Pesticides: The Chemical Weapon That Kills Life : (The USSR's Tragic Experience)

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LEV A. FEDOROV

ALEXEY V. YABLOKOV

Lev A. Fedorov graduated from the Moscow State University in 1965. First he worked at the Institute of Elementorganic Chemistry, then at the Institute of Geochemistry and Analytical Chemistry, USSR/Russian Academy of Sciences, Moscow. He is Dr. Chem., specialist in environmental contamination caused by dioxins and other substances toxic to the environment, the author of the book “Dioxins as an Environmental Hazard: A Retrospective and Prospects for the Future” (Moscow, 1993). In 1992, he was accused in “revealing state secrets” upon publication of an article about the Soviet chemical weaponry program. He is also the author of “Chemical Weapons in Russia: History, Ecology, Politics” (Moscow, 1994) and of “Undeclared Chemical War in Russia: Politics against Ecology” (Moscow, 1995). While studying the Soviet program for the development and production of chemical weapons, Dr. Fedorov revealed its intimate ties with the problem of pesticides. He is the founder (1993) and President of the NGO “Union for Chemical Safety” and, until recently, he was co-chairman of the International Social Ecological Union (2000–2003). Alexey V. Yablokov graduated from the Moscow State University in 1956. He is Dr. Biol., for many years he worked at the Koltzoff Institute of Developmental Biology, USSR/Russian Academy of Sciences, Moscow. He was Deputy Chairman of the Ecology Committee of the USSR Parliament (1989–1991), advisor on the environment and health to Russian President (1991–1993), chairman of the Interagency Commission on Environmental Security, State Security Council of the Russian Federation (1993–1997). He is the founder (1993) and President of the Center for Russian Environmental Policy, Corresponding member of the Russian Academy of Sciences, Honorary member of the American Academy of Art and Science, Vice President of the World Conservation Union (2000–2004). At present he focuses on the problems of population biology, of environmental policy and of environmental human rights. Among his more than 20 monographs, several like “Population Biology”, “Variability of Mammals”, “Nuclear Mythology”, “Phenetics”, “Poisonous Additive: Problems of Pesticides and Ecologizing Agriculture”, “Conservation of Living Nature” have been translated in the USA, Germany, Japan and some other countries.

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Lev A. Fedorov & Alexey V. Yablokov

PESTICIDES The chemical weapon that kills life

Russian, Ukrainian, Moldovan, Azerbaijani, Uzbekistani, Tajikistani, as other former Soviet republics’ experience with pesticide use are necessary to understand the causes and effects of disseminating pesticides throughout the world. Never, in any country, there has so much medical and biological research on the consequences of pesticide use been seen as in the USSR in the 1970–80s. These data had remained mostly secret until the 1990s. The book presents part of this material to Western readers for the first time. Among discussed problems are: regulation, control, and economics of pesticides in the USSR agriculture; air, water and soil contamination; transformation of pesticides in the environment and in food products; human and animal poisoning by different types of pesticides; morbidity and mortality connected with pesticides, genetic effects, and effects on reproduction, endocrine and other systems; bioaccumulation; pesticides as poisons for cultivated plants; pesticide resistance in target species; connections of chemical weaponry plants with pesticide production.

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(THE USSR’S TRAGIC EXPERIENCE)

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1

THE CENTER FOR RUSSIAN ENVIRONMENTAL POLICY

Lev A. Fedorov, Alexey V. Yablokov PESTICIDES – THE CHEMICAL WEAPON THAT KILLS LIFE (THE USSR’S TRAGIC EXPERIENCE)

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PESTICIDES — THE CHEMICAL WEAPON THAT KILS LIFE

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Lev A. Fedorov, Alexey V. Yablokov

PESTICIDES THE CHEMICAL WEAPON THAT KILLS LIFE (THE USSR’S TRAGIC EXPERIENCE)

SOFIA–MOSCOW 2004

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PESTICIDES – THE CHEMICAL WEAPON THAT KILLS LIFE (THE USSR’S TRAGIC EXPERIENCE) © Lev A. Fedorov & Alexey V. Yablokov Translated by Lilia P. Poger

First published 2004 ISBN 954-642-205-3

© PENSOFT Publishers All rights reserved. No part of this publication may be reproduced, stored in a retrieval system or transmitted in any form by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior written permission of the copyright owner.

Pensoft Publishers, Acad. G. Bonchev Str., Bl.6, 1113 Sofia, Bulgaria Fax: +359-2-870-45-08, e-mail: [email protected] www.pensoft.net

Cover and book design: Zheko Aleksiev Layout: Teodor Georgiev

Printed in Bulgaria, February 2004

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CONTENTS PREFACE

7

INTRODUCTION

9

CHAPTER 1. PESTICIDES IN THE USSR 1.1. SCOPE OF USE

11

11

1.2. REGULATION AND CONTROL 1.3. STORAGE AND DISPOSAL 1.4. ECONOMICS OF USE

13

25

26

CHAPTER 2. PESTICIDES IN THE ENVIRONMENT 2.1. AIR CONTAMINATION

29

29

2.2. WATER CONTAMINATION 2.3. SOIL CONTAMINATION

31 34

2.4. TRANSFORMATION OF PESTICIDES IN THE SOIL, AIR, AND WATER

36

2.5. PESTICIDES IN GLOBAL PROCESSES CHAPTER 3. PESTICIDES, THE STATE AND HUMANS 3.1. ACUTE POISONING

38 39

40

3.2. OCP POISONING

42

3.3. OPP POISONING

47

3.4. OMP POISONING

52

3.5. POISONING BY OTHER TYPES OF PESTICIDES 3.6. MORBIDITY AND MORTALITY

59

3.7. PESTICIDES’ GENETIC EFFECTS

64

3.8. EFFECTS OF PESTICIDES ON PREGNANT WOMEN AND CHILDREN

66

3.9. PESTICIDES AND FOOD PRODUCTS 3.9.1. REALIZATION OF THE PROBLEM

75 75

55

6


3.10. PESTICIDE TRANSFORMATION…IN THE KITCHEN 3.11. POISONING OF THE COUNTRY

85

CHAPTER 4. PESTICIDES AND THE NATURAL ENVIRONMENT 4.1. BIOACCUMULATION

84

89

89

4.2. THE DESTRUCTION OF PLANTS NOT TARGETED BYPESTICIDES

92

4.3. THE DESTRUCTION OF ANIMALS NOT TARGETED BYPESTICIDES

93

4.4. PESTICIDES AS DESTROYERS OF THE NORMAL LIFE PROCESSES OF ORGANISMS

101

4.4.1. PESTICIDES AS MUTAGENS AND CARCINOGENS

101

4.4.2. EFFECTS ON REPRODUCTION

103

4.4.3. THE DESTRUCTION OF THE ENDOCRINE SYSTEM

107

4.4.4. PESTICIDE TRANSFORMATION IN THE NATURAL ENVIRONMENT CHAPTER 5. PESTICIDES AND AGRICULTURE

109

113

5.1. PESTICIDES AS POISONS FOR CULTIVATED PLANTS

113

5.2. OTHER NEGATIVE CONSEQUENCES OF PESTICIDE USE IN CROP PRODUCTION

113

5.3. PESTICIDE RESISTANCE IN TARGET SPECIES CHAPTER 6. PESTICIDES: LESSONS LEARNED BIBLIOGRAPHY APPENDIX (A)

122 129

121

117

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PREFACE Chemist Lev Fedorov and biologist Alexey Yablokov are the authors of an outstanding book entitled PESTICIDES — CHEMICALS THAT KILL LIFE: THE USSR’s TRAGIC EXPERIENCES. Their thorough study of pesticide consequences, the first from the USSR, contributes to our growing knowledge of pesticide usage and gives us much valuable information about evaluating the risks of these chemicals. In particular, they document problems of incomplete information in pesticide regulations and describe a lack of education about pesticides, which resulted in the tragic experiences of the USSR. Further, the authors have carefully examined and documented the public health and environmental impacts of pesticide use in the USSR. The USSR was the largest country by territory in the world and the use of pesticide here was enormous. As the authors have shown, this happened mostly because the USSR’s Communistic rulers decided at the end of the 1960’s — to turn all chemical weaponry plants (constructed in the beginning of the cold war) to pesticide production. With rich government subsidies, pesticides were distributed through all collective farms The Soviet official policy, the “chemicalisation” of agriculture, was an attempt to overcome its prominent ineffectiveness in crop production. The scale of pesticide application in the USSR was great, at an annual average up to more than 2 Kg per hectare (2,7 Kg per person) in the 1980’s up to 70 Kg per Hectare were applied in some areas of Turkmenistan (Central Asia), Armenia (Caucasus) and Moldova (Eastern Europe) and up to 237 kg/ha in Azerbaijan (Caucasus). Public health consequences were so serious, that in the 1970’s there was a special secret governmental decision to conduct wide scale investigations of the public health problem. Following this decision, about 75 medical and scientific institutions studied the health consequences of the widespread pesticide use. This was one of the most widespread investigations of such kind over the globe. To date, the majority of more than 400 Ph.D. dissertations are kept in secret storage at the VNIIGINTOX (former All-Union Institute of the Genetic Toxicology) in Kiev, Ukraine.Fortunately, hundreds of thesis dissertations were opened” at the beginning of the 1990’s and were made available to the authors of this book. The results of this investigation are shocking because of the significant public health and environmental effects reported. Unfortunately, similar types of assessments are not available for most nations. Over decades, pesticide applications have contributed to increasing agricultural yields in the production of many crops in the USSR and, in

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indeed, throughout the world. However, according to a recent report from the World Health Organization concerning the use of pesticides worldwide, there are an estimated 26 million human non-fatal pesticide poisonings, with about 220,000 deaths annually. These data emphasize that human health problems associated with pesticide usage still exist. In the demographic catastrophe, which now faces all former USSR countries, there may be a role played by pesticides. Undoubtedly a steadily growing number of newborn abnormalities in Russia during last 20-30 years are partly the result of enormous pesticide use in Soviet agriculture. The growing concerns about the public health and environmental impacts of pesticides have led many in the general public and the government to question whether all the benefits of pesticides, such as the perfect red apple, are worth the associated costs of environmental pollution, human illness and loss of life, bird kills, and the destruction of other beneficial natural organisms. Indeed, some agriculturists have been viewed as primarily concerned with promoting commercial interests rather than protecting public health and the environment. Certainly serious ethical and moral investigations of the social policies related to pesticide use must consider all the risks as well as the benefits. To regain public trust, difficult questions regarding our scientific responsibilities concerning pesticide use need to be investigated and evaluated. Sound, safe, pesticide use policies need to be implemented to reduce pesticide use without reducing crop yields. Some nations, like Sweden and Indonesia, already have instituted changes in pest control. These changes have reduced pesticide use by approximately 65% without reducing crops yields, and with some crops, yields have actually increased. Reduced pesticide use policies were implemented in Russia after the collapse of the USSR. Without state subsidies, the use of pesticides has been declining. The scientific community is indebted to Alexey Yablokov and Lev Fedorov for carefully examining the pesticide impact on public health and the environment. Their studies add to our knowledge and their results suggest ways that public health and environmental pesticide related problems could be avoided. Given the food security needs of the rapidly expanding world human population, a safe and a productive agriculture are vital for the future. David Pimentel College of Agriculture and Life Sciences, Cornell University, USA

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INTRODUCTION In the beginning, “pesticides” meant any chemical formulation (substances and their compounds) which was used to combat living organisms whose presence on agricultural and non-agricultural lands was undesirable, and which humans called “pests” and “weeds,” i.e. insects, rodents, plants, fungi, etc. With time, the understanding of pesticides was expanded, and subsequently included chemical substances used not only to destroy, but also to regulate the lives of, organisms:plant growth regulators (stimulators and inhibitors) and animal behavior managers (attractants, repellants, and sterilizers). Humans try to regulate over 80,000 different species. For example, the potato has 240 known “enemies,” including 23 strains of viruses, 6 bacteria, 38 fungi, 128 insects, and 68 worms. There are known to be about 30,000 disease-causing agents (fungi, viruses, nematodes, bacteria) in 3,000 types of cultivated plants. More than 10,000 species of arthropods (insects, ticks, arachnids) affect agricultural plants and animals. Along with agriculture, pesticides are also widely used in forestry and fisheries, in energy and railroads (to clear plants), in construction (to protect wood structures), etc. There are approximately 700 individual chemical substances that are used as pesticides in the world, out of which several thousand formulations can be made. Pesticides were massively used, especially in the first decades after WWII, thus becoming one of the largest risk factors to human life and health, as well as to the entire natural environment. In 1962, Rachel Carson [2] described the terrible consequences of using pesticides in a way that the general public could understand for the first time. She also showed the most important difference between pesticides and other pollutants:pesticides are not production waste, but are introduced into the environment deliberately. For the first time, the well-founded hypothesis was stated that, with time, poisonous and foreign chemical substances could make the Earth uninhabitable. In the USSR in the 1970-80s, there was an unprecedented amount of research on the consequences of pesticide use. More than 70 scientific institutes participated in a secret program, studying the consequences of pesticide use on human health. Several hundred masters theses and doctoral dissertations were written, the majority of which are still inaccessi-

10


ble today. However, during the “glasnost” period in Russia in the 1990s, abstracts of these dissertations passed into the public domain. These abstracts were widely used in this book. This work is not an attempt to look at the past and future of the pesticide problem from the environmental point of view. After the general discussion of pesticides’ properties and use in the USSR (Chapter 1), we look successively at the unexpected consequences of pesticide use, for the natural environment, humans, and for agriculture itself.This work concludes with “Lessons Learned from Pesticides,” food for thought for policymakers, ecologists, and farmers. This book is an abridged English version of the publication Pesticides: The Toxic Impact on the Biosphere and Humans (Moscow, “Nauka,” 1999, 462 pp., Center for Russian Environmental Policy seria’ “Lessons of the XXI century”). Authors are sincerely grateful to many people in Russia and other countries who have made possible the writing of this book. They helped us to collect new material, encouraged us to familiarize ourselves with results that had been inaccessible, and supplied us with new literature at a time when Russia’s scientific libraries were suffering from the financial crisis in Russian science, and were not receiving information. The authors are grateful to the Wallace Genetic Foundation, which has made it possible to prepare and publish this book and Ms. Julia P. Poger for enormous work with the translation of the book. Any questions and comments may be sent to the authors at The Center for Russian Environmental Policy (Moscow, 119991, Vavilov Street, 26; fax: (095) 952-80-19; e-mail: [email protected]; [email protected]).

Chapter 1. PESTICIDES IN THE USSR

11

CHAPTER 1 PESTICIDES IN THE USSR This chapter briefly looks at some general characteristics of using, regulating, monitoring and controlling pesticides in the USSR. This information will help Western readers better understand the unique state system of pesticide production, dispersal and use that existed in the USSR. 1.1. Scope of Use Approximately 3,000 tons of pesticides were produced in the USSR in 1938. DDT and HCH (hexachlorocyclohexane) started being produced immediately following WWII, and organophosphate pesticide (OPP) production began in the 1950s. Pesticides in the Soviet Union were poured out on fields in an evergrowing stream. In 1989, 88% of agriculturally cultivated land was treated with pesticides. Table 1.2 gives us an idea of the volume of pesticide use. Table 1.2. Growth in the number of pesticides used in the USSR [3]

Years

Area of pesticide use, millions of hectares

% of all fields

Average in the regions of use, kg/ha

Average per capita, kg

1970

103

45

1.5

0.75

1976–80

159

70

1.6

1.0

1981–85

182

80

1.8

1.3

1989

200

88

2.1

1.7–2.7

Several regions in the USSR received a much more serious “pesticide impact” (table 1.3). Undoubtedly, pesticide production in the USSR was stimulated to some degree by the creation of a huge and powerful chemical weapons industry in the 1940–50s. When it became clear at the end of the 1960s that more than enough chemical weapons were being produced in the USSR, the question arose of what to do with the factories, the hundreds of thousands of workers, and the many scientific centers that had all been created to produce those chemical weapons (for details, see L. A. Fedorov. The Undeclared Chemical War in Russia: Policies Against the Environment. Published by The Center for Russian Environmental Policy (M., 1995, 304 pp.). The leadership of the CPSU, which determined the entire life of the country, felt that pesticide production was a good solution. This decision was also facilitated by the virtual collapse of the soviet and collective farm (sovkhoz and kolkhoz) system,

12


Table 1.3. Average annual pesticide exposure, 1980–84, by active substance (a.s.) in several USSR Regions [3] Exposure range, kg/ha of pasture Regions

Region

Separate farms

Krasnodar Krai

4.9–15.2

19.6

Rostov Oblast

0.2–11.6

20.4

Russia

Ukraine Western and Southern Regions

9.2–38.5

Northern and Eastern Regions

2.9–3.6

Moldavia

3.4–36.5

75.5

Armenia

0.06–80.1

97.3

Azerbaijan

4.8–237.5

Turkmenistan (Ashkhabad Oblast)

37.8–87.7

Tajikistan

3.4–13.5

Uzbekistan (Djizak Oblast)

0.8–20.7

Kirgiztan

1.0-3.6

6.4

which had produced very little, and was not able to ensure food sufficiency for the country. Pesticides played a key role in using more chemicals in agriculture, which was officially adopted as the main way to develop the agro-industrial sector. As a result, by the middle of the 1980s the USSR became one of the world leaders in pesticide use (per hectare and per capita). This “spending” practice reigned supreme in the USSR agro-industrial complex, as the main indicator of development was the amount of spending, not increasing harvest size or decreasing agricultural production costs. The USSR created special institutions called plant protection units. Their success was not determined by harvest size, but by fulfilling the plan for chemically treating the fields. In the search for weighty accounting figures, sometimes pesticides were just transported out and dropped by the side of the fields. Planning any pesticide use took place much earlier than the actual use, sometimes by two or three years, without considering specific fields or seasonal conditions. The kolkhozes and sovkhozes procured pesticides at a large discount that was determined by huge state subsidies, sometimes for a tiny fraction of the real cost (often on credit, which was officially written off their accounts the next year). Pesticides were normally used in much larger quantities and much more often than recommended. Instead of pesticides


13

being used on some fields, they were used on all of them. Aviation was widely employed, not because of production necessity, but because there were no appropriate land-based delivery systems. In 1987, over 96 million hectares were treated from the air, more than 63% of the overall volume of the area treated with pesticides. In so doing, the rules for treating fields from the air were almost always violated. Even according to official, clearly exaggerated, data, no more than 20% of the area treated with pesticides had been treated in accordance with regulations. Pesticides were being used 2-3 times more than recommended in instructions as a rule, not as an exception. In 1988, an evaluation showed that 25% of the collective farms exceeded specific rules for pesticide use. 1.2. Regulation and Control In 1954, the Committee on the Study and Regulation of Pesticides was created under the USSR Ministry of Health’s (Minzdrav) State Sanitary Inspection; the Committee was mandated to direct research on pesticide use regimes. However, open information about this organization’s activities is scanty. MPC (maximum permissible concentration) — the highest concentration of a harmful substance in the environment (air, water, and soil), where this substance does not act unfavorably in the human body over an unlimited length of time. ASLI (approximate safe level of impact) — the temporary approximate health regulation of the content of harmful substances in the air of workplaces and population points, in the water in reservoirs, and in food products. Used for preventive health supervision. Established using mathematical equations. The State Commission (Goskomissia) on Chemical Methods for Combating Pests, Disease, and Weeds was created in the USSR in 1960. Although formally located in the USSR Ministry of Agriculture (further Minselkhoz), in practice it was given interagency status and included representatives of the USSR Ministry for the Chemical Industry (Minkhimprom), Minzdrav, and the USSR State Planning Agency (Gosplan), along with representatives of Minselkhoz. Goskomissia’s main task was to determine how advantageous it would be to produce and use each new pesticide in the USSR; however, in actual fact, Goskomissia sharply weakened the role of the Minzdrav Committee created earlier. In 1964, a special state center to carry out the above work was created in Kiev (Ukraine):the “All-Union Scientific Research Institute on the Health and Toxicology of Pesticides, Polymers, and Plastics” (VNIIGINTOKS). In 1969, a

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clinic was even opened within VNIIGINTOKS to study and treat human pathologies of chemical etiology. FD50 (average fatal dose) is a lethal (fatal) dose causing death in 50% of laboratory animals. FC50 is a lethal (fatal) concentration causing death in 50% of laboratory animals when the pesticide is absorbed through the respiratory tract (inhalation) as a steam or aerosol. The lower the fatal dose or concentration of a pesticide (i.e. the values for FD and FC), the higher its toxicity. The analogue to FD50 for plants would be, in Russian, ED50, the dose of herbicide that will decrease the plant mass by 50%. From the 1960-80s, about 50 state medical institutes throughout much of the USSR, coordinated by VNIIGINTOKS, evaluated the toxicological and health characteristics of pesticides. Pesticides’ hygiene and toxicology was widely researched, not only in Kiev, Tashkent and Moscow, but also in Dushanbe and Tbilisi, Erevan and Minsk, Ashkhabad and Samarkand, Lvov and Leningrad, Bishkek and Alma-Ata, Ryazan and Saratov, as well as in other cities. Let us give two examples concerning organochlorine pesticides (OCPs) and OPPs. From the time it was “banned” in the USSR in 1970, the official presence of DDT in meat, oil, milk, and eggs was “not allowed” [4]. In practice, DDT never disappeared from the Soviet diet. It was always detected by the services monitoring food products, especially in eggs, meat, and dairy products; however this information became accessible to the public only in the 1990s. The USSR Health and Epidemiological Service practiced a system of temporary permitting. One example is the “temporary” maximum permissible level (MPL) for DDT content in food products. Fifteen years after the “ban,” standards were the following (in mg/kg) [3, 5]:milk – 0.05 (temporary), children’s and health food products – 0.05 (temporary), eggs – 0.1 (temporary), meat – 0.1 (temporary), fish – 0.2 (temporary), and canned fish – 0.2 (temporary). Twenty years after the “ban” there are even more stringent “temporary” hygienic standards (in mg/kg) [6]:milk and dairy products – 0.005, meat – 0.005, and eggs – 0.005. A second example concerns thiometon, an OPP.Back in 1964, information showed that milk containing 0.001 mg/l of thiometon was toxic for calves [3]. At the same time, and for several years, the standard for the “acceptable content” of thiometon in food products for humans was 500 times larger (!) – 0.5 mg/kg. The situation was the same for many pesticides. Table 1.4 gives an idea of how different standards for pesticide content and presence in food products evolved. As a rule, we can see that the standards only become stricter. The most deplorable fact is that, in many cases (40%) the new


15

health standards were especially strict – they generally did “not permit” the presence of pesticides in food products using existing measurement methods (blacked out). This shows the methodological helplessness of those who were developing and prescribing these standards in the beginning. The issue of how well pesticide presence in food products was monitored, a task given to the Health and Epidemiological Service of Minzdrav, merits particular study. Monitoring and controlling started on a serious scale only in Table 1.4. Evolution of stricter standards for pesticide content in food products in the USSR/Russia in 1977-97. Hygienic Standard, mg/kg [4,7,8,9,10] PRC1

MPL1

# times

(1977-81)

(1992-97)

stricter

Pesticide

Food Product

Formothion

citrus

0.2

0.04

E5

Diazinon

beets

0.5

0.1

E5

meat fat

0.7

0.01

E70

potatoes

2.0

0.1

E20

vegetables, corn

2.0

0.5

E4

apples, grapes

2.0

0.05

E40

0.5-2.0

Not permitted

∞

0.8

0.01

E80

potatoes

0.05

0.006

E8

sugar beets

0.05

0.0006

E83

corn

0.1

0.0006

E167

apples

0.05

0.0001

E500

cabbage, cucumbers,

1.0

0.5

E2

1.0

0.1

E10

Insecticides, Acaricides

Lindane

cereals Tetrachlorovinphos

grapes, gooseberries, strawberries

Chlorpyrifos

Malathion

tomatoes, apples Dicofol

cucumbers, tomatoes, fruit, grapes

Fenitrothion

mushrooms

0.1

Not permitted

∞

Methoxychlor

potatoes

7.0

0.3

E23

Tedion

grapes

0.7

0.1

E7

citrus

0.7

0.2

E3.5

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Table 1.4. Continued. Toxafene

potatoes

0.1

Not permitted

¥

Phosalone

potatoes, soy

0.2

0.1

E2

Dimethoate

potatoes, cereals

0.4

Not permitted

∞

sugar beets, apples, grapes cabbage

0.15

Not permitted

∞

Phosmet

sugar beets

1.25

0.25

E5

Trichlorfon

cabbage, tomatoes, melons,

1.0

0.1

E10

1.0

0.05

E20

cucumbers, potatoes, cereals, beans beets, carrots, eggplants, onions Herbicides Daminozide

apples

30.0

3.0

E10

Atrazine

corn

0.1

0.03

E3.3

Dactal

plant products

3.0

Not permitted

Diuron

grapes, fruit, citrus

0.05

Not permitted

Monolinuron

potatoes

0.1

Not permitted

∞ ∞ ∞

Simazin

cereals, corn

1.0

0.1

E10

Trifluraline

carrots

0.5

0.01

E50

0.35

Not permitted

∞

1.0

0.02

E50

2.0

Not permitted

∞

cereals

1.0

0.2

E5

potatoes

0.6

0.1

E6

Fungicides, Seed Protectant Captan

vegetables, fruit, melons, berries

Metiram

cereals, beets, vegetables, fruit, berries

Folpet

potatoes, apples, tomatoes, pears, cherries, gooseberries

Zineb

Legend: 1 PRC: Permissible Residual Concentration; MPL: Maximum Permissible Level

the 1980s. This is how the work was carried out: in Russia in 1984, only 12% of the area treated with pesticides was monitored by the plant protection unit laboratories; the remaining pesticides were monitored only in 3.4% of agricultural production [3]. In Moldavia, one of the regions that was most contaminat-


17

ed by pesticides in the USSR, there was no unit to observe contamination levels [11]. In many regions, pesticides were not analyzed in food products, or were analyzed randomly. The overall number of pesticides monitored went from 17 (!) in Azerbaijan to 127 in Ukraine. In any case, a large number of pesticides that were used were not monitored. Under these conditions, if there is no data on the presence of a particular pesticide in food products, this does not mean that there was no contamination by that pesticide. In 1987, only 800 of 3400 rural regions in the USSR could boast analytical state Agroprom laboratories, in which agricultural products were checked in some way for pesticide content. Even so, these checks covered no more than 5% of all products. The Minzdrav system was no better: in 1988, only 1453 (26.4%) of 5500 health and epidemiological stations in the country were supposed to monitor for pesticide content in food. Nevertheless, in 1987 Minzdrav included only 126 pesticides, and in 1988 only 152 of 262 different types of food products [3]. It is significant that in a large number of cases in the USSR, the reasons pesticides contaminated food products were never discussed. The reasons why 5090% of food products were contaminated by pesticides were not discussed in Azerbaijan, Armenia, Belorussia, Georgia, Kirgizia, Latvia, Moldavia and Ukraine. Moreover, this list shows not only that the Health and Epidemiological, and Agrochemical, Services were unprepared, but also that they did not wish to detect the reasons for food products becoming contaminated by pesticides. For example, the 1988 VNIIGINTOKS report looked at the contamination of products designated for children’s food, while in 1989 this section of the report was absent [3]. The actual percentages of food products contaminated by pesticides were the following: 1987 – 1.85%, 1988 – 2.5 %, 1989 – 2.7 %. In other words, food products overall in the entire country did not become less contaminated, but more so. The long-term widespread use of DDT over a number of years demonstrates one typical Soviet trick – abusing loopholes in the rules: DDT was actively used for decades, while not being on lists of permitted substances, a situation condoned by the Health and Epidemiological Services and their on-site agencies. Pesticide use systematically was not in accordance with the permissible standards in the USSR. In 1976 the USSR introduced a “System of Labor Safety Standards: Harmful Substances, Classification and Overall Safety Requirements,” according to which all harmful substances were broken down into four risk classes, taking into account several different indices (table 1.5). According to VNIIGINTOKS, potent toxic agents (PTA), “where the fatal dose (FD50) is less than 50 mg/kg, are not introduced into agriculture, are not produced in the USSR, and are not imported from abroad” [12]. In actual fact, Risk Class I OPPs with an FD50 for laboratory animals of less than 50 mg/kg were not only actively used, but were also produced in the USSR for many years (including such OPPs as parathion, demeton, octamethyl pyrophosphoramide, methyl ethyl

18


Table 1.5. Classification of chemical substances according to their human risk factor (State Standard GOST 12.1.007-76) Index FD50 when

Average fatal

Risk

Degree

introduced into the

MPC in workplace

concentration

Class

of Risk

stomach, mg/kg

air, mg/m3

in the air, mg/m3

I

Very High

50000

parathion, methyl parathion, and pirofos). The practice of widely using pesticides from Risk Class I still goes on: in 1991, 7% of 125 permitted individual pesticides, and 16 mixed formulations were classified as being on the Risk Class I list [13]. It was often the case in the USSR that pesticides were used and even produced before, sometimes even without, developing health protocols. This is seen when we analyze Tables 1.6 and 1.7, where a number of pesticides were used for many years, in essence illegally. Health protocols for different environments were never formulated until the pesticide was banned. The negative consequences of using each pesticide in practice were not gauged on laboratory animals, but on their interaction with humans and the environment. This practice went on until recently. Four hundred eighty-one formulations and compounds were included in the official list of pesticides “permitted for use in agriculture from 1986-90” [14]. In 1990, the MPC and other health protocols were developed for only 127 pesticides in food products, 105 pesticides in bodies of water used for hygiene and drinking, 78 pesticides in fishery reservoirs, 31 pesticides in farm animal feed, 81 pesticides in the soil, and 119 pesticides in work zone air [1]. There were no MPCs for the remainder of the pesticides permitted for use and, according to existing rules, they should not have been used. Nevertheless, they were. It was usual in the USSR that, even when strictly complying with the MPC, neither environmental nor human safety were ensured. Table 1.6 shows MPC examples of the water from reservoirs where the Health and Epidemiological Service needed to toughen MPCs in later years because several factors had been neglected. Shaded pesticides in this table (as well as following tables) were subsequently officially banned. In the USSR, permitting and banning pesticides took place without considering human or environmental interests. Fig. 1 illustrates this trend; you can clearly see the spikes in pesticide banning in the USSR/Russia.


19

Table 1.6. Evolution of MPC changes in waters of reservoirs used for hygiene and drinking [3] MPC in reservoirs used for hygiene and drinking, mg/l Pesticide

1972

1983-85

# of Times 1992

Stricter

Herbicides DEF

0.01

0.0003

2,4-D-Butyl

0.5

0.5

0.002

x250

Dalapon

2.0

2.0

0.04

x50

Diquat

0.02

0.002

x10

Diuron

1.0

0.06

x17

Monolinuron

0.5

0.05

x10

3.0

0.002

E1500

0.3

0.004

x75

1.0

0.01

x100

Chlorpyrifos

0.02

0.002

x10

Iodfenphos

0.05

0.01

x5

Prometrin

3.0

x33

Insecticides, Acaricides Diazinon Dichlorvos

1.0

Methyl Parathion

0.02

0.02

0.002

x10

Methylnitrophos

0.25

0.25

0.006

x42

Trichlorfon

0.05

Etaphos

0.05

0.01

0.05

0.0004

x5 E125

Fungicides Captan

2.0

0.2

x10

Mankozeb

0.015

0.003

x5

In general, a pesticide was banned because of an accumulation of data on negative effects, effects that were not observed or were considered acceptable at the time the permit was issued. Table 1.7 contains a list of popular pesticides, and gives an idea of how our government changed its thinking towards them. Here, as in other tables, the names of those pesticides banned after many years of use are shaded. Each pesticide used in the USSR had the same history: permit, realization that a mistake was made, ban. The only variable in all of these histories was the length of time required to understand that a mistake had been made when the permit was issued. When removing the pesticide from circulation, officials cited several reasons: “very high toxicity” (aldrin, dieldrin, parathion, demeton,

20


Numberof of Banned Banned Pesticides Number Pesticides 110

90

70

50

30

10 95 19

19 95

93 19

19 93

91 19

19 91

89 19

19 89

87 19

19 87

85 19

19 85

83 19

19 83

81 19

19 81

79 19

19 79

77 19

19 77

75 19

19 75

73 19

19 73

71 19

19 71

69 19

19 69

67 19

19 67

-10

Fig. 1. Dynamics of banning pesticides in the USSR/Russia

octamethyl pyrophosphoramide, aldicarb, vamidothion); “high toxicity” (heptachlor, thiometon, methylmercaptophos, phenkapton); “carcinogenic” (DDT, HCH, diuron, linuron, maneb, monolinuron, polychlorpinen, 2,4,5-”); “mutagenic” (maneb, 2,4,5-”); “teratogenic” (DEF, maneb, nitrophene, 2,4,5-”); “embryotoxic” (DEF, DDB, nitrophene); “gonadotoxic” (nemagon); and “remote neurotoxicity” (dichlorfenthion, leptophos). In actual fact, the “bouquet” of environmental ramifications caused by each of these pesticides that are banned today is much richer (for more detail, see Chapters 3, 4, and 5). Soviet society had no information on the pesticide poisoning of its people and environment. Rachel Carson’s prophetic work [2] was translated and published in a limited number “for official use”: we did not learn from others’ mistakes, but only from observing our own. Thus, for example, there was very little accessible data, some of which was contradictory, on OPP toxicity until the 1990s. In 1967 people still mentioned that demeton was banned for agricultural use; in 1980 there was silence. The 1980 Official Handbook [4] recommended, besides demeton, several other pesticides that had also been banned long before (octamethyl pyrophosphoramide, thiometon, vamidothion, phenkapton). When republishing the handbook in 1985, among those pesticides “permitted for use” in agriculture in the USSR were OPPs that already were banned five years before (octamethyl pyrophosphoramide, thiometon, vamidothion, phenkapton) [8]. The same happened in practice as well: Lindane and the HCH


21

Table 1.7. Evolution of Pesticide Use in the Soviet Union/Russia [3] Pesticide

Popularized and recommended in the USSR [3,4,5] 1966 1980 1985

1990

Minzdrav final decision

1997

[8,15,16]

Organochlorine Pesticides Aldrin

+

-

-

HCH - mix of 8 isomers +

+

+

+

Ban, 1990

HCH (tech grade)

+

+

+

Ban, 1986

+

Ban, 1972

Heptachlor

+

+

+

Ban, 1986

DDT

+

-

-

Ban, 1970

Dieldrin

+

-

-

Ban

Gamma-HCH

+

+

+

Polychlorpinen

+

+

Toxafene

+

+

+

Chlordan

+

+

-

Endosulfan

+

+

+

+

Ban, 1990 Ban, 1981

+

Limited, 1986; Ban, 1991 Ban

+

+

Limited, 1984

Mixed Organochorine and Organophosphorus Pesticides Bromophos

+

+

+

Ban, 1991

Iodfenphos

+

+

+

Ban, 1991

Fenchorophos

+

+

+

+

+

+

Dichlorvos

+

+

Naled Tetrachlorovinfos

+

Chlorpyrifos Trichlorfon

+

Etaphos

+

+

Ban, 1994 Ban, 1991

+

+

+

+

+

+

+ +

+

+

+

+

+

+

Limited, 1984 Limited, 1986 Ban, 1994

Organophosphorus Pesticides Formothion

+

+

+

+

Diazinon

+

+

+

+

DEF

+

+

+

Ban, 1986

Thiometon

+

+

+

Ban, 1978

Malathion

+

+

+

Vamidothion

+

+

+

Fenthion

+

+

+

Demeton

+

+

-

+

+ Ban, 1994

+ Ban, 1978

+

Ban, 1994 Ban, 1967

22


Table 1.7. Continued. Methyl Parathion

+

+

+

Methylmercaptophos

+

+

+

Fenitrothion

+

+

+

octamethyl

+

+

+

Menazon

+

+

+

Parathion

+

+

+

Limited, 1986 Ban, 1986

+

Ban, 1994 Ban, 1978

pyrophosphoramide + Ban, 1972

Phenkapton

+

+

+

Phosalone

+

+

+

+

+

Ban, 1978

Dimethoate

+

+

+

+

+

Limited, 1986

Phosmet

+

+

+

+

+

Limited, 1986

Phenthoate

+

+

+

+

+

Other pesticides Dinobutone

+

+

Aldicarb

+

+

Atrazine

+

Chlordimeform

+

Ban, 1990 Ban, 1986

+

+

+

-

+

Ban, 1978

Ban, 1994

Diuron

+

+

+

Ban, 1987

Linuron

+

+

+

Ban, 1986

Maneb

+

-

-

Ban, 1986

Monolinuron

+

+

+

Ban, 1986

+

+

Ban, 1986

Nitrophene Pentachlorophenol

+

+

+

+

Prometrin

+

Ban

+

+

+

Propachlor

+

+

+

Fenvalerat

+

+

+

Ban, 1994

+

+

+

Ban, 1994

Thiram

+

2,4,5-T

+

Ban, 1994 +

Limited, 1986

Ban, 1970

mixture itself were banned before the beginning of the 1990 season in March, whereas this ban was not reflected in actual practice (Table 1.8). In this case we can hardly say that the remaining HCH was being used “as an exception.” Here we see agricultural workers disregarding the ban. Materials from Minzdrav’s 1987 examination of Uzbekistan are a good


23

Table 1.8. Use of HCH in several Russian regions after its official ban in March 1990 [17, 18] Used, in tons Regions

1990

Altai Krai

1991

1992

23.8

46.5

71.4

Irkutsk Oblast

7.3

No data

15.4

Kurgan Oblast

24.4

17.2

2.2

Krasnodar Krai

22

No data

No data

Lipetsk Oblast

380.9

No data

78.5

Penza Oblast

149.1

No data

No data

Rostov Oblast

211.1

No data

No data

Samara Oblast

48.7

90.4

17.4

Stavropol Krai

34.0

No data

No data

Tambov Oblast

158.6

60.1

47.1

Ulyanov Oblast

33.3

2.8

1.7

Volgograd Oblast

29.8

No data

No data

illustration. When walking along the farmyards, you could see pesticides banned for sale almost everywhere [3]. As could be seen even in official (and most likely seriously understated) data [17], DDT was used much later in Russian agriculture than when it was officially banned in 1970: Region

Year

Belgorod Oblast

1978

Kursk Oblast

Amount, tons 1.83

1982

28.9

1978

14.5

1982

19.9

Lipetsk Oblast

1978

8.4

Samara Oblast

1987

2.9

1988

0.4

1978

36.6

1979

23.4

Tambov Oblast Tatarstan

1987

0.07

Voronezh Oblast

1982

4.1

24


In 1987-89, DDT was found quite often when checking the composition of food products throughout the entire country. In the USSR, monitoring and controlling the presence of pesticides and their metabolytes was a much slower process than the process by which pesticide use was expanded. In spite of the fact that the Health and Epidemiological Control, the State Committee for Hydrometeorology, the Agrochemical Service, and others all formally monitored pesticides, the USSR showed active negligence. The shaded box below gives a quote from a 1989 dissertation that generalizes the experience accumulated over several decades of “monitoring and controlling.” “As seen from the data received in the Sysin Scientific Research Institute (NII) for General and Communal Health Protocols of the Academy of Medical Sciences (AMN) of the USSR, and in the Kiev-based A.N. Marzeev NII for General and Communal Health Protocols (G.I. Sidorenko, M.A. Pinigin, M.G. Shandala, et al), • Physiological and biochemical changes in the human body are observed when MPC rates in the air are exceeded by a factor of 3-4, • Clear changes in health are registered when the MPC is exceeded by a factor of 8, • Acute poisoning is possible when the MPC is exceeded by a factor of 500 or more.” From the dissertation, “Health Justifications for Measures Taken to Prevent Unfavorable Effects from Toxic Fogs when Using Pesticides in Cultivating Beets.” Kiev, 1989, 113 pp. [107]. As can be seen from the boxed quote, monitoring and controlling pesticides both in the environment and the biosphere could not have been taken seriously: government representatives were prepared ahead of time to act only in response to acute poisoning. In 1986, in the Rostov Oblast, laboratories evaluating water contamination were equipped to account for only 20 of the 128 pesticides that were found in the water. In Moldavia, the Health and Epidemiological Service was monitoring and controlling only 43 of the 130 formulations used [3]. Overall throughout the USSR at the end of the 1980s, fewer than 30 of the more than 400 formulations permitted for use were being monitored and controlled in the environment i.e. in the soil, water, and air [1]. A system for monitoring and controlling pesticide contamination of the environment and, in particular, of the soil, began within the USSR State Committee for Hydrometeorology (Gosgidromet) only in 1974 [17]. In the beginning, they worked with only a very tiny number of the pesticides


25

actively being used. However, even in the beginning of the 1990s, the on-site subdivisions of the Hydrometeorological Service analyzed only 6-10 pesticides apiece: the Northern Department (Arkhangelsk Oblast and the Republic of Komi) analyzed six OCPs (DDT, DDD, DDE and three HCH isomers); the North-Western Department (Leningrad Oblast) analyzed 6 OCPs, the Far East Department analyzed 6 OCPs, the Baikal Department analyzed 6 OCPs, the Krasnoyarsk Department analyzed 6 OCPs, the Yakutsk Department analyzed 6 OCPs, etc. [17]. The Hydrometeorological Service was not able in principle to give an objective picture of environmental pesticide contamination with this amount of knowledge. 1.3. Storage and Disposal The pesticide storage situation in the 1960-70s was typical of what was found in Uzbekistan: only 40% of 1082 storehouses met health and hygiene requirements [A62]. Towards the end of the 1980s, only 75% of the pesticides used in the USSR were provided with storehouses [1]. A significant number of the chemical substance storehouses (20% in Russia, 23% in Ukraine) did not meet elementary health requirements. In Azerbaijan, there were no specialized storehouses for pesticides at all – these chemicals were being stored together with mineral fertilizers [19]. From that time on, very little has changed. Pesticides produced in the USSR were usually supplied to farms in extremely inconvenient sizes and packaging (in 100- to 200-liter containers, or in 20- to 50-kilogram bags), with labels that were not in accordance with international standards. The concentration of working solutions of pesticides did not hold up. The pesticide delivery technology did not meet requirements. Because of insufficient packaging and specialized technology, up to 20% of the pesticides were lost on the way to the field. Because sprayer construction was of low quality, 30% of the pesticides used were lost. Pesticide storehouses were examined in five regions of the Astrakhan Oblast because of the rise in the Caspian sea level and the possibility of flooding in 1993-95. Only eight of 39 storehouses were standard; however, even they did not meet construction standards, and most were in terrible condition. Residual pesticides contaminated the land surrounding many of these storehouses. In the Volodarsk Region, the maximal values for contamination were: atrazine at 1330 times MPC; DDT at 53 times MPC, methyl parathion at 1330 times MPC, trifluraline at 8000 times MPC, and phosalone at 107 times MPC. In the Kamyzyak Region, trifluraline exceeded the MPC by 3333 times. The most contaminated areas were storehouses on farms in the Privolga Region, where pesticide content was: DDT at 133 times MPC; methyl parathion at

26


3333 times MPC; trifluraline at 2500 times MPC; and phosalone at 1000 times MPC [3]. In the Odessa Oblast (Ukraine), more than 890 tons of banned or unsuitable pesticides were amassed by the end of 1987. In Uzbekistan, 7000 tons of the banned pesticide DEF had accumulated by 1989. The usual method for disposing of pesticides in the USSR was walling them into spent quarries and mine shafts. For example, more than 3000 tons of pesticides were walled into unfitted vertical boreholes in the Krasnodar Krai. The complete destruction of pesticides has become a large environmental problem, comparable in scale to the problem of destroying chemical weapons stocks. About 40,000 tons of unused pesticides (banned or too old to be used) had accumulated in the countries of the former Soviet Union, about half of which are located in Russia. 1.4. Economics of Use While in 1960 103 different pesticides were permitted for agricultural use, in 1990 the number of permitted formulations had grown to more than 667 (including 217 insecticides). Table 1.9 gives an idea of the pesticide production and supply dynamics in the USSR. By the middle of the 1980s, the USSR produced more than 300,000 tons of pesticides in approximately 60 different nomenclatures (about 100 formulations). In 1989, only 40% of the pesticides produced met world standards. In the USSR it was thought that 1.2-1.3 billion rubles a year were spent on pesticides, while 7-8 billion rubles a year of additional agricultural product were produced (i.e. a 5.8-6.2 ruble return on 1 ruble spent in prices from the end of the 1980s) [1]. However, reality was different. There is every reason to speak not so much about profits earned by pesticides, but about the direct damage to rural and forestlands, to human health, etc. caused by the large-scale use of pesticides. Let us look at just one example. Analyzing the consequences of developing the rice industry in the Krasnodar Krai (southern Russia) showed that as a Table 1.9. Pesticide production, supply and imports in the USSR (100% calculations by active substance) [6] Volumes per year, thou. tons Production

1960

1970

1980

1985

1986

1987

30.6

163.8

281.8

346

332

327

46.7

111

145

147

145

Including herbicides Supply

-

170

279

362

346

333

Including herbicides

-

50

127

160

172

169

100

24.1

34.6

42.5

39.9

35.4

Import, as % of supply

1989

330


27

result of the pesticide poisoning of the reservoirs from 1952-75, the fisheries of the region lost valuable fish worth more than 2 billion rubles. At the same time, the entire profit from rice produced during that same period was less than 1.5 billion rubles. In this way, considering only the fishing industry, pesticide use caused economic losses and was dangerous. Along with these calculated losses, we should also add in the uncalculated damage caused to human health. In the 1980s, about 5 million people were living in the Krasnodar Krai, including half in rural areas. No fewer than half of all agricultural workers (about 800 thousand people) were annually poisoned by pesticides. There was an exceptionally high level of infant mortality, retarded children, and children with diminished development in the rice-growing regions of Krasnodar Krai. There were years when the regional military draft office could not send anyone (!) for military service because of the poor health of the draftees. The experience of the USSR in pesticide use is of interest to the entire world because it is an object lesson of the lack of a direct correlation between the amount of pesticides used and the growth in harvest size. In the USSR, pesticide use in practice did not affect harvest increases. Pesticide production in the USSR from 1960-85 grew more than ten times, their use in agriculture from 1960-86 grew seven times, while the cereal harvest stayed the same, in spite of the use of fertilizers and pesticides. The large growth in pesticide supplies to agriculture clearly did not correlate with growth in harvest size. For example, in Ukraine and Kazakhstan, the cereal harvest for 1970-85 stayed the same or even decreased, in spite of the fact that pesticide use doubled. A particular object lesson can be found in Tatarstan (Russia), where for 20 years pesticide use grew 15 times, while harvest size remained the same or, in many cases, decreased. In Russian rice-growing regions (the Far East and Krasnodar Krai), harvests fell simultaneously with the growth of pesticide use. In the Primorsk Krai, harvests decreased from 25 hundredweight per hectare in 1966-79 to 20.4 cwt/ha in 1981-85 [1, 3]. There are two possible explanations for this phenomenon: either the majority of species suppressed by pesticides were not a factor limiting harvest size, or pesticides were not effective enough in suppressing the number of regulated species. In either case, the assertion of how important it is to use pesticides to increase agricultural productivity is not founded in fact (see also Chapter 5). While DDT and toxafene were manufactured in one stage from the available raw materials, parathion and aldrin were manufactured in two stages, as a result of which they were 2-3 times more expensive to produce than the former. Dieldrin and endrin, manufactured in 3 stages, were 2.5 - 3 times more expensive to produce than parathion. Pyretroid allethrin is manufactured in 13 stages, which makes it 40 times more expensive to produce than parathion. On

28


average, modern, more effective formulations were approximately 100 times more expensive to produce than DDT [20]. Often, up to 60 rubles/ha were spent on chemically protecting the plantings, when the planned production cost of cereals was 6.4 rubles/cwt (in prices from the end of the 1980s). Thus, if the harvest was 30 cwt/ha, then the cost of chemical treatment was over 30% of the cost of the cereals. In the USSR, pesticide use was an economic loss even without considering negative effects on human health and environmental damage. Using pesticides to cultivate cereals under conditions in the USSR might somehow be justified economically (though not environmentally!) when the harvest was over than 45-50 cwt/ha (in the USSR the average harvest was 14-17 cwt/ha). We must also consider the damage that pesticides cause to human health, as well as to the condition of fisheries, the unavoidable increase in soil erosion, the decrease in the amount of humus in the soil, the destruction of the soil’s flora and fauna, and the damage to the natural environment (for more detail, see Chapters 3 and 4). Pesticide supporters’ assertions that pesticides are economically highly effective are incorrect, since supporters are only considering the expenses of producing a specific agricultural product in a specific growing season, and not the other factors accompanying pesticides’ use. *** This chapter gave examples of some known, collateral, and unexpected negative effects of using pesticides. The specter of such consequences only grows with each year.

Chapter 2. PESTICIDES IN THE ENVIRONMENT

29

CHAPTER 2 PESTICIDES IN THE ENVIRONMENT Pesticides are one of the main environmental contaminants of the 20th Century. Only a small amount of the pesticides used actually reaches their targets. About 3% of herbicides and insecticides do so; the rest is lost, falling on untargeted plants and animals, and into bodies of water. In other calculations, pesticides reach only about 0.1% of their targets. 2.1. Air Contamination Pesticides (and their stable metabolites) that do not reach their targets are dispersed by air currents, and are the primary air contaminant. When sprayed from the air, an average of 82% of OPPs (organophosphorous pesticides) are lost because particles drift in solution; however, these losses may reach as high as 99% [21]. The distance pesticide aerosols may travel when sprayed using land-based methods is also considerable: when sprayed manually, drops of solution can be found at a distance of 500 m, and when sprayed mechanically, up to 2,000 m from the treated field [21]. An air mass with a dangerously high concentration of pesticides may disperse up to 10 km from where the pesticides were used, i.e. pesticides are able to move a significant distance away from the area that the regulations envisage [22]. Secondary air contamination is caused because pesticides on plant and soil surfaces convert into steam, or disperse by adsorbing on dust particles. Under certain conditions, up to 50% of such OCPs (organochlorine pesticides) as DDT, aldrin, and dieldrin move into the air during the week after a field is treated. DDT evaporates from a treated field at a rate of 10-50 kg/ha a year, depending on temperature, humidity, and air movement [3]. On the second or third day after treatment, OPP concentrations can be higher than on the first day as a result of pesticides converting into steam [22]. Table 2.1 shows the shocking research results for concentrations of the most used pesticides in Tajikistan in the 1970s. You can see that MPCs were exceeded by many times (up to 250 times) in all areas. The first day after cotton fields in Uzbekistan were treated with the OPPs demeton and DEF, the average daily concentration of these pesticides were tenths of a mg/m3 at a distance of 500-1000 m from the edge of the treated field, i.e. many times higher than levels that are safe for humans. When analyzing air contamination by pesticides, it is important to consider not only pesticides in their unchanged form, but also how they transform in the atmosphere, particularly through photochemical oxidation (photolysis). In many cases, photolysis creates products that remain in the environment for a

30


Table 2.1. Average data on pesticide content of work zone air and population points in Tajikistan in the 1980s [A86] Pesticide Concentrations in mg/m3 Zones

Methylmercap

Thiometon

HCH

DDT

-tophos (solution)

(solution)

(powder)

(powder)

Airplane Cabin

0.55

0.43

5.6

-

Fuel Point (airport)

0.37

0.84

5.4

-

Signaler

1.44

0.76

4.6

-

Tractor Driver

0.9

1.1

-

3.6

Manual Spraying

-

1.08

-

4.7

Field Treatment

(at breathing level) Air in Work Zones

0.23

0.36

0.38

0.26

MPC [9]

0.1

0.1

0.01

0.1

Air in Population Points

0.17

0.25

-

-

MPC [9]

0.001

0.001

0.03

0.001

long time. Along with these photochemical transformations, some pesticides can change through hydrolysis and oxidation, forming stable and dangerous metabolites. A 1989 dissertation [A107] may illustrate one of the unexpected physical processes tied to pesticide air contamination. This work appeared decades after dissertations [A72, A74, A81], which described how the insecticide polychlorpinen poisoned numerous groups of beet-growers in the Ukraine. It is known that pesticide aerosols, formed when the pesticide steam settles on surfaces of miniscule droplets of water, are much more toxic than the steam form of the same pesticide. This circumstance turned out to be extremely important. Table 2.2 gives an idea of how dangerous pesticides are to humans when we ignore the role of factors such as atmospheric humidity. Data from Table 2.2. Danger of Pesticides Adsorbed on Droplets of Fog [108] Amount of Adsorbed

MPC in the

MPC Exceeded by

Pesticides in mg/m3

atmosphere in mg/m3

How Many Times

Lindane

62.0

0.03

x2065

Methyl-Parathion

41.3

0.001

x41300

Malathion

46.2

0.015

x3300

DIAZINON

44.7

0.01

E4470

Dichlorvos

48.0

0.002

x23975

Pesticide


31

[A107] are cited only for one situation (where the liquid water content in a fog was 2.0 g/m3, the diameter of the water droplets in the fog was 2 mkm, and the overall droplet surface area in 1m3 of air equaled 6,28 m2). In 1988, instructions were issued by Minzdrav of Ukraine: The Methodology of Predicting the Formation of a Toxic Fog When Using Pesticides in Beet Farming with the Goal of Preventing Poisoning. It is difficult to say why instructions were linked specifically to Ukraine and sugar beets. After all, this is an important physical phenomenon with tragic consequences, with no specific link to the territory, pesticide (or other toxic substance), or even time intervals. A very heavy rain in an area where pesticides (even those with low toxicity) are used is a direct guarantor of trouble. After it rains, the pesticide’s real concentration per cubic meter of air may be millions of times higher than is usually officially calculated from the ideal gas law. All that is needed for this to take place is for there to be a low wind speed and an inversion temperature in the layer of air closest to the earth, i.e. that does not allow this layer of air to rise. It is practically impossible to predict the appearance of such a toxic fog ahead of time. Based on the real scale of pesticide use in the world, the dispersal of pesticides in dangerous concentrations in the atmosphere over large territories is inevitable. 2.2. Water Contamination Pesticides have a constant effect on the hydrosphere, i.e. on surface and underground water. The contamination of internal bodies of water with OCPs has become global. OCPs are stable in water, are able to accumulate in hydro-organisms and bottom sediment. Instructions say that toxafene remains in the water for up to a month, and for up to 150 days in treated plants [15]. In actual fact, after lakes have been treated, toxafene has been observed in the water and hydro organisms for 6-7 years [3]. The Volga and Kuban river basins, as well as the Azov and Black seas, are the watersheds most seriously contaminated by pesticides in Russia (table 2.3). No matter how small the numbers in the table may seem (“micrograms”), they are always higher than standards permit. Since these rivers are also used for fishing, a bioaccumulation of micrograms of DDT and HCH in a liter of river water turns into milligrams of these OCPs in a kilogram of commercial fish. Table 2.3 shows how dirty the Volga is. This is the river most contaminated by stable OCPs in Russia. Pesticides are present almost constantly in the water, bottom sediment, and hydro organisms of the downstream Volga and its deltas, and pesticide content sometimes exceeds MPC by a factor of thousands [1]. In Lake Baikal, the largest fresh water reservoir in the world, DDT content has also reached dangerous levels. According to 1988 data, 254

32


Table 2.3. Dynamic of Stable OCP Contamination of Several Rivers in Russia [13, 18, 23] Maximum Concentrations, in mkg/l SDDT

SHCH

Watershed

1986

1990

1993

1986

1990

1993

Volga

10.1

2.70

0.6

23.5

19.7

6.0

Ural

0.26

1.43

0.47

0.33

1.53

0.68

Don

1.74

0.73

No Data

1.13

0.5

No Data

Kuban

1.11

0.11

0.56

0.06

0.03

0.12

Lena

0.15

0.51

Not Observed.

0.04

0.71

0.09

Ob

3.46

0.54

1.21

1.35

2.78

3.86

Enisei

0.50

Not Observed

Not Observed

1.76

0.21

0.2

Amur

1.47

0.15

0.09

4.45

1.53

0.19

MPC [24] 1 2

100

20

Absent

Absent

Bodies of water: 1 – domestic water supply, 2 – fisheries.

tons of DDT and its metabolites (åDDT) are already dissolved in the waters of the lake, including 63 tons of DDT itself. Annually, the Baikal receives 900 kg of åDDT that falls from the air, and 1.5 tons from rivers and streams [25]. More than 80% of Moldavia’s bodies of water in 1985-86 were dangerously contaminated with pesticides. The level of pesticide contamination was high in the main rivers of Ukraine: the concentrations of DDT and its metabolites in the Dnepr reached 0.384 mkg/l [23]. At the end of the 1970s, OCPs were found in the waters of Belorussia’s rivers: the Dnepr, Western Dvina, Pripyati, and Nemana. Of the 960 analyzed samples, 82.7% contained DDT, and 81.6% contained HCH. Concentrations of the herbicide 2,4-D (amino salt) in drainage runoffs reached 1400 mkg/l (standards in those years were 200 mkg/l, and today are 2 mkg/l) [3]. In 1976-78, OCPs were detected without exception in every body of water studied in the Caucasus region (lake Sevan, the Mingechaursk Reservoir, and the Razdan, Inguri, Kura, and Rioni Rivers). DDT was found in 77.3% of samples, HCH in 96.4%, and granosan in 100%. The problem of OPP contamination of the bodies of water of Central Asia became relevant after OPPs started to be widely used together with OCPs in intensively treating irrigated fields. A large amount of the water used for irrigation returned to the rivers and canals. According to instructions, OPPs supposedly


33

decompose rapidly in water; however, existing data showed the contrary [3]. For example, phosalone was detected in sludge (up to 8.10 mg/kg), water plants (up to 1.86 mg/kg), and fish (up to 20 mg/kg). Phosmet was also detected: in sludge (up to 1.33 mg/kg), water plants (up to 0.8 mg/kg), and fish (up to 3.08 mg/kg) [26]. When examining the Syrdarya and Amurdarya watersheds in 1979-80, it was found that DDT concentrations reached 0.119 mkg/l, and lindane concentrations reached 0.076 mkg/l [23]. In the cotton-growing regions of Uzbekistan in the beginning of the 1960s, concentrations of DDT in the canals and ditches reached 5.4 mg/l, of Aldrin reached 1.2 mg/l (600 times higher than the acceptable level), and of HCH reached 2.52 mg/l [A49, 27]. The concentration of methylmercaptophos reached 9.2 mg/l (900 times the acceptable level) in the water sources of the Khorezm Oblast of Uzbekistan [28]. In Tajikistan when cotton plants are sprayed from aircraft during planting, the concentration of methylmercaptophos in the canal water reached 9.3 mg/l, and of thiometon reached 5 mg/l, hundreds and thousands of times higher than MPCs adopted in 1972 for bodies of water (MPC is 0.01 mg/l for methylmercaptophos, and 0.001 mg/l for thiometon). According to 1980 data, DDT, long banned by that time, was found in 27% of water samples from small canals [3, A86]. Pesticides contaminate not only surface water, but also ground water and aquifers. By 1990 in the USSR, 15% of all pesticides used were detected in underground water [29]. Pesticides were detected in 86% of samples of underground water in Ukraine in 1986-87 (including DDT and its metabolites, HCH, dimethoate, phosalone, methyl parathion, malathion, trichlorfon, simazin, atrazine, and prometrin). In actual fact, the number of pesticides was apparently larger, but the laboratory was able to determine the content of only 30 of the 200 pesticides used at that time in Ukraine [29]. In the 1960s, in the Tashkent and Andizhan oblasts of Uzbekistan, the methylmercaptophos content in the water of studied well shafts was, by clearly underestimated data, 0.03 mg/l (MPC was 0.01 mg/l), of DDT was 0.6 mg/l (MPC was 0.1 mg/ l), and of HCH was 0.41 mg/l (MPC was 0.02 mg/l) [A49]. Monitoring and controlling pesticides in water (the way it was done in Russia and all other countries) does not give a true picture of the danger of pesticides in bodies of water, since it does not take into account the distribution of pesticides within the water mass layers [1,3]. The concentration of pesticides in the thin layer of water near the surface can be hundreds (!) of times higher than in the rest of the water mass. The role of the surface layer is exceptionally important, not only for substance exchange between the atmosphere and the water, but also for the lives of many hydro organisms. Even if a miracle happened, and all pesticides stopped being used completely as of today, the problem of their contaminating bodies of water, hydro organisms, and bottom sediment would be current for many decades to come.

34


2.3. Soil Contamination Moving into the deep layers of soil, accumulating and transforming there (in some circumstances rising to the surface again), pesticides may be found where no one expected them a long time after they were used. A residual amount of DDT penetrating the soil’s deeper layers may remain for many years. DDT’s half-life (i.e. the decay of 50% of the original quantity) in soil on average is about 20 years [6]. HCH has been found in soil 22 years after it was used [6]. The 1980 Soviet handbook states that toxafene “is almost completely broken down by soil microorganisms, with the molecules decomposing to their simplest substances in the course of 1.5-2 years” [4]. In actual fact, toxafene has been found in soil 14 years after it was used [13]. Heptachlor has been known to have been detected in soil 14 years after it was used [3]. Even five years after it was used, the heptachlor concentration in the soil reached 0.4 mg/kg – 8 times higher than MPC [30]. Ninety percent of aldrin remains in the soil for a year, and 80% for three years [15]. Quintozen can remain in the soil up to four years [A84]. Sym-triazines and dinitro-o-cresol act in the soil sometimes for more than two years after being used [3]. Atrazine is considered to be stable in soil for about a year; therefore, crops could be sown in fields treated with atrazine 12 months later [20]. However, eight years after atrazine was used once, the soil was found to contain atrazine in large quantities (0.9 mkg/kg), along with atrazine’s breakdown products of the same class: di-ethylatrazine, isopropylatrazine, hydroxyatrazine, chlordiaminoatrazine, etc. [31]. Cases are known of how propazine negatively affected crop rotation five years after its use [32]. Official Soviet science considered that OPPs did not remain in the soil for very long, and the products resulting from its decay were of low toxicity [21, 30]. In fact trichlorfon, for example, decays slowly in acid soils. It more actively dehydrochlorinates in alkaline media, but it then forms highly toxic dichlorfos [33]. Parathion may remain in soil for up to 16 years [34]. Cases are known when phosalone and chlorpyrifos remain in soil for up to two years [3, 20]. Methyl parathion and trichlorfon were detected in the Kilmez region of the Kirov Oblast in an underground chemical repository 20 years later [3]. Humidity, temperature, the water regime, and soil structure and content all affect how long pesticides may remain in soil. It is practically impossible to state that in a certain field, a certain pesticide will disappear a specific amount of time after being used. For example, depending on the soil, the halflife of propachlor varies from 1 - 3.5 years [31]. “! decays more slowly in acid soils, leading to the danger of residual amounts having a negative impact on crops [31]. It takes 25% longer for the amino salt 2,4-D to break down completely in the northern regions of Belorussia than it does in the southern regions. In rainy years, this herbicide completely breaks down in the soil in 45


35

days, whereas in dry years it takes at least 75 days [31]. 2,4-D also breaks down more slowly when other pesticides are present in the soil [31]. By the end of the 1980s, Moldavia, Azerbaijan, Armenia, Uzbekistan, and some regions of Tajikistan were among those regions with the largest area of soil contaminated by pesticides. In these regions, 40-80% of the soil studied was contaminated, with the average contamination level was from 2 – 6 times MPC. Large territories of Russia (the Primorsky Krai, the Central Chernozem Oblast, the Central Volga region, and the Northern Caucasus), as well as Kirgizia, Turkmenistan, Georgia, and Ukraine were among regions with a medium amount of soil area contaminated by pesticides. Western Siberia, the Upper Volga region, and the Moscow, Omsk, Kurgan, and Irkutsk Oblasts, as well as Kazakhstan, all had a small area contaminated by pesticides, with the amount not exceeding 10%, and with an average pesticide content in soil of up to 0.5 MPC. The threat of pesticides’ impact on the environment in Russia and other CIS countries has not diminished because they were used less in the 1990s. The long-term influence of pesticides on the soil not only has not decreased, but has become more apparent. Until recently, OCP soil contamination, significantly exceeding MPC, has been observed in the Krasnodar Krai, in the Republics of Central Asia, Moldova, Kazakhstan, in Ukraine, and in other regions [35]. DDT and its metabolites cause the most significant environmental problems, especially where perennial and industrial crops are grown. More than 20 thousand tons of DDT was used annually from 1950-70, its period of intensive use in the USSR. However, the amount of soil contamination by DDT/DDE remained practically unchanged even during the long years after the “ban” (1970); this contamination was detected on average in 15-20% of the areas studied [36]. To date, 50 – 80% of the soil of Azerbaijan, Uzbekistan, and Kirgizia are contaminated with DDT and its metabolite DDE [31]. Although from 1981-84 the volumes of DDT used were decreased in cotton-growing regions, DDT content in the soil in specific cases reached 4485 times MPC (MPC for the sum of all types of DDT at the time was 0.1 mg/ kg). Considering DDT’s stability, as well as the significant total exposure to each hectare of soil (reaching 85 kg/h), the problem of contaminated territories in the former Soviet Union will remain for many years. The soils of Moldova today contain about 1000 tons of DDT (mostly in old gardens) [11]. HCH soil contamination in the Irkutsk oblast was found in 7-10% of the studied areas; in Moldova the area grows to 37%, and in Turkmenia to 50% [31]. In one of a series of measurements made in the 1970s in Ukraine, lindane was found in 26% of 136 soil samples taken from different places, with the range in its concentration being from 0.1-5 mg/kg ( MPC is 0.1) [3]. In the 1983 grain harvest, 16 mg/kg of lindane was detected [3], while the MPC does “not permit” its presence [8]. In the Moscow oblast, where lindane content in the soil was 0.6-1.2 mg/kg, the

36


concentration of lindane in feed oats reached 0.15 mg/kg [3]. When cotton was processed in Uzbekistan, aldrin was found in the soil at concentrations up to 40 mkg/kg (cotton plant leaves accumulated Aldrin, reaching 4 mg/kg) [27]. The systematic monitoring and controlling of OCP soil contamination at a background level started in the USSR at the end of the 1970s. In 1977-81, the detection of OCPs in samples from the surface soil layer in nature preserves and other background regions showed that contamination was everywhere. Table 2.4 shows that DDT concentrations in the soil in the background regions of Central Asia made up 14-27 mkg/kg, 1.5-2 times higher than in soil from other parts of the former USSR. Annually, about 100g of DDT fell from the air on each square kilometer of soil in the European part of the USSR, and about 30 g in the Asian part. Pesticides, especially OCPs, remain a constantly active factor in soil contamination for many years. 2.4. Transformation of Pesticides in the Soil, Air, and Water All pesticides introduced into the natural environment undergo transformations. Sometimes the metabolites produced are more toxic than the original substance. Table 2.4. Background OCP soil concentrations in the USSR (according to 1980-87 data for biosphere preserves) and their fluxes [6] Density of OCP flux

OCP concentration in soil

from atmosphere,

surface layer, in mkg/kg

g/km2 per year

of dry mass

∑DDT

∑HCH

Astrakhan

38

26

13

3

10

Berezinsk

83

48

15

10

5

Caucasus

226

122

7

3

3

Prioksko-Terras

105

94

7

3

6

Tsentralno-Lesnoy

71

28

10

2

4

Overall European

101

62

10

4

6

54

38

20

7

5

27

4

5

Biosphere preserve

∑DDT Gamma-HCH

Alpha-HCH

territory of the USSR Barguzinsk Repeteksk Sary-Cheleksk

36

448

25

4

4

Chatkalsk

35

355

14

5

4

Overall Asian territory

33

110

15

5

5

of the USSR


37

There are many examples of OCPs that undergo transformations in the natural environment. One is industrial 1,2,3,4,5,6-hexachlorocyclohexane (HCH): this is a mixture that includes eight stereoisomers. Gamma-isomer HCH (the insecticide lindane) may transform in the environment into mostly alpha-, as well as beta-, isomers [31]. The untargeted ballast isomers of HCH (those having little effect on insects) introduced into the environment in the HCH mixture together with the working isomer lindane negatively affect the environment and humans. For example, the alpha-isomer is carcinogenic to some types of warm-blooded animals, and the beta-isomer causes chronic poisoning in the same animals. The toxicity of both isomers is increased by their cumulative abilities, i.e. they accumulate in fatty tissues. The insecticide heptachlor oxidizes in the soil, and becomes a more toxic epoxide, capable of remaining for a long time. The insecticide aldrin transforms in the soil into dieldrin, maintaining its toxicity [15, 30]. Mirex (FD50=300-600 mg/kg), used to fight ants, just like kelevan (FD50=255-325 mg/kg), used to fight the Colorado beetle, transform in the soil into the more toxic chlordekon (FD50 decreases to 95-140 mg/kg) [30]. The OPP cotton defoliant folex (merphos) is relatively toxic to mammals. However, under natural conditions, it oxidizes in atmospheric oxygen, creating another defoliant that is more toxic to mammals and fish – DEF [20, 30]: (C4H9S)3P ⇒ (C4H9S)3PO. The insecticide phosalone oxidizes and creates the corresponding thiophosphate – the more highly toxic = – an analogue to phosalone [30, 33]. The insecticide malathion was the “hero” in the 1976 tragedy in Pakistan. Poisoning started after measures were taken to fight malaria. At least 2800 of the 7500 workers in this area were poisoned [37]. When studied, the more highly toxic iso-malathion was found together with malathion in their bodies. It is known that iso-malathion transforms into the more highly toxic malaoxon, both in storage and directly in the environment. Some of the metabolites arising from the breakdown of trifluraline (an herbicide used to treat cotton, soy, sunflowers, etc.) are far more stable and have a significant antibacterial expression. The most toxic of the pesticides used in the USSR was the systemic insectoacaricide aldicarb (FD50=0.93 mg/kg), which breaks down in the soil, forming the also highly toxic sulfoxide and sulfone. The herbicide propanile transforms in the soil into a dioxin-like substance [38]. Along with those cases we understand, where pesticides transformed without it being desired, there are other cases where humans introduced components of the necessary chemical processes directly into the natural environment. The soil sterilizer metham (sodium methyldithiocarbamate) may act simultaneously as a fungicide, a nematodicide, and an herbicide [4, 5, 30, 41]. Metham itself is relatively toxic (the FD50 is 285 mg/kg for white mice, and 820 mg/kg for

38


rats [30]); however, when it decays, it gives off methylisothiocyanate (MIT), whose toxicity is 2-2.5 times higher. Developers recommend pouring water on the soil after it has been treated with metham, so as to ensure that the MIT exuded from the humid soil starts fumigating. Metham is unstable when stored, and will break down to form the same MIT in the warehouse. Moreover, humans may be poisoned either through inhalation of MIT’s fumes or through direct contact with the skin. In the future, we must expect ever-newer types of pesticide transformations in the environment, which will be accompanied by unpredicted consequences. It is practically impossible to guess what these consequences may be. 2.5. Pesticides in Global Processes Contamination of the biosphere by stable OCPs (DDT, HCH, aldrin, dieldrin, heptachlor, and toxafene) has become a global phenomenon. With global transfer, pesticides may reach countries that never produced or used them. In the northern hemisphere, where winds tend to blow from west to east, the rate of the wind in the boundary layer between the troposphere and the atmosphere is approximately 35 m/sec. Pesticide particles may completely orbit the Earth in approximately 12 days. Over this time, the probability of the particles falling to Earth may vary, and depends on the height of their orbit: at a height of 3 km above sea level, particles will remain in the atmosphere for about seven days; at a height of 6 km, for 30 days; at a height of 30 km, for two years [31]. In spite of the fact that in the 1970s, many countries cut back their use of DDT and other OCPs, these pesticides will remain in the biosphere in huge quantities for many years to come. In particular, about 2/3 of the 3.5-4 million tons of DDT produced in the world by the middle of the 1980s (almost 1 kg per each inhabitant of the Earth) is still circulating in the biosphere. If the year 2000 level of DDT use is maintained until 2010, the fluxes of DDT from the atmosphere and its concentration in the air and fall-out will increase by approximately a factor of 1.5-2. Under these conditions, DDT concentration in the soil will grow by 10%. Since DDT falls into the ocean at a rate of 40-50 thousand tons a year, aggregate DDT content in the ocean will reach 500-600 thousand tons in 2010. In the most optimistic scenario (a complete ban on DDT use everywhere), a sharp decrease in the level of DDT in atmospheric fall-out should take place, along with a specific decrease in the amount in the soil (by 30% over 10 years). However, even in this case, total DDT content in the ocean will only decrease to 300-400 thousand tons. Contamination of the environment with DDT and other OCPs will remain a global phenomenon for many years to come. No one is protected from pesticide exposure, especially from exposure to OCPs. Thus, in the near future, all biochemical processes in living organisms will take place under unprecedented complex and practically unpredictable conditions.

Chapter 3. PESTICIDES, THE STATE AND HUMANS

39

CHAPTER 3 PESTICIDES, THE STATE AND HUMANS At the end of the 1950s, as pesticide use grew in many countries, the first information appeared about acute and, especially chronic, poisoning in humans. Soon the World Health Organization (WHO) started looking at pesticide poisoning as one of the new, significant factors affecting human health. According to WHO calculations, in the 1970s, up to 50,000 people died annually from pesticide poisoning worldwide, and several million became sick. However, these data did not include information from the USSR, which, beginning in the 1950s, considered them secret: the truth was too frightening to discuss openly. Information about the true state of affairs started appearing in the open press only after 1986. Finally it became known that at the beginning of the 1970s, a secret CPSU Central Committee resolution was adopted, following which the USSR carried out apparently the widest-ranging research on the effects of pesticides on human health. More than 70 institutes in Ukraine, Uzbekistan, Russia, Kazakhstan, Moldavia and other union republics were brought into this research. Official accounts have remained secret to this day. This chapter presents a portion of this huge fund of material. There is a significant amount of data from other countries on the effects on human health of large-scale pesticide production and use, in particular of OPPs and OCPs. Even one-time, accidental contact with some OCPs and OPPs such as dieldrin, malathion, and parathion, can lead to changes in the encephalogram (which remain for a year after exposure), disruptions of sleep patterns and memory, loss of libido, and difficulties in concentration [3]. Global practice shows that all pesticides are toxic to humans. The WHO classifies the population exposed to the risk of pesticide poisoning into three categories [39]: 1) personnel in a plant producing pesticides and their formulations, 2) workers who use pesticides, and 3) inhabitants of private housing treated with pesticides. This WHO classification is unsuitable for the former USSR, since almost all of the rural population suffered from pesticide poisoning, including those who were in no way in professional contact with pesticides. There is no place in this classification for population groups that ingested pesticides in their food products, nor for people who were poisoned by pesticides that had somehow leached into the ground water from old pesticides that had been buried. The official Soviet point of view on the safety of pesticide use acknowledged that pesticide poisoning took place only when safety techniques, instructions and standards were ignored. From the 1970s, scientific articles stopped quoting absolute numbers of sufferers, and replaced them with percentages;

40


even the names of the oblasts and regions where health research took place disappeared. Strict Soviet censorship came into play. Dissertations on the toxicology and health standards for pesticide use began to be defended in closed scientific councils. Even dissertations on other countries’ negative experience in pesticide use [A54] were defended in 1972 in “closed” session. In 1960-80s in the USSR, much research took place, mostly within the Minzdrav system, and many dissertations were defended on the effect of pesticides on different organs and systems in the body [5, 12, 21, 22, 24, 26, 27, 32, 43, 47, 48, 53, 60, 63, 64, 67, 70, 71, 73, 76, 82, 89, 98, 104]. However, very few of the research results are accessible to the population, even to this day. Moreover, these data have not yet been generalized. Let us look at some of this material, first of all by basic pesticide groups, and then by geography. 3.1. Acute Poisoning In the 25 years up to 1970, there were 42,500 incidents of acute pesticide poisoning in 69 different countries; in the USSR for 10 years during that period, there were 8,100 incidents [A54]. If we recalculate per capita, there was one incident per 200,000 people worldwide, with one incident per 20,000 in the USSR: in other words there were ten times more incidents in the USSR than in the rest of the world. Unlike other countries where the majority of pesticide poisoning was due to OCPs and OPPs, in the USSR an overwhelming number of incidents were due to OMPs (organomercury pesticides) (Table 3.1). A number of studies were written on the “regime of using” OMPs and their negative consequences [6, 9, 10, 12, 15, 20, 25, 57]. The percentage of fatalities from pesticide poisoning (3.2%) introduced in paper [134] was not confirmed in the next dissertation [A78]; this latter indicated that over the 20 years from 195675, fatalities due to pesticide poisoning in the USSR were on average 5%, in some Table 3.1. Distribution of acute pesticide poisoning in the USSR in the 1960s by degree of danger [54] Number of acute pesticide poisonings Pesticide

Most

Relatively

Least

GROUP

Total

dangerous

dangerous

dangerous

OMP

5036

5036

-

-

OCP

1097

740

357

-

OPP

1022

550

426

46

Other types of

218

6

147

65

7373

6332

930

111

pesticides Total


41

years reaching 34%. Dissertation [A78] analyzed not only acute, but also chronic, pesticide poisoning; an idea of the results is given in Table 3.2, which includes data on only two groups of sufferers, and does not discuss health damage to other population groups. For example, city dwellers linked to pesticide production are not considered. Rural inhabitants not directly linked to pesticide use are also not reflected, though they certainly suffered from pesticides’ effects. The importance of the last case is easy to see in the example of two regions where pesticides were used especially intensively. In the 1970s in Tajikistan, only 23.9% of the population suffering from acute pesticide poisoning was Table 3.2. Data on pesticide poisoning in the USSR from 1956-75 [78] Occupational poisoning of Pesticide supply in agriculture, Year

agricultural workers

products with

Acute poisonings # of

# of

Poisoning by food residual pesticides

Chronic

thous. tons Sufferers Incidents poisonings

# of

# of

Sufferers

Incidents

1956

88.6

38

14

No data

1024

2

1957

90.2

59

41

No data

264

8

1958

68.6

60

33

No data

335

16

1959

78.7

383

183

No data

222

25

1960

97.7

235

200

No data

62

9

1961

103.6

167

121

No data

18

3

1962

149.7

306

166

No data

134

17

1963

173.2

292

148

No data

430

21

1964

213.9

833

261

No data

263

28

1965

232.9

1157

362

No data

397

23

1966

229.3

431

280

52

183

14

1967

231.6

344

88

75

581

18

1968

281.6

231

82

83

679

11

1969

313.7

425

67

71

300

14

1970

292.4

288

133

38

1083

21

1971

253.9

513

142

55

608

17

1972

274.6

249

138

37

510

5

1973

321.8

212

120

52

50

3

1974

336.0

295

117

109

15

3

1975

407.2

387

133

56

Not registered

6845

2829

Total

7158

257

42


working with pesticides [A86]. In Uzbekistan in 1960-72, “a significant number of incidents of acute poisoning ” by pesticides was registered; however, only 25.9% (practically the same figure as Tajikistan) of the incidents were linked to their occupation. The remaining 74.1% of acute poisoning incidents took place among people not working with pesticides (29.6% were sent to harvest cotton before the end of the quarantine period; 10.5% accidentally entered a pesticide cloud when an area was treated from the air; 19.0% were poisoned because aircraft did not respect established protective health zones; and 15% ingested poisoned water and fruit) [A62]. When analyzing the data from Table 6.2, one must keep in mind that as of the beginning of the 1970s, data collection on chemical poisoning statistics was transferred from Minzdrav’s general Health and Epidemiological Service to an independent Third Main Directorate in the same Ministry – a secret division linked to defense work in the nuclear and chemical industries. 3.2. OCP poisoning All OCPs are polytropic, parenchymatous poisons, afflicting the central nervous system, liver, kidneys, the heart muscle, the stomach and intestines, and the endocrine system (mostly the adrenal glands, thyroid, and ovaries). Morphological changes in warm-blooded creatures poisoned by OCPs vary from insignificant disruptions in circulation and reversible dystrophy to focal necroses; these effects depend on the organism, the dose of OCP, how long the OCP remains active, as well as on other factors [9, 39, 40, A47, A79]. Among the most toxic OCPs are aldrin, dieldrin, lindane, polychlorpinen, chloroindan, and DDT [45]. When introduced into the body, the majority of OCPs are carried in the bloodstream and accumulate in the fatty tissues, liver, spleen, heart, brain, kidneys, adrenal glands, and lungs [32]. OCP poisoning causes dystrophic and necrobiotic changes in nerve cells (especially in the cerebellum and the medulla oblongata), dystrophic changes in the liver, kidneys and heart muscle, and inflammatory changes in the liver, lungs and the gastro-intestinal tract (in HCH poisoning). In the endocrine system, OCP poisoning, in particular by DDT, aldrin and dieldrin, causes focal swelling with necrobiosis of the adrenal gland cortex, spermatogenic epithelia, and epithelia of the thyroid. An increase in plethora and focal dystrophic changes in the endocrine system matches clinical observations of changes in adrenal and thyroid function, as well as changes in local and general vascular dystonia, all detected in humans poisoned by OCP. Morphological changes in the brain’s nerve cells conform to information on the disruption of reflex activity in the early stages of OCP exposure. Morphologically expressed protein and fatty dystrophy of the liver and kidneys, and a depletion of glycogen in the liver, are all evidence of the


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disruption in the metabolizing of protein, fat, and carbohydrates that emerges in OCP poisoning (in particular DDT poisoning). Detected discoordination and fits are an expression of the diffuse dystrophic processes in nerve cells, especially within the cerebellum and the medulla oblongata [40]. DDT (like the defoliant 2,4,5-T and the fungicide nemagon) affects sexual functions. Acute poisoning was frequently observed during use of HCH [42], polychlorpinen [72, 81, 43], and toxafene [44]. There is a large amount of data on the chronic influence of OCPs. For example, a group of female collective farm workers was poisoned with HCH after they had been sent to manually thin sugar beet sprouts immediately after a morning rainshower (this took place in the beginning of the 1980s, and the number of sufferers was not given) [42]. The day before, the neighboring field had been treated with HCH; on that day the women saw air move from the treated field “in the form of a fog,” and smelled an unpleasant odor. Poisoning symptoms showed up immediately after they started work (headache, overall weakness, burning in the nose and throat, sandy and scratchy eyes, numbing of the tongue, burning and dryness in the mouth). Nevertheless they continued to work, and on the following day the symptoms worsened (nausea, vomiting, shaking in hands and feet, stomach cramps, liquid stools, and a body temperature of 37,5-39oC). At the time they were hospitalized, HCH soil content was 0.84 mg/kg, and air content over the field was 0.4-0.5 mg/m3 (data have most likely been underreported). One third of the women were detected to have enlarged livers, one half – to have pain in their gall bladder, epigastric area, and also in the large intestine. The cause of the poisoning was trivial: according to regulations, people were not permitted to enter a field treated with HCH for four days after treatment, and when the field being worked was covered with dense vegetation, for two weeks. We should emphasize that in 1980 a dissertation [A81] on the effect of polychlorpinen and HCH on workers in sugar beet production suggested that HCH not be used. Unfortunately, HCH was banned only in 1990. In the book “The Safe Use of Pesticides While Intensifying Agricultural Production” [21], the paragraphs on polychlorpinen in beet fields were lost among data linked to OCP contamination of breast milk in Japan, the USA, and Sweden; the dangers to the inhabitants of Italy from herbicide contamination of the Po river; the poisoning of the inhabitants of the USA and Canada by watermelon from a plantation treated with pesticides; and many other facts. Here is the text on the beet fields: “Mass poisonings of the population were registered when people manually planted sugar beets in fields treated with pesticides, most often during the first days after polychlorpinen or other OCP use. There were also incidents of later poisoning.

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“Research has shown that when polychlorpinen, ammonium nitrate, and superphosphate are present together in the soil, phosgene, carbon monoxide, nitric oxide, hydrochloric acid, ammonia, hydrocyanic anions, ozone, hydrogen fluoride and phosphide, etc. could appear in the air over the beet fields. Photooxidants could also appear. Airborne toxic compounds over this crop were noted in areas after precipitation with little wind, and with an air temperature of over 20o!. The combined and complex activity of pesticides and other chemical compounds led people who manually sowed beets to develop symptoms of poisoning.” [21] An objective statement about the most frequent incidence of acute mass poisoning by polychlorpinen is understandable: this is when people are knowingly sent to the sugar beet fields before the end of the “quarantine period” required by regulations. Health workers did not predict incidents of poisoning taking place at later times. The box below gives as an example a list of 11 events taking place in beet fields in three oblasts within Ukraine: Nikolaevsk, Vinnitsk, and Kiev. Nikolaevsk Oblast [72] 1. On May 14, 1971, 154 female collective farm workers from the Ilyich Collective Farm in the Krivoozersk Region started work in a beet field one hour after treatment with polychlorpinen. Acute poisoning took place immediately. 2. On May 20, 1971, 52 female collective farm workers from the Kuybyshev Collective Farm in the Krivoozersk Region started working in a field 12 hours after treatment with polychlorpinen. They were not able to finish their work. 3. In the summer of 1972 in the Kuybyshev Collective Farm in the Krivoozersk Region, a field was fertilized with ammonia solution 14 days after treatment with polychlorpinen. Twenty-seven female collective farm workers went into the field on the following day (the 15th after treatment with polychlorpinen), and were immediately poisoned. Seven days later they were sent again to the same field, with the same result. 4. On April 25, 1972, a field from the “Banner of Communism” Collective Farm in the Bratsk Region was treated with polychlorpinen. Thirty-three female collective farm workers, working in this field from May 5-21, did not complain about conditions. On May 22, two to three hours after a wind carried over amino salt 2,4-D from a neighboring field that had been sprayed at the time, all 33 displayed symptoms of acute poisoning (the concentration of polychlorpinen in the air over the field was only 0.03-0.001 mg/m3 two days after the poisoning).


5. On May 1, 1972, a beet field from the Gorky Collective Farm in the Krivoozersk Region was treated with polychlorpinen. Seventy people worked there ten days later and returned with no signs of poisoning. On May 20, the field was fertilized with carbamide, and that night there were light showers. Eight people from the same work brigade of 70 went into the field on May 21 (i.e. the 21st day after the field was treated with polychlorpinen); 1-1.5 hours later they showed signs of acute poisoning. 6. On May 1-2, 1974, a field from the Zhdanov Collective Farm in the Krivoozersk Region was treated with polychlorpinen. On May 15-25, 57 female collective farm workers worked in this field with no complaints. From May 30-June 6 the field was fertilized with ammonium nitrate, and on June 8 it rained. When, on June 11, the same 57 women worked in this field again, by 2pm all developed acute gas poisoning (the concentration of polychlorpinen in the air over the field three days later was only 0.04 mg/m3). 7. On a sugar beet field at the Chapaev Collective Farm in the Krivoozersk Region on March 20, 1974, a superphosphate and potassic fertilizer was used; on April 4, the field was treated with hexachloran; on May 1 with trichlorfon; and on May 2, 1974 with polychlorpinen. When 32 female collective farm workers went into the field on May 12, they immediately started complaining, and were evacuated due to acute poisoning. Seven suffered vomiting and nosebleeds (the concentration of polychlorpinen over the field was 0.069 mg/m3 three days after the poisoning). Vinnitsk Oblast [75] 8. An acute group polychlorpinen poisoning of 11 fieldworkers took place at the beginning of the 1970s in the sugar beet field at the Telman Collective Farm in the Lipovetsk Region. The accompanying circumstances were high air humidity and mineral fertilizer in the soil. “Symptoms of poisoning noted in people on the seventh day after pesticide use were not characteristic of polychlorpinen activity.” Kiev Oblast (“Ukraine” Collective Farm, Mironov Region) [81] 9. Female collective farm workers suffered acute poisoning 2.5 hours after the last polychlorpinen treatment of the field. 10. A mass poisoning of female collective farm workers while weeding the sugar beet field took place eight days after the last polychlorpinen treatment (with high soil humidity). 11. A mass poisoning of female collective farm workers took place after a rainfall 28 days after the last polychlorpinen treatment of the field.

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From the 11 described incidents of mass poisoning it is possible to conclude that there are chemical and physical causes for the poisoning. The mixture of polychlorpinen and mineral fertilizer in a natural environment may form toxic gases: phosgene, carbon monoxide, hydrogen fluoride, cyanogen chloride, nitric oxide, and others [A72, A81]. The concentration of cyanogen chloride over the fields concerned in mass poisonings from incidents Nos. 9-11 was very high: 0.6; 0.46; and 0.25 mg/m3. Let us emphasize that after incident No. 10, the author also detected phosgene in the air (at a concentration of 0.26 mg/m3) [A81]. Phosgene and cyanogen chloride were military poison gases from WWI. The USSR did not ban cyanogen chloride for many years after WWII, and phosgene was in Russian military stocks even very recently. In the Official Handbook published in the same year of 1980, it was stated impersonally that polychlorpinen “is broken down by soil microorganisms, with the molecules decomposing to their simplest substances in the course of 1.5-2 years” [4]. Since we now know some of the names of these “simplest substances” (phosgene, cyanogen chloride), it is easier to judge how unbiased the supporters of pesticide use were. One more example of acute polychlorpinen poisoning occurred in the Ukraine around 1969-70, when 27 women aged 26-49 were sent out to sow collective farm fields three days after the fields had been treated with polychlorpinen. A warm rain washed the pesticide from the soil, and the pesticide evaporated intensively. All the women showed symptoms of acute poisoning 2040 minutes later: eight lost consciousness, and nine had fits. The poisoned women spent from 3-25 days in the regional hospital, after which they all went to the VNIIGINTOKS clinic with disruptions of the neural and cardio-vascular systems, as well as of the digestive tract over the next 9-13 months [43]. Only a narrow circle of people knows of polychlorpinen’s “contribution” to human health when cultivating sugar beets: these dissertations [A72, A81, A75] are not accessible even to specialists. The consequences of toxafene use in beet growing were studied systematically [26]. At the time when these observations began (the summer of 1970), standards for toxafene’s regime of use were already established [A3, A16]. In a field treated using tractor-based sprayers, the concentration of toxafene in the air 5-8 hours later was 20 mg/m3, 4-6 days later 0.8-0.4 mg/m3, and on the 10th day 0.2 mg/m3(the standard for toxafene in work zone air varies depending on the work [4, 8, 44]: from 0.2 mg/m3 and 0.5 mg/m3 to 0.005 mg/m3, with all these amounts coming from official sources). Secondary air contamination was detected due to contaminated soil and plants in the days immediately following treatment. A group of 95 people treating the sprouts had health checks; 84% were women aged up to 50 (all had worked with pesticides for over five years). After going to weed on the third day after chemical treatment, the women spoke


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of various complaints (insomnia, pains in the heart area, blistering rashes on their wrists with hyperemia and edema of the skin, high blood pressure, pain and fits in the large intestine, extrasystoles, etc.). Sinus arrhythmia in ECGs was observed in one-third of those studied. After just two weeks of work on the treated field, many had anomalies in their blood makeup. This group was observed for the next three years, and conclusions were not reassuring: 1) the cause of the poisoning was the decrease in the period between toxafene treatment and work in the field; 2) people affected by residual toxafene for three years were observed to have a dysfunction in the sympathetic adrenal system due to the cumulative effect [26]. Thirty-five (out of 85) people weeding sugar beets after the field was treated with toxafene in 1972 were observed to have symptoms of acute poisoning. Damage to the hypothalamus with subsequent disruption of the sympathetic adrenal system [44] are clinical symptoms of toxafene poisoning. At that time, a quarantine period of 21-40 days after use had already been established in many countries (Sweden, Switzerland, the Netherlands, the USA, Italy and France) [45]. In the USSR “expediency” reigned, as a consequence of which the health of tens of thousands of people was ground down from their work in fields of sugar beet, potatoes, peas, etc. immediately following treatment with toxafene. In one of the regions of Uzbekistan, a group of people processing cotton was acutely affected by aldrin. Its concentration in the air was 0.8-0.9 mg/ m3, i.e. it exceeded the MPC 80-90 times. In the fields where people suffered, the concentration of aldrin in the soil was 0.2-0.5 mg/kg, in the cotton plant leaves it was 2.5-3 mg/kg, and in the irrigation network it was from 0.08 to 0.9 mg/l [A29]. Results are described from three years’ observation of 88 people in Uzbekistan who had contact with aldrin over 2-3 years [A29]. This group consisted of men aged 26-53. Aldrin contact was especially high in 1964, when its concentration exceeded the MPC 100-300 times during treatment (even two months later the level had decreased only to 10-15 times the MPC). Thirty-six people from the group were observed to have disruptions of the central nervous system, a sign of poisoning. Especially marked disruptions were observed in six people who manifested diencephalic epilepsy (fits and loss of consciousness). Along with changes in the nervous system, toxic hepatitis and myocardiodystrophy were also observed. 3.3. OPP poisoning There are as many incidents of poisoning by OPPs as there are by OCPs [12, 40, 46, A8]. All OPPs are polytropic poisons. Changes are observed in the brain nerve cells of victims of acute OPP poisoning. Acute poisoning accompanied by diffuse damage to the central nervous system causes attacks similar to epileptic fits when symptoms of clinical poisoning have already

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disappeared. OPPs cause changes to cardiac activity and blood pressure. Poisoned workers producing OPPs (demeton, trichlorfon, methyl parathion, and methyl ethyl parathion) displayed characteristic electrocardiogram changes [47] connected to anticholine esterase activity and OPPs’ direct blocking influence on cellular oxidation processes. Even light chronic OPP poisoning gives rise to the precursor forms of liver disease, which, with more marked damage, develops into explicit forms of chronic hepatitis [A58]. Acute OPP poisoning causes disruption of renal functions [3, A58]. OPPs even influence morphological and biochemical blood composition, for example in acute methylmercaptophos poisoning [A28]. Acute OPP poisoning may be accompanied by complications such as pneumonia, purulent tracheobronchitis, asthenic syndrome, and toxic polyneuritis [12]. After contact with OPP, neurasthenic syndrome returned two years after treatment. When examining victims 2-4 years after acute OPP poisoning, an asthenic condition, irritability, touchiness, acute weakness, rapid fatigue, and insomnia were all identified [47]. Asthenic syndrome with headaches, irritability, anxiety, and insomnia were observed in 62 of 130 people working with OPPs for more than five years [48]. Most displayed decreased blood cholinesterase activity. Many were observed to have affective syndromes (anxiety, fear, aggression), sometimes accompanied by symptoms of depression. Disruption of memory was noted. Vision problems are also caused by long-term contact with OPPs [A64]. In cotton growing regions with intensive OPP use, the number of spontaneous miscarriages and stillbirths was higher than elsewhere [3]. Women working in contact with DEF more frequently gave birth to children with abnormal development, and showed a higher level of spontaneous miscarriages, as well as of pathologies during pregnancy and birth [A70]. DEF’s toxicity to embryos is known [3]. DEF not only damages the central nervous system, but also affects the liver, heart, kidneys, intestines, endocrine system, and other organs and systems [A66]. DEF and other OPPs damage immunological response, and decrease the body’s resistance to infectious diseases, especially in children [A68]. This defoliant has caused an especially large number of problems among the inhabitants of cotton growing regions in the former Soviet Union [19, 33, 66, 68, 70]. Over the course of one to two weeks in Uzbekistan, practically every cotton plantation underwent pesticide treatment, mostly using DEF sprayed from aircraft. The underreported data (measurement means were inadequate) on DEF concentrations in the air in the 1960s were as follows: up to 0.95 mg/m3 using airborne sprayers, and up to 2.5 mg/m3 in the signaler’s breathing zone [A33] (the standards were 0.2 mg/m3). DEF was banned only in 1986-87. However, this “ban” was widely violated. Demeton poisoning causes neutrophilic leucocytosis, an increased number of erythrocytes, and various other types of blood damage [49, 50]. Asthenic


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syndrome with exhaustive psychic processes is described as complications of demeton poisoning [51]. Tractor drivers who worked with demeton for long periods have been observed to suffer sleep disorders (nightmares), decreased memory, increased irritability, and anxiety. Trichlorfon poisoning causes disruptions in normal functions – from slight deafness to hallucinations, and asthenic-autonomic syndromes that can last 2-3 months. The first research on demeton use took place in 1955 in the Andizhansk Oblast (Uzbekistan) on cotton [50], and in the Stavropol Krai on the destruction of harmful shield bugs [A2]. Many cases of poisoning in humans were described [A11, 49-53]. Demeton use was accompanied by concentrations reaching: 2.5 mg/m3 with aircraftbased spraying [46], 7.4 mg/m3 with tractor-based spraying [46], and 4.0 mg/ m3 in the signaler’s breathing zone [A55]. Acute demeton poisoning was distributed among inhabitants of one of the cotton growing regions in the following manner: 50.9% when treating from aircraft, 40.1% when cultivating cotton on treated fields, 9% when using canal waters [52]. Officially confirmed MPCs for work zone air, established much later than this research, was 0.02 mg/m3 and remains so today [54]. Thus, acute demeton poisoning is inevitable when MPCs are exceeded hundreds of times. It is impossible to use demeton while upholding safety regulations such as, for example, a four-hour workday on hot days. Nevertheless, demeton continued to be used for more than 10 years. Let us note that back in 1959-60, it was discovered that when working with demeton over the course of 4-9 days, marked changes in the autonomic nervous system take place, and the conclusion was drawn that demeton “is highly toxic for workers, and it should be banned” [55]. Officially, use of demeton stopped in 1961 [53], but in practice the Health and Epidemiological Service of the USSR permitted it to be used in agriculture until 1967. Health standards for demeton could be found even in the 1997 Official Russian Handbook, though with no mention of the inadmissibility of its use [10]. Methylmercaptophos poisoning is also known. Pregnancies and menstrual cycles are more often disrupted in regions where cotton plants are intensively treated with methylmercaptophos [A48]. In the 1960s in the Ternopol Oblast (Ukraine) [53], a group of 36 collective farm workers, in violation of regulations, were sent to thin sugar beet plants in a field that had been treated with methylmercaptophos the night before. Symptoms of poisoning emerged 2-7 hours later. All suffered from disruptions in their psyche (depression, lassitude, nightmares, memory decrease). The ECGs of all victims of medium (28 people) and high levels of poisoning showed signs of toxic damage to the myocardium. In particular, methylmercaptophos penetrated the body through the skin of the hands that had pulled up beet plants (even in the days following treatment, the plant’s juice transforms methylmercaptophos into sulfoxides and sulfones with heightened toxicity).

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The authors of work [56], “not noticing” methylmercaptophos in the air over the cotton fields 48 hours after treatment, concluded that people could work in fields two days after treatment. This proposal featured in guidelines drafted in 1964. However, acute poisoning continued to affect hundreds of people annually. In 1966 in the Andizhansk Oblast of Uzbekistan, the quarantine period before cotton workers could work in the field was increased to 6-7 days, as a result of which the number of acute poisoning incidents when cultivating cotton in 1966-67 decreased by a factor of 8-15 when compared with figures for 1964-65. In 1968 all farms adopted these quarantine periods, so that in 196869 only a few poisonings were recorded, not hundreds [57]. Workers’ safety was never ensured when using methylmercaptophos on cotton plants, even when all rules and regulations were followed. The pesticide’s concentration in the air reached 4 mg/m3 (including up to 2 mg/m3 in the signaler’s breathing zone) [A33] and 0.97-1.76 mg/m3 in the cabin of airplanes not equipped with external poison pods (the standard was 0.1 mg/m3)[A35]. The range of methylmercaptophos concentrations in the air observed [49] with tractor-based spraying was 0.15-6.1 mg/m3. Methylmercaptophos was identified at a distance of up to 250 m from the treated field, and it was recommended that work going on in neighboring fields should be banned at a distance of no less than 500 m [A6]. Even with all these conditions, workers were observed to have a decreased level of blood cholinesterase [A11]. Methylmercaptophos was banned in the USSR only in 1986. However, the standard in force earlier for work zones (0.1 mg/m3) has been maintained to the present [54], and allows for “exceptions” to the ban. In the mid-1950s, octamethyl pyrophosphoramide was tested on wheat in the Stavropol Krai, and in the Kiev Oblast on gardens [A2]. Octamethyl pyrophosphoramide concentrations were 1.0-3.0 mg/m3 when fruit trees were manually sprayed, and 0.5 mg/m3 in the signaler’s work zone when sprayed from the air [58]. The MPC, established considerably later, was much lower: 0.02 mg/ m3. When spraying cotton from the air in Tajikistan, the concentrations were 0.81.5 mg/m3 in the air of the field airport, and 3.0 mg/m3 in the signaler’s work zone. Workers were observed to have decreased cholinesterase activity. Working conditions were studied in one of the collective farms in Tajikistan where vamidothion was used to fight spider mites in cotton [A52]. The vamidothion concentration in work zone air when it was sprayed from airplanes and tractors reached 0.9 mg/m3, according to underreported data (the public health standard was 0.1 mg/m3)[12]. In 1978, vamidothion was banned; however, the 1997 Official Handbook of the Health and Epidemiological Service of Russia [10] still lists this pesticide, with no mention of the ban! The concentration of the highly toxic systemic insecticide thiometon in work zone air with both air- and tractor-based spraying reached 2.3 mg/m3 (with a standard of 0.1 mg/m3) [A11]. In fact, concentrations in the air when


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treating cotton fields exceeded MPCs up to 200 times, and in water, 50 times [A36]. Dissertation [A8] concludes that work could commence in fields 24 hours after treatment, based on measurements of thiometon vapor in the air after spraying. These data were based on the moderate climates of Ukraine and Russia, and then transferred to the hot conditions of Uzbekistan. As a result, after many incidents of poisoning in 1978, thiometon had to be banned [57]. Parathion poisoning was observed to cause disruptions in liver functions: chronic hepatitis, and changes in protein forming functions [3, A27]. Changes in blood makeup observed in people affected by fenitrothion were explained by a disruption in the liver’s protein forming functions [A26]. Workers producing malathion showed changes in biochemical blood indicators [A67]. People who came into contact with dibromochloropropane showed a higher fatality level from malignant tumors (mostly lung cancer) [15]. Let us give several examples of poisoning by OPPs that have not yet been banned. The insecticide methyl parathion has been actively used for several decades, and regulations allow workers to re-enter a field 24 hours after treatment [A4]. At the same time, the practice of using methyl parathion shows that when loading the product in powder form onto an aircraft, and when signaling, its concentration reached 11 mg/m3 (the standard [10] is 0.1 mg/m3) [59], so that chronic human poisoning was inevitable. Health standards were exceeded even in the pilot’s breathing zone [58]. When dispersing the insectoacaracide dimethoate, widely used even today, from tractor-based sprayers, air concentration reached 9.0 mg/m3, a level unacceptable for humans (the old public health standard was 0.3 mg/ m3; the standard was then rounded up to 0.5 mg/m3 [10]). People are still permitted to carry out manual work in fields just 10-20 days after dimethoate treatment [7, A13]. Concentrations of the insectoacaracide dichlorvos were researched in real conditions when during treatment of grain storage and milling equipment, and disinfestations of housing and ancillary accommodations [A30]. The largest concentration was found in the applicators’ breathing zone (2.7-3.3 mg/m3); the ancillary workers’ breathing zone (0.8-3.0 mg/m3) and the loaders’ breathing zone (1.7-2.1 mg/m3) had lower concentrations. The clothing and hands of people using dichlorvos were also markedly contaminated. Workers affected by dichlorvos at concentrations of 1.9-3.0 mg/m3 (the standard is 0.2 mg/m3) saw their blood cholinesterase activity decrease to 23%. When treating fruit trees with phosmet using tractor-based ventilator spraying, it was observed [A34] that permissible concentrations in the tractor driver’s breathing zone were exceeded (the concentration was 3.2-6.1 mg/m3, with a public health standard of 0.15 mg/m3; the standard today has been rounded up to 0.3 mg/m3 [10]).

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Data exist on trichlorfon concentrations in production and working conditions (the regulated health standard is 0.5 mg/m3): during trichlorfon solution preparation, the concentration reaches 4 mg/m3; in aircraft cabins it reaches 5 mg/m3; in tractor cabins – 4 mg/m3; in applicators’ breathing zones while spraying with a hose – 8 mg/m3; and in signalers’ breathing zones when spraying from the air – 6 mg/m3. These violations of course left traces: these people suffered from decreased cholinesterase activity, serious headaches, dizziness, and loss of appetite [A17]. Pathological and anatomical research showed that poisoning takes place with potent toxic agents (demeton [8], octamethyl pyrophosphoramide [2], and methyl parathion [4]); with substances of high toxicity (methylmercaptophos [6,28], dichlorvos [30], thiometon [8], dimethoate [13], phenkapton [38], vamidothion [52], phenthoate [88], phosmet [34], and phosalone [60]); with substances of medium toxicity (DEF [19], trichlorfon [17], fenitrothion [26], and methyl acetophos [32]); and with substances of low toxicity (tetrachlorvinfos [56]). OPPs all cause similar morphological damage [12]. This conclusion shows once more that the division of OPPs into classes of danger is no more than a convention. Experience has shown that, whether the poisoning is acute or chronic, humans suffer similarly. We can only deplore that this lamentable experience was not gained so much through experimentation on laboratory animals, but through the participation of living human beings. In concluding this section, we would like to emphasize that some OPPs, just like OCPs, have an explicit ability to accumulate. After examining the large amount of data and the deplorable results on the health of large groups of people, we must emphasize yet again that OPPs not only are not “safe for human health,” but will never be so, whether or not the regulations for their use have been followed. 3.4. OMP Poisoning OMP damage was studied in the USSR in much more detail than in other countries [40, 60, 1, 7, 10, 12, 20, 79]. OMP poisoning causes disruptions in hemodynamics, and marked dystrophic changes in the neural system and in internal organs. Hemodynamic disruptions are morphologically expressed in venous engorgement, stasis, thrombosis and perivascular edema [40, 58]. Circulation disorders and changes in blood vessel walls arise. General exhaustion and uneven blood supply to organs are observed as well (an abundant supply of blood is found in the brain, intestines, kidneys and liver; a significantly decreased blood supply is found in the skeletal muscles). Dystrophic changes in neural cells are seen more often in the cerebellum and medulla oblongata. Vascular disruptions are observed in internal organs, such as venous engorgement, tissue edema, and multiple


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hemorrhages. A brown pigment is observed both inside and outside blood vessels, which is a consequence of hemoglobin transformation through erythrocyte decay within blood vessels. A multiplication of adventitious cells is observed, showing that the permeability of the blood vessel barrier has been disrupted. Swelling, and sometimes fatty degeneration of the heart muscle, is observed, as well as vacuolar dystrophy of liver cells. Granosan also causes inflammatory changes in the heart muscle, liver and kidneys. With chronic OMP poisoning, more acute circulation disorders are noted: dystrophic changes are observed in the liver, lungs, and spleen; and hyperemia of brain tissue and matter in the central neural system. Long-term contact causes wasting, dizziness, a weakening of memory, salivation, fear, aural and visual hallucinations, disruptions in the menstrual cycle, and spontaneous miscarriages. The risk group (children, the elderly, pregnant women) is particularly vulnerable to poisoning. Between 1958-64, health and epidemiological, as well as clinical, studies were carried out on incidents of the granosan poisoning of 422 inhabitants of the Perm Oblast [A15]. These people suffered individual and group acute and chronic poisoning. The initial stages were not recognized during the first examination, so that patients were treated under other diagnoses. In the Novosibirsk Oblast, sunflower seeds treated with the seed protectant granosan poisoned 69 children (mostly boys). The digestive organs of 80% of the children were damaged (toxic stomatitis, gastritis, gastroenteritis); the cardiovascular system was affected in 66% of the children (mostly by disruptions in the extracardial regulation of heart activity); and changes in the neural system were observed in 33% of the children (micro-mercury poisoning). Residual phenomena were observed in 37% of the patients three years later [A57]. Apart from the 69 children who showed clear indications of poisoning, the dissertation also mentions 283 children with mercury in their urine but no clinical symptoms of the disease. However, children from both groups showed similar changes in their blood: anemia on the background of reticulocytosis, a disruption in the leukocyte profile, and thrombocytopenia. Thus, this group of 283 children also included children who were actually poisoned by granosan but whose signs of poisoning had been “wiped out” [A57]. Both the small and large groups of children from Novosibirsk were treated with unithiol [A57]. It is clear that not all children poisoned by granosan received such treatment: there were many different groups who showed no outward indications of disease, and were therefore not considered. Dissertation [A12] discusses the results of studying 57 children from the Oshk Oblast of Kirgizia, who were chronically poisoned by granosan. A mass poisoning of 45 children took place because they ate bread made from grain that had been treated with the same protectant. Two were poisoned through

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breast milk, and ten in the uterus. The poisoning caused crude changes in the brains of the poisoned children, and defects in their mental and physical development. Of the 47 children, 18 developed acute poisoning, and 29, while seemingly healthy, saw a gradual growth in the symptoms of chronic poisoning (with a shortened incubation period). The simultaneous observation of both groups of children and adults showed that chronic poisoning is a more serious problem in children. While only 17 out of 76 adults displayed more serious symptoms, 25 of the 47 children had more marked problems, with eight fatalities [A12]. From dissertation [A12], it follows that chronic granosan poisoning damages both the central and peripheral nervous systems. Toxic encephalitis syndrome was observed in 38 of the group of 47 children, encephalomyelitis in four, and encephalopolyneuritis in five of the group. Children where poisoning was chiefly localized in the brain stem and subcortex, developed the most serious symptoms, sometimes resulting in fatalities. Children having brain stem encephalitis who suffered marked poisoning saw disruptions to respiratory functions and cardiovascular centers. Poisoning progressed rapidly: two of the eight fatalities occurred on the 7-8th day after the first symptoms appeared, three on the 10-11th day, and the rest from the 18th to the 60th day after the first symptoms appeared. All other incidents of OMP poisoning had the same social background: hunger and ingestion of food made from grains treated with protectants. Only the geography and the type of seed treated with granosan changed. Thus, in Kirgizia, pea and hemp seeds treated with granosan poisoned a group of 55 children [61], the majority of whom were observed to have skull and brain nerve damage. In the Chelyabinsk Oblast, sunflower seeds treated with granosan poisoned 58 children, six of whom had acute damage (with two fatalities), and 15 developed symptoms of medium gravity. Liver damage was found in 13 children [62]. Unfortunately, granosan in the USSR was regulated not through knowledge of its toxicology, but through negligence towards humans. If scientific knowledge had been employed, granosan would have been banned after a 1960 dissertation [A7]. In any case, at a scientific conference in Kiev in June 1957, the future degree candidate L.I. Medved’ stated that granosan “should be replaced” with a less toxic pesticide [63]. The same conclusion followed from dissertation [A31], defended in Tbilisi, which convincingly showed granosan’s toxic effects on embryos and gonads, as well as its cytogenetic effect. In order to understand the picture of events in the USSR more fully, we should recall similar events in Japan. There, the first signs of poisoning by organomercury compounds were noted in 1956; 12 years later all OMPs were banned without exception.


55

Therefore, we emphasize again that mass human poisoning by OMPs, and in particular by granosan, is a purely Soviet phenomenon. Over the last half-century, the USSR did not ban granosan. No ban has since been introduced in Russia. 3.5. Poisoning by Other Types of Pesticides Pesticides that are not part of the OCP, OPP, and OMP groups also caused much damage, especially chronic, to humans. Let us give some examples. Studies of the effects of the fungicide thiram, widely used in agriculture to protect corn and sugar beet seeds from disease, lasted for many years [A91, 64]. In 1971, 119 people were reported to have been poisoned, all of who had contact with thiram in their work treating seeds [64]. Thiram concentrations in the workplace reached 20.4 mg/m3 (the MPC has different values, from 0.01 mg/m3 to 0.5 mg/m3 [4, 8, 39]). Of those poisoned, 52.1% reported headaches, 20.0% dizziness, 22.6% sleep disruptions, and 12.6% irritability; moreover, there were other symptoms of neural system disruptions. The frequency of illness increased with the length of exposure to thiram. The most evident changes in the neural system (diencephalic syndrome, encephalopathy, sclerosis of blood vessels in the brain) were observed in those who treated seeds with the fungicide, and those who packaged them [62]. However, it appears that this experience was not enough; ten years later, the same author defended a dissertation on the state of the neural system of subjects working with thiram [A91]. The number of those tested grew to 475; 82.3% of this group had neural pathologies. But the ban on thiram and its formulations took place only ten years later, in 1994. Propanile use creates concentrations of 0.2-8 mg/m3 in agricultural workers’ breathing zones (the public health standard was 0.1 mg/m3 in the summer of 1967). This herbicide was detected in the water used to wash the signalers’ kerchiefs and gloves. In experiments with rats and cats, propanile in concentrations of 5.6 mg/m3 caused blood chemistry changes, methemoglobin formation, and an increase in the weight coefficient of lungs and adrenal glands. When examining the animals, destructive deviations were observed, and with another dose of propanile at the same concentration of 5.6 mg/m3, there were some fatalities. People continued working. Conclusions were unsurprising: when working with propanile, one must use individual protective equipment and take precautionary measures [3]. Let us look separately at working conditions in greenhouses [A94, A102]. Compared with working conditions in the open, pesticide migration paths in greenhouses are acutely complicated. Greenhouse working conditions are characterized by long human contact with an environment that has become contaminated by pesticides (air, plants, soil) in a heated microclimate, and with

56


physical exposure. Protective equipment is not able to protect humans – pesticides get inside this clothing rather quickly. As a result, safety standards valid under usual conditions are not acceptable for use in greenhouses. Health standards must be made considerably more stringent. Thus, using pesticides in greenhouses effectively means either decreasing the amount used, which leads to inefficiencies, or maintaining the amount used, with patent damage to humans. The latter reigned. Twenty-four hour quarantine periods were established after pesticide treatment in greenhouses; this amount of time [A94] was not acceptable from the safety point of view. According to data from a mass examination [A102], 82% of the deterioration in both human health and the objective status of workers in greenhouses was caused by violating these quarantine periods. A large portion of those people who worked for many years in greenhouses using pesticides were observed to have pathological changes in their liver and bile passages, and in their cardiovascular system [3]. Workers also displayed a marked growth in the frequency of chromosomal aberrations in the lymphocytes of peripheral blood [A102]. With the widespread use of pesticides, it is difficult, and sometimes impossible, strictly to enforce technological production processes. Therefore, commercial forms of pesticides made up of a single compound can in actual fact differ significantly in their properties from those verified in laboratory tests. It is even more difficult to create an invariable compound in those cases when the pesticides are made up of complex chemical cocktails. Different components in these mixtures differ in their environmental stability, and in their toxicity. As examples, the insecticides toxafene and polychlorpinen are made up of more than 100 components. Commercial-grade HCH produced industrially is a complex mixture of isomers. In this mixture, only lindane acts on the target; the other seven isomers have no effect on insects, but negatively affect the rest of the natural environment. This situation does not simply create difficulties in identifying pesticides in the environment, but also excludes the possibility of identifying an objective mechanism by which pesticide mixtures influence living organisms. Additives contained in many pesticides are also highly toxic. In particular, a series of pesticides (especially the phenoxyherbicides 2,4,5-”, 2,4-D, etc.) contain polychlorinated dioxins as constant additives, which, in miniscule quantities, can be teratogenic, carcinogenic, and mutagenic [38]. Sulfoteppe is seen in the mixture of many different OPP formulations, such as diazinon and malathion, chlorpyrifos and phosalone, phensulphothion and disulfoton, demeton and terbuphos [31]. Sulfoteppe is a poison [12] that is often stronger than the pesticides in which it hides. There is an especially significant amount of sulfoteppe in demeton (from 3-4% [31]), which explains the large spread in demeton’s FD50 values – from 2.5 to 12 mg/kg [12]. Demeton caused a


57

number of illnesses and fatalities in humans [A49] for a long time before the necessary public health standards were established. Sulfoteppe not only actively operated (through diazinon), but is continuing to act (through chlorpyrifos, phosalone and malathion) from its pesticide underground. The famous herbicide “agent orange” contained as an additive 2,3,7,8tetrachlordibenzo-p-dioxin (2,3,7,8-TCDD), the most toxic chemical substance created by mankind. Dioxin makes up about 150-160 kg. in 24,000 tons of herbicide 2,4,5-T. This additive is enough to allow us to continue to discuss the consequences to humans and the environment in Vietnam from not one, but two wars: the herbicide and the dioxin [65]. Herbicide 2,4,5-T was not alone. We do not know the fate of the toxic dioxins that spread throughout the USSR in the formulations of different pesticides: 2,4,5-trichlorophenol, 2,4,5-trichlorophenol copper salts, 2,4-D, pentachlorphenol, propanile, and many other formulations made up of various components. Many dioxins were, and still are, introduced into the environment together with phenoxyherbicides – derivatives of 2,4,5-T and 2,4-D. Therefore, the general toxic background created by these herbicides may be much higher than expected, since they can contain many other dioxins as additives along with 2,3,7,8-TCDD. Moreover, these compounds can evolve dioxins when transformed in natural conditions. Thus, the danger of all such pesticides must be measured in two ways: by the content of highly toxic dioxins, and by the dioxin precursors [38]. For many years, hexachlorophene (HCF; the chemical name is bis-3,5,6trichlor-2-hydroxyphenylmethane) was thought of as a bactericide and fungicide that effectively protects humans from bacterial contamination. However, this particular formulation in its time introduced toxic 2,3,7,8TCDD directly to many people in different countries. At the end of the 1950s, the USSR started to use HCF as an antibacterial formulation during surgery on wounds and in treating burns [66]. It was thought that this substance had no side effects when used on the skin, and it showed promise in curing many illnesses, including pyodermia and epidermophytosis. By the end of the 1960s, the Moscow Textile Institute created a material that was an inoculated cellulose copolymer and poly-1,2-dimethylpyridinium that chemically attached HCF, in this way maintaining the material’s antibacterial activity [38]. HCF was especially widely used in Western countries. Until 1972, it was included as an active component in soaps, cleansing creams, shampoo, deodorants, creams, and toothpastes. HCF was used for medical purposes, to control staphyllococcus contamination, in particular in maternity hospitals and in the cosmetics industry; it was also used as a preservative, etc. It was used in agricultural formulations as well [67]. Although HCF’s toxicity was

58


often mentioned, there was a radical change only in 1971. In the USA, it was noted in experiments with rats that HCF causes cerebral hemorrhages, brain damage, and paralysis of the hind legs [38]. Soon 2,3,7,8-TCDD was detected in American and French samples of HCF. In France in 1972, 36 children died from nervous system damage after using dusting powder containing HCF as a bactericidal additive [68]. This tragedy showed the amount of real danger from spreading 2,3,7,8-TCDD as a microadditive in HCF. Events in 1971-72 in the USA and France ended with the adoption of measures that strictly limited its sphere of medical use [38, 67]. No lessons were learned by the USSR from the Western experience. In the USSR, HCF was produced in Shop No. 15 of the Rubezhansk enterprise PO “Krasitel” (35-ton-per-year capacity and, after reconstruction in 1987, 120-tonper-year capacity). The raw material was 2,4,5-trichlorophenol from the PO “Khimprom” enterprise (Ufa). Measurements of 2,3,7,8-TCDD concentrations in the Ufa trichlorophenol were not envisaged and did not take place before the end of the 1980s. Nevertheless, no consideration was given to the fact that, through predioxin transformation, 2,3,7,8-TCDD content could grow when synthesizing HCF. From 1981 the USSR launched industrial production of an antibacterial cloth treated with HCF using a radiation and chemical method [69, 70]. Minzdrav’s secret Biophysics Institute, and its subsidiary in the city of Angarsk, coordinated the testing and use of this cloth. Maternity hospitals in Ivanovo, Moscow, Obninsk and other cities started to use it in 1977 [69, 70]. Even wider introduction of antibacterial cloth into medical practice in the former USSR started in the second half of the 1980s, with the beginning of large-scale production in the city of Noginsk [38]. The methodology of introducing HCF onto the cloth did not take into account at all the existence of the 2,3,7,8-TCDD dioxin. Monitoring and controlling 2,3,7,8-TCDD content were not envisaged in 2,4,5-trichlorophenol, nor in HCF, nor in the cloth treated with HCF [69, 70]. Consumers of antibacterial cloth could only use methods of trial and error, in the absence of data on 2,3,7,8-TCDD and other toxic dioxins. Navy medics, seeing the growth of illness among sailors and submariners, stopped using the bactericide linens in the Soviet Navy. Although the world press continued to refer to 2,3,7,8-TCDD in connection with the medical use of HCF, in the USSR a “dioxin silence” reigned [38]. HCF production began, and the antibacterial cloth using this substance was developed, tested, and supplied for mass production. In 1987, Minzdrav’s Biophysics Institute published a monograph called “Antibacterial Materials in Medicine” [70] without any mention of the negative consequences well known at that time. In 1988, in the HCF produced for many years by the Rubezhansk PO “Krasitel” and in powdered HCF, whose technological production regulations provided for drying at temperatures of 100 0 ! for 21,5-22.5


59

hours, dioxin concentrations reached 102 mg/kg; i.e. the dioxin concentration was a thousand times higher than known concentrations for other industrially developed countries. The concentration of 2,3,7,8-TCDD in the antibacterial cloth, even after the cloth had been cleaned and ironed once, grew sharply. All this showed very clearly the absence of any dioxin and predioxin elimination, even in the production of the original 2,4,5-trichlorophenol at the PO “Khimprom” (Ufa). Moreover, it was observed that even self-emulsifying oil containing HCF, and different cosmetic formulations – for example, a formulation to protect against insects – were introduced without toxicological research. In 1988, the production and use of HCF were banned. In spite of the ban, at the end of 1988 Minzdrav permitted the use of the antibacterial cloth “on an exceptional basis” in hygienic napkins in Armenian maternity hospitals. The napkins played their own role – 37 newborns died in the Scientific and Research Institute for Obstetrics and Gynecology of Armenia in January 1989 [71]. Only a year after the “ban” was there an open discussion on the danger to human health presented by HCF contaminated by 2,3,7,8-TCDD. 3.6. Morbidity and Mortality Pesticides’ marked influence on the health not only of those who used them, but of the entire population, was seen in all the Republics of the former USSR: Azerbaijan [72], Armenia [A99], Kirgizstan [3], Belorussia [A105], Moldavia [11, 73, A42], Russia [3], Tajikistan [A11, A86, A87, A95], Turkmenistan [3], Uzbekistan [57, A19, A33, A44, A49, A59, A62], and the Ukraine [3, A79]. Above, we looked at this issue from the point of view of how different groups of pesticides act. In this section we discuss two further aspects: the geographical and medical-environmental (epidemiological). When analyzing the problem from the geographical standpoint, considering recent data, it is evident that the greatest growth in human illness linked to the immoderate use of pesticides is seen in Moldavia, Tajikistan, and Uzbekistan [1]. In Moldavia, people who were in contact with pesticides in their work had higher indicators of overall illness. In population centers where chemical use was maximal, the indicators for overall illness were up to 3.5 times higher than the same indicators for those with minimal chemical use. The growth in illness is due in general to pathologies of the respiratory organs (acute respiratory illness, pneumonia), inflammatory processes in epidermal and dermal cells, and congenital developmental abnormalities. A direct correlation was observed between territorial pesticide exposure and the damage to human health caused by tuberculosis, infant mortality, and also by cirrhosis of the liver and chronic hepatitis [1]. The situation in Tajikistan was the same; the amount of pesticides used in the 1970s per hectare of sown fields was 20.6 times higher than

60


world levels (4.7 times higher than average levels in the Soviet Union, and 3.5 times higher than levels in the USA). OCPs were in first place, followed by OPPs. Pesticide concentrations in the air not only of work zones, but also of population centers, exceeded MPCs by many times. Such OCPs as DDT and HCH were found in concentrations higher than MPCs allowed in the canal water used for drinking [A865]. Table 3.3 gives an idea of how “pesticide pressure” directly affected human health. The data from this table are from 1974-77. The author of dissertation [A86] divided Tajikistan into several zones with differing levels of pesticide use. Illness levels in cotton growing regions were significantly higher than in mountainous and foothill regions. This same group of cotton growing regions had the largest number of infectious diseases among children. Table 3.3. Illness indicators in regions of Tajikistan in 1974-77 from zones with differing pesticide exposure [86] Indicators of overall illness and infant mortality Infant Pesticide Amounts Zone REGION

Mortality, SOMATIC

Infectious

< 1 Year, per

in kg/h

Children

Adults

Children

Adults

1000 Births

I

Aininskiy

2.6

18.7

39.4

45.2

37.2

92.5

II

Ganchinskiy

5.8

23.2

17.2

38.4

22.3

83.0

III

Ashtskiy

30.9

20.3

14.3

43.3

33.5

IV

Proletarskiy

42.1

52.7

21.5

70.5

43.0

88.7

V

Parkharskiy

44.6

35.8

18.9

105.5

61.7

117.8

One of the regions of the USSR that suffered most from pesticide use was Uzbekistan, where a large amount of work took place in the 1960s without even elementary knowledge, and with chronic and mass violations of existing regulations and standards [A49]. “Pesticide poisoning incidents from 1959-68 in Uzbekistan were analyzed. The acute poisoning analysis permitted us to divide sufferers into three groups: the first includes workers who have direct contact with pesticides; the second includes collective farm workers who worked in the fields shortly after the crops were treated; and the third includes people who suffered the effects of pesticides introduced into their bodies through water, food, and inhalation.


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“The wide use of pesticides in the republic started in 1959 when 30% and 60% mercaptophos started to be used for the first time in the fight against cotton pests. In 1959-61, the number of incidents of poisoning, especially in the first group, was 23% of all incidents over the ten-year period; 7% of those poisoned suffered fatalities. “As a result of replacing mercaptophos with methylmercaptophos, the number of registered poisoning incidents from the first group decreased by a factor of two in 1962 and 1963. Methylmercaptophos poisoning was detected in general among collective farm workers (59.8%) aged 17-45. In acute methylmercaptophos poisoning, most often a lower level of poisoning (in 75.9% of incidents) was observed; the number of grave incidents was insignificant (2.4%); and there were no fatalities. The decrease in blood cholinesterase activity varied from 15-51%, and was noted in 45% of subjects. “The growth in poisoning incidents in 1964 (31.5%) was explained by the use of highly toxic mixtures of aldrin and methylmercaptophos in the fight against cutworm and cutworm moths. The ban on aldrin decreased the number of acute poisoning incidents, but nevertheless their number remained high. “The results of the pesticide poisoning analysis showed that, while in 1959-63 in general only poisonings connected with professional activity were registered, from 1964-68 60-70% of poisoning incidents took place among the second group, those working in collective farms (pruning, weeding, irrigation, etc.), and 20-30% among the inhabitants of regions using pesticides. While before 1964 the main cause of poisoning was the violation of safety rules, more recently the causes of poisoning have been: violating quarantine periods when returning to treated fields, violating health protection zones, and ingesting water and food products contaminated by pesticides” (emphasis ours – authors). From the doctoral dissertation by R.A. Yakubova “Issues of Water Health and Protecting Reservoir Health During Pesti At the end of the era of intensive cotton farming in Uzbekistan, 40% of the population of some regions that used pesticides intensively had disruptions to their nervous system and liver [1]. Table 3.4 gives results for the first half of the 1960s and for different types of illnesses. As can be seen, the cotton growing regions felt the main impact from mass OPP and OCP use. In another research paper [215] covering the health status of 2745 inhabitants of Uzbekistan working with OPPs and

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Table.3.4. Illness in the rural population of Uzbekistan (adults and children) by nosological forms in the 1960s (per 1000 population) [49] Akkurganskiy Region

Parkentskiy Region

(intensive pesticide use)

(control)

ILLNESS

1961

1963

1965

1961

1963

1965

Chronic Bronchitis

7.19

8.06

12.67

0.24

0.32

0.37

Chronic Gastritis

6.60

9.98

14.82

1.50

2.28

3.23

Gastroenteritis

4.27

6.20

7.82

1.40

0.64

1.14

Chronic Hepatitis

1.01

0.66

1.39

0.45

0.20

0.29

Neuritis, Neuralgia

2.64

2.41

4.05

0.07

0.12

0.37

Sciatica

4.86

8.57

15.33

2.44

1.38

4.15

Spontaneous Miscarriages

2.57

9.91

32.24

4.61

7.43

12.2

OCPs, different types of clinical deviations in the nervous system were observed: asthenia (23.6%), asthenoautonomic syndrome (28.1%), and autonomic vascular disruptions (34.5%); almost 40% suffered from an enlarged liver, 33.8% from toxic hepatitis, and 84.2% from disruptions in kidney functions. The state of the cardiovascular system was researched in the 1970s in Ukraine, using two groups of people as test subjects [A69]. One group consisted of 1101 disinfectors (1003 of whom were women) who worked with combinations of OPPs and OCPs for an extended period. The second group consisted of 87 people producing OCPs. The disinfectors worked with pesticides 3-4 days a week, seven hours a day, in closed rooms (their protective equipment included coveralls, head kerchiefs, rubber gloves, and surgical masks). Complaints covering various cardiovascular problems were noted in 79.5% of the first group, 51.4% of the second (16.5% of the control group). The most commonly encountered cardiovascular pathology was myocardial dystrophy: 56.0% of the first group, and 42.5% of the second (9.3% of the control group). More often than not, hypertension was observed in people working with pesticides for 1115 years (36.6%), or more than 15 years (42.9%). The combined effect of OPPs and OCPs on the human cardiovascular system is much more serious than the effect of OCPs alone. The upper respiratory tract was studied in 686 inhabitants of Ukraine who came into contact with OCPs in the middle of the 1960s [6]: 205 produced DDT and its formulations; 51 produced HCH; 216 came into contact with OCPs in agriculture. Respiratory tract disruptions were observed in 302 subjects, and olfactory disruptions in 178, i.e. in 44.4% of those having contact with pesticide combinations, 41.1% of those producing


63

DDT, and 31.4% of those producing HCH. The frequency and gravity of the olfactory disruptions grew with the length of exposure to OCPs. In the 1960-70s, pathologies of the central nervous system were studied in 1136 inhabitants of the Ukraine, 937 of whom were examined in clinics; these pathologies were caused by OCPs and OMPs separately, as well as by combinations of pesticides (OCPs, OPPs and OMPs) when chemicals were increasingly used in agriculture [A79]. The author clinically classified pesticide damage to the nervous system, separating out four types of pathologies, and seven groups of damage. In 1966-72, 683 agricultural workers from Uzbekistan who had come into contact with OPPs and OCPs had their vision studied [A64]. Chronic pesticide poisoning affected 663 people, 20 acutely; 81% of those examined complained of worsened vision (20% in the control group). The real situation was even worse: 89.2% displayed pathological changes in their visual organs (12.1% in the control group). Of those suffering chronic poisoning, 95% had disruptions in color perception (8% in the control group), 93% disruptions in cornea sensitivity (< 22% in the control group), 53.4% a reduction in visual acuity, and 48.2% a narrowing of the achromatic field of vision. The combined effect of OPPs and OCPs led to greater damage in the visual organs. Chronic skin disease linked to pesticides affected 47.9% of 4329 cotton workers who had worked on several farms in the Tashkent Oblast of Uzbekistan in the 1960s, and had come into contact with OCPs and other pesticides [A46]. In the 1970s, the oral cavity was studied in 4246 inhabitants of the Galabinsk (cotton growing) region of the Tashkent Oblast, where OCPs and OPPs were used especially widely [A92]. The largest amount of dental illness was seen in subjects who had contact with pesticides at work. Those with pesticide poisoning showed a particularly high incidence of dental illness: 78.3% had cavities (48.7% in the control group), 22.2% dental erosion (0% in the control group), 82.2% paradontosis (15.4% in the control group), 62.7% stomatitis (6.4% in the control group), 63.2% damage to the lips (3.8% in the control group), and 51.3% damage to the tongue (5.0% in the control group). In several regions of Belorussia [A105], a correlation was observed between liver and gall bladder disease among people using pesticides at work, and the pesticide exposure of a given territory. Statistically, this correlation became apparent at levels of pesticide exposure of 2 kg/h and higher. The average annual indicators for stillbirths in Uzbekistan are 1.5 times higher in regions with intensive pesticide use, in Kirgizia 1.6 times higher, and in Moldavia 1.2 times higher [A109].

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“An analysis of materials on human illness of those people living in zones with varying levels of “pesticide contamination” permitted us to establish a correlation between the illness and the level of pesticide contamination in elements of the outside environment. “A direct correlation was established between the volume of pesticides used and the indicators for death and infectious disease” (emphasis ours – authors). From the doctoral dissertation by A. Yakubov “The Regime of Using Pesticides in Different Climatic and Geographical Zones of Tajikistan.” Dushanbe, 1980 [A86]. It was established in the Kursk Oblast that malignant tumors of the stomach and milk glands are directly linked to the volume of pesticides introduced into the environment. Comparable results were recorded in the Bryansk Oblast. It was found that of all types of cancer, that of the milk glands is the most sensitive indicator of pesticide contamination in the environment [6]. A direct correlation was also observed between the indicator for territorial pesticide exposure and the number of fatalities among the adult population from cirrhosis of the liver and chronic hepatitis. Similar facts show that WHO data (in the 1980s about 50,000 people died annually throughout the world from pesticide poisoning) were underreported by several times for acute poisoning, and by hundreds of times for chronic poisoning. 3.7. Pesticides’ Genetic Effects Since all pesticides are mutagenic, there must be long-term genetic effects accompanying their direct and immediate consequences. A cytogenetic examination of a group of women poisoned by toxafene [15] established a growth in the level of chromosomal aberrations. There are data on the increasing frequency of chromosomal aberrations among people producing dactal [A100] and zineb [A97], and among people having contact with the insecticide pirimor [A97]. This increase was established in those suffering from acute OPP poisoning. A reliable increase in the level of embryonic mortality and the number of congenital abnormalities in progeny was also established in this same population group [74]. The frequency of chromosomal disruptions increased in many cases: in personnel producing zineb in Ukraine [A97], and GCBD and dactal in Russia [A100]; in regions with high pesticide exposure in Uzbekistan, Moldavia and Azerbaijan [1, 3, A97]; and in greenhouse workers in Simferopol (Ukraine) after working with the aphicide pirimor [A102]. Table 3.5 gives some generalized data on pesticides’ genetic consequences to humans.


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Table 3.5. Some of pesticides’ genetic consequences to humans [1, 75] Effect

Pesticide

Increase in the frequency of

Captan, toxafene, folpet, DEF, foxim, phosmet,

chromosomal aberrations

tetrachlorvinfos, malathion, phosphamidon, trichlorfon, carbaryl, mankozeb, thiram, zineb, 2,4D, 2,4,5-”, maleic hydrazide, aldicarb

Increase in the number of

Nitro-aldicarb, bavistin (carbendazim), malathion

daughter chromatid changes, lengthening of the cell cycle Suppression of mitotic activity

Trichlorfon, carbaryl, thiram, nitro-aldicarb

Increase in the number of mitoses Trichlorfon Disruption of mitotic component

Propham

figures, change in DNA synthesis Potential mutagenic danger

DDT, dichlorvos, sulfallat, triallat, carboxide, trifluraline

Cytogenetic research showed that the average group frequency of cells with chromosomal aberrations in lymphocytes is many times higher in personnel producing the fungicide zineb (5.53%, with fluctuations from 4.00-8.50%) than in the control group (0.95%) [A97]. Blood was studied in a group of virtually healthy adolescents aged 14-17 from two localities in the Ukraine, where pesticide exposure differed by a factor of three, though the pesticide content in food products, drinking water, air and soil in the experimental zone was not higher than public health standards permitted. In Azerbaijan there was a difference of 100 times in the amounts of pesticides used in the experimental and control localities, while the pesticide contamination of elements of the environment and food products in the experimental zone was 2-50 times higher than acceptable levels [A97]. Table 3.6 shows the results. In the Ukraine, there was an increasing trend in the average population level of spontaneous chromosome mutations among adolescents from the experimental zone; however, the difference in the basic cytogenetic indicators between the experimental and control zones is not yet statistically reliable. In Azerbaijan, the average frequency of metaphases with chromosomal aberrations differed significantly, statistically, from the control and average population values. However, it is characteristic that in Azerbaijan, the frequency of cytogenetic disruptions in the control group is also higher than the level characteristic for natural (spontaneous) mutation processes in human lym-

66


Table 3.6. Results of cytogenetic examination of adolescents from agricultural zones with differing intensity of pesticide use [97] Ukraine Characteristic Avg. frequency of

Azerbaijan

Experim’tal Control Experim’tal Control

Spontaneous Value

2.12

1.74

7.35

4.48

1.19

0-6.0

0-4.5

1.0-14.0

1.0-9.0

0-6.0

Studied

0.022

0.018

0.090

0.061

0.012

Aberrant

1.09

1.08

1.19

1.37

1.00

% of subjects with >2%

33.30

28.60

91.30

78.27

11.6

metaphase with aberrations, % Scope of individual fluctuations in the group, % Number of aberrations per metaphase

aberrant cells

phocytes. In other words, in Azerbaijan at the time of the research, there were no zones clear of pesticides – there simply was no territory not genetically “colored” by pesticide exposure. One does not need to be a prophet to foresee with certainty the surge in hereditary disruptions in all agricultural regions of the world that are intensively using pesticides. 3.8. Effects of Pesticides on Pregnant Women and Children Acute and chronic pesticide poisoning (the latter being much more frequent) has serious effects during pregnancy and birth. Women who have been in contact with toxafene have an increased estrogen level in the initial period of the menstrual cycle. Moreover, there was no clear phase change, which shows that hormonal regulation was disrupted [15]. The negative impact of even low doses of OCPs on pregnancy has been proved, especially in the third trimester [1]. It has been shown many times that there is a correlation between embryo death and pesticide content in the mother’s body [1]. We will now quote several results of the study of pesticides’ effects on pregnancy and birth. The accumulation of OCPs causes poisoning in expectant women [A37, A45]. Four hundred three Ukrainian women, aged 19-30 who had recently given birth were examined in two groups, one having had contact with DDT, the other not. DDT was found in 270 (74.6%) of 370 samples of breast milk


67

taken from women who had had no contact with DDT. The DDT content in the breast milk of women working with this pesticide did not significantly differ from its concentration in the rest of the women. The following data give an idea of DDT concentrations in breast milk in the 1960s in the USSR [A45]: 7.3% of samples contained from 400-3200 mkg/l, 18.1% from 200-300 mkg/l, 34.9% from 30-150 mkg/l, and 14.3% showed trace amounts. In the Kherson Oblast (Ukraine) in 1965, DDT was found in 90.5% of breast milk samples, with an average concentration of 820 mkg/kg [A77]. In the Kiev Oblast at the end of the 1960s, DDT content in the milk of breastfeeding mothers was on average 20 mkg/l (the result was clearly underreported). None of the examined women who had given birth had contact with pesticides. The explanation showed that DDT content in cow’s milk reached 300 mkg/l (and HCH content reached 600 mkg/l) [3]. In the Angara River basin (Russia) in 1968, in the region where bodies of water were treated with mineral-oil DDT emulsions [A61], this formulation was observed in 90% of breast milk samples in women who had just given birth (the average was 180 mkg/l), and DDE in 60% (with an average of 110 mkg/l). Table 3.7 shows comparative data on DDT content in breast milk in different countries. The USSR could claim some kind of primacy among civilized countries (for the period after 1970, when DDT was “banned” in the USSR). However, the real picture is more complicated. A UNEP report published in 1987 [77] contained other numbers for DDT and DDE contamination of breast milk (Table 3.8). Table 3.7. Average DDT content in breast milk samples from different countries (in mkg/l) [76] Country

Years

# Samples

∑DDT

Canada

1975

16

35

Sweden

1977-79

300

47

Finland

1982

50

31

USSR

1984

112

82

Table 3.8. DDT content (mkg/l) in breast milk in several countries [77] Country

Years

DDT

DDE

FRG

1981

280

1200

Great Britain

1982-83

10

1300

Japan

1980-81

200

1800

1981

100

960

1979-81

150

2200

Sweden USA

68


Therefore Table 3.9, constructed from Soviet data on DDT and HCH, although it includes more detailed observations, does not allow us to come to a final conclusion. It seems that the results were clearly underreported. Stillborn children, who were discovered in the 1960s during a study of DDT’s effects on pregnancy and birth, had a noticeably higher quantity of DDT+DDE in their subcutaneous fatty tissues [A37, A45]. It thus became clear that DDT actively penetrates the placenta barrier. Overall, the average DDT content in fetal subcutaneous fatty tissues (3100 mkg/kg) differed very little from the DDT content in the subcutaneous fatty cellulite of adults who had operations (4330 mkg/kg) [A37]. The DDT concentration in the livers of stillborn children was on average 820 mkg/kg [A45]. Women with high DDT concentrations in their breast milk displayed more frequent pathologies during pregnancy, along with premature and pathological births [A37]. Mothers with high DDT concentrations in their breast milk delivered low-weight children, children not carried to full term (26.5±2.7%), and children with developmental defects, more often than mothers whose breast milk contained no insecticide (13.1±3.7%) [37]. HCH also penetrates the placenta barrier [A96, A101]. Complications during pregnancy occurred 1.5 times more frequently in the 213 women whose blood contained HCH than in the 89 women with no signs of this insecticide (78.3% and 58.4% respectively). It is especially significant that twice as many women with HCH in their blood spontaneously miscarried during the first trimester as those without HCH (7.5% and 3.4% respectively). Causal factors included disruptions in prenatal fetal development, and disruptions in women’s hormonal systems under the effect of HCH [A96]. Postpartum complications in women who had HCH in their blood were 2.5 Table 3.9. Average stable OCP content in breast milk in 1984, in several regions of the USSR [76] REGION

# of

Amount of OCP, mkg/l

samples

ï ,ï ’-DDT

ΣDDT

γ-HCH

ΣHCH

Moscow

4

8

87

46

Penza

4

9

63

34

Rostov

11

14

128

66

Baikalsk

5

10

45

53

Uzbekistan

64

18

120

51

Djambai Region

16

32

191

0.6

136

15

16

84

1

86

Russia

(intensive OCP use) Pai-Aryk region (“clean”)


69

times more frequent than in those without (52.4% and 20.8% respectively). The percentage of asphyxiations among newborn babies (12.0%) was twice as high in women with HCH in their blood as in women without. First-time mothers with HCH in their blood had many more children with abnormal development (2.56%, with 0.15% in the control group) [A96]. Health data for women of childbearing age in Uzbekistan are presented in several papers from different periods [48, 70, 89, 96]. Around 1969-70, 204 post-partal women were examined; they lived in the Khorezm Oblast, a region where cotton was treated with methylmercaptophos and DDT. Even without any visible signs of poisoning, their blood cholinesterase activity could be seriously depressed (by 50% or more). Spontaneous miscarriages were seen in 12-13% of the women (5.9% in the control group), and premature births in 3-4% (0.4% in the control group) [A48]. Two hundred mothers were examined from the Namangansk and Khorezm Oblasts of Uzbekistan, where lindane, DEF, and other types of OCPs and OPPs were widely used in growing cotton in the beginning of the 1970s. Of these women, 75.5% had early toxicosis during pregnancy (19.8% in the control group), 32.1% complications during birth (10.6% in the control group), and 7.9% stillbirths (1.7% in the control group) [A70]. At the end of the 1970s, 409 (or 52.8%) out of 775 women were observed to have chronic gynecological illnesses in regions where HCH, dimethoate and their mixtures were used in the Tashkent and Khorezm Oblasts. When comparing pregnancies and their outcomes between a group of mothers from a cotton growing region of the Samarkand Oblast (not linked to pesticides, but possibly having undergone their effects), and a group of mothers from a grain growing region (no pesticide use) from 1972-85, it turned out that health indicators for the group from the cotton growing region were significantly worse than for its grain growing counterpart [A96]. Pregnancy, birth, the postpartum period, gynecological pathologies, and the status of the fetus and newborn were all studied in 665 women from the Ukraine (Vinnitsk Oblast) living in a zone affected by pesticides (90 women were in the control group) [A103]. Of these 665 women, the menstrual cycle of 179 (26.9%), who had contact with pesticides, was disrupted three times more often than in the control group; inflammatory genital illnesses (39 incidents, or 5.86%) and erosion of the cervix (47 incidents, or 7.1%) occurred more frequently; 503 of the women (75.6%), who had contact with pesticides, had 3.3 times more illness and complications during pregnancy than those in the control group; and childbirth with no surgical intervention took place in only 45.0% of cases (92.3% in the control group). Of 674 children, 47 (7.12%) were born with grave intrauterine asphyxiation and died (2.2% in the control group); neonatal mortality occurred in 3.1% of cases (21 compared with 0 in the control group); perinatal mortality was

70


4.6 times higher than in the control group; and there was a noticeably lower birth weight (on average 3.04 kg versus 3.47 kg in the control group). The presence of OCPs in the pregnant women and the fetuses leads to disruptions in immunological response and in protein metabolism [A103]. It is known that female and male sexual glands are highly sensitive to the impact of OMPs. Children born to mothers suffering from acute and subacute granosan poisoning were often weak and not viable. Many of them were observed to have encephalopathy, paresis of the cranial nerves, and/or an underdeveloped brain with grave damage to brain structure [15]. None of the 12 mothers poisoned by granosan (10 of them conceived three months after acute poisoning, two during poisoning) had normal pregnancies, births, or normal children. One mother, poisoned by granosan and suffering encephalopolyneuritis, breast fed her daughter for eight weeks with breast milk that was observed to contain a mercury concentration of 0.04 mg/l. Only subsequent artificial feeding saved the baby’s life [A12]. In the Oshsk Oblast (Kirgizia) in the 1960s, 65 children born to women with chronic granosan poisoning were observed to be retarded in their physical and mental development, ill, and/or unviable [A25]. At the PO “Khimprom” plant (city of Pervomaisk in the Kharkov Oblast of the Ukraine, in 1973-77), 166 women, all working in a shop that treated seeds with combined chemical protectants, had various pregnancy complications 3.5 times more often than in the control group. “In the placentas of women working in close contact with chemicals, histological study showed destructive changes (heart attacks, obliteration of blood vessels, etc.), decreasing their functional capabilities, which is one of the causes of perinatal pathologies.” “Women working producing pesticide combinations had disruptions of the liver even before pregnancy” [A74]. A decade-long study [A83] of the pathology of 920 pregnant women, who produced herbicides of the 2,4-D group at the PO “Khimprom” plant in Ufa showed that 21.7% suffered toxicoses during the second half of pregnancy (4.05% in the control group); 17.4% gave birth prematurely (5.4% in the control group); 13.04% had their waters break early (4.05% in the control group); 5.5 % spontaneously aborted (1.8% in the control group); 10.6% had disruptions in their menstrual functions (4.8% in the control group); 4.4% produced congenital abnormalities in the fetus (0.8% in the control group); and 10% of newborns asphyxiated (5.5% in the control group). The risk of acute, more likely chronic, poisoning by different pesticides concerns not only this small number of children who are in one way or another linked to pesticide use, but also the larger number of children with no link whatsoever to pesticides. The danger of pesticides’ effects on children and their mothers is examined in many different papers [12, 37, 45, 48, 57, 70, 89, 90, 93, 96, 101, 103].


71

Pesticides affect children’s genes and heredity, and are transferred from mother to child through breast milk. Finally, pesticides are introduced to children by the state and society, through a contaminated environment. The average daily amount of lindane and DDT derivatives ingested by newborns in Kiev in 1981-82 through the breast milk of their mothers, who were not working with these insecticides, in many cases was 3-5 times higher than provisional acceptable FAO/WHO standards [A108]. The lindane concentrations in the blood of newborns in Kiev were three times higher than in their mothers’ bodies [A101]. Newborns are especially vulnerable to pesticides’ effects, since they do not have a fully developed immune system and adaptation mechanisms, or detoxification systems for foreign chemicals. A direct correlation between overall pesticide exposure in a given territory and primary illness in newborns [A101] was traced into even those territories of the Ukraine where the volumes of pesticides used were not extreme. The clearest expression of the “pesticide exposure – primary newborn illness” correlation is seen with pesticides of the second risk class (by toxicity), while the correlation is less clear for pesticides of the third and fourth categories. The most dangerous pesticides of all types for newborns are OCPs, with OPPs a close second [A101]. In rural regions with maximal pesticide exposure, children more often suffer the following illnesses before the age of 14 [A109]: iron-deficit anemias (10 times more often in Turkmenia, 4 times in Armenia, 2.5 times in Azerbaijan, 2 times in Uzbekistan, and 1.4 times in Moldavia); active tuberculosis (2 times in Moldavia, 2.3 times in Kirgizia, 1.6 times in Armenia and Azerbaijan); viral hepatitis (23.7 times in Turkmenia, 2.4 times in Armenia, 2 times in Azerbaijan, 1.2 times in Kirgizia); and acute upper respiratory tract infections (21 times in Turkmenia, 1.4 times in Kirgizia). We will provide data by region. The indicator for infant mortality in children up to one year of age in Armenia turned out to be significantly higher in those regions that actively used pesticides than in those where pesticides were less actively employed [A99]. Pesticides have a statistically reliable effect on children in zones where OCPs are intensively used (in the Salyansk region of Azerbaijan, the amount of OCPs introduced into humans exceeded public health standards by up to 7.7 times). Primary illness of the endocrine system increased 3.1 times in children up to age 15 (over a five year observation period); in disruptions in diet and metabolism, the nervous system, and the sensory and respiratory organs; in increased frequency of illness (over five years) in children up to age 15 (an overall increase by 3.6 times, and by class of illness, from 2.2-7.6 times); in the prevalence of pathological disruptions according to data from medical examinations of children from 8-14 years (an overall increase by 2.3 times, and by class of illness by 2.0-8.4 times); in

72


the decreased number of healthy children (by 3.4 times), and the increased number of pathological disruptions in health during the compensation phase (by 1.6 times) and the subcompensation phase (by 3.3 times); in increased frequency of functional disruptions to different organs and systems in children aged 8-14 related to the II group (healthy children with some morphological and functional disorders). The data received were used to develop “tables (standard and evaluative) to examine children’s physical development, taking into account the unfavorable effects of pesticide contamination of the environment” [A93]. The course of viral hepatitis A was studied in regions with mass OCP and OPP use in Uzbekistan (Samarkand Oblast, Narpaisk region) from 1958-76. The contamination in regions where children lived was characterized by the following data: in 1968-74 the amount of DDT and HCH in the soil reached 3.2 mg/kg and 10.8 mg/kg, respectively (MPCs are 0.1 mg/kg and 0.1 mg/ kg), and in water sources reached 2.7 mg/l and 2.9 mg/l (MPCs are 0.1 mg/kg and 0.02 mg/kg). The concentration of methylmercaptophos in the air of population points varied from 1.9 mg/m3 at a distance of 100 m to 0.085 mg/ m3 at a distance of 2000 m (the MPC is 0.001 mg/m3). The residual quantity of DDT in onions, potatoes, and carrots reached 14.8 mg/kg, and of methylmercaptophos reached 2.6 mg/kg in tomatoes and 1.46 mg/kg in apples [A90]. Air contamination in population points 100 m from the fields reached 1900 times the MPC. In the control region, cotton was not cultivated, and pesticides were not observed in the environment and food products [A90]. In the region with pesticide contamination where subjects contracted viral hepatitis A, the pre-jaundice period was 4.2 days (in the control area, 5.1), the jaundice period lasted 32 days (22.4 in the control area), the liver enlarged more than in the control area and took longer to return to normal size, there was a larger number of patients who also had an enlarged spleen, there was more frequent damage to the nervous and cardiovascular systems (1.5-2 times higher than in the control area), mixed syndrome was observed more often (45% of the time, compared to 12.6% in the control area), and the illness was more frequently serious. In 1971-75, the health of a group of 2473 children aged 1-14 was studied in several farms of the Khorezm Oblast (Uzbekistan), where HCH, phosalone and DEF were used to grow cotton. Overall illnesses among children in the region where the air was contaminated with pesticides were three times higher than in the control region [A85]. In 1970-75, the health of 2972 children aged 1-14 was studied in the Fergana Oblast, where OPPs were widely used. Overall illnesses among children were 2.4 times higher than in the control region of the Tashkent Oblast, where pesticides were virtually unused. Moreover, children aged 4-7 years were the most sensitive to air contamination. The OPP formothion,


73

found in 1969-70 in the Akkurgansk region of the Tashkent Oblast (in a concentration lower than the MPC – 0.5 mg/m3), was generally toxic [A65]. In the 1970-80s, in regions of the Krasnodar Krai where rice was intensively grown, a linear correlation was found between the amount of territorial pesticide exposure and a series of children’s illnesses, including: a higher level of chronic tonsillitis and adenoids in children up to the age of 14 and adults, and frequent upper respiratory tract illnesses, neuroses, and psychopathies among adolescents aged 15-17. In zones with an average annual pesticide exposure of 14.7 kg/ha, when compared with a zone featuring a 5.3 kg/ha exposure, there is a higher incidence of infectious and parasitic diseases among children, as well as tuberculosis, viral hepatitis, illnesses of the nervous system, eyes, ears, respiratory and digestive organs; there are a decreased number of children with normal physical development, and an increased number with a body mass deficit of the I degree; the number of children with retarded physical development grows; more children aged 0-14 are in the II and III health groups; and there is a decrease in lysozyme activity in children’s saliva [3]. In Moldavia, in zones where chemicals were used intensively in agriculture, primary illness in children in the 1980s was 3.5 times higher than the same indicators in zones with a minimal level of pesticide use [1]. An examination of 5550 boys and 5496 girls in Armenia showed a marked worsening of physical development indicators among rural newborns as pesticide exposure grew. These indicators were worst in families where the parents worked in contact with pesticides. In all studied cases, children in these families were more retarded in their physical development than children whose parents had no contact with pesticides. Children were most retarded in their physical development where both parents worked with pesticides [A99]. Separate research carried out in the USSR from the beginning of the 1970s shows the correlation between the intensity of pesticide use and the frequency of complications in newborns, of poorer development indicators, and of poorer health among children [1]. Overall in the former USSR, children aged up to 15 years in regions with intense pesticide use show clearly worsened or poor physical development, 14-57% of the cause for which was due to the effects of pesticides. Pathologies in pregnant women and difficult gynecological case histories occur 15-18% more often in zones of intense pesticide use than in zones with limited pesticide use [3]. There are data on the jump in infant mortality in the pesticide-saturated cotton growing regions of Central Asia [1]. Central Asia and Moldavia had the largest number of newborns with congenital defects in the former USSR; these were regions with the largest pesticide use per capita. An analysis of epidemiological research materials permitted us to identify some general trends for the regions that were studied: “…in regions with

74


intense pesticide use, children up to 14 years of age are more often diagnosed with iron deficit anemia, active tuberculosis, viral hepatitis, and acute respiratory viral infections. Illness among newborns, and stillbirths, took place more often” [3]. This research again showed the correlation between the amount of pesticides used and indicators for children’s physical development in a series of cases (in Moldavia, Armenia, and Kirgizstan), as well as the correlation between pesticide use and the indicator for infant mortality [78]. Table 3.10 gives official data describing children’s health in several regions of the USSR where pesticides were used especially intensively. Table 3.10. Average annual number of illnesses (per 10,000) established for the first time in children up to age 14 in rural regions of the USSR in 1980-84 in territories with differing pesticide exposure [3] Illness in Regions Using Pesticides REPUBLIC, OBLAST

Minimum

Maximum

Iron Deficit Anemia Turkmenistan (Ashkhabad Oblast)

1.3

12.7

Armenia

1.7

7.3

Azerbaijan

4.5

10.9

Uzbekistan (Djizaksk Oblast)

27.6

54.0

Moldavia

33.1

45.1

Active Tuberculosis Azerbaijan

0.6

1.0

Armenia

0.8

1.3

Moldavia

1.1

2.2

Kirgizia (Chuysk Valley)

1.3

3.0

Uzbekistan (Djizaksk Oblast)

3.1

3.5

Turkmenistan (Ashkhabad Oblast)

1.0

23.7

Armenia

4.8

11.5

Azerbaijan

15.5

29.5

Kirgizia (Chuysk Valley)

45.7

57.2

Viral Hepatitis

Acute Upper Respiratory Tract Infections Turkmenistan (Ashkhabad Oblast) Armenia Kirgizia (Chuysk Valley)

30.3

646.4

483.4

555.4

1892.7

2765.0


75

Thus, it follows from the facts that an increase in pesticide exposure also increases the frequency of different types of illness. 3.9. Pesticides and Food Products Mankind has known of the dangers of food products being contaminated by pesticides for several decades. It is possible that this fact was stated earliest and most frankly in Rachel Carson’s famous book [2]. As early as 1963, the World Health Organization (WHO) published a report called “Principles of the Safe Use of Food Products Containing Residual Pesticides.” PUBLIC HEALTH STANDARDS, RUSSIA (food products) MPL (Maximum Permissible Level) – the maximum concentration of harmful substances in food products that does not cause illness or deviations in the health of those ingesting these products, or cannot negatively affect the next generation. PDD (Permissible Daily Dose) – the dose that can be ingested every day for a person’s entire life not causing harmful effects to the body [8]. Earlier, instead of MPL, the term PRQ was used (Permissible Residual Quantity). Unfortunately, the warning was not heard everywhere, or immediately. By the time this, and later, warnings began to be heeded, it was realized that an ever growing number of agricultural products ingested around the world (and in our country) were to some degree dangerous to our health. 3.9.1. Realization of the Problem In 1979, the joint center for three international organizations (UNEP, FAO, and WHO) monitoring food product contamination started collecting relevant data. Generalized information covered the period from 1971 onward; it was collected widely, from Australia, New Zealand and Japan to Great Britain, Canada, and the USA [79]. The Soviet Union did not feature on this list! The USSR adopted two government programs for the mass examination of food products in different regions. One of these programs was coordinated by VNIIGINTOKS (Kiev) [80], and the other by the Nutrition Institute of the Academy of Medical Sciences of the USSR [81]. All results from these examinations are still considered secret; however, several facts give an idea of their nature. In Belorussia in 1965, 1727 products were analyzed, mostly of vegetable origin. Pesticides were found in 10.4% of cases, and in 6.5% with levels exceeding MPCs (grain, grain products, sugar beets, fresh cabbage, etc.). In 1966, the number of products analyzed grew to 2100 (pesticides were found in 8.6% of cases). Pesticides

76


most often found were: HCH (23.8%), trichlorfon (23.5%), parathion (22.3%), and polychlorpinen (21.7%). Those vegetable food products that were most often found to be contaminated were: sugar beets (30%), potatoes (21.8%), apples and pears (21%), and fresh cabbage (14%). Ninety percent of potato samples with DDT turned out to be from the Grodnensk Oblast, where chemical treatment took place on a large scale. Dairy products were similarly affected: of all samples of milk, butter, and farmer’s cheese where DDT was found, 97% were from Grodnensk [3]. In Lithuania in 1964-66, 1394 food product samples were studied from farms in 15 regions of the Republic. DDT was found in 39% of samples in 1964, 24.3% in 1965, and 29.1% in 1966. HCH was found in 37%, 71.4%, and 43.7% of samples respectively. The amount of HCH in carrots was 4.6 mg/kg, in cabbage 2.2 mg/kg, in onions 2.1 mg/kg, and in apples 2.0 mg/kg [A51]. In Moldavia, the data from 1964-67 (Table 3.11) show the significant levels to which pesticides had accumulated in food products. Only 15% of these cases followed violations of pesticide use regulations; in all other cases, regulations were followed [82]. The conclusion that with existing application methods, pesticides accumulate in food products in unacceptable quantities [82] was not drawn. Research on pesticides in food products carried out in 1965-66 in Khersonsk Oblast (Ukraine) detected HCH in 80% of vegetable product samples, and DDT in 74.3% (in products of animal origin, these figures were 10% and 93.8%, respectively). The daily diet of subjects from Group I intensity work contained 2.31 mg of DDT [A77]. Stable OCPs were not the only pesticides found in food products, as was inevitable for the USSR in the 1960s; all types of OPPs were also detected, including phenkapton [38] and dichlorvos [30], menazon [41] and phenthoate [50], trichlorfon [14], phosalone [60] and tetrachlorvinfos [56]. The growing concealment of medical data during this period meant that the problem of food product contamination by pesticides disappeared from discussion. Over three five-year periods (from 1970 to the middle of the 1980s), Soviet society was almost completely deprived of information on human poisoning by food products contaminated with pesticides. However, the trend itself did not weaken. In the beginning of the 1970s, HCH concentrations reached 0.2 mg/l in samples of milk from the city of Namangan’s dairy factory (Uzbekistan). In the Namangan and Khorezm Oblasts DEF was found in large quantities of vegetables and fruits in gardens neighboring cotton fields from which this defoliant migrated: in cabbage and carrots (up to 0.6 mg/kg), pears (0.59 mg/kg), and grapes (0.41 mg/kg) [A70]. Inevitably, in the middle of the 1980s the issue of pesticides contaminating food products resurfaced. The organization of this process was initiated by a Resolution of the Council of Ministers of the USSR on April 2, 1984, “On


77

Table 3.11. Food product contamination by pesticides in Moldavia, from 1964-69 [82] # of

%

Observations Identified

Product

Pesticide

Apples

2

Public Health

mg/kg

Standard, mg/kg

1

2

PRQ

MPL

(1977-81)

(1992)

[49,52]

[42]

1

2

DDT

356

515

HCH

65

217 24.04 18.4 0.6 0.13

0.05

Trichlorfon

85

200

0.1

Methyl

1

Content,

70.7 39.3 2.25 0.28 25.2 55.5 0.48 1.74

55

25.4

0.76

Parathion Carbaryl

Not

Not

permitted permitted 32

96

3.1

32.2 0.2 0.44

Not permitted

Fruits

DDT

261

HCH Trichlorfon

582

66.2 19.4 0.66 0.14

422 54

Methyl

179

14.2

0.15

40.7 43.0 0.44 0.50

34

44.1

0.44

Parathion Carbaryl Vegetables DDT

Not

Not

permitted permitted 17

37

140

862

HCH

0

13.5

0

0.12

35.7 8.93 0.49 0.20

579

19.5

0.29

Trichlorfon

151

553 20.05 25.7 0.65 2.05

Methyl

17

60

58.2 58.3 0.19 0.51

Parathion

Grains

0.1

0.1-0.5 0.1 Not

Not

permitted permitted

Polychlorpinen

56

31

Carbaryl

40

229

DDT

164

and Beans HCH

359 108

75.0 35.5 3.93 2.18 0

43.1

0

0.12

34.7 19.7 0.28 0.26 55.6

0.27

Not permitted

Trichlorfon

80

15

Legend:1. Observation period - 1964-67; 2. Observation period - 1968-69.

50.2 73.4 0.65 1.1

0.1

78


Table 3.12. Pesticide Content in Food Products in the USSR from 1966-69, considering MPCs [81] Vegetable Products

Animal Products

Detection of Pesticide, % Pesticide

# Samples

Detection of

Within MPC Exceeding MPC # Samples Pesticide, %

DDT

7478

22.7

6.7

2962

14.6

HCH

6754

17.2

0.8

1893

18.1

Carbaryl

4211

-

22.0

Trichlorfon

2260

8.4

1.0

Parathion

1334

-

1.4

Additional Measures to Increase Monitoring of the Use in the Economy of Pesticides and Plant Growth Regulators with the Goal of Not Permitting Harmful Effects to Public Health.” As a result, a comparatively wide-scale verification of food products for their pesticide content started from 1984. In 1987-89, the Minzdrav Health and Epidemiological Service carried out a mass survey for pesticide contamination in agricultural and food products; a portion of their results became accessible to specialists and the general public [3]. In 1987, about 600,000 products were analyzed, in 1988 about 730,000, and in 1989 about 770,000. Table 3.13 gives an overall idea of the scale of pesticide contamination in food products in the USSR during the second half of the 1980s. The steady growth in contamination is evident. Firstly, throughout the entire USSR, the most contaminated class of basic food products was that of vegetable Table 3.13. Indicators of average pesticide content in food products in the USSR [3, 109] Samples with

% Samples Exceeding MPL

pesticides, %

to Overall # Samples

Exceeds

Fruits and

Year

Total

MPL

Dairy

Meat

Berries

Vegetables

Other

1984

3.10

1.25

1.01

0.83

1.34

1.90

1.33

1985

3.40

1.30

1.26

0.98

1.22

1.55

1.35

1986

4.02

1.37

1.22

1.05

1.43

1.71

1.36

1987

5.26

1.85

1.18

1.58

2.0

2.61

2.12

1988

7.70

2.68

2.08

2.08

3.21

3.37

2.44

1989

7.87

2.79

2.23

1.85

3.28

3.10

3.87

1990

6.78

1.99


79

origin, followed by dairy and meat products. Secondly, the percentage of products where pesticides were detected did not fall, but grew, from year to year. The amount of pesticides in food products grew more than 2.5 times (from 3-7.87%) over the five years from 1984-89. Thirdly, it was discovered that during the same period, the amount of residual pesticides grew from 1.5-3 times in food products from the basic diet: dairy, meat, vegetables, fruits and berries [3]. The data in Table 3.14 have undoubtedly been underreported. This is evident, if only from the results of pesticide surveys in separate republics of the former USSR. In our opinion, the fact that republics where a very large amount of pesticides were used, such as Azerbaijan, Tajikistan, and Turkmenistan, all were reported to be those with the most favorable levels of pesticide content in food indicates the data were falsified. It is also surprising that, according to official data, in Moldavia only 9% of samples containing pesticides had levels exceeding MPLs. At the same time, the frequency of pesticides being detected in food products grew from year to year, and from 1983-87 made up 3.99%, 5.59%, 5.79%, 8.93%, and 7.96% of the studied samples [1]. According to official data, around 1989-90 more than 10% of food products studied in the USSR contained pesticides, while 3-4% exceeded MPLs established Table 3.14. Pesticide content in food products in Union Republics of the former USSR in 1987-90 [3, 109] Positive Samples, %

Samples Exceeding MPL, %

Republic

1987

1988

1989

1990

1987

1988

1989

1990

Armenia

1.01

1.53

1.72

1.44

0.35

0.50

0.72

0.30

Azerbaijan

0.83

3.36

1.81

0.96

0.72

1.92

1.19

0.65

Belorussia

5.62

4.78

5.59

3.2

1.20

1.47

1.95

0.87

Estonia

14.92

15.76

11.16

19.71

1.75

1.18

0.15

0.16

Georgia

3.18

9.87

8.46

8.01

1.47

3.04

2.78

2.99

Kazakhstan

4.34

7.22

5.86

5.40

1.16

2.09

1.87

1.78

Kirgizia

2.46

3.16

3.55

2.69

0.93

1.27

1.28

0.63

Latvia

14.07

16.05

11.89

8.69

5.54

2.03

2.79

1.38

Lithuania

7.14

6.87

7.95

7.04

3.63

2.09

2.21

1.58

Moldavia

8.33

17.66

22.75

19.83

0.76

1.89

1.77

1.26

Russia

9.16

8.34

8.65

6.76

3.40

3.29

3.50

2.09

Tajikistan

0.77

1.26

4.38

4.19

0.82

1.15

2.82

1.88

Turkmenistan

0.91

4.12

1.20

6.51

0.42

2.52

0.52

4.79

Ukraine

3.29

6.24

7.11

6.31

1.42

2.33

2.56

1.76

Uzbekistan

8.18

13.08

11.37

10.56

2.63

4.26

4.12

3.57

80


by Minzdrav. The real numbers were significantly higher since, firstly, Minzdrav took into account only a small amount of the pesticides used, and secondly, methods for analyzing pesticides in food products at the time were archaic. Table 3.15 gives some idea of the trends in pesticide contamination of different food products. As should have been expected, fatty dairy products, Table 3.15. Residual Pesticides in agricultural and food products in the USSR exceeding MPLs in 1988-89 [3]

Products

Samples exceeding

# of Pesticides

Total

MPL, %

Detected

sample #

1988

1989

1988

1989

1988

1989

9

5

74

69

Dairy Products Butter, diet

41.89

27.54

Sour Cream 30%

30.77

16.67

5

5

26

24

Powdered Milk, children’s food

53.85

21.05

2

11

26

19

Sweetened condensed milk

12.90

7.59

4

8

31

79

Sweetened condensed cream

33.33

Breast milk

37.86

8

2

103

3

Fish Products Fish from reservoirs

15.20

21.60

30

21

329

514

Freshwater fish

15.81

24.87

26

35

487

985

Herring

11.63

7.46

12

13

43

67

Dried fish

16.67

0

7

4

12

12

Other Products Currants

16.81

7.91

30

20

220

278

Gooseberries

4.55

12.50

16

20

44

48

Preserved mushrooms

14.29

9.30

26

20

56

43

Neaps

17.76

11.30

17

24

107

115

Turnips

11.36

10.53

13

19

44

38

Wine (from grapes)

11.98

Malt for brewing beer

17 13.75 7.14

192 28

17

30

80

Mandarins

10.34

87

196

Marrow feed meal

15.38

12

39

Linen

44.44

5

18

Cotton

2.94

29.17

13

18

34

24

Grain for storage

25.0

20.0

2

7

4

5

Coffee concentrate

100

50.0

2

2

2

2


81

fish, and several different garden vegetables were the products that tended to accumulate the greatest amount of pesticides. From these data, it is clear, for example, that in spite of being “banned” in agriculture in 1970, DDT contaminated food products on an especially wide scale for some time. HCH contamination in food products was just as high, but it had yet to be banned. Extreme contamination, i.e. that exceeded MPL by more than five times, occurred in at least six samples of the same product (Table 3.16). In Table 3.16, shaded pesticides are those detected in products where they should have been absent, because: 1) they were banned (DDT, heptachlor); 2) their presence in all food products was banned (methyl parathion, 2,4-D, etc.); 3) they were not permitted to be present in particular food products (trichlorfon in meat and dairy products); and 4) they were not permitted to be used with particular crops. Unfortunately, practically the entire table is shaded, which shows that all regulations were violated. The reasons for mercury pesticide poisoning deserve especially close analysis. OMPs were detected not only in cereals where they could be found since they were used, but also in fish products. We must keep in mind that according to existing public health standards, in principle, granosan (active ingredient: ethyl mercury chloride), and especially OMPs (in the mixtures mercury benzol and mercury hexane, the active ingredient is also ethyl mercury chloride), presence in food products is banned [5]. Therefore, the notation “exceeds MPL” is not appropriate. It is characteristic to see pesticide contamination of a range of food products. Thus, in Moldavia, 62.5% of grape samples exceeded MPLs for OMPs. The insecticide dicofol was present in concentrations exceeding MPLs in 25% of mandarin orange samples from Georgia. In Uzbekistan, 22% of onion samples, and 36% of dairy products contained gamma-HCH that exceeded MPLs. In Kazakhstan, 19% of watermelon samples contained trichlorfon exceeding MPLs, and 28% of pork contained methyl parathion (residual quantities of this OPP in food products were not permitted [5]). About 30% of cabbage in Lithuania was contaminated with dimethoate. In the Ukraine in 1988, MPLs were exceeded by an extremely high amount for 28.6% of cabbage samples in the Dnepropetrovsk Oblast and 30% of samples in the Kiev Oblast; for 44.4% of cucumber samples in the Lvov Oblast; 41.1% of juice samples, fruit and berry products, and 46.7% of vegetable juice samples in the Dnepropetrovsk Oblast; and for 43.8% of freshwater fish samples in the Odessa Oblast. This list is far from exhaustive. It characterizes the situation as a whole not only in the former USSR, but also in today’s CIS. Children’s food and its contamination by pesticides deserve special examination. In 1987, more than 31% of the children’s canned food that was

82


Table 3.16. Specifics of extreme contamination by some pesticides of several food products in the USSR in 1988-89 [3] % of Samples

PRODUCTS

PESTICIDE

with Extreme

Total # of

Contamination

Samples

1988

1989

1988

1989

Field Crops Winter Wheat

Methyl parathion

3.06

359

Granosan

4.06

247

Flour, Grains Cereals

Mercury compounds

9.7

5.73

176

192

Flour

Lindane

5.7

23.26

212

215

Meat and Dairy Products Milk

Polychlorpinen

11.3

Toxafene 2,4-D

204 6.33

7.0

Chlorpyrifos

3.38

758 5351

32.0

35

Trichlorfon

1.06

1.41

22731

20517

Dichlorvos

4.13

1.08

1984

1849

7.31

198

Children’s Powdered Milk DDT

30.0

Cream

2,4-D

9.1

Trichlorfon

1.07

652

Sour Cream

2,4-D

5.8

173

Light Butter

DDT+DDE

17.0

Butter

2,4-D

16.5

176

Cheese, Feta

Mercury compounds

13.6

66

Eggs

Granosan

10.0

100

Poultry Sausage Subproducts

4439

20

52.38

106

219

21

2,4-D

5.7

Trichlorfon

0.77

1.70

1293

193 1176

2,4-D

7.9

7.59

127

158

Trichlorfon

0.78

0.70

1032

859

Heptachlor

11.5

61

2,4-D

8.1

348

Mercury compounds

7.0

630


83

Table 3.16. Continued. Fish Freshwater River Fish

Granosan

69.23

Mercury compounds

32.53

Freshwater Reservoir Fish Granosan

30.00

117 166

25.0

490 52

Mercury compounds

38.0

34.47

100

253

Freshwater Lake Fish

Mercury compounds

27.39

12.05

65

166

Saltwater Fish

Mercury compounds

17.57

13.25

74

83

Berries, Fruits Grapes

Methyl parathion

10.45

134

Watermelon

Dichlorvos

45.5

22

Cypermetrin

23.08

39

Raspberries

Methyl parathion

25.0

28

Currants

2.4-D

38.7

31

Bayleton

38.46

26

2,4-D

39.5

38

Methyl parathion

3.94

Phosmet

32.0

25

2,4-D

31.7

41

Phosmet

17.4

16.30

92

92

Dimethoate

14.6

19.68

1691

2205

Decametrin

6.3

1.49

553

1077

Methyl parathion

2.05

2.01

1465

1787

Vegetables Tomatoes Cucumbers Cabbage

Potato Onion

Garlic

2,4-D

533

6.21

539

145

Phosmet

4.76

2.35

336

553

Dimethoate

5.8

3.06

894

1143

2,4-D

19.6

51

Phosmet

21.8

32

Dimethoate

21.1

Phosmet

75.0

2,4-D Radish

1.67

Dimethoate Methyl parathion

10.53

76

114

8 53.85

13.1

13 92

6.25

112

84


studied was highly contaminated by gamma-HCH and, in 42.5% of cases, children’s dairy products contained pesticides exceeding MPLs. It is difficult to justify the fact that children’s food products were found to have such high levels of stable and “banned” OCPs such as DDT and polychlorpinen. It is quite simply incredible that vegetable juices for children contained OCPs such as endosulfan if, according to regulations, even residual quantities are not permitted in either tomatoes or cucumbers [5] (endosulfan was banned in 1984 for overall use in vegetable and fruit crops [8]). On the whole, 68.7% of 262 types of agricultural and food products that were studied in the USSR in 1988 were contaminated by pesticides in unacceptable quantities. The basic pesticide types led the list: OCPs such as DDT (38.8% of 250 types of products studied) and HCH 37.3% of 255 products), OPPs such as methyl parathion (26.5% of 170 products) and trichlorfon (28.4% of 236 products), 2,4-D (43.8% of 144 products), and OMPs (31.0% of 129 products). 3.10. Pesticide Transformation… in the Kitchen The growth regulator daminozide is used in apple orchards to increase the number of apples, to change the ripening period, and to increase the density of the apples’ flesh. Although daminozide itself has been known since 1965, there usually is no information on its effects, or else the reader is assured that “following a quarantine period of two months, there are no significant toxicological problems and the environment is not contaminated as a result of using this relatively unstable compound” [32]. In Russian handbooks [4, 41] it was noted that daminozide is made through the interaction of succinic anhydride and N,N-dimethylhydrazine without, of course, adding that the latter is toxic missile fuel. The authors of the handbook omitted that in apple juice, when thermally processed, the reverse process takes place: daminozide breaks down into malic acid and toxic missile fuel. The insecticide trichlorfon is well known. The list of insects that it is used to fight is a long one: the harmful shield bug (on grasses) and beet armyworms (on cotton), European corn borer and frit fly (on corn), nodular weevils, pea weevils, and pea codling moth (on legumes), linen coddling moth and gamma (moth) (on linen), Colorado beetle and potato stem borers (on potatoes), alfalfa stem borers and alfalfa moths (on perennial grasses), and beet webworm (on sunflowers). It is suggested that the insecticide acts in two ways: both directly, and also by forming another insecticide. In this process, trichlorfon (of medium toxicity) transforms through dehydrochlorination into a highly toxic contact insecticide (trichlorfon ⇒ dichlorvos). Dichlorvos is a much more effective cholinesterase suppressor (toxicity grows from 10-15 times, from FD50=440-900 mg/kg to FD50=23-87 mg/kg) [12, 31, 58]. Trichlorfon is also


85

extremely dangerous to humans when used to fight animal parasites, in particular the subcutaneous botfly. A special formulation has been created for this latter instance: a solution of trichlorfon in mineral oil and isopropyl alcohol [30]. The recommended methods are simple: spray the animals with the trichlorfon solution; wrap the cattle in burlap soaked in the pesticide solution; or simply introduce it into their feed. However, this treatment does have consequences, both for the parasites and for humans. Independently of how the animal (cow, sheep) was treated, an hour later trichlorfon is found in its blood, muscles, and internal organs. Thus, 7-8 days after treatment, trichlorfon is found in the animal’s milk. The more trichlorfon a cow receives during treatment, the longer it appears in her milk. An especially large amount of trichlorfon was found in milk after the cow was wrapped in burlap treated with trichlorfon [83]. When milk is thermally treated, trichlorfon always transforms into dichlorvos, and the milk inevitably becomes more toxic. Simply heating milk becomes dangerous. At the present time, the MPC for trichlorfon in food products has been lowered from 1 mg/kg to 0.05-0.2 mg/kg for all products except meat and dairy products, and forest berries, where it is completely banned [8]. We should note that trichlorfon has been literally poisoning our existence for more than 30 years. 3.11. Poisoning of the Country In 1959-60, it became clear in the USSR that humans may be chronically poisoned by the long-term effects of OPPs, even in small doses. Instances of demeton poisoning taking place with significant disruptions in the central and autonomic nervous systems were described back in 1959 [50]. Soon afterwards, a clinical picture was described for chronic human poisoning by such OPPs as parathion, demeton, methylmercaptophos, trichlorfon, and methyl parathion [47]. Symptoms were autonomic dystonia, functional disruptions in the cardiovascular system, liver, and the digestive tract [43, 49]. An especially large number of poisoning cases was observed during the production of various OPPs, with workers suffering severe effects. During production, MPCs were exceeded, as the author of the report – who has a tendency to self-censorship – affirms, by several times [47]. Starting in the second half of the 1960s, and only in Uzbekistan, just 12.8% of 2745 people working with OCPs and OPPs were considered effectively healthy, while 23.2% were diagnosed with chronic poisoning, 29.7% were found to have been suffering acute OCP and OPP contamination for a long period of time (since terminology was not precise, this group could have been merged with that suffering chronic poisoning), and 34.3% had specific indications of acute or long-term pesticide effects [A58].

86


The number of those suffering from chronic pesticide poisoning is not several thousand, as compared with those suffering acute poisoning, and not several hundred, as a dissertation written by a high level candidate avers [A78]. There are tens of millions of people suffering from chronic pesticide poisoning. In the former Soviet Union, more than two million people worked as machine operators in agriculture. A large number of these worked with chemicals as well. The average life expectancy for someone in this latter category in the former USSR was no longer than 56 years, i.e. 10 years less than the average for the country. After 10 years of work, machine operators who worked with pesticides suffered increased levels of arterial hypertonia, autonomic blood vessel dystonia, cerebral artereosclerosis, pathology of internal organs and the nervous system. The number of gynecological illnesses also increased sharply [3]. At the end of the 1980s, the USSR carried out wide-ranging research on the effects of pesticides on human health. The Government Resolution of April 2, 1984, “On Additional Measures to Increase Monitoring of the Use in the Economy of Pesticides and Plant Growth Regulators with the Goal of Not Allowing Harmful Effects to Public Health,” tasked Minzdrav with researching all facets of pesticide effects on health. In 1985-86, the effects of pesticides had been studied in nine republics (Russia, Ukraine, Uzbekistan, Azerbaijan, Moldavia, Kirgizstan, Tajikistan, Armenia, and Turkmenistan). Twenty-eight scientific research and medical institutes participated, and collected data on 275 rural regions, and ten experimental and control villages situated in identical conditions, differing only in the amount of pesticide use. Minzdrav put the research results together in 1987. A large amount of material covering tens of thousands of people in different regions of the USSR, as well as comparisons of experimental and control zones that differed many times in the amount of pesticides used, forced everyone to consider the research data objective and reliable enough to compare human health in territories with differing pesticide exposure levels [3]. This research not only confirmed earlier data on the danger of pesticides to human health, but also showed that the danger was even greater than earlier had been supposed. Human health was worse in regions with higher pesticide use in all cases when control and experimental zones were compared, as well as when zones with different average annual pesticide exposure were compared within one republic or oblast. The consequences of pesticide effects in different geographic regions were: 1) the development of anemia, active tuberculosis, viral hepatitis, and acute infections of the upper respiratory tract;


87

2) increased illness among newborns, and an increased frequency of stillbirths; 3) an increased number of psychological illnesses. Administrative regions differed from each other by factors of ten. In those cases when data were received on indicator dynamics over a five-year period, in those regions that used pesticides intensively between 1980-84, the number of incidents of still births, infant mortality, psychological problems, active tuberculosis, bronchial asthma, viral hepatitis, rheumatism, and diabetes all grew significantly. A more detailed comparison of human health in 10 specific villages in one region, with significant differences in pesticide exposure and identical values for other factors, showed that in those villages with a large amount of pesticide exposure (in the indicated number of incidents), the following illnesses all increased: In Children Respiratory Organs 7 Nervous System 5 Infectious Disease 4 More Children in Health Group III-IV 4 Parasitical Illnesses 3 Dermal and Epidermal Cellulite 3

In Adolescents and Adults Respiratory Organs Nervous System Infectious Disease

4 7 1

Cardiovascular System 4 Complications in Pregnancy and Birth 3 3 Dermal and Epidermal Cellulite 3 3 Sensory Organs 3 3 Urinogenital System 2 3 1 Overall Illness 1 1 1 1 1

Sensory Organs Digestive System Body Mass Deficit Metabolism Overall Illness Illness Among Newborns Infant Mortality Congenital Abnormalities Urinogenital System Decreased Number of Infants up to One Year Old with Normal Weight 1

The most significant difference in human health indicators between the experimental and control villages was in Uzbekistan (with 18 indicators), Armenia (13 indicators), Azerbaijan and rice growing regions of the Krasnodar Krai in Russia (11 indicators), and Moldavia (10 indicators). The lowest number of differences (with only 3-4 indicators) was detected in the Rovensk and Vinnitsk Oblasts of Ukraine. It is important to emphasize that the

88


differences in illness between the groups were seen even with comparatively small differences in pesticide use (0.77-3.93 kg/h in the Vinnitsk Oblast, 1.26.0 kg/h in the Rovensk Oblast, 0.88-6.4 kg/h in the Chuysk Valley of Kirgizstan, and 2.2-3.8 kg/h in the Cherkassk Oblast of Ukraine). This allows us to suppose that pesticides do not have a lower threshold of action [1]. The facts of pesticides’ negative effect on human health, especially in rural areas, show that there is no coincidence of, and no underestimating, some factors – the range of effects is too large. “Pesticide impact” has affected the health not only of agricultural workers using pesticides, but also the health of those who did not. General results are the following: during the period of very high pesticide use, one out of every ten people who worked with pesticides was seriously ill [1]. In the USSR in agriculture, mortality among workers from pesticide poisoning was 18-20 times higher in 1988-89 than in 1976-85 [3]. Overall, tens of millions of inhabitants of the Soviet Union suffered pesticide overexposure for many years and inevitably were acutely or chronically poisoned.

Chapter 4. PESTICIDES AND THE NATURAL ENVIRONMENT

89

CHAPTER 4 PESTICIDES AND THE NATURAL ENVIRONMENT Most problems linked to the environmental consequences of wide pesticide use are due to the fact that almost all pesticides are xenobiotic (from the Greek xenos – foreign, and bios – life), i.e. they are chemical substances that are foreign to the natural environment. Materials from the USSR confirm all the concerns about pesticides’ dangerous effects on the natural environment. 4.1. Bioaccumulation When pesticides and their transformation products enter the environment, they move along the food (trophic) chain. During this process, they may be stored in living organisms (bioaccumulation), increasing in concentration many times (up to hundreds of thousands or a million times). Even those pesticides and their transformation products that are not detected using modern methods of monitoring water, air or soil may become dangerous to living organisms because of accumulation. Because pesticides accumulate in living organisms, animals and fish may become harmful to human health. Different classes of pesticides accumulate in living organisms to different degrees. Hydrophobic pesticides, especially OCPs (organochlorine pesticides) and their metabolytes, concentrate in the fatty deposits of living organisms. The degree to which they accumulate is determined by the efficiency of two processes: absorption and excretion. Absorption predominates over excretion in stable pesticides and their metabolytes. In this case, the bioaccumulation coefficient (the ratio of the concentration of the pesticide or its metabolite in the body to its concentration in the environment or the previous link in the food chain) may be very large. We should look at Russian examples from the second half of the 1960s (Table 4.1). Even when considering contemporary Table 4.1. Average DDT concentrations (mkg/kg) in the ecosystems of the Angara and Ilima Rivers [61] Element

DDT

DDT+DDE

Water

12

Sludge

420

520

Water plants

1514

1854

Body cavity fat

2412

3715

Liver

2128

4189

Muscles

755

864

Fish

90


weak analytical techniques, these results give some idea of the concentrations of DDT and its metabolite DDE in the environmental chains of Siberian rivers. Another example is Lake Baikal, where the water is cleaner than other bodies of water. In this case, the bioaccumulation coefficient for DDT in the water ⇒ zooplankton ⇒ fish ⇒ seal chain exceeded one million (Table 4.2). Table 4.2. DDT Content in Baikal ecosystem links (data from 1989) [25] Pesticide concentration, mkg/l (kg)

DDT Bioaccumulation

DDT

∑DDT

Lindane

Surface

0.003

0.008

0.010

800 m depth

0.002

0.013

-

Plankton

6.0

14.8

5.0

x1850

Benthos

7.6

13.0

6.6

x1625

6.5

21.5

3.3

x2687

Element

Coefficient (in water)

Water:

Omul (fish): Muscles Brain

17.0

54.0

7.5

x6750

Seal, fat

4000

9200

60

x1150000

Table 4.3. DDT content in the environment and in living organisms (according to 1994 data) [84] DDT Content, mg/kg (mg/l) Element

Typical

Maximum levels

Atmosphere Air

0.000004

0.0000561

Hydrosphere Fresh water

0.00001

0.000109

Plankton

0.0003

5

Marine invertebrates

0.001

151

Salt-water fish

0.5

136

Predatory birds (fish-feeding)

10.0

194

Land Agricultural cropland soil

2.0

131

Invertebrates

4.0

40

Insect-feeding mammals

0.05

126

Grass- and insect-feeding birds

2.0

55.6


91

Table 4.3 gives an idea of the scale of DDT accumulated in different links of the food chain compared with natural environments. DDT is not the only pesticide that easily accumulates in biological organisms. HCH has similar properties. We can distinguish heptachlor from among other types of OCPs; it accumulates in slime and hydro-organisms (the accumulation coefficient may reach 1000 and higher), from where it enters other organisms. Thamnophis garter snakes died in North American territories contaminated with heptachlor; study showed that those Thamnophis sauritus that died had a heptachlor concentration in their tissues reaching 18.5 mg/kg, while those that survived had no more than 7.9 mg/kg [6]. Heptachlor accumulates in the milk of cows that have eaten feed contaminated by heptachlor [15]. A predator eating a victim that has accumulated pesticides in its tissues may die from secondary pesticide poisoning. For example, newts died when they ate tadpoles poisoned by OCPs. Frogs may die as a result of eating poisoned caterpillars [85]. Table 4.4 shows an example of the accumulation levels of different OCPs in inhabitants of the northern regions of the world, including Russia. The data in Table 4.4 show the result of global pesticide contamination. These pesticides were never used in the Arctic; nevertheless, they were found in humans. It is notable that pesticide concentrations in human blood were several times higher (and in the case of beta-HCH, 17 times higher) in Russia than in Sweden and Norway. The official ban on DDT in the USSR (in 1970) had practically no effect on the amount found in women’s bodies. The content of DDT and its derivatives in the Ukraine from 1965-81 changed very little, and was on average 3120 mkg/kg (from 520 to 14160 mkg/kg). The average content of all HCH isomers was 780 mkg/kg (from 30 to 2140 mkg/kg) [A106]. Table 4.5 gives an idea of Table 4.4. OCP content in blood plasma of inhabitants of several northern regions (according to 1997 data) [86] OCP concentration in blood plasma, mkg/l Country

DDT

Chlordan

HCB

Beta-HCH

Swedish North

0.9

0.1

0.2

0.1

Norwegian North

0.7

0.1

0.2

0.1

Nikel

3.4

0.1

0.5

-

Salekhard

0.7

0.5

0.4

-

Norilsk

0.9

0.5

0.4

1.7

Russian North

92


Table 4.5. OCP concentration in breast-feeding mothers in Kiev from 1981-83 [106] OCP (metabolite)

OCP concentrations Breast milk, mkg/l

Fatty tissues, mkg/kg

Blood, mkg/l

7

743

62

DDD

0.2

31

8

DDE

22

2079

32

ΣDDT

33

3125

127

Alpha-HCH

0.4

16

2

Gamma-HCH

0.3

32

8

Beta-HCH

7

727

10

ΣHCH

8

781

25

Ï ,ï ’-DDT

how much pesticides contaminated humans at the end of the period when OCPs were used most enthusiastically. The situation was analogous in Uzbekistan. When examining Tashkent inhabitants in the 1980s, the total concentrations of “banned” DDT and permitted lindane in children’s blood were close (0.60-49.57 and 0.53-50.70 mkg/l, respectively) [A 106]. However, OCPs were not alone; bioaccumulation characterizes pesticides of several other classes. As a result of pesticide bioaccumulation, not only high, but low, levels of contamination are dangerous for living organisms, even if the contamination is close to background level. The full scale of the danger faced by all living things from pesticide bioaccumulation is not yet known. 4.2. The Destruction of Plants Not Targeted by Pesticides All herbicides not only destroy “weeds,” but also other, non-targeted, plants. It is either an error or a lie for herbicide developers to state that their product is selective (i.e. it supposedly acts only on targeted species). The mechanisms by which herbicides act are the same for all plants [87]. Photosynthesis inhibitors penetrate the chloroplast and prevent the plant from capturing electrons using ferredoxin, in this way disrupting the process of restoring NADP – a coenzyme of nicotine amide dinucleotide phosphate in photosystem I (examples include dipyridyl salts – paraquat, diquat, etc.); or else the inhibitors prevent the transfer of electrons to the plastoquinone in photosystem II (aryl carbamides, sym-triazines 1,2,4-triazinones, uracils, hydroxybenzonitriles, and pyridazinones). Disruptors of plant respiratory functions dissociate the chain of oxidizing phosphorylation and depress the formation of ATP (nitrophenols, halogen phenols). Cellular division inhibitors, when introduced into the soil, suppress the growth of seeds and roots (N-


93

aryl carbamides, dinitroanilines). Plant growth regulators model their action on natural auxins, i.e. plant growth hormones, for example on heteroauxin (examples include derivatives of arilhydroxycarboxylics, hydroxycarboxylics, and picolinic acids). Herbicides of other groups may suppress the synthesis of vitally important substances (nucleic acids, proteins, lipids), as well as biosynthesis and the transportation of natural catalysts for these processes. It is impossible to differentiate a useful plant from a “weed:” no plant is protected from the effects of herbicides. 4.3. The Destruction of Animals Not Targeted by Pesticides Background pesticide contamination of the natural environment affects most animal species, mainly influencing their behavior and physiology [1]. For example, white rats’ natural resistance to plague is weakened by even the smallest dose of warfarin (0.075 mg per individual over 24 days). There are many such examples [88]. Table 4.6 gives an idea of how dangerous pesticides are to fauna. The table shows data on several highly toxic pesticides used to limit the numbers of completely different targeted species (the shaded pesticides are those that the Soviet (Russian) Health and Epidemiological Service was obliged to ban after long use, i.e. after they had poisoned the natural environment and humans for a lengthy period of time). The groups of animals most affected by pesticides are (in ascending order by degree of damage): invertebrates, fish, birds, mammals, and finally, microorganisms [1]. Different groups of animals, and different species within those groups, display differing sensitivity. Sensitivity may even differ depending on the species’ stage of development. Today’s level of knowledge is not sufficient to allow us to determine a given pesticide’s effect on a representative of different groups of fauna based only on data received in controlled experiments, even for several species of laboratory animals. Thus it is significant that for such sym-triazine herbicides as simazine, atrazine, etc., the health and hygiene MPC (toxicity to warm-blooded animals, including humans) and phytotoxic MPC (toxicity to plants) differ by more than an order of magnitude: 0.2-0.5 mg/kg for warm-blooded animals, and 0.01 mg/ kg for plants [89]. Warm-blooded animals and arthropods have a difference in sensitivity to many pyretroids that can reach tens of thousands of times [90]. It is now practically impossible to find a pesticide that does not affect at least one system in living organisms, be they genetic, immune, endocrine, reproductive, or nervous systems. Moreover, all risk assessments of pesticide effects on living organisms made until now all concentrate on their carcinogenic and mutagenic effects. This is analogous to the fact that when we increase the number of test subjects, all pesticides without exception show a mutagenic

94


Table 4.6. Pesticide Toxicity in Animals [85] FD50, mg/kg Mammals

FC50, mg/l Birds

Fish

Fallow Deer, Pesticides

Mice, Rats,

Domestic

Mallard

Rabbits

Goat

Duck

Trout, Pheasant

Guppies

Insecticides Lindane

150-230

Endosulfan

40-100

Toxafene

50-70

139

70

40

0.1

Carbaryl

310-850

300

2180

2000

1.75

5

6

0.4

4.2

0.28

Carbofuran

200

200

0.02

33

0.01

Diazinon

76-130

3.5

4.3

8.0

Methyl Parathion

100-180

10.0

8.2

3.0

Dimethoate

100-230

Fenitrothion

470-516

56.0

8.6

5000

0.25

200

42.0

727 Fungicides

Benomyl

10000

Captan

12000

5000

Folpet

1500

2000

Zineb

1850

2000

2000

40.0

Herbicides 2,4-D (Na salt)

1200

5000

5000

1160

Dalapon

9250

5000

5000

340

Simazine

4100

5000

5000

100

Monuron

3700

5000

5000

10

Diquat

227

5000

3750

91

effect; therefore, if we expand the scope of study, there will be no pesticide that does not affect some organ or organ system. Pesticides, and especially OCPs (DDT and its metabolytes, HCH isomers, aldrine, dieldrin, heptachlor, etc.), are seen everywhere in mammals. Table 4.7 gives data on the death of higher vertebrates from causes linked to agricultural production in the USSR. About 40% of the accidental deaths of animals, and about 80% of birds, are due to pesticides. It is difficult to evaluate how many mammals in the environment die from pesticide contamination, since sick and weakened individuals fall prey to predators [6].


95

Table 4.7. Causes of accidental death among mammals and birds in the European part of the USSR in the 1980s (in %) [3] Upland Fowl, Ducks, Cause

Moose, hare, boar

Geese, Bustards

41

13.7

39.1

77.1

Herbicides

22.4

19.2

Other pesticides

16.7

57.9

19.9

9.2

Poisoned by fertilizer and seeds treated to resist disease Poisoned by pesticides, including:

Vehicles

The negative role of pesticides in mammal life became clear several decades ago. OCP concentrations in the subcutaneous fat of seals (Pusa baltica) from the Baltic Sea reached 300 mg/kg. Marine mammals living in the median latitudes of the northern hemisphere are more contaminated by DDT than animals of the southern hemisphere because of industrial development [6]. Even after a single treatment of different ecosystems with carbaryl, this insecticide became a permanent component in the habitats and feed of wild animals not its targets for at least one or two years [91]. The targeted use of pesticides against mammals is no less dangerous. To this day, up to 1 kg of DDT is introduced into marmots’ (Marmota bobac) burrows in plague prevention in Russia and Kazakhstan and in field disinfestations. As a result of this practice, DDT accumulated and increased its presence many times in the skin and fat of young marmots for many years. DDT is then widely spread through both the food chain, through predator feeding on marmots, and through the soil, through the marmots’ natural death and decomposition [3]. Mammals may die from pesticide poisoning not immediately, but many months later, when they more actively use their fat deposits, for example, when waking up after hibernating; they are then poisoned by “deposits” of toxic substances in their fat [3,6]. Stable lipotropic OCPs and their metabolytes present a danger to mammals not only through acute exposure, but also through chronic exposure to small doses. In recent years, intensive study of the effect of small doses of contaminants [92] shows that small, and super small, doses (i.e. doses that are thousands, and tens of thousands, of times smaller than those causing acute effects) of biologically active substances affect living organisms in a “delayed” way, over a protracted amount of time. The disappearance of songbirds described by Rachel Carson became noticeable in the 1970s in the USSR, when the number of larks, starlings, and

96


other songbirds sharply decreased (in places to extinction) in the European part of Russia. That this is linked to the “pesticidization” of agriculture is shown by the fact that the birds disappeared first of all in areas where pesticides were used intensely [1]. We know of many cases where treating fields or seeds with OCPs, OPPs, and OMPs (in particular with parathion, dieldrin, endosulfan, aldrine, endrin, heptachlor, etc.) led to the death of grain-feeding birds, as well as birds that feed on insects that, in their turn, had pesticides in their systems [32]. When the number of insects falls sharply, birds may simply die from hunger. Many pesticides, such as malathion, fenitrothion, HCH, etc., cause shifts in blood indicators, change the proteins in blood plasma, and lower cholinesterase activity in birds and mammals [3]. OPPs change birds’ behavior, change their hormone levels and resistance to cold, and affect excretion of minerals, growth, and embryonic development. When the eggs of the Zeravshansk subspecies of pheasant were incubated in the natural conditions of Uzbekistan, where pesticides and defoliants were widely used, 25% of baby birds hatched with congenital defects: deformation of their extremities, malformed bills, and other changes [74]. OCPs and their metabolites have an especially negative effect on birds. By the beginning of 1980, DDT, DDE, HCH, oxychlordan, heptachlor epoxide, heptachlor, dieldrin, etc. started to be observed in the bodies and eggs of birds living in many regions of the world [6]. At least three reasons for problems with bird reproductive success were governed by OCPs: 1) eggshells became thinner, which led to eggs breaking and embryos dying; 2) bird behavior was changed, which led to both eggs and baby birds dying; and 3) embryos and baby birds died during development because of the metabolization of nutrients poisoned by OCPs [93]. Just like mammals, birds have a “delayed reaction” to lipotrophic pesticides such as OCPs and their metabolites. These toxic substances dissolve and accumulate in the fatty tissues of well-fed birds, and are comparably harmless in this form. However, once the bird starts using the stored fat (at the end of a long flight or when laying eggs), the substances are carried through the bloodstream to the brain, liver, or yolk of the egg, and poison all the systems [1]. In particular, well-fed raptors have lower DDE concentrations in their liver (0.5 mg/kg) than less well-fed (3.5 mg/kg) and emaciated birds (7.3 mg/kg) [6]. Numerous data exist on the indirect effect of pesticides on birds. When the number of insects and all invertebrates decreases due to insecticide use, the number of birds falls in regions of active planting and gardening [32]. The destruction of “weeds” using herbicides leads to serious consequences for birds [32]: a decrease in the number of birds feeding on these plants and their seeds or fruit, as well as of birds feeding on caterpillars (cuckoos, orioles, nightingales, and warblers) feeding on the “weeds.”


97

The deliberate poisoning of “harmful” birds leads to unexpected consequences. In three districts of the former GDR in 1964-65, corn was sprayed with methyl parathion and grain with zinc phosphide to fight rooks. As was expected, a large number of birds died, but rooks made up only 3% of the total [32]. In this way, and decades after the first notice was given, pesticides remain an important reason for the mass death of birds in the wild, in spite of all the systems for their “safe” use. Pesticides are the second factor (after industrial pollution) in fish population decrease in many countries of the world [3]. For example, in Tajikistan in 1980, more than 10% of local fish species were threatened by extinction as a result of poisoned bodies of water [3]. In the Nizhegorodsk oblast, 21 of 57 fish species disappeared by 1980, mainly due to the effects of agricultural run-off. On average, about 30% of the cases of fish death in freshwater reservoirs in the central belt of Russia are due to pesticide contamination of those bodies of water [1]. Table 4.8 summarizes data on how acutely toxic several pesticides are to fish (the FC50 is the concentration in water that is fatal to half of the population of a given fish species). It can be seen that OCPs are more toxic to hydro-organisms than OPPs [85]. The shaded pesticides are those that our Health and Epidemiological Service was forced to ban after many years of use. Table 4.8 shows that the FC50 concentration can be different even for the same fish species, and varies significantly within a species — from several to Table 4.8. Acute toxicity to fish of some pesticides dissolved in water (FC50, mkg/l) [30] Pesticide

Fresh-water ecosystems

Marine ecosystems

Organochlorine Pesticides DDT

5-16

0.4-2

Methoxychlor

30-75

55

Pentachlorphenol

52-110

-

Lindane

27-87

30

Toxafene

11-18

0.01-5.5

Aldrine

5.2-8.2

2.8

Dieldrin

1.4-2.8

5.5-7.1

Endrin

0.4-8.6

0.6-2.6

Chlordan

7.8-40

5.5

Heptachlor

8-19

3.3-25

Endosulfan

12

0.6

98


Table 4.8. Continued. Mixed Organochlorine and -phosphorus Pesticides Dichlorvos

480

550

Chlorpyrifos

3.3

70

Trichlorfon

260-1400

1000

14

150

240-320

320

Methyl Chlorpyrifos Trichloronate

Organophosphorus Pesticides Demeton

81

550

Disulfoton

50

740

Parathion

470-2000

65

14-52

5.5

2700-5700

1000

Ethion

230

69

Diazinon

2-90

250

Azinfos-Methyl Methyl Parathion

Fenitrothion

700

1000

Naled

80-330

550

Malathion

103-170

570

Carbamates Aminocarb

-

1000

Carbofuran

280

-

Methiocarb

110-640

550

Propoxur

8200

1000

Carbaryl

4340-11200

1750

several dozen times (in the case of endrin). We should look at just the first line of this table: the influence of OCPs. OCPs strongly affect water plants through cellular biochemical processes (photosynthesis, the formation of nucleic acids, and the biosynthesis of proteins and lipids), changing plant growth and productivity. Crustaceans are especially sensitive to OCPs and other pesticides, because of their filtering activity, the high penetrability of their shells, and the design of their respiratory organs. Lower crustaceans and water insect nymphs are more sensitive to OCPs than fish, dying from water contamination at the ng/l level. The fish most sensitive to DDT are in the salmon family, such as trout [6]. When researching DDT content in the biota of Lake Sevan (Table 4.9) and the


99

Chardarinsk Reservoir (Table 4.10) in the middle of the 1980s, DDT and its metabolytes DDD and DDE were observed in large quantities in fish [603]. In water, the concentration of DDT is usually higher than that of its metabolytes; in phytoplankton the ratio is close to that observed in water; in zooplankton, there is more DDT present than its metabolytes. In fish, the ratio usually changes in favor of the metabolytes: in organs and tissues, DDD, and especially DDE, concentrations are at the same level, if not higher, than that of DDT (Table 4.10). OCPs paralyze the nerves of fish, which leads to disruptions in coordination and in the feeding reflex; this in turn causes the fish to become emaciated. OCPs also disrupt the metabolizing of carbohydrates, proteins and lipids, and affect the reproductive cycle. All of these factors lead to many fish species weakening and dying out [6]. We have never seriously evaluated how dangerous pesticide contamination in bodies of water is for hydro-organisms. Modern knowledge has led us to draw a very important conclusion: background environmental concentrations of several pesticides have almost risen to a level that seriously affects several species’ viability. It seems that we are on the edge of a veritable pesticide catastrophe for hydro-organisms. Practically all OCPs are toxic for a wide group of invertebrates, especially insects. However, invertebrates differ significantly in their sensitivity to pesticides. After appearing in the agricultural ecosystem, DDT content increased over the first eight days by 5-40 times in different groups of insects (orthopterous, homopterous, and beetles), notwithstanding the insect diet. Carnivorous insects, for example ladybirds, had higher levels of contamination than plant-feeding (phytophagous) cicadas and grasshoppers. Predatory spiders had 200-400 times more DDT in their bodies than plant-feeding insects [6]. Table 4.9. Average DDT+DDE content in fish from lake Sevan (Armenia) in 1984, in mg/kg of raw mass [94] Tissues

Whitefish

Carp

Muscles

0.124

0.102

Skin

0.290

0.769

Gills

0.398

0.388

Brain

1.677

0.328

Sexual Organs

2.211

0.138

Liver

4.099

No Data

Body cavity fat

7.884

7.013

MPL for fish - “none” (temporary - 0.2)

100


Table 4.10. DDT concentration in fish from the Chardarinsk Reservoir (Kazakhstan) in 1985, in mg/kg of raw mass [94] Tissues

n,n’-DDT

n,n’-DDD

o,n’-DDT

n,n’-DDE

ΣDDT

Carp (Ciprinus carpio) Gills

0.038

0.122

0.015

0.212

0.388

Skin

0.047

0.287

0.021

0.412

0.769

Brains

0.043

0.135

0.018

0.133

0.328

Body cavity fat

1.156

1.697

0.738

3.422

7.013

Amur Chub (Pseudaspius leptocephalus) Gills

0.141

0.334

0.144

0.793

1.413

Skin

0.107

0.445

0.096

0.994

1.642

Brains

0.026

0.085

0.008

0.229

0.348

Body cavity fat

0.157

0.747

0.103

1.809

2.817

Pike-Perch (Lucioperea lucioperea) Gills

0.448

0.266

0.187

1.563

2.692

Skin

0.211

0.249

0.087

0.821

1.534

Using more chemicals, irrigation, and mechanization in agriculture gave rise to the dangerous illusion that soil biota plays a decreasing role in maintaining soil productivity. In fact, when decreasing the number of soil organisms, humans are irreversibly decreasing natural soil productivity. In the floodplains of the Nechernozem even recently, you could find up to 300 earthworms per square meter. Annually, up to 100 t/ha of soil passed through these worms. Now, the number of worms has decreased by a factor of 100 because of the effects of chemicals [3]. As a result of the long-term use of herbicides, the soil’s natural capacity for recovery is decreasing irreversibly. Today, many hundreds of soil organism species are decreasing in number and changing their composition because of pesticides. Cases are known where, due to long-term pesticide and fertilizer use, microorganisms that are highly toxic to cultivated plants have taken over, and soil became poisonous to crops [3]. For example, it became impossible to grow crops on 3,000 ha because of immoderate herbicide use in Moldavia [11]. Overall, insecticides seriously affect invertebrates in the soil, especially insects, but affect microorganisms much less [3,6]. The most toxic OCPs for soil invertebrates are heptachlor and chlordan. They sharply decrease the numbers of almost all invertebrate groups, including insects, earthworms, and ticks [6].


101

By sharply decreasing biodiversity in the soil ecosystem, pesticides negatively affect all soil organisms on which soil productivity depends. Pesticides affect the biological activity in soil, especially through long-term use and accumulation (or accumulation of their residues). *** All groups of animals suffer from pesticide use. Although the groups targeted by pesticide use are usually invertebrates, these are not the only ones to have suffered from chemical use in agriculture; all groups of vertebrates and, though less attention is paid to them, microorganisms, also suffer. Pesticides are one of the main factors threatening biodiversity on the planet. In the near future, pesticide effects on animals will not lessen, but grow; background concentrations of some pesticides have almost reached levels that seriously affect life processes. 4.4. Pesticides as Destroyers of the Normal Life Processes of Organisms Pesticide developers have declared that their “brainchildren” must “not cause any remote consequences when entering the human and animal food chain, or serious environmental consequences for different species of useful living organisms” [95]. In the light of present data this seems utopian, especially if we consider not only pesticide effects that take place immediately, but also consequences that take place later in time. For many years, the downstream effects of pesticides did not attract the necessary attention. These include not only carcinogenic and mutagenic effects on living organisms, but also the many different effects of pesticides on progeny, on different organs and systems of the body, on pathological processes, etc. [9]. 4.4.1. Pesticides as Mutagens and Carcinogens With careful checking, all pesticides show a mutagenic effect (causing inherited changes) on the natural environment, including on humans. Using only one test system, mutagenic activities are seen in only 40-50% of pesticides studied; however, when using five different test systems, more than 90% of the pesticides studied are observed to have mutagenic activity [96, 97] (Table 4.11). This example illustrates the difficulty of showing pesticides’ mutagenic activity. For example, mutagenic activity was clearly expressed not in the sym-triazine herbicides atrazine and cyanazine, but in their transformation products formed in corn husks! Naturally, no standard test system can cover the practically unlimited number of cases when a given pesticide may prove to be mutagenic. Pesticides are among the most mutagenic substances introduced by humans into the environment [75]. Mutagenic activities are inherent to an

102


Table 4.11. Pesticide mutagenic effects observed using different numbers of test systems [96,97] Number of Test

Number of

Mutagens

Systems Used

Pesticides Studied

Observed, %

1

208

42.8

2

77

76.6

3

44

93.2

4

31

93.5

5

19

94.6

6

13

92.3

7

15

100.0

approximately equal degree in all classes of pesticides (distributed by toxicity). This conclusion is illustrated clearly in Table 4.12. Pesticide mutagenic activities are usually ascertained much later than the inception of active use in agriculture and forestry [3]. This is because pesticideproducing companies are not interested in detecting mutagenic affects in their products, and do not conduct the long, expensive, comprehensive research needed to do so. In the best case, they comply with the prescribed health test standards for mutagenic activities in new pesticides – which normally use only three test systems (as is done, for example, in the USA). We should emphasize once more – every pesticide, when studied using a number of test systems, displays mutagenic activity. All pesticides are dangerous mutagens for the natural environment. The carcinogenic activity of chemical substances is important as well. They are present in pesticides of different classes: OCPs (DDT, aldrine, heptachlor, methoxychlor), thiocarbamates (thiram, zineb, ziram), carbamides (monuron) [3], etc. Even if the official description of a given pesticide does not denote its carcinogenic (mutagenic, teratogenic, embryotoxic, etc.) activity, this merely means that this particular pesticide was not studied sufficiently. Table 4.12. Percentage of observed pesticide-mutagens among pesticides of different toxicity classes [97] Pesticide Classes

# Pesticides Studied

% Mutagens Observed

Extreme Toxicity

37

73

High Toxicity

32

75

Medium Toxicity

66

63

Low Toxicity

165

61


103

4.4.2. Effects on Reproduction Among the most serious consequences of introducing pesticides into the environment are their effects on the reproductive system of living organisms. These have several effects: gonadotoxic, embryotoxic, and teratogenic. Science did not discover this immediately. For example, when using the OCP dicofol in experiments on mice, deformities were seen not in the first or second generations, but only in the third [6]. Introducing the OPP parathion into the feed of laboratory rats led to a mortality rate of up to 81%, but only in the third generation. It is clear that conclusions on the effect a given pesticide has on the reproductive function of humans can be drawn only 40-50 years later [98]. Gonadotoxicity is one of pesticides’ serious side effects. This means the ability of extraneous chemicals to cause not only morphological, but also functional, damage to gonads and reproductive cells. As a result, the ability to have progeny is lessened or disappears altogether, which may be due to many causes: damage to spermatogenesis, the death of the majority of spermatozoids, damage to the estrous (menstrual) cycle and to embryogenesis, and the death of the majority of embryos at different stages of development [39]. Gonadotoxicity is characteristic for a large number of pesticides (Table 4.13). Several pesticides are embryotoxic; i.e., they pathologically affect the developing fetus. For example, it was established in long-term experiments on animals that polychlorpinen, phosalone and trichlorfon are embryotoxic to mammals, leading to stillbirths [A103]. Besides being embryotoxic, many pesticides are teratogenic, which is why progeny are born with various deformities. Assumed (i.e., not inherited) developmental defects appear, caused by the harmful effects of pesticides; these defects may begin with damaging exchanges, and finish with necrosis of tissues that help form a given organ in the embryo. This effect alone confirms the possibility that toxic substances penetrate the placental barrier from mother to embryo. Substances that act selectively on the embryo, in doses not toxic to the mother, are the most dangerous [9, 39]. There are many known examples, and they are unexpected. Pesticides accumulate in fetal cells and reproductive organs in mammals, birds, and fish due to biochemical processes. This is noted especially often for OCPs, which were observed in large amounts (up to 6.8 mg/kg) in, for example, the sexual organs of hares, rabbits, pheasants, green-winged teals, and in white-eyed and red-headed ducks. They were found in animal embryos, as well as in black thrush eggs and in pheasant embryos and amniotic fluid (up to 73.0 mg/kg) [3]. The carbamate carbaryl, migrates through elements of the natural ecosystem and penetrates living organisms; it is distributed through many

104


Table 4.13. Downstream consequences of some pesticides (data from 1988) [75]; (shaded pesticides were banned after many years of use) Pesticide

Type of Biological Activity

Name

Type

1

2

3

4

Ziram

Fungicide

+

++

+

+++

Carbaryl

Insecticide

+

++

++

++

Thiram

Protectant

++

++

+

+

Maneb

Fungicide

++

+

++

+

Ferbam

Fungicide

+

+

+

+

Zineb

Fungicide

+

+

+

++

Methylmercaptophos

Insecticide

+

+

+

Dinitro-o-cresol

Herbicide

+

+

+

HCH

Insecticide

+

+

+-

Lindane

Insecticide

+

+

Molinat

Herbicide

++

++

Thidazuron

Herbicide

+

+

Granosan

Protectant

+

+

Milbex

Insecticide

+

+

DDT

Insecticide

++

+

+

Atrazine

Herbicide

+

+

+

Simazin

Herbicide

+

+

+

-

+

Trichlorfon

Insecticide

+

+

+

2,4,5-”

Herbicide

+-

+

++

Chloridazon

Herbicide

+

+

Malathion

Insecticide

+

+

Methiram

Fungicide

+-

+-

2,4-D (dichlorophenoxyacetic

Herbicide

++

++

2,4-D-butyl

Herbicide

+

+

Polychlorpinen

Insecticide

+

+

Diazinon

Insecticide

acid amino salt)

+

Fenchlorophos

Insecticide

+

Daminozide

Regulator

+

Propanile

Herbicide

+

Fluometuron

Herbicide

+

Chlordekon

Insecticide

+

Nemagon

Nematocide

+

+


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Table 4.13. Continued. Chlormequat

Herbicide

+

Carbendazim

Fungicide

-

Prometrin

Herbicide

+

Diquat

Herbicide

+

Fenthion

Insecticide

+

DEF

Defoliant

+

Parathion

Insecticide

+

Leptophos

Insecticide

+

Phosmet

Insecticide

+

Trifluraline

Herbicide

+

Butocarboxim

Insecticide

+

Diuron

Herbicide

+

Polymarzin

Fungicide

+

Mankozeb

Fungicide

Folpet

Fungicide

-

+

+ +

Methoxychlor

Insecticide

-

+

EPTC

Herbicide

-

+-

Methylmetiram

Fungicide

+

Paraquat

Herbicide

+

Heptachlor

Insecticide

+

Metoalachlor

Herbicide

+

Mirex

Insecticide

+

Aldrine

Insecticide

+

Dimethoate

Insecticide

-

+

Chlordan

Insecticide

+

Barban

Herbicide

+

Zectran

Insecticide

+

Diallat

Herbicide

+

Triallat

Herbicide

+

Rotenone

Insecticide

+

Nitrophene

Herbicide

Quintozen

Fungicide

Fenuron

Herbicide

+

Endrin

Insecticide

+-

Legend:1 - gonadotoxic, 2 - embryotoxic, 3 - teratogenic, 4 - carcinogenic.

+ -

-

-

+

106


animal organs and tissues: the liver, muscles, kidneys, spleen, womb, ovaries and testicles. Carbaryl concentrates in mammals’ reproductive organs in large amounts (it was found in 97% of animals studied in the treated territories). Carbaryl lowers the reproduction frequency of wild mammals that constantly inhabit contaminated territories [91]. In experiments on five generations of white rats, carbaryl was found to affect reproductive functions. In doses of 2 mg/kg it was not detected in the parent or first generation; negative effects were observed only in succeeding generations [99] (with the establishment of health standards [A18] this phenomenon was not noted). A correlation between the dose of carbaryl and its effects on gonads was shown [A31]. In a long-term experiment, the threshhold gonadotoxic dose was 1 mg/kg: changes in animals’ estrous cycle and a decrease in fertility were noted six months after carbaryl was introduced daily. Residues of the herbicides benthiocarb and propanile, as well as OCPs, were observed in fish feeding of different things: in predatory pike and perch, in tench feeding on mollusks and small invertebrates, and in rudds feeding on seaweed. Moreover, benthiocarb was present in fish gonads a year after it had been used. Only one percent of the spawn of several plant-eating fish from many Central Asian bodies of water contaminated by pesticides developed normally [1,3]. The derivatives of sym-triazine (prometrin, semeron etc.) affect spermatogenesis in rats. For example, simazin in doses of 62.8 mg/kg lowers the relative level of normal spermatogonia in mammals, and increases the number of spermatic tubules with damage to the epithelius of the fetus [9]. Fungicides from the dithiocarbamate group (zineb, maneb, thiram) affect the function of mammals’ gonads as well [A40]. Thiram, the seed protectant from the dithiocarbamate group, and the insecticide HCH both damage spermatogenesis in mice and rats [75]. A significant decrease in mammal fertility was detected due to granosan and other OMPs, widely used to treat seeds as a fungicide. Data showed how gonadotoxic granosan is [A31]. Chronic poisoning (a dose of 0.2 mg/kg) caused structural changes in animals’ ovaries and testicles, damage to the follicles and death of egg cells, death of spermatogenic epithelia, and other damage to spermatogenesis [A31]. The threshhold of granosan’s gonadotoxicity turned out to be 5-10 times lower than the general toxicity level [5]. Other pesticides are also gonadotoxic, including: the plant growth regulator daminozide, the retardant chlormequat, the herbicide fluometuron, the mixture of the contact acaricide milbex, the defoliant thidazuron, etc. [71]. Although the gonadotoxic effect has not yet been found in all pesticides, judging by their influence on the reproduction of different animal


107

groups, there is still every chance that pesticides that have not been studied for this effect will also show it. The ability of many pesticides to penetrate the placental barrier is a very important and dangerous characteristic. This phenomenon has already been proved for insecticides from the OCP group, such as DDT and its metabolytes [A37], and HCH [A108]. It is known also for granosan, a seed protectant from the OMP group [A25]. The fungicides captan and folpet penetrate the placental barrier with ease [52]. In so doing, diquat is embryotoxic (resulting in stillbirths and a decrease in the number of progeny) [A103]. The insecticide carbaryl also penetrates mammal embryos [91]. Phosmet (from the OPP group) and its metabolytes also pass through the placental barrier [A82]. Generalizing the data we have already, we can confirm that all pesticides negatively affect the reproduction of at least some animals. 4.4.3. The Destruction of the Endocrine System Life on Earth continues because, whatever changes happen around us, the male sperm finds the female egg. From the birth of the first ovum to the formation of a new organism, reproduction is governed by the endocrine system, the “chemical post office,” the mechanism for passing information between cells in different parts of the body. In mammals, the starting point is the pancreas, where sexual hormones are created. These hormones carry command signals, and control the birth and early development of a new life. The main actors are the female hormone estrogen and the male hormone testosterone. When one of these encounters its receptor, each of the sexual hormone molecules gives commands to “its” part of the biological system, i.e. what to do and when to do it. Estrogen initiates some processes, testosterone others. In other words, fundamental changes in the body such as the birth of a new life take place only in those cases when the chemical command is received. For many years it was considered impossible to falsify commands and influence this process from the outside, since these hormones and receptors, which are complex in their chemical structure and form, fit each other like a key in a lock. This mechanism guaranteed that there would be no possible interference in creating a new life by any of the thousands of chemical substances found in living organisms and in the environment. In 1992, a group of Danish authors systematized the data from 61 scientific papers describing the sperm count in healthy males from 21 countries of North America, Europe, South America, Asia, Africa and Australia, starting with 1938 and moving forward [100]. On average the number of spermatozoids decreased by 50%. Subsequent research confirmed these conclusions [101]. Moreover, it turned out that with the passage of years, two effects became increasingly evident: the

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number of spermatozoids decreased, and the number of spermatozoid abnormalities grew. The “negative effect on male fertility” covered two generations and could not be due to genetics. It was linked with serious changes in the environment [100], i.e. with foreign chemical molecules affecting natural male reproductive processes. Several “picklock” molecules are already known that imitate the activity of the female hormone estrogen, interfere with relations that arise when male and female sexual cells meet, and change the interrelation between the sexes that are regulated by hormones in the newly created organism, as well as interfering with the full development of these organisms before their birth. In the light of this discovery, the various reproductive pathologies, which are increasingly described in every country, have become explicable. These “picklock” molecules are chemical substances that humans released into the biosphere. Pesticides, the organohalogen dioxin substances (formed when using pesticides from organohalogen production and other technologies), and substances resembling dioxins of the polychlorbiphenyl (PCB) class are the substances that most harm the endocrine system [101, 102]. Among the pesticides that are suspected as part of this list are DDT, DDT’s metabolites such as DDE, as well as its structural relatives, in particular the “harmless” dicofol and methoxychlor. “Picklock molecules” also include all HCH isomers including lindane, HCB, and chlordekon [103108]. This list may lead to the idea that we are talking mostly about OCPs. In fact, the list of substances that damage the endocrine system include those “not dangerous to humans,” such as synthetic pyretroids [3], simtriazine herbicides, and many others [101, 102, 107]. Thus, this is a global phenomenon of fundamental importance for life on Earth: many pesticides and/or their transformation products may substitute their activity for the hormonal system. Many earlier known examples of pesticide activity take on a dire new side in light of these views. Let us provide some illustrations: Russian examples include the population of lake frogs in the Northern Caucasus and the Lower Volga Region. Pesticides accumulated in their systems, leading to asynchronous development of gonads in both the males and females. This meant that successful reproduction was impossible among some of the frogs, and the population growth rates changed. Of course, it is not so important that the population of a specific species decreases; this is an example of how unexpected pesticides’ effects can be, and how close danger comes to many animal species [1]. Practically all species suffer from the unbidden action of pesticide molecules. The data received now allow us to list the first group of chemicals that damage the endocrine system of living organisms (table 4.14).


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Table 4.14. Pesticides that have already been found to negatively affect the reproductive and endocrine systems (1996 situation; shaded pesticides were earlier used widely in the USSR but are now banned) [101,107] Insecticides

Herbicides

Beta-HCH

Acetochlor Amitrol (Aminotriazol)

Lindane

Atrazine

Heptachlor and its epoxide

2,4-D

DDT and its metabolites

Metribuzin

Dieldrin

Nitrophene

Dicofol

2,4,5-T

Methomyl

Trifluraline

Methoxychlor

Fungicides

Mirex

Benomyl

Transnonachlor

Vinclosalin

Oxychlordan

Hexachlorbenzene

Pyretroids (synthetic) Carbaryl Endosulfan Parathion

4.4.4. Pesticide Transformation in the Natural Environment Penetrating through the respiratory and intestinal tracts, and the integument, pesticides undergo a dual transformation [6]: both chemical transformations (oxidation, reduction, hydrolysis), and the formation of complex compounds with biochemical components in the body. The insecticide heptachlor (FD50 for mice is 82 mg/kg [4]) oxidizes into an epoxy-product in living organisms; this product is twice as toxic for practically all species [21, 35]. The insecticide aldrin (FD50 is 40-50 mg/kg) oxidizes in plants, insects, and invertebrates, as well as in the soil; it thus transforms into the seed protectant dieldrin (FD50 is 25-50 mg/kg), which is equally as dangerous to humans [15] aldrin ⇒ dieldrin. OPPs that enter living organisms may transform in especially varied and dangerous ways. One example is the biological transformation of dicrotophos (Bidrin), a wide-spectrum insecticide and acaricide. It transforms into two teratogenic substances: monocrotophos (Azodrin) and its amide analog [1]. There are hundreds of known examples of pesticides becoming poisonous substances inside living organisms. The examples studied make up only a

110


portion of all the transformations that exist. The problem may be understood by looking at Table 4.15, which was published as long ago as the 1960s. OPPs metabolize in warm-blooded organisms in two opposing ways. The first is the usual detoxification, i.e. the breakdown of a substance into simpler and less toxic compounds. Together with detoxification, many OPPs become more actively anticholinesterase, and more toxic subtances. One of the most important mechanisms for toxification in many thionic and thiophosphoric esters is oxidizing desulfuration, during which an atom of sulphur in the P=S link is replaced by an atom of oxygen (P=S ⇒ P=O). As a result of this process, more toxic cholinesterase inhibitors are formed directly in the living organism. The mechanism by which toxicity is increased directly in living organisms has been proved for parathion, methyl parathion, dimethoate, fenitrothion and others. When fenitrothion becomes fenitrooxon, toxicity grows, with the FD50 decreasing from 420-516 mg/kg to 20 mg/kg [31]. OPPs’ anticholinesterase activity grows significantly in many cases, in particular by almost 10,000 times for methyl parathion, malathion, the thionic isomer of demeton, and parathion (the data were collected in 1967) [12]. In the case of malathion, together with changing into the more toxic malaoxon, it also becomes the toxic iso-malathion (see above). Toxification rates may vary. For example, when humans are acutely poisoned by the systemic insecticide menazon, there is an “incubation” period (of up to one day) and a slow growth in the anticholinesterase activity when the PS-form with low toxicity becomes the active PO-form [A17]. Another way for OPPs to transform in mammals is linked to their direct oxidation, accompanying the formation of sulfoxide and sulfone, more toxic products. This takes place particularly when using the insecticide fenthion [21]. The systemic insecticide and acaricide demeton is an interesting case. Table 4.15. Comparative toxicity of pesticides and their metabolites (for rats) [80] FD50, Pesticide

mg/kg

Demeton

7.7

Parathion

13.0

FD50,

Growth in Toxicity,

mg/kg

# of times

Sulfoxide

2.0

3.9

Paraoxon

3.0

4.3

30-55

~8-15

100

2.5-6

Metabolite

Dimethoate

250-800

P=O – Dimethoate

Dimethoate

250-600

Thiolate

Trichlorofon

560-633

Dichlorvos

76-80

~8

Heptachlor

60-169

Heptachlor epoxide

34-88

~2

400

3.1

Ziram

1230

Tiram


111

Demeton is a potent toxic agent, and is made up of a mix of isomers. When direct oxidation takes place in humans, first sulfoxides form (as a consequence of the oxidation of the ethyl mercaptoethyl portion of the molecule), which then change into sulfones. Sulfoxides and sulfones from demeton have a high anticholinesterase activity and are very toxic. Next, demeton’s oxidation products undergo oxidizing sulfuration (during which the anticholinesterase activity of the sulfoxides and sulfones from the thion isomer again increases by three and six times respectively), and only then does hydrolization into nontoxic substances take place [12, 58]. These data were collected back in the 1960s, and were not included in the official USSR 1987 handbook [30], although the pesticide itself had been banned in the USSR as long ago as 1967 due to the large number of poisonings. Let us give several examples of pesticide transformation during other types of reactions. Octamethyl pyrophosphoramide oxidizes in mammals and forms phosphorous amino oxide. This oxidized compound has a much higher level of anticholinesterase activity [58]. Nevertheless, this OPP was banned in the USSR only in 1978, almost two decades after production started. The contact and systemic insecticide formothion not only oxidizes in mammals, but is also reduced, creating the insecticide and acaricide dimethoate (during this process, toxicity increases from FD50 = 350 mg/kg to FD50 = 220 mg/kg) [12, 39, 58]. Dimethoate in its turn may undergo oxidizing sulfuration with the appearance of products that are even more toxic. Trichlorfon, an insecticide of medium toxicity, may serve as an example of the dehydrochlorination reaction when it transforms in the body into the highly toxic contact insecticide dichlorvos (see section 4.2.6) [12, 31, 58]. The transformation and metabolism products of pesticides in plants may not only be of acute toxicity, but also may have other properties. Phosmet, for example, transforms into phthalimide and phthalic acid, teratogenic substances [21]. This transformation into more toxic substances directly in living organisms is characteristic for pesticides of other classes as well. For example, the highly toxic dinobutone, widely used in greenhouses as an acaricide and fungicide to fight powdery mildew, may transform in the body into the insecticide and herbicide dinoseb [5], the toxicity of which more than doubles (the FD50 changes from 140 mg/kg to 60 mg/kg) [30]. The metabolism of the systemic fungicide triadimephon (Bayleton) in mushrooms and plants leads to its transforming into the mixture of diastereomers of triadimenol, whose fungicidal properties are higher than those of the original product. In mushrooms’ mycelium, the process takes place very rapidly, and the concentration of triadimenol in the mycelium is 20-30 times higher than its concentration in other elements of the environment. This type of transforma-

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tion takes place the same way in mushrooms both sensitive and resistant to fungicides. This process in mammals is also accompanied by the hydroxilization of the tertiary butyl group with consequent oxidation to an acid [30]. The widely used insecticide carbaryl (FD50=270 mg/kg) transforms in oxidizing processes into 5-oxynaphthyl-N-methylcarbamate, a substance that is as toxic as carbaryl itself (FD50=297 mg/kg) [30, 33]. One of the metabolites of the fungicide benomyl, the methyl ester carbamino acid (BMK, carbendazim), is also toxic to fungi [33]. Several fungicides of the dithiocarbamate series, for example zineb, maneb and metiram, when transforming in plants, food products, and simply in the environment, form the stable volatile metabolites ethylene thiourea, and ethylene thioammonia sulfide. They are two to ten times more toxic than the original substances. Some metabolites stay in plants and food products, for example in grapes and cherries, for up to two months, when the fungicides themselves are no longer detected [21, 33]. The herbicide atrazine, as well as triazine derivatives, affected by plant enzymes form substances that are much more mutagenic than the originals [75]. This list is far from exhaustive. However, it convincingly demonstrates the spectrum of the dangerous transformations pesticides may undergo in living organisms, with which humans, unprepared, must contend when they use pesticides.

Chapter 5. PESTICIDES AND AGRICULTURE

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CHAPTER 5 PESTICIDES AND AGRICULTURE Pesticides were created as a new, progressive and effective technology for agriculture and other sectors. At first glance, these expectations were justified to some degree. Today we can say that this advance was a two-edged sword. 5.1. Pesticides as Poisons for Cultivated Plants After use, herbicides decompose slowly, and so affect cultivated plants for many years. In 1990, investigations in many regions of the USSR detected herbicides’ phytotoxic effects, especially among the sym-triazine class, on different cultivars in many varied situations [13]. These symtriazine herbicides, such as protrazin, simazin, atrazine, metazin, and prometrin, were used in different oblasts of the Ukraine, Kirgizia, Kazakhstan, Russia and Moldavia in previous years, especially on corn. Residual herbicide aftereffects led to the suppression and death of crops such as winter wheat, oats, barley, rye, potatoes, beets and sugar beets, linen, onions, watermelons and other melons, and sunflowers. Allegedly, insecticides have no negative effect on cultivars. However, it is known that lindane, for example, noticeably suppressed barley development [31]. There are more and more facts that show that, after they have been exposed to pesticides such as granosan, carbaryl, and captan, living organisms are more sensitive to the subsequent effects of these and other pesticides. This is one reason for the rapid degradation of high-yield crops – a dangerous phenomenon that spreads together with pesticide use. Because herbicides have been used for many years, soil will almost always simultaneously accumulate residual amounts of several stable pesticides. The number of possible combinations of residual pesticides is so great (hundreds, maybe even thousands), that it is impossible theoretically to predict the effect. However, it is theoretically possible to draw a general conclusion founded in fact: the consequences of using any pesticide are always more varied and dangerous than the regulations state. 5.2. Other Negative Consequences of Pesticide Use in Crop Production Species targeted by pesticides usually make up only several tenths of a percent of the total number of species in an agricultural environment. Natural enemies and parasites usually decrease a species’ mass reproduction reliably. Destroying, or sharply decreasing the number of, such enemies through pesticide use often leads to a population explosion in the suppressed species; chemical protection thus creates a greater threat to the protected cultivars [1].

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Pesticide use in agriculture creates favorable conditions for the mass reproduction of forms that existed in insignificant quantities before the pesticides were used – a serious, negative consequence. We propose just a few examples among the many that exist. The use of DDT in gardens to fight “harmful” insects led to an explosion in the spider mite population; spider mites had not been harmful to garden plants before their number grew so rapidly. In another case, when pesticides were used to destroy pierid caterpillars, a number of other arthropod predators were also destroyed; in this way, the pierid population returned and expanded [85]. One negative effect of pesticide use is how they stimulate suppressed species. For example, DDT and several other pesticides may accelerate the development of suppressed species (just as they did with the spider mites) and increase the frequency with which new generations are born. Sublethal doses of dieldrin and parathion do not decrease the Colorado beetle’s egg production – they increase it by 33-65% in a way we do not yet understand [3]. Data from 1976 showed that using carbofurans increased the Colorado beetle population in several U.S. states [20]. Trichlorfon also stimulates the Colorado beetle’s development at specific dose levels. Some insecticides may in this way change the age-sex structure of a population, leading to the remaining individuals producing larger numbers of progeny. For example, after pesticides decimated the Colorado beetle population, the remaining beetles started producing a sharply increased number of eggs [109]. Many examples have shown that rodents return to their original numbers faster after their population had decreased due to rodenticide use than after decrease due to natural factors. Other examples show that pubescence in gray marmots (Marmota baibacina) takes place faster in populations exposed to pesticides. A higher percentage of females reproduce in all age groups in the first two years after the use of rodenticides. In many cases, the growth rate of these rodents was faster in populations exposed to pesticides [3]. Another negative consequence of pesticide use is that special means must be used to protect harvests from unwanted pesticide actions: adsorbents, plant antidotes, microbiological detoxification means, etc. This does not only make agricultural production more expensive, but also increases the agricultural environment’s exposure to chemicals, an altogether more serious consideration [3]. Pesticides affect the content of microelements and other substances in plants, thus changing their nutritive value, as well as their ability to be stored. This was detected for OCPs in grain and legume harvests. For example, wheat crops treated with some fungicides (zineb, bayleton, and propicanazol) to fight stem rust (Puccinia) produce a lower quality of bread [3].


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Sometimes herbicides may change a plant’s taste, which can have dangerous consequences. After treatment of inedible ranunculus with herbicide 2,4-MCPA, livestock began to eat it in large quantities, which led to cases of poisoning and fatalities. There have been incidents where treating fields with herbicides made economically important crops accessible to beetles and leaf-eating insects [1]. Pesticides may sharply change the agrotechnical qualities of cultivated crops by affecting processes that take place within and between plant cells. For example, herbicides of the sym-triazine group and carbamide derivatives block the transport of electrons during photosynthesis, leading to changes in plants’ vegetative character. Prometrin suppresses symbiotic nitrogen fixation, and contributes to legumes moving to a mineral type of nitrogen nutrient. As a result, the value of legumes as nitrogen fixers is sharply decreased. Another negative consequence of pesticide use is the risk of destroying modern, high-yield crops that are genetically unsustainable because they rapidly accumulate mutations [110]. For example, the use of such herbicides as linuron, fluometuron, toluene and TCAN on cotton plants rapidly destroys their genetic structure [75]. The same effect is seen when using dichlorvos, phosmet, simazin, and trichlorfon on certain types of wheat, as well as dilor, malathion, and thiram on tomatoes (in this latter case, the genetic consequences are seen only from the second generation) [1]. Pesticides may not only change the genetic structure of a plant population, but also cause damage, sterility, and malformed outgrowths (morphoses) of the autonomic and reproductive organs. For example, up to 70% of barley plants treated with pesticides were observed to have ear malformation. Using 2,4-D and foxim on barley increased the number of plants with morphoses by a factor of 18-24 [3]. Pesticides often suppress the immune system of agricultural plants. Thus, after corn had been treated with herbicide 2,4-D, its nitrogen content increased, leading to an increased number of aphids on the plant. One of the little studied, but terrible, consequences of pesticide use is the spread of viruses that earlier did not cause great damage. The spread of several pathogens among sunflowers, the rhizomania pathogen in sugar beets, the Sharkey plum virus, the barley yellow dwarf pathogen, several pathogens in wheat, and bean yellow mosaic in lupines are all direct results of using herbicides on these plants [3]. After introducing recommended amounts of terbutrin and chlortoluron, wheat suffered more seriously from downy mildew. Monolinuron and simazin affected winter wheat similarly. Herbicides such as 2,4-MCPA, ioxynil, dicamba, and several others increased the amount of root rot damage to winter wheat on average by 60% when compared with the control crop. Treating grain crops using

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2,4-D created favorable conditions for the development of downy mildew and purple blotch. Herbicides of the sym-triazine group that have a strong effect on corn also stimulate the dangerous illness common smut (Ustilago maydis) [31]. Pesticides may change the soil’s element content. Some pesticides may increase plants’ micro- and macroelement content, such as nitrogen, phosphorus, calcium, potassium, magnesium, manganese, iron, copper, barium, aluminum, strontium and zinc, whereas others decrease these or other elements. Pesticides may cause ammoniac compounds to accumulate in the soil. Dimethoate and fluometuron increase nitrates in the soil, while DDT, carbaryl and HCH sharply decrease them. When prometrin was used, soil nitrate content decreased by 30-40% [3]. A serious and underestimated negative effect of herbicide use is acutely increased soil erosion. The lack of an herbaceous cover leaves the soil with no defense against wind, rain, and snowmelt. Erosion rapidly develops on slopes of just 1-2% when the soil has no covering. Herbicide use in forestry causes mineralization, thus decreasing the amount of organic compounds in the soil, as well as the overall nitrogen and calcium content. It is an immutable fact that pesticides negatively effect agricultural crops. And this influence is much more serious and varied than pesticide proponents believe. More than 20% of insects are pollinators. Bees alone pollinate more than 50 agricultural crops [111]. When fully pollinated, fruit and berry plants grow 30-40% more, and melons and squash twice as much, or more. Bees increase harvest size 3-4 times in feed grass like alfalfa, red clover, and vetch [111]. However, the number of bees and other plant pollinators sharply and universally decreased in regions of the USSR where chemicals were used in agriculture in the middle of the 1980s. Because of this decrease, harvest size of some plants has noticeably decreased (for example, buckwheat and melons). Bees are poisoned directly when they feed on fields treated with pesticides. OCPs cause stupor, paralysis, and abnormal, disconnected, circular motion in bees. They become aggressive when poisoned by lindane and OPPs [111]. A sublethal dose of parathion causes bees to make mistakes when determining the direction and distance to feeding grounds, and to lose their sense of time. The queen’s behavior changes when she is contaminated by pesticides brought back to the hive by the worker bees in contaminated pollen: she becomes depressed, she starts to lay eggs in unprepared cells, etc. [112]. Even more honeybees may die after a given region is treated with herbicides, not only because the bees were directly poisoned, but also because bees that return to the hive from contaminated regions are then ejected from the hive. Apart from their direct effect on bees, pesticides are dangerous because they accumulate in honey [84]. As early as 1973, residual quantities of


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lindane, dieldrin, DDT and DDE were detected in 90% of commercial types of honey in the USSR [3]. Pesticide contamination of honey takes place even in regions where pesticides are not used [32]. Carbaryl and HCH can remain in honey for up to a year [111]. 5.3. Pesticide Resistance in Target Species As a result of chemical treatment, target species may acquire resistance to the pesticides used against them. Chemists – pesticide developers – failed to consider the natural environment’s most important law: natural selection. When a given species with a large population undergoes pressure from an unusual factor, individuals survive who have characteristics that accidentally allow them to be less sensitive to that factor. If “less sensitivity” is genetic, then the entire next generation will be less sensitive to this factor. This is exactly how the evolutionary process has worked for many millions of years. In populations, this process is called microevolution. The speed with which adaptations appear, such as, for example, resistance to pesticides, depends on the pressure of selection. When using pesticides, the pressure is practically 100% and, therefore, new characteristics appear very rapidly, in just 2-3 generations. The speed with which resistance appears depends also on the population size of the target species: the larger the population, the more probable that resistance will appear in some members of the first generation. The populations of target species are always large; otherwise there would be no reason to try to suppress them. Therefore, in each suppressed population, there will inevitably be more resistant individuals. In natural circumstances, at least one individual in 10,000 carries an unusual mutation, which, if “fixed” by selection, may turn into a new characteristic. Insensitivity to a chemical substance that has not been seen over millions of years of evolution is a rare characteristic, and the frequency of such mutations is not 104, but closer to 107 or even 109. If there are over one billion individuals in the population of the target species, then less sensitive members will always be present in the first generation. They will survive, and will have progeny. Three to four generations later, the population of the target species will be the same size as, or even larger than, it was before pesticide use; however, the majority of individuals will be less sensitive to the pesticide. There are many examples of this effect of pesticide use, which can seem unexpected at first glance. Epidemiologists’ achievements in using pesticides to suppress malaria-carrying mosquitoes are well known. Before pesticide use, 40 million people contracted malaria in India annually; after mass pesticide treatments in the 1950s, this number decreased to 40,000 annually. However, 10-15 years later, the mosquitoes showed resistance to

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all the pesticides used. At the end of the 1990s, the overall number of people contracting malaria reached 59 million annually [3]. The resistance of the Transcarpathian population of the Colorado beetle to the insecticides DDT, lindane and polychlorpinen grew sharply over the course of several years [109]. This process can be seen universally (Table 5.1). We should note once again: the general mechanism by which resistance appears in target species is natural selection. Many factors may accelerate or slow this process: a growth in frequency or number of resistance alleles; their dominance, ability to penetrate, and expressivity; their interaction with various genes; the speed with which generations are replaced; the number of individuals in each generation; the character of the reproductive system (sexual or asexual); and a host of other factors [113]. There are many further factors which facilitate the appearance of resistance in target-species: growth in sensitivity to, and successful avoidance of, insecticides; growth in the ability to detoxify insecticides; decrease in integument penetrability to pesticides; growth in fertility; and change in the development rate at different stages of the life cycle. All of these features may be “fixed” by selection, and in just a few generations may ensure that the target species population is insensitive to the pesticide or pesticide cocktail used. Often, if pesticides or their cocktails are changed, the process of developing resistance may be slowed in the target species. Slowed, but not stopped. One result of pesticide use is the growth in the number of target species (“pests”) that have become resistant to pesticides. From 1970 to 1984, the number of resistant arthropod species doubled – from 224 to 447. These include 25 species of beetles, mites, and caterpillars that attack Table 5.1. Growth in pesticide resistance among various insect families [1] Family

Pesticide

Growth in Resistance, # of Times

Organophosphorus Pesticides (OPPs) Phytocciidae

Phosmet

E10

Coecinelidae

Methyl parathion

Chrysomelidae

Azinfos-methyl

E100

Phytocciidae

Diazinon

E119

Phytocciidae

Parathion

E103-152

Tetranylchidae

OPPs as a whole

E180-550

Phytocciidae

Azinfos-methyl

E100-1000

E10-35

Carbamates Phytocciidae

Carbaryl

Chrysomelidae

Carbofuran

E25-77 E450


119

cotton (by 1984 they were resistant in 36 countries). By 1984, resistance also grew in 100 pathogens in agricultural crops, 55 species of “weeds,” two species of nematodes, and five species of rodents [114]. At this juncture, about 1000 suppressed species of animals, plants, and microorganisms have acquired resistance to the pesticides used, and this process continues. In the middle of the 1980s in the USSR, approximately 150 species acquired resistance to one of the various OCPs and OPPs used [3], and now require more complicated means of suppression. For example, until the 1950s, weevils and boll weevils were the main pests damaging cotton. After the widespread use of OCP insecticides – DDT, toxafene, and others – cottonworms, tobacco tortricids, tobacco aphids, spider mites and loopers must now be fought as well. Their number jumped after suppression of the first two target species. In fields where some “weeds” were cleared using herbicides, other, more herbicide-resistant, species have appeared, such as common horsetail, coltsfoot, foxtail, wild oats, false wheat, etc. As a result of herbicide use, scratchweed, which cannot be destroyed by any herbicide, is making inroads into cereal crops, and chamomile has taken over rapeseed [6]. Using herbicides on rice fields caused the spread of wild, pesticide-resistant, low-yield forms of red-grain rice. Resistant “weeds” may appear and spread with the intensive use of herbicides; these are plants whose root systems are found in the deep layers of the soil, and are damaged by herbicides to a lesser degree [3]. Thus, as a result of the intensive use of pesticides, the number of target species increases rather than decreases. Another important result of the appearance of resistant target species is the increase in the number of pesticides to which “pests” acquire resistance. Resistance develops to all the pesticide groups used (Table 5.2). Table 5.2. Pesticide groups to which agricultural “pests” have become resistant [1] Pesticide Groups

Number of Resistant Species 1970

1980

DDT

98

229

Cyclodienes

140

269

OPPs

54

200

Carbamates

3

51

Pyretroids

3

22

Fumigants

3

17

Other Groups

12

41

OCPs

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When a species becomes resistant to a pesticide, larger doses of that pesticide must be used, as well as ever-newer formulations. In this way agriculture, having started down the path of pesticide use, just like a drug addict, has fallen into the trap of pesticide addiction. This addiction is tragic, since it becomes stronger and stronger. Therefore, pesticide supporters appear naïve in their statements, saying “the expanding assortment of pesticides is necessary…as a consequence of having to avoid the appearance of especially resistant races of harmful organisms” [115]. We should emphasize once again that pesticide resistance in suppressed target species inevitably appears. By the beginning of the 1990s, houseflies, Colorado potato beetles, cockroaches, peach aphids, cabbage moths and several other insect species became insensitive to all the insecticides used. One more consequence of pesticide use is that old target species expand to new territories. Because of the intensive use of herbicides, barnyard millet has not only survived, but has spread to fields of corn and other crops for thousands of hectares, entering agricultural environments where it had never grown before [11]. Almost all target species that are monitored and controlled develop resistance to the pesticides used. As early as 1984, the US National Academy of Science gave an international conference on the issues of resistance; it was admitted that, both in theory and practice, there are no satisfactory and universal methods of fighting pesticide resistance. The situation has not changed in the decades since. *** The spread of new “weed” species, the decrease in crop harvest size, the destruction of high-yield crops’ genetic system, the change in agricultural product quality, the increase (not decrease) in the population of suppressed species, and finally, the dangerous increase of chemical exposure in agricultural ecosystems and in the environment as a whole – these are only some of the negative consequences of using pesticides in agriculture. If the rate at which resistance appears is maintained, all 2000 main species of “weeds” and “pests” will become resistant to the pesticides used in 30-40 years. If the biosphere’s pesticide exposure doubles, by 20152020, all target species could become universally resistant. But with such chemical contamination, pesticides would then affect the entire biosphere, including human health.

Chapter 6. LESSONS OF PESTICIDE USE

121

CHAPTER 6 LESSONS OF PESTICIDE USE Summarizing the data in this report, we can see that the history of pesticide use has taught civilization several extremely important lessons. LESSON 1. WITH ANY PESTICIDE USE, FURTHER DANGEROUS CHEMICAL CONTAMINATION OF THE ENTIRE BIOSPHERE IS INEVITABLE. PESTICIDES ARE ALREADY FOUND IN DANGEROUS CONCENTRATIONS IN ALL CORNERS OF THE EARTH. LESSON 2. ALL LIVING SPECIES, NOT ONLY THE TARGET SPECIES, ARE DAMAGED BY PESTICIDES. LESSON 3. HUMANS INEVITABLY SUFFER ACUTE AND, MUCH MORE OFTEN, CHRONIC, POISONING FROM PESTICIDE USE. LESSON 4. SINCE PESTICIDES HAVE EXISTED, NEW, UNPREDICTABLE DANGERS AND CONSEQUENCES HAVE CONSTANTLY ARISEN FROM THEIR USE. IT BECAME CLEAR ONLY IN RECENT YEARS, THAT PESTICIDES NOT ONLY CAUSE CANCER, CONGENITAL DAMAGE, AND DEFORMITIES IN NEWBORNS, BUT ALSO AFFECT THE IMMUNE AND ENDOCRINE SYSTEMS. WE DO NOT YET KNOW ALL THE DANGERS OF PESTICIDE USE. LESSON 5. PESTICIDE USE, THOUGH CONFERRING SOME LOCAL AND SHORT-TERM ADVANTAGES, IS ECONOMICALLY DISADVANTAGEOUS, AND CAUSES MORE PROBLEMS THAN IT SOLVES. THE ONLY PARTIES WHO DERIVE A STABLE AND SIGNIFICANT ADVANTAGE FROM PESTICIDES ARE THE CHEMICAL COMPANIES THAT PRODUCE THEM. LESSON 6. THE WIDESPREAD USE OF PESTICIDES IS PRIMARILY DETERMINED NOT BY AGRICULTURE, FORESTRY, THE FISHING INDUSTRY, OR MEDICINE, BUT BY THE INTERESTS OF THE CHEMICAL COMPANIES THAT PRODUCE THEM. THE INTERESTS OF MILITARY AND POLITICAL CIRCLES PLAY AN IMPORTANT ROLE IN PESTICIDE PRODUCTION, AS THEY WISH TO MAINTAIN AND BUILD BASES TO DEVELOP AND PRODUCE CHEMICAL WEAPONS.

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APPENDIX (A) 1. Trakhtenberg I.M. K toksikologii organicheskikh soyedineniy rtuti – etilmerkurfosfata i etilmerkurkhlorida (Towards a Toxicology of Organic Mercury Compounds – Ethyl Mercury Phosphate and Ethyl Mercury Chloride): Dissertation (Dis.)...Candidate of Sciences. Kiev, 1950. 267 pp. 2. Buriy V.S. Materialy po gigienicheskoy i toksikologicheskoy kharakteristike insektitsida oktametiltetramida pirofosfornoy kisloty (oktametila) (Materials on the Health and Toxicology Characteristics of the Insecticide Octamethyl Tetramide Pyrophosphoric Acid (Octamethyl)): Dis. ...Candidate of Medical Sciences. Kiev, 1957. 264 pp. 3. Voytenko G.A. Toksikologicheskaya kharakteristika insektitsidov khlortena i polikhlorpinena i ikh gigienicheskoye normirovaniye (Toxicological Characteristics of the Insecticides Chlorothen and Polychlorpinen, and Their Health Standards): Dis. ...Candidate of Medical Sciences. Kiev, 1958. 257 pp. 4. Brakhnova I.T. Materialy po toksikologii metofosa i gigiene truda pri ego primenyenii (Materials on Metaphos Toxicology, and Workplace Health and Safety During Use): Dis. ...Candidate of Medical Sciences. Kiev, 1959. 220 pp. 5. Osetrov V.I. Materialy po toksikologicheskomu i gigienicheskomu normirovaniyu novogo insektitsida geptakhlora (Materials on the Toxicological, and Health Standards of the New Insecticide Heptachlor): Dis. ...Candidate of Medical Sciences. Kiev, 1959. 184 pp. 6. Statsek N.K. Materialy po toksikologii metilsistoksa i ego gigienicheskomu normirovaniyu (Materials on the Toxicology of Methylsystox and Its Health Standards): Dis. ...Candidate of Medical Sciences. Kiev, 1960. 243 pp. 7. Medved’ L.I. Gigiena truda pri primenyenii rtutnoorganicheskikh fungitsidov (Workplace Health and Safety When Using Organic Mercury Fungicides): Dis. ...Doctor of Medical Sciences. Kiev, 1960. 558 pp. 8. Kagan Yu.S. Toksikologiya ryada fosfororganicheskikh insektitsidov i gigiena truda pri ikh primenyenii (Toxicology of Several Organophosphorous Insecticides and Workplace Health and Safety During Use): Dis. ...Doctor of Medical Sciences. Kiev, 1961. Vol.1/2. 673 pp. 9. Balashov V.Ye. Toksikologo-gigienicheskaya otsenka insektofungitsida merkurana (Evaluation of the Toxicology and Health Implications of the Insectofungicide Mercuran): Dis. ...Candidate of Medical Sciences. Kiev, 1962. 233 pp. 10. Trakhtenberg I.M. Mikromerkurializm kak gigienicheskaya problema: (Vopr. Gigieny truda, eksperim. toksikologii i profilaktiki) (Micro-Mercury Poisoning as a Health Issue: Questions of Workplace Health and Safety, Experimental Toxicology, and Prevention): Dis. ...Doctor of Medical Sciences. Kiev, 1963. Vol.1/2. 589 11. Yakubov A.Ya. Gigiena truda pri primenyenii fosfororganicheskikh insektitsidov v khlopkovodstve (Workplace Health and Safety When Using Organophosphorous Insecticides in Cotton Cultivation): Dis. ...Candidate of Medical Sciences. Dushanbe, Kiev, 1963. 266 pp. 12. Mekhtarova N.D. Sostoyaniye nervnoy sistemy v rannem i otdalennom periodakh khronicheskoy intoksikatsii granozanom (State of the Nervous System in Initial and Successive Periods of Chronic Granosan Poisoning): Dis. ...Candidate of Medical Sciences. Frunze, 1964. Vol.1. 275 pp. Vol.2. 219 pp. 13. Pan’shina T.N. Materialy po toksikologii fosfamida i gigienicheskomu normirovaniyu ego soderzhaniya v vozdukhe rabochey zony (Materials on Phosphamide Toxicology, and Health Standards for Work Zone Air Content): Dis. ...Candidate of Medical Sciences. Kiev, 1964. 14. Krasil’shchikov D.G. Materialy k toksikologo-gigienicheskoy otsenke khlorofosa i normirovaniyu ego ostatochnykh kolichestv v pishchevykh produktakh (Materials on the Toxicology and Health Assessment of Trichlorfon, and Establishing Standards for Its Residual Quantity in Food Products): Dis. ...Candidate of Medical Sciences. Tashkent, 1965. 195 pp.

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15. Sivkov I.G. Alimentarniy granozanoviy toksikoz i ego preduprezhdeniye (Nutritional Granosan Toxicosis (Slows) and Its Prevention): Abstract of Dis. ...Candidate of Medical Sciences. Leningrad 1965. 20 pp. 16. Spynu Ye.I. Toksikologiya khlororganicheskikh pestitsidov dienovogo sinteza i gigiena truda pri ikh primenyenii (The Toxicology of Diene Synthesized Organochlorine Pesticides and Workplace Health and Safety During Use): Dis. ...Doctor of Medical Sciences. Kiev, 1965. 519 pp. 17. Tsapko V.G. Materialy po toksikologii i gigienicheskomu normirovaniyu khlorofosa (Materials on the Toxicology and Health Standards of Trichlorfon): Dis. ...Candidate of Medical Sciences. Kiev, 1965. 227 pp. 18. Yakim V.S. Eksperimental’nye dannye po toksikologii sevina i gigienicheskomu normirovaniyu ego v vozdukhe rabochey zony (Experimental Data on Sevin Toxicology, and Establishing Health Standards in Work Zone Air): Dis. ...Candidate of Medical Sciences. Kiev, 1966. 199 pp. 19. Akhmedova R.A. Toksikologiya butifosa i gigiena truda pri ego primenyenii v khlopkovodstve (The Toxicology of Butifos and Workplace Health and Safety During Use in Cotton Cultivation): Dis. ...Candidate of Medical Sciences. Tashkent, 1966. 269 pp. 20. Borisenko N.F. Osnovnye voprosy gigieny truda pri rabote s nekotorymi rtutnoorganicheskimi pestitsidami (agronal, radosan, granosan) (Main Issues of Workplace Health and Safety When Working with Some Organomercury Pesticides (Agronal, Radosan and Granosan): Dis. ...Candidate of Medical Sciences. Kiev, 1966. 308 pp. 21. Nazaretyan K.L. Khronicheskoye otravlyeniye granozanom v sudebno-meditsinskom otnoshenii: (Kliniko-eksperimental’noye issledovaniye) (Chronic Granosan Poisoning in Forensics: Clinical and Experimental Research): Dis. ...Doctor of Medical Sciences. Yerevan, 1966. Vol.1. 317 pp. Vol.2. 78 pp. 22. Onikienko F.A. Sostoyaniye nekotorykh storon uglevodnogo obmena i okislitel’nykh protsessov vozdeystvii na organizm otdel’nykh khlororganicheskikh insektitsidov (The State of Some Aspects of Carbohydrate Metabolism and Oxidizing Processes When Physiology is Affected by Specific Organochlorine Insecticides): Abstract of Dis. ...Candidate of Biological Sciences. Kiev, 1966. 18 pp. 23. Yakim V.S. Eksperimental’nye dannye po toksikologii sevina i gigienicheskomu normirovaniyu ego v vozdukhe rabochey zony (Experimental Data on Sevin Toxicology, and Establishing Health Standards in Work Zone Air): Dis. ...Candidate of Medical Sciences. Kiev, 1966. 199 pp. 24. Atabayev Sh.T. Gigienicheskoye izucheniye obyektov vneshney sredy pri primenyenii pestitsidov v usloviyakh zharkogo klimata i ozdorovitel’no-profilakticheskiye meropriyatiya (Studying the Health Implications for the Outside Environment When Using Pesticides in a Hot Climate, and Health and Prevention Measures): Dis. ...Doctor of Medical Sciences. Tashkent, 1967. 456 pp. 25. Goloma Ye.A. Sostoyaniye gemodinamiki pri khronicheskoy intoksikatsii granozanom (v klinike i eksperimente) (The State of Hemodynamics with Chronic Granosan Poisoning (Clinic and Experiments): Dis. …Candidate of Medical Sciences. Frunze 1967. 229 pp. 26. Matyushina V.I. Toksikologiya metilnitrofosa i voprosy gigieny truda pri ego primenyenii v sel’skom khozyaystve (Methylnitrophos Toxicology and Issues of Workplace Health and Safety During Use in Agriculture): Dis. ...Candidate of Medical Sciences. Kiev, 1967. 190 pp. 27. Paramonchuk V.M. Funktsional’noye sostoyaniye pecheni u lits, podvergayushchikhsya vozdeystviyu nekotorykh khlororganicheskikh soyedineniy v usloviyakh ikh proizvodstva (The Functional State of the Liver in Persons Undergoing the Effects of Some Organochlorine Compounds During Production): Dis. ...Candidate of Medical Sciences. Kiev, 1967. 295 pp. 28. Tarashchuk V.V. Nekotorye biokhimicheskiye i morfologicheskiye izmenyeniya v nervnoy sisteme i perifericheskoy krovi pri ostrom otravlenii metasistoksom: (Eksperimental’noye issledovaniye) (Some Biochemical and Morphological Changes in the Nervous System and Peripheral Blood in Acute Metasystox Poisoning: Experimental Research): Dis. ...Candidate of Medical Sciences. Ternopol’, 1967. 267 pp.

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29. Atabayev Sh.T. Gigienicheskoye izucheniye obyektov vneshney sredy pri primenyenii pestitsidov v usloviyakh zharkogo klimata i ozdorovitel’no-profilakticheskiye meropriyatiya (Studying the Health Implications for the Outside Environment When Using Pesticides in a Hot Climate, and Health and Prevention Measures): Dis. ...Doctor of Medical Sciences. Tashkent, 1967. 456 pp. 30. Sasinovich L.M. Materialy po toksikologii dimetildikhlorvinilfosfata (DDVF) i po gigienicheskoy kharakteristike usloviy ego primenyeniya (Materials on the Toxicology of Dimethyldichlorovinylphosphate (DDVP) and Its Regime of Use): Dis. ...Candidate of Medical Sciences. Kiev, 1968. 279 pp. 31. Vashakidze V.I. Vliyaniye granosana i sevina na generativnuyu funktsiyu i potomstvo v usloviyakh eksperimenta: (K probleme otdalennykh posledstviy deystviya pestitsidov) (The Effects of Granosan and Sevin on the Reproductive Function and Progeny Under Experimental Conditions: Towards the Issue of Remote Consequences of Pesticide Activity): Dis. ...Doctor of Medical Sciences. Tbilisi, 1969. 505 pp. 32. Vygovskaya L.I. Toksikologiya metilatsetofosa i voprosy gigieny truda pri ego proizvodstve (The Toxicology of Methyl Acetophos and Workplace Health and Safety Issues During Production): Dis. ...Candidate of Medical Sciences. Kiev, 1969. 339 pp. Dis. ...Candidate of Medical Sciences. Tashkent, 1969. 318 pp. 33. Gurevich B.E. Sanitarno-gigienicheskaya kharakteristika usloviy truda i meropriyatiy po ikh uluchsheniyu pri aviatsionno-khimicheskikh obrabotkakh khlopchatnika v Uzbekistane (Workplace Health and Safety, and Measures for Improvement During the Chemical Treatment of Cotton Plants from Aircraft in Uzbekistan): Dis. ...Candidate of Medical Sciences. Tashkent, 1969. 318 34. Danilenko L.P. Toksiko-gigienicheskoye issledovaniye fosfororganicheskogo insektoakaritsida ftalofosa (Research on the Toxicology and Health Implications of the Organophosphorous Insectoacaricide Phthalophos): Dis. ...Candidate of Medical Sciences. Kiev, 1969. 215 pp. 35. Drobyshevskaya (Asribekova) T.A. Gigiena truda pri khimicheskoy zashchite rasteniy s pomoshch’yu samoletov i vertoletov (Workplace Health and Safety During Chemical Protection of Plants Using Airplanes and Helicopters): Dis. ...Candidate of Medical Sciences. Kiev, 1969. 360 pp. 36. Ibragimova G.Z. Gigienicheskaya otsenka zagryaznyeniya vneshney sredy yadokhimikatom M-81 (A Health Assessment of the Outside Environment Contamination by Pesticide M-81): Dis. ...Candidate of Medical Sciences. “., 1969. 161 pp. 37. Komarova L.I. Nositel’stvo DDT i nekotorye storony ego vliyaniya na organizm (The Carrier State of DDT and Some Aspects of Its Effects on Physiology): Dis. ...Candidate of Medical Sciences. Kiev, 1969. 229 pp. 38. Lyubenko P.Kh. Eksperimental’nye dannye po toksikologii fenkaptona i voprosy gigieny v svyazi s primenyeniyem ego v sel’skom khozyaystve (Experimental Data on the Toxicology of Phenkapton and Issues of Food Health in Connection With Its Use in Agriculture): Abstract of Dis. ...Candidate of Medical Sciences. Kiev, 1969. 23 pp. 39. Russkikh V.A. Gigienicheskaya kharakteristika usloviy truda v proizvodstve granozana i puti ikh ozdorovleniya (Health Characteristics of Working Conditions During Granosan Production and Methods of Improvement): Dis. ...Candidate of Medical Sciences. Gor’kiy, 1969. 324 pp. 40. Martson’ L.V. Sravnitel’noye izucheniye vliyaniya nekotorykh pestitsidov, proizvodnykh ditiokarbaminovoy kisloty, na embrional’noye razvitiye i generativnuyu funktsiyu zhivotnykh (A Comparative Study of the Effects of Some Dithiocarbamic Acid Derivative Pesticides on Animal Embryo Development and Reproductive Functions): Dis. ...Candidate of Medical Sciences. Kiev, 1970. 171 pp. 41. Medovar A.M. Toksikologiya A09D>A0 i gigienicheskiye reglamentatsii usloviy ego primenyeniya v sel’skom khozyaystve (Sayfos Toxicology and Regime of Use Regulations in Agriculture): Abstract of Dis. ...Candidate of Medical Sciences. Kiev, 1970. 42. Suvak L.N. Nositel’stvo DDT sredi naseleniya Moldavii, ne kontaktiruyushchego s pestitsidami, i nekotorye storony ego neblagopriyatnogo deystviya (The Carrier State of DDT

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in the Moldavian Population With No Pesticide Contact, and Some Aspects of Its Unfavorable Effects): Dis. ...Candidate of Medical Sciences. Kishinyev, 1970. 171 pp. Ustanova I.Ya. Immunye reaktsii organizma pri vozdyeystvii khlor- i fosfororganicheskikh pestitsidov (Immune Response to the Effects of Organochlorine and -phosphorous Pesticides): Dis. ...Candidate of Medical Sciences. Tashkent, 1970. 135 pp. Khuriyev B.B. Gigienicheskaya otsenka zagryaznyeniya atmosfernogo vozdukha metilmerkaptofosom pri primenyenii ego v sel’skom khozyaystve Uzbekistana (A Health Assessment of Air Contamination by Methylmercaptophos During Use in the Agriculture of Uzbekistan): Dis. ...Candidate of Medical Sciences. Tashkent, 1970. 232 pp. Vasykovskaya L.F. Khimiko-biologicheskaya kharakteristika nakoplyeniya i raspredeleniya DDT v organizme cheloveka (Chemical and Biological Characteristics of DDT’s Accumulation and Distribution in the Human Body): Dis. ...Candidate of Biological Sciences. Kiev, 1971. 192 pp. Karimov A. Sostoyaniye kozhnykh pokrovov khlopkorobov pri primenyenii DDT, GKhTsG, tsianamida kal’tsiya, khlorata magniya, TKhFM i TMTD v usloviyakh Uzbekskoy SSR i mery profilaktiki dermatozov (The State of Cotton Growers’ Epidermis During Use of DDT, HCH, Calcium Cyanamide, Magnesium Chlorate, TCFM and TMTD in the Uzbek SSR, and Dermatosis Prevention Measures): Dis. ...Candidate of Medical Sciences. Tashkent, 1971. 175 pp. Krasnyuk Ye.P. Klinicheskaya kharakteristika khronicheskikh professional’nykh intoksikatsiy khlororganicheskimi soyedinyeniyami (Clinical Characteristics of Chronic Poisoning by Organochlorine Compounds in the Workplace): Dis. ...Doctor of Medical Sciences. Kiev, 1971. 427 pp. Saraimoanova Z.S. Vliyaniye nekotorykh yadokhimikatov na polovuyu sferu (klinikoeksperimental’noye issledovaniye) (Effects of Some Pesticides on the Sexual Sphere: Clinical and Experimental Research): Dis. ...Candidate of Medical Sciences. Tashkent, 1971. 200 pp. Yakubova, R.A. Problemy gigieny vody i sanitarnoy okhrany vodoemov v svyazi s primeneniem pestitsidov v Uzbekskoy SSR (Issues of Water Health and Protecting Reservoir Health During Pesticide Use in the Uzbek SSR): Abstract of Dis. …MD Tashkent, 1971. 35pp. Zor’yeva T.D. Materialy po toksikologii i gigiene pri primenyenii tsidiala: (Kompleksnoye gigienicheskoye normirovaniye) (Materials on Cidial Toxicology and Regime of Use: Comprehensive Health Standards): Dis. ...Candidate of Medical Sciences. Kiev, 1972. 287 pp. Lazumka F.A. Gigiena truda pri primenyenii pestitsidov v Litovskoy SSR (Gigienicheskoye issledovaniye primenyeniya pestitsidov i eksperimental’no-toksikologicheskoye izucheniye isnektitsidov anabazin-sul’fata i nikotin-sul’fata) (Workplace Health and Safety During Pesticide Use in the Lithuanian SSR: Health Research on Pesticide Use, and An Experimental and Toxicological Study of Anabasine-Sulfate and Nicotine-Sulfate Insecticides): Dis. …Doctor of Medical Sciences. Vilnius, Kiev, 1972. 332 pp. Pak L.V. Toksikologo-gigienicheskoye issledovaniye novogo fosfororganicheskogo insektoakaritsida kil’valya (Toxicology and Health Research on the New Organophosphorous Insectoacaricide Kilval): Abstract of Dis. ...Candidate of Biological Sciences. Moscow., 1972. 20 pp. Pismopulo A.I. Diagnostika otravlyeniy metafosom v sudebno-meditsinskom otnoshenii (Diagnosis of Metaphos Poisoning in Forensics): Abstract of Dis. ...Candidate of Medical Sciences. Alma-Ata, 1972. 14 pp. Pol’chenko V.I. Prichino-sledstvenniy analiz otravlyeniy pestitsidami i problemy ikh profilaktiki (A Cause and Effect Analysis of Pesticide Poisoning and Problems of Its Prevention): Abstract of Dis. ...Doctor of Medical Sciences. Kiev, 1972. 38 pp. Rusyaev V.A. Vliyaniye fosfororganicheskikh pestitsidov (khlorofosa, malationa i trikhlormetafosa-3) na organizm belykh myshey razlichnogo vozrasta: (Eksperimental’noye issledovaniye) (The Effects of Organophosphorous Pesticides (Trichlorfon, Malathion, and Trichlormetaphos-3) on the Physiology of White Mice of Different Ages: Experimental Research): Dis. …Candidate of Medical Sciences. Minsk, 1972. 149 pp. Bolomniy A.V. Toksikologiya novogo fosfororganicheskogo insektitsida gardony i obosnovaniye gigienicheskikh reglamentov ego primenyeniya (The Toxicology of the New Organ-

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57. 58.

59. 60. 61. 62.

63.

64.

65.

66.

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68. 69.

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ophosphorous Insecticide Gardona and the Rationale for Its Regime of Use Regulations): Dis. ...Candidate of Medical Sciences. Kiev, 1973. 258 pp. Bychkova N.A. Klinika i lecheniye intoksikatsii granozanom u detyey (Granosan Poisoning Manifestations and Treatment in Children): Abstract of Dis. ...Candidate of Medical Sciences. Novosibirsk, Omsk, 1973. 15 pp. Katsenovich L.A. Klinika i iskhody intoksikatsii, razvivayushchikhsya pri sovmestnom i posledovatel’nom primenyenii khlor- i fosfororganicheskikh pestitsidov (Manifestation and Outcomes of Poisoning Developing During Joint and Consecutive Use of Organochlorine and -phosphorous Pesticides): Dis. ...Doctor of Medical Sciences. Tashkent, 1973. 265 pp. Mel’nikova S.V. Gigiena truda pri primenyenii merkaptofosa v usloviyakh zharkogo klimata Uzbekistana (Workplace Health and Safety During Mercaptophos Use in the Hot Climatic Conditions of Uzbekistan): Abstract of Dis. ...Candidate of Medical Sciences. Kiev, 1973. Man’ko N.N. Gigiena primenyeniya i toksikologiya fozalona (benzofosfata) (Phosalone (Benzophosphate) Regime of Use and Toxicology): Dis. ...Candidate of Medical Sciences. Kiev, 1973. 247 pp. Vrpchinskiy K.K. Tsirkulyatsiya pestitsidov v vodoyemakh kak gigienicheskaya problema (The Circulation of Pesticides in Bodies of Water as a Health Problem): Abstract of Dis. ...Doctor of Medical Sciences. L’vov, 1974. 54 pp. Iskandarov T. Gigiena primenyeniya i toksikologiya pestitsidov, ispol’zuemykh v khlopkovodstve v usloviyakh zharkogo klimata (Pesticide Regime of Use and Toxicology in Cotton Cultivation in Hot Climatic Conditions): Abstract of Dis. ...Doctor of Medical Sciences. Tashkent, 1974. 40 pp. Kuz’minskaya Y.A. Biokhimicheskaya kharakteristika subkletochnykh kul’tur pecheni pri pestitsidov: (K mekhanizmu deystviya khlororganicheskikh i karbamatnykh pestitsidov) (Biochemical Characteristics of Subcellular Liver Cultures Under the Effects of Pesticides: Towards an Organochlorine and Carbamate Pesticide Mechanism): Dis. ...Doctor of Medical Sciences. Kiev, 1974. 367 pp. Nuritdinova F. Sostoyaniye organa zreniya u lits, s intoksikatsiyey pestitsidami, rabotayushchikh v sel’skom khozyaystve Uzbekistana: (Klinicheskoye i eksperimental’noye issledovaniye) (The State of Visual Organs in Subjects Poisoned by Pesticides and Working in Agriculture in Uzbekistan: Clinical and Experimental Research): Dis. ...Doctor of Medical Sciences. Tashkent, 1974. 296 pp. Pankrat’yeva T.B. Gigienicheskaya otsenka zagryaznyeniya atmosfernogo vozdukha insektitsidom antio pri primenyenii v usloviyakh Uzbekistana i ego vlianiye na organizmy cheloveka i zhivotnykh (A Health Assessment of Air Contamination by the Insecticide Antio During Use in Conditions in Uzbekistan and Its Effects on Human and Animal Physiology: Abstract of Dis. ...Candidate of Medical Sciences. Tashkent, “., 1974. 33 pp. Perkhurova V.P. Issledovaniye po toksikologii karbofosa i kombinirovannomu deystviyu promezhutochnykh produktov ego proizvodstva (Research on Carbophos Toxicology and the Combined Effects of Its Intermediate Products of Production): Dis. ...Candidate of Medical Sciences. Kuybyshev, 1974. 187 pp. Khalpaev O.Sh. Gigienicheskaya i toksikologicheskaya kharakteristika vozdeystviya malykh doz i kontsentratsiy fozalona i butifosa (Health and Toxicology Characteristics of the Effects of Small Doses and Concentrations of Phosalone and Butifos): Abstract of Dis. …Candidate of Medical Sciences. Tashkent, 1974. 30 pp. Bakhtiyarova R.S. Immunologicheskoye sostoyaniye organizma pri vozdeystvii butifosa i vysokoy temperatury (The Immunological State of the Body Under the Effects of Butifos and High Temperatures): Abstract of Dis. ...Candidate of Biological Sciences. Tashkent, 1975. 20 pp. Gorskaya N.Z. Sostoyaniye serdechno-sosudistoy sistemy u lits, rabotayushchikh s kompleksom khlor- i fosfororganicheskikh pestitsidov (The State of the Cardiovascular System in Subjects Working With Complex Organochlorine and –phosphorous Pesticides): Abstract of Dis. ...Candidate of Medical Sciences. Vinnitsa-Kiev, 1975. 29 pp.

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70. Kasymova R.A. Vliyaniye yadokhimikatov (butifos, geksakhloran et al.) na techeniye beremennosti i rodov u zhenshchin, prozhivayushchikh v sel’skikh rayonak Uzbekistana (The Effects of Pesticides (Butifos, Hexachloran, etc.) on Pregnancy and Birth in Women Living in Rural Areas of Uzbekistan: Dis. ...Candidate of Medical Sciences. Tashkent, 1975. 130 pp. 71. Khakimov A.M. Sostoyaniye vestibulyarnogo analizatora u rabotayushchikh s khlororganicheskimi i fosfororganicheskimi pestitsidami: (Klinicheskoye i eksperimental’noye issledovaniye) (The State of the Vestibular Analyzer in Subjects Working with Organochlorine and –phosphorous Pesticides: Clinical and Experimental Research): Dis. ...Candidate of Medical Sciences. Tashkent, 1975. 150 A 72. Altareva L.A. Prichiny intoksikatsii pri rabote na sveklovichnykh polyakh posle primenyeniya polikhlorpinena (Reasons for Poisoning During Work on Beet Fields After Polychlorpinen Use): Dis. ...Candidate of Medical Sciences. Nikolaev, Kiev, 1976. 135 pp. 73. Levkovskaya Ye.N. Abortivnoye deystviye nekotorykh fosfororganicheskikh i karbamatnykh pestitsidov i ikh vliyaniye na funktsional’noye sostoyaniye matki (The Abortive Action of Some Organophosphorous and Carbamate Pesticides, and Their Effects on the Functional State of the Womb): Abstract of Dis. ...Candidate of Medical Sciences. Kazan, 1977. 20 pp. 74. Verzhanskiy P.S. Vliyaniye kombinirovannykh pestitsidov (fenituram, khometsin et al.) na reproduktivnuyu funktsiyu i profilaktika oslozhnyeniy u zhenshchin, rabotayushchikh na khimicheskom predpriyatii (Effects of Combined Pesticides (Fenthiuram, Kuprozan, etc.) on Reproductive Function and Prevention of Complications in Women Working in Chemical Plants): Dis. ...Candidate of Medical Sciences. Kharkov, 1978. 232 pp. 75. Dunaiskiy V.B. Materialy po toksikologii polikhlorpinena i gigienicheskaya kharakteristika usloviy ego primyeneniya dlya bor’by s vreditelyami sakharnoy svekly (Materials on Polychlorpinen Toxicology and Regime of Use in Fighting Sugar beet Pests): Dis. ...Candidate of Medical Sciences. Vinnitsa, 1978. 140 pp. 76. Shafeyev M.Sh. Vliyaniye nekotorykh pestitsidov i ikh kombinatsiy na pokazateli immuniteta i nespetsificheskoy reaktivnosti organizma (Effects of Some Pesticides and their Combinations on Indicators for Body Immuno- and Unspecified Response): Dis. ...Candidate of Medical Sciences. Kazan, 1978. 139 pp. 77. Damaskin V.I. Gigienicheskoye obosnovaniye profilakticheskikh meropriyatiy v svyazi s primenyeniyem pestitsidov v stepnoy zone yuga Ukrainy (Health Implications for Preventive Measures Connected With Pesticide Use in the Steppe Region of Southern Ukraine): Dis. ...Candidate of Medical Sciences. Kiev, 1979. 24 pp. 78. Loranskiy D.N. Gigienicheskiye aspekty okhrany zdorov’ya naseleniya v svyazi s primenyeniyem pestitsidov (Regime of Pesticide Use Aspects of Population Health Protection): Dis. ...Doctor of Medical Sciences. Moscow, 1979. 315 pp. 79. Mukhmarova N.D. Patalogiya nervnoy sistemy, vyzvannaya vozdeystviyem chlor-, rtut’organicheskikh i kompleksa pestitsidov v usloviyakh khimizatsii sel’skogo khozyaystva: (Klassifikatsiya, klinika, diagnostika, reabilitatsiya) (Nervous System Pathologies Caused By Organochlorine, Organomercury, and Combinations of Pesticides During Chemical Use in Agriculture: Classification, Manifestations, Diagnosis, Rehabilitation): Dis. ...Doctor of Medical Sciences. Kiev, 1979. 278 pp. 80. Azizova O.M. Morfologicheskiye izmenyeniya v golovnom mozge pri khronicheskoy intoksikatsii pestitsidami (Morphological Changes in the Brain During Chronic Pesticide Poisoning): Dis. ...Doctor of Medical Sciences. Samarkand, 1980. 161 pp. 81. Bruy G.F. Gigiena truda pri vozdelyvanii sakharnoy svekly v usloviyakh intensivnogo primenyeniya khlororganicheskikh pestitsidov (geksakhlorana, gamma-izomera geksakhlortsiklogeksana i polichlorpinena) (Workplace Health and Safety During Sugar beet Cultivation and Intensive Use of Organochlorine Pesticides (Hexachloran, Gamma-Isomer of Hexachlorcyclohexane, and Polychorpinen)): Dis. ...Candidate of Medical Sciences. Kiev, 1980. 184 pp.

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82. Voronina V.M. Embriotoksicheskoye, teratogennoye i gonadotoksicheskoye deystviye ftalofosa i ego metabolizm v organizme laboratornykh zhivotnykh: (K probleme gigienicheskoy reglamentatsii pestitsidov) (The Embryotoxic, Teratogenic, and Gonadotoxic Effects of Phthalophos and Its Metabolism in Laboratory Animals: Towards the Question of Regime of Pesticide Use Regulation): Abstract of Dis. ...Candidate of Biological Sciences Moscow, 1980. 24 pp. 83. Yelina V.A. Sostoyaniye spetsificheskikh funktsiy rabotnits proizvodstva gerbitsidov gruppy 2,4-D (The State of Specific Functions of Female Workers Producing Group 2,4-D Herbicides): Dis. ...Candidate of Medical Sciences. Ufa, 1980. 143 pp. 84. Khaidarov S.A. Gigienicheskaya otsenka zagryzneniya obyektov okruzhayushchey sredy i nekotorye aspekty biologicheskogo deystviya metationa i PKhNB (A Health Assessment of Environmental Contamination and Some Aspects of the Biological Activity of Metathion and PCNB): Dis. ...Candidate of Medical Sciences. Tashkent, 1980. 163 pp. 85. Khasanov T.S. Gigienicheskaya otsenka zagryaznyeniya atmosfernogo vozdukha geksakhloranom, fozalonom i butifosom pri odnovremennom i posledovatel’nom primenyenii ikh v sel’skom khozyaystve (A Health Assessment of Air Contamination by Hexachloran, Phosalone, and Butifos During Their Simultaneous and Consecutive Use in Agriculture): Dis. ...Candidate of Medical Sciences. Tashkent, 1980. 286 pp. 86. Yakubov, A. Gigiena primeneniya pestitsidov v razlichnykh klimato-geographicheskykh zonakh Tadjikistana: (K probleme rayonirovaniya sel’skoy mestnosti po stepeni zagryaznyeniya pestitsidami vneshney sredi): (The Regime of Using Pesticides in Different Climatic and Geographical Zones of Tajikistan: Towards the Question of Redistricting Rural Areas by the Degree of Pesticide Contamination of the External Environment): Dis. …M.D. Dushanbe, 1980. 284 pp. 87. Babaev I.I. Gigienicheskoye obosnovaniye primenyeniya gerbitsidov na posevakh ovoshchnykh kul’tur i vinogradnikakh v usloviyakh Tadzhikskoy SSR (The Rationale Behind the Regime of Herbicide Use on Vegetable Crops and Grapevines in the Tajik SSR): Dis. ...Candidate of Medical Sciences. Dushanbe, 1981. 279 pp. 88. Sasinovich L.M. Osnovy uskorennogo gigienicheskogo normirovaniya fosfororganicheskikh i khlororganicheskikh pestitsidov v vozdukhe rabochey zony, toksikodinamika i lecheniye otravleniy imi (The Rationale Behind an Accelerated Establishment of Health Standards for Organophosphorous and –chlorine Pesticides in Work Zone Air, Their Toxicology Dynamics, and Poisoning Treatment): Dis. ...Doctor of Chemical Sciences. Kiev, 1981. 445 89. Sattarova S.Sh. Vliyaniye nekotorykh pestitsidov na polovuyu sistemu, reproduktivnuyu funktsiyu, vnutriutrobnoye razvitiye, razvitiye ploda i potomstva (Effects of Some Pesticides on the Sexual System, Reproductive Functions, Prenatal Development, and Development of the Fetus and Progeny): Dis. ...Candidate of Medical Sciences. Tashkent, 1981. 128 pp. 90. Shukrullaev I.Sh. Osobennosti techeniya infektsionnogo gepatita u vzroslykh i detey, podvergshikhsya vozdeystviyu pestitsidov (Characteristics of the Development of Infectious Hepatitis in Adults and Children Affected by Pesticides): Abstract of Dis. ...Candidate of Medical Sciences. Samarkand, Moscow, 1981. 22 pp. 91. Yurchenko I.V. Sostoyaniye nervnoy sistemy u lits, rabotayushchikh s tetrametiltiuramdisul’fidom (The State of the Nervous System in People Working with Tetramethylthiuram Disulphide): Dis. ...Candidate of Medical Sciences. Kiev, 1981. 203 pp. 92. Zhumanov U. Sostoyaniye organov polosti rta pri vozdeystiivii na organizm khlor- i fosfororganicheskikh pestitsidov (The State of the Oral Cavity When Affected by Organochlorine and –phosphorous Pesticides): Dis. ...Candidate of Medical Sciences. Tashkent, 1982. 226 pp. 93. Baida L.K. Sostoyaniye zdorov’ye detyey, prozhivayushchikh v sel’skikh mestnostyakh s intensivnym primenyeniyem pestitsidov (The Health State of Children Living in Rural Areas With Intensive Pesticide Use): Dis. ...Candidate of Medical Sciences. Kiev, 1983. 269 pp. 94. Raevskiy V.A. Kombinirovannoye deystviye pestitsidov i mineral’nykh udobreniy v usloviyakh sovremennogo teplichnogo khozyaystva (The Combined Effects of Pesticides and Mineral Fertilizers in Greenhouse Conditions): Dis. ...Candidate of Medical Sciences. Kiev, 1983. 167 pp.

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Pesticides: The Chemical Weapon That Kills Life : (The USSR's Tragic Experience)

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Pesticides: The Chemical Weapon That Kills Life : (The USSR's Tragic Experience)

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The Kills

The Kills

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The Weapon

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The Weapon

Chemical Pesticides - Mode of Action and Toxicology

The Weapon

The Weapon

Chemical Pesticides Mode Of Action And Toxicology

Chemical Pesticides: Mode of Action and Toxicology

The SPIW: The Deadliest Weapon That Never Was

Fluff the Tragic Dragon

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Weapon

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The Deadlier Weapon

The Ultimate Weapon

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Fluff the Tragic Dragon

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Silent Kills

Near Life Experience

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