Public Healft Polyy Fonim Cancer: An Approach to Cancer Etiology and ControL New York: Academic Press; 1975:225-238. 8. Dol R, Peto R. The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today. JNatl Cancer Inst. 1981;66:1191-1308. 9. Ames BN, Gold LS. Chemical carcinogenesis: too many rodent carcinogens.
Proc NatlAcad Sci USA. 1990;87:7772-
7776. 10. National Research Council. Environmental Epidemiology. Vol. 1. Public Health and Hazardous Wastes. Washington, DC: National Academy Press; 1991. 11. Peto R, Lopez AD. Worldwide mortality from current smoking patterns: WHO consultative group on statistical aspects of to-
bacco-related mortality. In: Durston B, Jamrozik K, eds. Tobacco and Health 1990: The Global War. Perth, Western Australia: Proceedings of the 7th World Conference on Tobacco and Health, April 1990. 12. Doll R. Progress against cancer: an epidemiological assessment.AmJEpdemiL In press. 13. Doll R. Are we winning the war against cancer? In press. 14. KnoxEG, Lancashire RJ.Epidemio1ogyof congenital malformations. London: HMSO; 1991. 15. International Clearinghouse for Birth Defects Monitoring Systems. Congenital malformations worldwide. Amsterdam: Else-
vier Science Publishers; 1991. 16. World Health Organization. World Heakh Statistics Annua4 1991. Geneva: World Health Organization; 1991. 17. Kerr RA. Ozone destruction worsens. Science. 1991;252:204. 18. Myers N. Mass extinctions: Palaeogeography, palaeoclinatology, palaeoecology. Amsterdam: Elsevier Science Publications; 1990. 19. Peto R, Lopez AD. Tobacco-attributable mortality: global estimates and projections. In: Tobacco Alert. Geneva: World Health Organization; January 1991:4-5, 7. 20. Commission on Health and the Environment. Our planet, our health. Geneva: World Health Organization; 1991.
Commentary: Environmental Disease-A Preventable Epidemic Phili J. Landngan, MD, MSc
Intrduton
...........~~~~~~~~~~~~~~~~~e..>..
}XO'
.........:..>.
;..e;DK! S' :es:-^yX
-
Disease caused by toxic chemicals in the environment is a substantial yet highly preventable cause of morbidity and mortality in the United States and around the world. Consider: 0 Leadpoisoning. Lead poisoning is epidemic among young US children. The Centers for Disease Control (CDC) estimates that 3 to 4 million American preschool children have blood lead levels above 10 Fg/dl.l Blood lead levels in this range in young children have been shown to cause depression of neurological and psychological function,24 effects that appear to be permanent. o Asbestos. Asbestos in the work environment has created an absolute disaster.5 Although the hazards of asbestos were known in the 1930s, billions of tons ofasbestos were used in the United States from then until the 1980s. Millions of workers were exposed, and tens of thousands of homes, schools, and other public buildings were contaminated.6 Bytheyear 2000, an estimated 300 000 American workers will have died of the diseases caused by asbestos: principally, asbestosis, lung cancer, and malignant mesothelioma. It is anticipated that deaths will continue to occur well into the 21st century.7 With the overseas spread of asbestos-contaiing building materials, the pan-
demic is now extending to the Third World. * Occupational disease. Studies conducted in New York State have estimated that 50 000 to 70 000 US workers die each year of chronic occupational disease resulting from past exposures to toxic substances.8 These diseases encompass a broad range: besides the lung cancer and mesothelioma of asbestos workers,5 they include cancer ofthe bladder in dye workers9; leukemia and lymphoma in workers exposed to benzene10 and ionizing radiation11; chronic bronchitis in workers exposed to dusts12; disorders of the nervous system (including possibly dementia, Parkinson's disease, and motoneuron disease) in workers exposed to pesticides, solvents, and certain other neurotoxins13; renal failure in workers exposed to lead14; and cardiovascular disease in workers exposed to carbon monoxide15 and carbon disulfide.16 A major impediment to assessing the contribution of synthetic chemicals to the causation of cancer and other workplace diseases is the fact that only 20% of the Philip J. Landrgan is professor and chair in the Department of Community Medicine, Mount Sinai School of Medicine, New York, NY. Requests for reprints should be sent to Philip J. Landrigan, MD, MSc, Department of Community Medicine, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10009.
American Journal of Public Health 941
Pubc HedM PdUlly Fon
approximately 60 000 industrial chemicals in commerce have ever been tested for their carcnogenic, neurotoxic, immunotoxic, or other toxic potential.17 Millions of American workers are therefore exposed to chemical agents of unimown toxicity. * ChiWhood asthma. Among chiidrenworldwide, morbidity, disability, and mortality from asthma are increasing.18 In 1987, an estimated 585 American children died of asthma,19 and 150 000 were hospitalized.20 In American inner cities, asthma is the leading cause of hospital admissions for chlldren 5 to 15 years old, and rates are highest among African-American and Hispanic children. The causes of recent increases in asthma are not known. However, these increases coincide with substantial rises in summertime peak levels of atmospheric ozone and with year-round increases in oxides of nitrogen (NOx), two pollutants derived principally from automotive emissions.21 Recent epidemiologic data suggest that ozone and NOx have contrbuted to the increasing incidence and prevalence of childhood asthma.22 * Cancer. Between 1950 and 1988, for US Whites, age-adjusted incidence for all forms of cancer rose by 43.5% and ageadjusted cancer mortality increased by 2.9%.23 These overall increases in incidence occurred despite declines in cancer mortality among younger persons as a result of remarkable improvements in treatment.U.Z.26 Explanations for these increases do not exist. They do not appear to be attnbutable solely to changes in cigarette smoking.27 Although smoking remains the most important of the known preventable causes of cancer (accounting for as much as 40%o of all human malignancy), mortality rates for lung cancer as well as for cardiovascular disease have actually begun to decline among men in the United Kingdom and United States, due principally to decreases in cigarette consumption.2S,N Several ofthe cancers forwhich increased incidence (at all ages and in mortality above age 55) have been noted in a number of industrialized nations are not known to be related to smokig; these include multiple myeloma, brain cancer, cancer ofthe breast, testicular cancer, and
non-Hodgkin's lymphoma.27 Changes in competing
causes of death,28 improved access to health care, and alterations in diagnostic technology29 also do not appear to account entirely for the observed changes in cancer incidence and mortality. The possible contribution
942 American Journal of Public Health
to recent cancer trends of the substantial worldwide increases in chemical production that have occurred since World War II (and the resulting increases in human exposure to toxic chemicals in the environment) has not been adequately assessed.17 It needs to be systematically evaluated.30 The tragedy of environmental diseases is that they are highly preventable. Toxic environmental diseases arise as a direct consequence of human activity and can therefore, in theory, be prevented throgh modification of that activity. The control of toxic disease does not require changing the behavior of millions of addicted or habituated individuals, only the containment of common sources of exposure to chemical toxins. Such containment is demonstrably achievable through legislation, regulation, and other well-understood mechanisms of communal action. Children must be protected from exposure to lead. Automotive and industrial atmospheric emissions must be curbed. Dangerous chemicals in the work environment must be replaced with safe substitutes; hazardous processes must be enclosed and ventilated; and workers and consumers must be provided with knowledge, training, and protective equipment.31 Premarket testing of new chemicals and processes constitutes a very effective approach to the prevention of toxic disease. In this issue of theJownal Sir Richard Doll considers the role of the environment in the etiology of human disease.32 He correctly recognizes the pervasive influence of the environment-defined broadly as the conditions under which people live-on human health and the causation of disease. He speaks compellingly of the need to combat the use of tobacco and to reduce excess consumption of alcohol and fatty food. These are areas of public health in which Doll has contributed enormously and is a muchhonored pioneer. Doll also speaks of the perils of unchecked population growth and of humnkind's changes to the global climate. His points here are well taken, and his counsel deserves close heed. However, Doll does not adequately address the role of chemical toxins in the causation of human disease, therefore overlooking important opportunities for disease prevention. In my view, the following points in his analysis need to be set
right. Doll speaks of "the few cases of mesothelioma"32(P") that have resulted from the dispersal of asbestos. This com-
ment is not consistent with epidemiological data that already have been accumulated, nor does it jibe with projections of future mortality.7 It is anticipated that, by the end of this century, hundreds of thousands of workers in the United States and around the world will have died of asbestos-related diseases, mesothelioma prominent among them. This issue is far from
trivial. Doll asserts that recently observed increases in mortalityfrom cancer "can be accounted for in all industrialized countries by the spread of cigarette smoking."32(p936) However, this does not appear to be the whole story, because it does not account for the increases noted earlier in incidence and mortality for some cancers that are not known to be related to smoking.27.28 His comment also does not consider the possible etiologic significance ofwidespread population exposure, since World War II, to tens of thousands of synthetic chemicals of unknown and untested carCinogenic potential.17 Doll states that the contamination of foods with toxic pesticide residues is not an issue of health concern. He refers to a recent commentary by Ames and Gold33 in which the authors claim that naturally occurring pesticide residues pose by far the greater threat. However, this analysis appears to be premature. Of particular concern here are recent data from the US Environental Protection Agency (EPA) showing that infnts and young children are permitted to have dietary exposures to potentially crcingeni and neuotoxc pesticides in amounts that exceed published standards by a factor of more than 1000.M4 This iswe requires further assessment. Finally, Doll's opinion that modern industry has given rise to "the dispersal of small amounts of potenfially toxic chemicals"32(94) considerably understates the sad reality. The EPA's Toxic Release Inventory reports that in 1989 American industries released 3.56 billion pounds of chemical agents into the environment.35 These releases include carcnogens, neurotoxins, reproductive toxins, and thousands of chemicals of unknown toxicity. Moreover, releases in Europe, Japan, and the developing nations are likely to be at least as large as the United States', given the past 20 years' experience in Seveso, Minimata Bay, Chenobyl, and Bhopal. Public health workers and the makers of public policy must recognize that toxic chemicals in the environment are important, widespread, proven causes ofhuman disease. Eachyear preventable exposures to chemical toxins sicken and kill thou-
July 1992, Vol. 82, No. 7
Public Health Policy Fonrm
sands of persons of all ages in the United States and around the world. These hazards must be confronted. They cannot be wished away.36 Reduction of exposures to chemical toxins will prevent thousands of deaths and will improve the quality of hundreds of thousands of lives. Reuel Stallones, in whose honor Doll spoke at the University of Texas, fully recognized the importance of toxic chemicals in the causation of disease. In 1979, in an analysis of cancer in the work environment, Stallones and Downs calculated that toxic factors encountered at work were responsible for at least 20% of all human cancer.37 From firsthand knowledge, Stallones described the asbestos pandemic as "horrifying" and as a "public health catastrophe." He concluded his report by arguing "that reduction of exposures to carcinogens in the course of employment can certainly be expected to effect major reductions in the frequency of occurrence of cancer. [It] is one of the most promising applications of preventive medicine."37 0
References 1.
PreventingLeadPoisonigin Young Chiddren. Atlanta, Ga: Centers for Disease
Control; 1991. 2. Bellinger D, Leviton A, Waternaux C, Needleman HL, Rabinowitz M. Longitudinal analyses of prenatal and post-natal lead exposure and early cognitive development. New Engl J Med 1987;316:10371043. 3. Dietrich KN, Krafft KM, Bornschein RL, et al. Low-level fetal lead exposure effect on neurobehavioral development in early
infancy. Pediatrics. 1987;80:721-730.
4. McMichael AJ, Baghurst PA, Wigg NR, Vimpani GV, Robertson EF, Roberts RJ. Port Pirie cohort study: environmental exposure to lead and children's abilities at the age of four years. New EngIJMedL 1988;
319:468-475. 5. Selikoff IJ, Hammond EC, Churg J. Asbestos exposure, smoking and neoplasia. JAMA. 1968;204:100-112. 6. PJ Landrigan, H Kazemi, L Selikoff, eds. The third wave of asbestos disease: exposure to asbestos in place. Public Health Control.Ann NYAcad Sci 1991;643. Special issue. 7. Nicholson WJ, Perkel G, Selikoff U. Oc-
July 1992, Vol. 82, No. 7
cupational exposure to asbestos: populations at risk and projected mortality1980-2030.AmJIndMedL 1982;3:259-311. 8. Landrigan PJ, Markowitz S. Current magnitude of occupational disease in the United States: estimates from New York State. Ann NYAcad ScL 1989;572:27-45. 9. Rehn L. Blasengeschwuelste bei Fuchssinarbeitern. Arch Jiir Klinische Chi'wgie. 1985;50:588-600. 10. Rinsky RA, Smith AB, Hornung R, Filloon TG, Young RJ, Landrigan PJ. Benzene and leukemia-an epidemiologic risk assessment. New Engl J Med 1987;316:1044-
1050. 11. March HC. Leukemia in radiologists. Ra-
diology. 1944;43:275-278.
12. Parkes WR. Occupational Lung Disordes. 2nd ed. London: Butterworths; 1982. 13. National Research Council. Environmental neurota2cology. Washington, DC: National Academy Press; 1992. 14. Landrigan PJ, Goyer RA, Clarkson TW, Sandler DP, Smith TH, Thun MJ, Wedeen RP. The work-relatedness of renal disease. Summary of the working group on renal disease. Arch Environ Health. 1984;39: 225-230. 15. Kleinman MT, Davidson DM, Vandagriff RB, Caiozzo VJ, Whittenberger JL. Effects of short-term exposure to carbon monoxide in subjects with coronary artery disease. Arch Environ Health. 1989;44: 361-369. 16. Hemberg S, Partanen C, Nordman CH, Sumari P. Coronary heart disease among workers exposed to carbon disulphide. BrJ Ind Med. 1970;27:313-325. 17. National Research Council. Toxicity Testing-Strategies to Detennine Needs and Pnorities. Washington, DC: National Academy Press; 1984. 18. Sly RM. Increases in deaths from asthma.
AmAllegy. 1984;53:20. 19. National Center for Health Statistics. Vital Statistics ofthe United States. 1987. Washington, DC: US Government Printing Office; 1989; 11, part B. US DHHS publication PHS 89-1102. 20. Graves EJ. National Hospital Discharge Swvey:Anual Swmnmary, 1987. Vital and health statistics; series 13, no. 99. Hyattsville, Md: National Center for Health Statistics; 1989. US DHHS publication PHS 89-1760. 21. National air quality emissions trnds repo??s. Research Triangle Park, NC: US Environmental Protection Agency; 1990. EPA report 450/4-90.002. 22. Lippmann M. Health effects of ozone: a critical review. JAirPollut ControlAssoc.
1989;39:672-695. 23. Ries LA, Hankey BF, Miller BA, Hartman AM, Edwards BK. Cancer Statistics Review 1973-78. Washington, DC: US Dept of Health and Human Services; 1991. DHHS publication NIH 91-2789. 24. Doll R. Progress against cancer: an epidemiologic assessment. Am J Epidemiol.
1991;134:675-688.
25. Devesa SS, Silverman DT, Young JLJr, et al. Cancer incidence and mortality trends among whites in the United States, 194784. JNatl Cancer Inst. 1987;79:701-770. 26. Davis DL, Hoel DG. Figuring out cancer. IntemationalJHlth Senvices. 1992;22:447453. 27. Hoel DG, Davis DL, Miller AJ, Swerdlow AJ, Sondik E. Trends in cancer mortality in 15 industrialized countries, 1969-1986. J Natl Cancer Inst. 1992;84:313-320. 28. Lopez AD. Competing causes of death: a review of recent trends in mortality in industrialized countries with special reference to cancer. Ann NYAcad Sci 1990; 609:58-76. 29. Davis DL, Hoel DG, Fox J, Lopez AD. International trends in cancer mortality in France, West Germany, Italy, Japan, England and Wales, and the United States. Lancet. 1990;336:474-481. 30. Davis DL, Magee BH. Cancer and industrial chemical production. Science. 1979;
206:1356-1358.
31. National Institute for Occupational Safety and Health. Occupational Diseases: A Guide to 7heir Recognition. Washington, DC: US Department of Health, Education and Welfare; 1977. 32. Doll R. Health and the environment in the 1990s. Am J Public Health. 1992;82:933941. 33. Ames BN, Gold LS. Chemical carcinogenesis: too many rodent carcinogens. Proc. NatlAcad ScL 1990;87:7772-7776. 34. Fisher UJ. Communication to the Chairman, Committee on Labor and Human Resources, United States Senate. Washington, DC. 30 March 1992. 35. Toxacs in the Community: National and Local Perspectives. The 1989 Taoics Re-
leaseInventoryNationalRepoti. Washing-
ton, DC: US Environmental Protection Agency; 1991. 36. Abelson PH. Cancer phobia. Science. 1987;237:473. 37. Stallones RA, Downs T. A critical review of estimates of the fraction of cancer in the United States related to environmental factors. Prepared for the American Industrial Health Council. Houston: University of Texas School of Public Health; 1979.
American Joumal of Public Health 943
Proc NatlAcad Sci USA. 1990;87:7772-
7776. 10. National Research Council. Environmental Epidemiology. Vol. 1. Public Health and Hazardous Wastes. Washington, DC: National Academy Press; 1991. 11. Peto R, Lopez AD. Worldwide mortality from current smoking patterns: WHO consultative group on statistical aspects of to-
bacco-related mortality. In: Durston B, Jamrozik K, eds. Tobacco and Health 1990: The Global War. Perth, Western Australia: Proceedings of the 7th World Conference on Tobacco and Health, April 1990. 12. Doll R. Progress against cancer: an epidemiological assessment.AmJEpdemiL In press. 13. Doll R. Are we winning the war against cancer? In press. 14. KnoxEG, Lancashire RJ.Epidemio1ogyof congenital malformations. London: HMSO; 1991. 15. International Clearinghouse for Birth Defects Monitoring Systems. Congenital malformations worldwide. Amsterdam: Else-
vier Science Publishers; 1991. 16. World Health Organization. World Heakh Statistics Annua4 1991. Geneva: World Health Organization; 1991. 17. Kerr RA. Ozone destruction worsens. Science. 1991;252:204. 18. Myers N. Mass extinctions: Palaeogeography, palaeoclinatology, palaeoecology. Amsterdam: Elsevier Science Publications; 1990. 19. Peto R, Lopez AD. Tobacco-attributable mortality: global estimates and projections. In: Tobacco Alert. Geneva: World Health Organization; January 1991:4-5, 7. 20. Commission on Health and the Environment. Our planet, our health. Geneva: World Health Organization; 1991.
Commentary: Environmental Disease-A Preventable Epidemic Phili J. Landngan, MD, MSc
Intrduton
...........~~~~~~~~~~~~~~~~~e..>..
}XO'
.........:..>.
;..e;DK! S' :es:-^yX
-
Disease caused by toxic chemicals in the environment is a substantial yet highly preventable cause of morbidity and mortality in the United States and around the world. Consider: 0 Leadpoisoning. Lead poisoning is epidemic among young US children. The Centers for Disease Control (CDC) estimates that 3 to 4 million American preschool children have blood lead levels above 10 Fg/dl.l Blood lead levels in this range in young children have been shown to cause depression of neurological and psychological function,24 effects that appear to be permanent. o Asbestos. Asbestos in the work environment has created an absolute disaster.5 Although the hazards of asbestos were known in the 1930s, billions of tons ofasbestos were used in the United States from then until the 1980s. Millions of workers were exposed, and tens of thousands of homes, schools, and other public buildings were contaminated.6 Bytheyear 2000, an estimated 300 000 American workers will have died of the diseases caused by asbestos: principally, asbestosis, lung cancer, and malignant mesothelioma. It is anticipated that deaths will continue to occur well into the 21st century.7 With the overseas spread of asbestos-contaiing building materials, the pan-
demic is now extending to the Third World. * Occupational disease. Studies conducted in New York State have estimated that 50 000 to 70 000 US workers die each year of chronic occupational disease resulting from past exposures to toxic substances.8 These diseases encompass a broad range: besides the lung cancer and mesothelioma of asbestos workers,5 they include cancer ofthe bladder in dye workers9; leukemia and lymphoma in workers exposed to benzene10 and ionizing radiation11; chronic bronchitis in workers exposed to dusts12; disorders of the nervous system (including possibly dementia, Parkinson's disease, and motoneuron disease) in workers exposed to pesticides, solvents, and certain other neurotoxins13; renal failure in workers exposed to lead14; and cardiovascular disease in workers exposed to carbon monoxide15 and carbon disulfide.16 A major impediment to assessing the contribution of synthetic chemicals to the causation of cancer and other workplace diseases is the fact that only 20% of the Philip J. Landrgan is professor and chair in the Department of Community Medicine, Mount Sinai School of Medicine, New York, NY. Requests for reprints should be sent to Philip J. Landrigan, MD, MSc, Department of Community Medicine, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10009.
American Journal of Public Health 941
Pubc HedM PdUlly Fon
approximately 60 000 industrial chemicals in commerce have ever been tested for their carcnogenic, neurotoxic, immunotoxic, or other toxic potential.17 Millions of American workers are therefore exposed to chemical agents of unimown toxicity. * ChiWhood asthma. Among chiidrenworldwide, morbidity, disability, and mortality from asthma are increasing.18 In 1987, an estimated 585 American children died of asthma,19 and 150 000 were hospitalized.20 In American inner cities, asthma is the leading cause of hospital admissions for chlldren 5 to 15 years old, and rates are highest among African-American and Hispanic children. The causes of recent increases in asthma are not known. However, these increases coincide with substantial rises in summertime peak levels of atmospheric ozone and with year-round increases in oxides of nitrogen (NOx), two pollutants derived principally from automotive emissions.21 Recent epidemiologic data suggest that ozone and NOx have contrbuted to the increasing incidence and prevalence of childhood asthma.22 * Cancer. Between 1950 and 1988, for US Whites, age-adjusted incidence for all forms of cancer rose by 43.5% and ageadjusted cancer mortality increased by 2.9%.23 These overall increases in incidence occurred despite declines in cancer mortality among younger persons as a result of remarkable improvements in treatment.U.Z.26 Explanations for these increases do not exist. They do not appear to be attnbutable solely to changes in cigarette smoking.27 Although smoking remains the most important of the known preventable causes of cancer (accounting for as much as 40%o of all human malignancy), mortality rates for lung cancer as well as for cardiovascular disease have actually begun to decline among men in the United Kingdom and United States, due principally to decreases in cigarette consumption.2S,N Several ofthe cancers forwhich increased incidence (at all ages and in mortality above age 55) have been noted in a number of industrialized nations are not known to be related to smokig; these include multiple myeloma, brain cancer, cancer ofthe breast, testicular cancer, and
non-Hodgkin's lymphoma.27 Changes in competing
causes of death,28 improved access to health care, and alterations in diagnostic technology29 also do not appear to account entirely for the observed changes in cancer incidence and mortality. The possible contribution
942 American Journal of Public Health
to recent cancer trends of the substantial worldwide increases in chemical production that have occurred since World War II (and the resulting increases in human exposure to toxic chemicals in the environment) has not been adequately assessed.17 It needs to be systematically evaluated.30 The tragedy of environmental diseases is that they are highly preventable. Toxic environmental diseases arise as a direct consequence of human activity and can therefore, in theory, be prevented throgh modification of that activity. The control of toxic disease does not require changing the behavior of millions of addicted or habituated individuals, only the containment of common sources of exposure to chemical toxins. Such containment is demonstrably achievable through legislation, regulation, and other well-understood mechanisms of communal action. Children must be protected from exposure to lead. Automotive and industrial atmospheric emissions must be curbed. Dangerous chemicals in the work environment must be replaced with safe substitutes; hazardous processes must be enclosed and ventilated; and workers and consumers must be provided with knowledge, training, and protective equipment.31 Premarket testing of new chemicals and processes constitutes a very effective approach to the prevention of toxic disease. In this issue of theJownal Sir Richard Doll considers the role of the environment in the etiology of human disease.32 He correctly recognizes the pervasive influence of the environment-defined broadly as the conditions under which people live-on human health and the causation of disease. He speaks compellingly of the need to combat the use of tobacco and to reduce excess consumption of alcohol and fatty food. These are areas of public health in which Doll has contributed enormously and is a muchhonored pioneer. Doll also speaks of the perils of unchecked population growth and of humnkind's changes to the global climate. His points here are well taken, and his counsel deserves close heed. However, Doll does not adequately address the role of chemical toxins in the causation of human disease, therefore overlooking important opportunities for disease prevention. In my view, the following points in his analysis need to be set
right. Doll speaks of "the few cases of mesothelioma"32(P") that have resulted from the dispersal of asbestos. This com-
ment is not consistent with epidemiological data that already have been accumulated, nor does it jibe with projections of future mortality.7 It is anticipated that, by the end of this century, hundreds of thousands of workers in the United States and around the world will have died of asbestos-related diseases, mesothelioma prominent among them. This issue is far from
trivial. Doll asserts that recently observed increases in mortalityfrom cancer "can be accounted for in all industrialized countries by the spread of cigarette smoking."32(p936) However, this does not appear to be the whole story, because it does not account for the increases noted earlier in incidence and mortality for some cancers that are not known to be related to smoking.27.28 His comment also does not consider the possible etiologic significance ofwidespread population exposure, since World War II, to tens of thousands of synthetic chemicals of unknown and untested carCinogenic potential.17 Doll states that the contamination of foods with toxic pesticide residues is not an issue of health concern. He refers to a recent commentary by Ames and Gold33 in which the authors claim that naturally occurring pesticide residues pose by far the greater threat. However, this analysis appears to be premature. Of particular concern here are recent data from the US Environental Protection Agency (EPA) showing that infnts and young children are permitted to have dietary exposures to potentially crcingeni and neuotoxc pesticides in amounts that exceed published standards by a factor of more than 1000.M4 This iswe requires further assessment. Finally, Doll's opinion that modern industry has given rise to "the dispersal of small amounts of potenfially toxic chemicals"32(94) considerably understates the sad reality. The EPA's Toxic Release Inventory reports that in 1989 American industries released 3.56 billion pounds of chemical agents into the environment.35 These releases include carcnogens, neurotoxins, reproductive toxins, and thousands of chemicals of unknown toxicity. Moreover, releases in Europe, Japan, and the developing nations are likely to be at least as large as the United States', given the past 20 years' experience in Seveso, Minimata Bay, Chenobyl, and Bhopal. Public health workers and the makers of public policy must recognize that toxic chemicals in the environment are important, widespread, proven causes ofhuman disease. Eachyear preventable exposures to chemical toxins sicken and kill thou-
July 1992, Vol. 82, No. 7
Public Health Policy Fonrm
sands of persons of all ages in the United States and around the world. These hazards must be confronted. They cannot be wished away.36 Reduction of exposures to chemical toxins will prevent thousands of deaths and will improve the quality of hundreds of thousands of lives. Reuel Stallones, in whose honor Doll spoke at the University of Texas, fully recognized the importance of toxic chemicals in the causation of disease. In 1979, in an analysis of cancer in the work environment, Stallones and Downs calculated that toxic factors encountered at work were responsible for at least 20% of all human cancer.37 From firsthand knowledge, Stallones described the asbestos pandemic as "horrifying" and as a "public health catastrophe." He concluded his report by arguing "that reduction of exposures to carcinogens in the course of employment can certainly be expected to effect major reductions in the frequency of occurrence of cancer. [It] is one of the most promising applications of preventive medicine."37 0
References 1.
PreventingLeadPoisonigin Young Chiddren. Atlanta, Ga: Centers for Disease
Control; 1991. 2. Bellinger D, Leviton A, Waternaux C, Needleman HL, Rabinowitz M. Longitudinal analyses of prenatal and post-natal lead exposure and early cognitive development. New Engl J Med 1987;316:10371043. 3. Dietrich KN, Krafft KM, Bornschein RL, et al. Low-level fetal lead exposure effect on neurobehavioral development in early
infancy. Pediatrics. 1987;80:721-730.
4. McMichael AJ, Baghurst PA, Wigg NR, Vimpani GV, Robertson EF, Roberts RJ. Port Pirie cohort study: environmental exposure to lead and children's abilities at the age of four years. New EngIJMedL 1988;
319:468-475. 5. Selikoff IJ, Hammond EC, Churg J. Asbestos exposure, smoking and neoplasia. JAMA. 1968;204:100-112. 6. PJ Landrigan, H Kazemi, L Selikoff, eds. The third wave of asbestos disease: exposure to asbestos in place. Public Health Control.Ann NYAcad Sci 1991;643. Special issue. 7. Nicholson WJ, Perkel G, Selikoff U. Oc-
July 1992, Vol. 82, No. 7
cupational exposure to asbestos: populations at risk and projected mortality1980-2030.AmJIndMedL 1982;3:259-311. 8. Landrigan PJ, Markowitz S. Current magnitude of occupational disease in the United States: estimates from New York State. Ann NYAcad ScL 1989;572:27-45. 9. Rehn L. Blasengeschwuelste bei Fuchssinarbeitern. Arch Jiir Klinische Chi'wgie. 1985;50:588-600. 10. Rinsky RA, Smith AB, Hornung R, Filloon TG, Young RJ, Landrigan PJ. Benzene and leukemia-an epidemiologic risk assessment. New Engl J Med 1987;316:1044-
1050. 11. March HC. Leukemia in radiologists. Ra-
diology. 1944;43:275-278.
12. Parkes WR. Occupational Lung Disordes. 2nd ed. London: Butterworths; 1982. 13. National Research Council. Environmental neurota2cology. Washington, DC: National Academy Press; 1992. 14. Landrigan PJ, Goyer RA, Clarkson TW, Sandler DP, Smith TH, Thun MJ, Wedeen RP. The work-relatedness of renal disease. Summary of the working group on renal disease. Arch Environ Health. 1984;39: 225-230. 15. Kleinman MT, Davidson DM, Vandagriff RB, Caiozzo VJ, Whittenberger JL. Effects of short-term exposure to carbon monoxide in subjects with coronary artery disease. Arch Environ Health. 1989;44: 361-369. 16. Hemberg S, Partanen C, Nordman CH, Sumari P. Coronary heart disease among workers exposed to carbon disulphide. BrJ Ind Med. 1970;27:313-325. 17. National Research Council. Toxicity Testing-Strategies to Detennine Needs and Pnorities. Washington, DC: National Academy Press; 1984. 18. Sly RM. Increases in deaths from asthma.
AmAllegy. 1984;53:20. 19. National Center for Health Statistics. Vital Statistics ofthe United States. 1987. Washington, DC: US Government Printing Office; 1989; 11, part B. US DHHS publication PHS 89-1102. 20. Graves EJ. National Hospital Discharge Swvey:Anual Swmnmary, 1987. Vital and health statistics; series 13, no. 99. Hyattsville, Md: National Center for Health Statistics; 1989. US DHHS publication PHS 89-1760. 21. National air quality emissions trnds repo??s. Research Triangle Park, NC: US Environmental Protection Agency; 1990. EPA report 450/4-90.002. 22. Lippmann M. Health effects of ozone: a critical review. JAirPollut ControlAssoc.
1989;39:672-695. 23. Ries LA, Hankey BF, Miller BA, Hartman AM, Edwards BK. Cancer Statistics Review 1973-78. Washington, DC: US Dept of Health and Human Services; 1991. DHHS publication NIH 91-2789. 24. Doll R. Progress against cancer: an epidemiologic assessment. Am J Epidemiol.
1991;134:675-688.
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