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#411 - Birth Defects -- Part 2: Why Birth Defects Will Continue To Rise, 12-Oct-1994

Last week we saw that 29 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 REHW
#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; new york times; los angeles times; 20/20; tv;
journalism; news media;