of September, had water from the Broad Street pump. The inner dotted line on the map shews the various points which have been found by careful measurement to be at an equal distance by the nearest road from the pump in Broad Street and the surrounding pumps; and, if allowance be made for the circumstance just mentioned respecting the pump in Marlborough Street, it will be observed that the deaths either very much diminish, or cease altogether, at every point where it becomes decidedly nearer to send to another pump than to the one in Broad Street (109).

These circumstances being taken into account, it will be observed that the deaths either very much diminished, or ceased altogether, at every point where it becomes decidedly nearer to send to another pump than to the one in Broad Street (46–47). a

We italicize every difference and boldface those significant to the maps.

included sewer gases escaping from new sewer lines in the parish among the unquestionable factors possibly responsible for the local outbreak.36 The Cholera Inquiry Committee in the parish obtained a copy of the GBH map and was given permission to reproduce it in its report, published late in the summer of 1855.37 The CIC as a whole concluded that impure water from the Broad Street pump had caused the outbreak: “Contamination of the water in the well in Broad Street by filtration from a cesspool during the time of the Cholera outbreak is rendered certain by the result of Mr. York’s investigations made in April” (75). In addition, Reverend Whitehead discovered the likely index case, the infant listed as dying from diarrhea at 40 Broad Street. Snow had not included her death among the four bars he placed at that address on both of his spot maps. The GBH investigators must have decided that her diarrhea was premonitory of cholera and added a fifth bar on their map. Whitehead reached a similar conclusion and requested another excavation (the earlier one, undertaken at Snow’s request, had found no evidence of contamination). This time, York’s team had found decayed brickwork between the pump well and the drain into which water from soiled diapers had been emptied. Although Whitehead had come to accept Snow’s water-borne hypothesis, the CIC waffled: “All the facts seem to point to the introduction, importation, or invasion [of the pump] of a material agent, either gaseous, liquid or solid, having specific

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Figure 12.7. (left) Snow’s spot map, detail of area around the Broad Street pump (from MCC2). (right) Snow’s spot map, detail of area around the Broad Street pump. The finely dotted Voronoi line is in the lower half; the symbol for the Broad Street pump—circle around black dot—has been repositioned to its correct location opposite no. 40 Broad Street (from CIC, between 106 and 107).

poisonous properties” (85). At Whitehead’s suggestion the CIC modified the GBH map by inscribing a circle with a radius of 210 yards around the Broad Street pump (Fig. 12.8) to depict the “Cholera area” within which the vast majority of the cases were clustered (16).38 What sort of medical cartographer was Snow? Today a considerable part of his reputation hinges on his role in mapping the Broad Street outbreak, so it is essential that the historical assessment be accurate. When Snow modified his original map for the CIC, he introduced a substantial cartographic innovation by explicitly indicating the line of equidistance among the pumps. (Ironically, his CIC map is much less well known today than the more common and less accurate version of the map in MCC2.) Overall, however, Snow viewed his mapping activities as a minor aspect of his investigation of cholera. He never used his map as a true investigative tool, unlike Cooper and von Pettenkofer, whose theories of cholera transmission are today discredited. The structure of MCC2 makes clear that Snow intended his south London study to be the centerpiece in supporting his theory. In essence, the Broad Street investigation was merely preparation for the main event. It is due largely to the connection between Broad Street and a visually appealing icon, the map, that


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Figure 12.8. The General Board of Health map used by CIC, with Whitehead’s “cholera area” indicated by a circle (CIC, between 96 and 97).

today’s reader often gets it backward and attributes to the Broad Street investigation an importance that Snow never assigned to it in comparison with the much more extensive and conclusive study of the south London data.

Notes 1. Snow, “On the mode of propagation of cholera,” 559. 2. UK GBH, Cholera of 1848 & 1849, appendix B (by R. D. Grainger), map opposite 200. In Grainger’s “tinted cholera map” the “depth” of the “tinting” showed the “amount of mortality”; Ibid., 31–32. Grainger was an anticontagionist; see “Mr. Grainger and the cholera,” Lancet 1 (1849): 106–07, issue of 27 January 1849. 3. Also suspended in the room at the meeting of the Epidemiological Society was a statistical table, copied from the 12 January 1850 Weekly Report of Births and Deaths, depicting cholera mortality in the 1848–1849 epidemic. 4. “Map 1. Showing the deaths from cholera in Broad Street, Golden Square,” MCC2, viii; inserted between 44 and 45. Map 2 was a boundary map showing districts south of the Thames and their water supply, akin to the one from the Health of Towns Report he displayed before the Epidemiological Society. 5. Although MCC2 was not printed until late December 1854 or early January 1855, the opening passage reads as follows: “The most terrible outbreak of cholera which ever occurred in this kingdom, is probably that which took place in Broad Street, Golden Square, and the

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adjoining streets, a few weeks ago” (38)—actually, the first two weeks of September. Further on Snow wrote, “The deaths which occurred during this fatal outbreak of cholera are indicated in the accompanying map, as far as I could ascertain them. There are necessarily some deficiencies . . . [although they] probably do not detract from the correctness of the map as a diagram of the topography of the outbreak” (45). 6. “Epidemiological Society,” Lancet 2 (1854): 530–31; MTG 9 (1854): 629. 7. We offered a slightly different interpretation of these maps in Brody et al., “Mapmaking and myth-making in Broad Street,” Lancet 356 (2000): 64–68. 8. See Barrett, Disease & Geography; A. Robinson, Early Thematic Mapping; Jarcho, “Yellow fever, cholera, and medical cartography”; and Gilbert, “Pioneer maps of health and disease.” 9. Petermann, Cholera Map, “Statistical notes,” 1. 10. Ibid., 2. Petermann had traveled to Scotland in 1845 to assist in making an atlas. The Royal Geographical Society elected him a fellow in 1846, before he moved to London. In 1852 Queen Victoria gave him an appointment as physical geographer and engraver in stone at her court. 11. Seaman, “Inquiry into yellow fever in New York.” 12. Jackson, Spasmodic Cholera. 13. Ibid., 170. 14. Shapter, Cholera in Exeter in 1832. 15. He allowed for person-to-person transmission as a contingent factor; Ibid., 230. 16. Later Snow used the parish of St. Edmund as evidence that a pure water supply would protect residents from cholera despite elevation and cholera’s prevalence in nearby districts (MCC2, 99–100). 17. “Reviews,” Lancet 2 (1849): 317. The reviewer added that “an admirable map of the city, indicating the points at which the disease prevailed, . . . add to the value of the work.” Many decades later Underwood called attention to the existence of Shapter’s book—”a mine of information, and it must be one of the best descriptions extant of an historical epidemic”; British Medical Journal (1933): 620. Unlike the Lancet reviewer, Underwood did not mention the map. 18. Petermann, Cholera Map. The inset for London represented varying percentages of cholera deaths in six tints, from pink to red. Grainger also used this tonal shading method (see Fig. 12.1); UK GBH, Cholera 1848 &1849, appendix B, 200. Both had adapted Adolph Quételet’s system of continuous tonal shading, with increasing mortality represented by increasingly darker shades; see A. Robinson, Early Thematic Mapping, 160–61. 19. Mills and Pearce, Victorian Census, 1; Glass, Numbering the People, 94. Petermann also produced two demographic maps of England, one in 1848 that made use of 1841 census material and the second to illustrate the 1851 census. 20. Petermann, Cholera Map, “Statistical notes,” 4; Farr, Cholera in England, 1848–1849, lxi–lxv. 21. Petermann, Cholera Map, “Statistical notes,” 4. 22. Lancet 2 (1848): 595. 23. Hatton, “Sanitary condition of Chorlton-Upon-Medlock.” 24. Blue was used to indicate places where cholera was present in only one or two houses. This map was probably destroyed during the aerial bombing of Munich in July 1944; see Barrett, Disease & Geography, 375. 25. Hume, Max von Pettenkofer, 58. 26. Barrett brought this map to our attention and supplied a copy. 27. Cooper, “Report,” 3. 27a. Ibid., 3–4. 28. Snow, “The Cholera near Golden Square, and at Deptford” (1854).


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29. Shapter’s map of cholera in Exeter may have influenced Snow to substitute bars for dots to represent cases. In 1849 Snow noted that Shapter “kindly furnished me with information concerning the sewers, and maps of their position,” in Exeter; PMCC, 751. However, Snow never cited Shapter’s spot map. In addition, Cooper employed bars, and there is no indication he was influenced by Shapter. 30. Snow, “Dr. Snow’s report,” CIC, 109. Some of the alterations are also noted by McLeod, “Our sense of Snow,” 931–32. 31. The revised spot map in CIC, between 106–07. 32. Such an equidistant line dividing a map into areas is today called a Voronoi diagram. McLeod considers Snow the first disease cartographer to use such a device; “Our sense of Snow,” 932; see also Brody et al., “Map-making and myth-making in Broad Street.” 33. E. A. Parkes made this point in a review of MCC2 for British and Foreign Medico–Chirurgical Review 15 (1855): 458. Parkes also noted that there were so many street pumps in this neighborhood that no matter where the noxious vapors had originated, there was certain to be a pump nearby, but Parkes’s review appeared after Snow had written his report for the CIC and reconfigured the map of Golden Square. 34. Of the 194 cases (33.8% of the total) outside the equidistant demarcation line, Snow made additional inquiries early in December 1854 and was able to show that at least a quarter of them either drank Broad Street water or contracted cholera at a point nearer to that pump than the alternative closer to where they lived; “Dr. Snow’s report,” CIC, 110–16. In his earlier investigations he had shown this to be the case for only four victims; MCC2, 47–48. 35. UK, GBH, Report of Committee for Scientific Inquiries, 1854. 36. Ibid., appendix, 143. 37. CIC, map between 96–97. The virtual identity of the GBH and CIC maps—the CIC added a circle at Henry Whitehead’s behest—was established via a point-by-point comparative analysis. 38. This circle was Whitehead’s second effort to represent the “cholera area” in spatial terms. In the fall of 1854 he had drawn an irregularly shaped polygon to indicate what he took to be the boundaries of the area most afflicted; Cholera in Berwick Street, 1–2.

Chapter 13

Snow and the Sanitarians

NOW’S WORK AS A SCIENTIST and physician in the 1840s was concurrent with some significant formulations of sanitary theory. Edwin Chadwick’s Inquiry into the Sanitary Condition of the Labouring Population of Great Britain (1842) and two reports by the Parliamentary Commissions on the Health of Towns (1844 and 1845) proposed that the endemic and epidemic diseases ravaging the poor of Great Britain could be controlled only by government action. The ultimate results of the sanitary reform movement—publicly-financed water supplies and sewerage in cities, disposal of garbage, and a public health infrastructure— produced profound public health benefits, but not during Snow’s lifetime.1 Later in the century, when the sanitary reform movement eventually adopted the insights from epidemiology that it had initially spurned, and also accepted the new bacteriology that it had been slow to acknowledge, great improvements in public health did take place. Sanitary reform would have borne fruit much sooner, however, had it linked disease to class distinctions, slum housing, and industrial exploitation of the working classes.2 Sanitarianism in Snow’s time retained the humoral notion that health was the result of a harmonious relation between every body’s unique internal components and the external environment. As such, the sanitary reform movement was based on a comprehensive view of the relationship of humans to their natural and social environments rather than a theory of fever causation.3 The immediate consequence of

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such views was to reject narrow or specific theories such as Snow’s. It seemed to defy common sense experience for him to insist that cholera, always and everywhere, was caused by one particular method of transmission: the fecal–oral spread of the specific cholera particle or agent. It seemed equally obvious to his critics that cholera was sometimes caused by one factor, sometimes by another, depending on local conditions and the history of the individual patient. To a sanitarian Snow’s simple reforms for the prevention of cholera were pure nonsense; why bother to institute reforms that might not prevent other disorders?4 By comparison William Budd’s claims that cholera was usually spread by contaminated water, although inhaled effluvia was a possibility, were more readily acceptable to a multifactorially inclined audience.5

The Sanitarian Establishment The participants in the GBH’s several investigations and committees included a crosssection of London’s leading physicians, surgeons, apothecaries, scientists, and public health officials. The professional leadership of all three medical corporations in London, the queen’s physicians Clark and Arnott, the paleontologist Richard Owen, the public health leaders Farr and Simon, Hassall the microscopist, Babington, president of the Epidemiological Society of London, and many others supported the board’s miasmatic interpretation of cholera. They shared a common understanding of the etiology of epidemic disease, even though they differed at times as to the proper ways to achieve particular sanitary goals. Snow’s views on the nature and spread of epidemic diseases such as cholera differed fundamentally from those of the leading sanitarians of his time. The essence of the disagreement was the all-encompassing nature of Snow’s cholera theory and its dependence on two singularities. First, cholera was a singular disease; only a case of cholera could give birth to another case of cholera. Cholera bred as true as any species of animal or plant. Local impurities, whether acting by themselves or in concert with atmospheric conditions, and no matter how foul, could not produce a case of cholera. Second, cholera had a singular route of transmission. With minor and rare exceptions, the only way the cholera agent could be introduced into the body was by swallowing the dejecta of another case of cholera. Even to think of “routes of transmission” was to conceptualize the agent of cholera in a radically different way. By late 1854 Snow assumed the cholera agent had to be a form of live matter and suggested that it probably took the form of a cell, analogous to the morbid material that caused smallpox and cowpox (MMC2, 15). It could produce its pathology only by interacting with a specific tissue, the intestinal lining, and therefore needed to be transported to that location. He did not see the cholera agent, as the sanitarians did, as a local atmospheric phenomenon that in the presence of common toxic gases arising from putrefaction was inhaled and absorbed into the bloodstream, where it chemically combined with unspecified human material to

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produce its pathology. Snow emphasized the singularities of the nature of cholera and its fecal-oral and waterborne route of transmission. But this advocacy included a negative dimension—an intense skepticism of the alternative explanation, the gaseous-miasmatic concept of cholera origin. His skepticism of miasma theory, which stemmed in part from his understanding of anesthetic gases, ultimately proved more troubling to sanitarians than did his cholera theory and its link to water supplies. Both Snow and the sanitarians recognized that their differences in the theoretical construction of the nature of cholera and its agent were not idle speculations in pure science about which gentlemen could disagree. Their divergent theories had profound implications for public health action. Snow believed that the sanitarian focus on the elimination of fictitious air-borne cholera agents was either useless in the prevention of cholera or inadvertently promoted spread of the disease. He believed the sanitarians were especially mistaken in their desire to rid cities of sewage by flushing it into the same waterways that served as the sources of municipal water supplies. This practice was a major plank in the sanitary program of the Metropolitan Commission of Sewers (MCS) in London.6 One of the commission’s recommendations was to eliminate London’s estimated 200,000 cesspools, replacing them wherever possible with water closets directly connected to the sewers. In Snow’s mind such a program essentially meant that cholera evacuations would be routed into the Thames and then recirculated in the piped water supply to be ingested by an unsuspecting populace. Chadwick was one of the twenty-three original commissioners appointed in 1848, and it seems clear that the MCS was influenced by the recommendations on drainage he had formulated earlier in the decade when writing Sanitary Condition of the Labouring Population. Chadwick believed that substituting water closets for latrines and cesspools, laying sewer drains, and then using great volumes of water to flush urban filth and refuse into nearby rivers would eliminate the foul smells he considered predisposing for epidemic diseases. Joseph Bazalgette, the chief engineer of the MCS and the designer of the nineteenth-century sewage system that continues to serve London, noted that, “within a period of about six years, thirty thousand cesspools were abolished, and all house and street refuse was turned into the river. . . .”7 Success in achieving this goal was largely due to an MCS recommendation that all new housing be outfitted with flushable water closets,8 but the “arrival of the water closet was a giant step forward for personal hygiene and two steps backward for public sanitation.”9 Snow’s theory predicted that unless the water supply was protected from recycling raw sewage, the new system, appealing though it might be to the olfactory sense, would exacerbate the severity of future cholera outbreaks. Despite their theoretical disagreements, Snow maintained cordial personal relations with most of the sanitarians, participating amiably, for example, in meetings of the sanitarian-dominated Epidemiological Society, of which he was a founding member. In return they generally accorded him a respectful hearing, seldom rejecting his arguments out of hand. In turn Snow avoided ad hominem attacks when he


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considered it necessary to criticize the sanitary agenda. During the 1849 epidemic, for example, he was gently ironic in commenting on high mortality in Rotherhithe, where many inhabitants obtained their drinking water directly from ditches of Thames water that were refilled at each high tide: “Rotherhithe is less densely populated than many parts of the metropolis which have been comparatively free from cholera, and those ditches, it should be remembered, are not very offensive to the smell; being only Thames water rendered a little richer in manure; being, in short probably equal to what Thames water would be if certain of our sanitary advisors could succeed in having the contents of all the cesspools washed into the river” (PMCC, 748). However, five years later his criticism had an edge to it: There is one circumstance, however, that ought to prevent any expression of blame or recrimination for the propagation of cholera in this way; it is this— that the persons who have been more instrumental in causing the increase in cholera, are precisely those who have made the greatest efforts to check it, and who have been loudest in blaming the supineness of others. In 1832, there were few water-closets in London. The privies were chiefly emptied by night men, a race who have almost ceased to exist; or a portion of the contents of the cesspool flowed slowly, and after a time, into the sewers. By continued efforts to get rid of what were called the removable causes of disease, the excrement of the community has been washed every year more rapidly into the river from which two-thirds of the inhabitants, till lately, obtained their supply of water. While the fæces lay in the cesspools or sewers, giving off a small quantity of unpleasant gas having no power to produce specific diseases, they were spoken of as dangerous and pestilential nuisances; but when washed into the drinking-water of the community, they figured only in Sanitary Reports as so many grains of organic matter per gallon.10 In his mind it was obvious that cholera epidemics in London were getting worse, and he held misguided sanitarian reformers chiefly responsible.

The Nuisance Trades On 5 March 1855 Snow provided his testimony to Parliament on the proposed Nuisances Removal and Diseases Prevention Act. This act sought to control factory processes, such as tanning and soap making, which depended upon animal products and were associated with unpleasant smells. For miasmatists such as Chadwick, who adhered to the notion that all stink is disease, the smells emanating from these factories were exciting or contributory causes of epidemic disease. But Snow believed that medical concern about such odors was a complete waste of time, so he agreed to present his views on epidemic disease in support of the manufacturers whose

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factories were threatened by the pending legislation.10a The testimony sparked editorial denunciation from the Lancet, accusing Snow of joining forces with filth and disease and abandoning the sanitary cause.11 Had Snow been thinking solely of politics, he would surely have avoided presenting this testimony. Had he wished to win the sympathies of the sanitarians, he would have avoided taking the side of the nuisance trades. He was later characterized by his friend and fellow student Joshua Parsons as someone who cared solely about truth and gave not a jot about what others might think of him. Still, the Snow who loved truth must have been bothered by the Lancet editorial. After giving his testimony Wakley accused him of “riding his hobby . . . down a gully-hole” and being unable to extricate himself.12 He assumed that Snow was so enamored of his theory of the diffusion of gases that he could not smell what was right under his nose and so failed to reach the common sense, sanitarian conclusion that anything as patently offensive as the nuisance trades would have to have an injurious impact on health. In Wakley’s view, Snow had deviated from his usual scientific practice. He had presented conclusions without experimental evidence or statistics to back them up. Snow seems to have taken that portion of Wakley’s criticism to heart. The following year he submitted a paper on the nuisance trades to the Lancet.13 He made no reference to the harsh words meted out by Wakley, nor did he attempt to justify his decision to testify on behalf of a consortium of manufacturers. Instead, he presented evidence that workers in offensive trades did not suffer more ill health than did other urban workers. Snow presented mortality rates by occupation derived from Weekly Returns published during the previous eighteen months. The overall mortality for men over twenty was 241 per 10,000, while for men over twenty in the offensive trades it was 205. If the category was enlarged to include all who worked with dead animals (i.e., poulterers, butchers, and fishmongers) the mortality rate was 201. Snow listed fifteen offensive trades in which at least one death occurred, trades that give a wonderful sense of the early industrial world of urban London—tripe dealer/dresser, tallow chandler, comb maker, soap boiler, music string maker, bone gatherer, bone worker, carrier, tanner, fellmonger, grease dealer, cat meat purveyor, skinner, parchment maker, glue and size maker.14 Snow was aware that age distributions above twenty might well vary in the several occupations and cited Farr to that effect when discussing the data from which his numbers came, but Snow dismissed age as an explanation for his findings. Compared to the total population of men over twenty, Snow reasoned, the ages of men in any specified occupation ought to be greater because the trades might be joined at any age over twenty, thereby excluding younger men from the occupational tally. The higher average age of any occupational group ought to have produced higher mortality, and thus the lower rate found in the offensive trades was yet more impressive evidence of their healthiness. By way of comparison, Snow mentioned that the mortality rate among keepers of beer shops was a relatively high 373. However much Snow the teetotaler might have been tempted to attribute this high death rate to the evils of alcohol, Snow the scientist pointed out that it was common for older men who had become unfit for


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more active occupations to take up the beer trade. The higher mortality rate reflected the average age and earlier health of the workers and not the inherent danger of the trade. He thought that the nuisance trade figures should be reasonably accurate with regard to health hazards because he knew of no biasing tendencies for men of any certain age group to enter or to leave those trades. Although his argument rested mainly on numerical data, he reiterated the view that the laws of diffusion of gases directly contradicted miasmatic theory: “As the gases given off by putrefying substances become diffused in the air,” he noted, “the quantity in a given space is inversely as the square of the distance from their source. Thus, a man working with his face one yard from offensive substances would breathe ten thousand times as much of the gas given off, as a person living a hundred yards from the spot.”15 Mention of gas laws drew Wakley from his den. A week later the Lancet responded with an editorial that also drew on data and conclusions published by the RegistrarGeneral. The editorial noted the documented hazards to the respiratory system caused by the air of London, contaminated as it was by “mechanical impurities in the shape of fine dust, composed of a variety of organic and inorganic matters.” Although the public health issue in question was not quite the same as that dealt with by Snow in his article and testimony, the Lancet used this tangible evidence of the ill effects of air to cast aspersion, once again, on Snow’s science. Speaking of the “variety of noxious gases and vapours” in the London air, the editorial suggested that, “There can be no doubt that they exert a most efficient and malignant influence in the causation and aggravation of disease. They are evolved so fast in many districts, that the ordinary rate of circulation of the air and the action of that beautiful law of the diffusion of gases are altogether insufficient to dilute them rapidly enough to deprive them of their poisonous properties.”16 Snow did not respond to this editorial, or to a letter that appeared the following week from a Dr. John W. Tripe, the medical officer of health for the borough of Hackney. Dr. Tripe could not agree with Snow’s conclusions about the offensive trades, arguing that the census figures Snow used were not adjusted for the increase in population since the 1851 census and that the problem of age differences might not have favored Snow’s view. One needed youth and strength for these kinds of work, so the deaths of older, retired workers from these trades might not be classified with them.17 Dr. Tripe was considering a possibility that Snow had dismissed, that diseases caused by constant exposure to noxious gases would be either delayed in onset or else slow to develop and chronic in nature. But Snow’s testimony had focused only on acute fevers and epidemic disease, while his paper included deaths from all causes and concluded that there was no elevation in mortality.

Responding to the GBH Snow turned next to a critique of government reports on the cholera epidemic of 1853–1854. The Committee for Scientific Inquiries of the GBH had concluded that

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cholera was the result of an atmospheric ferment that interacted with the existing organic impurities in the residences and neighborhoods of the poor.18 In a series of reports published in mid-1855 and illustrated with the map developed from the laborious house-to-house survey conducted by Fraser, Hughes, and Ludlow, the committee dealt with concerns about impure water by incorporating them into their general miasmatic framework. They attributed the epidemic to the accumulation of decaying animal and vegetable matter interacting with the “epidemic influence” (a seasonal change in atmospheric conditions). They described the unknown choleracausing agent as acting “after the manner of a ferment,” so that “the stuff out of which it brews poison must be air or water abounding with organic impurity. . . . Either in air or water, it seems probable that the infection can grow. Often it is not easy to say which of these media may have been the chief scene of poisonous fermentation; for the impurity of one commonly implies the impurity of both; and in considerable parts of the metropolis (where the cholera has severely raged) there is a rivalry of foulness between the two. But, on the whole evidence, it seems impossible to doubt that the influences, which determine in mass the geographical distribution of cholera in London, belong less to the water than to the air.”19 The Committee was aware of Snow’s writings but were unpersuaded by his theory or the evidence he presented that the pump in Broad Street was the source of the Golden Square outbreak : “After careful inquiry, we see no reason to adopt this belief. We do not find it established that the water was contaminated in the manner alleged; nor is there before us any sufficient evidence to show whether inhabitants of that district, drinking from that well, suffered in proportion more than other inhabitants of the district who drank from other sources.”20 Snow responded with a paper presented to the London Epidemiological Society in May and June of 1855. After reiterating themes (sometimes using the very same words) made in MCC2 and his report for CIC, he noted specific points of disagreement with the GBH reports.21 He considered Dr. John Sutherland’s contribution especially problematical. Sutherland, too, had implicated bad water, but only as a predisposing cause; it weakened the constitution, making people more susceptible to the effects of cholera-carrying effluvia than they would be otherwise. He did not accept Snow’s theory that a specific cholera agent must be in bad water for a person to come down with the disease. Snow warned his listeners at the Epidemiological Society that his views on water-borne transmission of cholera required the presence of a transmissible agent: “The division of my views on cholera which refers to its communication through the means of drinking water, has apparently obtained a greater amount of attention from the Profession, than my views respecting its more immediate communication by the cholera poison being swallowed without the water. While I speak on this division of the subject, however, I must beg the Society to bear in mind also the other part of my views, first alluded to, for I am well aware that the part which relates to polluted water will not of itself explain the whole progress of the disease as an epidemic.”22 Nevertheless, Sutherland, the board’s chief


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sanitary inspector, took a pragmatic view of the influence of impure water. He believed that it did not really matter whether one viewed water as containing the “specific poison of cholera” as long as it was recognized that “impure water is injurious to the public health.”23 Even so, Snow was not tolerant of this apparent tilt toward his theory: “It seems very curious that Dr. Sutherland should not have perceived that this question, as to whether or not the water contains the specific cause of cholera, involves the entire question of the cause and prevention of the malady, and also the approval and condemnation of nearly all the so-called sanitary measures which have been adopted with respect to cholera, since it was first expected in 1830.”24 Only water rendered impure by the admission of cholera evacuations could cause the disease, so the central question was whether sanitary reforms reduced or exacerbated that possibility. Snow found errors in several parts of the board’s work, errors that generally stemmed from a lack of knowledge of the water supply. He alleged that the board’s analysis of mortality from cholera in Christchurch, the model lodging houses in Lambeth Square and Park Road, and Jacob’s Island was either mistaken or misleading. The board credited sanitary improvements for lower than expected mortality at each of these locations, whereas Snow argued that the information he had collected during his analysis of metropolitan water supply showed precisely the opposite. For example, he argued that lower mortality in the new lodging houses, with their water closets and good ventilation, was artificial because the board had not taken into account that some cholera victims were removed to distant hospitals. Snow also criticized the board for using the concept of disease predisposition too loosely. In his mind “a predisposing cause is one which is supposed to prepare the patient to be acted upon by some more direct cause; and it must, therefore, require a certain time for its operation.”25 The information he had gathered in south London and Golden Square clearly showed that some individuals who had not been in the habit of drinking water from a contaminated source did so on one occasion and promptly came down with cholera. “[These] circumstances show that the water did not act as a predisposing cause, but must have contained the real and efficient cause of the cholera.”26

Snow and Simon The differences between Snow and the GBH on the causes of cholera epidemics were more subtle than his disagreement with local miasmatists like Milroy, because the board agreed that impure water could pose health hazards. Hence, Snow’s response in the immediate aftermath of the 1853–1854 epidemic was a series of emphatic clarifications that his theory required fecal–oral transmission of the cholera agent; it must be swallowed, and the vehicle could be food as well as impure water. The differences between his views and the GBH’s became even blurrier when, in mid-1856, the latter published a “Report on the cholera epidemics of London as affected by the

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consumption of impure water,” written by the medical officer to the privy council, John Simon.27 This report virtually replicated Snow’s analyses of London water supply in MCC2. Moreover, Simon practically appropriated his description of the natural experiment offered by the comingled water supply in south London.28 The report was well received in the medical and popular press,29 but Snow bit his tongue. He wrote a letter to the Times at the end of June in which he summarized his views and then embarked on a scientific paper for the journal of the Epidemiological Society published in October 1856. He began the former with a laconic assessment: “This report, although valuable in some respects, contains, from the nature of it, only an approximation to the truth.”30 Next he told the truth, as he saw it: “The population supplied with the impure water of the Southwark and Vauxhall company suffered a mortality from cholera in the late epidemic not [as Simon would have it] merely three and a half times as great as that supplied by the Lambeth Company, but six times as great; and even this fact expresses the influence of the impure water in an inadequate manner, unless the different periods of the epidemic are considered separately.” Snow then gave a brief history of his own investigation, the assistance he had received from Farr’s office, and his conclusions. It was a letter to establish his priority. It was also an opportunity to tout the validity of his theory and distance himself from the sanitarians: “I should like to say, in conclusion, that many other diseases, beside cholera, can be shown to be aggravated by water containing sewage, and that since the Southwark Water Company has obtained a supply almost equal in purity to that of the Lambeth Company the mortality of the south districts of London had greatly diminished.” The centerpiece of Snow’s article in the JPH&SR was the predictive mathematical model of south London mortality by subdistricts (discussed in Chapter 10), which Simon’s report enabled him to complete, for it contained what he had been hoping to see since August 1854: a breakdown by subdistricts of the number of houses supplied by the Lambeth and Southwark and Vauxhall companies.31 He also used the article to outline four problematical aspects in Simon’s report that diminished the mortality differences between customers of the two water companies. Snow pointed to 1. Imperfectly drawn subdistrict boundaries resulting in a misclassification of the water supply to some houses 2. Failure to enumerate streets in which no death took place, resulting in an underestimate of the risk of death from cholera 3. Apparent failure to ascertain the correct address for each death 4. Failure to account for the transfer of cholera patients to workhouses and other locations Although each error was relatively minor, their net effect was to dilute the difference in mortality among customers of the two water supplies—from six-fold to threeand-a-half throughout the entire epidemic, as he had already noted in the letter to


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the Times. In essence, Snow was arguing the statistical principle that random misclassification biases towards the null.32 He thought it worth emphasizing this difference in calculated cholera mortality because sanitarians could point to Simon’s lower figure as confirmation that impure water was only a predisposing factor. A six-fold difference overall (and even higher during the early weeks) was more consistent with true causation. Although Snow never objected in public to Simon’s unwillingness to credit him for the original investigation of the south London water supply, a handful of Snow’s friends in the sanitary movement did so on his behalf. At the 1856 meeting of the British Medical Association held in Birmingham, Dr. T. Bell Salter presented an address, “A summary of our present knowledge of the laws of epidemics.”33 Benjamin W. Richardson created an opportunity to support his friend, proposing (as recorded in the minutes) “That the cordial thanks of the meeting be given to Dr. Bell Salter for his learned address.” In proposing this vote, Dr. Richardson was anxious to state that the author of the paper had, as he thought, made an accidental omission in speaking of the Report of the Board of Health on the influence of the Southwark and Vauxhall water supply on cholera, in the last epidemic of that disease in London. It was well known to all who were acquainted with the subject in its fulness, that the discovery of the connexion between water supply and cholera in no way belonged to the Board of Health, but exclusively to one of our own associates—Dr. John Snow. [Hear, hear.] The Board of Health had, indeed, up to a late period, ignored to a great extent this important question; and it was not until Dr. Snow had, with unwearied industry, with that true genius for observation which so characterises his labours, and at great pecuniary cost, placed the question beyond dispute, and had been seconded in this respect by Dr. Budd of Bristol, that the Board took up the matter. . . . The Report itself was nothing more than a corroboration of Dr. Snow’s important and original views; and he (Dr. Richardson) thought it by no means fair that, while the views of other men were referred to, the claims of our associate were entirely overlooked. [Hear, hear.] He thought it was but honest to put the meeting fully in possession of these facts; and regretted that he should have been obliged to digress from the simple business of proposing the resolution placed in his hands. Dr. Lankester seconded the resolution. . . . Dr. Budd said he could not let the occasion pass without expressing his entire concurrence in the remarks . . . from Dr. Richardson. . . . He considered the [GBH] Report decidedly unfair. He had himself laboured at the subject of the diffusion of cholera by means of water, and by the excreta of cholera patients; but he was proud to have that opportunity of stating, that the entire

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priority of this inquiry rested with Dr. Snow. [Hear, hear.]. . . . Certainly, in regard to the spread of cholera by water, [the GBH] had only declared an opinion when the question had been satisfactorily proved by others; and he regretted exceedingly to see that Dr. Snow’s great labours had been so completely unrecognized. [Hear, hear.] The motion was carried unanimously.34 This occasion may have been the only time in Snow’s lifetime that his study of cholera received a “Hear! Hear!” from a medical audience.

Later Cholera Writings After the 1856 article that finalized his south London study and commented on Simon’s report, Snow published seven more items on cholera. One article (and a followup letter) discussed a neighborhood-level cholera outbreak in Abbey-row, West Ham. He made personal inquiries into the layout of the dwellings, water supply, and drainage. At the time of the outbreak, 115 inhabitants received their water supply from one pump in the middle of the row of houses. According to the inhabitants, “The impurity of the water of this pump-well was a chronic affair, and therefore, as mere impurity, would not account for the remarkably sudden and circumscribed outbreak of cholera which has occurred around it. Moreover, mere impurity in the water was never known to cause, or even aggravate, cholera. In all the sudden outbreaks of cholera which I have been able to connect with impure water, and have related in previous volumes of this Journal [MTG], and the two Journals from which it sprung [LMG and MT], there has always been either absolute proof or strong presumption that the evacuations of a cholera patient had entered the water.”35 In addition to this aside at the expense of the sanitarian obsession with all impure water, Snow explained how the evacuations from a cholera patient in one of the houses could have seeped into the pump-well and spread it to other inhabitants of Abbey-row. He counseled patience to anyone who expected a documented index case and cited an example of delayed confirmation: “In the fearful outbreak of cholera near Golden-square, . . . I could myself only bring forward statistical and other evidence of the effect of the water, not having the power to open the well and adjoining drains; but when this was done by the parish authorities, at the suggestion of the Rev. Henry Whitehead, six months afterwards, the pump-well which caused the outbreak was found to be the recipient of the overflow from a cesspool, into which the evacuations of a child ill of cholera had been emptied within three days before the great irruption of the disease.”36 Nonetheless, the British Medical Journal published an article in which the author accused Snow of presenting a tendentious interpretation of the outbreak. Snow responded firmly: “I should like to say,” he wrote in a letter to the editor, “that I have not clipped or shaped this outbreak of cholera to fit the bed I had made for it; on the contrary, it came and shaped itself exactly to the


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conclusions which I had drawn from the observance of previous epidemics.”37 Thereafter, he clarified facts relating to this incident that he considered indisputable, rehearsed parallel examples he had described in earlier writings, and noted the recent changes in the water supply of London that made future epidemics at the metropolitan level unlikely: “At present no water company draws its supply from any part of the Thames which is within reach of pollution by the shipping, or the sewers of the town.”38 Consequently, any cases of cholera introduced from outside London were unlikely to cascade to epidemic proportions. Nonetheless, he “beg[ged] the reader to remember that, although I find it necessary to write most on that part of the subject which concerns the communication of cholera through the medium of water, its propagation by swallowing the morbid poison without this medium, plays a very important part in its progress, more especially in the crowded habitations of the poor.”39 On three occasions Snow used the medical journals to assert his priority over William Budd in developing a new theory about the mode of communication of cholera. The first (in December 1855) was a letter to the editor of the Edinburgh Medical Journal in which he took issue with Dr. William Alison’s statement that “Dr. Budd of Bristol” was the first to propose “the communication of cholera by dejections.”40 Snow noted that MCC was published in advance of Budd’s essay and that Budd had already “made a full and handsome acknowledgement of my priority. . . .”41 However, the editor appended a note to Snow’s letter: “his theory that it is chiefly or almost exclusively by swallowing that the poison of cholera is taken in, can scarcely be supposed.”42 Alison’s article apparently prompted Sir James Kay-Shuttleworth to make a similar misattribution in the Association Medical Journal. Snow read it the day it appeared, and he was again quick to respond, sending a letter of correction that included verbatim phrases from the letter he had sent to the Edinburgh Medical Journal. In the process he distanced himself from Budd’s willingness to consider multifactorial explanations for “the propagation of cholera through the air, by means of the excretions,” and conditional acceptance “that some kind of change or fermentation is necessary in the peculiar excretions of cholera to enable them to propagate the disease.”43 Otherwise, he and Budd were in complete agreement on the pathology and mode of communication. The last publication of Snow’s life, published only weeks before his death, was a two-part paper that gives a picture of where Snow’s thinking might have gone had he lived longer.44 After reviewing much familiar material on the relation of the water supply to cholera and repeating his disagreement with sanitarian and local miasmatic reasoning, he examined the relation of water supply to overall mortality. The metropolitan part of the county of Surrey corresponded quite closely to the southern reaches of the water supplies of the Lambeth and S&V companies. In July 1855 S&V had established a new water intake at the village of Hampton, remote from the sewage of London. Leaving out the cholera years (from July 1853 to December 1854), Snow tabulated total mortality in metropolitan Surrey and in the remainder of London before and after this change. He found that mortality in Surrey, consistently

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higher than in the rest of the metropolis before S&V changed its supply, dropped below average in the succeeding two and a half years. Even greater relative reductions were apparent if attention was paid to deaths from diarrhea and typhus.45 He concluded the article with a disquisition on water closets, which he considered a threat to public health. Flushing required enormous quantities of water, often forcing towns to tap the very rivers into which the sewage was drained. If water closets were to be continued, Snow advised the development of separate water supplies— one for flushing, in which purity was not an issue, the other for drinking water, drawn from pure sources.46

Snow, Public Health, and Social Class Whereas most of the London sanitarians came from the middle classes, Snow’s origins were in the laboring classes. Strikingly absent in his writings on cholera is any mention of the ostensibly “vicious habits” of the poor mentioned by some of his colleagues. Nothing he wrote or said in a medical society meeting approximates Chadwick’s conclusion that “adverse circumstances [poverty] tend to produce an adult population short-lived, improvident, reckless, intemperate, and with habitual avidity for sensual gratifications.”47 Unlike most sanitarians, Snow did not incriminate drinking as a predisposant to cholera, even though he was a teetotaler. While Snow acknowledged that cholera could spread rapidly through the slum neighborhoods of London and Glasgow, he never attributed this fact to moral degeneracy of the victims. Instead, he pointed out that the residences of the lower classes were poorly lit, making it difficult to notice contamination, and that they lacked sanitary facilities for hand washing. Moreover, cholera could spread like wildfire in a mine not because the miners were poor, but because the owners did not provide them separate facilities in which to defecate and consume their food. Long shifts forced them to eat some meals underground. One of the simplest ways to prevent cholera in mines, therefore, was to reduce the length of the shifts so food need not be taken below (PMCC, 929). Snow gave further evidence of his concern for public health problems among the poor in an article on rickets in children. At his death his thinking on the subject was still preliminary, but it is evident that he intended to attack this problem with methods similar to those he had used to study the transmission of cholera. The beginning of the article is typical Snow: He established the prevalence of rickets, the suffering it was causing, and its tendency to afflict children from the disadvantaged classes. Next he offered an epidemiological observation: Rickets was less prevalent in urban areas of the north of England than in metropolitan London, even where overcrowding and sanitary conditions were equally bad. What causative factor, he wondered, was present in the south of England but not in the north. As was his inclination, he looked first for a chemical explanation: “[I]n rickets the phosphate of


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lime in the bones is known to be deficient.”48 One possibility, therefore, was that infants in London received less of this vital nutrient (calcium phosphate) in their diets, but Snow rejected it because milk was just as often in short supply in the north as in the south. He had suspected for some time that the bread eaten by Londoners was less than ideal. A report by Liebig in which the chemist showed that phosphoric acid forms a very stable compound with alumina turned Snow’s attention to a common practice among bakers of adulterating bread with alum. In the north of England, however, where coal was cheaper than in the south, many poor and laboring families baked their own bread using flour that contained no alum. Here was a geographical difference that might explain why so many children in London developed rickets: The alum in their bread interacted with phosphate of lime to form sulfate of lime and phosphate of alumina, neither of which provided the necessary nutrients for growing bones. “The subject is capable of being decided by an exact numerical investigation,” and Snow imagined a natural experiment comprised of two large orphanages, or similar institutions, one of which served homemade bread and the other serving its wards adulterated bread from a local baker. So far, every institution he had consulted said it used only bread containing alum. He had heard, however, of two towns in Cornwall situated a few miles apart in which the inhabitants of one generally purchased their bread from commercial bakers, whereas townsfolk in the other baked their own. Supposedly, rickets was absent in the latter town but prevalent in the former. “[B]ut as my inquiries have been only of a colloquial nature, I hesitate to mention places and persons.”49 Perhaps with the critics of his cholera theory in mind, he immediately offered a caveat to his hypothesis on rickets in children: “It does not follow, if my conclusions are correct, that every child eating bread adulterated with alum ought to have rickets, or that every child fed with good bread ought to be free from the complaint.” Children fed bread containing alum might obtain adequate calcium from other parts of their diet, while some children fed homemade bread could be sickly and unable to absorb nutrients adequately. Probabilistic evidence, not certainty, would be the most that anyone should expect. As he had done on several other occasions, he decided to publish his hypothesis before he had the desirable confirmatory evidence in the event that others would find it instructive and pursue it further. On that basis he offered suggestions for testing the alum content of bread.50 Snow in some ways resembles another group of public health reformers of the early nineteenth century—physicians, mostly Scottish, who sought the causes of epidemic and zymotic diseases in destitution, factory work, and other evils of the capitalist industrial revolution rather than in the filthy habits of the poor. William Alison of Edinburgh was perhaps the leading advocate of this point of view and has been described by Hamlin as having provided a “medical critique of industrialism and capitalism the like of which did not appear until the twentieth century.”51 In Observations on the Management of the Poor in Scotland, and its Effects on the Health of Great Towns (1840), Alison was skeptical of a purely miasmatic interpretation of

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fever and expressed sentiments similar to Snow’s in 1855, when he dismissed the importance of “dead animal and vegetable matter” in his testimony before the select committee investigating the nuisance trades. Hamlin has documented that several other writers, including William Tait of Edinburgh, Alexander Tweedie of London, and William Budd, expressed similar viewpoints in the 1840s. Hamlin also notes that Chadwick stripped such radical content from the reports submitted by medical men in Scotland and Ireland before including them in his own Report on the Sanitary Condition of the Labouring Population.52 By comparison, Snow never developed a systematic critique of industrialism. His critique of the sanitarians was made on scientific grounds only.53

Sanitary Reform in 1858 While the sanitarians of the era from 1830 to 1850 relied on a miasmatic theory of disease causation and spread, sanitary reform was not logically tied to it. Actually, a new scientific model was emerging during the last years of Snow’s life, although full acceptance of his theories by the public health establishment would not come for many years. In part, acceptance of a new model reflected the success of Farr’s zymotic theory. Farr had gradually shifted toward the view that specific “ferments” could produce specific diseases. As zymotic theory gained ascendency, Snow was no longer such an outlier in insisting that cholera was caused by a particle or agent specific to that disease. The demise of miasmatic reasoning was also hastened by the summer of the Great Stink. In June and July of 1858 a horrible stench emanated from the Thames, but there was no outbreak of epidemic diseases. Chadwick’s notion that stench equaled disease could not survive such a dramatic disproof. For all the lack of credit Snow received during his lifetime, his work was part of the evolution in sanitary thinking and hastened the day when sanitary reform could be placed on a more modern scientific footing.54

Notes 1. “The plain truth of the matter is that is that in 1875, the death rate stood at almost exactly the same level as it had in 1838 when civil registration began and Chadwick first sent his poor law medical investigators into the London slums. . . . Infant mortality . . . scarcely began to fall before the end of the century”; Finn, “Introduction” to Sanitary Reform, 7. 2. Hamlin emphasizes the essential conservatism and pro-industrialism of Chadwick and most sanitary reformers; see Public Health and Social Justice in the Age of Chadwick, and “John Sutherland’s Epidemiology of Constitutions.” 3. Baldwin, Contagion and the State, 127-29, and Worboys, Spreading Germs, 31–37. “Health and disease were seen as consequences of the total environment. The conditions of city life—


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the stale and vitiated air, the uncleanliness, crowdedness, alcoholism, poor food and foul water—acted collectively to undermine health; the combined effect of all these ‘predisposing causes’ was virtually the disease itself ”; Hamlin, Science of Impurity, 106. According to W. M. Frazer, the sanitarian idea was rooted in “the principle that the material environment exercises a profound effect on the physical, and indeed, the mental well-being of the individual”; Frazer, History of English Public Health, 15. 4. In a speculative vein, in CMC (1853) Snow suggested that several other diseases besides cholera might be spread by the fecal–oral route and by contaminated water. It was not until the very end of his life, however, that Snow claimed to have evidence that cleaning up drinking water could prevent other diarrheal diseases and not cholera only; “Drainage and the water supply in connexion with the public health” (1858). 5. Several contemporary historians and epidemiologists believe that the sanitarians’s multicausal view of public health has much to recommend it to a modern temperament, whereas Snow’s focused researches sometimes seem less appealing. This was Pelling’s main point in comparing Snow’s “exclusivity” unfavorably to Budd’s “inclusivity” within the context of nineteenth-century medicine; Cholera, 275–81. Hamlin generally agrees with this assessment; Science of Impurity, 107. Likewise, Eyler compares Snow unfavorably with Farr: “Judged by the standards of his time Snow was the dogmatic contagionist and premature reductionist”; “Changing assessments of cholera studies,” 230. Another way to interpret the schism between Snow and his sanitarian contemporaries is to note that whereas they argued that the social environment could increase cholera incidence by “lowering general health,” his theory proposed that social environments determined “patterns of exposure”; Davey Smith, “Behind the Broad Street pump,” 929. 6. The MCS established in 1848 was an amalgamation of seven autonomous commissions of sewers (with a total of 1,065 commissioners) in existence since the days of Henry VIII. Parliament extended MCS authority over drainage and house construction in London and its suburbs. On the history of London sewage generally, see Trench and Hillman, London under London, and Halliday, The Great Stink of London. 7. Bazalgette, Metropolitan System of Drainage, 6. 8. The water closet was first invented in the seventeenth century by Sir John Harington, refined in the eighteenth century by Alexander Cummings and Joseph Bramah, and developed into its modern form by Hopper and Crapper in the nineteenth century. Trench and Hillman, London under London; Halliday, Great Stink of London. 9. Trench and Hillman, London under London, 65. Hamlin has more sympathy for Chadwick’s sanitary program. Chadwick was no supporter of sewage-contaminated water and eventually envisioned a London water supply drawn from pure sources other than rivers, as well as the recycling of sewage. The problem was that one part of the sanitarian agenda could be accomplished quickly (flushing sewage into the Thames) while the other part (supplying pure drinking water) was still decades away; personal communication. But Hamlin also shows that in 1850 Chadwick was relatively more concerned with the hardness of London water and less with the degree of organic contamination from sewage; Science of Impurity, 108. 10. Snow, “On the communication of cholera by impure Thames water” (1854), 366. 10a. UK HoC, “Select committees on medical relief and public health,” 328–30. 11. The key portions of Snow’s testimony and the Lancet’s critique are reprinted in Lilienfeld, “John Snow: The first hired gun?” See also Vandenbroucke, “Invited commentary: The testimony of Dr. Snow,” and Sandler, “John Snow and modern-day environmental epidemiology.” Interestingly, these modern epidemiologists largely echo the Lancet’s position. The latter two authors see Snow’s opposition to miasmatic effects of disease as evidence of narrowmindedness, Sandler citing his lack of evidence for the innocuousness of factory fumes and

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Vandenbroucke his “unreasonableness.” The three authors fail to distinguish between toxic factory exposures as causes of chronic diseases of the twentieth century and as agents of the epidemic communicable diseases during the nineteenth. 12. Editorial, Lancet 1 (1855): 635. 13. Snow, “On the supposed influence of offensive trades on mortality” (1856). Snow did express dismay at the manner in which the medical press characterized his Parliamentary testimony; [Open] Letter to the Right Hon. Sir Benjamin Hall (1855). 14. A fellmonger was a dealer in skins or hides of animals, especially of sheep. 15. “On the supposed influence of offensive trades on mortality,” 96. Snow also could not resist telling the reader that in two London subdistricts full of nuisance trade establishments but supplied with sewage-free water, there were hardly any cholera deaths in 1853 or 1854, while in two districts almost totally free of nuisance trades but supplied with sewage-contaminated water, the death rate had been much higher. 16. Lancet 2 (1856): 139–40. 17. John W. Tripe was a member of the London Epidemiological Society and is listed, along with Snow, as having taken part in the discussion of a paper on cholera in the Baltic fleet by Babington; “Influence of offensive trades on health,” Lancet 2 (1856): 177, and Babington, “On the cholera which visited her majesty’s Black Sea fleet in the autumn of 1854,” Lancet 2 (1856): 225–26. 18. Farr had provided in 1852 an open-minded review of several cholera theories, including those, such as Snow’s, that were not miasmatically based. Farr on that occasion referred to Snow’s theory as “in many respects the most important theory that has yet been propounded” and endorsed Snow’s preventive recommendations; Farr, Cholera Mortality in England, 1848–49, lxxvi. However, the only theoretical contribution in the 1855 Board of Health Scientific Appendix, by Neal Arnott, considered solely the miasmatic perspective and focused its recommendations on ventilation and air exchange: “[O]bservation has now clearly ascertained that the travelling morbific cause, whatever it may be, can no more produce a true pestilence, unless it meet with much filth of decomposing animal and vegetable matters—of which air which has served for respiration is one kind—than coal gas can produce an explosion without being mixed with many times its volume of common air. . . . It thus appears that the ravages of Cholera may be prevented, by preventing the local accumulation of organic impurities”; Arnott, “Memorandum on Asiatic cholera and other epidemics as influenced by atmospheric impurity,” in UK GBH, Report of the CSI, appendix, 168. 19. UK GBH, Report of the CSI, 48. 20. UK GBH, Report of the CSI, 52. The dates of publication suggest that the CSI did not have access to the St. James Cholera Inquiry Committee report, and especially Whitehead’s findings, when their own report was written, although it is unclear whether that would have changed their opinions in any way. For more on the CSI report see Paneth et al, “Rivalry of foulness.” By contrast, Snow’s theory received a somewhat kinder reception from another quarter. MCC2 and the CIC report were reviewed together in the Lancet 2 (1856), 524–25, with the anonymous reviewer disagreeing on several points with Snow but stating that “these books must exert considerable influence on sanitary reform, and in fact prove the position, hitherto scarcely demonstrated, that zymotic diseases are, to a certain extent, removable by sanitary measures.” 21. The paper was later published as “Further remarks on the mode of communication of cholera” (1855). 22. Ibid., 32. When contrasting the cholera theories of Snow and the sanitarian John Sutherland, Hamlin argues that “to explain cholera among those who have not consumed the water, one can posit supplementary modes of transmission through person to person contact or fomites,” and attributes this strategy to Snow; Hamlin, “John Sutherland’s Epidemiology,” 918.


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In doing so, however, Hamlin reverses the order of Snow’s logic; person-to-person transmission by the fecal-oral route is the fundamental route of transmission, public water supplies only one means of its extension. Thomas Snow understood his brother’s theory quite well and asked readers of the Times not to be misled by commentators who claimed that it limited the spread of cholera to waterborne transmission; “Propagation of Cholera,” Times (26 September 1885), and “Dr. Snow on the Communication of Cholera,” Times (20 November 1885). 23. UK GBH, Letter of the President (1855), 40. 24. Snow, “Further remarks on the mode of communication of cholera,” 84. 25. Ibid., 34. 26. Ibid., 35. 27. Snow’s name for the report; see “Cholera and the water supply in the south districts of London in 1854” (1856), 245. 28. Snow wrote in MCC2, “[N]o experiment could have been devised which would more thoroughly test the effect of water supply on the progress of cholera. . . . The experiment too was on the grandest scale. No fewer than 300,000 people of both sexes, of every age and occupation, and of every rank and station . . . were divided into two groups . . . one group being supplied with water containing the sewage of London, and amongst it, whatever might have come from the cholera patient, the other having water quite free from such impurity” (75). Simon’s language a year later was, “An experiment . . . has been conducted during two epidemics of cholera on 500,000 human beings. One half of this multitude was doomed in both epidemics to drink the same faecalized water . . . while another section—freed in the second epidemic from that influence which had so aggravated the first, was happily enabled to evince . . . the comparative immunity which the cleanlier beverage could give”; Simon, Report of the Last Two Cholera Epidemics (1856), 9. 29. An MTG editorial reported favorably on Simon’s report and rehearsed conclusions that also supported MCC2, but the journal would not give Snow’s “hypothetical views” an unqualified endorsement because he did not consider effluvial infection a cofactor; “Impure water a source of disease,” MTG 13 (1856): 15–16. See also the article on Simon’s report; Times (25 June 1856). 30. Snow, “Cholera and the water supply” (26 June 1856). 31. While Simon had possession of the subdistrict data that Snow had been unable to obtain for the previous two years, he did not preempt Snow in carrying out any sophisticated predictive modeling using those data and made no particular statistical use of them in his own report. 32. On the random misclassification principle, see McMahon and Trichopoulos, Epidemiology, 248; Kelsey, Thompson, and Evans, Observational Epidemiology, 294; Brownson and Petitti, Applied Epidemiology, 53. Snow phrased it thus: “For these reasons it follows that, in comparing the lists of the water supply with the list of deaths, many errors must have occurred; and as the deaths were six times as numerous in the houses supplied by the Southwark and Vauxhall company as in those supplied by the Lambeth company, the evident result would be that out of every six mistakes, five would transfer a death from the former company to the latter, and only one would transfer a death from the latter company to the former”; “Cholera and the water supply in the south districts of London in 1854” (1856), 249. 33. The Provincial Medical and Surgical Association changed its name to the British Medical Association at this meeting. 34. “Twenty-fourth annual meeting of the British Medical Association,” AMJ 4 (1856): 683. Budd took issue with the reporter’s accuracy in a letter to the editor two weeks later. He claimed that he had not, at the Birmingham meeting, referred to his own work on cholera at all but had simply wished to assert the priority of “Dr. Snow’s admirable, long prior, and entirely

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original researches” over any claims by Simon and the GBH; Budd, “Dr. Snow and the Board of Health,” AMJ 4 (1856): 730. 35. Snow, “On the outbreak of cholera at Abbey-Row, West Ham” (1857), 418. 36. Ibid. 37. Snow, “On the origin of the recent outbreak of cholera at West Ham” (1857), 934. 38. Ibid. 39. Ibid., 935. 40. Snow, “On the mode of communication of cholera,” (1856), 668. 41. Ibid., 669. 42. Ibid., 670. 43. Snow, “The mode of propagation of cholera,”(1856). He sent a similar letter to the Lancet after it published Kay-Shuttleworth’s address; it was published under an identical title to the one in AMJ. 44. Snow, “Drainage and water supply in connection with the public health” (1858). 45. Typhus is not water-borne, but Snow points out that cases of typhoid fever were included in this category. 46. Snow indicated that his preferred solution was rather to recycle the human waste as agricultural manure, which was impractical if it was diluted with large quantities of water. He apparently did not consider the possibility that agricultural use might also lead to the spread of disease. 47. Chadwick, Report on the Sanitary Condition of the Labouring Population, 370. 48. Snow, “Adulteration of bread,” 4. 49. Ibid., 5. 50. To prevent adulteration it was essential to have an accurate chemical test for the presence of alum in bread. Snow described the method used by his microscopist–sanitarian acquaintance Hassall that involved incinerating the bread and testing the ashes and warned that the failure to use that method would result in underdetection of alum. Four months after his paper appeared Snow sent a letter to the Lancet calling attention to evidence by a Belgian researcher that supported his hypothesis; “The adulteration of bread as a cause of rickets” (1857). 51. Hamlin, Public Health and Social Justice, 81. 52. Ibid. Tweedie was Southwood-Smith’s senior at the London Fever Hospital, while KayShuttleworth had studied with Alison, who was sympathetic to the water supply hypothesis in the broader formulation he attributed to Budd. 53. Snow’s work could have provided strong support for the more radical public health perspective then in circulation among the Scottish physicians, but there is little evidence that the two streams of thought ever converged. 54. On the importance of the Great Stink and the evolution in the scientific base for sanitarianism, see Hamlin, Science of Impurity, 128–32. Hamlin seems ambivalent as to whether Snow actually helped to bring this change about or merely reflected the changes occurring around him. See also Wohl, Endangered Lives, 81, 247, 251.

Chapter 14

Further Developments in Anesthesia

OHN SNOW MAY HAVE BEEN THE FIRST physician to “specialize” in anesthesia.1 In principle if not always in practice, his approach mandated that anesthesia should be performed by a trained physician exclusively dedicated to its safe administration. A surgeon or dentist operating on a patient had too much to do to take on the responsibility of inducing, monitoring, and reviving the chloroformed or etherized patient. In the 1850s surgeons began performing longer and more complex procedures that could not have been done without anesthetics. Surgery without pain made surgery both more popular and more common. Procedures that were formerly an excruciating last resort—amputations, removal of tumors, abdominal surgery—were now offered and performed routinely and repeatedly. Snow worked frequently with William Fergusson, an early practitioner of conservative surgical interventions (such as excision of joints or removal of dead bone tissue) that would have been impossible without anesthesia. During a span of five Saturdays in the autumn of 1848, Snow gave chloroform four times to one little boy for repeated surgeries on an “un-united fracture” of the humerus requiring resection (CB, 22–26).2 Such a series of procedure would have been unimaginable two years earlier. Looking back on the impact of chloroform on surgery, Snow commented in On Chloroform that surgeon–patient relations were fundamentally altered because the surgeon could now obtain “the ready assent of his patient” for many painful operations in which previously “it would either not be obtained at all,

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or not at the most favorable time.” Chloroform also made pediatric surgery possible: “Many operations take place in children which could not be performed in the waking state” (OC, 263).3 Snow administered chloroform to children as young as eight days old and participated in dozens of infant surgeries, especially for repair of harelip. The symbiotic relationship between surgery and pain relief naturally led to increased demand for anesthesia. In 1849, the first full year in Snow’s extant Case Books, he administered chloroform in roughly 250 cases. By 1857, the last full year on record, he logged roughly 550 cases, and he was on track in June 1858, when he suffered his fatal stroke, to reach more than 600 cases. Today, when we think of specializing we often imagine a narrowing of medical experience to a more uniform type of patient, but Snow’s specialization brought him into contact with all kinds of patients and conditions. His was something of a superpractice in which he traversed the metropolis of London seeing the complete range of patients and conditions, from the queen to the chimney sweep to the stable-boy, from breast cancer to strabismus to venereal warts to delirium tremens.

Going Under: The Vagaries of the Organism Through chloroform Snow had become more intimately acquainted with the nature of pain and its relation to degrees of unconsciousness than any man in London. Pain requires a more or less orderly consciousness. Once the mind becomes disorganized the usual signs of pain take on ambiguity. In a waking state cries and flinching are sure signs of discomfort. Under anesthesia these signs might indicate that sensation, neural activity, and consciousness are returning but are not necessarily experienced as pain. Sometimes chloroform functioned like posthypnotic suggestion, erasing all memory of the operation; at other times it had no such effect. Some patients, upon recovering from surgery, inquired as to when the operation would begin. Other patients, although clearly under the influence of chloroform, would, in the most reasonable way imaginable, and without flinching or stirring, request that they be given more chloroform. Snow is remembered as a systematic thinker, a man who cleverly calculated blood solubility ratios for anesthetics and laid out with great precision the degrees through which the anesthetized body travels. But the study of anesthesia reveals the unpredictability of the human organism. In his Case Books, therefore, Snow provides a record that points not only to the laws of these powerful agents but to the vagaries of human experience. The microphenomena of the hypnagogic states he recorded seem unexplainable by physiology; they can be glossed only as the fugitive reactions of the disorganized consciousness, the random effects of chloroform on the human subject. That Snow fashioned a rational system to gauge and categorize the phenomena of anesthesia testifies to his diagnostic acumen and his skill at


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building models. That he handled so many cases so well speaks to his ability to handle uncertainty and unpredictability on a practical level, to balance phenomena and epiphenomena. Anesthesia also suited his temperament. His utterly sober demeanor was perfect for the Victorian period, especially as it would become his calling to dispense narcotic inhalants and thereby control consciousness. One feels this love of control in Snow’s discipline, in his abstemious habits, in his knowing remarks about a patient’s ignorance that an operation had taken place, even in his preference for fast-acting chloroform. His temperance sprang from a desire for bodily self-possession unalloyed by piety or faith, which was relatively unusual for the era. When Snow took anesthetics or even alcohol (when exploring its anesthetic properties or using it medicinally), it was in the name of science. Throughout these autoexperiments he stared intently at his stopwatch until the hands disappeared or he lost consciousness. He made a point of recording his observations the moment he recovered, exerting the force and will of his mind over the volatile matter. It was no accident that James Clark tapped Snow to give chloroform to the queen—there may have been no safer, more prepossessing, more self-controlled individual in all the kingdom. Snow observed, but did not interpret, the anesthetized mind and body: There is generally a sense of dizziness, with singing in the ears and tingling in the limbs. Many persons have a feeling like that of rapid travelling, and as an appearance of darkness sometimes comes on from the failure of the sight, whilst there is also a loud noise in the ears, it not infrequently happens that a person feels as if he were entering a railway tunnel, just when he is becoming unconscious. . . . In the second degree of narcotism, there is no longer correct consciousness. The mental functions are impaired but not necessarily suspended . . . [the patient] usually appears as if asleep . . . but if his eyelid be raised, he will move his eyes in a voluntary manner. There are occasionally voluntary movements of the limbs; and although the patient is generally silent, he may nevertheless laugh, talk, or sing. Persons sometimes remember what occurs whilst they are in this state, but generally they do not. Any dreams that the patient has, occur whilst he is in this degree. OC, 36–37 He thought that people tended to react differently to chloroform, and there is class and gender inflection to his explanations for the wide variety of behavior he encountered as people went under. He felt that “brain workers”—people with cultivated mental faculties—retained their consciousness longest, whereas “certain navigators and other labourers” no sooner took a whiff than they would “get into a riotous drunken condition.”“Hysterical females” would very quickly start to dream (OC, 36). Chloroform could reveal the nature of one’s upbringing. Snow’s experience indicated that patients who had been treated kindly were highly suggestible in the early stages

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of chloroform. If such patients grew restless, as they often did, “a few kind words” might calm them and render them “tractable,” but had they been used to harsh treatment from birth, they would commonly require “a little restraint.” This difference seemed often to fall along sex lines. Women were raised with kindness and care; men were more likely to have been brutalized from a young age (OC, 38). Chloroform might thus reveal glimpses of the harshness of growing up in Victorian London. As chloroform seemed to provide a means of identifying, or at least confirming, a particular type of patient, particularly the “hysterical female,” it could also be used by Snow to delve into obscurities of hysterical paralysis as a diagnostic category. This might mean using chloroform to detect feigning. Snow recorded a case from December 1851 involving a servant of the marquis of Cholmondley, a young woman who had been in bed in Charing Cross Hospital for two months. She “kept her left knee in a semi-flexed position, and would not allow it to be moved.” Reluctantly, she inhaled the chloroform. Once unconscious, she exhibited the telltale symptoms of hysteria, fitful breathing and sobbing. As unconsciousness deepened the leg “went down flat on the bed, the knee being quite moveable.” While the leg was unbent, the doctors bound the leg with a splint to keep it straight. A few days later the bandages grew slack, but Snow was skeptical. He thought the patient “contrived to get her leg bent again. She was the domestic servant of a nobleman. It was evident that there was nothing the matter with her limb, and that it was only influenced by her volition, which was perverted by the hysteria under which she was labouring” (OC, 339; CB, 209). In another case an unmarried woman was suspected of feigning paralysis in the left arm and leg and the inability to speak. She communicated by nodding or writing on a slate. Under chloroform she, too, “breathed in a sobbing and hysterical manner.” Her right side moved a great deal as well as her left side and limbs, but much less so. Her jaws remained firmly closed, but Snow opened them with his fingers, prying with “a moderate degree of force.” The chloroform was allowed to wear off and was given again with same results, and a cork was slipped in between her teeth in an attempt to keep her mouth open. Somehow the cork slipped out. The patient did not open her eyes or answer questions for six days. When Snow raised her eyelid on the seventh day, “she turned her eye about, as if endeavouring to hide the pupil under the lid.” The next day she answered questions by nodding her head or writing in chalk. Snow concluded that the patient truly believed her limbs were actually paralyzed. “I looked on the woman as a sick person, and not a mere impostor; for although she appeared to exaggerate her symptoms, and to have a good deal of pretence and affectation, this circumstance arose, no doubt, from her complaint” (OC 339–41; CB 204). The mixture of skepticism and credulity, sympathy and force, in Snow’s dealings with hysterical patients testifies to Snow’s belief in chloroform’s power to reveal bodily states. It offered a way of drawing the line between mind and body. He regarded the first patient as deceitful because she willed her body into a deformity, but he considered the second sick because, at the deepest stages of chloroform anesthesia, paralysis remained and provided physical basis for the patient’s belief.


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Delirium, Tremors, Spasms Snow recognized that anesthesia provided a model for other unconscious states. Not surprisingly, the clinical picture of Snow presented in his Case Books reveals a willingness to make connections between narcotism and other physiological and mental phenomena. In July 1848 he attended a man in his neighborhood who had been run over by a cab. The man appeared to have a concussion, and Snow suggested that “he was in a state resembling the ‘second degree of narcotism’” (CB, 4). In “On narcotism” Snow had drawn analogies between anesthesia and alcoholic intoxication; now he used the degrees of narcotism to illuminate the nature and severity of mental confusion resulting from concussion. In the stages of ether and chloroform anesthesia, when voluntary motion had ceased, it was common for some patients to experience trembling, spasms, rigidity, and, in rare cases, convulsions. Snow believed these reactions were especially likely in “robust” individuals, people who were particularly fit or used to physical labor. Just as brain workers were more likely to retain consciousness longer under chloroform, he believed that body workers, “where the muscles have been much exercised,” were more likely to exhibit disorganized nervous activity (OC, 39). This phenomenon was more common in men, in the active than in the sedentary, and in the lean than in the fat. It was never found in infancy, rarely before puberty, and diminished in frequency with age. Chloroform seemed to both induce and abolish spasms, tremors, and delirium, and Snow frequently administered it in attempts to counter these symptoms. As early as May 1849 he gave chloroform with some success to a girl with epilepsy. The royal physician, Sir James Clark, and James Todd, a colleague with special expertise in treating seizures, were in attendance. In April 1857 Snow gave ether and chloroform to a middle-aged surgeon and colleague, William Hooper Attree, over a ten-day period. Attree had been suffering for six years from “a spasmodic affection of the muscles of the right side of the neck which draws the head down to the shoulder” (CB, 471). The anesthetics eased the spasms and put him to sleep, when Snow “pressed the head over towards the other side as much as I could,” in an attempt to manually correct what the spasms had deformed. He gave chloroform to young children with laryngismus stridulus, a spasmodic contraction of the laryngeal folds, with good success. He also gave it for cases of croup, whooping cough, and asthma (OC, 331–33). He tried it on patients in the throes of delirium tremens. In December 1851 he gave chloroform to a forty-fiveyear-old silversmith, who had not slept for four days and had been placed in a straitjacket. The man had become enraged, spitting out medicine, and violently casting about. Snow took the silversmith’s pulse and found it rapid and weak. The man was bathed in sweat. When Snow brought out the chloroform inhaler, the man objected vehemently, but Snow compelled him to take it; soon he was unconscious. When the man awoke a minute or two later he was terrified, delirious, and convinced he was

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being injured. Snow continued administering chloroform and kept the silversmith under for more than a half hour. At the same time the attending doctors gave him spoonfuls of an opiate, which were easily swallowed despite the unconscious state. Snow stayed for another hour and fifteen minutes, observing the straitjacketed man, who was sleeping relatively peacefully. He woke totally free from his delirium but “had a slight relapse 2 or 3 days afterwards” (CB, 208). Snow could resort to force in order to administer chloroform; it could be an agent of force, sleep, and reason, and in cases of delirium tremens, it was an effective inhaled sedative.

Alleged Fatality Less than a week after treating the silversmith, Snow gave chloroform to Major Evans, a tall, heavy-set gentleman from Herefordshire. The man was seventy-odd years old and had undergone the same procedure for lithotripsy three or four times in the past year. He had taken chloroform on these occasions, but this time Snow was particularly pleased with the outcome: “No sickness or other sequelae. The operation was performed before breakfast” (CB, 209). Ten days earlier, however, when Major Evans had had a lithotripsy performed after breakfast with a different anesthetist administering the chloroform, he “was very much depressed [syncope] a few minutes after it” and vomited. Snow’s better anesthetic outcome seemed to vindicate his methods. His liberal use of chloroform, even in patients like Major Evans, whom Snow suspected “had disease of the heart,” was justified because the risk of chloroform was smaller than the risk of performing surgery without anesthesia.4 Four days later, Snow and Caesar Hawkins, the surgeon, repeated the lithotripsy with identical results, and the major returned to the countryside relieved of his stone. It was the same patient, same surgeon, and same procedure done three times within two weeks. In the first instance the patient almost died, but in two others the operations went smoothly. The only difference was the anesthetist. It is no wonder Snow had confidence in his method. However, Major Evans redeveloped bladder stones and returned to London for an operation nine months later. He again consulted Mr. Hawkins, who asked Snow to give chloroform during yet another lithotripsy on this elderly man. This time, however, things did not go well. The patient was anesthetized and all seemed normal until Snow observed that the patient’s face and lips were growing pale. Immediately, he allowed him to inhale air unmixed with chloroform for two minutes, at which point the major’s face reddened, and he began to strain as if “beginning to feel the operation.” Snow gave him a little more chloroform, the patient taking two or three breaths of it with the air valve one-third open. “He appeared to be merely holding his breath” (this sometimes happened with chloroform), and Snow felt sure he would begin breathing again any second. When he searched for a pulse, however, he found none. He put an ear to Major Evans’s chest, but he heard nothing. Suddenly, the


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patient took a deep breath, when Snow thought he heard some cardiac activity. More silence ensued, punctuated by a few feeble gasps. After thirty seconds all signs of life ceased. Artificial respiration was performed to no avail. The postmortem examination revealed “a good deal of fat” on the surface of Major Evans’s heart, thinning of the ventricular walls, and “a calcareous incrustation in one of the aortic valves.” Microscopy revealed fatty degeneration of the heart’s fibers.5 Snow wrote a detailed case report, which was published in MTG on 10 October 1852. The title, “Death from chloroform in a case of fatty degeneration of the heart,” suggested that Snow may have believed chloroform was the cause of death. But Snow was in fact uncertain, and he signalled his intent in this paper to undertake research as to “whether, in cases of presumed fatty degeneration of the heart, it is more desirable to give chloroform or ether,—to operate without anæsthesia, or to leave the patient without surgical assistance.”6 Snow revisited the case three years later and said that although he had “thought it best at the time [1852] to designate the death as one from this agent [chloroform],” he was now “by no means sure that this patient died from the effects of chloroform.” He felt that the straining effort of the patient while holding his breath may have caused death. “I am quite unable to tell whether it was the effort of straining, or the influence of the chloroform,” he conceded.7 By the third iteration of this case, he had thoroughly exculpated chloroform. The posthumously published book On Chloroform contains a comprehensive inventory of every fatal case of chloroform inhalation reported through mid-1858, but Snow placed the Major Evans case in a section entitled “Alleged fatal cases of inhalation of chloroform.” “I am of opinion that this patient did not die from the direct effects of the chloroform” (OC, 208). George Pollock, the surgeon–anesthetist for the first procedure when the major had fainted and then vomited his breakfast, witnessed the fatal operation. He concurred with Snow’s assessment that death should be attributed to heart disease rather than chloroform. In fact, Snow argued that the chloroform afforded relief that actually added months to this obviously sick man’s life (OC, 208–09). Snow had overcome his brief uncertainty about the safety of chloroform.

Amylene By November 1856 Snow had been working with anesthetics for almost ten years, and he had done almost all that a single individual could imaginably do with them in that span. He had developed inhalers for their controlled administration and calculated blood solubility ratios and safe mixtures of gas to air. He had laid out the physical signs that accompany their use and published guidelines for safe usage of anesthetics in dental and surgical operations and obstetrics as well as in the therapeutic treatments of some diseases. He had used these agents in thousands of cases, yet, although he had placed ether and chloroform among a wide spectrum of

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anesthetic agents and had experimented with many other inhalants, from Dutch liquid to chlorated muriatic ether (ethyl chloride) to benzene, he had yet to introduce an anesthetic agent that might supersede ether or chloroform. While confident in his abilities to administer ether and chloroform safely in most circumstances, experience and experiment had made Snow painfully aware of their shortcomings. Ether was readily available and nonfatal in use, but it could be explosive and relatively slowacting. Its pungency made it hard to inhale, and it generally caused expense, delays, and struggles with difficult patients. It frequently caused excessive salivation, spasms in healthy athletic patients, and, most distressingly, vomiting, sickness, and disorientation. Chloroform was much faster-acting than ether and less expensive to use, but it shared some of the latter’s unpleasant effects. Snow had calculated doses that provided a margin of safety, but he was increasingly aware that both ether and chloroform, especially chloroform, were capable of arresting breathing and paralyzing the heart. He was determined to find a better anesthetic. In the early months of 1857, he began to think he had found what he was looking for in the pentene hydrocarbon amylene. It had been discovered in 1844 in Paris, but Snow only learned of its existence in the fall of 1856. It had a chemical structure similar to other agents he had studied. Introducing the agent to the Medical Society of London, Snow explained that amylene was made from fusel oil (which contains amyl alcohol) and zinc chloride and that the chemical relation between amylene (C5H10) and amyl alcohol (C5H12O) was the same that “olefiant gas, or ethylene [C2H4], bears to common alcohol [C2H5OH].”8 Ethylene and amylene were both alcohols stripped of a water molecule. Because Snow had long been aware of the anesthetic properties of alcohol and olefin hydrocarbons, it was a good guess that the amyl form would possess similar properties. As he had done with all the other agents he investigated, Snow put amylene through his own set of chemical and animal trials, establishing boiling points, blood-solubility ratios, and air saturation tables. Very little amylene had to be absorbed into the blood to produce insensibility. Snow explained, however, that “when considered in relation to the quantity which is consumed during inhalation in the ordinary way, it is very far from being powerful.” Amylene’s “great tension and small solubility” made it difficult for the lungs to absorb. Snow thought it resembled “the nitrogen gas of the atmosphere, with which the lungs are always four-fifths filled, while the blood contains but a few cubic inches.” Although amylene was more powerful than chloroform and ether, more of it was needed to create its effects. Snow thought this might be an ideal combination: a powerful agent that was hard to overdose because it was hard to absorb. Amylene seemed to promise the power of chloroform with the safe absorption levels of ether.9 Amylene possessed other advantages. It smelled like naphtha—some liked this smell, others did not—but it lacked the pungency of ether and chloroform. Patients did not gag or choke upon first inhaling. Almost no rigidity or spasms occurred. In January 1857 Snow administered amylene to a patient having plastic surgery on his nose who, a few weeks before, had received chloroform with a great deal of


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“rigidity and struggling.”10 The anesthetic powers of amylene seemed to be stronger as well. Snow wrote that the “absence of pain has been obtained with less profound coma than usually accompanies the employment of ether or chloroform.” Patients would wake up more quickly under amylene. Flinching and crying without any signs of consciousness were common signs that ether and chloroform were wearing off, but with amylene patients “have more frequently begun to look about and to speak before showing any signs of pain.”11 Perhaps most promising of all, amylene did not produce excess salivation or sickness. Snow was aware that the question of amylene’s safety was far from settled, and much more clinical experience would have to be obtained. Nevertheless, bringing it to public notice in this way was precisely the means to extend its clinical use; perhaps greater demand would spur chemists to produce it in greater quantities, thereby reducing its cost. Whatever doubts he may have had, he was very sanguine in the winter of 1857 that amylene might answer to the disadvantages of ether and chloroform. He had a sense that he was inaugurating a new era of medical discovery. He took a step he had not taken with Dutch liquid or any other anesthetic agent he had worked with since chloroform, designing a new inhaler apparatus specifically for use with amylene.12 He began his first paper on amylene in January 1857 by rehearsing the history of inhaled anesthetics, which appeared to his eyes to be largely an accidental affair. He observed that Humphrey Davy had brought the pain relieving properties of nitrous oxide to the public’s attention at the beginning of the nineteenth century, remarking that “it may probably be used with advantage during surgical operations in which no great effusion of blood takes place,”13 but it took forty-four years for Horace Wells, an American dentist, to take up that suggestion. Snow also noted that sulphuric ether’s “exhilarating effects” had been generally known since 1818 and had been regularly inhaled by medical students. Not until 1846, however, was its surgical applicability established at Massachusetts General Hospital. Snow went on to note, “A medicine called chloric ether has been in use since 1831.”14 Jacob Bell used it to prevent pain in early 1847 at several London hospitals. This medicine was actually twelve percent chloroform dissolved in spirits. David Waldie, a Liverpool chemist, explained these circumstances to the obstetrician James Young Simpson in Edinburgh in 1847, and chloroform in an undiluted state came into use. Snow’s point was that all of this had occurred more or less by chance: Ever since the introduction of chloroform I have been of opinion that other agents would be met with more eligible for causing anesthesia by inhalation. It seemed improbable that this one, which happened to be standing on the shelf of the Pharmaceutical Chemist for another purpose, should be better than all the very numerous volatile compounds which organic chemistry is daily bringing to light; and the continued use of chloroform is probably due to the circumstance, that hardly any one has made anæsthesia by inhalation a subject of constant and protracted investigation.15

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All the hubris and wisdom of Snow show in this passage. He is at once the protocorporate spokesperson for better living through chemistry, and the hard-nosed scientist requiring protracted investigation before adopting new anesthetics, but his claim that an agent discovered by systematic organic chemistry would be better than one found on the laboratory shelf reveals both insight and insensitivity. After all, who can say whether or not chance discovery will yield better or worse results? Undoubtedly, organic chemists have washed down their drains many a compound that later turned out to be quite useful, but Snow was confident that when one knew how to set about looking the day would come when a better agent was discovered. In amylene he thought he had a very good candidate. The desire to find a safer anesthetic may have had its roots in a dream of rational scientific discovery, but it was also prodded by continuing public concerns about chloroform. Stories of more fatal and near-fatal accidents with chloroform continued to be reported in the press. In February 1857 a nine-year-old boy died under chloroform in the care of Mr. James Paget, who laid the case before the medical public in a report published in MTG.16 This was, by Snow’s count, the forty-eighth case of fatality since the use of chloroform began a decade before. He lashed out at those who used handkerchiefs: “It must be quite obvious that a handkerchief, or cotton wool, or lint can afford no adequate means of properly regulating the amount of vapour in the inspired air.”17 He doubted that “fear on the part of the patient is a cause of death from chloroform. If this were so, accidents would be extremely common; for many patients inhale it, unfortunately, with great fear, only because they have still greater fear of pain; children, also, are usually afraid of anything so strange, yet accidents have seldom happened to them. . . . Excessive fear and an overdose of chloroform may either of them cause sudden death, just as infancy and old age both predispose to bronchitis; but they cannot combine to cause an accident in the same case. In fact, as soon as a patient becomes unconscious from chloroform, the effects of fear on the pulse quickly subside.”18 Despite Snow’s scoldings, however, accidents continued to occur. By early April 1857 Queen Victoria was in the last month of her ninth pregnancy, and Snow was well aware that he might be called in any day to administer chloroform as he had done in 1853. By this time he had amassed more than 140 cases of amylene administration, with results admirably consistent with his preliminary findings. Some sickness had arisen in some cases, but it was hardly of the severity he found with ether or chloroform. So far, he had only “had leisure to administer amylene in two cases of labour.” In both instances the anesthetic removed labor pains, allowed the mother to retain consciousness between pains, and produced “no interference with the progress of the labor. I look forward with some interest to a more extended experience of amylene in midwifery.”19 On Tuesday afternoon, 7 April, Mr. William Fergusson requested Snow’s services at Maddox Street near Regent Street. The thirty-three-year-old Mr. Wellington required repair of an anal fistula. According to Snow, he was in good health, “though he had lived somewhat freely.”20 Perhaps because Wellington was strong and such


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patients often flinched during this procedure, Snow opted for amylene and poured six fluid drachms (about 21 ml) into the inhaler. At 4:46 P.M., the man lay down on his right side in bed and they commenced. His “pulse was pretty good” as he started inhaling, and Snow gradually advanced the valve over the opening in the face-piece until it was 3/4 covered. Within two and a half minutes the patient was unconscious. Fergusson probed Wellington’s backside, testing for any signs of feeling. Finding none, he picked up the bistoury and began to open the fistula. Patients typically flinched in these situations, and Snow held the man’s thigh. The patient did not flinch but held his legs tense and still. When Snow returned his gaze to the patient’s face, he observed that the oxygen-intake valve was shut. This was not uncommon with amylene. Because the patient was still unconscious, Snow discontinued the inhalation as the surgeon completed the operation with a single incision. “Out of constant habit and from a scientific curiosity,” Snow felt for Wellington’s pulse. He could not find it, even though the patient’s breathing was good and he seemed to be waking up. Snow grew alarmed. The patient’s insensibility was deepening and his breathing growing slower and deeper. Snow called out to Fergusson, who was washing his hands and preparing to leave after another successful operation. They dashed cold water in Wellington’s his face, which caused him to begin gasping for breath. They tried artificial respiration, but it was no use. By 5:02 P.M. the patient was dead. After the postmortem examination, Snow concluded that he could not “attribute the patient’s death to any other cause than the amylene.”21 The following Tuesday Snow was summoned to Buckingham Palace. The Queen’s labor had begun at two that morning, but was progressing slowly. At 10 A.M. Dr. Locock, the royal accoucheur, gave the queen powdered ergot to advance the labor, thereby increasing the pains. Snow began administering chloroform at 11 A.M. The chloroform was given on a handkerchief in minute quantities. Prince Albert had been administering it in this fashion before Snow arrived. The queen was in great pain, and she called out for more of the chloroform. As if to make a compromise between the lay and professional modes of administration, Snow poured half a milliliter of chloroform onto a cloth and folded it in a conical shape for each pain. Victoria expressed “great relief from the vapour,” and she asked for even more. When the time came to bear down, she complained that she could not make the effort. Just as Snow had seen in other cases, and as is commonly known today, the anesthetic was inhibiting the delivery to some degree. The gas was left off, and three or four pains later a princess was born (CB, 471). This was not the time to test amylene as a substitute for chloroform. Despite young Wellington’s death and the letters of criticism that ensued, Snow continued to use amylene and advocate its use throughout the spring and summer of 1857, even sending a sample to John Gay Orton, a physician in Binghamton, New York.22 One bad outcome did not worry him at the time: The “accident [with Wellington] happened in the 144th case in which I have administered amylene. It is impossible to form an average from a single case. I do not know any reason why an

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accident like the above might not have occurred in one of the early cases in which I was giving chloroform, or, on the other hand, why I might not have been able to go on for four or five years at a time administering amylene, without any approach to an accident.”23 However, in late July 1857 another patient died under amylene administered by Snow. It was the 238th case in which he had used the agent, and “in the ninety cases and upwards in which I administered amylene between these two accidents, I never had occasion to feel a moment’s uneasiness about it” (OC, 416). After the second death we hear no more of Snow using amylene in clinical practice, but he had not given up on it, noting a few weeks after the death, “I still believe, that if amylene were exhibited, by measured quantity . . . a sudden accident would not happen.”24 He had in mind a change in the mode of administering it, not its discontinuance: “In the future cases in which I employ amylene, it is my intention to administer it from a bag or a balloon.” (OC, 416).25 As such, Snow anticipated the apparatus and recirculating techniques later developed by Joseph Clover, but Snow died before he could put them into practice.

Notes 1. Shephard, JS, 9. 2. Ellis, Case Books of Dr. John Snow, cited parenthetically in the text as CB. 3. Snow, On Chloroform (1858), cited parenthetically in the text as OC. This was Snow’s posthumously published monograph on chloroform and the entire family of narcotic agents, which included many case reports but did not expand the scientific base of narcotism beyond what Snow had published in his ON series in 1848 through 1851. 4. Snow, “Death from chloroform in a case of fatty degeneration of the heart” (1852), 361. Here he explained the “weakness” noted in CB as syncope. 5. Ibid. 6. Ibid., 362. For a slightly different interpretation, see Shephard, JS, 112. 7. Snow, “On the employment of chloroform in surgical operations” (1855), 361. 8. Snow, “On the vapour of amylene” (1857), 61. 9. Ibid., 62. 10. Ibid., 83; see also CB, 444–45. 11. Ibid., 83. 12. Snow, “Further remarks on amylene” (1857), 379–80. The apparatus was only slightly modified from his chloroform inhaler, providing a deeper chamber to allow for the greater volume of amylene required. 13. Snow, “On the vapour of amylene” (1857), 60, quoting Davy, Researches concerning nitrous oxide, 556. 14. Ibid., 61. 15. Ibid. 16. James Paget, “Administration of chloroform was fatal,” MTG 35 (7 March 1857): 236–37. Paget, whose memoirs were cited in earlier chapters, was then assistant surgeon to St. Bartholomew’s Hospital. 17. Snow, “On the recent accident from chloroform,” (1857), 283. 18. Ibid.


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19. Snow, “Further remarks on amylene” (1857), 359. 20. The description of this operation and its outcome are synthesized from accounts in Snow, “Further remarks on amylene” (1857), 381–82; and CB, 469. 21. Snow, “Further remarks on amylene” (1857), 381. 22. Snow, “Mr. A Prichard on amylene” (1857); John G. Orton, “Amylene,” Boston Medical Surgical Journal 56 (1857): 457. 23. Snow, “Further remarks on amylene” (1857), 382. 24. Snow, “Case of death from amylene” (1857), 134. 25. Richardson thought differently: “These deaths affected him very seriously, and his sudden and early demise may, in some measure, be attributed to their effects upon him. . . . He had not in amylene accounted sufficiently for its insolubility, and it was not until I ventured to show him separation of amylene in the blood, a separation which looked like the formation of minute plugs, that he fully realized the danger”; Vita Medica, 284. Snow never mentioned anything about Richardson’s microscopic investigations, although he had at least a year to have recorded any debt he owed his younger colleague and friend.

Chapter 15

Common Ground: Continuous Molecular Changes

HE THATCHED HOUSE TAVERN in St. James’s Street was a five-minute walk from Snow’s Picadilly residence. In the eighteenth century it had been the home of a fine arts society, the Dilettanti. In the nineteenth century it was a fashionable meeting place for artists and writers and featured a large room for public gatherings, where members and visitors of the Medical Society of London assembled to celebrate its eightieth anniversary on Tuesday, 8 March 1853. The annual oration was scheduled for 5:00 P.M., with a dinner to follow. The orator for the year was John Snow.1 His address was cumbersomely entitled, “On continuous molecular changes, more particularly in their relation to epidemic diseases” (CMC). Given the standards of the time, most of Snow’s communications were narrowly focused, addressing one issue or a single set of observations. An oration, however, offered him an unusual opportunity to speak in a speculative way and with unprecedented breadth “on the chief phenomena of living beings” (CMC, 147).2 This work, therefore, provides a rare glimpse of Snow’s scientific thought as a whole, illustrating connections not discernible in his papers on anesthesia and cholera. It is a deeply interdisciplinary, synthetic essay, a focal point at which the rays of Snow’s thought converged and his two specialities were joined, albeit tenuously. Snow thought serially and by accretion, and CMC was the apotheosis of this style.

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In the 1850s debates over the fundamental nature of life and living processes were still quite common. Vitalism, the doctrine that life was sustained by forces distinct from chemical and physical forces, was no longer popular in the medical circles in which Snow traveled, but fundamental questions remained about what distinguished living entities from the nonliving. Some believed it was possible for nonliving materials to become living under certain circumstances, a view with special implications for those who believed that epidemic diseases were caused by immaterial particles in miasmatic or effluvial suspension. This debate found Snow in the familiar place of straddling a line between life and death. He had investigated this borderland of medical research for at least fifteen years, whether by reanimating asphyxiated guinea pigs or by studying the patterns by which chloroform shuts down human consciousness. He had long been interested in the chemistry of respiration and oxidation, subjects of crucial concern to the animal physiology of Liebig and Magendie, upon whom Snow often relied and from whom he occasionally departed. Snow was no vitalist, but he maintained a major distinction: vital molecular processes were continuous, nonvital were not. He believed in a chain of continuity from one living being to another and intended his oration to show that apparently disparate living phenomena share common properties, common patterns of action, and common continuities of action. His ultimate goal on this occasion was to convince local miasmatists that one could not conclude from the blurred line between vital and nonvital that one disease or disease-causing agent could change into another. In his mind epidemic diseases should ultimately be understood on a molecular level. In this way the title was meant to signal the common ground represented by a unification of chemistry and epidemiology. He believed that the molecular action of organic chemistry, essential to all natural processes, was linked to the biological processes of individual living beings and to the diseases that attacked whole populations—that is, epidemics, especially cholera. The reach of Snow’s argument was vast, from the interactions of atoms to the interactions of a global populace. In short, his oration was a “think piece,” inviting his colleagues to consider that the same laws that regulate the behavior of molecules also regulate the patterns of epidemic diseases. If they agreed, Snow had found a common ground with local miasmatists, from which the medical establishment could launch concerted preventive measures.

Continuity, Change, Molecules It is likely that the concept of “continuous molecular changes” appeared immediately relevant to Snow in the context of his anesthesia investigations. In his asphyxia study of 1841, he had commented on the continuity of respiration and its fundamental chemical nature. Similarly, Justus von Liebig had expressed his own wonderment at the exhaustion and replenishment entailed in the chemistry of respira-

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tion: In living organisms “an unfathomable wisdom has made the cause of a continual decomposition or destruction, namely, the support of the process of respiration, . . . the means of renewing the organism.”3 Thereafter, the administration of ether and chloroform to living organisms had impressed upon Snow the ways in which the inhalation of nonliving molecules could create specific effects on the living system—both shutting it down in a definite sequence and reducing the rate of respiration, or the amount of CO2 exhaled. That is, the controlled duration of anesthesia pointed to ways in which the continuity of molecular action could be regulated. When Snow turned his attention to cholera in the fall of 1848, he was interested in the action of the agent and its discrete impact on the human organism. In his view cholera was a local affection of the intestinal tract, and in his first essay on the subject he employed the concept of continuous molecular change to explain the pathological process involved: Being led to the conclusion that the disease is communicated by something that acts directly on the alimentary canal, the excretions of the sick at once suggest themselves as containing some material which, being accidentally swallowed, might attach itself to the mucous membrane of the small intestines, and there multiply itself by the appropriation of surrounding matter, in virtue of molecular changes going on within it, or capable of going on, as soon as it is placed in congenial circumstances. Such a mode of communication of disease is not without precedent. The ova of the intestinal worms are undoubtedly introduced in this way. . . . The writer, however, does not wish to be misunderstood as making this comparison so closely as to imply that cholera depends on veritable animals, or even animalcules, but rather to appeal to that general tendency to the continuity of molecular changes, by which combustion, putrefaction, fermentation, and the various processes in organized beings, are kept up. MCC, 8–9 Snow’s explanation does not seem straightforward to modern readers. He associates two processes—putrefaction and fermentation—with molecular change, but then seems to exclude the microorganisms we now understand to cause these processes, bacteria and yeast. To grasp Snow’s meaning, therefore, requires us to imagine a time before germ theory, when it was still unclear whether fermentation was a vital or nonvital process. Putrefaction and decomposition in urine were considered self-propagating processes, but it was unclear what drove these changes. Contemporary medical researchers could accurately measure inputs and outputs and employ litmus tests to indicate acidity or alkalinity of the fluids and gases that living beings regularly exchanged, but “we have no instrument, like the thermometer,” Snow reminded his colleagues, “with which we can measure the force that communicates the change to substances in contact with those in which it is taking place” (CMC, 150).


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In 1849 Snow was uncertain whether the cholera agent was a microscopic organism or some undetermined, specific animal poison. Parasitic worms, an established example of an agent whose germinal cells (eggs) could be accidentally swallowed and eventually reproduce in the intestine, provided a useful analogy. He conjectured that the agent that caused cholera lodged in the mucus membrane of the intestine and then proceeded to divert materials intended for the body’s sustenance to its own reproduction. Cholera, like ether or chloroform, was a chemical agent that altered the body’s metabolic processes, but unlike these anesthetics, cholera redirected those processes to make more of itself.4

Animal Chemistry Snow structured CMC in three parts. In an opening theoretical section he addressed the general questions of vital and nonvital processes and the chemical basis for biology. Next, he presented a theory of the nature of epidemic diseases and defended his own views on cholera transmission. In the concluding section he substantiated his general theory of epidemic diseases and drew practical implications from it. “Molecular changes,” for Snow, alluded to the forces that constantly act on all particles of matter, whether they exist in life forms or in test tubes. For him molecular meant “atoms of matter.”5 Flux occured on a molecular level in all matter, organic as well as inorganic. Matter in living and nonliving things is always changing—changing state, forming new compounds, decaying, oxidizing, reproducing, combusting, and fermenting. It was also known that crystallization and “cohesion” were the result of forces that occur at a molecular level. Snow knew his usage of the term continuous molecular change would call to mind Liebig’s book on Animal Chemistry, which had been translated into English in 1850 and was repeatedly mentioned in medical journals. Liebig frequently used the phrase continuous molecular action, and Snow adopted Liebig’s terminology for organic chemical processes.6 For Snow molecular was the word that most effectively “express[ed] all that refers to the attraction which exists amongst the particles of matter at insensible distances”—distances too minute to be perceived by the senses (CMC, 145).7 Besides the etymological link with anesthesia, “insensibility” was at the heart of the dispute over cholera transmission. In arguing for his fecal–oral theory and his hypothesis of water-borne spread, Snow regularly found himself opposed by those who believed that disease arose from sensible causes such as foul odors and visible filth. Some of Snow’s would-be allies, such as Frederick Brittan, Joseph Swayne, and William Budd, were prepared to consider a cholera poison that acted the way Snow predicted only if they could see the particle under the microscope. To the contrary, Snow wished such colleagues to embrace the idea that processes that occur at insensible levels of size and organization might explain the sensible phenomena all of them observed at the bedside.7a As Liebig put it, “The discovery of the laws of

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vitality, cannot be resolved, nay, cannot even be imagined, without an accurate knowledge of chemical forces; of those forces which do not act at sensible distances.”8 By invoking this respected Continental authority, Snow hoped to establish consensus that an understanding of molecular structure developed in the laboratory would permit medical men to make new predictions of how matter should behave at “sensible” orders of scale. Just as he had done with his investigations of ether and chloroform, Snow sought to create a scientific approach that melded laboratory medicine, bedside medicine, and a numerical, or quantitative method.

The Vital and Nonvital: Commonality and Difference Snow also modeled his reasoning on Liebig’s to argue for a common ground between the organic and inorganic. Molecular changes were characteristic of both realms: “All changes of composition whatever, whether occurring in a test-tube, or in a living brain, are properly included amongst chemical changes; and all that takes place in living structures has a right to be called vital, whether it differs from what occurs elsewhere or not. Thus, whilst the terms chemical and vital have each a separate signification, they have a certain ground in common, since changes of composition in living beings are at once both chemical and vital, and belong to both chemistry and physiology; just as fossil animals belong to both the mineral and animal kingdoms, and to the sciences of geology and zoology at the same time” (CMC, 145–46).9 In other words, Snow’s common ground was the biochemical nexus; at the molecular level vital changes entail chemical ones. He recast vital and morbid processes in biochemical terms, insisting that “the chief phenomena of living beings” could be thought of as “a number or collection of continuous molecular actions” (CMC, 150–51). In his mind “there is no distinct line of demarcation between vital processes and those which are not vital” (CMC, 151). With respect to zymotic changes (fermentation), he acknowledged that “many persons would doubtless say that the formation of the [yeast] sporules is a vital process, and the production of alcohol and carbonic acid a chemical process inseparable from it. . . . [However,] it must be remembered that the decomposition of sugar into alcohol and carbonic acid is as closely connected with a process of organization as are the sensibility and contractility of animal tissues” (CMC, 152).9a Such statements warned his audience not to assume that vitality was something other than its processes nor that some processes were necessarily more vital (or fundamental to vitality) than others. Snow cited another Continental researcher, Matthias Schleiden, in support of the view that “we must regard the whole process of [vegetable] cell-formation as simply a chemical act. The gathering together of granules of mucus to form a cytoblast we can as little explain as that, when we form a solution of two salts, if we throw into the mixture a crystal of one or other salt, that salt alone crystallizes around it” (CMC 152).10 Snow’s work on the degrees of narcotism induced by anesthetic agents had indicated


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ways in which chemical agents affected nervous activity and suspended sensibility in tissue, which confirmed for him the chemical nature of such complex vital functions.11 This interpretation of the biochemical nexus also offered an explanatory mechanism by which a cholera poison could rapidly reproduce in the mucous membrane of the alimentary canal. Whereas “molecular changes” characterized both vital and nonvital processes, “continuous molecular changes” were characteristic of vital processes alone. For Snow a continuous chemical process could not begin de novo and always required the pre-existence of a similar vital process: “Combustion, putrefaction, and numerous other molecular actions, although capable of self-propagation, commence anew, under the requisite circumstances, without any contact with matter undergoing the same change. There are, however, changes of a more complicated nature—those to which plants and animals owe their development and continuance—that have never commenced anew within the experience of man. The most characteristic property, indeed, of vital actions probably is, that they are always caused by similar processes which have preceded them, whilst all other molecular changes may arise, occasionally at least, from other causes” (CMC, 150).12 He allowed one exception, combustion, which he considered a bridge between nonvital and vital processes. It could occur spontaneously, but it was also the process by which animal life breaks down foodstuffs.13

Oxidation Oxidation was the common ground for Snow’s work on anesthesia and cholera. In the last installment of ON (1851), he had noted (following a train of thought suggested by Charles Philippe Robin in Paris) that a range of narcotic agents, from ether and chloroform to benzine and arsenic, possessed antiseptic properties. All appeared to preserve animal matter from putrefaction. He linked their various antiseptic powers to a common capacity to inhibit oxidation, “probably in direct proportion to their narcotic strength,” and he noted the bridging nature of combustion: “Substances which have the property of limiting and preventing oxidation in the living body, have also the property of limiting and preventing that kind of oxidation which constitutes ordinary [that is, nonvital] combustion” (ON, 18: 1091). Continuous molecular changes that maintained biological functioning were oxidative processes, or partly so. Consequently, narcotic anesthetics could interrupt those processes if administered in proper doses. Communicable diseases disrupted normal oxidative processes and, like anesthetics, became irreversible if not arrested in time, but whereas anesthetics induced molecular changes, communicable diseases did their “mischief ” via continuous molecular changes, commandeering the nutritional and maintenance processes of the healthy body for the task of manufacturing more of the disease agent, infecting others, and starting the process anew.14

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To explain why the interruption of oxidation in the case of anesthesia might be readily reversible when the disruption produced by communicable diseases might not be, Snow introduced the idea of chemical counteraffinity. He described a series of experiments in which he found that the nitrogen that makes up eighty percent of the air is not inert in relation to atmospheric oxygen. Some of the experiments involved nonliving material, such as a red-hot iron wire and a burning candle, both of which combined more readily with oxygen when the nitrogen was absent. He also experimented on birds and other animals and noted that they died more quickly in oxygen-deprived atmospheres with high concentrations of nitrogen. He considered it “evident, then, that the nitrogen of the air exerts an influence over the combination of oxygen with other bodies. This depends chiefly on the affinity between the nitrogen and the oxygen—an affinity which is not great enough to cause their combination under ordinary circumstances, but is sufficient to counterbalance, to a certain extent, the affinity between oxygen and other bodies. It is on this kind of counteraffinity, as it may be called, that the action of most narcotic and antiseptic agents on living and dead animal substances depends” (CMC, 149).15 The key to effective narcosis was manipulation of this counteraffinity in such a manner that it was speedily induced and just as speedily reversed. Hence, Snow’s interest in continuous molecular changes and chemical affinity had emerged from investigations of the mechanism by which anesthetics inhibit oxidization.16 According to Richardson, Snow’s “greatest deduction . . . [was] that the action of volatile narcotics is that of arresting or limiting those combinations between the oxygen of the arterial blood and the tissues of the body, which are essential to sensation, volition, and all the animal functions.”17 The point of the “farthing candle” experiment (see Chapter 6) was to demonstrate counteraffinity: The process of adding chloroform vapor to the bottle removed none of the oxygen from the air it contained, although the candle acted as if it were burning in an atmosphere that contained less oxygen than normal air.18 Along with his experiments on oxygen and nitrogen, the farthing candle experiment bridged the vital–nonvital divide by positing a biochemical nexus.

From Contagion to Communication After his discussion of oxidation and counteraffinity, Snow gave examples of how his general theory of continuous molecular changes explained the action of various epidemic diseases. Such diseases resulted from the multiplication and spread of specific agents—in short, they were “continuous.” By this reasoning disease agents could not arise spontaneously in the atmosphere or from the putrefaction of vegetable matter, because any molecular changes involved therein were not capable of reproducing the same agent. The common ground Snow had in mind, therefore, did not accommodate hard-core anticontagionists. Instead, he directed his remarks to contagionists and contingent contagionists and hoped to shape a new consensus with


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a term that had fallen out of fashion in all the hubbub over Asiatic cholera: communicable diseases. Snow’s gambit began with a definition. The communicable diseases were “an extensive group of maladies, each case of which is caused by some material that, as a general rule, has been produced in the system of another individual” (CMC, 155). His term included diseases such as “syphilis, small-pox, measles, scarlet-fever, typhus, typhoid and relapsing fevers, erysipelas, yellow-fever, plague, cholera, dysentery, influenza, hooping-cough [sic], mumps, scabies, and the entozoa” (CMC, 156). He considered the term communicable preferable to contagious or zymotic because communicability can be direct as well as indirect, and it emphasized the process of change.19 Communicable was flexible and inclusive; it should be acceptable to contact contagionists, swallowing contagionists, and contingent contagionists (who accepted inhalation of infectious agents produced by the sick). It did not distinguish among modes of communication; he lumped syphilis, influenza, and entozoa (intestinal worms) into the same category.20 Plus, it had another advantage that made it seem appropriate for a generation of medical men trained to believe that medicine was connected to collateral sciences like chemistry: It brought to mind a set of patterns of molecular change peculiar to living beings. The organized matter . . . which induces the symptoms of a communicated disease . . . possesses one great characteristic of plants and animals—that of increasing and multiplying its own kind. . . . The molecular changes taking place in the materies morbi of some diseases resemble the changes in many living beings in another respect also: they permit of being suspended, under certain circumstances, and recommence at the point at which they ceased. . . . There is always a definite period . . . before the illness commences, which is called the period of incubation. As regards the materies morbi itself, this . . . is a period of reproduction. . . . [C]ommunicable diseases . . . are apt to be extremely prevalent at particular times and places . . . which arises strictly out of their communication from individual to individual.” CMC, 156–57 Every communicable disease followed a particular pattern, often involving a period during which its characteristic molecular changes appeared discontinuous to the medical observer but when the disease agent actually was reproducing inside the host. CMC represented a turning point in Snow’s thinking about the mathematics of epidemics. Four years earlier, he had suggested that the mode of communication of epidemic diseases might explain the shorter duration of outbreaks in villages, compared to cities, and had noted that an epidemic dies out “for want of fresh victims” (PMCC, 928). Snow expanded on these insights in CMC by arguing that the mathematics of an epidemic outbreak are explainable entirely by reference to the

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transmission characteristics of the disease in a population. Referring to epidemic diseases, he asserted that their extreme prevalence at times “arise strictly out of their communication from individual to individual” (CMC, 157). While “various irruptive fevers” are constantly present in London, cholera “has been twice spread over the world . . . and seems to be dying out a second time everywhere but in the South of Asia. . . . It is so difficult to support that the world seems scarcely large enough for it, and, were it not for its pastures in India, it would be in danger of passing altogether out of existence, like the Dodo in Mauritius” (CMC, 158). Snow may have been the first to recognize the complete dependence of the rise and fall of human epidemics on the need to sustain the chain of human transmission, and that that chain in turn depends entirely upon the changing prevalence in the population of susceptibles and immunes.21 He offered an example: “syphilis, for instance, keeps a pretty even course in this metropolis, because there is a steady amount of vice for its support; and a still greater amount of virtue to keep it in check; but when it is introduced amongst a community of savages, indulging in promiscuous intercourse, it rages as a fearful epidemic” (CMC, 157–58). His point was simultaneously social and pathophysiological. Social practices can encourage or prevent communicable diseases from becoming epidemic. The epidemiological thrust of the concept of communicability lay in its attention to discrete social pathways as well as discrete pathogenic agents, but one did not need to identify the latter in order to posit socioecological equations of disease.22 It was sufficient to know that in a communicable disease the victim had to receive the “materies morbi”specific to that disease from another person. Thereafter, the “suitable materials” (which some called the infectious “virus”) resumed the process of reproduction, incidentally causing the symptoms of disease in its new host, at the point where it had been suspended when the particles were excreted by the previous individual. By virtue of the principle of continuous molecular change, the “virus” could replicate only itself; cases of syphilis would only produce more syphilis, and so on, regardless of the route or conduit by which the “virus” entered the body. Some communicable diseases seemed to be transmitted through the air: “It is not improbable,” Snow speculated, “that the specific cause of influenza and measles is drawn in with the breath, as these diseases affect chiefly the respiratory organs, and spread almost equally amongst all classes of the community” (CMC, 168).23 The alimentary canal offered another mode of communication.24 Cholera, in his view, was spread by accidental “swallowing of the morbid excretions of the patients” carried by “drinking water, or other articles of diet” (CMC, 168–69).25 Poverty, filth, and overcrowding often facilitated the transmission of morbid materials from person to person, but Snow believed that they could not, in the terminology of the day, be predisposing factors that actually caused someone to come down with a communicable disease. The underlying process was still unknown, but “as we have analogy to guide us, we are warranted in concluding that when the morbid matter of any disease is received into the system, in the way required in that particular disease, it is almost


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certain to produce its specific effects, except in the instances in which the patient has gained an immunity by a former attack. . . . There is no reason to invoke a supposed predisposition, or predisposing causes, to account for its existence in the persons in whom we find it. To be of the human species, and to receive the morbid poison in a suitable manner, is most likely all that is required” (CMC, 161). It was inconsistent with the notion of continuous molecular change to imagine that any “disease has taken on contagious properties which it did not previously possess” (CMC, 171). To suppose, for example, that yellow fever was caused by marsh miasmatas in some locations and elsewhere transmitted from person to person “amounts to nothing more or less than supposing that some material produced in marshy ground, without any connection with the human body, can be reproduced and grow in the system of the patient. I believe we know nothing in nature analogous to this, and it is therefore an opinion which should not be adopted till there is strong evidence in its support. It is most likely that yellow fever was always a communicable disease” (CMC, 171–72).

Continuous Molecular Change as Social Theory Snow insisted that the study of communicable diseases should consider sociological and cultural factors in addition to the physiological. For example, medical controversy about the question of contagion often turned contentious because of “the great pecuniary interests involved . . . on account of its connection with quarantine” (CMC, 173–74). In his formulation the notion of continuous molecular change demanded the addition of a sociocultural level to the systems thinking he was using to explain the communication of cholera (see Table 8.2).26 Culture, education, literature, emotions, and, most strikingly, memory exhibit the continuity of suspended activity in vital organisms. Cultural transmission is a form of vital replication: “In the human species, enjoying the faculties of speech, [the] connection between succeeding generations is much more intimate. . . . In our own profession it has been truly said to last to the end of life, and institutions like this Society have the effect, not only of preserving and transmitting the knowledge of one generation of medical men to the next, but of increasing the boundaries of the science they cultivate, and rendering it more perfect and useful.” Language, as a medium of communication, is also subject to the natural laws underlying continuous molecular change: “The communication of certain molecular changes taking place in the brain . . . extends collaterally in all directions, by means of vibrations in the air, or in the ethereal medium which pervades space. . . . The faculty of speech gives to man a power of communicating his complex feelings and ideas, far exceeding that of lower animals; and the invention of literature has greatly increased this power in civilized nations. By speech, not only can fresh sensations and ideas be communicated, but also that continuation of them called remembrance, by which

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they revive after, it may be, a long interval of suspended action” (CMC, 154–55). In this vision memory is analogous to the dormancy period characteristic of communicable diseases. There are other analogies as well. One person’s idea (“a particular state of molecular action” within the brain), conveyed by a suitable medium (oral speech or writing) to another person, can set up the same process of molecular action in the recipient’s brain.27 For Snow the notion of continuous molecular change explained animal behavior as well as animal physiology and the communicability of epidemic diseases.28 His speculative oration painted an intricate web of social, chemical, and biological communication. Three years previously he had said that simply because influenza seems to break out somewhere in many people seemingly at the same time, this is not evidence for miasmatic causation. An illusion was at work, for influenza travels no faster than bad news, which is clearly communicated by the breath.29 The sociocultural vision in CMC shows that Snow’s earlier comment was no verbal byplay. Bad news was not bad because the breath was bad; the breath was the neutral medium for the transmission of a specific sort of information, just as it could transmit the agent that caused influenza. Similarly, drinking water, as such, was not disease inducing, but it could be a neutral medium by which the continuous molecular action of the cholera agent was transmitted. Snow concluded his remarks by urging all members of the Medical Society of London to increase their investigations into the “modes of propagation” and the “means of prevention” of communicable diseases. He invoked the example of Edward Jenner, a former fellow of the society, and his smallpox vaccine as one of the surest paths to the advancement of the society and the profession. Perhaps Snow considered this example apposite, because (like himself studying cholera) Jenner had not been deterred by the “insensible” nature of the causative agent of cowpox or by the fact that the science of his day could not reveal the mechanism by which cowpox protected against smallpox. Two years after delivering this oration, Snow became president of the Medical Society of London. In his inaugural address he gave an assessment of the state of the medical profession in England and his sense of how the society could promote its advancement: We are all agreed that the medical profession does not hold that position in the country that we should wish. . . . The chief reason, in my opinion, is that the science of medicine itself is not in the position in which we could wish to see it. . . . There is a right time for the advancement of every science. Medicine could not approach to perfection till the collateral sciences were first advanced; but the time has probably now arrived when medical science may advance in the same rapid manner that chemistry has advanced within the last seventy or eighty years. . . . I do not mean that we shall find a cure for every disease, but that we shall have a rational knowledge of it, and know what to


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expect from treatment. . . . If the profession should then not have quite the position in society that we could wish, it will, at all events, not be placed beneath the other professions; and we shall not see the civil engineer and the chemist placed over the medical man, in matters that belong exclusively to his own profession.30 This passage reveals Snow’s abiding conviction that medicine ought to derive its value and power from its foundations in basic research undertaken in the “collateral sciences,” particularly chemistry.31 He called for professional consensus built around principles derived from chemistry and physics. This notion that professional identity should be based on scientific knowledge echoed the reformist rhetoric of other medical men in Snow’s intellectual generation, such as Benjamin Brodie, William Farr, Marshall Hall, Robert Liston, and James Johnson. Snow’s language was characteristic of the London institutions in which Snow received his medical training.32 Each collateral scientific field, such as chemistry, could illuminate medical concerns, but medicine was constituted by the totality of the collateral sciences and practical bedside medicine. Scientific medical practitioners knew how to employ the collateral sciences to enhance their therapeutic abilities. Snow also expressed frustration at the lack of influence in public health matters exerted by the medical profession generally and perhaps himself in particular, but the profession was certainly partly at fault. For a quarter century they had engaged in contentious debates over the fundamental nature of epidemic diseases such as cholera, with no resolution in sight. It was no wonder nonmedical reformers like Edwin Chadwick found a clear path to power.33 CMC was Snow’s attempt to forge a medical consensus about epidemic diseases, but it had no discernible effect in his lifetime. Although members of the Medical Society of London applauded his learned oration that March evening in 1853, his colleagues proved unwilling to share the common ground he had offered them.34

Notes 1. “Medical Society of London,” Lancet 1 (1853): 253–54; MTG 6 (1853): 282–83; AMJ 1 (1853): 218. On the Thatched House Tavern, see Cunningham, Hand-Book of London, 492. 2. Snow, On Continuous Molecular Changes (1853). We cite the published version parenthetically in the text as CMC. 3. Liebig, Chemistry and its Application, 123. 4. In the early 1850s Snow decided that the “morbid poison” causing cholera was probably cellular. He was not alone in this shift in thinking. In 1852 Farr stated that cholerine was the likely “zymotic cause of malignant cholera.” He redefined a term previously used for milder diarrheal symptoms during outbreaks of summer cholera; see the OED. 5. CMC, 147. Although Liebig and other Continental researchers used molecular, it was not in common use among British scientists. It does not appear in the index to a 900-page textbook, Brande and Taylor’s Chemistry.

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6. For a discussion of the scope and nature of Liebig’s influence, see Eyler, Victorian Social Medicine, 27–33. Throughout the period of Snow’s development as a chemist and anesthetist in the 1840s, Liebig had advocated the chemical analyses of animal tissues, stressing the inferential power of what he called the “quantitative method.” He had spoken to the British Association in Glasgow in 1840 and toured Great Britain in 1843 lecturing on the application of organic chemistry to agriculture. In 1845 he sent his student August Hofmann to head Prince Albert’s new Royal College of Chemistry. If one followed Liebig’s method, carefully measuring “what went in (food, water, oxygen) and what came out in excretions and exhalations (urea, various salts and acids, water, carbon dioxide), much could be inferred about chemical processes inside the animal (or human) organism”; Bynum, Science and the Practice of Medicine, 96. Snow could have accepted Liebig’s general approach without subscribing to his pathological theories, which had some currency in London in the 1840s and 1850s as seen from the frequent references to Liebig’s work in the medical journals. Snow, for example, appears not to have accepted Liebig’s assertion that yeast was a nonliving particle; Liebig, Chemistry and its Application, 121–27. 7. The word “insensible” disturbed a reviewer of Snow’s published oration. This person believed that an “insensible” distance was real and conceivable, even if the measuring apparatus of the day could not deal with it; “Bibliographical notices,” AMJ 1 (1853): 484. 7a. The miasmatic-oriented GBH was unconvinced that insensible micro-organisms could cause disease. When commenting on the many “living animal and vegetable forms” in London water detected by Hassall, the GBH emphasized in 1855 that “where . . . parasites are the cause of disease, they exist as a palpable morbid product occupying some considerable share of the affected body.” In the muscardine of silkworm, for example, the entire insect is destroyed by the disease. Parasitic infestations in humans also indicated to them that “the causative thing, remains as a material shaped body, susceptible of ocular demonstration, side by side with its effects, and having bulk proportionate to them”; UK GBH, Report of CSI, 46. Since such sizable and visible effects were manifestly not the case for cholera, the GBH did not find Snow’s theory or his analogy to intestinal parasites persuasive. 8. Liebig, Animal Chemistry, vi. 9. Like Snow, Liebig was a multilevel scientific thinker: “My object in the present work has been to direct attention to the points of intersection of chemistry with physiology, and to point out those parts in which the sciences become, as it were, mixed up together”; Liebig, Animal Chemistry, viii. 9a. In this passage, Snow shares Liebig’s view of the chemical nature of all vital processes, rather than the one offered independently more than a decade earlier by Theodor Schwann and Charles Cagniard Latour that fermentation was caused by a living fungus-like organism. 10. Snow cited Schleiden, Principles of Scientific Botany, 35. The idea that the body is, in effect, a chemical machine had been proposed nearly fifty years earlier by Jöns Jacob Berzelius (1779–1848): “Unreasonable as it may seem . . . our judgment, our memory, our reflections, as well as other functions of the brain, are organic chemical processes as well as, for instance, those of the abdomen, the intestines, the lungs, the glands, etc . . .”; quoted in Nordenskiöld, History of Biology, 372–73. 11. For a summary of this research, see OC, 34–48. 12. Snow did not assume that his audience would agree with him that all complex vital processes arose from preexisting, similar vital processes, and the reviewer for AMJ did not. This person differed from Snow on one major issue, asserting that because at some point in the world’s history the first vital process must have emerged from nonvital chemistry, analogy of process required that each time a new living being was formed, it must arise by the same


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chemical process by which the species first arose, that is, spontaneous generation; “Bibliographical notices,” AMJ 1 (1853): 486. 13. “[R]espiration has been compared to combustion, and the lungs to a furnace; but as we have seen that the carbonic acid is really produced in the capillary circulation of the system, and only evolved in the lungs, the whole body ought to be compared to the furnace, and the lungs to the draught and chimney department . . .”; Snow, “On asphyxia, and on the resuscitation of still-born children” (1841), 223–24. 14. Toward the end of his life Snow appears to have been trying to extend this idea further. Richardson states that had Snow lived, he would probably have proceeded to the formal investigation of cancer based on the concept that cancer represented a local disruption of the body’s nutrition; L, xxxiii. Perhaps Snow thought of communicable diseases and cancer as two ways that continuous molecular changes might hijack the body’s normal metabolic processes. In the former case the result was the multiplication of the disease “poison,” which could cause the disease in others. In the latter case the result was the proliferation of an abnormal tissue that could ultimately kill the person through the diversion of nutrition and substance but which could not be communicated to others. The nearest contemporary analogy may be a computer virus, which seems to have been the modus operandi that Snow envisaged as the disease agent in cholera. 15. See also Snow, ON, 18: 1092. Neither his theory of counter-affinity, nor his thesis that anesthetics were anti-oxidative and antiseptic, appear to have a basis in modern science. 16. S. Snow recounts one of Snow’s contributions to the discussions of the Westminster Medical Society that may help us date the origins of this concept. In the fall of 1838 he joined the debate over the death of a night watchman from the vapors of a new type of stove, claiming that the death was due not to carbon dioxide but to lack of oxygen, the absorption of which by the lungs was prevented by the presence of carbon dioxide “owing to the affinity which one gas bore to another”; JS-EMP, 206, quoting Lancet 1 (1838–39): 419. Three months later, however, Snow recounted further animal experiments he had done that had changed his mind, and he now thought that carbon dioxide could kill via a mechanism different from the exclusion of oxygen. Thus, Snow seems to have been working on the precise mechanism of counteraffinity among gases as early as 1838. 17. Richardson, L, xvi. 18. Ibid., xvii. It is likely that Snow actually said something very close to Richardson’s account. Snow referenced Graham’s experiments on phosphorus (cited below) and described a similar experiment; ON, 18: 1092. Zuck thinks it possible that Graham’s demonstration triggered Snow’s experimental work on inhalation anesthetics in late 1846 to early 1847; Zuck, “Thomas Graham.” Shephard believes that Snow’s model anticipated some aspects of the modern theory of anesthetic action, with the anesthetic molecule exerting its counteraffinity effect at the level of the cell membrane; JS, 145. 19. Snow considered zymotic pathology one form of communication among a set of possibilities. He disagreed with Farr’s inclusion of acute rheumatism and scurvy in the class of zymotic diseases without evidence that they were, in fact, communicable, as well as for the more basic reason that zymosis accepted miasmatic origin and diffusion of disease. He wondered what Farr meant by zymotic with respect to direct or indirect communication because he took fermentation to be, in and of itself, a communicable process; CMC, 156. For the contrary view that Snow followed Liebig in accepting zymotic pathology, see Hamlin, Science of Impurity, 127–51. 20. Also see Farley, “Parasites and the germ theory of disease.” 21. A similar insight a century later eventuated in the eradication of smallpox. The principle that Snow here sets out is true, however, only of diseases like cholera and smallpox that have no animal reservoir.

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22. For a similar point, see Shephard, JS, 263–64. In the passage on syphilis, Snow refers implicitly to the systems concepts of feedback loops and homeostasis. 23. Snow devoted a great deal of research, summarized in the early chapters of OC, to determining if there were any means by which the administration of chloroform might possibly be construed as pathogenic. This research allowed him to rule out air itself as a cause of communicable disease. This would not by itself refute miasma theory but would give Snow a good grasp of how any airborne substance or particle might be expected to behave. 24. The type of medication that would arrest an attack of cholera if administered during the premonitory diarrheal stage was the sort of substance that would arrest putrefaction or fermentation, thus showing its property of “destroying low forms of organized beings.” One such substance was chloroform, which “has gained some reputation as a remedy for cholera, when introduced into the stomach.” Because chloroform had no curative powers when inhaled, this confirmed for Snow his hypothesis that the poison of cholera was confined to the alimentary tract, was not inhaled, and did not invaded the bloodstream; “The principles on which the treatment of cholera should be based” (1854), 181. 25. On this mode Snow’s speculation proved a stretch. He said that there “is evidence tending to show that typhoid fever, yellow fever, and plague, as well as cholera, are communicated by accidentally swallowing the morbid excretions of the patients”; CMC, 168. 26. Earlier in the essay he had said that the reproduction and dissemination of species of plants and animals were all examples of the process of continuous molecular change; CMC, 150–51. 27. Snow’s thinking may be compared to that of the theologian and philosopher David Hartley (1705–1757), who explained the mechanism of the mind by drawing on the Newtonian idea of the transmission of vision by atomic vibrations in the nerves. He suggested that experiences, sensations, and memories were stored in the brain as “vibrationuncles” that were associated with impressions of pleasure or pain. The “vibrationuncles” were subsequently activated by repetitions of the appropriate experiences, generating responses by association; Hartley, Observations on Man. 28. Once again the analysis suggests an analogy between Snow’s interdisciplinary, multilevel approach and the biopsychosocial model; Engel, “Need for a new medical model”. It seems a safe assumption that Snow was able to make analogies between processes that occurred at the molecular and at the social levels of organization (i.e., continuous molecular changes with human language and speech). It also seems safe to say that Snow had at least a rudimentary notion that some type of information transfer might be the common element at these disparate levels of organization—hence our willingness to employ a term like “molecular memory” in elaborating Snow’s thought. However, one would not want to go beyond that and claim that Snow had somehow anticipated the mid-twentieth-century sciences of cybernetics and information theory, which formed part of the theoretical basis for the biopsychosocial model in the 1970s. Still, just as the biopsychosocial model was fundamentally an antireductionist model, the social sweep of Snow’s thinking in CMC and elsewhere seems clearly to indicate that Snow was not a simple reductionist. By saying that human communication and culture were kinds of continuous molecular changes, he did not intend to say that these phenomena were nothing but chemical processes or that they could be appropriately studied in the test tube. He showed in CMC that his multilevel, interdisciplinary mode of thinking sought functional analogies at all levels of organization from the molecular to the social and viewed knowledge at any level of organization as potentially helpful in elucidating the problems of disease. 29. “Chemical researches on the nature and cause of cholera,” Lancet 1 (1850): 155. His comment occurred at a meeting of the Royal Medical and Chirurgical Society. Compare Snow


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on influenza and bad news with the first sentence in Daley and Gani, Epidemic Modelling: “This monograph is designed to introduce probabilists and statisticians to the diverse models describing the spread of epidemics and rumours in a population.” 30.”Medical Society of London,” Lancet 1 (1855): 292. 31. The phrase “collateral sciences” was an allusion to London Medical Gazette being a weekly Journal of Medicine and the Collateral Sciences, which Snow had been reading since he was a medical student from 1836 to 1838 and contributing to regularly in more recent years. In 1851, however, the subtitle was dropped when LMG merged with MT to become MTG. 32. Warner, “Idea of science in English medicine.” 33. In the utilitarian civil engineering solutions of the sanitary reformers, who held great sway with Parliament, medical investigators figured marginally as collectors of data. Chadwick and his circle were relatively uncritical of the evidence on which they based their pathological and etiological assumptions. It was just these areas that Snow targeted as the foundation of a cultural authority based on, in Christopher Lawrence’s phrase, “a new medical science of disorder, the promotion of medically informed solutions and the advancement of the claims of the medical expert”; C. Lawrence, Medicine in Modern Britain, 49–50. See also Bynum, Science and the Practice of Medicine, 74–75. 34. To judge from the reaction of the author of the only contemporary review of CMC we have found, Snow accomplished his task as orator well. The reviewer praised him for the richness and originality of his ideas; “Bibliographical notices,” AMJ 1 (1853): 484–89. That the reviewer went on for five pages and dealt with Snow’s various points seriatim and in detail indicates his level of interest in the oration. For more recent interpretations of CMC, see Pelling, Cholera, 210, and Winkelstein, “New perspective on Snow.”

Chapter 16

Snow’s Multiple Legacies

N WEDNESDAY, 10 June 1858, John Snow had his mind on his magnum opus, On Chloroform. He was working from his case notes dating back to the summer of 1851, when he had tried out chlorated muriatic ether (ethyl chloride) on patients at King’s College Hospital. The substance had worked fairly well and might have proved safer than chloroform, but it was unstable and difficult to obtain. Snow had procured only enough for operations on twenty patients, and that pint had to be brought specially from Paris. Although the cases were old and small in number, it was important to give the substance its own chapter. Perhaps some other chemist or anesthetist might find a better way to synthesize this agent and bring it into common use. It was all part of Snow’s long search for a safer, better anesthetic. In a matter-of-fact way he was listing cases, describing all the types of surgery in which the drug had been used. He had just penned the name of Fergusson, a surgeon he had worked with from the beginning of inhaled anesthesia and a name he must have written in his casebooks a thousand times when he was stricken and fell off his chair.1 He told his housekeeper that he did not understand the nature of his complaint. He appeared to have suffered a stroke and tried to treat himself, resting on a couch for a day, selfmedicating with ether for the pain, and hoping that whatever was wrong would soon right itself.

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It did not. Friday morning he began vomiting blood. Dr. George Budd and Dr. Charles Murchison were called in.2 Paralyzed on his left side and moving in and out of delirium, he expressed hope in his lucid moments that he would recover and resume his professional activities and expressed a wish to see a colleague, Dr. James Todd, who had expertise in epilepsy and neuralgia. He lingered for five more days and died on 16 June. He was forty-five years old. An autopsy revealed his kidneys to be shrunken, granular, and encysted. There was scar tissue from old bouts of tuberculosis. He had died from a stroke. His excitability and somnolence may have been the result of some chronic illness, rather than vegetarianism, as his carnivorous medical school friend Joshua Parsons would have it. Regular exposure to a variety of toxins in his search for the perfect anesthetic may have hastened his end, but it is just as likely that his renal troubles had brought on the hypertension and stroke. John Snow today is viewed as a pioneering figure in both anesthesia and epidemiology. He has also been identified as a sort of patron saint within the subdiscipline of medical cartography. In each of these fields, Snow’s legacy has assumed a very different form.

The Anesthesia Legacy More controversy over the safety of chloroform occurred during the summer and fall after Snow’s death. Catastrophic accidents at Epsom and Dorking had re-ignited calls for abandoning the anesthetic agent. The Times printed several letters that made uninformed claims about the dangers of chloroform; had Snow been alive he would surely have responded with lucid rebuttals. Others had taken up his message, however, and it was being heard. In articles published by the Lancet, Robert M. Glover and Henry Potter, a long-time colleague of Snow’s at St. George’s Hospital, offered cautions about the safe administration of chloroform that reflected Snow’s precepts. In fact, the Lancet had emerged as the self-styled champion of Snow’s anesthesia legacy. Its editorials seconded his long-standing concerns about the hanky method and endorsed his inhaler: “Chloroform on a napkin is a dangerous and uncontrolled agent; administered through Snow’s inhaler, it is robbed of half its danger, by the more perfect manner in which we can control its inhalation.” The journal greeted with enthusiasm the posthumous appearance of On Chloroform and Other Anæsthetics (OC) in October 1858, and took a stand on its merits in advance of formal reviews: “We strongly recommend to thoughtful perusal the valuable monograph on the subject of Anaesthesia which [Snow] has bequeathed to the profession. No one can rise from reading this valuable digest of a wide experience and the observation of ten years of scientific and practical labour, without a feeling of regret that so much carelessness should still prevail in the administration of this most potent vapour, and a sense of necessity for a more extended instruction in the principles of anestheti-

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zation.” In addition, the Lancet extracted a quotation from the departed-but-nowundisputed master chloroformist on the necessity of gradual induction and Snow’s crucial insight that the induction of anesthesia is “not caused so much by giving a dose as by performing a process.”3 When the review of OC did appear in the Lancet the following month, it contained assessments of Snow and his work strikingly different from the vituperative ad hominem remarks that the journal had carried just three years earlier after Snow’s testimony before the Parliamentary committee investigating the nuisance trades. “We have nothing but good to say of Dr. Snow, living or dead,” gushed the reviewer. Consequently it would have been “only graceful and becoming” if the memoir of Snow’s life that Richardson had prefixed to OC had “alluded to the active part taken by the Lancet, in bringing Dr. Snow’s merits before the professional world at a time when such encouragement was all-important to him—when he was comparatively unnoticed and unknown, and struggling at the painful commencement of what must always be an arduous career.” Indeed, the Lancet had published Snow’s earliest letters and articles periodically throughout his career. It seems that in rushing to embrace a dead colleague, it forgot the scolding it had dished out when he gave Queen Victoria chloroform. Perhaps the pique directed at Richardson was a reaction to the fact that he had given prominence to the role MTG had played in Snow’s career. Or perhaps the Lancet’s changing attitudes betokened professional jealousy or unease that the very journal associated with medical radicalism had not been as consistently supportive during Snow’s improbable rise from a hard-scrabble GP to a pioneer in inhalation anesthesia as had its rivals, especially LMG (which amalgamated with MT to form MTG in 1852). When the Lancet reviewer turned to the substance of OC, his praise remained unalloyed as he focused on Snow’s methods for promoting safe inhalation and preventing fatalities. These methods were the key to Snow’s success as an anesthetist for more than a decade: “It was from his hands that the sufferer, whether alone in the curtained bedroom, or publicly on the hospital table, could best obtain the full advantage of this greatest and most beneficent discovery of modern medical science.”4 Across class lines, in public hospitals and in private rooms, Snow had administered chloroform safely and effectively. None could match this record. The review that appeared in the British Medical Journal in December 1858 was more interested in assessing OC ’s potential contributions to medical literature than in lionizing its author. Nonetheless, the reviewer graciously suggested that an untimely death prevented Snow from correcting drawbacks attributable to incomplete revising and unfinished argumentation. It ends abruptly during Snow’s discussion of ethyl chloride, an apparently deliberate choice by the editor, Richardson, to preserve the precise point at which Snow had suffered his fatal collapse (OC, 423). There was no better work on the subject, according to this reviewer, despite the fact that Snow had neglected a growing body of knowledge on local anesthetics. In addition, he was unconvinced by Snow’s arguments for the absolute safety of chloroform and wondered why Snow had not used ether for patients, such as Major Evans, in whom


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he suspected heart trouble. In fact, the reviewer suspected that the major had died of chloroform, not fatty degeneration of the heart. Why, wondered the reviewer, had Snow not entertained this possibility?5 Persistent doubts about the safety of chloroform eventually led to its abandonment, but the principles Snow established guide inhalation anesthesia to the present day. Snow left behind colleagues and advocates but no real disciples in anesthesia. Joseph Thomas Clover (1825–1882) inherited Snow’s mantle as the most influential anesthetist in London practice.6 Clover followed his teaching in one important way by developing the balloon method (started by Snow) by which one could give a constant concentration of chloroform without worrying about its evaporation into the room air as it was being given. And Richardson, despite his role in editing OC for publication, writing a biographical sketch, and retaining possession of all scientific papers belonging to the deceased, never took up the inquiries Snow left dangling. Richardson’s primary contribu-tion to the field during his later life was to go on to discover some seventy additional anesthetic agents, although none were major improvements over ether or chloroform.7 For several decades after Snow’s death it seemed as if the field was moving in quite the opposite direction from his research and practice. The commitment to scientific study of the physiological and pharmacological basis of narcotism and the reliance on controlled dosages by means of his apparatus, which defined Snow’s method, was replaced by lack of interest in laboratory work. He would have been chagrined to learn that many anesthetists, who preferred the fast and easy handkerchief to an apparatus, had safety records as good as his own.8 The originality and creativity of his experimental work was not recognized again until the mid-twentieth century, when the journal British Anesthesia reprinted On the Inhalation of Ether (1847). The response was so positive that the journal proceeded to reprint OC in the same format. Even if Snow’s scientific accomplishments could not be fully understood until the middle of the twentieth century, his scientific deficiencies were revealed much earlier, although, even here, it was many decades after his death before the field was sufficiently advanced to take issue with any of his major findings. In 1911 A. Goodman Levy demonstrated the mechanism of cardiac failure under chloroform.9 Using cats he showed that injecting a small amount of adrenaline could cause sudden ventricular fibrillation in an animal very lightly anesthetized with chloroform. Indeed, he showed that lighter doses of chloroform might produce more cardiac irritability than did heavier doses. In retrospect, those who suggested that fear or emotional excitement during the beginning stages of chloroform anesthesia might cause death had some justification; Snow, insisting that only an overdose could cause death, had been wrong. Levy’s work did more than reveal how Snow, dazzled by his comprehensive theory of the family of narcotic agents, ignored bits of data that might have revealed the truth. Levy also showed, in retrospect, that Snow was no experimental physiologist in the modern sense. Levy used the methods made famous by Claude Bernard about a decade after Snow and was able to isolate the effects of chloroform in dif-

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ferent doses on different organs in a living animal system.10 Snow could do no more than observe the behavior of the intact animal during life and then try to look for more clues by dissecting the animal after death. Later in the twentieth century more sophisticated machines for administering anesthesia supplanted Snow’s primitive apparatus, even as they relied on similar principles. Both ether and chloroform were replaced by a variety of newer agents. (Besides its risk of cardiac toxicity, chloroform was later shown to be both a liver toxin and a cause of cancer.) Snow’s concept of the five degrees of narcotism is still valid, and today’s practice has not moved beyond it as a way to use bedside observations to identify the depth of anesthesia, but his crude ideas of interference with oxidative processes and counteraffinities were eventually replaced by theories of specific cell membrane receptor sites for specific molecules—ironically, a model perhaps even more in keeping with Snow’s idea of continuous molecular changes and fully consistent with his notion of molecules as small, traveling packets of information, even if he could not possibly have foreseen the chemical details of the modern theory. In the end, Snow’s place in the world of anesthesia is symbolized by the handsome stone erected on his grave in 1951 by the Association of Anaesthetists of Great Britain and Ireland to replace the original stone, which had been destroyed during the Blitz (Fig. 16.1).10a Snow is revered as a pioneer and father figure, even if the modern practice of anesthesia retains only traces of his science or techniques. Members of the History of Anaesthesia Society have been especially keen researchers and guardians of Snow’s significance in the development of this medical specialty.

The Epidemiological Legacy At Snow’s death in 1858, few people working in public health and sanitation believed his theory of the cause and transmission of cholera, yet today he may well be the most recognized figure in the history of public health. The American Public Health Association joins the Royal College of Anaesthetists in supporting an annual John Snow lectureship to honor a distinguished member of its profession.11 A major public health consulting firm in Boston is named John Snow, Inc. At the U.S. Centers for Disease Control in Atlanta, when an epidemiological problem requires a rapid, straightforward solution, staff have been heard to ask, “Where’s the handle to this Broad Street pump?”12 It is virtually impossible to find a contemporary textbook of epidemiology that fails to give Snow a prominent place.13 The transition to public health icon began with the fourth cholera epidemic to strike England, in 1866. This epidemic affected mainly east London, claiming about 4,000 victims in the late summer and early fall. Earlier the Rev. Henry Whitehead, Snow’s colleague in the investigations of the Broad Street outbreak of 1854, had reacted to the news that cholera was again headed toward England by writing two


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Figure 16.1. Snow’s gravestone, Brompton Cemetery, Westminster, London. The base reads, “Inscription restored in 1938 by members of the Section of Anaesthetics of the Royal Society of Medicine and Anaesthetists in the United States of America. The original memorial to John Snow was destroyed by enemy action in April 1941. This replica was erected by the Association of Anaesthetists of Great Britain and Ireland in September 1951” (photograph by Zuck).

articles in a popular magazine that reminded the English reading public of Snow’s cholera investigations and theories.14 A young epidemiologist, John Netten Radcliffe, read these articles and invited Whitehead to accompany him in an investigation of the outbreak in the east London districts.15 The two men traced the cause of the outbreak to uncovered reservoirs at Old Ford that became contaminated with cholera evacuations during July 1866. The reservoirs belonged to the East London Water Company, which only tapped them during emergency water shortages. In an appendix

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to a report to Parliament by the Privy Council, Radcliffe cited Snow’s theory with approval and mentioned the Broad Street investigation as a model for examining localized outbreaks,16 but his superior, John Simon, made no mention of Snow’s theory or writings on the 1848–1849 and 1854 epidemics, neither in his introduction to the report nor in a postscript.17 He made amends seven years later in an annual report to the Privy Council: “Indeed, with regard to the manner of the spread of the entero-zymotic diseases generally, it deserves notice that the whole pathological argument which I am explaining grew among us in this country out of the very cogent facts which our cholera-epidemics specially supplied, and to which the late Dr. John Snow, twenty-five years ago, had the great merit of forcing medical attention: an attention at first quite incredulous, but which, at least for the last fifteen years, as facts have accumulated, has gradually been changing into conviction.”18 The Lancet was quicker in making amends. Near the end of the 1866 cholera epidemic, it stated that “the researches of Dr. Snow are among the most fruitful in modern medicine. He traced the history of cholera. We owe to him chiefly the severe induction by which the influence of the poisoning of water-supplies was proved. No greater service could be rendered to humanity than this; it has enabled us to meet and combat the disease, where alone it is to be vanquished, in its sources or channels of propagation. . . . Dr. Snow was a great public benefactor, and the benefits which he conferred must be fresh in the minds of all.”18a William Farr’s analysis of cholera mortality during the 1866 epidemic as well as Radcliffe’s report on east London did what MCC2 had not—it made Farr a nearly complete convert to Snow’s theory. In an interesting reinterpretation of the local miasmatic conclusions presented by the GBH in 1854, he wrote: “The final report of the scientific committee proved conclusively the extensive influence of water as a medium for the diffusion of the disease in its fatal forms. The zymotic theory was established, and Dr. Snow’s view that the cholera-stuff was distributed in all its activity through water was confirmed. The special report of Dr. David Fraser, T. Hughes, and Mr. J. M. Ludlow inculpated the Broad-street pump to some extent in the terrible outbreak of the St. James’ district. But the subject was further and more conclusively investigated by a committee, aided by Dr. Snow and by the Rev. Henry Whitehead.”19 Further evidence of acceptance and a subsequent enhancement of Snow’s reputation as an epidemiologist appeared in an early work on the history of British sanitary reform.19a Alexander Stewart and Edward Jenkins made some fun of the “eager pertinacity” with which Snow put his views forward, “amusing to some and irksome to many.”20 While disagreeing with some aspects of Snow’s theory, Stewart and Jenkins nevertheless described the south London data as “startling” and the Broad Street investigation by that “indefatigable inquirer” as “such as to compel the assent of the most incredulous to the proposition that [the outbreak] was mainly attributable to the contamination of the water. . . . “21 Government acceptance followed somewhat more slowly. The Local Government Board stated in its 1886 review of cholera,


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“the remarkable and shrewd observations of Dr. Snow, demonstrat[ed] incontrovertibly the connexion of cholera with a consumption of specifically polluted water, startl[ed] the profession with the novelty of his doctrine, and inaugurat[ed] a new epoch of etiological investigation.”22 Near the end of his life John Simon again admitted that the 1856 government report on impure water had followed in the wake of Snow’s pioneering investigation in south London.23 Well before the end of the century, British public health authorities were describing Snow’s work in mythic terms.23a Snow’s theory was being discussed and approved in America at about the same time that his reputation was being reinvigorated in England, but his theories received virtually no attention on the Continent, where the “soil theory” of Max von Pettenkofer of Munich remained dominant in cholera thinking.24 While neither the United States nor Great Britain experienced a major cholera epidemic after 1866, 10,000 lives were lost to cholera in Hamburg in 1893.25 Since that outbreak in Hamburg, however, there has been no serious challenge to Snow’s explanation of the water-borne basis for metropolitan-level cholera epidemics. Snow’s role as an exemplary figure in epidemiological research was first suggested by the American public health expert William T. Sedgwick (1855–1920). He devoted thirteen pages of a 1902 textbook to Snow’s investigation of the Broad Street pump, which he considered “one of the most famous, and one of the most instructive cases of the conveyance of disease by polluted water.”26 Because his account was based on the CIC Report, it was accurate, comprehensive, and credited Whitehead’s role in the investigation. Sometimes referred to as “the Father of Epidemiology in the United States,” Sedgwick guided his textbook through four reprints between 1902 and 1914.27 Subsequently, Snow was championed in the United States by Wade Hampton Frost (1880–1938), the first professor of epidemiology at the Johns Hopkins School of Hygiene and Public Health, who did much to shape modern academic epidemiology in America. In 1936 he prepared Snow on Cholera, a reprint of MCC2, CMC, and the abbreviated version of Richardson’s Life of Snow; this edition, itself reprinted, made a small part of Snow’s writings on cholera readily available to American readers.28 Frost characterized Snow’s reasoning in MCC2 as “a nearly perfect model” (ix) and added, “His account should be read once as a story of exploration, many times as a lesson in epidemiology” (xiv). When epidemiology education expanded in the 1950s and 1960s, the writers of the next generation of textbooks took Frost’s advice to heart, so that it is hard to find an epidemiologist educated between 1960 and 2000 who was not introduced as a student to the Broad Street pump episode as an exemplary case study.29 To today’s epidemiologist Snow demonstrated the success of the epidemiological method—the search for confirmation of theories of disease origin in observations made at the population level—both as science and as the basis for public health policy. Snow showed that seeking to understand the mode of transmission of disease, a phenomenon observable only in the field, could be more important than identify-

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ing the specific agent that causes the disease under controlled conditions in the laboratory. Snow approached public health research in a hypotheticodeductive manner that permitted him to draw conclusions with a quantitative firmness typically associated with laboratory investigations. No stranger to the world of the laboratory, Snow was able to make the crucial imaginative leap to incorporate population and public health data into an experimental mind-set. Snow’s contemporaries Ignaz Semmelweis, who showed the means by which puerperal fever was communicated, and William Budd, who worked out the mode of transmission of typhoid fever, were also members of the scientific fraternity that eventually led to modern epidemiology, but neither Semmelweis nor Budd performed the sorts of comprehensive analyses for which Snow is now known. Snow’s scientific followers include Sir Ronald Ross, who discovered in 1895 that the Anopheles mosquito is the vector of malaria, and Charles Nicolle, who found in 1909 that typhus was louse-borne. Walter Reed likewise uncovered in 1900 the way in which yellow fever is transmitted. Snow had shown that not just the causes of disease, but their routes of transmission, are highly specific. In addition, he modeled public health action by inferring that the corollary of that specificity is to interrupt these routes. He pointed out that cholera can be controlled by nothing more complicated than making sure that the discharges of cholera patients are not spread to others. After Snow, typhus proved controllable via the wearing of clean clothes, and yellow fever mortality was virtually eradicated by isolating patients and interfering with the breeding of mosquitos. As the first scientist to display the power of the epidemiological method, Snow helped to pave the way for the great sanitary triumphs that massively reduced infectious disease mortality during the twentieth century, and he did so using tools of investigation and analysis that can be recognized as “modern” by today’s epidemiologists.

The Cartographic Legacy Snow is a historical icon in anesthesia and a case study in modern epidemiology, but his legacy in medical geography and medical cartography consists of a paradoxical replacement of his illustrative use of disease mapping by mythical caricatures of his methods and actions. The first reappearance of a Snow map occurred in Sedgwick’s 1902 textbook on public health. He redrew the map of cholera mortality in Golden Square that Snow had included in the CIC Report. Although the legend included the phrase “after the original,” the changes were significant. Sedgwick replaced the bars representing each cholera death with dots. He retained Snow’s Voronoi-like diagram of equidistant walking access to two nearest pumps, but he did not comment on its significance.30 A half century later E. W. Gilbert redrew Snow’s map of the Golden Square outbreak from MCC2 and included it in a 1958 article on pioneer disease maps in Great Britain. Like Sedgwick, Gilbert replaced Snow’s bars with dots.


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Unlike Sedgwick, Gilbert radically simplified the map by omitting many of the streets, and the caption misleadingly read “Dr. John Snow’s map (1855) of deaths from cholera in the Broad Street area of London.”31 As a result Snow’s altered map became staples in articles and books about medical cartography, although readers were probably unaware that they were viewing modified recreations rather than reprints of the original. Between 1952 and 2001 Snow’s map or some recreation of it was reprinted in at least forty books and articles on medical cartography (Fig. 16.2). It gradually made its way beyond technical publications into school textbooks, such as the 1993 National Geographic Society resource guide for middle and high school geography teachers.32 The capacity to misrepresent Snow’s map increased with the advent of geographic information system (GIS) technology in the 1990s.33 GIS combines two capacities of computers: graphic ability to draw highly detailed and elegant maps and computational capacity to handle vast quantities of numerical data that can be tied to geographic locations. One may, for example, feed in the home addresses of all new cases of cancer in one region over the last decade and then plot the cases to ascertain whether there is any geographical association between these cases and the location of power lines. GIS is an extremely powerful tool in identifying associations that may be important in the causation of disease, but it is just as capable of being employed to reveal spurious associations that can seem extremely convincing when plotted on a highly detailed map. For example, GIS was behind claims for the existence of so-called cancer clusters, which eventually proved to be random occurrences.34 The GIS community has declared John Snow to be virtually its patron saint.35 It is a simple matter to interpret Richardson’s account that Snow “had fixed his attention on the Broad-street pump as the source and centre of the calamity” during the 1854 cholera outbreak to make it seem that he used disease mapping as an inductive, analytical tool. It is also satisfying to accept Richardson’s heroic portrait of Snow’s subsequent actions: “He advised the removal of the pump-handle as the grand prescription. The vestry were incredulous, but had the good sense to carry out the advice. The pump-handle was removed, and the plague was stayed. There arose hereupon much discussion amongst the learned, much sneering and jeering even; for the pump-handle removal was a fact too great for the abstruse science men who wanted to discover the cause of a great natural phenomenon in some overwhelming scientific problem.”36 This mythical Snow seems an attractive figure to those GIS aficionados who see themselves as standing up for the public health in the face of the jeering throng and as rushing out into the real world to save real lives while the stodgy, plodding scientists fussily demand more evidence before they are willing to act. Maintenance of this Snow myth also has survival value for GIS. Advocates of disease mapping can point to no other incident in which the construction of a map played a pivotal role in identifying the cause and cure of a disease. The desire for a foundational myth in medical cartography, particularly GIS, contributes to the


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remarkable persistence of false versions of the Broad Street incident and Snow’s role as an investigator and public health figure. There is irony in the promulgation of this Snow myth. Modern GIS bears greater resemblance to the methods used by mid-nineteenth-century sanitarians than to the real Snow. He implicated the Broad Street pump because he had a coherent, multilevel theory of the pathology and mode of transmission of cholera. The theory was essential; the map was an illustrative device to support his reports of the outbreak, added several months after he had completed his investigations. The sanitarians, by contrast, had no equally detailed and coherent theory of how effluvia caused disease. They relied on superficial observations and associations. For example, Edmund Cooper pointed to a drainage map of Golden Square to show that cholera cases were not clustered near sewer vents, whereas inspectors from the GBH used a nearly identical map to determine that effluvia escaping from the sewers were the cause of the outbreak. Similar reliance on chance spatial associations by GIS advocates allies them with these sanitarians instead of their purported hero.

* * * Snow’s life in medical science proceeded like a series of continuous molecular changes, one idea engendering the next. It was to his profession that he devoted his life. Ironically, the professionalization and specialization that his career advanced, as well as the reverence with which he is held by members of their respective epidemiological and anesthesiology societies, eventuated in a fracturing of the unity of his work. Richardson included his memoir of Snow’s life in On Chloroform, thereby linking that life to his contributions to anesthesia. The soundness of his epidemiological theory was eventually acknowledged, but it came with little recognition that his work in anesthesia was compatible and, in fact, critical in its formulation and substantiation. Snow’s writing is often a model of lucidity, but his argument has often been taken out of context to make him appear “ahead of his time.” By modern standards some of his views were wrong, just as our successors will find errors in our thinking. Ultimately, however, the limits and staying power of Snow’s thought seem less significant to us than its complex integration of available knowledge in European medical sciences during the first half of the nineteenth century.

Figure 16.2. Family tree of authors who have recreated Snow’s maps as published in MCC2 and the CIC Report. Four authors actually redrew Snow’s original MCC2 map, and two electronically digitized them for computer analysis purposes. All maps published since 1964 are copies of these initial redrawings. The maps noted in four boxes with thick black borders were used for teaching GIS.

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Notes 1. This is our reconstruction of events based on OC, 420–23; CB, 185–93; and Richardson, L, xli–xliv. Richardson wrote that Snow had “written the last printed sentence” of the book just before he was struck down; L, xlii. “Fergusson” is the last word in the printed text of OC. 2. George Budd was the brother of William Budd of Bristol. Snow sent George Budd a complimentary copy of MCC2; see his letter of thanks, 3 January 1855, Clover/Snow, VIII.4.i. 3. The Lancet printed a short notice of Snow’s death, noting that he had made contributions to inhalation anesthesia; Lancet 1 (26 June 1858): 635. On deaths from administration of chloroform, see Times (4–11 September 1858). On Snow’s first advocates, see H. Potter, “Cautions in the administration of chloroform,” Lancet 2 (1858): 32, 34, 289; and R. M. Glover, “Report on anesthesia and anesthetic agents,” Lancet 2 (1858): 369–70, 393–95, 416–18. For the critique of the hanky method, see “Chloroform in surgery,” Lancet 2 (1858): 314. For the endorsement of OC, see “Chloroform and its administrators,” Lancet 2 (1858): 407. 4. “Review,” Lancet 2 (1858): 555–56. 5. “Review,” British Medical Journal 2 (1858): 1047–49. OC begins with a history of anesthetics, focusing more on ancient medicine than on the recent past. Thereafter, Snow included discussion of inhalation as a route for administering medications of all classes; a brief history of chloroform and a description of its chemical and physical properties; the stages of narcotism and related key experiments from the ON series; practical aspects of preparing the patient, administering chloroform, and treating aftereffects; a long section on deaths from chloroform describing his theory of the mechanism of death and analyzing fifty case reports of fatalities; and administration of chloroform in different types of operations. Shorter sections of the book addressed ether, amylene, and an agent similar to Dutch liquid. 6. Clover trained as a surgeon before deciding to become a specialist in anesthesia. He exerted his influence primarily by serving on various study commissions and speaking at society meetings. Like Snow, he was resourceful in designing and applying new apparatuses based on scientific principles; unlike Snow, he did no research himself on the physiology and pharmacology of anesthesia. His death left a leadership vacuum in British anesthesia, and the field suffered a brief period of decline; Duncum, Inhalation Anesthesia, 26, 241–46, 457–59. 7. Some are discussed in Ibid., 264, 385–86. 8. There were anesthetists with equivalent safety records, despite use of the handkerchief, such as Syme in Scotland; Duncum, Inhalation Anesthesia, 204. 9. Levy, Chloroform Anæsthesia. 10. In Snow’s own day only Pierre Jean-Marie Flourens (1794–1867) exemplified this experimental method and thus became one of the few contemporaries upon whom Snow actually relied for experimental evidence. Snow cited with approval Flourens’s experiments early in 1847 to show the order in which the various portions of the central nervous system came under the influence of inhaled anesthetics and to show that chloroform was capable of acting directly on peripheral nerves. Flourens was an associate of Magendie, who had earlier experimented on dogs to isolate the respiratory center within the medulla of the brain (1842). He was thus well poised upon the advent of ether anesthesia to perform the studies necessary to isolate the effects of ether on specific centers within the brain; Duncum, Inhalation Anesthesia, 159–61. 10a. In the spring of 1859, Richardson undertook an appeal for funds for “a plain, but durable monument” to be placed over Snow’s grave in Brompton cemetery as a “simple tribute to the memory of our late estimable and distinguished brother in science”; “Monument to the late Dr Snow,” Lancet 1 (1859): 548, and British Medical Journal 3 (1859): 411, 415.


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11. In September 2001 the University of Durham opened a new residential college named the John Snow College, adapting a depiction of a water pump as the college’s distinctive badge. At the time of his death, a few contemporaries did praise Snow’s “immense labours in the cause of sanitary science”; SR&JPH 4 (1858): opposite table of contents. In a presidential address at the Royal Medical-Chirurgical Society in March 1859, Charles Locock noted that Snow “paid great attention to the investigation of cholera, and published some papers on his views of the effect of drinking impure water as propagating that disease”; Proceedings, RM-CS 3 (1858–61), 47. 12. Dr. David Satcher, then director of the Centers for Disease Control and Prevention (later surgeon general) allegedly would say, “Look for the ‘Broad Street pump’ for good public health”; FP Report 3 (1997): 7. 13. For examples see Brownson and Petitti, Applied Epidemiology, 5; Friis and Sellers, Epidemiology for Public Health Practice, 15–22, 138, 324; Gordis, Epidemiology, 9–10, 257; Kelsey, Thompson, and Evans, Observational Epidemiology, 85, 213–14, 236; McMahon and Trichopoulos, Epidemiology, 8–10, 69, 72–73, 86, 327; J. N. Morris, Uses of Epidemiology, 3, 142, 144; and G. Stewart, Trends in Epidemiology, 7–8. 14. Whitehead, “The Broad Street pump,” and “The influence of impure water on the spread of cholera.” 15. Whitehead recalled these events in the farewell speech he made on leaving the London ministry in 1874; Rawnsley, Henry Whitehead, 226–27. John Netten Radcliffe (1830?–1884) was a Yorkshireman like Snow and received his medical education at Leeds. He was employed by the Privy Council between 1865 and 1869 to investigate and write reports on sanitation and worked under the supervision of its medical officer, John Simon. Later Radcliffe served as medical inspector to the Local Government Board and wrote on plague and enteric fever. He was an officer of the Epidemiological Society of London and was eulogized by the society; Transactions of the Epidemiological Society of London 4 (1884–85): 1. See also Brockington, Public Health in the Nineteenth Century, 262–64. When Thomas Snow defended his late brother’s reputation in a letter to the Times, he claimed that MCC2 had been as full of specific facts, of an equally decisive character, as Netten Radcliffe’s observations were in 1866; T. Snow, “Propagation of cholera,” Times (20 November 1885). See also T. Snow, “Dr. Snow on the communication of cholera,” Times (26 September 1885). 16. UK Parliament, Ninth Report of the Medical Officer of the Privy Council, appendix 7.f. “Mr. J. Netten Radcliffe on cholera in London, and especially the eastern districts,” 264–367. 17. Ibid., see particularly 22 and 295–96. 18. Simon, “Supplementary report,” Annual Report of 1874 to the Local Government Board, in Public Health Reports, 460. 18a. Lancet 2 (1866): 363–64. The editorial also endorsed an application, prepared by Benjamin Richardson and Thomas Snow, to have “the sisters of the late Dr Snow . . . [who] are, in fact, almost if not entirely without means,” added to the civil list for a state pension. “We cannot conceive a more fitting case for the exercise of Royal and national bounty,” stated the editors at the Lancet. The Medical Society of London and the British Medical Association followed suit, and the pension was approved. 19. Farr, “Report on the cholera epidemic of 1866 in England,” xi. Later in the introduction he wrote: “It is well known that the Broad-street explosion was traced to a pump, which drew its water from a well into which the dejections of a child found their way in a circuitous route”; xxxiii. 19a. Eyler argues that by the 1860s, increasing reliance on biological rather than chemical evidence in medical research provided the theoretical context which led Farr to be increasingly receptive to Snow’s line of thinking; “Changing assessments of cholera studies.”

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20. Stewart and Jenkins, Sanitary Reform, 9–10. According to Finn, this book was “a key document in the whole process of sanitary reform which unfolded from 1866 to 1875”; “Introduction” (to reprint edition), 24. 21. Ibid., 11. They did not accept, however, that cholera was spread exclusively via the oral route. 22. “General report of the results of the sanitary survey made in anticipation of cholera, 1885–86,” UK Local Government Board, 15th Annual Report, 110. 23. Simon, English Sanitary Institutions, 241, 261, 263. 23a. Richard Thorne Thorne, principal medical officer of the Local Government Board and president of the Epidemiological Society of London wrote, “it was during this epidemic [of 1854] that the circumstances occurred which have made the pump in Broad Street, Golden Square, historic in the annals of English cholera”; Thorne Thorne, Progress of Preventive Medicine, 56. Rollo Russell claimed that “the large part taken by infected water in the propagation of cholera is established beyond all question by the inquiries of Dr. Snow”; Russell, Epidemics, Plagues and Fevers, 77. An early textbook on public health describes the Golden Square outbreak as “the celebrated instance of the Broad Street pump”; Notter and Horrocks, Theory and Practice of Hygiene, 31. For the view that Snow was essentially unrecognized as a significant contributor to public health until 1936, see Vandenbroucke, “Changing images of John Snow in the history of epidemiology,” and Vandenbroucke, et al., “Who made John Snow a hero?” 24. Among the cholera investigators in the U. S. who praised Snow’s work, see Peters, Notes on Cholera, 47–50; Peters agreed that cholera was caused by a specific poison found particularly in cholera discharges and largely conveyed by water supplies. McClellan wrote that “the investigations of Dr. Snow in London during the epidemics of 1849, 1853, and 1854 prove that cholera may be actively distributed through the medium of drinking water”; History of the Cholera Epidemic, 58. See E. Goodeve’s chapter on epidemic cholera in Reynolds and Hartshorne, A System of Medicine, 389, and Wendt, Treatise on Asiatic Cholera, 120. Billings lists fourteen of Snow’s writings on cholera in Bibliography of Cholera. 25. R. Evans, Death in Hamburg. 26. Sedgwick, Principles of Sanitary Science, 170–82. 27. Jordan, Whipple, and Winslow, A Pioneer in Public Health, 62. Sedgwick founded a program in public health at MIT in 1883 and then developed the first joint program for training public health officials at Harvard in 1912. 28. Frost, Snow on Cholera. 29. In the 1960s Milton Terris, professor of preventive medicine at New York Medical College, developed a set of epidemiological exercises based on historical readings that were widely used in programs in epidemiology, public health, and medicine. The exercise based on MCC2, initially drafted by Clark and Gelman, revised by Terris, covered both the south London study and the Broad Street investigation; E. Clark and Gelman, “Epidemiology exercise: Snow on cholera.” 30. Sedgwick, Principles of Sanitary Science, ix. For more on the Voronoi concept and its formulation, see Okabe et al., Spatial Tessellations, 6–12. 31. Gilbert, “Pioneer maps of health and disease in England.” See also Rosenberg, Explaining Epidemics, 119. 32. National Geographic Society, “Fighting cholera with maps,” in TC Tool Kit. 33. Geographic information systems are “automated systems for the capture, storage, retrieval, analysis, and display of spatial data”; Clarke, Analytical and Computer Cartography, 11. GIS can be thought of as software that is used to organize and manage georeferenced data and then to display this information on areawide maps. GIS therefore comprises two closely integrated databases, one statistical, the other geographical. The latter contains coordinate data


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usually obtained from maps, fieldwork, and/or from airborne or satellite remote-sensing imagery. The data can be in the form of points (such as cholera deaths, houses, clinics), lines (roads, rivers), and polygons (residential suburbs, health districts). The attribute database contains data about the characteristics of the geographical features, such as demographic data on age and sex distribution, socioeconomic profiles, immunization coverage, and type of road access; see Maguire, “An overview and definition of GIS,” 9–20; Richards et al., “Geographic information systems and public health: Mapping the future”; Clarke et al., “On epidemiology and geographic information systems: A review and discussion of future directions”; and Loslier, “Geographical information systems (GIS) from a health perspective.” In 1995 GIS was identified as one of the top-ten most notable new developments in epidemiology; Waller, “Epidemiologic uses of geographic information systems (GIS)”; and Naphtali, “GIS in healthcare: When geography matters.” 34. S. Sachs, “Families are gathering clout in study of cancer clusters,” Dallas Morning News (27 September 1998); R. Perez-Pena, “Critics question overdue plan to track cancer and pollution,” New York Times (18 January 1998). 35. Snow’s Broad Street map has been called “one of the first uses of a rudimentary GIS . . .”; P. Forster, “Come the next pandemic . . . will we be prepared?” The Daily Telegraph (25 March 1999). Currently, the Broad Street pump incident features prominently in training exercises and programs for GIS; see, for instance, an internet exercise: http://www.esri.com/news/arcuser/0499/umbrella.html (accessed January 2001). 36. Richardson, L, xxi.

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Index Abbey-row, 350 Abstinence pledge, 47, 53n43 Acetone, 164n40 Ackerknecht, Erwin H., 193nn59–60 Acomb, 17, 18f Addison, Thomas, 244 Addison, William, 86, 107n66 Ague, 9, 167, 248, 396 Albion Terrace, 208–10, 208f, 209f, 212–13, 225n22, 226n31, 257–58 Albumin, 85–86 Alcohol (C2H5OH) chloroform, ether and, 157–58, 164n40 narcotism and, 158–59 physiological action of, 157–58 Aldersgate Street School, 64, 100–01, 146, 165, 185, 238 Alison, William, 3, 12n5, 351, 353–54, 358n52 All Saints North Street baptismal records of, 33n10, 33n12, 34nn14–15 Church of, 14–16, 15f , 21–23 Parish of, 17–18, 22–23, 33n4 Alum, 353, 358n50 American Public Health Association, 392 Ampthill Square, 251n11 Amyl alcohol (C5H12O), 366 Amylene (C5H10), 365–70, 370n12 deaths from, 369–70, 371n25 in midwifery, 368 “Anasarca Which Follows Scarlatina,” 104n30 Anatomy Act of 1832, 30, 37n54, 77n17 Andrew, John, Jr., 47–48, 54n45 Anesthesia. See Ether; Chloroform Anglesey, Lord, 233–34 Angus, Alexander, 82 Animal(s) chemistry, 375–76 experiments on, 1, 3–5, 71–72, 90, 94, 98, 123–24, 126–27, 137n56, 141, 146, 148–50, 150t, 151, 161, 366, 391 Animal Chemistry (Liebig), 157, 375 Animalculae, 176, 290 Anticontagionists. See also Miasma maps and, 320, 337n2

and quarantine, 191n38, 192n44, 212, 226n30 theories of, 167, 172–75, 175f, 178t, 192n44, 210, 223n8, 274, 378–79 Antivitalism, 5 Apothecaries, 4, 24–28 Act of 1815, 25, 77n13 Hall (AH), 58t, 60f hospital, 68 Licentiates of the Society of (LSA), 28, 68 pre-1815 medical men, 36n44 surgeon-apothecaries, 4, 6, 28 (Worshipful) Society of, 24–25, 56–59, 58t, 77n14 Archbishop Holgate’s Grammar School, 34n21 Arnott, Neal, 341, 356n18 Ash & Sons (manufacturer of dentists’ materials), 297 Ashley, Lord, 238 Askham, Mary, 17–18, 33n6 Askham Bryan, 18f Askham-Empson genealogy, 19f Askham-Snow genealogy, 20f Asphyxia, 1–3 causes of, 93–94, 123 definition of, 94 in infants, 2–4, 90–95 oxidation theory, 160–62 Snow’s research on, 2–4, 12n7, 93–98 Association Medical Journal (AMJ), 243–44, 351 Association of Anaesthetists of Great Britain and Ireland, 392, 393f Asthenia, 45 Astrakhan, 169 Atkinson, Anne, 130 Attree, William Hooper, 363 Aubing, 328 Autoexperiments, 124, 141, 159–60, 164n43, 178, 193n60, 201, 211, 232, 251n3 Babington, Benjamin Guy, 239, 252n19, 341 Bacon, Francis, 74–75, 260 Baldwin, Peter, 172,192n44 Bancroft, Edward N., 13n29

421

422 Barber-surgeons, 24–28, 26t Barker, Thomas Jones, 251n11 Barrett, Frank, 338n27 Bateman’s Buildings, 75, 77n12 Bath, 56 Battersea, 210, 244, 264 Bavaria, 328 Bayle, Gaspard L., 79n57 Bazalgette, Joseph, 342 Beauchamp, Mrs. Proctor, 253n29 Bell, G.H., 170, 187–88, 189n17, 190n18, 191n41 Bell, Jacob, 118, 142, 163n3, 226n25, 227n39 Bennet, William, 233 Bentham, Jeremy, 171–72, 190n26 Benthamite, 171–72, 174, 181 Benzin (benzene, C6H6), 151–52 Bermondsey, 249 Bernard, Claude, 105n45, 132, 391–92 Berners Street, 283, 318 Berwick Street, 285 Berzelius, J.J., 384n10 Bibliocholera, 189n4 Bichat, Marie Francois Xavier, 3, 12nn5–6, 79n55, 93 Bigelow, Henry, 134n1 Bigelow, Jacob, 134n1 Binghamton, 369 Biopsychosocial model, 229n46, 386n28 Bird, Golding, 71–72, 79n47, 86, 90, 105n34, 107n66, 109n87 Birmingham, 349 Bisulphuret of carbon (carbon disulphide, CS2), 151–52 Blackall, John, 104n30 Blackfriars, 245 Blenkinsopp, 203 Blisters, 43–44, 51n16, 52nn18–19 Blood-letting, 86, 188 Blue Coat Charity School, 22, 34n21 Board of Governors and Directors of the Poor, 292–93, 296 pump handle removal by, 294–95, 313n31, 313n37, 331 Snow’s meeting with, 294, 313n31 Board of Health. See Central Board of Health; General Board of Health Boards of Guardians, 171 Boden theory, 328 Böhm, Ludvik, 181, 185 Bonaparte, Napoleon, 79n57 Bootham School (Friends’), 35n24 Bootham Ward, 32n2 Boott, Francis, 110 Borough Road, 155, 276 Boston, 110

Index Botany, 63 Brande, William, 144–45 Bread, rickets and, 353, 358n50 Breath Breathalyzer, 158 detection experiments for, 158–60 Brentford, 255 Brera, V.L., 206 Bridge Street, 245, 288 Bright, John, 66 Bright, Richard, 85–86, 98 Brighton, 298 Bristol, 215, 231, 400n2 Bristol Microscopical Society, 227n38 British Anesthesia, 391 British Association in Glasgow, 384n6 British and Foreign Medical Review, 104n29, 138nn66–67 British Medical Association, 349–50, 357nn33–34, 401n18a British Medical Journal, 350, 390–91 Brittan, Frederick, 216–17, 227n39, 231, 375 Broad Street, 284f, 293f, 297, 309f, 311n3, 314n44. See also Golden Square Benjamin Hall on, 290, 309 40 Broad Street, 283–84, 290, 293f, 294–96, 306, 307f, 307, 309f, 310, 311n4, 314n40, 336f, 394 General Board of Health (GBH) and, 308f, 309–10, 337f, 346 Grand Junction Water Company and, 288 New River Water Company and, 288, 298 pump handle myths about, 397, 315n54, 320, 402n23a Snow’s maps of, 302–03, 309f, 316n75, 320, 331–37, 332f, 333f, 334–35, 336f water pump at, 284–85, 289f, 290, 294, 301–03, 310, 313n31, 316n78, 336f, 339n34, 397, 401n19, 402n23a Brodie, Benjamin C., 70, 93–94, 128, 229n49, 244, 383 Bromoform (HCBr3), 142, 151–53 Brompton, 234 Cemetery, 400n10a Broussais, J.V., 216, 196n82 Brown, John (Brunonian system), 45, 49, 85, 188 Brown, P.E., 223n9, 224n12, 228n43 Bryson, Alexander, 239, 246 Buchanan, Andrew, 148 Buckingham Palace, 242, 369 Budd, George, 389, 400n2 Budd, William, 192n46, 216, 228n42, 341, 354, 396, 400n2 effluvial transmission of cholera, 216, 316n72

Index fungus theory of, 215–19, 217f, 228n42 parasites and, 227n36 Snow’s hypothesis and, 218, 349, 351, 355n5, 375 typhoid fever and, 216, 227n35 as village epidemiologist, 226n24 Burling Slip, 321 Burne, John, 66 Burnop Field, 42–45, 51n15 Burnopfield Colliery, 43 Burnopfield Hall, 42 Busk, George, 216 Cabanis, Pierre, 79n55 Cairo, 196n87 Camberwell, 233 Cambridge Street, 283–85 Cambridge University, 76, 77n13, 99, 237 Campbell, Lord, 156–57, 235 Campleshon, 22 Canterbury, Archbishop of, 243 Cantharides, 51n16 Carbonic acid gas, 88, 90 Cardiopulmonary resuscitation (CPR), 1–2 Carlisle, Anthony, Sir, 66 Cartography, medical, 321–23, 397. See also Maps Case Books (CB) (Snow), 43, 78n27, 83, 252n28, 270, 360, 363. See also Snow, John Caspian Sea, 169 Census of 1841, 81 of 1851, 310n1 Centers for Disease Control, 392 Central Board of Health, 42 Chadwick, Edwin, 171–72, 175, 255–56, 290, 294, 342, 354n1, 355n9, 383, 387n33 Chambers, W.F., 190n19, 190n23 Charing Cross Hospital, 99, 108n78, 362 Chartist Movement, 170 Chelsea Water Company, 247, 273, 277n4, 281n33 Chemistry, 64t, 97, 223n8 Chester Street, Belgravia, 40 Children. See also Infants chloroform and, 363–64 rickets and, 352–53 Chloric ether, 142 Chloroform, 4–5, 109n85, 133, 140, 143, 236, 366 alcohol, ether and, 157–58, 164n40 chemical properties of, 142 children and, 363–64 as cholera treatment, 165–66, 188n1, 250 criminal use of, 155–57, 235–36

423 deaths while under, 145–47, 165, 364–65, 368, 370n4, 400n5 early experiments with, 150t Hannah Greener and, 143–47 inhalers, 154, 154f modus operandi of, 157–60 as new letheon agent, 141 in midwifery, 8, 240–44 ON experiments with, 149–50, 150t, 153 pharmacology of, 141–43, 153 physiological effects of, 153–55, 234 quantity of, 141t respiration and, 148–49 Simpson and, 142, 240–41 Snow on, 141–43, 141t, 146–47, 153–55, 360–62, 400n5 various responses to, 361–62 Chlorophobia, 155–57, 235–36 Choler, 189n16 Cholera Albion Terrace outbreak of, 208–10, 208f, 209f, 212–13, 225n22, 226n31 anticontagionist theory of, 167, 172–75, 175f, 176f , 178t, 192n44 Asiatic, 41–42, 169, 173, 178–79, 190nn18–19 asphyxia, 200, 223n5, 250 atmosphere and, 191n32, 191n38 biblio, 189n4 Broad Street/Golden Square outbreak of 1854, 8, 283–310, 293f, 309f, 310, 328–37, 394, 402n23a, 403n35 chloroform and, 165–66, 188n1, 200, 386nn23–24 CMC and, 374–75 contagionist theory of, 166, 175–77, 176f, 178t contingent contagionist theory of, 167 deaths from, 191n42, 207, 209, 269–77, 276t, 308f at Edinburgh, 169, 174 English, 168, 195n76 epidemic of 1831–1832, 7, 33n4, 48, 70, 166, 169–70, 176, 178, 185, 187, 194n71, 196n86, 198n104, 201, 215, 248, 321–23 epidemic of 1848–1849, 7, 11, 166, 171, 175, 187, 199–200, 206–10, 215, 229n50, 248, 256, 260, 288, 319f , 320 epidemic of 1853–1854, 7, 166, 175, 187, 259–77, 263f, 276t epidemic of 1866 and, 12, 316n78, 394 etymology of, 190n18 excessive drinking and, 211 fomites and, 166 fungus theory and, 215–19, 217f, 227n39, 228n40, 231–33

424 Cholera (continued) Garrod on, 185, 205, 224nn14–15, 232, 244 Horsleydown outbreak of, 207, 213 immorality and, 174 influenza and, 173, 232, 379–80 mapping, 318–39. See also Cartography; Maps; Snow, John morbus, 169t, 189n16, 323 mortality rates for, 189n17 in Newcastle, 169, 248, 273, 277n7 in North Street, 45 oxidation and, 377–78 pathology of, 40, 185–88 and population size, 215 prevention of, 203, 211–12, 248–49, 296 published works on, 166 saline treatments for, 186–87, 198n102, 198n104, 224n15, 250 Snow’s theory of, 148, 202–10, 203f, 224n13, 226nn28–29 Snow’s treatments for, 200, 249–51 spasmodic, 168f, 169, 189n13, 322f stages of, 168, 185, 186, 386n24 stomach acid and, 211 symptoms, 168, 186 terminology, 168, 169t transmission of, 175–77, 176f, 192n54, 193n60, 201, 204–05, 379–80 treatments for, 166, 185–88, 197nn94–95, 197n97, 199–200 vibrio cholerae, 303, 193n60, 228n40 water treatment for, 186–87 “Cholera and the London Water Supply” (Farr), 259 Cholera Inquiry Committee (CIC), 301–10. See also Snow, John; Whitehead, Henry Chorlton-Upon-Medlock district, 327 Chowne, William D., 93 Christchurch, 272, 275, 347 Church of England (National Society), 22–23, 34n21 Churchill, John (publisher), 137n64, 281n35, 302–03 “Circulation in the Capillary Blood-Vessels,” 97, 107nn69–70 Clapham, 6, 270, 280n29, 281n39a Clark, E. Gurney, 402n29 Clark, James, 242, 252n27, 341, 361, 363 Clark, William Stephenson, 24, 36n36 Clarke, Mansfield, 70 Clover, Joseph Thomas, 135n13, 370, 391, 400n6 Clutterbuck, Henry, 108n84, 165–66, 188n1, 238 College of Physicians, 25, 26t. See also Royal College of Physicians

Index Combustion, 377, 385n13 Commissioners Inquiring into the State of Large Towns and Populous Districts, 33n4, 171, 340. See also Health of Towns Committee on Scientific Inquiries. See General Board of Health Company of Grocers, 26t “Condition of Surrey Court, Horsleydown,” 207–08 Contagionists, 166 theories of, 166–67, 175–77, 176f, 178t, 201, 223n9 Contingent contagionists, 181, 194n63, 210 GBH and, 180, 194n63 Johnson’s theory and, 178–79, 180f sanitary reforms and, 179–80 theory comparisons and, 176t Continuous molecular changes. See On Continuous Molecular Changes; Snow, John Cooper, Astley, 65, 68, 106n57 Cooper, Edmund, 295, 300, 314n52, 315nn53–54, 328–31, 330f , 336, 399 Copland, James, 177, 223n5, 232–33 Corbyn, Frederick, 195n74 Cornwall, 353 Corvisart, Jean N., 79n57 Court of Queen’s Bench, 156 Cow yards, 284, 311n5 Cowdell, Charles, 196n82, 198n104 Cowen, William, 130 Cowpox, 341, 382 Cronstadt, 278n15 Cullen, William, 44–49, 52nn25–26, 54n50, 85, 107n70, 136n30, 188, 194n69, 232 Curling, T.B., 225n19 Cutler, William, 138n71 Dalton, John, 116, 136n30 Danish, 15 Darwin, Charles, 80n58, 193n60 Darwin, Erasmus, 193n60 Davey Smith, George, 280n26b, 281n39a David Copperfield, 140 Davidson, Dr., 96 Davies, David, 145 Davison, Robert, 213 Davy, Humphrey, 367 de Martine, Collard, 90 de Martingny, Collard, 12n5 “Death from Chloroform in a Case of Fatty Degeneration of the Heart,” 365 Demarquay, Jean Nicholas, 151 Dentistry, 6–7, 110, 129–30 Diamond, Hugh W., 82 Diapnetics, 97, 113

Index Dictionary of Practical Medicine (Copland), 232 Dilettanti, 372 Dilution, 150 Disease mapping. See Maps Diseases classification of, 79n56 febrile, 11, 44, 173, 188, 200 mental, 98 Distillation of water, 40 Diuretics, 97 Dodsworth, John, 23 Dodsworth Schools, 23, 35n25, 36n28 Donovan, Catherine, 155 Dorking, 389 Dosimetric technique, 138n81 Dropsy, 104n30 Drummond, J.L., 225n19 Dulwich, 262 Dumeril, Auguste, 151 Dumfries, 257 Duncum, Barbara M., 135n21 Dunglison, Robley, 190n18 Durham, 28, 41–42 Dutch liquid (1,2-dichloroethane C2H4Cl2), 151–53, 400n5 Dysentery, 173, 379 Easson, Kay, 38n57 East India Company, 168 East London Water Company, 209, 255, 393 Edgware Road, 292 Edinburgh, 5–6, 30, 140, 169, 174, 367 Edinburgh Medical Journal, 351 Edwards, William Frédéric, 3, 12n5 Effluvia, 9–10, 173–74, 177, 216, 223n8, 232, 313n39. See also Miasma; Anticontagionists; Contingent Contagionists Elementary schooling in England, 22, 34nn20–21, 35nn22–23, 35n25 Eley, Susannah (the Hampstead widow), 285–87, 297–98, 315n62, 333 niece of, 297–98 servant of, 298 sons of, 285, 290 Eley’s Percussion Cap Factory, 285, 287, 297, 311n7 Ellis, Richard, 35n23 Embleton, Dennis, 213 Emigrant Refuge Hospital, 190n19 Emmet, Thomas Addis, 190n19 Empson, Charles, 24, 31–32, 32f, 38nn59–60, 51n14, 56, 251n11 Empson, John, 17–18, 33n6, 34n13 Empson-Askham genealogy, 19f

425 Engel, George, 229n46 English Poor Law of 1601, 42, 52n20 Enlightenment, 74, 88 Entozoa, 224n17, 225n19, 227n36, 379. See also Worms Epidemic constitution, theory of, 44, 167 Epidemic curve, 222 Epidemiological Society of London, 229n50, 238–40, 246–48, 302, 316n73, 318–20, 332, 337nn3–4, 341–42, 346–48, 356n22, 401n15, 402n23a Epidemiologist, village, 208, 212–13, 226n24 Epidemiology, 6 clinical, 138n68 shoe-leather, 266, 285–310 Epps, John, 61, 63, 70, 76n10, 78n41 Epsom, 389 Erysipelas, 44–45, 379 Ether, 110–39 administration of, 113, 131, 134n11, 138n81 alcohol, chloroform and, 157–59, 164n40 as anesthesia, 110, 134n2, 366 animals and, 124, 126–27, 137n56, 150–51 cerebral functions and, 124 chloric, 142 inhalers, 112–14, 117–22, 119f, 120f, 121f, 131, 136n39, 137n54 midwifery and, 135n17 modus operandi of, 157–60 respiration and, 113, 148–49 sponge, 131, 138n81 sulphuric, 143 vicissitudes of, 131–34 volatility of, 116 Etherization four degrees (stages) of, 124–27, 135n13, 363–64 Ethyl bromide (C2H5Br), 151–53 Ethylene (C2H4), 366 Evans, Major, 364–65, 390–91 Everett, Edward, 134n1 Everitt, David, 71, 79n45 Eyler, John M., 355n5, 401n19a Exeter, 187, 215, 258, 323, 324f, 339n29 Farley, John, 206, 225n18 Farr, William, 181–85, 182f, 191n42, 196n82, 265, 291, 383 contingent contagionist theory of, 183f on crucial experiments, 259–60 elevation theory of, 184f , 259–60, 274, 278n18, 327 and Henle, 195n79 on Snow’s theory, 259–60, 278n18, 394, 401n19

426 Farr, William (continued) theories of, 356n18 water supply inquiry of 1854 and, 261f, 262, 267, 270, 273, 279n23, 282n41, 285, 348 on zymotic diseases, 181–85, 195nn78–79, 259–60, 278n18, 354, 383n4, 385n19, 394 Farrell, Mr., 301 Farringdon Street, 288 Febrile diseases, 44, 52n26, 173, 200 Ferguson, Daniel, 118, 121, 128 Fergusson, William, 138n71, 242, 359, 368–69, 388 Fermentation, 374–76, 384n9a Fevers, 44–45, 52n26 Fife, George, 30 Fife, John, 30, 144 Finn, M.W., 402n20 First Reform Bill of 1831–1832, 5, 45 First Report of the Metropolitan Sanitary Commission, 280n32 Flourens, Pierre Jean-Marie, 126–27, 132, 161, 165, 400n10 Flourens’s theory, 147 Fog Close House, 46 Fox, W.D., 80n58 Fracastorius, 176, 192nn49–50 Fraser, Alexander, 30 Fraser, David, 294–95, 297–301, 334–35, 346, 394 Frazer, William M., 354n3 French, John G., 251n6, 310 Frerichs, Ralph R., 225nn21–22 Friendly Societies, 82 Frith Street, 75, 81–82, 102n2, 234, 251n8 Frost, Wade Hampton, 395 Galbraith, N. Spence, 33n6, 33n10, 51nn14–15, 76n1 Garrod, Alfred Baring, 100–01, 185, 205, 224nn14–15, 232, 244, 250 Gateshead, 41, 248 Gay-Lussac, Joseph-Louis, 116 Gazetta Medica Italiana Toscana, 303 Gelman, Anna, 402n29 Genealogy Askham-Empson, 19f Askham-Snow, 20f General Board of Health (GBH), 166, 171, 175, 192n46, 244, 268, 279n25, 280n31, 312n24 anticontagionism of, 294–95, 384n7a Broad Street/Golden Square outbreak of 1854 and, 289–91, 301, 308f , 309–10, 310n1, 312n17, 314n40, 315n53, 316n75, 337f

Index Committee on Scientific Inquiries of (CSI), 294–95, 297–305, 309, 311n5, 313n35, 314n48, 314n52, 334, 316n76, 356n18, 394 contingent contagionism and, 180, 194n63 disagreements with Snow, 346, 349 precautions against cholera by, 296, 298 Snow’s critique of, 275–77, 345–47 General practitioners (GP), 6, 80n64, 82–83, 103n12 General Register Office (GRO), 171, 181, 259, 265, 270, 291–92, 319f, 327, 331. See also Farr, William; Registrar-General; Weekly Returns of Births and Deaths in London Geographic Information Systems (GIS), 397–99, 402n33, 403n35 George Street, 238 Germ theory, 11, 196n82 Gilbert, E.W., 396–97 Gilbert, Pamela, 312n17, 312n26 Glasgow, 244, 257, 352 Gloucester Road, 251n11 Glover, Robert M., 142–44, 389 Golden Square, 8, 82, 277, 283–85, 287–88, 292, 297, 330f . See also Broad Street disease mapping of, 300, 302, 309, 328–37, 332f, 333f, 336f Goodeve, Professor, 87 Goodman, John, 87 Gould, John, 291 Gotfredsen, Edvard, 135n14, 138n65, 138n67 Graham, Thomas, 385n18 Grainger, Richard D., 318, 319f, 337n2, 338n18 Grand Allies, 41 Grand experiment, 264–67. See also Natural experiments; Snow, John, experimenta crucis of and grand experiment of Grand Junction Water Company, 255, 288, 298 Grant, John, 207–08, 225nn21–22, 226n31, 247, 257 Grant, Robert, 77n14 Great Exhibition of 1851, 156 Great Stink, 354, 358n54 Greek Street, 297 Greener, Hannah, 143–47, 155 Greenhow, Thomas Michael, 30, 41, 37n56, 50n8, 191n38, 198n108, 198n110 Greenwich, 254 Grocers’ Company, 25 Gurthrie, George, 66 Guy’s Hospital Medical School, 60f, 71, 159 Guyton-Morveau, L.B., 195n79 Hackney, 345 Hague, Howard, 108n78

Index Hall, Benjamin, 9–10, 13n29, 290, 294, 309, 312n23 Hall, Marshall, 145, 383 Hamburg, 395 Hamlin, Christopher, 80n63, 224n10, 228n44, 278n19, 353–54, 354n2, 355n5, 355n9, 356n22, 358n54 Hampstead, 285, 287 Water Company, 254 Hampstead widow. See Eley, Susannah Hampton, 351 Hanover Square, 6, 238, 292 Hardcastle, William, 24–31, 38n60, 42, 67, 75, 104n28 Harnold, John, 203 Hartley, David, 386n27 Harvard University, 402n27 Harvean Prize Essay, 142 Hassall, Arthur Hill, 195n72, 247, 281n33, 290, 303, 341, 358n50, 384n7a Hatton, John, 327–28 Haughton’s School, 34n21 Hawkins, Caesar, 128, 138n71, 364 Health of Towns Bill, 191n28 Report, 318, 337n4 Henle, Jacob, 195n79, 204 Henry VIII, King, 25 Herefordshire, 364 Herschel, John, 74–75, 78n38, 80n58, 222 Higgins, Margaret, 155 Hill, James, 188n1 Hird, Francis, 199–200 History of Anaesthesia Society, 392 Hoffman, August, 384n6 Holland, Henry, 134n1 Holmes, Oliver Wendell, 135n25 Hooke, Robert, 136n30 Hooping-cough, 379 Hôpital Necker, 79n57 Horsleydown, 207–10, 213, 257 Hospital for Clinical Midwifery, 63 Hospital for Consumption and Diseases of the Chest, 234 Household Words, 140 Huggins, Edward, 298 Huggins, John, 298 Hughes, Thomas, 294–95, 299–301, 334–35, 346, 394 Hull, 30, 215, 258 Humber estuary, 14, 258, 273 Humidifier, 119, 136n36, 136n42 Humors, 51n17, 172, 321 Hungerford, 279n24 Hunter, John, 73–74, 94

427 Hunter, William, 73–74 Hunterian School of Medicine, 4–6, 60f, 61–64, 69, 73–74, 79n54, 84, 99, 100 Theatre of Anatomy (Lower Windmill School), 60f, 63 Huntington, 18 Hutchinson, Mr., 245, 288 Hyde Park, 94 Hydrocyanic acid, 152 Hypothetico-deductive reasoning, 75, 229n49, 396 Ideologues, 74, 79n55 Illustrated London News, 112 Indentures, 28–30, 36n35 Index case, 303, 316n73, 327, 335, 350, 401n19 India, 167–69, 189n12 cholera in, 167, 170, 178, 201 physicians in, 191n41, 193n59, 196n89 Industrial Revolution, 15, 32n2 Infants artificial respirator and, 2–3 asphyxiation and, 2–4, 90–95 Influenza, 44, 177, 199, 232, 379–80 cholera and, 173, 379–80 Snow on, 173, 229n47, 379–80 Inhalers amylene, 367, 370n12 chloroform, 154, 154f, 243, 253n29 ether, 5, 117–22, 119f, 120f, 121f, 135n21 Inoculations, 177 Inquiry into the Sanitary Condition of the Labouring Population of Great Britain (Chadwick), 171, 340, 342, 354 Iodoform, 142 Jackson, James, 323 Jackson, Robert, 193n60 Jackson, Samuel, 189n14, 198n104 Jacob’s Island, 347 James I, King, 25 James, James H., 195n74 Jeffreys, Julius, 118–19, 136n36, 136n42 Jenkins, Edward, 394, 402n20 Jenner, Edward, 238, 382 Jewell, Dr., 63, 77n14, 84 Jewett, Frederick Hardy, 155 J.L. Curtis and Co., surgeons, 82 John Snow College, 401n11 John Snow, Inc., 392 Johns Hopkins School of Hygiene and Public Health, 395 Johnson, George, 186–87, 198n104, 198n109 Johnson, Henry C., 138n71

428 Johnson, James, 178–79, 190n20, 383 Jones, G., 65 Jones, Harry, 311n13 Jones, N. Howard, 197n96 Jopling, Charles, 155 Journal de Chemie Medicale, 159 Journal of Public Health and Sanitary Review (JPH&SR), 239, 275, 348 Kay-Shuttleworth, James Phillips, 170–71, 351 Kennington, 266–67, 266t, 280n30 Kent Water Company, 254 Killingworth, 31, 41–42, 166, 169 King, Dr., 304 King’s College Hospital, 59, 60f, 186, 388 King’s Ling, 280n27 Kircher, Athanasius, 176 Knight, Henry, 7–8 Knott, Samuel, 30 Koch, Robert, 195n79, 228n40, 316n66 Kouwenhoven, William, 1 Laboratory Investigation Division (Privy Council), 103n13 Laennec, René T.H., 79n57 Lamarckian evolutionary biology, 5 Lambe, William, 39 Lambeth Church, 275 Lambeth Palace, 243 Lambeth Water Company, 247, 254, 260, 348, 351 districts supplied by, 262–64 Snow’s subdistricts’ investigation and, 262–73, 266t, 278nn16a-17, 348, 357n32 Lancet, 10–11, 13n29, 166, 169, 344–45, 356n20, 394 on anesthesia and midwifery, 243, 253n35 on arsenical candles, 72 on bedside medicine, 197n94 on chloroform, 140, 144–45 on ether, 118, 128, 131 on the hospital apothecary, 68–69 on hospital medicine, 66–67, 78n27 on medical schools, 61 medical schools, requirement listings of, 57, 58t Petermann’s cholera map and, 327 Shapter’s map and, 338n17 on Snow’s legacy, 389–90, 394, 401n18a Snow’s Parliamentary testimony and, 10–11, 355n11 on treatments for cholera, 186, 197n94 on zymotic theory of diseases, 195n78 Lane, John Hunter, 63, 69, 77n13

Index Lankester, Edwin, 79n57, 180n72, 195n72, 216, 227n39, 233, 311n5, 315n60, 316n72, 316n78, 349 on Cholera Inquiry Committee (CIC), 301–03, 307–10 Laryngoscope, 252n19 Lassaigne, Jean-Louis, 148 Latour, Charles Cagniard, 384n9a Latta, Thomas, 187, 198n102 Laudanum, 156 Lavoisier, Antoine Laurent, 2, 105n42 Laycock, Thomas, 33n5 Laycock, William, 48 Layerthorpe, 48 Lawrence, Christopher, 387n33 Leather Market, 275 “Lectures on the Entozoa or Internal Parasites of the Human Body,” 225n19 Lee, Henry, 250 Leeds, 248, 401n15 General Infirmary, 53n35 Leopold, Prince, 8, 242 Letheon. See Ether Letter to the Right Honorable Sir Benjamin Hall, 13n29 Lettsom, John, 84–85 Levy, A. Goodman, 391 Lewis, Sarah, 295, 305, 310n1, 314n40 daughter of (Lewis infant), 283–87, 307, 314n40 Lewis, Thomas, 284, 294, 296, 310n1 Licentiates of the Royal College of Physicians (LRCP), 237 Licentiates of the Society of Apothecaries (LSA), 28, 54n44, 58t, 59, 68, 76n3 Liebig, Justus, 157–58, 181–85, 223n9, 229n48, 249, 373–74 on continuous molecular action, 375, 383n5 Lincoln College, 286 Lincoln’s Inn Fields, 68 Lind, James, 193n60 Lindsay, W. Lauder, 174, 186–88 Linnaean tradition, 107n70 Lion Brewery, 298–99 Liquor ammoniae, 200 Liston, Robert, 65, 110–11, 128–30, 134n3, 134n7, 135n13, 138n71, 383 Literacy, 33n9 Lithotripsy (lithotrity), 6–7, 364 Liverpool, 56 Liverpool-Manchester Railway, 31 Lloyd, Dr., 247 Lloyd, Mr., 144 Local Government Board, 394–95, 401n15, 402n23a

Index Locock, Charles, 242–43, 252n27, 401n11 Loimometer, 194n63 London, 14, 25 Bridge, 155 Fever Hospital, 173, 358n52 Hospital, 46 medical schools in, 59–63, 60f, 62t, 100–01 sewage disposal in, 255–56 Snow’s comparative mortality analysis of, 7, 271–73, 281n39a water quality in, 255–56 London Corporation of Surgeons. See Royal College of Surgeons London Epidemiological Society. See Epidemiological Society of London London Medical and Surgical Journal, 76n10, 77n13 London Medical Directory, 105n36 London Medical Gazette (LMG), 68, 72–73, 87–89, 140, 191n28 amalgation with MT, 148, 350, 387n31 on ether, 111–12, 133, 134n11, 135n17 Snow and, 139n91, 233, 390 Longet, François-Achille, 126, 138n66 Lonsdale, Miss, 110 Loughborough Dispensary, 145 Louis, Pierre, 74, 79n57, 220t, 227n35 Lucas, P. Bennet, 63, 77n13 Lucretius, 194n70 Ludlow, J.M., 294–95, 299–301, 334–35, 346, 394 Ludwig, Karl, 105n45 Lumleian Lectures, 149–50 Lying-in Hospital, 4 Lyon, B., 66 Maddox Street, 368 Magendie, François, 12n5, 86–88, 105n42, 105n45, 196n82, 373, 400n10 Magnus, Heinrich, 2 Malaria, 9, 167, 248, 396 Manchester, 280n30, 288, 327 Medical Society, 105n38 Map(s) cholera, 50n8, 318–37, 325f–26f Cholera Inquiry Committee and, 316n75, 333f , 337f Committee on Scientific Inquiries/GBH and, 309–10, 316n75, 337f , 399 Cooper and, 300, 316n75, 329, 330f, 334, 339n29, 399 Golden Square disease and, 320, 328–37, 330f, 333f, 336f Grainger/Board of Health’s, 318, 319f, 320 London metropolitan, 225n21, 255f, 318, 319f

429 progress, 322–23, 322f, 326t shaded/cross-hatched, 319f, 324, 325t, 327–28, 337n2, 338n18 Snow and, 302, 309f, 316n75, 318–20, 332f , 339n29, 396–99, 403n35 spot/dot, 302, 320–23, 325t, 328–29, 332 Voronoi network diagram and, 333f Marshall, Peter, 82–84, 98, 104n21, 108n75, 246, 297 Marshall Street, 299–300 Marylebone, 155 Massachusetts General Hospital, 134n1, 138n81, 367 Institute of Technology, 402n27 Medical Society, 323 Materia medica, 58t, 59, 63–64 Mauritius, 233 McClellan, Ely, 402n24 McIntyre, James, 29–30 Measles, 10, 379–80 Medical Act of 1815, 27t Medical assistants, 42, 51n13 Medical corporations (orders), 5, 26t–27t Medical Officers of Health, 171–72 Medical radicals, 5, 70, 77n14, 170, 172 Medical Society of London (MSL), 8, 84–85, 163, 240, 401n18a amalgamation with WMS, 85, 238 chloroform, cholera discussed at, 165–66, 186 Snow and, 238, 249, 372, 383, 387n34 Medical Times (MT), 148, 166, 350, 387n31 Medical Times and Gazette (MTG), 13n29, 148, 248, 273, 297, 303–04, 312n15, 350, 357n29, 368, 387n31 Medicine academic posts in, 98–99 apprentices in, 28–30, 37n49 Bachelor of (MB), 99, 99t collateral sciences of, 74–75, 97, 222, 383 bedside, 44, 97, 113 depersonalization of, 139n82 forensic, 63, 100, 109n85, 146, 159 hospital, 66–69, 73–75, 78n24 Hunterian School of, 5–6, 60f, 61–63 and hypotheticodeductive method, 229n49, 396 as an inductive science, 229n49 laboratory, 113 military, 125, 131–32 Medico-Botanical Society of London, 71 Medico-Chirurgical Review (M-CR), 178 Medico-Chirurgical Society of Edinburgh, 140 Meggison, Thomas, 144–46 Merchants’ Hall, 48 Merriman, Mr., 246

430 Mesmerism, 111, 134n6 Metropolitan Commission of Sewers (MCS), 207, 295, 342, 355n6 Cooper and, 300, 314n52, 328–31 Metropolitan Free Hospital, 77n13 Miasma, 41. See also Anticongationists; Effluvia; Sanitarians; Sanitary reform movement anticontagionists and, 167, 174–75, 210 in contingent contagionist theory, 167, 232 influenza and, 177 local, 167, 173–75, 179, 347, 373 theory of disease, 7–10, 323, 343, 345, 354 Micklegate Stray, 22 Micklegate Street, 14 Micklegate Ward, 14–17, 16f , 22, 32n2 Microscopes, 107n71 Microscopical Society of London, 216 Middlesex Hospital, 60f, 187, 287, 311n14 Midwifery, 58t, 63–64, 135n17, 240–41 Hospital for Clinical, 63 Millbank Prison, 273 Mills, Mary, 129 Milroy, Gavin, 210, 240, 258, 260, 272, 274, 347 Moderation pledge, 47 Monk Ward, 17, 32n2 Monmouth House, 77n12 Moor Street, 241 Morens, David M., 196n86 Morgagni, Giovanni, 79n55 Morton, William Thomas G., 89, 111–13, 131, 134n1, 136n26 Müller, Johannes, 88, 105n45 Mumps, 379 Munich, 395 Murchison, Charles, 389 Murphy, E.W., 142 Naphtha, 366 Napoleonic Wars, 178 Narcotism, 126–27, 126t alcohol and, 158–59 antiseptics and, 377 degrees (stages) of, 159–60, 363–64, 392 Flourens’ theory and, 147 meaning of, 147 modus operandi of, 157–60 process of, 150 Snow’s oxidation-asphyxia theory and, 160–62 ON studies and, 148–60, 150t National Gallery, 124 National Geographic Society, 397 Natural experiments, 207, 260–72, 278n14 Naturphilosophie, 88

Index New Burlington Street, 303 New Jersey, 31 New Poor Law, 171, 294, 303 New River Water Company, 254–55, 288, 298 New Slip, 321 New York City, 190n19 New York Hospital, 321 New York Medical College, 402n29 Newburn, 41, 213 Newcastle, 4, 14, 24, 28–29, 29f , 37n50, 41–42, 213, 196n89, 248, 277n7 Infirmary, 30, 143, 226n27 Literary and Philosophical Society, 31, 38n57 Lying-in Hospital, 4, 24 Medical School at, 30, 37n54 Newton, John Frank, 39–41, 49nn1–3, 50n4, 50n7, 201, 212 Nicolle, Charles, 396 Nidderdale, 46 Nightingale, Florence, 187, 192n43, 198n107, 287, 311n14 Nitric ether (ethyl nitrate, C2H5ONO2), 151–52, 164n28 Noncontagion, 166–67. See also anticontagionists Nooth’s apparatus, 110–11, 134n8 Norfolk, 280n27 North London Hospital, 60f, 65, 77n21 North Sea, 14, 279n24 North Street, 14, 16–21, 23, 33n4, 33n11 Northumberland, 41–42 Norwood, 262 Nottingham General Hospital, 122 Nuisance trades. See Offensive trades Nuisances Removal and Diseases Prevention Act, 343 Nun Ings, 22 Nysten, Pierre Hubert, 12nn5–6 Observations on the Management of the Poor in Scotland, and Its Effect on the Health of Great Towns (Alison), 353–54 Offensive trades, 7–11, 13n29, 255, 284, 343, 356n15 Olefiant gas, 366 On Chloroform (OC) (Snow), 140, 143, 234, 359–60, 365, 370n3, 388–89, 386n23, 400n5 On Continuous Molecular Changes (CMC) (Snow), 163, 227n34, 355n4, 372–83, 395 as concept, 373–75 epidemic diseases and, 372, 378–81 Liebig and, 375–76, 384n6, 384nn9–9a, 385n19

Index oxidation and, 377–78, 385n15, 385nn16–18 as social theory, 381–83, 386nn27–28 vital vs. nonvital, 376–77, 384n12 “On Narcotism by the Inhalation of Vapours” (ON) (Snow) chloroform experiments of, 149–50, 150t installments of, 148–60, 234 On the Alternation of Generations (Steenstrup), 206 “On the Infectious Origin and Propagation of Cholera” (Bryson), 246 On the Inhalation of Ether. See On the Inhalation of the Vapour of Ether in Surgical Operations On the Inhalation of the Vapour of Ether in Surgical Operations (Snow), 114, 126, 128, 133, 140, 391 On the Mode of Communication of Cholera (MCC) (Snow), 6–7, 200–23, 227n33, 257–59, 304, 351 as Snow’s cholera hypothesis, 203f, 205–06, 213, 219, 224n17, 224n14 supporting evidence in, 206–10, 208f, 209f, 222, 225n18 On the Mode of Communication of Cholera, Second Edition (MCC2) (Snow), 259, 262, 263f, 264–65, 273–75, 281n35, 301, 312n15, 312n25, 315n63, 332, 332f, 356n20, 394–95, 400n2, 401n15 contents of, 271t, 277, 277n8, 278n16, 280n31 maps in, 320, 332f “On the Mode of Propagation of Cholera” (Snow), 239, 246 “On the Pathology and Mode of Communication of Cholera” (PMCC) (Snow), 200–01, 212–23, 258–59 presentation at WMS, 212–13, 227n39, 231–33 prevention of cholera in, 211–12 as Snow’s cholera theory, 213, 224n15, 227n33 supporting evidence in, 213–15, 214t, 222–23, 273 Operating theaters, 110–13, 128–29 Opium, 83 Orton, John Gay, 369 O’Shaughnessy, William Brooke, 185, 187, 196n89, 198n104, 224n15, 232 Overy, Caroline, 104n25 Owen, Richard, 341 Oxford University, 76, 77n13, 99, 237 Oxidation anesthesia and, 377–78, 385n14, 385n18 asphyxia theory and, 160–62

431 Pacini, Filippo, 228n40, 303, 316n66 Paget, James, 64, 67–68, 100, 368, 370n16 Pallister, W.A., 47, 54n45 Paracentesis, 95–96, 106n65, 107n66 Parish of Tanfield, 43 Parasites. See Entozoa; Worms Park Road, 347 Parkes, Edmund A., 186, 191n36, 193n60, 194n68, 197n97, 198n104, 224nn14–15, 244, 250, 278n17, 280n26b, 315n62, 339n33 Parkin, John, 227n36 Parliament, 5, 7, 65, 256, 279n25, 290–91, 312n24 first reform (1832), 22, 170 Parsons, Joshua, 63–65, 98, 344, 389 Pathological Society of London, 238 “Pathology and Treatment of Cholera” (Hird), 199 Pelling, Margaret, 224n13, 225n18, 226n24, 228n40, 228n42, 355n5 Pentonville, 298 Perchloride of formyle. See Chloroform Peregrine, Thomas, 200 Pericarditis, 86 Pestgage, 194n63 Petermann, Augustus, 321, 327, 336, 338n10, 338n19 Peters, John C., 402n24 Pharmaceutical Journal, 142, 156, 227n39 Pharmaceutical Society, 118 Pharmacology, 151, 135n20 of chloroform, 141–43, 153 Philadelphia, 189n14, 198n104 Phillips, Richard, 71, 79n46 Philosopical Transactions of the Royal Society (Hunter), 94 Phosphorus, 123, 137n53 Phrenological Society, 76n10 Phrenology, 61 Phthisis. See Tuberculosis Physicians. See Royal College of Physicians. Physiological Society, 238 Physiology (Müller), 88 “Physiology of the Mechanical Action of the Heart” (Goodman), 87 Piccadilly Circus, 234 Pirogoff, Nikolai Ivanovitch, 135n13 Plague, 177, 379 pits, 300, 313n35 Plomley, Francis, 126 Poland Street, 290, 298–99 Workhouse, 251n6, 298, 314n46 Pollock, George, 365 Porter, Roy, 104n25

432 Potter, H.G., 30, 143–44, 389 Preliminary Discourse on the Study of Natural Philosophy, A, 70 Preston Temperance Society, 53n43 Prevention of Offences Act (An Act for the Better Prevention of Offences), 156–57 “Principles on Which the Treatment of Cholera Should Be Based” (Snow), 197n96 Privy Council, 103n13, 394, 401n15 Prout, William, 98 Provincial Medical and Surgical Association, 238, 357n33 Provincial Medical and Surgical Journal (PMSJ), 77n13 Prussic acid. See Hydrocyanic acid Public health, 6, 49 rickets and, 352–53 Snow and, 49, 69–72, 352–54 Public Health Act of 1848, 171–72 of 1859, 82 Puerperal convulsions, 142 Punch (magazine), 112 Purgation, 86 Putney, 268, 270, 276, 280n29, 281n39a Putrefaction, 161, 167, 374, 377 Pyrexia, 44 Pyroxilic spirit, 164n40 Quain, Richard, 138n71 Quarantine, 172, 174, 192n44, 212, 226n30, 381 Quarterly Journal of Microscopical Science, 227n39 Queen Street, 21t, 22, 45 Queen Victoria, 8, 242–44, 252n27, 253n29, 253n35, 361, 368–69, 390 Quetelet, Adolf, 327 Quick, Joseph, 279n24 Radcliffe, John Netten, 393–94, 401n15 Random misclassification principle, 349, 357n32 Rawcliffe, 21t, 22 Read, John, 93–96, 106n57 Reed, John, 213 Reed, Walter, 396 Rees, George Owen, 105n34 Reform Bill of 1832, 170 Regent Circus, 12n4, 93 Regent Street, 300, 312n17, 368 Registrar-General, 244–45, 302–03, 327. See also General Register Office Regnault, M.G., 164n43 Reid, Dr., 253n29

Index Reid, John, 3, 12n5 “Report on the Last Two Cholera-Epidemics of London as Affected by the Consumption of Impure Water” (Simon), 275, 348, 357n28 Report on the Sanitary Condition of the Labouring Population. See Inquiry into the Sanitary Condition of the Labouring Population of Great Britain Respiration, 1, 2 artificial, 12n4, 93–94 chloroform and, 148–49 circulation and, 146–47 combustion, 377, 385n13 ether and, 113, 148–49 Liebig on, 373–74 oxygen and, 162 physiology of, 89–90, 105n42, , 135n23, 137n53, 146 rate, 150, 374 Snow on, 89–96 Return to Nature: A Defence of the Vegetable Regimen (Newton), 39 Rheumatism, 100, 385n19 Richards, Samuel, 130 Richardson, Benjamin Ward, 49n1, 53nn35–36, 83, 99, 104n21, 104n25, 107n72, 112, 240, 349–50, 385n14, 390–91, 395, 397, 399, 400n10a, 401n18a on amylene, 371n25 on chloroform, 143, 151 farthing-candle metaphor, 161, 378 on multiple causation of cholera, 228n42 Richardson, James, 292 River Clyde, 257, 273 Lea, 209–10, 254–56, 255f Nidd, 46 Nith, 257, 273 Ouse, 14–17, 258 Swale, 14 Thames, 7, 155, 207, 254, 255f, 255–57, 273, 277n4, 319f Trent, 273 Tyne, 41, 248, 273, 277n7 Robin, Charles Philippe, 377 Robinson, James, 110–13, 134n2, 134n9 Roe, George, 66 Rogers, William R., 283–85, 287, 307, 316n73 Ross, Ronald, 396 Rotherhithe, 247, 268, 272, 275, 343 Royal Academy of Arts, 124 Royal College of Anaesthetists, 392 Royal College of Chemistry, 384n6 Royal College of Physicians, 6, 25, 26t, 149

Index Royal College of Surgeons of Edinburgh, 77n13 Royal College of Surgeons of London (RCS), 24, 26t-27t , 60f examinations for, 68, 78n33 member of (MCRS), 28 requirements of, 56–59, 58t, 76n3 Royal Humane Society, 3, 94 Royal Lying-in Hospital, 5, 63 Royal Medical and Chirurgical Society (RMCS), 85, 104n26, 116, 134n3, 318, 386n29, 401n11 Snow and, 238, 244 Russell, Rollo 402n23a Ryan, Michael, 63, 77n13, 84 Sackville Street, 6, 234, 235f, 288 Salpetrière, 79n57 Salter, T. Bell, 349 Sanitarians anticontagionist theory of, 172–75, 175f, 192n44, 399 and medical radicals, 172 Milroy and, 258–59 and quarantine, 172, 174, 191n38, 192n44 and sanitationism (Baldwin), 172 Snow and, 271–73, 340–43, 358n46, 387n33 Sanitary reform movement, 7, 17, 167, 170–75, 271–73, 340–43, 354, 396 Sannier, August, 82 Satcher, David, 401n12 Savage, Mr., 65 Scabies, 379 Scarlatina, 199 Scarlet fever, 85–86, 104n30, 379 Schleiden, Matthias, 376, 384n10 Schoolpence, 22, 34n21 Schwann, Theodor, 384n9a Scott, James, 70–71 Scottish medical graduates practicing in England, 77n13 Scurvy, 385n19 Seaman, Valentine, 321, 323 Searle, Lucretia, 81 Searle, William, 81 Sedgwick, William T., 395–97, 402n27 Select Committee on Public Health and on the Nuisances Removal and Diseases Prevention Act, 7–10 Semmelweis, Ignaz, 396 Serpentine, the (Hyde Park), 94 Sewers, 255, 300, 328–31, 342, 355n8. See also Anticontagionists; Effluvia; Miasma; Metropolitan Commission of Sewers Shapter, Thomas, 197n94, 323–24, 324f, 329, 338n16, 339n29

433 Shephard, David A.E., 138n69, 224n13, 227n33, 229n48, 370n6, 385n18 Sibley, Mr., 311n14 Sibson, Francis, 122, 147, 232 Simon, John, Sir, 103n13, 275, 278n14, 341, 401n15 Snow and, 281n38a, 347–50, 357n28, 357n31, 394–95 Simpson, James Young, 112, 140–43, 145, 163n1, 240–41, 367 Skey, James, 100 Slaughterhouses, 284 Smallpox, 177, 179, 181, 341, 379, 382, 385n21 Smith, Elizabeth, 155 Smith, Protheroe, 223n9 Snow, Charles, 45 Snow, Frances (Askham), 17–21, 33nn5–6, 48 Snow, George, 45 Snow, Hannah, 18, 45 Snow, John. See also Animal experiments; Autoexperiments academic posts and, 98–101, 146 on ague, 248 alum in bread, 353, 358n50 on amylene, 365–70, 400n5 amylene inhaler by, 367, 370n12 analgesia and, 139n83, 154–55, 250 as anesthesia specialist, 6, 122–31, 359–70, 385n18 anesthesia legacy of, 389–92 anesthesia practice of, 115t, 128–31, 165, 233–34 antiseptics and, 377 apothecary, qualifies as (LSA), 75, 80n62 apparatus of, 90, 95–96, 138n75, 164n43 apprenticeship of, 23–24, 28–30, 37n48, 51n14 arsenic poisoning while dissecting and, 69–70, 73 arsenical candle investigation of, 70–72 asphyxiation research of, 2–4, 12n7, 93–98, 107n67 birth of, 21 blood solubility studies of, 146–53 on brandy treatment for cholera, 48, 54n51, 223n6 Bristol cholera fungus theory and, 218, 222, 228n43, 229n50, 231–33, 248 Broad Street/Golden Square investigation and, 285–310, 309f, 310, 314n43, 320, 337n5, 402n23a on Budd’s cholera theory, 228n41, 229n45 at Burnop Field, 42–45 calculated mortality during 1854 epidemic and, 275–77, 281n40, 282n42

434 Snow, John (continued) cartographic legacy of, 396–99, 398f Case Books (CB) of, 43, 78n27, 143, 237, 242, 252n28, 270, 314n51, 360, 363 on chemical affinity, 162–63 childhood/education of, 21–23, 35nn23–24, 36n28 on chloroform, 141–43, 141t, 146–47, 153–55, 236, 400n5 chloroform inhaler by, 154f and chlorophobia, 155–57, 235–36 cholera epidemic of 1831–32 and, 41–42, 50n8, 50n11, 201, 215, 226n27, 246 cholera epidemic of 1848–49 and, 199–219, 226n31, 244, 260, 282n41 cholera epidemic of 1853–54 and, 250, 259–77, 263f, 278n15, 347 and Cholera Inquiry Committee (CIC), 301–05, 307–10, 311n14, 312n15, 312n25, 315n60, 315n63, 334t, 335t, 395 cholera prevention and, 211–12, 248–49 cholera theory elaborations of 1849–53, 244–49, 273 cholera theory of, 148, 202–10, 203f, 220t–21t, 221–23, 226nn28–29, 233, 249–50, 341, 383n4 cholera transmission, ecological levels in, 256–57, 257t on cholera treatment, 200, 223n6, 224n15, 249–51, 257 and CMC, 372–83, 384n6 on continuous molecular changes, 249, 385n14, 386n26 dreams during anesthesia, 132–33 dental operations and, 129–30 early publications of, 86–89 epidemic diseases, general theory of, 8, 10, 13n29, 188, 318, 379–81, 385n14 epidemiological legacy of, 392–96, 401n11, 402n23a epidemiological perspective of, 130, 229n50, 265, 277, 281n40, 282n42, 396 Epidemiological Society of London and, 238–40, 246–48, 302, 318–20 ether, controlling dosage of, 114–17 ether inhalers by, 5, 117–22, 119f, 120f, 121f, 137n54, 163n1 ether research of, 112–17, 115t, 117f, 124, 131–34, 136n34, 138n66, 140, 400n5, 400n10 etherisation, degrees (stages) of, 124–27, 126t on exercise, 47 experimenta crucis of, 69–70, 260–65, 267, 271–72, 278n14 fatal illness of, 388–89

Index GBH and, 247, 346–47 as GP, 81–86, 234, 251n6, 251n11, 252n12 grand experiment of, 264–65, 267, 280n26b, 278n14 gravestone of, 393f, 400n10a handkerchief in chloroform administration, 241 on health of, 108n76 home laboratory of, 135n24 on homeopathy, 106n53 hospital apothecary, application for, 68 at Hospital for Consumption and Diseases of the Chest, 234 hypertension, suspected in, 108n77 inhaled gases, chemistry and physics of, 102 and Lancet, 13n29, 87, 138n80 later cholera writings of, 350–52 London medical training of, 56–69, 64t, 65t, 76n2, 100–02 as LRCP, 237–38 maps and, 226n23, 302, 309f , 312n25, 315n54, 316n75, 318–20, 331–33, 332f, 333f, 334t, 335t, 336, 336f, 337n4, 396–99 medical mistakes of, 138n78 Medical Society of London, orator of, 163, 238, 372, 387n34 Medical Society of London, president of, 8, 106n62, 382 metropolitan water supply/cholera thesis of, 256–60 and midwifery, 240–41, 253n31 on Milroy’s explanations, 210–11, 258, 260, 272, 274 on mind-body interdependence, 98 as modified contagionist, 201 as MRCS, 68, 252n12 narcotism and, 134, 147–53, 165 narcotism, degrees of, 126t natural experiments and, 207 at Newcastle medical school, 30 and Newton’s Return to Nature, 49n1, 49n3 and obstetrics, 100, 241–42 OC and, 388–90, 400n5 on occupations, 230n51, 344, 352, 356n15 ON and, 148–60, 150t, 370n3, 400n2 oxidation-asphyxia theory of, 160–62 paracentesis, instrument of, 95–96, 106n65, 107n66 Parliamentary testimony of 1855, 6–11, 13n29, 355n11 at Pateley Bridge, 45–48, 53n34 and the Pathological Society of London, 238 pathophysiology of, 256 pharmacokinetic model of, 142 pharmacodynamics and, 157–58

Index photograph of, 8f Physiological Society, president of 238 PMCC and, 200–01, 212–23, 214t, 227n33, 228n43, 231–33, 246, 273 portrait of, 101f, 124 practice of, 104n19, 104n21, 251n11, 252n12, 252n27 preserving meat, experiments with, 161 professional/social manner of, 83–86 Provincial Medical and Surgical Association and, 238 public health and, 49, 69–72, 352–54, 358n50 published research of, 91t–92t Queen Victoria and, 242–44, 368–69 respiration and, 89–96 residences of, 81–82, 234, 235f, 372 resuscitator invention of, 2–3, 12n4 on rickets, 108n78, 352–54 Royal Medical and Chirurgical Society and, 85, 104n26, 238 Royal Medico-Botanical Society and, 238 sanitarians and, 271–73, 340–54, 358nn45–46, 387n33 Simon and, 275–77, 281n38a, 347–50, 357n28, 357n31, 394–95 on smallpox, 181, 341, 379 and social class, 352–54 south London analysis of, 214, 222, 244, 247, 263f, 265–77, 266t, 276f, 279nn21–24, 279n26a, 281nn39–39a, 233, 336–37 as systems thinker, 219–23, 220t–21t, 229nn46–47, 381, 386n22, 386n28 on temperance and teetotalism, 46–49, 54nn48–49, 54n51, 98, 211, 344, 352 on therapeutic skepticism, 49, 55n52 on toxins, 142 on typhoid fever, 247 as village epidemiologist, 208, 212–13 as vegetarian, 40, 46–49, 83, 98 and Wakley, 87 Westminister Hospital and, 68–69 Westminister Medical Society and, 84–86, 104n24 Whiting and, 268–75 Snow, Mary, 34n15, 35n25, 45, 401n18a Snow, Stephanie, 228n44, 252n28 Snow on Cholera (Frost), 395 Snow, Robert, 35n25, 45, 248 Snow, Sarah, 35n25, 45, 401n18a Snow, Thomas, 34n15, 35n25, 45, 356n22, 401n15, 401n18a Snow, William (John Snow’s father), 18–20, 33n10, 45 occupational history of, 21–22, 21t, 23–24, 76n2

435 Snow, William, (John Snow’s brother), 35n25, 36n28, 45, 48 Snow-Askham genealogy, 20f Society of Apothecaries, 24, 65t, 77n14 Soho Square, 12, 81, 286 Somerset, 65 Somerset House, 259 South London Water Works, 254 Southwark and Vauxhall Water Company (S&V), 260, 262, 348–49, 351–52 districts supplied by, 262–64, 278n17 Snow’s subdistricts’ investigation and, 262–73, 266t, 280nn28–29, 357n32 Southwark Water Works, 244, 272 Smith, Thomas Southwood, 171–75, 175f, 185, 190n26 Spallanzani, Lorenzo, 93 Spasmodic cholera, 168f, 169, 189n13, 322f Spitalfields, 155 Spitta, Dr., 6–7 Spooner, E.O., 170, 179–81, 179n68, 185, 194, 195n72 Spontaneous generation, 206 Squire, Peter, 110, 118 Squire, William, 110 St. Anne’s, Soho, 81, 291 St. Bartholomew’s Hospital, 60f, 64 Medical School, 100–01, 108n84 St. Edmund, 323, 338n16 St. George’s Hospital, 60f, 83, 128–30, 141, 152, 163n1, 164n42, 285, 389 St. Giles, 312n26 St. James Palace, 312n26 St. James, Parish of, 283, 292–94, 312n26, 329 Cholera Inquiry Committee (CIC) and, 301–10, 311n14, 333, 333f, 335–36, 356n20 Paving Board (Commission) of, 301–02, 306 St. James Park, 312n26 St. James Street, 372 St. John’s Church, 28, 42 St. Luke’s Church, 290, 295 St. Mary, Bishophill Junior Church of, 23 Parish of, 21 St. Peter’s Grammar School, 34n21, 35n24 St. Petersburg, 135n13, 278n15 St. Saviour’s, 272 Stafford, 215 Stanhope, 42 Steenstrup, J.J.S., 206, 225n20 Stephenson, George, 31, 38n59 Stephenson, Robert, 31, 38nn59–60 Stewart, Alexander, 394, 402n20 Sthenia, 45 Streatham, 262, 268

436 Sulphuric ether, 143 Sunderland, 169 Surgeons, 5 surgeon-apothecary, 6, 24, 56, 58t Surgeon’s Square Cholera Hospital, 174 Surgery (the premises), 58t Surrey, 351–52 Surrey Court, 207, 257 Sutherland, John, 346–47, 356n22 Swayne, Joseph G., 195n72, 216–17, 227n39, 231–33, 375 Sydenham, 278n16a Sydenham, Thomas, 44, 52n24, 107n70 epidemic constitution, theory of, 167, 172–74, 186, 191n38 Hippocratic regimen, 49, 55n55, 172 Syphilis, 379–80 Tait, William, 354 Taylor, Alfred, 109n85, 159 Teddington Lock, 277n4 Teetotalism, 47–49, 54n42, 83 Temperance, 46–47, 53n36 Terris, Milton, 402n29 Thackery, Harriet, 46 Thames Ditton, 267, 275, 279n21 Thatched House Tavern, 372 Thomson. Robert D., 244–45, 253n37 Thorax, 96 Thorne Thorne, Richard, 402n23a Thrawl Street, 155 Times, 112, 157, 289–90, 295–96, 348–49, 356n22, 389 Todd, James, 363, 389 Tomes, Charles, 138n81 Toynbee, George, 82 Toynbee, Joseph, 82 Toynbee, Joshua, 72 Treatise on Verminous Disease (Brera), 206 Tripe, John W., 345, 356n17 Tuberculosis, 79n57 Tucker, J.H., 238 Turner, Richard, 53n43 Turpentine, 200 Tweedie, Alexander, 354, 358n52 Typhoid fever, 173, 177–79, 216, 227n35, 358n45, 379 Typhus, 10, 227n35, 358n45, 379 United Service Institution, 125, 128, 137n58 University College Hospital, 65–68, 77n21, 224n14 ether use at, 110–11, 128–30, 138n72 University College London, 60f, 77nn13–14, 99, 237

Index University of Durham, 37n54, 37n56, 401n11 University of Edinburgh, 30 University of London, 6, 77n21, 99t. See also University College Hospital Upper Poppleton, 18, 21–22 Ure, Andrew, 116, 136n30 Valentin, Gabriel, 150 Vegetarianism, 39–41, 46–49, 54nn50–51, 83 Venables, Robert, 65, 77n20 Vibrio cholerae, 303, 316n66 Victorian Values, 227n39 Vitalism, 2, 88, 373 von Helmholz, Hermann, 105n45 von Pettenkofer, Max, 328, 395 Voronoi network diagram, 333f, 339n32, 396 Wakley, Thomas, 87, 187, 138n81, 243 on medical men, 190n27 and Snow, 105n37, 344–45, 253n35 Waldie, David, 367 Wales, 56 Waller, A.D., 138n81 Walmgate Ward, 17, 32n2 Wandsworth, 6, 208, 270, 280n29, 281n39a Warburton, Joseph, 46, 53n35 Warburton, Joseph, Jr., 46, 53n35, 75 Wardrop, James, 77n14 Wardour Street, 297 Warsaw, 232 Warwick Street, 312n17 Water companies, private, 7, 208–10, 254–56, 259, 261f, 277n4, 279n25, 318, 351 filtering/settling of, 247–48, 256, 273 metropolitan supply of, 254–73 quality of Thames water, 255–56, 260, 269, 271–73, 277n4, 351 sewage contamination of, 207–15, 208f, 269, 271–73, 355n9 Water pump at Bridle Lane, 288 at Broad Street, 7, 284–85, 288, 289f, 290, 300–03, 310, 313n31, 316n78, 330f, 332–34, 336f at Marlborough Street, 288 St. Bride’s, 245, 288 at Vigo Street, 288 at Warwick Street, 288 Waterloo, 266t, 272, 280n30 Watkin, Marion, 251n8 Watson, Jane Toward, 42 Watson, John, 42–44 Watson, Thomas, 13n29, 190n19, 193n58, 194n65, 194n69

Index Wetherburn (Weatherburn), Jane, 82, 234, 251n8 Webster, John, 199–200, 232 Weekly Journal of Medicine and Collateral Sciences, A, 73, 387n31. See London Medical Gazette Weekly Returns of Births and Deaths in London, 209, 247, 250, 292, 329, 344 from November 1853, 259–62, 261f Snow’s grand experiment and, 261f, 264–65, 267–68 Snow’s subdistricts’ investigation and, 265–73 Wellington, Mr., 368–69 Wellington Row, 21, 34n15 Wells, Horace, 112, 134n1, 367 Wells, William Charles, 104n30 West Ham, 350 Western Literary Institution, 251n1 Westminister Abbey, 7, 65 Westminister Hospital, 60f, 65–69, 78n23 Westminister Medical Society (WMS), 5–6, 315n60 amalgamation with MSL, 85, 238 arsenical candle investigation of, 70–72 chloroform and, 141 cholera epidemic of 1832 and, 70 ether and, 114, 118–24 membership, 84–85 October 1849 meetings of, 212, 216, 227n39, 231–33, 251n3 PMCC and, 227n39, 231–33 Snow and, 2–4, 90–94, 173 West Moor colliery, 31 White, Anthony, 66, 68 Whitechapel Road, 155 Whitehall Yard, 137n58 Whitehead, Henry, 285–92, 295, 311n13, 314n43 on Broad Street water pump, 299, 314n49 Cholera in Berwick Street, 299, 314nn47–48 and cholera epidemic of 1866, 392–93, 401n15

437 and Cholera Inquiry Committee (CIC), 301–06, 307–10, 310n1, 315n60, 316n76, 335, 339nn37–38, 394–95 on pump handle removal, 313n37, 350 on Snow’s theory, 304, 314n49, 316n74, 335 Whiting, John Joseph, 268, 280n27 Snow and, 268–75, 285 Widder, Agnes H., 103n3 Williamson, Eleanor, 251n8 Williamson, Sarah, 82, 251n8 Wilson, Charlotte, 155 Wilson, James Arthur, 149–50 Wilson’s Green Coat Boy’s Charity School, 34n21 Winlaton, 144 Winslow, Forbes, 93 Worboys, Michael, 193n61, 227n34 Workhouses, 171 Worms, parasitic, 204, 206, 223n9, 224n17, 225n18, 225n20, 374–75 Worshipful Society of Apothecaries, 24–25, 56–59, 58t, 77n14 Wright, Thomas Giordani, 29–30, 37n51, 37n54, 38n57 Yellow fever, 177, 232, 321 York, 14–23, 17f, 45, 277n7 grazing privileges in, 22, 34n18 public sanitation in, 17, 33n4 schools in, 22–23 wards of, 32n2 Water Lanes of, 258 Waterworks, 16–17 York, Jehoshaphat, 299, 306, 307, 307f, 309, 335 York Minster, 15 York Moderation Society, 48 Yorkshire, 47 Zymotic diseases, 181–85, 195n78, 323, 353, 376, 379. See also Farr, William

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