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---October 13, 1994; revised October 16, 1994---
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Last week we saw that 30 types of birth defects are increasing steadily in the United States, some increasingly rapidly, others more slowly. Some of these increases are due to better diagnosis; however, many of the increases are real. This week we examine 10 reasons why birth defects are rising and will almost certainly continue to rise.

There is abundant scientific evidence that birth defects in laboratory animals and in humans have occurred as a result of exposure to five classes of pollutants: radiation; [1-2] pesticides; [3-9] metals (including mercury, cadmium, lead, and others); [10-14] solvents; [15-23] and dioxin-like chemicals including PCBs [polychlorinated biphenyls]. [24-27] From studies of pharmaceutical drugs found to cause birth defects, it is certain that other chemicals are teratogens (causing birth defects) as well. [28]

Because municipal landfills and toxic waste dumps are laced with pesticides, toxic metals, solvents, dioxin-like compounds, and sometimes even radioactive materials, at least seven studies have now reported finding unusually high numbers of birth defects in children born to parents residing near dumps. [29-35]

** The main reason why birth defects will continue to increase is that more than 500 new chemicals are introduced into commercial use each year. There will never be enough money available for independent scientists to conduct definitive (or even adequate) studies of all these chemicals to see if they cause birth defects in laboratory animals. For ethical reasons, chemicals cannot be tested in any organized way on humans (though, contrarily, most Americans don't object to the experimental exposures that occur routinely in the workplace, and in the home via consumer products). In addition to 500 new chemicals appearing each year, more than 50,000 chemicals already in commercial use have never been tested for their ability to cause birth defects.

** The prevailing American philosophy is that chemicals are innocent until proven guilty. Therefore, when new chemicals are released into the environment, the burden of proof rests on the general public to show that damage has occurred before scientific studies are undertaken to describe the damage in detail. This philosophy guarantees that people MUST BE HARMED before study can begin.

** Scientific studies can take years to complete. Even when an effect is grossly obvious, pinning down the cause can take a decade or longer. For example, mercury poisoned dozens of babies in the womb at Minamata, Japan, in 1955 but scientists did not clearly establish the cause for 15 to 18 years. [11]

** After research scientists are convinced, there is a long delay before the general public learns the facts, if it ever does. (As an anti-environmental viewpoint comes to dominate major media, such as the NEW YORK TIMES, LOS ANGELES TIMES, and 20/20 on ABC-TV, in many cases new information simply never gets widely disseminated).

** Furthermore, the results of studies may not be clear-cut, for many reasons: it is difficult to measure exposure so usually a "surrogate" for exposure is used, such as place of residence, or occupation; many birth defect studies rely upon mothers recalling what chemical exposures occurred during their early months of pregnancy and all such recollections are dubious; therefore it is difficult to absolutely rule out many possible causes of an observed effect.

** A society that demands scientific certainty before it will restrict the use of suspected teratogens, guarantees that the rate of birth defects will continue rising. Scientific certainty about anything involving humans is, and will remain, elusive and rare.

** Given the philosophical climate, public health officials are reluctant to raise an alarm on less-than-100%-certain data. As a practical matter, an official will get in much more trouble for raising a false alarm about a suspected chemical than for making the opposite error (which allows birth defects to continue). In the present philosophical climate (requiring scientific certainty), even well-justified alarm based on less-than-certain data draws an angry response from powerful monied interests. On the other hand, allowing birth defects to continue will only affect one family at a time. Individual, unorganized victims do not threaten a public health official's job security. [36]

** When studies reveal that a particular chemical probably causes birth defects, the producers and users of the chemical typically conduct a lengthy campaign to deny and obscure what is known. For example, the lead industry has known for at least 100 years that lead causes reproductive and developmental disorders in humans. But starting in 1925 medical doctors hired by the lead industry argued that lead occurs naturally in the human body and, therefore, the dangers of lead in gasoline were not worth worrying about, much less studying. This strategy was persuasive to the public health community for 40 years. [37]

** The public health community relies almost exclusively on a decision-making technique that cannot take into account multiple exposures and cumulative effects, a technique called "risk assessment." (See RHWN #393, #394, #395.) At its best, risk assessment can provide a ballpark guesstimate of a few of the many hazards created by a single toxic chemical. However in real life we are all exposed to multiple chemicals all the time, and risk assessment cannot account for cumulative effects and multiple interactions. Heavy reliance upon such an unrealistic tool for decision-making leads to decisions that harm public health.

** Finally, even the knowledgeable environmental community fails to fully adopt the clear requirements of a public health policy based on prevention of disease: persistent toxic pollutants must be banned. Recently when Environmental Defense Fund (EDF) and Physicians for Social Responsibility (PSR), followed separately by Greenpeace, published their recommendations for public policy on dioxin, they all argued that U.S. dioxin policy should be modeled on U.S Environmental Protection Agency's lead policy. [38] (Greenpeace set a goal of zero dioxins, but recommended the lead policy as a way to get there.) Over the last 20 years EPA's lead policy has forced a mere 8% reduction in total U.S. "consumption" of lead. At this rate it will take 3500 years for lead "consumption" to fall below 1000 pounds per year and thus disappear as a public health problem.
                                                                         --Peter Montague
[1] Niel Wald, "Evaluation of Human Exposure Data," in K.Z. Morgan and J.E. Turner, editors, PRINCIPLES OF RADIATION PROTECTION; A TEXTBOOK OF HEALTH PHYSICS (Huntington, N.Y.: Robert E. Krieger Publishing, 1973), pgs. 448-496.

[2] John W. Gofman, RADIATION AND HUMAN HEALTH (San Francisco: Sierra Club, 1981); see chapter 21.

[3] Anne Kricker and others, "Women and the environment: a study of congenital limb anomalies," COMMUNITY HEALTH STUDIES Vol. 10, No. 1 (1986), pgs. 1-11.

[4] M. Restrepo and others, "Prevalence of adverse reproductive outcomes in a population occupationally exposed to pesticides in Colombia," SCANDINAVIAN JOURNAL OF WORK, ENVIRONMENT AND HEALTH Vol. 16 (1990), pgs. 232-238.

[5] P. Rita and others, "Monitoring of Workers Occupationally Exposed to Pesticides in Grape Gardens of Andhra Pradesh," ENVIRONMENTAL RESEARCH Vol. 44 (1987), pgs. 1-5.

[6] David A. Schwartz and others, "Congenital Limb Reduction Defects in the Agricultural Setting," AMERICAN JOURNAL OF PUBLIC HEALTH Vol. 78, No. 6 (June 1988), pgs. 654-658.

[7] D.A. Schwartz and others, "Parental occupation and birth outcomes in an agricultural community," SCANDINAVIAN JOURNAL OF WORK, ENVIRONMENT AND HEALTH Vol. 12, No. 1 (February 1986), pgs. 51-54.

[8] T.E. Taha and R.H. Gray, "Agricultural pesticide exposure and perinatal mortality in central Sudan," BULLETIN OF THE WORLD HEALTH ORGANIZATION Vol. 71 (1993), pgs. 317-321.

[9] Jun Zhang and others, "Occupational Hazards and Pregnancy Outcomes," AMERICAN JOURNAL OF INDUSTRIAL MEDICINE Vol. 21 (1992), pgs. 397-408.

[10] Thomas W. Clarkson and others, "Reproductive and developmental toxicity of metals," SCANDINAVIAN JOURNAL OF WORK, ENVIRONMENT AND HEALTH Vol. 11 (1985), pgs. 145-154.

[11] Masazumi Harada, "Congenital Minamata Disease: Intrauterine Methylmercury Poisoning," TERATOLOGY Vol. 18 (1978), pgs. 285-288.

[12] H.A. Ragan and T.J. Mast, "Cadmium Inhalation and Male Reproductive Toxicity," REVIEWS OF ENVIRONMENTAL CONTAMINATION AND TOXICOLOGY Vol. 114 (1990), pgs. 1-22.

[13] Petter Kristensen and others, "Perinatal Outcome among Children of Men Exposed to Lead and Organic Solvents in the Printing Industry," AMERICAN JOURNAL OF EPIDEMIOLOGY Vol. 137, No. 2 (1993), pgs. 134-144.

[14] D.G. Wibberley and others, "Lead levels in human placentae from normal and malformed births," JOURNAL OF MEDICAL GENETICS, Vol. 14, No. 5 (October 1977), pgs. 339-345.

[15] Jorma Tikkanen and Ollie P. Heinonen, "Cardiovascular Malformations and Organic Solvent Exposure During Pregnancy in Finland," AMERICAN JOURNAL OF INDUSTRIAL MEDICINE Vol. 14 (1988), pgs. 1-8.

[16] Gary M. Shaw, "Maternal Workplace Exposures to Organic Solvents and Congenital Cardiac Anomalies," JOURNAL OF OCCUPATIONAL MEDICINE AND TOXICOLOGY, Vol. 1, No. 4 (1992), pgs. 371-376.

[17] Andrew F. Olshan and others, "Paternal Occupation and Congenital Anomalies in Offspring," AMERICAN JOURNAL OF INDUSTRIAL MEDICINE Vol. 20 (October 1991), pgs. 447-475.

[18] C. Loffredo and others, "Organic solvents and cardiovascular malformations in the Baltimore-Washington Infant Study [abstract]," TERATOLOGY Vol. 43 (May 1991), pg. 450. [19] Evert Hansson and others, "Pregnancy outcome in women working in laboratories in some of the pharmaceutical industries in Sweden," SCANDINAVIAN JOURNAL OF WORK, ENVIRONMENT AND HEALTH Vol. 6 (1980), pgs. 131-134.

[20] Stanley J. Goldberg and others, "An Association of Human Congenital Cardiac Malformations and Drinking Water Contaminants," JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY Vol. 16, No. 1 (July, 1990), pgs. 155-164.

[21] Anders Ericson and others, "Delivery Outcome of Women Working in Laboratories During Pregnancy," ARCHIVES OF ENVIRONMENTAL HEALTH Vol. 39, No. 1 (1984), pgs. 5-10.

[22] Sylvaine Cordier and others, "Maternal occupational exposure and congenital malformations," SCANDINAVIAN JOURNAL OF WORK, ENVIRONMENT AND HEALTH Vol. 18, No. 1 (February 1992), pgs. 11-17.

[23] Urban Blomqvist and others, "Delivery outcome for women working in the pulp and paper industry," SCANDINAVIAN JOURNAL OF WORK, ENVIRONMENT AND HEALTH Vol. 7, No. 2 (1981), pgs. 114-118.

[24] Hugh A. Tilson and others, "Polychlorinated Biphenyls and the Developing Nervous System: Cross-Species Comparisons," NEUROTOXICOLOGY AND TERATOLOGY Vol. 12 (1990), pgs. 239-248.

[25] Joseph L. Jacobson and others, "Effects of in utero exposure to polychlorinated biphenyls and related contaminants on cognitive functioning in young children," JOURNAL OF PEDIATRICS Vol. 116 (January, 1990), pgs. 38-45.

[26] Joseph L. Jacobson and others, "Effects of Exposure to PCBs and Related Compounds on Growth and Activity in Children," NEUROTOXICOLOGY AND TERATOLOGY Vol. 12 (1990), pgs. 319-326.

[27] Richard A. Albanese, UNITED STATES AIR FORCE PERSONNEL AND EXPOSURE TO HERBICIDE ORANGE, INTERIM REPORT FOR PERIOD MARCH 1984-FEBRUARY 1988 (United States Air Force: Brooks Air Force Base, Texas, Feb., 1988).

[28] Muin J. Khoury, "Epidemiology of Birth Defects," EPIDEMIOLOGIC REVIEWS Vol. 11 (1989), pgs. 244-248.

[29] L. Goulet and M. Goldberg, "Reproductive Outcomes among Women Living Near a Sanitary Landfill Site in Montreal, Quebec, Canada, 1979-1989 [abstract]," AMERICAN JOURNAL OF EPIDEMIOLOGY Vol. 138, No. 8 (1993), pg. 587.

[30] G. Shaw and others, "Congenital Malformations and Birthweight in Areas with Potential Environmental Contamination," ARCHIVES OF ENVIRONMENTAL HEALTH Vol. 47, No. 2 (March/April 1992), pgs. 147-154.

[31] Agency for Toxic Substances and Disease Registry, U.S. Public Health Service, U.S. Department of Health and Human Services, CALIFORNIA: BIRTH DEFECTS STUDY (Atlanta, Ga.: Agency for Toxic Substances and Disease Registry, 1990).

[32] G. Reza Najem and Lisa K. Voyce, "Health Effects of a Thorium Waste Disposal Site," AMERICAN JOURNAL OF PUBLIC HEALTH Vol. 80 (April 1990), pgs. 478-480.

[33] Nicholas J. Vianna and Adele K. Polan, "Incidence of Low Birth Weight Among Love Canal Residents," SCIENCE Vol. 226, No. 4679 (December 7, 1984), pgs. 1217-1219.

[34] Lynn R. Goldman and others, "Low Birth Weight, Prematurity and Birth Defects in Children Living Near the Hazardous Waste Site, Love Canal." HAZARDOUS WASTE & HAZARDOUS MATERIALS Vol. 2 No. 2 (1985), pgs. 209-223.

[35] Lawrence Budnick, and others. "Cancer and Birth Defects Near the Drake Superfund Site, Pennsylvania," ARCHIVES OF ENVIRONMENTAL HEALTH, Vol. 39, No. 6 (November/December, 1984), pgs. 409-413.

[36] David Ozonoff and Leslie I. Boden, "Truth and Consequences: Health Agency Responses to Environmental Health Problems," SCIENCE, TECHNOLOGY & HUMAN VALUES Vol. 12 Nos. 3 & 4 (Summer/Fall 1987), pgs. 70-77. In statistical terms, public health officials will get in less trouble for making a Type I error than a Type II error. Therefore, experiments are often designed to favor avoidance of Type I errors rather than Type II errors.

[37] Alan Loeb, "The First Federal Environmental Review: Its Long-Term Consequences," INTERNATIONAL SOCIETY OF EXPOSURE ANALYSIS NEWSLETTER (Fall 1993), pg. 3.

[38] Julia Moore and others, PUTTING THE LID ON DIOXINS (Washington, D.C.: Physicians for Social Responsibility, 1994); Joe Thornton, ACHIEVING ZERO DIOXIN (Washington, D.C.: Greenpeace, 1994). PSR and EDF failed to call for real prevention; instead they advocated that the major source of dioxin emissions (incinerators) be operated "at optimal conditions" rather than be shut down or phased out.

Descriptor terms: birth defects; congenital anomalies; radiation; pesticides; mercury; lead; cadmium; pcbs; dioxin; landfilling; minamata; japan; ny times; los angeles times; 20/20; tv; television; journalism; news media;

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