Carbon Monoxide and Human Lethality: Fire and Non-Fire Studies

CARBON MONOXIDE AND HUMAN LETHALITY: FIRE AND NON-FIRE STUDIES CARBON MONOXIDE AND HUMAN LETHALITY: FIRE AND NON-FIRE...

Author: M.M. Hirschler

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CARBON MONOXIDE AND HUMAN LETHALITY: FIRE AND NON-FIRE STUDIES

CARBON MONOXIDE AND HUMAN LETHALITY: FIRE AND NON-FIRE STUDIES Editor in Chief:

Marcelo M.Hirschler Safety Engineering Laboratories Rocky River, Ohio, USA Associate Editors:

Sara M.Debanne1, James B.Larsen2 and Gordon L.Nelson3 1

Case Western Reserve University, Cleveland, Ohio, USA University Southern Mississippi, Hattiesburg, Mississippi, USA 3 Florida Institute of Technology, Melbourne, Florida, USA

2

Project Sponsor: Society of the Plastics Industry, Inc., Washington D.C., USA

ELSEVIER APPLIED SCIENCE LONDON and NEW YORK

ELSEVIER SCIENCE PUBLISHERS LTD Crown House, Linton Road, Barking, Essex IG11 8JU, England This edition published in the Taylor & Francis e-Library, 2006. To purchase your own copy of this or any of Taylor & Francis or Routledge’s collection of thousands of eBooks please go to http://www.ebookstore.tandf.co.uk/. WITH 213 TABLES AND 59 ILLUSTRATIONS © 1993 ELSEVIER SCIENCE PUBLISHERS LTD British Library Cataloguing in Publication Data Carbon Monoxide and Human Lethality: Fire and Non-Fire Studies I.Hirschler, M.W. 615.9 ISBN 1-85861-015-X Library of Congress CIP Data applied for No responsibility is assumed by the Publisher for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions or ideas contained in the material herein. Special regulations for readers in the USA This publication has been registered with the Copyright Clearance Center Inc. (CCC), Salem, Massachusetts. Information can be obtained from the CCC about conditions under which photocopies of parts of this publication may be made in the USA. All other copyright questions, including photocopying outside the USA, should be referred to the publisher. 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 written permission of the publisher. ISBN 0-203-98681-4 Master e-book ISBN

ISBN - (OEB Format) ISBN 1-85861-015-X (Print Edition)

CONTENTS Chapter 1: Introduction MARCELO M.HIRSCHLER (Safety Engineering Laboratories) Chapter 2: Effects of Carbon Monoxide in Man: Exposure Fatality Studies GORDON L.NELSON (Florida Institute of Technology) Chapter 3: Effects of Carbon Monoxide in Man: Low Levels of Carbon Monoxide and their Effects GORDON L.NELSON (Florida Institute of Technology) Chapter 4: Physiological Effects of Carbon Monoxide JAMES B.LARSEN (University of Southern Mississippi) Chapter 5: Carbon Monoxide Determination in Human Blood GORDON L.NELSON (Florida Institute of Technology) Chapter 6: Carbon Monoxide and Fatalities: A Case Study of Toxicity in Man GORDON L.NELSON (Florida Institute of Technology) DENNIS V.CANFIELD (University of Southern Mississippi) JAMES B.LARSEN (University of Southern Mississippi) Chapter 7: Carbon Monoxide and Fatalities: Secular Trends SARA M.DEBANNE (Case Western Reserve University) DOUGLAS Y.ROWLAND (D.Y.Rowland Assoc.) Chapter 8: Lethal Carboxyhemoglobin Level: The Epidemiological Approach SARA M.DEBANNE (Case Western Reserve University) DOUGLAS Y.ROWLAND (D.Y.Rowland Assoc.) Chapter 9: Carbon Monoxide and the Toxicity of Fire Smoke MARCELO M.HIRSCHLER (Safety Engineering Laboratories)

1 3 63 117 175 181

200 215 232

Appendix Tables for the Data base in Chapter 6 A:

257

Appendix Tables for the Data base in Chapter 7 B:

338

Appendix Tables for the Data base in Chapter 8 C:

432

Appendix Carbon Monoxide Bibliography D:

452

Chapter 1 INTRODUCTION MARCELO M.HIRSCHLER Safety Engineering Laboratories, Inc., 38 Oak Road, Rocky River, OH, 44116, USA It has been known since about 1930 that one of the major causes of deaths in fires has been smoke toxicity. It was also known that carbon monoxide (CO), a highly toxic combustion product, was one of the major components of smoke derived from fires. Thus, it became likely that carbon monoxide was one of the primary causes of the lethality of smoke in fires. The way in which carbon monoxide caused poisoning was by combining with blood hemoglobin and generating carboxyhemoglobin. The levels of carboxyhemoglobin (COHb) found in the blood of a fatality were used by medical examiners to decide whether the victim had died of CO poisoning. It was soon decided that a 50% COHb level was the threshold to cause human lethality due to CO. In the period between the mid 1970s and the late 1980s, the issue of smoke toxicity took on a large importance in the public domain. This reflected two emerging trends. Firstly, small scale studies were being conducted, using tests of very dubious validity and animals (usually rodents) as models (and surrogates for man), to determine the toxicity of the smoke from burning materials. Great publicity was generated from the fact that one or two materials gave off smoke which appeared to be much more toxic than that of other materials. Secondly, as carboxyhemoglobin measurements became more widespread, some fire victims were found to have COHb levels of less than 50%. This created a fear of the presence of some “new” toxicants in fire atmospheres. It was feared that if such new toxicants existed they made fire atmospheres more toxic than traditional fire atmospheres. In 1984 the Society of the Plastics Industry, Inc. (SPI), in the United States, felt that the issue of the importance of carbon monoxide in the toxicity of fire atmospheres needed to be studied in greater detail. Moreover, the focus had to be human studies, especially lethality. Therefore, SPI commissioned a team headed by Professor Gordon L.Nelson, University of Southern Mississippi (USM), to carry out a study including the following tasks: 1. Analysis of the literature on carbon monoxide and toxicity, to include: (a) Effects of CO on man at low exposure levels (b) Studies of human fatality and exposure to CO. (c) Means of analyzing human blood COHb. (d) Physiological effects of CO to humans.

Carbon monoxide and human lethality

2

2. A case study, involving over 2,000 victims, of human fatalities associated with fires or with other exposures to CO. In 1986, the USM team presented a report to SPI where all the tasks were completed. On analysis of the results it was found that neither the population of fire victims nor that of victims of other exposures to CO were fully representative of the average human population. It was thus decided that a statistical analysis of the data needed to be carried out using epidemiological techniques. A team headed by Professor Sara M.Debanne, Case Western Reserve University (CWRU) was commissioned to carry out this investigation, using multivariate statistical techniques. They prepared a report which was presented to SPI in 1987. The victims included in the USM data base covered a large geographical area in the United States: data were collected in places as far apart as West Palm Beach, FL (Southeast), Seattle, WA (Northwest), Farmington, CT (Northeast) and Tucson, AZ (Southwest). Most of the victims analyzed for the USM data base, however, had died in fires which took place in the late 1970s and early 1980s. It was thus felt that it would be important to investigate whether the conclusions reached would change if data was collected for victims who had died earlier. Cuyahoga County (surrounding the city of Cleveland, OH) was not one of the contributors to the USM study. It was a very interesting location, however, because a very respected scientist, Dr. Samuel R.Gerber, was the county coroner during the period 1938–1979. This period started at a time when synthetic materials (e.g. plastics) were a rarity and concluded when plastics have become, as they are now, a fundamental part of life in the developed world. The total number of fatalities related to CO in that period exceeded 2,000 cases, which gave it good statistical validity. The CWRU team was thus commissioned by SPI to investigate all those fatalities and apply the same statistical analysis techniques they had used for the earlier studies. Their report was presented to SPI in 1990. Between 1990 and 1991 all of the various aspects that form the basis of this investigation were updated. Thus, chapters 2, 3 and 4 were written by Gordon L.Nelson and covered aspects 1(a), 1(b) and 1(c) of the original USM charter. Chapter 5 was written by James B.Larsen and covered aspect 1(d) of the USM charter. Chapter 6, written by Sara M.Debanne and Douglas Y.Rowland, covered the study of Cuyahoga County (OH) which became the CWRU data base. Chapter 7, written by Gordon L.Nelson, Dennis V.Canfield and James B. Larsen, presents the USM data base. Chapter 8, written by Sara M.Debanne and Douglas Y.Rowland, presents the multivariate statistical analysis of both the USM and CWRU data bases. The final piece needed to complete this puzzle was provided by Marcelo M. Hirschler. He analyzed data on smoke toxicity and on CO concentration from a variety of large scale and small scale fire tests, carried out by a variety of organizations. Using all of this information and the conclusions from the CO studies sponsored by SPI, he put together an overall analysis of the importance of CO in the toxicity (or lethality) of fire atmospheres as regards humans. Thus, Chapter 8 summarizes the implications of this entire study and puts into perspective the various smoke toxicity studies that are being made using animals as surrogates for humans.

Chapter 2 EFFECTS OF CARBON MONOXIDE IN MAN: EXPOSURE FATALITY STUDIES GORDON L.NELSON Florida Institute of Technology, College of Science and Liberal Arts, 150 West University Boulevard, Melbourne, FL, 32901–6988, USA ABSTRACT This report examines the various factors affecting carbon monoxide fatalities. Sources of carbon monoxide are examined. Effects of low oxygen, heat, carbon dioxide, hydrogen cyanide, alcohol, drugs, and disease are each discussed, as are time of exposure and level of activity. Human fatality data show that a significant percentage of exposed individuals die from carbon monoxide poisoning (automobile exhaust) at blood COHb levels thought by some to be less than “normal”, i.e, less than 50 percent COHb. Nearly 20% of individuals may die at such “low” levels. In the case of fire exposures, twice the number of victims are in the less than 50 percent category than for automobile exhaust victims, the two largest categories of CO exposure. Fire victims, however, have a very different age distribution and level of infirmity than do automotive exhaust victims. Carbon monoxide is the prime source of fire fatalities as well as automotive exhaust victims. In human carbon monoxide fatality cases the victims are predominantly male and alcohol is frequently present, regardless of the source of carbon monoxide. Individuals suffering from systemic hypoxemia (eg. anemia or cardiopulmonary (disease) or increased oxygen demand are at greater risk. In order to ensure meaningfulness of results special care is required in the determination of COHb in the blood victims, particularly from fire victims and for aged blood samples. Carbon monoxide is an ever present hazard which manifests itself in ways far more diverse than previously recognized. Many examples are provided.


4

2.1 GENERAL COMMENTS Carbon monoxide (CO) is a highly toxic, nonirritating gas. One of the products of combustion, it is invisible, odorless, tasteless, and slightly lighter than air. Carbon monoxide poisoning is not new. Man’s difficulties with CO date back to the time prehistoric man first used fire. Instances of CO poisoning have been found in early Greek and Roman literature. The increased use of coal for domestic purposes in the 1400s brought with it an increase in CO poisoning. The *

Note: In every case, if no further details are given, the venue for the study is the United States.

hazard was intensified by the introduction of illuminating gas, and later by natural gas, for heat, power, and light.1 The first understanding of the pathophysiology of CO dates from the work of Claude Bernard in 1857 when he ascribed the toxic effects to tissue hypoxia. In 1895 Haldane described the underlying mechanism for CO toxicity when he demonstrated that CO reversibly interacts with hemoglobin in the blood, blocking the binding of oxygen to hemoglobin, thus causing tissue hypoxia. He also demonstrated that rats poisoned with potentially lethal concentrations of CO survived if treated with hyperbaric (high pressure) oxygen, a treatment still used extensively for severely exposed CO victims today.2,3,4 Until recent years, concern over CO poisoning has been directed mainly toward the rather high concentrations sometimes found in closed spaces, such as homes, offices, factories, and mines. But with the increased use of motor vehicles, with their high CO emission rate, attention has also been focused on the more subtle effects of relatively low concentrations of CO that can often be found in outdoor environments, particularly in urban areas. In Stewart’s review of the effects of carbon monoxide in humans,4 he notes that humans have always been exposed continuously to small quantities of CO produced internally from the normal destruction of hemoglobin, with a minor fraction contributed by the breakdown of nonhemoglobin heme. In healthy male subjects at rest, the average rate of endogenous CO production is approximately 0.4 ml/h. During the progesterone phase of the menstrual cycle, endogenous CO production is approximately double that of the estrogen phase. The presence of these small quantities of CO in the blood results in a COHb saturation of 0.4–0.7 percent and is considered neither beneficial nor harmful. In patients with hemolytic anemia, COHb saturation may rise to 4–6 percent. Most environmental CO is produced from incomplete oxidation of carbon containing materials. Because complete combustion is seldom attained, varying concentrations of CO can be expected to be produced in most combustion processes. Tobacco smokers are the nonindustrial segment of the population most heavily exposed to carbon monoxide. The majority of cigarette smokers consuming one pack per day have blood COHb levels of 5–6 percent during their waking hours. Two- to three-pack-a-day smokers average 7.9 percent saturation, while heavy cigar smokers may reach peak saturations of 20 percent. The COHb saturation resulting from tobacco smoking is additive to that resulting from other CO sources in the environment. For example, a one-pack-a-day cigarette consumer

Effects of carbon monoxide in man

5

in one city would have a COHb saturation of 5.5 percent when nonsmokers in the same area had 1.2 percent, compared with a COHb of 6.5 percent in a second city when nonsmokers had 2.2 percent.4 The major environmental source of CO is the exhaust of motor vehicles, which accounts for approximately 67 percent of the total CO emissions per year. Exhaust tailpipe CO concentrations range from 0.5–7 percent, depending upon the year the automobile was manufactured, the state of engine tuning, and operation of pollution controls. A lethal CO concentration can be reached in a closed one-car garage in ten minutes. Concentrations of 25 ppm can be encoun-tered on expressways in major metropolitan areas during peak traffic periods.4 Fuel combustion in stationary sources, industrial processes, and solid waste disposal account for about 23 percent of total CO emissions. In the home environment improperly vented hot water heaters, furnaces, space heaters, and fire-places are the usual sources of CO exposure.4 Of course exposure to fire gases can provide very high levels of carbon monoxide in addition to other gases. CO concentrations up to 7 percent have been found in combustion gases during forest fires for example1. An unexpected indoor source of excessive CO exposure occurs following the use of a paint stripper whose basic ingredient is methylene chloride. Methylene chloride is metabolized in the body to CO, and a 3-hr exposure to paint stripper vapors in a well-ventilated room can result in COHb saturations of 8–16 percent.4 One frequently finds comments such as the following in texts and surveys: “Carbon monoxide is present in significant amounts in virtually all fires. It is highly toxic when inhaled, and acts by combining with hemoglobin in the blood to form carboxyhemoglobin (COHb). Hemoglobin’s function is to carry oxygen throughout the body, and it cannot do this if it is tied up, as COHb and, therefore, unavailable for oxygen transport. The level of carboxyhemoglobin in the blood of fire victims can be determined fairly easily. In the absence of other contributing factors a COHb concentration of 50 percent or greater is generally considered lethal.”5 Most medical discussions of carbon monoxide poisoning deal with “normal, healthy” individuals. However, the population is composed of a spectrum of individuals in a variety of environments. Conclusions for a small set of fatalities without reference to their detailed health can therefore be misleading. A number of studies have been reported which discuss carbon monoxide fatalities from specific sources. In this chapter focus will be on human exposure studies, largely analysis of exposure fatality cases. First carbon monoxide victims will be discussed in general and then fire victims in particular. Finally, the factors which affect carbon monoxide fatalities will be discussed.


6

2.2 CARBON MONOXIDE EXPOSURE STUDIES In 1977 CPSC presented a discussion of unvented space heater related deaths. Age and percent COHb are presented in Table 1.6 For 15 victims COHb levels were measured: 11 were males and 4 were females. Twelve (80 percent) of the victims were in their 20’s, 30’s or 40’s with an equal distribution of victims over the 3 age groups. Of the remaining 3 victims, one was age 52 and two were in their late 60’s. Twelve of the victims had blood COHb levels of 40 percent or more (10 of these victims were in the 40–59 percent range, and two were in the 70–79 percent range.) Three of the 15 victims had existing physical disorders; i.e., cardiovascular disease. Two of these victims exhibited blood COHb levels in the 30–39 percent range (a 23 year old male and a 69 year old male). The third victim’s

Table 1 Deaths from CO Poisoning from Unvented Gas Heaters6 Record of Death

Age of Victim

%COHb

x=CPSC file o=Dr. Davis

75%

x (76%)

37

70%

x (73%)

21

o (72%)

19 Fetus had 84%

65%

o (68%)

81 Coronary History

60%

o (60%)

21

55%

x (57%)

36

o (56%)

43

x (55%)

36

x (54%)

35

x (52%)

45

x (47%)

46

o (45%)

77

x (45%)

21

x (43%)

40

x (42%)

48

x (41%)

67-Hypertensive

x (40%)

22

50%

45%

40%

Comments

Heart Disease


35%

30%

25%

7

x (36%)

52

x (35%)

69-Arteriosclerotic Disease

o (33%)

49

x (33%)

23-Cardio. Resp. failure

o (26%)

54-Blood Alcohol 0.12%

20% 15% 10% 5% 0%

blood COHb level was 41 percent (a 67 year old male). Victims of carbon monoxide poisoning can exhibit a wide range of COHb levels.6 Additional cases were reported by CPSC based upon testimony given by Dr. Joseph H.Davis during unvented gas space heater hearings in Miami, March 29, 1978. Dr. Davis presented four incidents of CO poisoning associated with unvented gas space heaters that resulted in seven deaths. All of these deaths occurred in Dade County, Florida. Five of these victims were male, and two were female (one female was 41/2 months pregnant). Four of the seven victims ranged in age from 19–54 years; the remaining three were in their 70’s and 80’s. The blood COHb levels ranged from 26 percent (a 54 year old male whose blood alcohol level was 0.12 percent) to 72 percent (for the pregnant woman whose fetus’s blood COHb level was 84 percent). The COHb levels for the remaining 5 victims fell between 33.60 percent, and the ages ranged from 21 to 81. A pre-existing physical disorder was noted for one of these five victims (the 81 year old male was reported as having a coronary history). None of these victims had alcohol in their blood. Two married couples were represented in these four incidents. Within each couple, the spouses were close in age. In both incidents, the wife exhibited a higher tolerance for COHb than did her husband. (First couple, 21 year old male-60 percent COHb and 19 year old female-72 percent COHb; second couple, 79 year old male-33 percent COHb and 77 year old female-45 percent COHb).6 From this small sample of victims who died from CO exposure, it appears that tolerances to COHb levels can vary greatly, and may depend on age, sex, and pre-existing physical condition. Of 22 victims, 17 died with COHb levels less than 60 percent and 12 with less than 50 percent, the value frequently reported to be as “normal” for healthy adults. Other studies support the CPSC findings. Early work in New York reported a study of 68 cases exposed to carbon monoxide. Nearly one-quarter of the fatalities in this 1942 study had COHb levels less than 60 percent. Example data for the New York study are as follows7:


8

New York CO Fatality Study CASE %COHb 68

31.3 Each one of the 68 cases was found dead in a gas filled room or in a garage containing high concentrations of exhaust gases. 33.6

19

42.2

17

43.6

50

49.3

4

50.4

37

52.9

5

53.6

2

58.9

52

65.1

67

81.1

1

3% of the 68 cases died with 30–40% saturation 3% of the 68 cases died with 40–50% saturation 10% of the 68 cases died with 50–60% saturation 19% of the 68 cases died with 60–70% saturation 35% of the 68 cases died with 70–88% saturation


9

FIGURE 1. The Distribution of COHb Values Among Survivors and Fatalities8


10

FIGURE 2. The Age of Survivors and Fatalities in 1975–76 Study8 More recently, workers in Poland have reported data on carbon monoxide poisonings. While the source of CO was not discussed, 321 cases from 1975–76 were analyzed with 101 fatalities and 220 survivors. The distribution of COHb values for both sets of victims is shown in Figure 1. Some fatalities are in the 30–50 percent range, yet some survivors are in the 50–60 percent range.8 The ages of victims are shown in Figure 2. Older persons are more predominant in the fatalities than in the survivors. Differences by sex were also noted. Males predominated in fatalities, while females predominated in survivors (60 versus 41 for decedents and 66 versus 92 for survivors). The effects of blood alcohol showed no significant difference between those with 0.1 plus percent blood alcohol (26 victims, COHb mean 65 percent), and those without (75 victims, COHb mean 62 percent). Circulatory system problems were noted in 17 fatalities (COHb mean 59 percent). The mean COHb value was somewhat lower for those victims, than for those not showing circulatory system problems (COHb mean 63 percent). For fatalities, advanced age and severe arteriosclerosis led to lower COHb values.8 Another study of 304 fatalities due to carbon monoxide, largely exhaust fumes (287 cases), was performed by the Center of Forensic Sciences in Ontario, Canada. This study covered the years 1965–1968. The population was studied as the whole group, then divided into suicides, accidents, presence of alcohol and other drugs, and the presence of diseases. Data are shown as follows:9


11

%COHb

Category

Number of Cases Mean

Standard Deviation (±)

Minimum Maximum

Highest Single Frequency Range %

Majority Range

Whole group

304

51

12

23–89

45–59

(18)

40–59

Suicides

162

53

12

24–83

50–54

(19)

45–64

Accidents

135

49

12

23–89

45–49

(24)

40–59

Presence of Alcohol and Drugs

135

52

13

24–89

45–49

(16)

40–59

Presence of Pathological Conditions

25

46

17

23–89

35–39

(36)

30–44

The mean lethal percent saturation of carbon monoxide was found to be 51± 12 percent. COHb levels of 23 and 24 percent were found in two individuals in the survey. For a majority (approximately 68 percent) of the fatalities studied, the blood saturation of carbon monoxide ranged between 39 and 64 percent. The suicide group showed a somewhat higher mean lethal saturation than the accident group, 53.3 percent versus 49.4 percent,9 perhaps resulting from shorter exposure times for the suicide group. The category of fatalities in which alcohol or other drugs were found in addition to carbon monoxide, is of particular interest. The drugs involved were mostly alcohol and barbiturates, with blood concentrations ranging from traces to possibly lethal values. It is to be noted that the presence of drugs had no effect on the mean or the frequency distribution pattern of the lethal carbon monoxide saturations of this group. No evidence was found for enhancement of the toxicity of carbon monoxide by central nervous system depressants such as alcohol or barbiturates.9 The last category studied included carbon monoxide fatalities in which autopsy findings revealed cardiovascular, respiratory, or severe anemic disorders. The lowered mean lethal saturation and the generally lower distribution pattern in this category would appear to indicate that individuals with such diseases can succumb with somewhat lower saturations of carbon monoxide as compared with the whole group. It is to be noted, however, that individuals with low COHb levels are found in all groups, and not all individuals with pathological conditions have low COHb values.9 Carbon monoxide exposure in man must focus particularly on motor vehicle exposures. Over 1000 people die in the US annually from exhaust fumes. One study of unintentional CO poisoning is particularly revealing. Reports of victims in the state of Maryland during 1966–1971 were reviewed. The ages of the 68 victims were as follows10:


12

Ages of Persons Who Died AGE

PERCENT

14–19

13

20–29

35

30–39

24

40–49

25

50–59

6

60–69

4

70+

3

The percent carboxyhemoglobin measured in the blood of the victims was as follows7:

COHb of Victims COHb%

Number of Victims (%)

30–39

2

40–49

8

50–59

15

60–69

66

70–79

9

Severe arteriosclerotic coronary artery disease was noted in the person who died with a COHb saturation of 30 percent and in the one who died at 40 percent. Alcohol intoxication of four of the five persons with COHb in the 40–49 percent range was thought to have contributed to death at COHb saturations which the author of the study did not consider usually lethal. As shown below, alcohol over 0.1 percent was present in over one-quarter of the victims. Motor vehicles involved were statistically older than the population of registered vehicles.10

CIRCUMSTANCES OF EVENT AND BLOOD ALCOHOL CONCENTRATION Alcohol (% by wt.) Circumstances Sleeping

.00

.01–.09 0.10+ Unk. Total 6

3

11

0

20

17

8

3

2

30

Driving

3

0

0

0

3

Stuck in snow or mud

0

2

1

0

3

Couple Parking


13

Working on car

1

1

1

0

3

Warming car or changing battery

2

0

0

0

2

Other

4

1

2

0

7

33

15

18

2

68

TOTAL

A rusted body or exhaust pipes jammed against the body by a past accident so as to allow exhaust fumes to seep into the trunk are frequent automotive scenarios. A detailed report on several other cases in Maryland reveals the seriousness of these scenarios.11 Such accidents are common in late fall and winter in northern states, in rural regions, and in low income areas. Data follow:

Vehicular Carbon Monoxide Fatalities Age

COHb

CO Test of Vehicle Passenger Compartment

63 male

60 (heart patient)

0.045% at 10 min.

23 male

60 (0% alcohol)

0.02% at 30 min.

30 male

60 (0.14% alcohol)

0.02% at 30 min.

50 male

40 (0.11% alcohol)

0.045% at 30 min.

44 male

60 (0.12% alcohol)

0.02% at 25 min.

54 male

20±(0.17% alcohol)

0.005% at 45 min.

±vehicular crash

A review of 87 vehicular exhaust deaths for 1978–84 in West Virginia showed the typical victim to be male (78%), aged 15–34 years (64%), in a stationary passenger car, testing positive for blood alcohol (68%). Vehicles tended to be older, 10 years versus a state average of 6 years, with defective exhaust systems. Episodes generally occurred between midnight and 6 a.m. (76%). Of 14 episodes in garages, six had the main garage door open and 3 others occurred with an access door or window open, showing the ineffectiveness of passive ventilation to insure against carbon monoxide poisoning.12 In fact, three deaths have been reported by San Antonio, Texas, authorities involving incidents in a field or parking lot, with COHb results of victims, 58–81%.13 Two studies of mass carbon monoxide poisoning have been reported. In the first, carbon monoxide fumes began to enter the forced air heating system of a high school at 7:30 a.m., when the furnace was turned on, because a door to the exhaust chamber had been inadvertently left ajar. Soon both teachers and pupils throughout the school began to feel ill, complaining of headache, nausea, and weakness. Exposure ended at approximately 10:00 a.m., when a science teacher correctly associated the symptoms with carbon monoxide (CO) poisoning, the fire alarm was rung, and the school evacuated. Maximum time of exposure was two and a half hours. One hundred eighty-four persons were exposed; 160 (87 percent) became ill; 96 (60 percent) were transported to four hospitals for treatment. Carbon monoxide poisoning was confirmed by carboxyhemoglobin (COHb) levels measured on 66 persons that ranged from 4 percent to


14

28 percent saturation, with almost half falling between 21 and 25 percent. The mean COHb concentration was 18 percent. Atmospheric CO levels were assessed to have been fairly uniform throughout the school.14 The same week as the event, a questionnaire was prepared and circulated to all occupants of the school. A second questionnaire was circulated to physicians and administrators at the four hospitals where victims were treated, along with release forms for medical information. Symptoms reported are shown as follows14:

Symptoms reported by 159 persons who became ill from exposure to CO Symptom

Frequency (%)

Headache

90

Dizziness

82

Weakness

53

Nausea

46

Trouble Thinking

46

Shortness of Breath

40

Trouble with Vision

26

Loss of Consciousness

6

One hundred sixty of the 184 persons exposed (87 percent) reported becoming ill. One hundred (54 percent) first felt sick before the alarm was rung; 37 (20 percent), within one hour after the alarm; and 17 (9 percent), more than one after the alarm.14 Since victims arrived at school at irregular intervals throughout the morning, the duration of exposure varied from less than 30 minutes to 150 minutes. Those who reported they did not become ill had a mean duration of exposure of 71± 44 minutes; those who became ill but did not receive hospital care, 87±42 minutes; and those who were treated at hospitals, 107±34 minutes.14


15

FIGURE 3. Plot of percent COHb in blood versus duration of exposure for victims of a high school exposure incident.14 There were no significant differences between sexes or among age groups with regard to the kind or severity of symptoms, except that muscle weakness was more prominent among nonsmokers. There was no difference in the frequency of symptoms between smokers and nonsmokers. There was a strong correlation between most (but not all) symptoms and the duration of the exposure. A graphical representation of the association between duration of exposure and COHb concentration in the blood of 66 victims is shown in Figure 3. In order to estimate more accurately the actual COHb levels of victims at the time the alarm was rung, correction was made for the delay between exposure and the drawing of blood samples. The corrected mean COHb level was 20.7±7.0 percent. The points cluster very closely about the 500 parts per million isobar, suggesting that the concentration of carbon monoxide to which persons in the school were exposed was approximately 500 ppm.14 Of most significance for this work was the fact that, despite what were thought to be fairly uniform CO levels throughout the school, the results showed both significant variation among symptoms reported by victims with similar exposure times as well as different COHb levels in the blood, the latter of course complicated by differing activity levels of victims14. In a second case of mass exposure, 171 persons were involved when an exhaust pipe of a natural gas engine split apart in a sports arena in Anchorage, Alaska. CO was dispersed into the circulatory air. Of 316 exposed persons, 171 developed symptoms as shown below15:


16

Distribution of Illness Among Broomball Players, Hockey Players, and Adults Number Present Broomball Players

Number ill

Attack Rate Percent

247

131

53

Hockey Players

39

30

77

Coaches and teachers

30

10

33

316

171

54

TOTAL

Symptoms and Signs of Carbon Monoxide Poisoning Reported by 51 Ill Persons Present in the Sports Arena on March 20, 1969 Symptom

35 Broomball Players 7 Hockey Players Percent Percent

9 Adults Percent

51 Total Percent

Headache

91

57

100

88

Dizziness

77

43

11

61

Nausea

49

43

44

47

Tinnitus

43

14

0

31

Disorientation

31

14

0

24

Numbness of feet

26

29

11

24

Blurred vision

20

–

–

14

Numbness of hands

9

–

–

6

Vomiting

3

–

–

2

Loss of Consciousness

3

–

–

2

In this case 6 victims lost consciousness. It is estimated that the CO concentration was 900 to 1000 ppm. Exposure was varied both in time and circumstance. The hockey players were exposed earlier and for a longer period of time. Players were involved in more vigorous of action. COHb determinations were unfortunately not made. Again persons of seemingly similar exposure reported differing symptoms. Specific carbon monoxide exposure cases have been reported in the forensics literature. Several are worthy of mention. In one such case a 42-year-old intoxicated male arrived at his residence in the early morning. The male victim activated an automatic garage door opener and drove his fullsize automobile into the garage; he then placed the automobile in “park” and closed the garage door by once again using the remote control device. Sometime after this point,


17

while remaining in the vehicle, he became unconscious. The automobile’s engine was still running, all the windows were rolled up, and the headlights were left on.16 The two-car garage was located directly beneath the three bedrooms of the family dwelling, each of which was occupied. A 32-year-old female, wife by second marriage to the adult male victim, was sleeping in the north bedroom. An 18-year-old female, daughter by first marriage to the adult male victim, was sleeping in the southeast bedroom. A five-year-old male, son to the adult male by second marriage, was sleeping in the south central bedroom.16 Death occurred to the husband, wife, and daughter, with the five-year-old son surviving. Cause of death was confirmed as carbon monoxide asphyxiation in all three victims, who were otherwise in apparent good health. Carboxyhemoglobin data and blood alcohol data are shown below:16

Blood-alcohol analysis Victim

Age, years

Carboxy-hemoglobin, %

Blood Alcohol, %

Male (deceased)

42

69

0.240

Female (deceased)

32

59

0.000

Female (deceased)

18

57

0.000

5

–

–

Male (survivor)

The author of the study concluded that the male died earlier due to exposure to higher levels of CO. The reasons for the child’s survival were not altogether clear. Such cases of the survival of younger children are not unique.16 One case from New Zealand is also interesting. The bodies of a young married couple were found inside an unventilated caravan. It was established that they died from carbon monoxide poisoning. Field tests showed that fatal atmospheric levels of carbon monoxide were produced in the caravan by a poorly designed propane heater. The couple’s onemonth-old child survived even though he was exposed to the same carbon monoxide levels as the parents. COHb levels for the husband and wife were 75 percent and 65 percent, respectively.17 It was originally thought that the child must have been exposed to a lower CO concentration than his parents. However, the possibility of interference by a third party was ruled out and the caravan tests showed that very similar CO levels were established at three well-spaced sampling points. The child was therefore exposed to a CO level exceeding 800 ppm for ten hours. When found he as very hot and sleepy, but otherwise in no apparent distress. He had not been fed for more than twelve hours and was still on four-hourly feedings; this suggests he had an appreciable COHb level. He recovered quickly and had no apparent ill effects.17 In another case the body of a man was found near a defective gas stove. His wife’s body was found in an adjoining room, but their baby, lying beside his father, showed no signs of CO poisoning.17 Clearly, persons undergoing similar exposures can exhibit different outcomes. In a 1986 case in a Tennessee motel a 60 year old executive missed an early morning meeting. At 11 a.m., motel security opened his door and found the victim dead in the


18

floor (90% COHb) and his wife lying across the bed, comatose (35% COHb). That evening a 65 year old woman in a room directly below phoned a local relative and reported that she and her husband were ill. A search of other guest rooms found a fifth victim, comatose in a room adjacent to the room where the first patient had died. Subsequent investigation revealed that the source of carbon monoxide was the swimming pool heater. Exhaust fans above the building atrium maintained the building under negative pressure. There was thus potential for back draft from pool heater vents and subsequent carrying of CO into adjacent guest rooms.18,19 Indeed, a report from Denmark shows gas water heaters to be a frequent scenario.20 A Maryland study of heating victims showed COHb values ranging from 77 to 37%, with 2 of the 14 victims below 50% COHb.21 In a 1988 report a 27 month-old girl was brought to Johns Hopkins hospital after being the middle passenger in the backseat of a car that had been traveling from Washington, DC, to Baltimore. Two other children were in the backseat. The patient had repeatedly crawled down to the floor and back up to the seat in the 50 minute trip. She had fallen asleep 15 minutes before arrival. She was unresponsive with a COHb of 35%. Her 7 yearold sister who had been sitting to her right had a COHb of 34.7% but was largely asymptomatic. A 28 month old infant sitting to the left was totally asymptomatic despite a COHb of 33.6%. The front passengers (25 years and 72 years) showed COHb values of 18.4% (headache) and 16.1% (lightheadedness) respectively. The male driver of the car had dropped the passengers at the emergency room and had driven to work and felt fine. The driver’s window had been ajar during the trip. Again, persons with similar COHb values do not have identical symptoms.22 Sources of carbon monoxide in our environment are legion. The Utah Medical Examiners Office has reported several cases of carbon monoxide poisoning from the misuse of charcoal grills. Unrecognized by most individuals, charcoal produces substantial concentrations of carbon monoxide. Two of those cases follow.23 Case 1.—After cooking steaks outside their trailer on a cool evening, a husband and wife took their hibachi inside “to warm up the trailer.” The trailer was “closed up tight” because of the cool night. While asleep that evening the wife became nauseated, went into the bathroom in the trailer where she vomited and collapsed. When she awakened she found her husband dead in bed. The wife was hospitalized briefly and then released, without apparent effect. She reported that they had never before used the hibachi to heat the trailer. Autopsy of the husband revealed healed rheumatic heart disease. His heart blood contained 71 percent carbon monoxide. Case 2.—One day in late winter a father filed a missing persons report on his son. The following morning the father noticed the altered appearance of a stairway leading down to an old potato cellar near his property. Located at the bottom of the stairway was the only door and it was covered tightly with a plastic sheet. Inside the cellar on a foldaway type bed were his son and the son’s 18-year-old girlfriend, both covered to just below the shoulders by a sheet and a bedspread. The boy was unconscious. The girl was dead. The cellar measured approximately 10×8×6 feet. A nonusable oil stove stood on the floor. On top of it was a hub cap containing charcoal briquette ashes. Along-side the stove was a nearly empty bag of charcoal briquettes. Aside from the door covered by a plastic sheet, there was one small vent in the center of the ceiling. Autopsy revealed a


19

healthy girl whose heart blood contained 65 percent carbon monoxide and 0.054 percent ethanol. The boy survived without apparent effect. In a more recent report two hibachi cases were reported. In one, a 53 year old black male was found dead at his residence. He had moderate, generalized artereosclerosis. His blood COHb level was 41%. In the second case a 12-year old white male was found dead in his sleeping bag by his father who had been sleeping in the same tent. His blood COHb level was 30%.24 These cases demonstrate that a small volume of a seemingly harmless combustible can be fatal. Individuals exposed to the same atmosphere do not experience the same effects. And, victims of carbon monoxide poisoning can die at less than 50% COHb. 2.3 VARIATION BY SOURCE OF EXPOSURE It has been noted in the literature that the source of carbon monoxide makes a difference in the mean COHb at death. Data from Japan are as follows:25 Cause of Death Number of Cases Age Range COHb Range Mean City gas

15

4–50

64.3–83.1

74.8

Fire

12

1–87

40.1–68.5

54.9

Exhaust

10

19–46

50.3–81.6

64.6

It was speculated that oxides of nitrogen in exhaust gases led to a lower mean for these cases. For fire victims the four fatalities with the lowest COHb values were aged 67, 87, 78, and 1 respectively. Victim age plays a role. In another Japanese study the following data were presented.26 Cause of Death Number of Cases COHb Range City gas

4

64.2–79.5%

Fire

4

40.0–67.5%

Exhaust fumes

4

54.1–72.4%

City gas

3

71.9–78.7%

Fire

3

13.4–92.4%

Exhaust fumes

3

53.2–78.7%

From such data one might indeed conclude that fire is different and that perhaps even exhaust fume victims are different. In this latter study no data were presented on the age or health of victims. It is not surprising that exposure to fire gases might, on balance, lead to death at lower average COHb values. Fire gases, exhaust gases, and city gas are not pure carbon monoxide, although the concentrations of carbon monoxide are high in all three. For fire gases, elevated temperature and oxygen depletion are generally unassessable variables in addition to the presence of other gases such as hydrogen cyanide, aldehydes, CO2, etc.


20

Exhaust gases include oxides of nitrogen, and hydrocarbons. City gas includes hydrogen, methane, ethane, propane and carbon dioxide. However, city gas lacks the irritants such as aldehydes and oxides of nitrogen present in the other two. Wistar rats have been exposed to CO, and automotive exhaust gases from unleaded gasoline and 96% ethanol. The exhaust fumes were generated by two new identical Fiat engines. The LC50 values for 3 hour exposures were as follows: LC50 (ppm) Confidence Limits Gasoline

1968

1940–1992

Ethanol

2076

2042–2102

CO

2093

2068–2121

It was noted that high levels of aldehydes exist in ethanol exhaust which are absent in gasoline, while high levels of sulphur oxides exist in gasoline exhaust but are absent in ethanol. The LC50 value for ethanol exhaust was identical to CO while that of gasoline was somewhat less.27 The Institute of Forensic Medicine in Oslo has reported a study contrasting carboxyhemoglobin concentrations in fire victims (87 cases) with that from automobile exhaust victims (54 cases), mostly suicides. Their data are depicted visually in Figures 4 and 5. For the exhaust victims the mean fatal COHb was 70 percent. Little blood alcohol was found. The relationship between COHb and victim age is shown as follows:28

The Relationship Between Age and Post Mortem COHb Concentrations in Cases of Fatal Carbon Monoxide Poisoning (non-fire) Age

Number of Persons

Mean COHb concentration in % (Standard Deviation)

Less than 40 years

11

74 (5)

Between 40 and 50 years

12

74 (7)

Between 50 and 60 years

18

70 (11)

More than 60 years

13

65 (12)

The older group showed large variations in COHb concentrations and a lower mean. For fire victims 32% died with COHb concentrations below 45 percent. 54 percent of the victims were alcohol intoxicated. Figure 6 presents blood alcohol data for these victims. The distribution of victims with alcohol was the same as those without alcohol. Alcohol did not appear to alter the toxicity of carbon monoxide.


21

FIGURE 4. Post mortem carboxyhemoglobin concentrations in 54 cases of fatal carbon monoxide poisoning (non-fire).28

FIGURE 5. Post mortem carboxyhemoglobin concentrations in 87 fire victims.28


22

FIGURE 6. Post mortem carboxyhemoglobin concentrations in 54 alcohol intoxicated fire victims. The values within the columns indicate the post mortem blood alcohol con centration (percent×10).28

FIGURE 7. Post mortem carboxyhemoglobin concentrations in 72 fire victims with burns.28

FIGURE 8. Post mortem carboxyhemoglobin concentrations in 15 fire victims without burns.28 In Figures 7 and 8 carboxyhemoglobin data are given for fire victims who had burns and those who did not. A similar pattern is seen. Of the latter victims, five died with COHb values below 50 percent. In three of these cases heart disease was detected, in one case severe bronchopneumonia, and in the fifth case heavy alcohol intoxication. The authors of the Oslo study concluded that burns rather than carbon monoxide poisoning were the main cause of death in at least thirty percent of fire victims, that alcohol intoxication does not seem to influence the fatal COHb concentration, and that a low post mortem carboxyhemoglobin concentration is often found in victims suffering from disease.


23

Japanese workers have contrasted the COHb profiles of victims from carbon monoxide poisoning, mainly inhalation of city gas, with that of fire victims. Data from this study from the early 1960s are shown on facing page:29 COHb in Deaths from CO Poisoning (non-Fire) COHb Deaths in Fire COHb (%)

CO Fatalities Number

COHb %

Fire Fatalities

(%)

Number

%

10

–

–

10

12

7.2

20

3

1.3

20

15

9.0

30

–

–

30

12

7.2

40

7

3.0

40

17

10.2

50

11

4.7

50

22

13.2

60

26

11.2

60

30

18.0

70

52

22.3

70

22

13.2

90

115

49.4

90

34

20.4

90.1

19

8.1

90.1

3

1.8

Total

233

100.0

Total

167

100.2

Some nine percent of city gas victims have COHb values below 50 percent with another 11 percent in the 50 to 60 percent range. Fire victims show a substantially higher percentage at low COHb values, with 47 percent showing less than 50 percent COHb and another 18 percent in the 50 to 60 percent range. COHb values for fire victims in the Japanese work are lower than that reported in the foregoing studies. While fire victims clearly die with COHb levels less than exhaust or city gas victims, those exposed to carbon monoxide in these latter circumstances show a broad range of COHb values with upwards of 20 percent of the victims showing less than 60 percent COHb blood saturation. 2.4 FIRE GAS EXPOSURE STUDIES Having contrasted non-fire and fire carbon monoxide fatality studies, it is appropriate to discuss fire gas exposure studies in more detail. Data for two aircraft fires in the early 1960’s have been reported. The mean COHb value was 59 percent with a range of 25 to 85 percent for 85 victims.30 CO Values Found in Victims of Aircraft Fires Percent Carboxyhemoglobin

Number of Fatalities 0–20

0

21–30

4


24

31–40

9

41–50

16

51–60

18

61–70

19

71–80

16

81–85

3

TOTAL

85

A report on 15 persons from the 1940’s showed a range of 18 to 78 percent COHb with a mean of 48 percent.31 A study by the University Institute of Forensic Medicine of Copenhagen, Denmark is particularly interesting. Data were collected on 169 consecutive cases involving fire victims. Some 56 percent were men and 44 percent women, all autopsied at the Medicolegal Institute of Copenhagen. The data originated from two periods, 63 cases were from the years 1966 to 1971 and 106 cases 10 years later (1976–1981). The reason for this subdivision was to attempt to elucidate the possible role, if any, which might be played by the increasing amount of synthetic products, which are replacing natural products in the built environment. However, no difference occurred between the distribution of the carboxyhemoglobin levels in the two data sets, and they are consequently combined and dealt with as one.32 At autopsy, special attention was paid to the possible presence of soot particles in the respiratory tract, and blood was collected for the determination of carbon monoxide and of alcohol. The distribution of victims according to age proved to correspond to the age distribution of the entire population of Copenhagen with the exception of the 15–35 year group, where only half the number of fire victims expected according to the age distribution of the population was found. The explanation offered is the greater agility of young persons, enabling them to move more easily to escape a life threatening situation.32 More than half of the fire victims had a significant blood alcohol level (over 0.05 percent), and in well over 20 percent of the cases the blood alcohol level surpassed 0.2 percent. In these cases the ability to react adequately may have been reduced to such an extent that alcohol may be considered to have contributed substantially to the victim’s presence in the incident.32 The distribution of the fire victims according to the percent of carbon monoxide in their blood is shown in Figure 9. The Figure also shows the number of victims with soot in the respiratory tract. It is immediately apparent that the two findings are closely related so that there are very few cases with significant amounts of carbon monoxide in the blood and without soot in the airways. Half of the victims showed blood with more than 50 percent of carboxyhemoglobin.32 Of interest is the group showing no significant carbon monoxide in the blood (less than 10 percent saturation) and no soot in the airways, consisting of 12 cases. The autopsies indicated that death had occurred before the onset of fire in five of the cases (the dotted top of the column). There remain seven cases, where the authors felt that


25

causes of death may have been heat (neurogenic shock) or carbon dioxide poisoning/oxygen deficiency.32 Concerning the groups showing low or negligible carboxyhemoglobin levels, the Danish authors speculated that carbon monoxide was not evolved at the onset of the fire, but instead carbon dioxide, which accentuates the lack of oxygen. This is said to be the case in flash fires, where a sudden, large consumption of oxygen takes place. In flash fires the intense heat alone may also be considered the cause of death.32

FIGURE 9. Victim distribution according to carbon monoxide in the blood. The dark part of the columns indicates cases with soot in the respiratory tract The white top (- -) of the zero column signifies the number of deaths before the fire.32 The Danish workers plotted their COHb profiles versus those from two other studies (Figure 10). The profiles are quite similar but not identical, showing perhaps differences in the studied populations as well as differences in techniques of COHb determination.32

FIGURE 10. The distribution according to carboxyhemoglobin


26

levels of victims in three fire fatality studies: Anderson et al. (—–),33 Birky and Clarke (. . . .),34 and the Danish work (- - - -). 32 In the Danish study half of the victims died as a consequence of smoking in bed. Characteristic for this type of fire is initial smoldering with comparatively low heat at the beginning of the fire. The distribution of carboxyhemoglobin of the victims of smoking in bed proved to be the same as that for the other half of the victims. In a detailed British report some 58 fire fatalities were investigated and categorized as to their presence in the room of fire origin or remote from the room of origin. COHb data were available on 12 and 34 victims respectively. That data is plotted in Figure 11,35 which shows that 74% of victims were found away from the room of origin.

FIGURE 11. Plot of COHb percent versus fire victims age.35 For the 34 victims remote from the room of origin 19 had COHb levels over 65 percent, six between 50 and 65 percent and four between 40 and 49 percent. The remaining five, who all died in the same fire, had levels between 14 and 28 percent—the causes of death


27

being recorded as carbon monoxide and cyanide poisoning together with superficial burns.35 Thirty-six of the victims had lung or respiratory tract damage recorded in the postmortem reports. This typically comprised black soot and ash in, and severe inflammation of, the air passages, with lungs oedmatous or congested. Such information was not available for the remaining seven victims but there was no reason to suppose that similar damage did not occur. Most victims had burns ranging from superficial to severe although burns may have occurred after collapse or death.35Cyanide tests were carried out on the blood of 15 victims. Thirteen gave results ranging between 26 and 180 µg CN/100 ml of blood, and none was detected in the other two.35 Alcohol was present in the blood of victims of two of the fires (124, 47, and 43 mg alcohol/100 ml blood); in another fire blood alcohol determinations were performed on four victims but none was found. Children, only, died in three other fires. In the remaining six fires in which adults died no alcohol tests were performed.35 Overall the British author’s conclusions in this study were as follows: a) In nearly all fires investigated some firespread occurred beyond the item first ignited. Almost all the fatalities, both in and remote from the room of fire origin were overcome by, and died from, the effects of smoke and toxic gases. Of these, only about one quarter had burns considered a contributory cause of death. Despite this, most of them had external burns but these may have occurred after collapse or death. b) More than half the fatalities had COHb levels which alone were clearly high enough to account for death in healthy individuals. c) Nearly all the fatalities had lung and respiratory tract damage due to the effect of smoke and hot gases. d) Cyanide was found in measurable amounts in victims. Although these amounts were all below the minimum lethal level, cyanide may have been a contributory cause of death at higher levels. e) People who died at night in fires starting on the floor below were generally not overcome in their beds. In most cases they got up and moved around before collapsing. f) It was not possible to say whether alcohol played a part in the death of most of the victims. g) Once out of the house people were unable to re-enter to rescue others due to their injuries or to the rapid development of the fire. As the foregoing studies indicate, the fire environment is a complex environment. Indeed, hydrogen cyanide has been found in fire victims over the years. While it is beyond the scope of this report to focus on the causes of fire deaths in detail, it is perhaps useful to cite some of the more relevant human exposure studies on the interaction of hydrogen cyanide with carbon monoxide.


28

2.5 WITH HYDROGEN CYANIDE In 1966 the Wayne County Michigan Medical Examiner’s Office reported a study of 53 fire victims (38 adults and 15 children) taken over a 16 month period in 1964–1965. Forty-eight victims were either dead at the fire scene or dead on arrival at the hospital. Five victims lived for two hours or less. All victims had significant levels of carbon monoxide (17 to 90 percent COHb) in their blood. In addition, blood cyanide was found in 39 victims at levels of 17 µg/100 ml to 220 µg/100 ml (six above 100 µg/1100 ml). (A background level of up to 25 µg/100 ml blood cyanide is found in smokers and .5 µg/100 ml for non-smokers.) All values were less than the 300–500 µg/100 ml (3–5 µg/ml) lethal level. Of victims with blood cyanide, 27 also had COHb levels in excess of 50 percent. Sixty percent of the adult victims were intoxicated to a greater or lesser degree. It was noted that while the primary cause of death was likely to be carbon monoxide, the action of cyanide to cause respiratory stimulation and inhibition of the cytochrome system may have been a contributing factor to fire death in some cases.36 Three survivable, relatively low crash-force, air carrier accidents in the first half of the 1960’s were investigated. These accidents were the 11 July 1961 United Airlines DC-8 at Denver, the 23 November 1964 Trans World Airlines 707 at Rome, and the 11 November 1965 United Airlines 727 at Salt Lake City.37 Medical investigators conducted blood tests on the victims and found that carbon monoxide was present in amounts sufficient to have caused toxic incapacitation during the brief period available for emergency evacuation prior to the progressive destruction of the aircraft passenger cabin by fire. In connection with the accident investigations, investigators found that the acrid smoke caused laryngospasms and that this caused breathing difficulties. Carbon monoxide data are shown as follows:37 Passengers Passengers

Deceased Passengers

Tested for Carbon Monoxide

Carbon Monoxide (as blood COHb)

Denver DC 8

114

17

17

30–85% range (mean=62%)

Rome 707

62

45

24

3–49% range (mean=23%)

Salt Lake City 727

85

43

35

13–82% range (mean=37%)

105

76

Four accidents were reported which included cyanide analysis. These accidents were the 27 November 1970 Capitol International Airways DC-8 at Anchorage, the 7 June 1971 Allegheny Convair 580 at New Haven, the 8 December 1972 United Airlines 737 at Midway and the 20 December 1972 North Central DC-9 at O’Hare. These accidents also involved relatively low crash forces. During the emergency escape period fire and toxic smoke occurred.25


29

It was determined through blood analysis of the victims that cyanide was present in some cases in amounts which could be incapacitating, in combination with the carbon monoxide that was present. A summary of the accident investigation findings of these four accidents with respect to cyanide and carbon monoxide ranges is given below:37 Carbon Monoxide (as blood Cyanide in blood sample carboxyhemoglobin) in fatal victims Anchorage DC-8

19 positive (5–69% range)

18 positive (0.1 µg/ml to 2.26 µg/ml range)

New Haven 580

23 positive (9–49% range)


Chicago 737

Pilot 40%

Pilot 3.9 µg/ml

Chicago DC-9 9 positive (26–64% range)


It was noted in the FAA report, that incapacitation should occur at lower levels than death, and it was speculated that it may occur at half the fatal concentration. For example, the 30 percent blood carboxyhemoglobin range (coma and death begin to occur at the 60– 70 percent blood level range in “normal” healthy adults) was thought to produce severe headache, weakness, dizziness, dimness of vision, nausea, vomiting, and collapse. Cyanide alone causes death at about the 3–5 µg/ml blood level in mammals but incapacitation at about half that level might be anticipated. Thus together, assuming additivity, lethal effects could perhaps be anticipated with a blood carbon monoxide of 30 percent plus a blood cyanide of about 2 µg/ml (200 µg/100 ml).37 Despite such speculations as above, in fire fatality studies, victims with high COHb levels characteristically show high blood cyanide. Low COHb levels are seldom associated with high cyanide levels. Data for 10 victims of the Tennessee jail fire 34,38 are shown below:34

Correlation of Blood COHb with HCN Victim Age

Cyanide (µg/ml)

COHb%

45

0.05

59

37

0.30

61

18

0.35

76

25

0.42

64

20

0.43

58

22

0.59

60

26

0.93

45

19

1.06

58

59

1.64

58

18

1.83

77


30

Cyanide approaching 2 µg/ml in fact showed little effect on COHb values in these victims. Cyanide and other toxicants may play an intermediate role leading to incapacitation, preventing escape but the role of cyanide in conjunction with CO is unclear. In the 1983 Ramada Inn Central Fire, Fort Worth, Texas data for the five victims were as follows:39 Sex Female Male Male Male Male Age

27

25

54

46

26

Location within room

side of bed near bath wall

corner near window

bathroom

corner near window

Side of bed 5 ft from window

Burns (degree/% body surface)

2nd, 3rd/ 30%

2nd, 3rd/ 75– 2nd, 3rd/ 80% 15–20%

2nd, 3rd/ 60%

2nd, 3rd/ 10– 15%

Blood CO a) (Carboxyhemoglobin b) Normal: less than 1.5%)

79% Saturation 82%

77% Saturation 74%

62% Saturation 60%

75% Saturation 70%

28% Saturation 25%

Blood Ethanol

0.08%

0.02%

None Detected

None Detected

None Detected

Blood Cyanide

None Detected None Detected

3.0 µg/ml

4.5 µg/ml

2.5 µg/ml

a) (Normal: less than b) 0.2 µg/ml)

0.6

6.3

2.4

5.7

1.8

Two sets of COHb and blood cyanide data are shown. Four of five victims have COHb values greater than 60%, which is consistent with carbon monoxide poisoning being the primary cause of all fatalities. Blood cyanide is a factor of two different between the two sets of results provided, showing the difficulty of blood cyanide determination.39 The lethal cyanide level in man is higher than that in rodents. Esposito and Alarie have found a lethal blood cyanide level of 1 µg/ml at an LC50 concentration of 177 ppm and an LT50 of 29 minutes in mice,40 but a value of 2 µg/ml was found in rats41 by Levin and coworkers for a 30 minute exposure. Several reports note that the acute lethal blood cyanide level in man is 5 µg/ml.42,45,46 While Rieders notes that blood cyanide in fatal cases may be below 1 µg/ml on inhalation of hydrogen cyanide gas,43 yet fire data seem to show high cyanide levels only in conjunction with high blood CO levels. A study by Symington of 52 fire victims for example showed cyanide levels up to 3.5 µg/ml.44 In a study by Memon and Alarie of 177 fire cases, of 29 cases with blood cyanide over 1.5 µg/ml, all but five cases had COHb over 50%.47,48 In pure exposures, recovery has been noted in victims whose cyanide level in the blood reached 7.5 µg/ml.49 The estimated LC50 in humans for HCN alone on inhalation is 3400 ppm for 1-minute; HCN is listed as fatal at 270 ppm in 6–8 minutes, 181 ppm in 10 minutes, and 135 ppm in 130 minutes.50 The LCLo, the lowest concentration in air reported to cause death, is 166 ppm at 10 minutes and 100 ppm at one hour. In cats the LCLo for 30 seconds is 2075 ppm and in rabbits 1660 ppm.51 However, survival in man


31

has been reported for an individual exposed to 415 ppm HCN for approximately 6 minutes.52 While the concentrations of HCN in controlled human exposures have not exceeded 450–520 ppm, men employed in fumigation with HCN have been tested while at rest in 250 ppm for two minutes and 350 ppm for 1½ minutes but felt no dizziness. Other tests have exposed individuals to 500 ppm for about a minute without injury. A ten minute LC50 value of 539 ppm has therefore also been suggested for humans. Clearly humans are able to tolerate exposure to a given concentration longer than other mammals, including monkeys.53 The most comprehensive studies on rats would suggest that the effects of HCN and CO are additive36,54–59 rather than synergistic.60 However, in papers by Davis and coworkers using five minute rat exposures, the author examined HCN singly and in combination with CO, either during the exposure or within 20 minutes CO post exposure.61–62 No alteration in the time-to-death pattern of HCN was seen in the presence of CO (25% COHb). The five minute LC50 value was 503 ppm for HCN, while the HCN-CO combination produced an LC50 value of 467 ppm, a value within confidence limits of the HCN value. For mice an LC50 of 323 ppm was seen for HCN for 5 minutes alone and 289 ppm in combination with CO (25% COHb level). Their results were clearly less than additive. Pitt, et al., examined individual and combined effects of cyanide and CO on cerebral blood flow and on cerebral oxygen consumption. They found that cerebral blood flow increases with CO-hypoxia and with cyanide hypoxia and in combination. Cerebral oxygen consumption declines at 50% COHb and in combination with HCN. Test animals had 30 or 50% COHb with or without 1.0 µg/ml HCN or 1.5 µg/ml HCN. Their results were additive.63 Studies in monkeys by Purser have looked at the relationship between atmospheric HCN concentrations and time to incapacitation. HCN levels of 100–200 ppm can be extremely hazardous. Incapacitation occurred at blood cyanide levels of approximately 2.7 µg/ml (2.2–5.3 µg/ml). Unfortunately, no direct relationship was found between venous blood cyanide levels and atmospheric HCN concentrations over a 30 minute exposure period, nor a clear relationship between venous blood cyanide and time to, or degree of, incapacitation. There was a loose linear relationship between HCN concentration and time to incapacitation. It may be that blood cyanide measurements are poor predictors of the degree of incapacitation caused by cyanide and that the rate of uptake during the hyperventilatory stage is more closely related to incapacitation and subsequent death than is the actual blood level after a period of exposure.64,65 Instudiesexposing cynomolgus monkeys to fumes from polyurethane foam (HCN 115 ppm and CO 1016 ppm) and polyacrylonitrile (HCN 115 ppm and CO Oppm) times to incapacitation were 20 minutes and 22.5 minutes respectively. These experiments suggest only weak additivity between HCN and CO.66 Before proceeding further, two complications should be noted. While 67 percent carboxyhemoglobin generally results in death for “normal individuals” if untreated, levels of 16–20 percent may be lethal for victims with cardiovascular disease, anemia, lung disease, and increased metabolic rate. Such victims show far greater susceptibility to the toxic effects of carbon monoxide. As shown by the blood COHb values in CO victims as cited in Section 1.2, the identification of the role of carbon monoxide based upon a specific COHb loading is not straightforward. This will be discussed further in subsequent sections. Likewise, the role of hydrogen cyanide is not only complicated by


32

factors similar to those above, but also by recognized difficulties in obtaining valid blood cyanide measurements (increase or decrease in cyanide is observed on sample aging).67–71 2.6 LARGE FIRE FATALITY STUDIES In 1972, Zikria, et al., of Columbia University, reported on an extensive analysis of autopsy records of 311 New York City fire victims during 1966 and 1967. One hundred eighty-five survived less than 13 hours, and 72 over 12 hours with 54 not having survival time indicated. Smoke poisoning or asphyxia was the most common primary diagnosis in fire deaths under 12 hours.72–75 Carbon monoxide poisoning occurred in 79 percent of all victims with a primary diagnosis of smoke poisoning or asphyxia. Of the 185 victims surviving less than 12 hours, 59 percent of the 70 percent tested clearly had lethal or significant levels of carbon monoxide.72–75 Among the 105 victims with less than 40 percent body burns—who would not have been expected to die from surface burns alone—three-fourths also had respiratory involvement. In the total group, half clearly had carbon monoxide poisoning, almost as many had smoke poisoning or asphyxia, and over one-quarter had respiratory damage. In deaths under 12 hours, carbon monoxide poisoning was found almost equally in the presence or absence of body surface burns, in 50 percent of those with body burns and in 30 percent of those without body burns.72–75 Of particular interest in the Zikira work is that respiratory tract involvement was found in 70 percent of deaths under 12 hours and in 46 percent of victims who survived over 12 hours. Zikira noted that it is likely that the agents causing the tracheobronchial and pulmonary parenchymal damage of smoke poisoning in man are also the aldehydes such as acrolein, which are found in large quantities in smoke and combustion of wood, cotton, furniture, and nonsynthetic structural materials.72–75 However, from the data given in the preceeding sections carbon monoxide alone was the likely cause of deaths in more cases than Zikria recognized. The reason for the discrepancy is the excessively conservative lethal COHb level (50%) that the author used. One of the most detailed fatality studies reported to date is from Maryland. Research conducted from 1972 to 1977 by the Applied Physics Laboratory of Johns Hopkins University and the Maryland State Medical Examiner’s Office focused on 530 fatalities.21,76–79 The causes offires were as follows:76 Causes Fires Fatalities Percentage Smoking

135

184

44.4

Electrical

20

29

7.0

Heating Equipment

19

33

8.0

Stove

11

14

3.4

Matches

18

27

6.5

Candle

4

5

1.2

Flammable Substance

9

9

2.2

Cooking

10

16

3.9

Suicide

14

14

3.4


Arson/Suspicious

33

16

31

7.4

Other

3

4

1.0

Explosions

8

13

3.1

Set Fire

5

5

1.2

Automobile

11

14

3.4

Unknown

12

16

3.9

295

414

100.0

TOTAL

Fires caused by smoking were predominant in the list of causes. Also, the study indicated that smoking and alcohol were a bad pairing. A blood alcohol content of 0.1 percent (the intoxication limit in some states) was involved in 50 percent of all fire fatalities above age 20. Data show that about 25 percent of the fires in this study involved both alcohol use and smoking. This comprehensive study found a number of interesting differences in different populations.76 Location: Fire fatality data were available for three areas (Baltimore City, 4 large counties, 19 small counties) that represent, on the average, differing styles of living conditions (urban, suburban, rural). See Figure 12.69 A value of 1 in actual/ census indicates fatalities identical to population group proportion in census. In all three locations (and consequently in the state of Maryland as a whole), the distribution of actual versus census-predicted occurrences of fire deaths as a function of age of fire victims indicates a similar trend. The age group 50–60+ shows a substantial predisposition to being fire victims (approximately two times census expectation i.e., 2.0), whereas the age group 10–39 is well below the casualty rate predicted from census data alone (i.e., approximately 0.6). For the state of Maryland, on average, the age group 0–9 fatality rate agrees with the census prediction (observed casualties, 21.6 percent of the total; predicted casualties from census, 19.0 percent). However, the actual/census value for Baltimore City (1.39) is sufficiently different from the 19 small counties (0.74) that a location-specific cause may be indicated for the 0–9 age group.76


34

FIGURE 12. Fire fatalities as function of location and age. The ratios of observed fire fatalities compared to random occurrence based on population census are given for the state of Maryland and three subdivisions. Values greater than 1 indicated a greater than random chance of becoming a fire fatality in a given age group.76 Sex: The male-female distribution among fire fatalities as a function of age showed trends similar to the previously discussed overall distribution except for a pronounced minimum of female fatalities in the age group 30–39 (0.32 compared to 0.775 for men in the state of Maryland and observed in all three locations) and a noticeable increase in female fatalities (1.34) in the age group 0–9, compared to males (1.00).76 At all ages, the absolute number of male fire deaths exceeded that of females (on the average, by a factor of 1.5/1 and is particularly pronounced in the age group 30–60). Considerable fluctuations in the male-female ratios were observed in the various locations within the state. High consumption of alcohol by men, which has a profound effect on the probability of becoming a fire victim, is a key factor in the male/female ratio being substantially in excess of 1 beyond the age of 20.76 Race: The distribution of fire fatalities as a function of race and age shows a very substantial contribution to black fatalities in the age group 0–9 (1.66) which is well above


35

the census prediction, as compared to low values for white fatalities in the same age group (0.65). As a consequence, the age distribution curves for the black population have two age group peaks (0–9 and 60+), while the corresponding curve for whites has only one peak (50–60+). This pattern is particularly pronounced in Baltimore City and the four large counties.76

FIGURE 13. The involvement of alcohol on the absolute number of fire fatalities as a function of age and blood alcohol level. Alcohol of 0.1% represents the legal definition of drunkenness. For each age group, the fraction of fatalities with alcohol in excess of 0.1% and the male/female ratios are given. In the age group 30– 59, more than half of the fatalities have greater than 0.1%. Male deaths exceed female deaths in all instances where alcohol exceeds 0.1%.76 On an absolute basis, fatalities among the black population, averaged for the state of Maryland, always exceed the census-predicted values, with a particularly low value to predicted white/black ratio (0.13) in the age group 0–9. In some locations, however, such as in Baltimore City, this ratio is near or above 1 for the age group 30–65+, as are the ratios in most age categories of the 19 small counties. Indeed, the probability of being involved in fire is very situation dependent.76 Alcohol: The involvement of alcohol with fire fatalities is shown in Figure 13. With increasing age (up to 60), the fraction of casualties with blood alcohol levels in excess of 0.1 percent (the legal limit for drunkenness) raised rapidly to approximately 70 percent of


36

all fatalities in the age group 30–59, with a decline to 39 percent in the age group 60+. This pattern of very substantial consumption of alcohol prior to becoming a fire fatality parallels the substantially higher alcoholism rate of men in these age groups. Men account for more than two-thirds of the heavily intoxicated cases. Fifty percent of all fire fatalities above the age of 20 show an alcohol level above 0.1 percent. Drugs other than alcohol were rarely found in these fire victims.76 The fraction of fire victims in the Maryland study with carboxyhemoglobin (COHb) levels in excess of 50 percent was 60 percent This distribution is shown below:34

Distribution of Fire Victims According to Blood CO Saturation Levels COHb (%)

No. of Victims

%

0–9

48

9

10–19

42

8

20–29

37

7

30–39

38

7

40–49

43

8

50–59

58

11

60–69

79

15

70–79

111

21

>−80

74

14

TOTAL

530

100

Measurements of hydrogen cyanide showed that a substantial number of fire victims with high carbon monoxide intake had also been exposed to substantial amounts of hydrogen cyanide. Whether the cyanide intake makes a significant contribution to the final outcome was difficult to assess, since the time sequence of inhalation of the two gases was not known. However, concentrations that were considered possibly toxic by the authors (1–2 µg/ml) were found in 24% of the cases where determinations were made, and probably toxic concentrations (>2.0 µg/ml) were found in 10% of the cases.34 In the Maryland study, a number of the fire victims with COHb levels below 50 percent (and therefore thought not to have died from that cause alone) were found to have ingested substantial, but also subfatal, doses of hydrogen cyanide.76 A second cause of death cited from seemingly sublethal carbon monoxide uptakes was that the condition of the cardiovascular system of fire victims, expressed in terms of blood flow obstruction in the main heart blood vessels, which was substantially inferior to that of the comparable population at large.59 One of the surprising findings of the Maryland study was the amount of heart disease, expressed in terms of coronary artery stenosis, found in the fire victims and, in particular, in the youngest age group. The maximum narrowing found in the coronary arteries of the victims subdivided into age groups is as follows:34


37

CORONARY ARTERIAL NARROWING IN FIRE VICTIMS* Age

0–24%

25–49%

50–74%

75–89%

90–100%

Total

20–39

16

5

6

6

8

41

40–49

6

1

3

2

9

21

50–59

4

1

5

5

11

26

60–69

2

1

3

3

11

20

70+

1

0

2

0

8

11

29

8

19

16

47

119

TOTAL

(24.2%)

(6.7%)

(16.0%)

(13.4%)

(39.4%)

(100%)

*

Maximum observed in any one coronary branch.

Of the victims in the youngest age group (20 to 39 years), eight had more than 90 percent narrowing in at least one segment of their major coronary arteries. In addition to the unexpected amount of heart disease in the young, of the 119 victims, 40 percent had at least one location of 90 percent or more narrowing and more than half had greater than 75 percent narrowing.34 When the relationship between blood carbon monoxide levels and coronary artery stenosis was examined, however, no constant relationship between the two factors was found. More victims with significant heart disease achieved a higher than 50 percent carbon monoxide saturation than died with lower levels. Further to explore the relationship between blood carbon monoxide content and coronary artery narrowing, men and women were studied separately because of the reported different pattern of atherosclerosis in the sexes. Of the 85 men studied, 44 had significant heart disease and of these victims 13 succumbed to lower than 50 percent carbon monoxide levels. However, 31 of those with significant heart disease achieved greater than 50 percent carboxyhemoglobin levels before death, suggesting that those with cardiovascular disease do not necessarily succumb at a lower carboxyhemoglobin level.34 The authors suggested that preexisting heart disease contributes to inability to escape from the fire but does not necessarily contribute to early death. This incapacitated group would then continue to inhale and to increase their amount of carbon monoxide. This cardiac-based incapacitation would also explain the high incidence of heart disease because heart disease would “select” them to be fatalities.34 The contribution of inhaled soots and adsorbed materials or of irritating gases, such as a aldehydes or hydrochloric acid, was not known. Heavy concentrations of inorganic metals (lead, antimony, and others) and adsorbed pulmonary irritants were observed in the soots that were deposited throughout the trachea and lung tissues. Acetaldehyde was also recovered from lung specimens


38

FIGURE 14. Medical causes leading to fire fatalities. Shaded boxes indicate fatal out comes.76 of fire victims. The contributions of the soots and adsorbed materials to breathing difficulties (such as lung edema) are likely to be considerable, but their specific contributions to fatalities were not clear. They are probably a minor factor in the “rapid” fatality cases, but may be significant in “delayed” fatalities from pulmonary causes where the soot deposits may play a contributory role.76 A summary of the Maryland findings is shown in Figure 14. The available quantitative information concerning the numbers and nature of fire deaths that occur more than six hours after the fire exposure was labelled as approximate. However, the involvement of toxic gases is the primary cause of fire deaths, i.e., 75 percent of all fatalities are due to toxic gas ingestion.76 As seen from the above studies, fire fatalities are due largely to carbon monoxide, compounded by hydrogen cyanide, aldehydes, such as acrolein, other irritants, alcohol and heart disease. Run nearly parallel to the Maryland study was a study in the UK. This study contrasted data from Scotland with data from other parts of the UK. The project started in 1976, was carried out by the Department of Forensic Medicine and Science at the University of Glasgow. For the first five years the study was confined to the Strathclyde area of Scotland (surrounding the city of Glasgow, and hereafter called Glasgow); a total of 227 fire deaths were investigated, including both pathological and toxicological aspects. In 1981 it was extended to include a further 71 cases from other parts of the United Kingdom to validate the conclusions of the Glasgow study nationally.33,80–83


39

FIGURE 15. Frequency distribution of percent COHb in fire fatalities.80 Most of the deaths were in single fatality fires in dwellings, in which the fire was restricted to the room of origin. The fires occurred particularly during the winter and early spring, and often over the weekend. Old people were especially vulnerable.80 Severe burns had been sustained in about 80 percent of cases, although it was not possible in general to establish to what extent they had occurred after death or whether they were a cause of death. The respiratory tract was injured in more than 70 percent of the victims, and most had inhaled smoke and fire gases, leading to soot deposition in the airways and an increase in the level of carboxyhemoglobin (COHb) in the blood.80 The investigators concluded that carbon monoxide was the cause of death in 51 percent of cases in the UK study (with the assumption that lethal levels are those where COHb>50%) (54 percent in Glasgow), and was implicated in the death of 37 percent of the other UK cases (31 percent in Glasgow).80 COHb distribution for the Glasgow study is shown in Figure 15.80 The incidence of heart disease and surface burns versus COHb is shown in Figure 16. This figure indicates that 37% of the victims died with less than 35% surface burns.


40

FIGURE 16. Diagram showing the incidence of burn injuries versus percent COHb in fire fatalities. Fatalities with heart disease are indicated by open circles. The vertical line is set at 35% surface burns, considered the fatal threshold. The horizontal line is set at 50 percent COHb above which CO is considered probably fatal in normal healthy adults. The predominance of heart disease in less than 50 percent COHb cases was considered noteworthy.80 In the Glasgow study younger and older persons were more likely to be victims, while those aged 10–39 were much less likely to be victims of fire as shown as follows:80 Age No. No. % of % distribution of Scottish Group Males Females Fatalities population 0–9

11

8

20.4

15.8

10–19

4

1

5.4

17.8

20–29

0

2

2.2

13.8


41

30–39

3

1

4.3

11.6

40–49

6

3

9.7

11.5

50–59

7

4

11.8

11.5

60–69

14

5

20.4

10.2

70–79

6

6

12.9

6.0

80–

3

9

12.9

1.9

This shows once again the additional vulnerability of the very young and old in fires and is in agreement with other studies. Cyanide gas, produced in the course of most fires, was estimated to be a factor in 33 percent of the deaths in the UK study (24 percent in Glasgow). Although there were few cases in which cyanide might have caused death.80 One of the most important contributing factors in the deaths examined in Glasgow was alcohol: 50 percent of all fatalities had alcohol in their blood, and in 38 percent of the cases the level was above 150 mg/100 ml blood. This would have been enough to cause marked symptoms of intoxication and would have severely impaired the ability of those involved, either to fight the fire or to escape from it.81 In the UK segment of the study the percentage of victims who had alcohol in their blood was similar but the quantity of alcohol which had been consumed was much lower: only 14 percent had blood alcohol concentrations above 150 mg/100ml. It is probable that the Glasgow region is not typical of the UK as a whole and that the figures reflect the social pattern of that area. Data are given as follows:81

Blood alcohol concentrations in fire deaths Incidence Concentration mg/100 ml blood

UK Study No.

Glasgow Study

%

No.

%

Negative

38

54

113

50

50

15

21

10

4

50–100

5

7

10

4

100–150

3

4

8

4

150–200

5

7

14

6

200–300

4

6

42

19

300 and above*

1

1

29

13

71

101

227

100

Total * Highest concentrations observed:

UK study 376 mg/100 ml. Glasgow study 585 mg/100ml.


42

2.7 EFFECTS OF HEAT AND OTHER FACTORS The fire environment includes more than just carbon monoxide. It includes heat, oxygen depletion, carbon dioxide and other toxic gases. In this section these other factors are discussed in additional detail. Let us first examine heat. Indeed, many fire victims sustain burns. Unfortunately one can seldom determine whether death occurred before or after the victims sustained the observed burns or other effects of severe heat exposure. Heat over 50°C is life threatening. Heat enters the body mainly through the skin and usually increases the peripheral blood flow. This effect causes an increased heat conductivity of the periphery and, therefore, an increase of temperature of the body core. Profuse sweating, which usually commences a few minutes after heat exposure, may, through evaporation cooling, counteract the overheating with air temperatures up to 60°C. In moist air this limit will be reached at lower temperatures. The more heat enters the body, the greater the imbalance of physiological factors, such as the temperatures of different parts of the body or of the circulatory system. Signs of breakdown occur. The rise of the average body temperature is a valuable indicator of this stress.84 Concerning rescue from distress caused by heat, the “survival time” is a less decisive factor than the span of time in which man is still able to act, i.e., “escape time.” Figure 17 provides an estimation of escape time.84 The chart holds for dry, motionless air, with equality of air and radiation temperature. According to the authors, one must anticipate the possibility of incapacitation when the average body temperature rises by as little as one degree (C). Acclimation is possible since firemen frequently experience a 1–2°C body temperature rise in fires.85 The line of Figure 17 is calculated on the assumption of a subject with a heat capacity of 50 calories per degree (C), a projection surface of 1.2 sq. M., an evaporation from skin and lungs of 250 calories per hour, a metabolic heat production of 250 calories per hour and heat permeability of clothes (worn, above 80°C) of 5 calories per square meter per hour per degree (C). Figure 17 demonstrates the safe periods in which man is still able to act. This diagram is only approximate and restricted to passive overheating, including only moderate exercise, like standing or walking. Persons with fever or doing hard work may withstand a much higher increase of temperature, because the consequences of active and passive hyperthermia differ. With extremely high temperatures and correspondingly short period of heat tolerance, the heat capacity of thick clothing may lengthen periods by one minute or more.84 If a person is exposed to a hot environment, especially if the humidity is high and the person active, there is a danger of incapacitation and death due to hyperthermia. Incapacitation can occur for some people by breathing air as low as 65°C.86 Moritz and coworkers87–88 studied the effects on pigs of exposure to air temperatures ranging from 70°C to 550°C for varying lengths of time. In the extremes, exposures on the order of 15 minutes to an air temperature of 80°C or on the order of 30 seconds to air temperatures greater than 500°C were capable of causing acute hyperthermic death. During exposure the animals breathed air


43

FIGURE 17. Average “escape time” for lightly clad man in surroundings of high temperatures. Wall and air temperatures are equal: no wind except the natural uplift. The straight line is calculated on the assumption that a rise of one degree (C) of total body temperature is critical in determining the limit of escape time.84 at room temperature. At temperature extremes the mechanisms of death were different. In the long exposures at lower temperatures there was little or no cutaneous burning and death appeared to result from peripheral vascular collapse. In the case of brief exposure to high air temperature, there was severe general cutaneous burning with circulatory failure of central rather than peripheral origin. The cause of the central circulatory failure was traced to the rapid liberation of potassium from erythrocytes in the heated cutaneous and subcutaneous tissues, with consequent damaging effects on the heart of the liberated potassium. Figure 18 shows results of 71 individual pig exposures. For 49 pigs, 90% of


44

their cutaneous surface was exposed to heat. For 22 pigs, hot air was breathed as well, or larger animals were used, or animals were anesthetized after rather than before exposure. No significant differences were observed so all data were included on one chart.

FIGURE 18. Effect of Time Elevated Temperature on Injury to Pigs.86 The upper limits of exposures in which pigs survived without either cutaneous burning or total systemic hyperthermia are indicated by the first line (I). Exposures lying below this line failed to cause lasting effects. Exposures lying between the first and second lines resulted in mild or localized burning. The second line (II) represents the approximate threshold at which generalized hyperemic burning occurred. The third line III represents the threshold at which the burned skin and subcutaneous tissue underwent coagulation. The skin of most pigs that received exposures above this threshold was pale and the loss


45

of elasticity of the coagulated superficial tissues resulted in the formation of deep fissures when the extremities were flexed. The uppermost curve (IV) represents the approximate threshold at which rapidly fatal systemic hyperthermia occurred. Most pigs receiving exposures in excess of this threshold died within a few minutes after the oven had been lifted from their exposure platform, usually within 15 minutes.87 The most constant postmortem finding in animals that died of hyperthermic shock within thirty minutes of the exposure was the presence of hemorrhages throughout the internal viscera. These were seen most frequently and prominently beneath the endocardium of the right and left ventricle.87 It is interesting to note that pigs showed little pulmonary edema even on exposure to very hot gases. Dogs and goats, however, on similar exposure showed moderate to severe pulmonary edema which was a result of circulatory failure.87 In the tests with pigs, all pigs that died during the early post exposure period had rectal or heart’s blood temperatures of 42.5°C or higher. No pig whose rectal temperature rose above 44°C survived more than a few minutes. Eleven of fifteen animals with rectal temperatures 43–44°C died and four of thirteen animals with rectal temperatures 42– 43°C died.89–90 Cardiac dysfunction and edema have been noted in heat stroke patients whose body temperatures have reached 40°C.91 Work with monkeys has noted damage to intestine walls when core temperatures reach 40°C releasing a bacterial lipopolysaccharide (LPS) into the portal vein. That LPS not removed in the liver enters the systemic circulation causing vascular collapse, shock, and death.92–93 Morris, et al., have demonstrated bacterial translocation in studies of sheep exposed to smoke from cotton toweling and to thermal injury or to thermal injury alone. This was observed not only in the mesenteric lymph nodes but in liver and lung for thermal injury and liver, spleen, kidney, and lung for thermal injury plus smoke. This lends support to the theory that systemic infections may arise from the translocation of organisms across the wall of the intestine. Animals were sacrificed at 48 hours. Bacteremia combined with damage that occurs to the immune system in the shocked, traumatized patient would set the stage for multi-organ failure.94–95 Pain from the application of heat to the skin occurs when the skin temperature at the depth of 0.1 mm reaches 44.8°C. Human exposures at temperatures between 160° and 200°C result rapidly in intolerable pain. Figure 19 summarizes physiological effects of elevated temperatures. Exposures to fire gases at temperatures of 300 to 400°C would cause unbearable pain in less than 7 seconds, with collapse after taking a few steps.89 Heat can interact in combination with carbon monoxide. The combined effects of heat and carbon monoxide have been assessed in mice and rats.96 In mice the 1 hr LC50 was 2524 mg/m3 at 25°C and 836 mg/m3 at 36°C. Survival times at 25°C and 36°C were as follows:


46

FIGURE 19. Physiological Effects of Elevated Temperatures.88 CO Concentration (ppm)

Survival Time 25°C

(min) at 36°C

634

–

94

1005

–

40

1595

120

25


47

2525

51

8

4000

24

6

For rats, purebred males, weighing 170–220 g were subjected in groups of 16 animals to 600 ppm CO for 1 hr each day for 23 consecutive days. Data were as follows:

Blood COHb Concentration (X±SE) in Subacute Toxicity Experiment (%) Time Before Experiment

Group A (35°C+CO)

Group C (25°C+CO)

0.52±0.06

3.00±1.60

6.50±1.10 8.50±3.20 25.00±5.80 39.00±4.85 46.5±3.20

6.60±1.22 14.50±3.40 25.50±5.00 27.00±3.60 31.50±4.00

5 min 10 min 20 min 40 min 60 min

40.00±1.80 29.50±2.80 27.50±4.00 11.00+2.50 5.50±0.80

21.00±3.65 23.00±1.92 11.50±4.05 5.50±3.00 2.00±0.75

Before Experiment

0.27±0.06

0.72±0.08

42.67+2.10 31.58±2.16 23.31±2.56 22.75±1.38

30.92±1.99 26.92±2.92 22.42±1.85 22.32±2.10

During Experiment 5 min 10 min 20 min 40 min 60 min After Experiment

After Experiment Day 1 Day 7 Day 17 Day 23

Control animals were kept at each temperature. The animals exposed to CO at 36°C built CO to a higher level initially, but by the 23rd day both groups were equivalent. Hemoglobin increased significantly in rats exposed to heat and CO over the 23 day period, as animals built tolerance to the exposure conditions. The animals initially exposed to 36°C and CO showed a 2.5°C higher rectal temperature than controls at 36°C. By day 23 this had declined to 0.8°C. It is known though that rodents are particularly sensitive to temperature.96 Carboxyhemoglobin is not elevated in all fire victims. Flash fire victims die from thermal trauma, without elevation of blood carboxyhemoglobin or with COHb values at a low level if some smoke has been inhaled prior to a victim’s being engulfed in the flash fire.68,97–99 Fires can produce atmospheres low in oxygen and high in carbon dioxide. Approximate tolerance times for man for each are shown below:


48

Tolerance Times for Exposure to Reduced Oxygen Atmospheres Length of Exposure

Oxygen Limit %

5 min

9

30 min

11

2 hr

14

4–8 hr

15

24–72 hr

16

14 days

17

Tolerance Times for Exposure to Carbon Dioxide Length of Exposure

Carbon Dioxide Limit (In Air) %

5 min

5.0

30 min

4.0

2 hr

3.5

4–8 hr

3.2

24–72 hr

2.0

14 days

1.5

With low oxygen the respiration rate increases, then becomes irregular and compulsive, followed by collapse (Figure 20). Carbon dioxide induces asphyxia through exclusion of oxygen. In initial stages the respiration rate increases. CO2 at 3% doubles lung ventilation. The limit of CO2 tolerance is 10%, with unconsciousness in 10 minutes.89 Studies with rats show that low oxygen (14%) and elevated CO2 (to 5.4%) decrease the mean survival time but do not change the final COHb at death.59,100 In a crucial series of experiments goats were chosen for study because their body surface area to body weight ratio is nearly identical to man. Goats were exposed to inhalation of 3 percent oxygen, 2.7 percent carbon monoxide, and 3.0 percent oxygen plus 2.7 percent carbon monoxide plus 7.0 percent carbon dioxide. In some experiments body temperatures of subjects were raised to between 42.5 and 43.6°C (rectal). Carbon monoxide in conjunction with low oxygen showed a shortened time to death. The addition of CO2 slightly accelerated time to death. Increased temperature markedly increased the susceptibility of goats to anoxia and hastened the time of death from exposure to all gas mixtures studied. Most importantly, death of animals at elevated temperatures occurred at markedly decreased COHb levels, a result not seen with low oxygen plus carbon monoxide alone. Data are shown below:101 Number of Respiration Ceased Last Gasp %COHb at 5 Animals (@ min) (@ min) min. 2.7% CO/in air

5

3.0

7.2

86


49

2.7% CO/3.0% O2/in N2

9

1.9

4.8

90

3% 02

3

4.6

6.9

–

2.7% CO/3.0 % O2/7.0% CO2 in N2

5

1.3

4.1

91

4.2% O2/in N2/heat

4

2.1

3.7

–

2.7% CO/in air/heat

3

2.5

4.4

79

2.7% CO/3.0% O2/in N2/heat

8

1.3

2.9

38

2.7% CO3.0% 02/7.0% CO2 in N2/heat

2

1.1

2.8

49

A variety of factors can complicate human response to carbon monoxide poisoning. Physical activity of the victim, while hard to assess, also plays a role. It is known that in a healthy individual, severe toxic signs including collapse can occur at COHb levels of 30– 40 percent. An active individual would be severely affected at 25–30 percent, and with light physical activity, incapacitation at 27–37 percent. This is in addition to more rapid uptake of CO for an active individual. Also in fire, once victim knockdown occurs, high CO2 levels or oxygen depletion can play a role in time to death.64 Indeed, studies in monkeys show that the slow, insidious onset of CO intoxication may result in a victim being unaware of the predicament until he suddenly reaches the catastrophic stage where normal body functions can no longer be maintained, and the victim passes rapidly into a state of severe incapacitation and semiconsciousness. Whether or not such severe incapacitation occurs will depend upon the amount of CO inhaled and upon how active the victim is. Thus with animals sitting in chairs, it was noticed that when they were very quiet and relaxed they tended to reach the end of the exposure (30 minutes) with only minor signs of incapacitation, while if they were active, especially towards the end of an exposure, they were likely to pass into a state of semiconsciousness. In work where monkeys were placed in a chamber where they were active and free to move about, and trained to perform a behavioral task involving a certain amount of exercise and the application of psychomotor skills, the animals were found to be severely intoxicated after a 30 minute exposure to 1000 ppm CO with COHb levels of approximately 30 percent, while 40 percent COHb levels were normally necessary to produce severe intoxication in the chairbound animals.102


50

FIGURE 20. Effects of Reduced Oxygen Atmospheres. 89 2.8 EFFECTS OF DISEASE OR DRUGS As has been shown in earlier sections, diseases are clearly a factor in susceptibility to carbon monoxide. It is logical that individuals suffering from systemic hypoxemia (e.g., as in anemia, cardiopulmonary disease, congestive failure) or increased oxygen demand (e.g., thyrotoxicosis, fever) might suffer acceleration or aggravation of these pathologic processes under circumstances where carboxyhemoglobin might decrease their blood oxygen content or availability.103


51

Indeed groups at special risk include pregnant women, fetuses and young infants, the elderly, individuals with obstructed coronary arteries, individuals with congestive heart disease, individuals with peripheral vascular or cerebrovascular disease, individuals with anemia, individuals with genetically unusual forms of hemoglobin, individuals with chronic obstructive lung disease, individuals using CNS depressant drugs, and individuals newly at high altitude. Effects of cardiovascular disease on carbon monoxide poisoning have been discussed by Stewart.104 The acute effects of CO on myocardial function in healthy adults, in patients with coronary artery heart disease and in patients with non-coronary heart disease have been examined. A rapidly increasing COHb saturation to around 9 percent over 30–120 seconds in patients with no evidence of coronary heart disease results in increased coronary blood flow, increased oxygen extraction ratio by the myocardium and an insignificant decrease in coronary sinus oxygen tension. In patients with coronary heart disease the rapid increase in COHb did not result in a significant increase in coronary blood flow; but the oxygen extraction ratio by the myocardium was increased, the coronary sinus tension decreased significantly, and a significant decrease in the lactate extraction ratio and the pyruvate extraction ratio were observed. Thus a potentially serious state could result from the inhalation of CO by the patient with advanced coronary heart disease incapable of responding to the anoxic stress by increasing coronary blood flow.104 Investigators have demonstrated that in patients with advanced coronary artery disease, angina pectoris exercise tolerance is significantly decreased following exposure to low concentrations of CO sufficient to increase their COHb to 5 percent.104 Stewart carried the interpretation of these data one step further than did the original investigators by suggesting that there is no level of COHb which does not exert a significant effect upon a diseased cardiovascular system. Individuals with coronary heart disease will be stressed to some degree by any exposure sufficient to cause an increase in the COHb level. It is not possible therefore to set a “no effect” level of CO for such individuals.104 Stewart has provided a norm for healthy human response to various concentrations of COHb as follows.104

Human response to various concentrations of COHb Blood saturation % COHb

Response of healthy adult

0.3–0.7

Normal range due to endogenous CO production

1–5

Increase in blood flow to vital organs to compensate for the reduction in oxygen of the blood.

Blood saturation Response of healthy adult % COHb 2–9

Response of patient with severe heart disease

Heart patient may lack sufficient cardiac reserve to compensate for loss of the oxygen carrying capacity of the blood.

Response of patient with severe heart disease

Exercise tolerance reduced: Visual Less exertion required to induce chest


light threshold increased

52

pain in patients with angina pectoris

16–20

Headache; visual evoked response May be lethal for patients with severely abnormal compromised cardiac function

20–30

Throbbing headache, nausea; fine manual dexterity abnormal

30–40

Severe headache; nausea and vomiting; cyncope

–50–

Coma, convulsions

67–70

Lethal if not treated

Discussions in this report have already shown the approximate nature of such norms. A particularly interesting study is that of a survey of all deaths that were certified by the Cuyahoga County Ohio Coroner’s Office from the years 1958 through 1980, wherein asphyxia by carbon monoxide was the primary cause of death and a natural disease was the “other” diagnosis or vice versa. For the purposes of the study, the primary cause of death was defined as the disease or injury responsible for initiating the train of events, brief or prolonged, which produced the fatal end result. The “other” condition was that condition or conditions contributing to death but not related to the primary cause of death. The Cuyahoga County Coroner’s Office serves Cleveland, OH and its suburbs.105 During this 23-year period the Cuyahoga County Coroner’s Office certified 38 such deaths. These were divided into two groups. Group 1 consisted of 28 cases where all diagnosis including the levels of carboxyhemoglobin were documented by complete postmortem examination. All major coronary arteries were studied in detail to determine the severity (mild, moderate, and severe) and extent (focal or diffuse) of the atherosclerotic process, by cross-sectioning these arteries at about 2- to 5-mm intervals. A gross examination estimate of percentage occlusion was thus made. The myocardium was sliced at about 1-cm intervals to look for areas of acute or chronic myocardial infarction. Microscopic sections of the coronary arteries and myocardium were examined in all of these cases. The left coronary artery with its anterior descending and circumflex branches and the right coronary artery with its posterior descending branch were considered major coronary arteries for the purposed of this study. Group 2 consisted of ten cases where the diagnosis of the “other” condition was based on review of medical records, including results of coronary angiogram, serum enzymes, and clinical history. Autopsy was not performed on these ten cases. In all cases, hospital charts, office records of private physicians, and eyewitness accounts were reviewed.105 In cases where death occurred immediately following exposure, chemical tests were performed to determine the level of carboxyhemoglobin. In instances where death occurred several days following exposure to carbon monoxide, such tests were not carried out. Blood levels of ethyl alcohol were measured in all cases. Blood levels of drugs were measured in twelve cases belonging to Group 1 and in five cases belonging to Group 2.105 For a control group all deaths that were reported to the Cuyahoga County Coroner’s Office during the years 1958 through 1980 in individuals 35 to 86 years of age in whom the carboxyhemoglobin was 60 percent and more were reviewed. A complete autopsy had been performed in each of these cases. The coronary arteries and the hearts were


53

examined adhering to the techniques that are outlined for the examination of cases in Group 1. There was a total of 100 cases in the control group.105 The following is a summary of results:105

Summary of Victim Data Age

Carboxy hemoglobin %

Ethyl Alcohol Drugs 30 41 51 61 71 81 Sex Race 10 40 60 De Not Not to to to to to to M F W B to to and layed Pre Ab Tes Pre Ab Tes Total 40 50 60 70 80 90 30 50 More Death sent sent ted sent sent ted Group 1 1 28 Group 2 0 10 Control 22 100

7 10 5 4 17 11 24 4 14

4

0

10

2 4 2 2 9 1 7 3 5

3

0

2

28 10 6 3 59 41 68 32 0

0

100

0

5 23

0

2 10

16

2

8

0

0

5

5

48 52

0

9 72

19

Findings related to heart Number of Cases Heart Weight, g Coronary Atherosclerosis

Myocardial Infarct

Mild Moderate Severe

Recent

415 415 and Old More

History of Exertion Less Yes No Total

Group 1

2

2

24

1

4

20

8

2

26

28

Group 2

–

–

5

0

1

–

–

–

10

10

Control

89

5

6

0

2

13

87

0 100

100

*

Note: Diseased hearts tend to increase in weight.

These data show clearly that severe atherosclerosis is often present in fire victims with low COHb values.105 It should be noted from the Maryland study, however, that findings of coronary atherosclerosis do not necessarily reflect a low COHb case. The role of alcohol is interesting. Two studies, one on rats and one of humans, suggest that alcohol may be an antagonist to CO poisoning. In studies of rats, Hume concluded that if alcohol is present in sufficient quantity to produce a central nervous system depression, the survival time is longer. The depressant effect of alcohol decreases animal activity and thus the rate of CO uptake.106 In a study of records in the UK for 1976–81, carbon monoxide deaths were studied. Deaths were classified by zero blood alcohol, less than .150% and greater than .150 %.


54

The overall mean was .148%. The effect of alcohol was found to be an increase in the COHb percentage at which a given proportion of deaths occurred. For example, 50% of deaths occurred with a COHb concentration of 68% or less without alcohol, but with alcohol less than .150%, only 30% of deaths occurred with 68% COHb or less. Alcohol between .05 and .2% appeared to increase survival. The author speculates that other depressant drugs should have a similar effect.107 These data contrast with time to incapacitation results in rats exposed to 1947 ppm CO at levels of 1.2g/kg, 0.6g/kg and nil alcohol. The presence of alcohol shortened times to incapacitation.108 These latter observations perhaps correlate with those of Barillo and coworkers on a group of 39 fire victims in which victims found in bed had a mean blood alcohol level of .268% compared with a mean level of .88% for those victims found near an exit.109 A study of alcohol-CO interactions on driving performance has shown that alcohol and CO effects are additive and at 12% COHb the combined effects were greater than the sum of the effects of CO and alcohol alone.110 Animal studies also show that behavior can be affected by alcohol plus CO exposures.111–112 The direct role of other drugs in carbon monoxide poisoning in man remains unclear. In one animal study mice were pretreated with phenobarbital, chlorpromazine, or alcohol prior to exposure to 1900 ppm carbon monoxide (CO) or 7.5 percent oxygen O2 environments. Pretreatment for one hour with chlorpromazine or ethanol increased the lethality of mice exposed to both CO and 7.5 percent O2, while one-hour phenobarbital pretreatment had no effect on CO lethality but increased 7.5 percent O2 lethality. Slightly lowered carboxyhemoglobin concentrations (55 percent versus 63 percent) were observed only with chlorpromazine. Unfortunately time to effect was not reported. Studies of red blood cell 2.3-diphosphoglycerate concentrations and rate of carboxyhemoglobin formation in vitro showed that the apparent affinity of hemoglobin for oxygen and CO remained unchanged following drug or alcohol pretreatments. The different effects of the pretreatments on CO and 7.5 percent O2 lethality and the lack of correlation of CO lethality withs carboxyhemoglobin concentrations suggests that there are other factors besides extracellular events directly associated with oxygenation of tissues which are critical determinants of the lethal potential of CO or 7.5 percent O2. Data for one hour pretreatment exposures are shown as follows:113

Effect of 1 hr. Pretreatments on Lethality Associated with Carbon Monoxide (CO) or 7.5% O2 Environments CO lethalitya Dead/Total

%COHb

7.5% O2 lethalityb Dead/Total

Saline

17/30

63±2.0

5/12

Phenobarbital 80 mg/kg, ip

19/32

67±2.1

11/12

Chlorpromazine 20 mg/kg, ip

29/32

55±0.2

11/11

Water

18/30

64±1.9

3/10

Ethanol

25/30

66±4.0

10/10

Pretreatment


55

7.5 g/kg, po Saline

22/30

61±1.8

–

Phenobarbital 160 mg/kg, ip

20/30

69±0.9

–

a

Exposed for 4 hr to 1900 ppm CO. Exposed for 4 hr to 7.5% O2

b

Interestingly, longer pretreatments (24 hr and 3 day) with phenobarbital, chlorpromazine, or ethanol showed no increased toxic effect. 2.9 TIME OF EXPOSURE The time of exposure to carbon monoxide is known to be important. That relationship is difficult to ascertain in after-the-fact studies of human victims. The relationship between conditions of exposure to carbon monoxide and biochemical effects has, however, been investigated in experiments on rats. The magnitude and the time of biochemical disturbances in the tissues resulting from two different exposures consisting of 1 Volume percent CO for 4 minutes and 0.4 Volume percent for 40 min. respectively were compared. In both cases, at the end of exposure the same level of blood carboxyhemoglobin (about 50%) was reached. The biochemical determinations in the blood (pH, glucose, lactate, pyruvate) and brain tissue (lactate, pyruvate) were carried out immediately after termination of the exposure and after periods of recovery. CO exposure resulted in a decreased blood pH, increased level of blood glucose, as well as that of lactate and pyruvate both in blood and brain tissue. These changes were much more pronounced following the “longer-lesser” exposure than after the “shorter-intense” one, although blood concentrations of COHb were the same. The observed phenomenon puts some light on the lack of the correlation between COHb level in blood and field severity of CO intoxication.114 Of course, that different individuals have different behavior to a toxic agent is hardly surprising. Japanese work is particularly interesting. A toxicological study of carbon monoxide was carried out with special consideration to eliminate the effect of carbon dioxide expired by animals in the atmosphere. When 0.6 percent carbon monoxide in air was inhaled, mice did not manifest any toxic symptoms. When a one percent carbon monoxide-air mixture was inhaled, about 30 percent of the exposed mice died from respiratory failure following a violent convulsion within the first 30 minutes. Another 30 percent were alive at the end of 3 hours’ observation, while the remainder died with an almost even death rate in the course of the observation time. At a concentration of 1.5 percent carbon monoxide all the mice were killed within 30 minutes. Thus, the minimum lethal concentration was around 1.0 percent, but a normal distribution curve was not obtained for the death rate of mice by the inhalation of this concentration of carbon monoxide. With over 1.5 percent carbon monoxide, nearly 75 percent of mice died within ten minutes as shown in Figure 21, but others were alive two or three times longer. There were very susceptible, comparatively tolerant and very tolerant mice relative to the development of respiratory failure. Attempts were made to test whether the variance in the susceptibility was due to an intrinsic nature of the


56

FIGURE 21. Distribution of the death rate of mice in 1.0% (A) and 1.5% (B) carbon monoxide poisoning. Each column represents each death rate at ten minute intervals within three hours of exposure. The number of mice used is given in parenthesis.115 individuals or not. Surviving mice were exposed again to 1.0 percent carbon monoxide four weeks after the first exposure. The same susceptibility could not be reproduced in each animal. Furthermore, when the same trials were repeated with the animals having tolerated over three hours in 1.0% carbon monoxide, the distribution of death rate was similar to that at the first exposure. Therefore, the variance in the tolerance does not appear to be due to differences in the intrinsic nature of animals but to more subtle factors.115 2.10 CONCLUSIONS Several statements can be made in conclusion. While carbon monoxide exposure is seldom in its ultra-pure state, human exposure to city gas and exhaust gas, however, shows that a significant percentage of exposed individuals die from carbon monoxide


57

poisoning at COHb levels thought by some to be less than “normal,” i.e., less than 50 percent COHb. Nearly 20 percent of individuals may die at such levels. While persons with cardiovascular and other diseases are included in that group, it also includes other individuals who do not exhibit identifiable pathology. Persons with identifiable pathology do not necessarily die below 50 percent COHb. The length of time of exposure to CO is important, as are the level of victim activity and the age and the physical condition of the victims. Why do very young children occasionally survive although they had been exposed to the same atmosphere as their dead parents? Clearly carbon monoxide poisoning is much more complex than the simple percentage of COHb in the blood of the victim. Therefore, without additional information, a COHb value of X percent (below 50 percent) does not allow a ready conclusion for a given victim. For identical exposures different individuals exhibit different symptoms and outcomes. In the case of fire exposures, twice the number of victims are in the less than 50 percent COHb category than for automobile exhaust victims. Fire victims, however, have very different age distribution and level of infirmity than do automobile exhaust victims. Yet despite the presence of different materials in the environment the fire fatality/COHb profiles in Japan in the early 1960s, in Denmark in the late 1960s and 1970s, in the United States in the late 1970s, and in the UK in the late 1970s are all very similar. Despite population and environmental differences, the role of carbon monoxide in fire deaths is the same. Carbon monoxide is the prime source of fire fatalities. In fire victims males predominate and alcohol is a key factor. Most victims have burns. Clearly exposure to heat and hot fire gases plays a role, difficult to evaluate, yet known to markedly lower COHb levels essential for death. Finally, the determination of COHb in the blood of victims has a variety of opportunities for error. Care must be exercised in COHb determinations as well as in interpretation of results.

ACKNOWLEDGEMENT The tables on pages 10 (9), 19 (16) and 72 (105) are Copyright ASTM and are reprinted by permission. Figure 11 is British Crown Copyright 1978 and is reprinted by permission. The permission of publishers for tables and graphs is acknowledged with appreciation.

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29. K.Kishitani, “Study of Injurious Properties of Combustion Products of Building Materials at Initial Stage of Fire,” J. Faculty of Engineering, Univ. Tokyo, (B), 31, 1–35 (1971). 30. A.M.Dominguez, “Symposium-Fire and Incendiarism. Problems of Carbon Monoxide in Fires,” J. Forensic Sciences, 7(4), 379–393 (1962). 31. A.O.Gettler, and H.C.Freimuth, “The Carbon Monoxide Content of the Blood Under Various Conditions,” Am. J. Clin. Pathology, 10, 603–616 (1940). 32. H.Gormsen, N.Jeppesen, A.Lund, “The Causes of Death in Fire Victims,” Forensic Science Int., 24(2), 107–111 (1984). 33. R.A.Anderson, A.A.Watson, and W.A.Harland, “Fire Deaths in the Glasgow Area: 2 the Role of Carbon Monoxide,” Med. Sci. Law, 21, 288–294 (1981). 34. M.M.Birky and F.B.Clarke, “Inhalation of Toxic Products From Fires,” Bull.N. Y. Acad. Med., 57, 997–1013 (1981). 35. A.Silcock, D.Robinson, and N.P.Savage, Fires in Dwellings—and Investigations of Actual Fires, Part II: Hazards from Ground-Floor Fires, Part III: Physiological Effects of Fire. Building Research Establishment Current Paper, Department of the Environment, CP 80/78, December 1978. 36. H.R.Wetherell, “The Occurrence of Cyanide in the Blood of Fire Victims,” J. Forensic Sciences, 11(2), 167–75. 37. S.R.Mohler, “Air Crash Survival: Injuries and Evacuation Toxic Hazards,” Aviation, Space, and Environmental Medicine, 46(1), 86–88 (1975). 38. M.M.Birky, M.Paabo, and J.E.Brown, “Correlation of Autopsy Data and Materials Involved in the Tennessee Jail Fire,” Fire Safety Journal, 2, 17–22 (1979). 39. R.Cote, W.D.Wall, and T.Klem, “Investigation Report of the Ramada Inn Central Fire, Fort Worth, Texas, June 14, 1983,” National fire Protection Association, No LS-10, 44 pp.; and report of Southwestern Institute of Forensic Sciences to Institute of Forensic Medicine, Ft. Worth, TX, Nov. 14, 1983. 40. F.M.Esposito and Y.Alarie, “Inhalation Toxicity of Carbon Monoxide and Hydrogen Cyanide Gases Released during the Thermal Decomposition of Polymers”, J. Fire Sci., 6, 194–242 (1988). 41. B.C.Levin, J.L.Gurman, M.Paabo, L.Baier, L.Procell, and H.H.Newball, “Acute Inhalation Toxicity of Hydrogen Cyanide,” Toxicologist, 6, 59 (1986). 42. I.Sunshine and B.Finkle, “The Necessity of Tissue Studies in Fatal Cyanide Poisoning,” Int. Arch. Guverbepathol. Gewerbehyg. 20, 558–561 (1964). 43. F.Rieders, Methodology for Analytical Toxicology, CRC Press, 1971, p. 115. 44. I.S.Symington, et. al., “Cyanide Exposure in Fires,” Lancet, ii (July 8), 91 (1978). 45. S.Kays, Handbook of Emergency Toxicology, 4th ed., Charles C.Thomas, Springfield, IL, 1980, 255–256, 287. 46. “Toxicological Profile for Cyanide, Agency for Toxic Substances and Disease Registry,” U.S. Public Health Service, January 1988, p. 41. 47. A.R.Memon, and Y.C.Alarie, “Study of Fire Deaths for the Foundation for Fire Safety Programs,” Graduate School of Public Health, University of Pittsburgh, May, 1985, 72 pp. 48. Y.Alarie, R.Memon, and F.Esposito, “Role of Hydrogen Cyanide in Human Deaths in Fire,” in Fire and Polymers, G.L.Nelson, Ed., American Chemical Society ACS Symposium Series 425, 21–34 (1990). 49. A.Curry, Poison Detection in Human Organs, Charles C.Thomas Publishers, Springfield, IL: 1976, p. 98. 50. N.H.Proctor and J.P.Hughes, Chemical Hazards of the Workplace, J.B.Lippincott Co., Philadelphia, 1977, pp. 287–289. 51. R.J.Lewis and R.L.Tatken, Eds., Registry of Toxic Effects of Chemical Substances, Vol. I, U.S. Department of Health and Human Services, 1979 edition, Cincinnati, Ohio, September 1980. 52. J.L.Bonsall, “Survival Without Sequelae Following Exposure to 500 mg/m3 of Hydrogen Cyanide,” Human Toxicol. 3, 57–60 (1984).


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53. B.P.McNamara, “Estimate of the Toxicity of Hydrocyanic Acid Vapors in Man,” Edgewood Arsenal Technical Report, EB-TR 76023, August 1976, 25 pp. 54. G.E.Hartzell, W.G.Switzer and D.N.Priest, “Modeling of Toxicological Effects of Fire Gases: V. Mathematical Modeling of Intoxication of Rats by Combined Carbon Monoxide and Hydrogen Cyanide Atmospheres,” J. Fire Sciences, 3, 330–342 (1985). 55. T.Sakurai, “Toxic Gas Tests with Several Pure and Mixed Gases Using Mice,” J. Fire Sciences, 7, 22–77 (1985). 56. P.M.Smith, C.R.Crane, D.C.Sanders, J.K.Abbott and B.Endecott “Effects of Exposure to Carbon Monoxide and Hydrogen Cyanide,” Physiological and Toxico-logical Aspects of Combustion Products—International Symposium, National Academy of Sciences, Washington, D.C, 1976, pp. 75–88. 57. R.D.Lynch, “On the Non-Existence of Synergism Between Inhaled Hydrogen Cyanide and Carbon Monoxide,” Fire Research Station, Fire Research Note No. 1035 (May 1975). 58. Y.Tsuchiya, “On the Unproved Synergism of the Inhalation Toxicity of Fire Gases,” J. Fire Sciences, 4, 346–354 (1986). 59. B.C.Levin, M.Paabo, J.L.Gurman, and S.E.Harris, “Effects of Exposure to Single or Multiple Combinations of the Predominant Toxic Gases and Low Oxygen Atmospheres Produced in Fires,” Funaamental and Applied Toxicology, 9, 236–250 (1987); Toxicol., 47, 135–164 (1987). 60. J.C.Norris, S.J.Moore, and A.S.Hume, “Synergistic Lethality Induced by the Combination of Carbon Monoxide and Cyanide,” Toxicology, 40, 121–129 (1986). 61. L.C.DiPasquale and H.V.Davis, “The Acute Toxicity of Brief Exposures to Hydrogen Fluoride, Hydrogen Chloride, Nitrogen Dioxide, and Hydrogen Cyanide Singly and in Combination with Carbon Monoxide, Aerospace Medical Research Laboratory, Wright-Patterson Air Force Base, Ohio, December, 1971, AD-751 442, 13 pp. 62. E.A.Higgins, V.Fiorca, A.A.Thomas, and H.V.Davis, “Acute Toxicity of Brief Exposures to HF, HCl, NO2 and HCN with and without CO,” Fire Technology, 8, 120–130 (1972). FAA Report FAA-AM-71–41, July 1971. 63. B.R.Pitt, E.P.Radford, G.H.Gurtner, and R.J.Traystman, “Interaction of Carbon Monoxide and Cyanide on Cerebral Circulation and Metabolism,” Arch. Environ. Health, 34, 354–359 (1979). 64. D.A.Purser and W.D.Woolley, “Biological Studies of Combustion Atmospheres, J. Fire Sciences, 1, 118–144 (1983). 65. D.A.Purser, P.Grimshaw and K.R.Berrill, “Intoxication by Cyanide in Fires: A Study in Monkeys Using Acrylonitrile,” Archives of Environmental Health, 39, 394–399 (1984). 66. D.A.Purser and P.Grimshaw, “The Incapacitative Effects of Exposure to the Thermal Decomposition Products of Polyurethane Foams,” Fire and Materials, 8, 10–16, (1984). 67. R.J.Lokan, R.A.James and R.B.Dymock, “Apparent Post-Mortem Production of High Levels of Cyanide in Blood,” J. Forensic Science Soc., 27, 257–59 (1987). 68. B.C.Levin, P.R.Rechani, J.L.Gurman, F.Landron, H.M.Clark, M.F. Yoklavich, J.R.Rodriguez, L.Droz, F.M.de Cabrera, and S.Kaye, “Analysis of Carboxyhemoglobin and Cyanide in Blood from Victims of the Dupont Plaza Hotel Fire in Puerto Rico,” J. Forensic Sci., 35(1), 151–168 (1990). 69. B.Ballantyne, “The Forensic Diagnosis of Acute Cyanide Poisoning” in Forensic Toxicology, B.Ballantyne, Ed., John Wright and Sons, Ltd., Bristol, 1974, pp. 99–112. 70. B.Ballantyne, J.E.Bright, and P.Williams, “The Post-Mortem Rate of Transformation of Cyanide,” Forensic Sci., 3, 71–76 (1974). 71. B.Ballantyne, “In Vitro Production of Cyanide in Normal Human Blood and the Influence of Thiocyanate and Storage Temperature,” Clinical Tox., 11(2), 173–193 (1977). 72. B.A.Zikria, D.C.Budd, F.Floch, and J.M.Ferrer, “What is Clinical Smoke Poisoning?,” Ann. Sur., 1975, 151–156. 73. B.A.Zikria, J.M.Ferrer, and H.F.Floch, “The Chemical Factors Contributing to ‘Smoke Poisoning’,” Surgery, 71(5), 704–709, (1972). 74. B.A.Zikria, G.C.Weston, M.Chodoff, and J.M.Ferrer, “Smoke and Carbon Monoxide Poisoning in Fire Victims,” The Journal of Trauma, 12(8), 641–645 (1972).


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75. B.A.Zikria, et al., “A Clinical View of Smoke Poisoning,” Physicological and Toxicological Aspects of Combustion Products-International Symposium, National Academy of Sciences, (Washington, D.C., 1976) pp. 36–46. 76. W.G.Berl and B.M.Halpin, “Human Fatalities from Unwanted Fires,” Fire Journal, 1979, (Sept.) 105–123. 77. B.M.Halpin, E.P.Radford, R.Fisher, and Y.Caplan, “A Fire Fatality Study,” Fire Journal, 1975, (May) 11–13, 98–99. 78. E.P.Radford, B.Pitt, and B.Halpin, “Study of Fire Deaths in Maryland,” Physicological and Toxicological Aspects of Combustion Products-International Symposium, National Academy of Sciences, (Washington, D.C., 1976) pp. 26–35. 79. W.G.Berl, and B.M.Halpin, “Fire-Related Fatalities: An Analysis of Their Demography, Physical Origins, and Medical Courses,” Fire Standards and Safety, ASTM STP 614, A.F.Robertson, Ed., American Society for Testing and Materials, 1977, 26–54. 80. W.A.Harland and W.D.Wooley, Fire Fatality Study—University of Glasgow, Building Research Establishment Information Paper, 1P, 18/79, August 1979, 3 pp. 81. Cause of Death in Fire Victims, BRE News, 58, 8–9 (Winter, 1982). 82. R.A.Anderson, A.A.Watson, and W.A.Harland, “Fire Deaths in the Glasgow Area: 1 General Considerations and Pathology,” Med. Sci. Law, 21, 175–183 (1981). 83. R.A.Anderson, and W.A.Harland, “Fire Deaths in the Glasgow Area: 3 The Role of Hydrogen Cyanide,”Med. Sci. Law, 22, 35–40 (1982). 84. K.Buettner, “Effects of Extreme Heat on Man. Protection of Man Against Conflagration Heat,” J. Am. Med. Assn., 144(9), 732–738 (1952). 85. B.Dupont, “How Much Heat Can Firemen Endure?” Fire Engineering, Feb. 1960, pp 122–24, 173. 86. J.A.Zapp, “Fires, Toxicity, and Plastics,” Physiological and Toxicological Aspects of Combustion Products, International Symposium, National Academy of Sciences, Washington, D.C., 1976, pp. 58–74. 87. A.R.Moritz, F.C.Henriques, F.R.Dutra, and J.R.Weisiger, “Studies of Thermal Injury IV, Archives of Pathology, 43, 466–488 (1947). 88. The Committee on Fire Safety Aspects of Polymeric Materials, Vol. 3, Smoke and Toxicity, Publication NMAB 318–3, National Academy of Sciences, Washington, D.C., 1978, pp. 13–16. 89. A.J.Pryor and C.H.Yuill, “Mass Fire Life Hazard,” Report for the Office of Civil Defense, NTIS AD 642790, pp. 39–53 and 62–69. 90. P.J.Berenson and W.G.Robertson, “Temperature,” Chapter 3 in Bioastronautics Data Book, 2nd Ed., J.F.Parker, Jr. and V.R.West, Eds., NASA, Washington, D.C., 1973, pp. 65–148. 91. D.Zahger, A.Moses, and A.T.Weiss, “Evidence of Prolonged Myocardial Dysfunction in Heat Stroke”, Chest, 95, 1089–91 (1989). 92. P.Gathiram, M.Wells, D.Raidoo, J.Brock-Utne, and S.L.Gaffin, “Portal and Sytemic Arterial Plasma Lypopolysaccharide Concentrations in Heat-Stressed Primates.” Circ. Shock, 25, 223– 230 (1988). 93. S.L.Gaffin, “Heat Stroke, Cardiac Dysfunction, and Edema,” Chest, 97, 1503 (1990). 94. S.E.Morris, N.Navartnam, and D.N.Herndon, “A Comparison of Effects of Thermal Injury and Smoke Inhalation on Bacterial Translocation,” J. Trauma, 30, 639–645 (1990). 95. B.F.Rush, A.J.Sori, T.F.Murphy, S.Smith, J.J.Flanagan, and G.W. Machiedo, “Endotoxemia and Bactermia During Hemorrhagic Shock—A Link Between Trauma and Sepis,” Ann. Surg., 549–554, 1988. 96. L.Yang, W.Zhang, H-Z He, and G-G Zhang, “Experimental Studies on Combined Effects of High Temperature and Carbon Monoxide,” J. of Tongli Medical Univ., 8, 60–65 (1988). 97. C.S.Hirsch, R.O.Bost, S.R.Gerber, M.E.Cowan, L.Adelson, and I.Sunshine, “Carboxyhemoglobin Concentrations in Flash Fire Victims Report of Six Simultaneous Fire Fatalities Without Elevated Carboxyhemoglobin,” Am. J. Clin. Pathol., 68(3), 317–320 (1977). 98. C.S.Hirsch and L.Adelson, “Absence of Carboxyhemoglobin in Flash Fire Victims,” J. Am. Med. Assn., 210(12), 2279–2280 (1969).


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99. W.G.Eckart, “The Medical, Legal and Forensic Aspect of Fires,” Am J. Forensic Med. Pathol, 2, 347–357 (1981). 100. F.L.Rodkey and H.A.Collison, “Effects of Oxygen and Carbon Dioxide on Carbon Monoxide Toxicity, J. Combustion Toxicology, 6, 208–212 (1979). 101. J.A.Zapp, The Toxicology of Fire, Medical Division Special Report No. 4, Chemical Corps, Army Chemical Center, Maryland, April 1951, 106 pp. 102. D.A.Purser and K.R.Berrill, “Effects of Carbon Monoxide on Behavior in Monkeys in Relation to Human Fire Hazard,” Arch. Environ. Health, 38(5), 308–315 (1983). 103. B.D.Dinman, “Pathophysiologic Determinants of Community Air Quality Standards for Carbon Monoxide,” J. Occupational Medicine, 10, 446–463 (1968). 104. R.D.Stewart, The Effects of Low Concentrations of Carbon Monoxide on Man, Scand. J. Respir. Dis., 91, 56–62 (1974). 105. E.K.Balraj, “Atherosclerotic Coronary Artery Disease and ‘Low’ Levels of Carboxyhemoglobin; Report of Fatalities and Discussion of Pathophysiologic Mechanisms of Death,” J. Forensic Sciences, 29(4), 1150–1159 (1984). 106. A.S.Hume, B.H.Douglas, and K.Harden, “Effect of Ethanol on Carbon Monoxide Poisoning,” IRCS Med. Sci., 4, 300 (1976). 107. L.S.King, “Effect of Ethanol in Fatal Carbon Monoxide Poisonings,” Human Toxicol., 2, 155– 157 (1983). 108. W.E.Fitzgerald, D.S.Mitchell, and S.C.Packham, “Effects of Ethanol on Two Measures of Behavioral Incapacitation of Rats Exposed to Carbon Monoxide,” J. Combustion Toxicology, 5, 64–74 (1978). 109. D.J.Barillo, B.F.Rush, Jr., R.Goode, R.L.Lin, A.Freda, E.J.Anderson, Jr., “Is Ethanol the Unknown Toxin in Smoke Inhalation Injury,” Am. Surg., 52, 641–645 (1986). 110. T.J.Rockwell and F.W.Weir, “The Interactive Effects of Carbon Monoxide and Alcohol on Driving Skills,” Ohio State University Research Foundation, Columbus, Ohio, 1975, NTIS PB242266. 111. D.S.Mitchell, S.C.Packham, and W.E.Fitzgerald, “Effects of Ethanol and Carbon Monoxide on Two Measures of Behavioral Incapacitation of Rats,” Proc. West. Pharmacol. Soc., 21, 427– 431 (1978). 112. J.S.Kinsely, D.C.Rees, R.L.Balster, “Effects of Carbon Monoxide in Combination with Behaviorally Active Drugs on Fixed Ratio Performance in the Mouse,” Neurotoxicol. Teratol., 11, 447–452 (1989). 113. J.W.Winston, J.M.Creighton, and R.J.Roberts, “Alteration of Carbon Monoxide and Hypoxic Hypoxia-Induced Lethality Following Phenobarbital, Chlorpromazine, or Alcohol Pretreatment,” Toxicology and Applied Pharmacology, 30, 458–465 (1977). 114. J.A.Sokal, “Lack of the Correlation Between Biochemical Effects on Rats and Blood Carboxyhemoglobin Concentrations in Various Conditions of Single Acute Exposure to Carbon Monoxide,” Archives of Toxicology, 34, 331–336 (1975). 115. M.Hirata, M.Hioki, and K.Hashimoto, “Distribution of Death Rate in Acute Carbon Monoxide Intoxication in Mice,” Tohoku J. Exp. Medicine, 97, 67–73 (1969).

Chapter 3 EFFECTS OF CARBON MONOXIDE IN MAN: LOW LEVELS OF CARBON MONOXIDE AND THEIR EFFECTS GORDON L.NELSON Florida Institute of Technology, College of Science and Liberal Arts, 150 West University Boulevard, Melbourne, FL, 32901–6988, USA ABSTRACT This report discusses the effects of carbon monoxide on health, and human mental and physical performance from both acute and chronic exposures. Smoking and environmental exposures are discussed, with specific examples given. Carbon monoxide is commonly present in our environment. Build-up and downloading from the body depend upon a variety of factors including gender, activity, and physical health. Worker exposures leading to upwards of 32% COHb have been reported. The level at which carbon monoxide exposures lead to reduced performance in human subjects remains a matter of controversy. Examples from representative literature are presented. COHb levels of 30% are escapable for healthy subjects, with 40% required for incapacitation, depending upon exercise level, but levels as low as 20% can lead to fatalities in impaired subjects. While performance degradation at as low as 4–5% COHb has been reported in man, on the whole, data suggest that healthy individuals can tolerate 10% COHb with heavy physical work with minimal decrement in physical or mental performance and perhaps up to 20% COHb at rest. However, infants, the elderly and individuals with cardiovascular disease, anemia, lung disease, and an increased metabolic rate are at greater risk from CO than the healthy subjects normally addressed. It is also important to note that CO poisoning is not always recognized, given vague, non-specific but persistent symptoms. Diagnosis of carbon monoxide poisoning may require astute examination. Misdiagnosis can return the victims and others to a contaminated evnironment.

3.1 GENERAL COMMENTS In the previous chapter discussion was given of the factors involved in carbon monoxide fatalities, both fire and non-fire exposures. Given that carbon monoxide is ubiquitous, a large body of work has been done to elucidate the effects on health and human mental


64

and physical performance when man is subjected to non-fatal carbon monoxide exposures, both acute and chronic. At interest are *

Note: In every case, if no further details are given, the venue for the study is the United States. questions such as (a) does low CO exposure cause persons exposed in fire incidents to make decisions leading them to become victims, (b) does CO exposure in heavy traffic lead to accidents, (c) at what level does CO exposure cause serious performance deterioration, (d) is that performance deterioration assessable by COHb determination? The discussion is begun with an assessment of environmental exposure. 3.2 SMOKING AND CARBON MONOXIDE Sources of carbon monoxide are numerous, both natural and man-made.1–2 Carbon monoxide is always with us. Endogenous CO production in humans leads to COHb levels of 0.45 percent in adults and 0.30 to 0.35 percent in children under 10 years.3–4 In a study of blood donors from across the country average COHb values ranged from 3.2 to 6.2 percent for smokers and 1.2 to 2.0 percent for non-smokers. Data are provided below, showing effects of carbon monoxide from our urban environment:1

Median Carboxyhemoglobin (COHb) Saturation and 90% Range for Smokers and Nonsmokers

Location

Cigarette Smokers

No. of Nonsmokers

% of Nonsmokers With COHB Nonsmokers

>1.5%

Anchorage

4.7 (0.9–9.5)

1.5 (0.6–3.2)

152

56

Chicago

5.8 (2.0–9.9)

1.7 (1.0–3.2)

401

74

Denver

5.5 (2.0–9.8)

2.0 (0.9–3.7)

744

76

Detroit

5.6 (1.6–10.4)

1.6 (0.7–2.7)

1,172

42

Honolulu

4.9 (1.6–9.0)

1.4 (0.7–2.5)

503

39

Houston

3.2 (1.0–7.8)

1.2 (0.6–3.5)

240

30

Los Angeles

6.2 (2.0–10.3)

1.8 (1.0–3.0)

2,886

76

Miami

5.0 (1.2–9.7)

1.2 (0.4–3.0)

398

33

Milwaukee

4.2 (1.0–8.9)

1.2 (0.5–2.5)

2,720

26

New Orleans

5.5 (2.0–9.6)

1.6 (1.0–3.0)

159

59

New York

4.8 (1.2–9.1)

1.2 (0.6–2.5)

2,291

35

Phoenix

4.1 (0.9–8.7)

1.2 (0.5–2.5)

147

24

St. Louis

5.1 (1.7–9.2)

1.4 (0.9–2.1)

671

35

Low levels of carbon monoxide and their effects

65

Salt Lake City

5.1 (1.5–9.5)

1.2 (0.6–2.5)

544

27

San Francisco

5.4 (1.6–9.8)

1.5 (0.8–2.7)

660

61

Seattle

5.7 (1.7–9.6)

1.5 (0.8–2.7)

585

55

Vermont, New Hampshire

4.8 (1.4–9.0)

1.2 (0.8–2.1)

959

18

Washington, DC

4.9 (1.2–8.4)

1.2 (0.6–2.5)

850

35

It is found that CO exposed individuals show a larger hemoglobin mass than those lesser exposed, to compensate for the body’s anoxic stress.3 A comparison of smokers versus never smokers shows an increase in mean hemoglobin levels for smokers of 137+0.4g/1 versus 133±0.5g/1 for females and 156±0.4 to 152±0.5g/1 for men.5 Some non-smokers in urban situations can show COHb levels of 5 to 8 percent depending upon pollution and work environments. Tobacco smoke reaching the alveoli is approximately 200 ppm. Cigarette smoke contains high levels of CO, ca. 14mg per cigarette.6 Thus, rapid smoking can lead to COHb values of 10 percent. Coupled with occupational exposure, cigarette smoking cab drivers in New York City have shown up to 13 percent COHb.3 In a study of over 16,000 blood donors in Missouri/Illinois, smokers had a mean COHb saturation of 4.6 percent and non-smokers 0.9 percent. Smokers were 39 percent of the population; 43 percent of these had COHb values greater than 5 percent. There were 191 samples in excess of 10 percent with the highest being 18.2 percent. Thirty of the >10 percent samples came from the same site, people without apparent problem.7 A study was conducted in Finland of 21 smokers and 28 non-smokers. The smokers averaged 15 cigarettes per day. Seven tests were done in an unventilated room of 37.5m3. In each experiment three smokers and four non-smokers sat around a table for 90 minutes. Each smoker smoked a new cigarette every 15 minutes for a total of six during the test. The atmosphere in the room was approximately 30 ppm carbon monoxide at the end of the test. The room at the end of the test was very smokey with most subjects experiencing eye irritation. Smokers experienced an increase in COHb from 5.3 percent to 9.1 percent while the non-smokers showed an increase in COHb from 1.6 percent to 2.2 percent. While experimental conditions were identical for individuals, a great variation was seen individual by individual for CO uptake. One smoker showed an increase from 1.6 to 8.5 percent COHb over the 90 minutes while another showed 7.1 to 9.5 percent. Clearly smoking influences our indoor carbon monoxide environment and individual by individual experience is different.8 In another study of 19 smokers, this time in Britain, it was found that their initial COHb level in the mornings was 3.2 percent. Each cigarette caused a mean rise of 1.3 percent COHb. Levels fell between cigarettes with each subject establishing a mean COHb level which was then maintained. The half-life of CO unloading from the blood was 6.9 hours during sleeping and 3.1 hours during the day with normal activity. The half-life for women was 59 percent that of men. Nine subjects retired in the evening with mean COHb levels of 8 percent. One individual (male) had 11.8 percent, another 10 percent.9 The half-life of downloading of carbon monoxide is of some uncertainty, affected of course by a variety of factors. In one study of 39 separate experiments, the half-life of


66

COHb in the blood was found to range from 128 to 409 minutes, with an average of 320 minutes. Variations in the half-life of COHb in blood did not appear to be related to the amount of COHb in the blood, to the duration of exposure, to the number of exposures, or to the concentration inhaled. Other workers have reported half-lives of 2 to 2½ hours.10–11 Activity of smokers as well as amount of tobacco used is important in determining the COHb levels found in smokers. One study of a group of 63 smokers was carried out to examine those who exercise versus those who do not. Subjects were aged 24–27 and of apparent good health. Backgrounds were similar. Thirty were joggers and thirty-three seldom exercised. All smoked nearly three packs of cigarettes per day. Sedentary persons averaged 8.5 percent COHb with 10.1 percent maximum and 7.5 percent minimum from blood taken at 9 am and 3 and 8 pm. Joggers showed an average value of 4.7 percent with a maximum and minimum of 5.8 percent and 3.9 percent respectively. Effects of exercise were explained by more rapid gas exchange, increased capillary movement and adaptive carboxyhemoglobin transport to and from muscular tissue.12 In a study of 50 subjects, the effects of inhaling or not inhaling cigars or cigarettes were studied. The group consisted of 16 current non-smokers, 24 cigarette inhalers and 10 cigar inhalers. Data are presented below:

Carboxyhemoglobin (COHb), Oxygen Saturation (SaO2), and Hemoglobin (Hb) Determinations COHb (%)

SaO2 (%)

Hb (%)

Non-smoking control Subjects (n=16)

1.0

96.7

11.4

Cigarette inhalers (n=24)

4.6

93.0

13.5

Cigar inhalers (n=10)

8.4

88.4

14.2

Cigar inhalers showed COHb levels of 8.4 percent and measured oxygen saturation of 88.4 percent, less than the minimum 90 percent considered by some as healthful. Cigar inhalers had considerably higher carbon monoxide exposure than cigarette smokers.13 In a follow-on study of 130 subjects, cigarette, cigar, and pipe smokers were examined. Secondary smokers are those who originally smoked cigarettes. It is interesting that primary cigar smokers (i.e., always cigar smokers) here showed COHb levels of 13.8 percent with oxygen saturation levels of 85.7 percent. Data are shown as follows:14

Carboxyhemoglobin Level and SaO2 in 130 Subjects Grouped by Smoking Habit Group

No. of Subjects

COHb Level (%)

SaO2 (%)

Nonsmokers

16

1.0

96.7

Cigarette inhalers

41

5.6

91.8

3

13.8

85.7

Primary cigar inhalers


67

Secondary cigar inhalers

34

11.8

85.7

Primary cigar noninhalers

8

2.1

95.6

Secondary cigar noninhalers

4

1.9

96.4

Primary pipe inhalers

1

5.0

94.6

Secondary pipe inhalers

12

5.4

92.4

Primary pipe noninhalers

5

1.3

96.3

Secondary pipe noninhalers

6

2.5

96.3

Other studies of cigar and pipe smokers have shown similar results.15–16

FIGURE 1. Half-life of COHb in relation to alveolar ventilation rate. Adjustment has been made for the increase in transfer factor for CO with activity, taking a value from 30 ml min−1 mg−1 at rest to 50 ml min−1 mg−1 with strenuous exercise such as football. The energy expenditure for each activity is converted into alveolar ventilation rates using a 3.45 ml oxygen per calorie, a respiratory quotient of 0.8, and a mean alveolar CO2 concentration of 5.6%. It has been assumed that the inspired air contains no CO.17


68

A study of 9 cigarette smokers showed substantial variation in CO uptake depending upon number of cigarettes smoked, uptake per cigarette, and activity level. This is not unlike subjects exposed to CO in other circumstances. CO downloading is very dependent upon activity as shown in Figure 1.17 The equilibrium between CO in the atmosphere and in the bloodstream is heavily dependent on the time of exposure, activity level, level of smoking, and physical health of the individual. 3.3 ENVIRONMENTAL CARBON MONOXIDE The EPA standard is 9 ppm for 8 hours and 35 ppm for 1 hour. That standard is exceeded, however, in a variety of circumstances. A study was made of 38 parking garage attendants in 1967 in Dayton, Ohio. Air samples showed a range of 7 to 240 ppm with a mean of 59 ppm in 6 garages. Attendants were all male aged 18 to 50. Twenty of the 38 were smokers. Data are shown below:18

COHb and Hb of Exposed and Control Groups % of COHb Group No. Exposed

Range

Mean

Hb gm/100 cc Mean

38

15.8

8 am

0.4–6.9

2.4

5 pm

2.9–15.8

8.4

Controls

27

0.5–7.6

2.8

FIGURE 2A. Relationship of carboxyhemoglobin (COHb) level before and after shiftdue to methylene chloride (MeCl2) exposure of smokers and nonsmokers. (TWA=time-

15.0


69

weighted average,—=before-shift values,——=after-shift values.25

FIGURE 2B. Relationship of alveolar carbon monoxide (COA) level before and after shift due to methylene chloride (MeCl2) exposure of smokers and nonsmokers. (TWA= timeweighted average,—=before-shift values,——=after-shift values).25 From a mean of 2.4 percent COHb on entering work the subjects, on leaving at 5 pm, had a mean of 8.4 percent COHb, with a high of 15.8 percent. Garage workers who had been employed 6 months to 16 years had 0.8 percent more hemoglobin than the control group. Unexpected exposures are possible. A study of one office building showed eight hour averages of 26 ppm carbon monoxide in basement offices with up to 50 ppm late in the afternoon. The adjacent parking garage showed 100–200 ppm in the late afternoon. Activation of inoperative ventilation fans in the garage was found to reduce exposure in the offices by better than 50 percent.19 A study in London showed that sidewalk exposure can range as high as 360 ppm for short periods. Average concentrations were about 25 ppm. Between the hours of 9 am and 8 pm concentrations measured exceeded 50 ppm with a peak of 100 ppm at 6 pm. The UK workers also studied firemen and those in confined spaces, 295 subjects. Of most interest was the 31.9 percent COHb shown by a rotary cultivator operator working in a closed greenhouse, apparently without effect.20 A study of the urban atmosphere in Toronto revealed street levels of 10–50 ppm carbon monoxide with excursions to 170 ppm. A check of underground garages found children playing in excess of 100 ppm. A reading 13 feet from a car which was being adjusted showed 700 ppm. Those who habitually work on busy city streets were viewed as likely to be exposed periodically to 100+ ppm.21 It should be noted that in the U.S. Federal emission control standards have resulted in a reduction in the carbon monoxide content of automobile exhaust, from 8.5% in 1968 to 0.05% in 1980. This has resulted in about a 45% reduction of carbon monoxide in the


70

environment due to automobile exhaust (given older cars still on the road and more automobiles overall).22 One interesting source of carbon monoxide exposure is methylene chloride (23–26). Methylene chloride is converted in the body to carbon monoxide. Occupational employee exposures of 500 ppm methylene chloride are possible. In smokers that concentration would yield a COHb of 13 percent and about 8 percent in non-smokers as shown in Figure 2. In a 1974 study 100 men in the blast furnace department of an integrated steel works were studied in the UK. Blast furnace workers showed an increase of 2.6 percent COHb versus 0.2 percent for office workers. Four blast furnace individuals of the 100 showed increases of 10 percent COHb or greater. 20 men showed increases of 5 percent or more at the end of the shift. No subject complained of symptoms.27 A study in Finland was made of foundry workers. Air sampling in iron foundries was done in problem areas, with 76 percent of the samples near cupolas, 72 percent of the samples near casing areas and 67% in breathing zones of casters in excess of the 50 ppm TLV. Mean values were 240 and 110 ppm respectively. Blood COHb samples were taken from 145 workers at six foundries. Data are shown in Figure 3.28 In Japan factory workers were studied. COHb values were assessed versus observed CO concentrations in the workplace as shown as follows:29 Group 1

2

3

4

No. Examined

47

39

45

23

No. of Persons COHb% 0–1

0

0

12

9

1–5

5

2

27

12

5–10

7

4

5

2

10–15

12

5

1

0

15–20

10

8

0

0

20–25

8

11

8

8

25–30

5

7

0

0

15.5

19.5

3.0

2.3

Over 30 Average COHb (%)

CO p.p.m. by vol. in air Work place of group 1 50–250 Work place of group 2 60–1370 Work place of group 3 10–20 The office of the factory 4 below 20 Out-of-doors 4 below 10


71

FIGURE 3. Carboxyhemoglobin levels of carbon monoxide exposed iron foundry workers at the end of a work shift.28 While the investigator found a higher frequency of subjective symptoms in subjects exposed to carbon monoxide than in the controls, none of them felt ill. Despite COHb values to 30 percent, he reported that no grave cases of poisoning occurred. He observed that repeated and long term exposures to carbon monoxide had not caused disorders of the human health which might be diagnosed as “chronic poisoning of carbon monoxide” or even as “ill condition” by clinicians, and the workers thought themselves to be healthy without paying attention to complaints such as headache or forgetfulness.29


72

An extensive Swedish study has been performed on workers in ironworks, mines, gasworks, and motor repair shops. Carbon monoxide levels were measured and medical history and data obtained. Ironworks and mines produced the highest values, with a few subjects showing 20+ percent COHb. There were no significant differences between the groups of exposed and unexposed workers who had, in pairs, the same type of shift work. This was true of the group with the greatest degree of exposure and of that with the least, and of the two groups taken together. There were no significant differences in performance tests between exposed workers on shift work and unexposed workers on the day shift.29 The Swedish workers held the view that the absence of significant differences in the results of the performance tests in the exposed and unexposed groups of workers was evidence that exposure to carbon monoxide to the degree and duration present in the study did not have a detrimental effect on the variables measured by the tests used, or that such effects are at least insignificant. In the Swedish studies median COHb at work was approximately five to six percent. A scrutiny of Swedish National Health Insurance records for a period of ten years revealed no differences in the frequency of illness between the groups.29 In a study of fatal motor vehicle accidents, of 44 accidents studied, 13 had COHb values in excess of 10 percent with six showing blood alcohol in excess of 0.15 percent.30 In other work COHb concentrations of 10 to 28 percent in 23 percent of drivers who died in accidents in Dade County, Florida were reported. Twenty-seven victims (15.7 percent) had COHb concentrations of 10 to 20 percent, and 13 (7.6 percent) had concentrations of 20 to 28 percent. However, only nine of 423 victims in a California study had COHb concentrations of 10 to 15 percent. The pattern of alcohol plus carbon monoxide is interesting in its similarity to fire victims.30 Commuters are one group of the population who face daily carbon monoxide exposure. One study looked at commuters in the metropolitan Washington, D.C., area in the winter of 1983. Fifteen routes were chosen involving automobile, bus and rail. Sampling involved a total of 266 trips. Automobile travelers were exposed to means of 9–14 ppm with one evening route to 22 ppm. Trips took 40–70 minutes. Bus commuters were exposed to 4–8 ppm with one morning route at 10 ppm. Trips took 80–115 minutes. Rail commuters were exposed to means of only 2–5 ppm on trips of 27–48 minutes. These values contrast with ambient fixed site readings during the commuting hours of 1.8–3.1 ppm in the Washington area.31 Monitoring at city sites in El Paso, Texas, showed similar values to the Washington, D.C., study. Based on hourly averages for each month, high concentrations were at 7 am and 5 pm, with the highest hourly average being 13 ppm.32 The most comprehensive report of exposure to carbon monoxide is a study of disease mortality among bridge and tunnel officers in metropolitan New York City.33 The study population consisted of all male bridge and tunnel officers employed between January 1, 1952 and February 10, 1981, at one of nine major water crossings (two tunnels and seven bridges) operated by the Triborough Bridge and Tunnel Authority of New York City. Data available from personnel records contained name, Social Security number, sex, date of birth, date of hire, date of separation, and specific work history information identifying the bridge(s) or tunnel(s) at which the officers had worked. Information on race was obtained from the Social Security Administration. The primary duties of the bridge and tunnel officers included toll collections from booths, traffic observation within and outside the tunnels, and direction of traffic within the


73

tunnels and on the bridges when necessary (i.e., during rush hours or motor vehicle accidents).33 Continuous monitoring of carbon monoxide levels within the tunnels began in 1940 at the Queens Midtown Tunnel and in 1950 at the Brooklyn-Battery Tunnel. Measurements showed peak concentrations exceeding 400 ppm. In 1961, an investigation demonstrated 24-hour average carbon monoxide levels inside the tunnels of 53 ppm in the summer (with peaks of 200–300 ppm) and 49 ppm in the winter (with peaks of 100–200 ppm). In 1968, 24-hour average carbon monoxide concentrations measured inside the tunnels were 35–40 ppm. Carbon monoxide exposures measured during rush hour traffic were found to range from 120–165 ppm in the morning and 65–145 in the evening in the tunnel toll booths, and 15–45 ppm in the morning and 12–22 ppm in the evening in the bridge toll booths. During the same year, fresh-air ventilation systems were installed in all toll booths. In 1971, an increase in electrical service to the ventilation fans in the tunnels yielded an increase of approximately 15 per cent in tunnel ventilation capacity. Starting in 1971, officers were allowed one half-hour “air-break” for each day’s work, which consisted of two two-hour tours inside the tunnel. In 1977, ventilation equipment for the tunnels was linked electrically to continuously reading carbon monoxide monitors. In 1981, sampling found mean area levels of carbon monoxide of 38.3 ppm inside the tunnels and 23.0 ppm outside the bridge toll booths. Peak carbon monoxide levels measured in the traffic lanes of both the tunnels and the bridges and on the tunnel catwalks were frequently greater than 100 ppm and occasionally greater than 400 ppm. Exposure to contaminants for tunnel and bridge officers were 0.3 and 0.1 ppm for nitrogen dioxide, 0.07 and 0.02 mg/m3 for polycyclic aromatic hydrocarbons, 0.005 and 0.004 mg/m3 for lead, and 0.06 and 0.02 fibers/cm3 for asbestos.33 Carboxyhemoglobin levels measured in 1970 (before ventilation systems were installed in the toll booths) averaged 2.12 and 3.90% in nonsmokers and smokers, respectively, for bridge officers and 2.93 and 5.01% in nonsmokers and smokers, respectively, for tunnel officers. Post-shift carboxyhemoglobin levels measured in 1981 were not found to be significantly different between bridge (4.9% carboxyhemoglobin) and tunnel officers (4.5% carboxyhemoglobin), with pre- vs post-shift carboxyhemoglobin levels rising about 20 percent in nonsmokers and 10 percent in smokers.33 The status of each officer was ascertained as of December 31, 1982. For deceased officers, death certificates were obtained from the appropriate state vital statistics offices. Death rates for New York City were obtained for the years 1950–1984. The mortality experience of those officers employed only in tunnels and of those employed only on bridges was examined separately, because previous environmental sampling had indicated that carbon monoxide levels had been substantially higher within and around the tunnels than on the bridges. Because environmental sampling results for carbon monoxide were only available for a few years of the study, duration of employment was used for cumulative exposures. Two categories, less than 10 years and greater than or equal to 10 years employment, were used to ascertain effects from cumulative long-term vehicular exhaust exposures. For cancers only, an additional analysis by latency was performed.33 There were 4,317 bridge officers and 1,212 tunnel officers employed between January 1, 1952 and February 10, 1981, by the Triborough Bridge and Tunnel Authority. There were a total of 103,900 person-years at risk. As of December 31, 1982, 88 percent of the officers were alive, 9 percent were deceased, and 3 percent were lost to follow-up. Death


74

certificates were obtained for 97 percent (460 out of 474) of all known deaths. The percentage of tunnel officers who died (13 percent) was almost twice that of bridge officers (7 percent). On average, the bridge officers and tunnel officers were very similar in racial composition and calendar year of birth. On average, the tunnel officers had worked for five years at the Triborough Bridge and Tunnel Authority, while the bridge officers had worked there for only three years. Mortality data are shown in Table 1.

Table 1 Mortality (1952–1982), by duration of employment, among male bridge and tunnel officers, Triborough Bridge and Tunnel Authority, New York City133 Duration (years) of Employment Cause of Death

10 SMR

Obs

Exp

Total SMR

Obs

Exp

SMR

Bridge Officers All heart disease

78

96

0.82

30

33

0.91

108

129

0.84

ASHD

66

76

0.87

23

28

0.81

89

104

0.85

Lung Cancer

13

16

0.83

5

6

0.91

18

21

0.85

All other causes

154

223

0.69

34

37

0.93

188

259

0.73

All causes

245

334

0.73

69

75

0.92

314

409

0.76

Tunnel Officers All heart disease

35

36

0.98

32

19

1.722

67

54

1.243

ASHD

31

29

1.07

30

16

1.882

61

45

1.353

5

6

0.83

4

3

1.29

9

9

0.97

69

63

1.01

15

21

0.72

84

89

0.94

109

110

0.99

51

43

1.20

160

153

1.04

Lung cancer All other causes All causes

1 ASHD, arteriosclerotic heart disease; Obs, observed number of deaths; Exp, expected number of deaths; SMR, standardized mortality ratio (Obs\Exp). Expected number of deaths are based on the death rates for New York City rounded to the nearest whole number. 2 Significantly different from 1.00 (p45% COHb, however.26 Numerous factors affecting the loss of carbon monoxide from stored blood samples were identified in another recent study. Effects of temperature, surface area versus volume, initial COHb saturation, storage temperature versus volume of air, initial hemoglobin concentration, non-physiological versus post-mortem samples, and air versus oxygen versus nitrogen storage were all investigated. The exposure of CO-containing blood to an oxygen atmosphere will result in a decrease in COHb saturation. The rate is highest when the exposed surface area to volume of blood is large, when the temperature is not kept low, and when the initial saturation is high. In a sealed container with air, loss of CO to air will occur until equilibrium is reached between the air and the specimen. Use of a syringe technique to provide for total exclusion of air was recommended by the authors of the study. Storage at −20°C was not effective as the sole preservative condition. Very rapid loss of COHb was observed at 23°C.27 In studies of post-mortem blood Levin and coworkers have shown a drop of nearly 20% from initial values of 71.5% and 24.6% with 4 month storage at −20°C. On the day of analysis, the thawed blood was stored in an ice bath. The samples were in screw-top vials sealed with rubber septa and containing the anticoagulant sodium fluoride.13 Aged blood samples and blood samples from fire victims may contain sulphemoglobin (SHb) which will interfere with the determination of COHb by spectrophotometry and yield results approximately 10 percent low.28 One final concern is the effect caused by heat in victims with burns. Turbidity in blood samples, when samples are heated above 50°C, affects results. Above 70°C coagulation and hemoglobin degeneration results in accelerating errors in determined values. Methods can overcome these issues, but are not commonly in use.29 Indeed, determination of COHb is not without a multitude of opportunities for error.


178

REFERENCES 1. A.H.J.Maas, M.L.Hamelink, and R.J.M.Leeuw, “An Evaluation of the Spectrophotometric Determinations of HbO2, HbCO, and Hb in Blood with the COOximeter IL 182,” Clin. Chem. Acta, 29, 303–309 (1970). 2. K.A.Small, E.P.Radford, J.M.Frazier, F.L.Rodkey and H.A.Collison, “A Rapid Method for Simultaneous Measurement of Carboxy- and Methemoglobin in Blood,” J. Appl. Physiol., 31(1), 154–160 (1971). 3. C.A.Ainsworth, E.L.Schloegel, T.J.Domanski, and L.R.Goldbaum, “A Gas Chromatographic Procedure for the Determination of Carboxyhemoglobin in Post-Mortem Samples,” J. Forensic. Sci., 12, 529–537 (1967). 4. S.M.Ayers, A.Criscitello and S.Gianelli, “Determination of Blood Carbon Monoxide Content by Gas Chromatography,” Upsala J. Med. Sci., 77, 22–24 (1972). 5. A.M.Dominguez, H.E.Chrostensen, L.R.Goldbaum, and V.A.Stembridge, “A Sensitive Procedure for Determining Carbon Monoxide in Blood and Tissue Utilizing Gas-Solid Chromatography,” Toxicol. Appl. Pharmacol., 1, 135–143 (1959). 6. T.H.Allen, and W.S.Root, “An Improved Palladium Chloride Method for the Determination of Carbon Monoxide in Blood,” J. Biol. Chem., 216, 319–323 (1955). 7. K.G.Paul, and H.Theorell, “A Colorimetrical Carbonmonoxide-Hemoglobin Method of Determination for Clinical USe,” Acta. Physiol. Scand., 4, 285–292 (1942). 8. S.M.Horvath, and F.J.Roughton, “Improvements in the Gasometric Estimation of Carbon Monoxide in Blood,” Clin. Chem., 144, 747 (1942). 9. F.J.W.Roughton, and W.S.Root, “The Estimation of Small Amounts of Carbon Monoxide in Blood,” J. Biol. Chem. 147, 123 (1945). 10. R.F.Coburn, W.S.Danielson, W.S.Blakemore and R.E.Forster, “Carbon Monoxide in Blood. Analytical Method and Sources of Error,” J. Appl. Physiol., 19, 510–515 (1964). 11. H.W.Bay, K.F.Blurton, J.M.Sedlak, and A.M.Valentine, “Electrochemical Technique for the Measurement of Carbon Monoxide,” Anal. Chem. 46, 1837–39 (1974). 12. S.Kays, Handbook of Emergency Toxicology, 4th ed., Charles C.Thomas, Springfield, IL, 1980, 255–256, 287. 13. B.C.Levin, P.R.Rechani, J.L.Gurman, F.Landron, H.M.Clark, M.F. Yoklavich, J.R.Rodriguez, L.Droz, F.M.de Cabrera, and S.Kaye, “Analysis of Carboxyhemoglobin and Cyanide in Blood from Victims of the Dupont Plaza Hotel Fire in Puerto Rico,” J. Forensic Sci., 35(1), 151–168 (1990). 14. D.V.Canfield, private communication (1986). 15. Y.M.Katsumata, M.Aoki, M.Oya, O.Suzuki, and S.Yada, “Simultaneous Determination of Carboxyhemoglobin and Methemoglobin in Victims of Carbon Monoxide Poisoning,” J. Forensic Sciences, 25(3), 546–549 (1980). 16. Y.M.Katsumata, M.Aoki, K.Sato, M.Oya, S.Yada, and O.Suzuki, “A Simple Spectrophotometric Method for the Determination of Carboxyhemoglobin in Blood,” Forensic Sci. Int., 18, 175–9 (1981). 17. A.W.Freidrich, and D.Lanau, “Carbon Monoxide Determination in Post-Mortem Clotted Blood,” J. Forensic Sci., 16, 112–119 (1971). 18. O.Siggaard-Andersen, B.Norgaard-Pedersen, and J.Rem, “Hemoglobin Pigments, Spectrophotometric Determination of Oxy-, Carboxy-, Met-, and Sulfhemoglobin in Capillary Blood,” Clin. Chem. Acta, 42, 85–100 (1972). 19. D.J.Blackmore, “The Determination of Carbon Monoxide in Blood and Tissue,” Analyst, 95, 439–458 (1970). 20. K.M.Dubowski, and J.L.Luke, “Measurement of Carboxyhemoglobin and Carbon Monoxide in Blood,” Ann. Cln. Lab. Sci., 3, 53–65, (1973). 21. J.E.Hodgkin, and D.M.Chan, “Diabetic Ketoacidosis Appearing as Carbon Monoxide Poisoning,” JAMA, 231, 1164–1165 (1975).

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22. J.G.Guillot, J.P.Weber, J.Y.Savoie, “Quantitative Determination and Carbon Monoxide in Blood by Head-Space Gas Chromatography,” J. Anal. Toxicol., Nov–Dec, 264–266 (1981). 23. L.D.Hobbs, J.A.Jachimezyk, and E.L.Schloegel, “A Gas Chromatographic Integrator Procedure for the Determination of Carboxyhemoglobin Percent Saturation in Post-Mortem Samples,” J. Anal. Toxic., 4 181–184 (1980). 24. F.L.Rodkey, “Carbon Monoxide Estimation in Gases and Blood by Gas Chromatography,” Ann. N.Y. Acad. Sci., 174, 261–267 (1970). 25. B.J.Perrigo and B.P.Joynt, “Evaluation of Current Derivative Spectrophotometric Methodology for the Determination of Percent Carboxyhemoglobin Saturation in Postmortem Blood Samples,” J. Anal. Tox., 13, 37–46 (1989). 26. A.G.Costantino, J.Pack, and Y.H.Caplan, “Carbon Monoxide Analyses: A Comparison of Two CO-Oximeters and Headspace Gas Chromatography,” J. Anal. Tox, 10, 190–193 (1986). 27. D.H.Chace, L.R.Goldbaum, N.T.Lappas, “Factors Affecting the Loss of Carbon Monoxide form Stored Blood Samples,” J. Anal. Tox., 10, 181–189 (1986). 28. V.S.Rai and P.S.B.Minty, “The Determination of Carboxyhemoglobin in the Presence of Sulphemoglobin,” Forensic Sci. Int., 33, 1–6 (1987). 29. Y.Fukui, M.Matsubara, A.Akane, K.Hama, K.Matsubara, and S.Takahashi, “Determination of Carboxyhemoglobin in Heated Blood—Sources of Error and Utility of Derivative Spectrophotometry,” J. Anal. Tox., 9, 81–84 (1985).

Chapter 6 CARBON MONOXIDE AND FATALITIES: A CASE STUDY OF TOXICITY IN MAN GORDON L.NELSON Florida Institute of Technology, College of Science and Liberal Arts, 150 West University Boulevard, Melbourne, Fl, 32901–6988, USA & DENNIS V.CANFIELD AND JAMES B.LARSEN University of Southern Mississippi, Department of Biological Studies, Southern Station, Box 5018 Hattiesburg, MS, 39406–6018, USA ABSTRACT Carbon Monoxide exposure is common. Questions of interest are: What are the lethal levels of CO in man? How are these levels related to blood COHb? What are the roles of age, disease, drugs, alcohol, and gender? What is the relationship to the fatal event (fire, city gas, or exhaust fumes)? The present study involved data collection on 2241 fatalities and software manipulation to allow analysis of key parameters. Data were from the United States and Canada, and 98% of cases were from between 1976 and 1985. Cases with COHb greater than 20% were evaluated. Information was gathered on age, gender, method of COHb analysis, blood % COHb, blood% ethanol, presence of drugs, disease, source of CO, and physical condition, yielding 128 cross-tabulated contingency tables. For fire victims increased age and the presence of impairment were associated with low COHb levels. For non-fire victims the presence of ethanol was associated with decreased percentage of low COHb. The distribution of COHb levels for fire victims has a (2x) greater fraction below 60% COHb than does that of non-fire victims; however non-fire victims succumb at low COHb levels as well. Different segments of the exposed population exhibit different outcomes. A victim with 30% COHb can clearly be a case of carbon monoxide poisoning without other agents required, a fact of considerable importance in the analysis of carbon monoxide exposure cases.


182

INTRODUCTION Carbon monoxide (CO) is a toxic, nonirritating gas. One of the products of combustion, it is invisible, odorless, tasteless, and slightly lighter than air. Carbon monoxide poisoning is not new. Man’s difficulties with CO date back *

Note: In every case, if no further details are given, the venue for the study is the United States.

to the time prehistoric man first used fire. Instances of CO poisoning are found in early Greek and Roman literature. The increased use of coal for domestic purposes in the 1400s brought with it an increase in CO poisoning. The hazard was intensified by the introduction of illuminating gas, and later natural gas, for heat, power, and light. One frequently finds comments such as the following in texts and surveys: “Carbon monoxide is present in significant amounts in virtually all fires. It is highly toxic when inhaled, and acts by combining with hemoglobin in the blood to form carboxyhemoglobin (COHb). Hemoglobin’s function is to carry oxygen throughout the body, and it cannot do this if it is tied up, as COHb and, therefore, unavailable for oxygen transport. The level of carboxyhemoglobin in the blood of fire victims can be determined fairly easily. In the absence of other contributing factors a COHb concentration of 50 percent or greater is generally considered lethal.”1 Most medical discussions of carbon monoxide poisoning deal with “normal healthy” individuals. But the population is composed of a spectrum of individuals in a variety of environments. While one frequently sees conclusions given about a small set of victims without regard to other factors, conclusions which implicate particular combustible materials for example, such conclusions may not be justified given the full spectrum of expected human response to carbon monoxide exposure. Because of the general uncertainties about the detailed factors involved in carbon monoxide poisoning. A major descriptive forensic study of carbon monoxide poisoning in man has been undertaken. A summary of results are provided in this report. Data are from the United States and Canada. The vast majority of the cases studied are recent fatalities, 98% occurred between 1976 and 1985. This study involved data collection on over 2000 fatalities and software manipulation to allow analysis of some key parameters. The issues to be addressed include the following: What are the lethal levels of CO in man? How are these levels related to COHb? What are the roles of age, disease, drugs, alcohol, and gender? What are the mechanisms of CO toxicity? What is the relationship to the fatal event (fire, city gas, exhaust fumes)? Have fires changed over the years? Background Literature Survey More than 1300 papers were reviewed,2 from which several summary statements can be made. Whereas CO exposure seldom occurs with CO in its ultrapure state, studies of

Carbon monoxide and fatalities

183

human exposure to city gas and exhaust gas show that nearly 20% of exposed individuals die from CO poisoning at blood COHb levels less than the concentration thought by some to be required for lethality i.e. 0.05%

67.51

16.61

70

MALE FIRE >0.05% ETHANOL

60.61

18.50

70

FEMALE FIRE >0.05% ETHANOL

65.59

18.27

70

MALE NON-FIRE >0.05% ETHANOL

70.53

14.54

80

FEMALE NON-FIRE >0.05% ETHANOL

71.81

11.59

70

MALES ETHANOL

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