#411: Birth Defects -- Part 2: Why Birth Defects Will Continue To Rise

=======================Electronic Edition========================
RACHEL'S ENVIRONMENT & HEALTH WEEKLY #411
---October 13, 1994; revised October 16, 1994---
News and resources for environmental justice.
==========
Environmental Research Foundation
P.O. Box 5036, Annapolis, MD 21403
Fax (410) 263-8944; Internet: erf@igc.apc.org
==========
RACHEL-4CM = DIOXIN FOCUSED DIRECTORY Remote Access Chemical Hazards Electronic Library. Dioxinnz.com
========================Original Source========================

Last week#410  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;

#410: Birth Defects -- Part 1

=======================Electronic Edition========================
RACHEL'S ENVIRONMENT & HEALTH WEEKLY #410
---October 6, 1994---
News and resources for environmental justice.
==========
Environmental Research Foundation
P.O. Box 5036, Annapolis, MD 21403
Fax (410) 263-8944; Internet: erf@igc.apc.org
==========
RACHEL-4CM = DIOXIN FOCUSED DIRECTORY Remote Access Chemical Hazards Electronic Library. Dioxinnz.com
========================Original Source========================

The Birth Defects Monitoring Program (BDMP) is a U.S. government effort to monitor birth defects (congenital malformations) using data collected when newborn infants are discharged from the hospital. [1] The BDMP was initiated by the federal Centers for Disease Control (CDC) in 1974. The current BDMP database includes information on roughly 15 million births that have occurred at 1200 predominantly mid-sized community hospitals in the U.S. during the past 20 years.

The BDMP database is not comprehensive (it does not include information on every birth that occurs in the U.S.). Neither does it represent a randomly-selected sample of all U.S. births; therefore data from the BDMP cannot be considered representative of the entire "universe" of all U.S. newborns. In 1987 the BDMP received information on 15% of all U.S. births, which gives an idea of how comprehensive the coverage is. Because the data are mostly from mid-sized hospitals, we might expect that some of the largest hospitals in the largest cities are under-represented. Nevertheless, as the CDC says, the BDMP "represents the largest single set of uniformly collected and coded discharge data on congenital malformations in the United States." It is simply the best information available on birth defects in the U.S.

CDC says that the BDMP "functions primarily as an early warning system; however it can be useful also for correlating incidence [occurrence] patterns with such trends as the temporal [time-related] and geographic distribution of drugs, chemicals, and other possible human teratogens." A teratogen (from the Greek words meaning "monster producing") is anything that causes birth defects. Examples of teratogens are diseases such as German measles; infections; inherited genetic defects; radiation; and certain chemicals.

In 1990, researchers looked for trends in the BDMP database, examining records for 38 types of birth defects from 1979-80 through 1986-87. During this 7-year period, of the 38 types of birth defects, 29 increased; 2 decreased; and 7 remained stable (meaning they changed less than 2% per year during the 7-year period.)

Table 1 shows the annual percent change for 30 types of birth defects. All of them increased during the 7-year period (though some increased at a rate less than 2% per year, and are thus classified as "stable" by the CDC).

Table 1 contains 3 columns of numbers. The first two columns show the actual number of birth defects per 10,000 births; the first column shows data for the earlier period, 1979-80; the second column shows the later period, 1986-87. The third column shows the yearly percentage increase during the 7-year period.

Some of these increases are explained by better health care and better diagnosis. For example, some of the heart defects listed in Table 1 are so serious that an infant might not have survived such a defect 10 years ago but might survive it today. Likewise, some of the heart defects might be revealed by high-tech medical diagnostic machines today, whereas they might have gone unnoticed 10 years ago.

However, many of the increases in birth defects in Table 1 cannot be explained by better health care or better diagnosis. If a child were born 10 years ago with the iris missing from one or both of its eyes, chances are good that the mother or her doctor or a nurse would see it. (The iris is the part of the eye that makes blue eyes blue and brown eyes brown.) So the 5.2% ANNUAL INCREASE in "aniridia" (absence of an iris) is very likely a real increase.

The same can be said for birth defects of the central nervous system, facial clefts, musculoskeletal defects and some of the gastrointestinal and genitourinary defects. Most of these defects are so obvious that they would have been noticed as easily 10 years ago as today. Therefore, increases in these defects are very likely real increases.

Some of the increases shown in Table 1 are surprisingly large. For example, coloboma of the eye increased 9.6% each year during the 7-year period; this means the occurrence of this defect doubled during the study period. (Coloboma of the eye means a wedge-shaped piece is missing from the iris, or some other part of the eye is missing.) Other eye disorders (congenital cataract, for example) are increasing about 5% each year, thus doubling every 14 years. (The relationship of annually-increasing quantities to the doubling time was detailed in RHWN #197 and #199.)

Are most birth defects caused by the parents' genetic characteristics, or by something in the environment?

In July of this year an important study of birth defects in Norway appeared in the NEW ENGLAND JOURNAL OF MEDICINE. [2] It indicated that environmental factors may be more important than previously thought.

Norway has maintained a Medical Birth Registry since 1967; the registry now contains data on 1.5 million births. Norwegian and American researchers examined records of 371,933 women who had given birth to first and second children in Norway between 1967 and 1989. For the 9192 women whose first infant had a birth defect, they examined the risk of similar or dissimilar effects in the second infant. And they examined the risk of a birth defect in the second child among mothers who lived in the same municipality during both pregnancies vs. mothers who moved to a new municipality before the second child was born. (The control group was the 362,741 women whose first infant did not have a birth defect.)

The researchers found that 2.5% of all infants born in Norway have a birth defect. Examining 23 different kinds of birth defects, they found that in every category, mothers whose first infant had a defect were more likely to have a second infant with a defect, as would be expected if birth defects are genetic in origin. What was "surprising" to the researchers was that women who moved to a new city between pregnancies were only half as likely to have a second child with a birth defect. Mothers whose first child had a defect were 11.6 times as likely to have a second child with a defect (compared to mothers whose first child did not have a defect), but if a mother moved to a new municipality between pregnancies she was only 5.1 times as likely to have a second child with a defect. The researchers concluded, "...[W]e find strong, if indirect, evidence... suggesting that important environmental teratogens have yet to be discovered."

 --Peter Montague

===============

[1] Larry D. Edmonds, "Temporal Trends in the Prevalence of Congenital Malformations at Birth Based on the Birth Defects Monitoring Program, United States, 1979-1987," MORBIDITY AND MORTALITY WEEKLY REPORT, CDC SURVEILLANCE SUMMARIES Vol. 39, No. SS-4 (Dec., 1990), pgs. 19-23.

[2] Rolv Terje Lie and others, "A Population-Based Study of the Risk of Recurrence of Birth Defects," NEW ENGLAND JOURNAL OF MEDICINE Vol. 331, No. 1 (July 7, 1994), pgs. 1-4.

==========================================================
TABLE 1
Birth Defects: Annual Percent Change in Occurrence During 7-year
Period, 1979-80 to 1986-87, United States
==========================================================

DEFECT TYPE	Number of defects per 10,000 births		Annual Percent change in occurrence, 1979-80 to 1986-87
	------------------------
	1979-80	1986-87
CENTRAL NERVOUS SYSTEM
Hydrocephalus without spina bifida (fluid in the skull)	4.34	5.84	4.3%
Encephalocele (gap in the skull)	1.10	1.16	0.8%
Microcephalus (small head)	2.12	2.61	3.0%
EYES
Anophthalmos (absence of eyes)	0.57	0.68	2.6%
Congenital cataract (eye cataracts at birth)	0.71	1.02	5.3%
Coloboma of eye (eye parts missing)	0.21	0.40	9.6%
Aniridia (absence of the iris)	0.07	0.10	5.2%
HEART
Common truncus (undeveloped main arteries)	0.19	0.40	11.2%
Transposition of great arteries (reversal of main arteries)	0.87	1.45	7.6%
Tetralogy of Fallot (4 common defects simultaneously)	0.73	1.82	13.9%
Ventricular septal defect (opening between lower chambers)	11.34	20.49	8.8%
Atrial septal defect (opening between upper chambers)	1.16	3.69	18.0%
Endocardial cushion defect	0.34	0.95	15.8%
Pulmonary valve atresia and stenosis (obstructed blood flow)	0.58	3.44	29.0%
Tricuspid valve atresia and stenosis (obstructed blood flow)	0.16	0.36	12.3%
Aortic valve stenosis and atresia (obstructed blood flow)	0.22	0.79	20.0%
Hypoplastic left heart syndrome (undeveloped left side)	0.56	1.25	12.2%
Patent ductus arteriosus (pulmonary artery open to aorta)	17.87	35.43	10.3%
Coarctation of aorta (constriction of the aorta)	0.74	1.15	6.5%
Pulmonary artery anomaly	1.12	2.66	13.2%
Lung agenesis and hypoplasia (undeveloped lungs)	1.66	3.84	12.7%
FACIAL CLEFTS
Cleft palate without cleft lip	5.05	5.33	0.8%
Cleft lip	7.76	9.35	2.7%
GASTROINTESTINAL
Tracheoesophageal anomalies (upper airway problems)	1.86	2.49	4.3%
Rectal and intestinal atresia (blockage)	3.23	3.80	2.3%
GENITOURINARY
Renal agenesis and hypoplasia (one kidney or small kidneys)	1.23	2.34	9.6%
Bladder exstrophy (gap in abdomen, revealing bladder)	0.29	0.33	1.9%
MUSCULOSKELETAL
Reduction deformity, upper limbs (arms deformed or missing)	1.53	1.58	0.5%
Reduction deformity, lower limbs (legs deformed or missing)	0.78	0.83	0.9%
Congenital arthrogryposis (contracted or bent limbs)	1.33	1.93	5.5%

===========
Source: Larry D. Edmonds and others, "Temporal Trends in the Prevalence of Congenital Malformations at Birth Based on the Birth Defects Monitoring Program, United States, 1979-1987," MORBIDITY AND MORTALITY WEEKLY REPORT, CDC SURVEILLANCE SUMMARIES Vol. 39, No. SS-4 (December, 1990), pg. 22.
=========================================================
Descriptor terms: birth defects monitoring program; centers for disease control; cdc; bdmp; new england journal of medicine; norway; hydrocephalus; encephalocele; microcephalus; anophthalmos; congenital cataract; coloboma of the eye; aniridia; common truncus; heart; head; brain; tetralogy of fallot; ventricular septal defect; atrial septal defect; endocardial cushion defect; pulmonary valve atresia and stenosis; tricuspid valve atresia and stenosis; aortic valve stenosis and atresia; hypoplastic left heart syndrome; patent ductus arteriosus; coarctation of aorta; pulmonary artery anomaly; lung agenesis and hypoplasia; cleft palate; tracheoesophageal anomalies; rectal and intestinal atresia; renal agenesis and hypoplasia; reduction deformity; congenital arthrogryposis;

#412: A Turnabout for Cancer Policy?

=======================Electronic Edition========================
RACHEL'S ENVIRONMENT & HEALTH WEEKLY #412
---October 20, 1994---
News and resources for environmental justice.
==========
Environmental Research Foundation
P.O. Box 5036, Annapolis, MD 21403
Fax (410) 263-8944; Internet: erf@igc.apc.org
==========
RACHEL-4CM = DIOXIN FOCUSED DIRECTORY Remote Access Chemical Hazards Electronic Library. Dioxinnz.com =======================Original Source========================

The National Cancer Advisory Board (NCAB), an official body of the National Cancer Institute, last month issued a stinging indictment of the nation's cancer programs. Furthermore, for the first time in memory the Board said industrial chemicals, environmental chemicals that mimic hormones, and pesticides need to be investigated as causes of cancer. [1]

In 1971 the U.S. Congress declared "War on Cancer," but year after year many cancers have steadily increased. See Table I. In a blunt assessment of the failed War on Cancer, the NCAB last month said, "The alarming statistics are that one in three people in this country will be diagnosed with cancer during their lifetime; every minute, another person in the United States dies of cancer; in 1994, 1.2 million new cancer cases will add to the more than 8 million people in this country alive today who have already been diagnosed; and within five years, cancer will surpass heart disease as the leading cause of death," the NCAB said. [pg. 9]

"The great strides made in understanding the disease still pale in comparison to the problem. It is disturbing that since 1971 the overall incidence of cancer has increased 18 percent, and the mortality rate has grown by 7 percent. Tobacco use and inadequate health care access account for much of this alarming and wholly unacceptable increase," the NCAB said. [pg. 10]

"While individuals have a responsibility to change high-risk behavior, government and society have responsibilities to identify and prevent workplace and environmental hazards, restrict advertising of unsafe products, require accurate product labeling, and provide culturally targeted education about cancer risk and prevention," the NCAB said. [pg. 17]

Throughout its report, the NCAB makes reference to industrial chemicals, environmental chemicals that mimic hormones, and pesticides, as suspected causes of cancer. Until now, the National Cancer Institute has taken the official position that chemicals cause such a small percentage of cancers that they are not worth investigating.

In a turnabout, the NCAB now says, "The elimination or reduction of exposure to carcinogenic agents is a priority in the prevention of cancer. We are just beginning to understand the full range of health effects resulting from the exposure to occupational and environmental agents and factors." [pg. B-6]

And: "Lack of appreciation of the potential hazards of environmental and food source contaminants, and laws, policies, and regulations protecting and promoting tobacco use worsen the cancer problem and drive up health care costs." [pg. 6]

The report makes 13 recommendations for applying research dollars more effectively; recommendation No. I-5 says, "Examine and change laws and regulatory policies and practices, including those related to the environment and food supply, that contribute to the cancer problem and frustrate cancer prevention and control efforts." [pg. 21]

Furthermore, under "recommendations for translational research" (research to translate existing knowledge into practical benefits) we find, "Establish the role of hormones in the etiology [cause] and prevention of certain cancers." [pg. 26] And: "Develop cancer risk assessments for occupational and environmental carcinogens, based on sound epidemiologic evidence, potency of the carcinogen, and prevalence of human exposure." [pg. 26] Recommendation II-2(4) reads: "Establish the role of external hormones (e.g., from plant or environmental sources) in the etiology [cause] and prevention of certain cancers." [pg. 26]

The report says, "Cancers developing in reproductive tissues such as the breast, ovary, endometrium, and prostate account for approximately 30 percent of all cancers. These tissues are dependent upon an interactive network of various hormones (estrogens, progestins, and androgens) for their structural and functional development. In recent years, investigators have shown that there is a relationship between the level and duration of hormone exposure and tumor development in these hormonally sensitive tissues." [pg. B-5]

In an appendix, the NCAB report lists known and suspected causes of various cancers. Pesticides are listed for cancers of the female breast; the prostate; the stomach; the brain; and the lymph system (non-Hodgkin's lymphoma). As Table I shows, several of these are major killers and/or are rapidly increasing.

Perhaps most importantly, the report focuses on poverty as a major stumbling block to winning the war on cancer: "Unless proven advances in cancer prevention and care are made available to our people in all walks of life, the cancer burden will never be markedly reduced. Bringing existing knowledge and technologies to all of the people will achieve the greatest and most rapid impact on cancer incidence, suffering, and death," the NCAB says. [pg. 17]

"Over 38 million people have no health insurance at all; 50 million are uninsured at some time during the year. Eighty million more have health insurance insufficient to cover the costs of a catastrophic illness such as cancer," the NCAB says. [pg. 18]

"The problem of access is severe among the 35 million poor. African-Americans represent one-third of the poor although they comprise only 12 percent of the United States population. The poor, who typically experience substandard living conditions, lower educational levels, risk-promoting lifestyles, and insufficient access to health care, have a higher incidence of many cancers, are diagnosed with more advanced disease, and have lower survival rates than the more affluent. Even the poor on Medicaid may fare no better than the uninsured," the NCAB says. [pg. 18]

"Anecdotal evidence indicates that even those with insurance may delay seeking diagnostic and other medical care for fear of employment discrimination, future uninsurability, and financial ruin should cancer be discovered," the NCAB says. [pg. 18]

Lastly, the report says that "Current health care reform proposals" [i.e., the Clinton administration's proposals AND the Republicans' suggested alternatives] "are devastating to the War on Cancer" because they deny resources for research and for quality cancer care. [pg. 5]

In sum, the National Cancer Institute is showing definite signs of beginning to "get" the connection between environmental justice, economic justice, and cancer prevention. So far, however, there are no signs of an awakening in the White House or in Congress.

--Peter Montague

===============

[1] Paul Calabresi and others, CANCER AT A CROSSROADS: A REPORT TO CONGRESS FOR THE NATION (Bethesda, Md.: National Cancer Institute, September, 1994). Available free; phone 1-800-422-6237.

---

TABLE 1
U.S. Cancer Incidence (Occurrence) and Deaths in 1990, and the
Percent Change in Rates of Incidence and Death (Per 100,000
Population) During the Period 1950 to 1990.*

	-----ALL RACES------		----------------WHITES----------------
Cancer Type	Incidence in 1990	Deaths in 1990	Percent change in incidence, 1950-1990**	Percent change in deaths, 1950-1990
mouth & pharynx	30,500	8,405	- 32.2	-28.3
uterus	33,000	6,027	-3.8	- 66.3
stomach	23,200	14,072	-74.6	- 76.3
cervix	13,500	4,627	-75.1	- 73.6
esophagus	10,600	9,719	- 13.3	+9.4
colon/rectum	155,000	57,154	+9.9	- 28.2
larynx	12,300	3,709	+59.3	- 10.5
testicles	5,900	342	+124.7	- 68.6
bladder	49,000	10,340	+53.7	- 34.5
Hodgkin's	7,400	1,632	+26.9	- 65.8
childhood cancers	7,600	1,697	+1.3	-59.2
leukemia	27,800	18,725	+5.7	- 2.4
thyroid	12,100	1,026	+102.4	- 50.3
liver	14,600	8,511	+87.8	+18.3
pancreas	28,100	25,081	+11.8	+16.9
ovaries	20,500	12,566	+10.7	+1.0
lung	157,000	141,146	+258.6	+261.5
skin (melanomas)	27,600	6,419	+336.1	+156.0
breast (female)	150,000	43,389	+52.3	+4.0
prostate	106,000	32,376	+134.4	+17.8
kidney	24,000	9,843	+116.1	+33.3
brain	15,600	11,630	+73.6	+47.9
non-Hodgkin's lymphoma	35,600	18,461	+171.9	+113.7
multiple myeloma	11,800	8,896	+182.5	+189.8
All types excluding lung	883,000	364,149	+31.7	-14.4
All types	1,040,000	505,295	+45.6	+10.0

Source: Barry A. Miller and others, editors, CANCER STATISTICS REVIEW 1973-1990 [National Institutes of Health Publication No. 93-2789] (Bethesda, Md.: National Cancer Institute, 1993), Table I-3, pg. I.27.
* All data are age-adjusted to the 1970 U.S. population.
** Certain data are for all races combined, not just whites; specifically: all types; all types excluding lung; liver; brain; and childhood cancers. For other cancers, the National Cancer Institute says historical data for non-whites are not considered reliable.

---

Descriptor terms: national cancer advisory board; ncab; pesticides; solvents; cancer; carcinogens; hormones; estrogen; androgen; prevention; food safety; tobacco; reproductive system; cancer studies; cancer statistics; breast cancer; ovarian cancer; stomach cancer; brain cancer; lymph system cancer; non-Hodgkin's lymphoma; health insurance; health policy; cancer policy; poverty; African-Americans; health care reform; bill clinton; president clinton; congress; national cancer institute; nci;

#415: The Scientific Basis of Chemical Safety--Part I: Limits on Workplace Chemical Exposures

=======================Electronic Edition========================
RACHEL'S ENVIRONMENT & HEALTH WEEKLY #415 
---November 10, 1994---
News and resources for environmental justice.
==========
Environmental Research Foundation
P.O. Box 5036, Annapolis, MD 21403
Fax (410) 263-8944; Internet: erf@igc.apc.org ==========
RACHEL-4CM = DIOXIN FOCUSED DIRECTORY Remote Access Chemical Hazards Electronic Library. Dioxinnz.com =======================Original Source========================

In 1990, the American Public Health Association (APHA) estimated that each year 50,000 to 70,000 Americans die of diseases developed from toxic exposures on the job. Furthermore, APHA estimated that 350,000 new cases of occupational disease develop each year from toxic exposures. [1]

The federal government established standards for chemicals in workplace air for the first time in 1971, as required by the Occupational Safety and Health Act [OSH Act] of 1970. Prior to 1971, the U.S. had no enforceable federal standards for workplace air; instead, guidelines (which could be voluntarily adopted, or not) were set by a private organization called the American Conference of Governmental Industrial Hygienists (ACGIH). The ACGIH is a private group composed of industrial hygienists from state and local governments, plus academics and industry consultants.

In 1946 the ACGIH established a Committee on Threshold Limits, charged with developing "threshold limit values" (TLVs) for chemical exposures in the workplace. A threshold is an amount below which no damage is evident. The ACGIH says TLVs are average concentrations in air for an 8-hour workday, 40 hours per week, to which "nearly all workers may be repeatedly exposed, day after day, without adverse effect." [2]

In 1971 the U.S. government adopted all the ACGIH's TLVs as official government standards for workplace air. Since 1950, the ACGIH's TLVs have also been used to set government standards in Belgium, West Germany, Austria, Italy, the Netherlands, Portugal, Denmark, Sweden, Finland, Norway, Spain, Switzerland, England, Japan, and probably elsewhere.

Furthermore, during the 15 years after 1971, at least 37 of 50 states in the U.S. used the TLVs as the basis for setting ambient air pollution standards --not workplace standards, but standards for the general outdoor air. ("Ambient" means "surrounding" or "enveloping.") Often states have taken the TLVs, reduced them by some arbitrary "safety factor" like 100, and declared them "safe" for ambient air. Reasons for reducing TLVs by a "safety factor" are: (a) TLVs are established for only 40 hours of exposure each week, not continuous exposure 168 hours per week; (b) workers are assumed to be young, healthy, male, and employed (therefore, probably eating well, with access to health care) whereas the general population includes pregnant women, infants, the elderly, people with chronic ailments, people with special sensitivity to particular chemicals, and poor people who can't afford to eat well and rarely, if ever, see a doctor; (c) TLVs are set based on exposure to a single chemical, but in the real world everyone is exposed to numerous chemicals simultaneously. Since the "safety factor" is an arbitrary number, any "safety" in TLV-based ambient air standards must rely upon the safety of the underlying TLV itself. There is evidence that the role of TLVs is now being extended in the U.S., to setting standards for indoor air, standards for groundwater contamination, and standards for cleanup at Superfund [contaminated dump] sites.

For nearly 5 decades, no one critically examined the scientific data underlying the TLVs. Even the TLV Committee itself seems to have relied solely on the advice of individual Committee members who took responsibility for setting a TLV for a particular chemical. Those individual Committee members, it was revealed in 1988, were often employed by the same corporations that were the major producers of the chemicals having their TLVs set. For example, a Dow Chemical Company representative took responsibility for setting TLVs for at least 30 of Dow's halogenated hydrocarbons, pesticides, and other industrial chemical products. Furthermore, in 1988 it was learned that at least 104 TLVs had been set based, in whole or in part, on data that appeared in unpublished corporate communications. Those corporate communications were not available from the ACGIH, from the corporations themselves, or from individual members of the TLV committee. [3] Thus the basis of those TLVs was secret and not available for scientific peer review. (The Reagan administration's Occupational Safety and Health Administration [OSHA] responded to this information in 1989 by once again formally adopting all 600 of the TLVs, wholesale, as federal regulations. The OSH Act of 1970 had required the federal government to conduct its own research and set its own workplace air standards, but between 1971 and 1989 OSHA was able to set only 12 such standards of its own. Since there are roughly 60,000 chemicals now in commercial use, at this rate, OSHA would take 90,000 years to set standards for all chemicals.)

Despite the absence of open scientific process underlying many TLVs, many other TLVs had been set based on published literature, and in those cases, the TLVs were still assumed to be valid. However, in 1990, independent researchers compared many TLVs to the scientific reports upon which these TLVs are supposedly based. [4] They found that, in numerous cases, the TLVs had been set at levels higher than the levels shown to cause effects in humans, ranging from eye and nose irritation to permanent changes in bodily structure and outright disease. (They also found TLVs based on data that was 50 years old; TLVs based on examination of as few as 3 individuals; and TLVs set to protect against hearing loss, based on studies of eyes, noses and throats but not ears.)

The 1990 report on the scientific underpinnings of the TLVs is worth reading. Using a uniform format, it contrasts the effects that the TLV is supposed to prevent, against the actual scientific study of those effects in humans which the TLV Committee says it relied upon. Here we reprint excerpts from that 1990 report readers can see for themselves the way scientific information has been used in setting many TLVs. We are quoting the 1990 report verbatim, including material both inside and outside quotation marks, and including the original use of ... to indicate omissions; our only editing has been to remove italics from some words. (In what follows, the notation m**3 means "cubic meter of air.")

Acetaldehyde:

EFFECT.

"The TLV, 100 ppm, is recommended to prevent excessive eye irritation and potential injury to the respiratory tract." [ACGIH, 1976]

VALIDATION? 

"Several of 12 volunteers objected... strenuously even at 25 ppm... A majority... experienced... eye irritation at 50 ppm." [Silverman and others, 1946]

Benzene:

EFFECT.

"A TLV of 25 ppm is believed low enough to prevent serious blood changes." [ACGIH, 1976]

VALIDATION?

In "a study... of the benzene exposure of workers in the rubber coating industry... the measured benzene vapor concentrations averaged 18 ppm and 6 of 47 employees showed a lowered hemoglobin of below 13.5 grams." [Pagnotto and others, 1961]

Butyl Alcohol:

EFFECT. 

"In view of the apparent potential of n-butyl alcohol to increase hearing loss in the younger age group of workers and to impair vestibular [ear] function at levels somewhat below 110 ppm, a TLV of 50 ppm as a ceiling value is recommended." [ACGIH, 1976]

VALIDATION?

"Butyl alcohol, at 25 ppm irritated the eyes, nose, and throat of the majority of 10 volunteers... At 50 ppm there was a unanimous feeling of pronounced throat irritation, in 10 volunteers." [Nelson and others, 1943]

Chlorine dioxide:

EFFECT. 

"The recommended limit of 0.1 ppm is... to prevent irritation and possible bronchitis." [ACGIH, 1976]

VALIDATION?

"At a factory for the production of sulfite-cellulose... extensive investigations... showed the occurrence of slight bronchitis in 7 of 12 workers exposed to chlorine dioxide... at concentrations lower than 0.1 ppm." [Gloemme and Lundgren, 1957]

Chlorodiphenyl--42% chlorine: 

EFFECT.

"It is believed that this limit, 1 mg/m**3, will offer reasonably good protection against systemic intoxication but may not guarantee complete freedom from chloracne [a disfiguring skin disease]." [ACGIH, 1976]

VALIDATION?

"In a chemical plant concerned with organic chemical production where the chlorinated diphenyls in the actual breathing zone of the workers were 0.1 mg/m**3 of air... seven cases of mild to moderate chloracne of the face and head occurred among 14 chemical operators exposed..." [Meigs and others, 1954]

Ethyl Ether:

EFFECT.

"Regular exposure at this concentration (400 ppm, the TLV) should cause no demonstrable injury to health nor produce irritation or signs of narcosis among workers." [ACGIH, 1976]

VALIDATION?

"Complaints of nasal irritation began at 200 ppm in the majority of 10 volunteers." [Nelson and others, 1943]

Fluoride as F [Fluorine]:

EFFECT.

"The limit, 2.5 mg/m**3, is sufficiently low to prevent irritative effects and to protect against disabling bone changes." [ACGIH, 1976]

VALIDATION?

At a factory where the concentration of fluorides ranged from 0.14 to 3.13 mg/m**3, "radiological [x-ray] examination revealed signs of osteosclerosis [abnormal hardening of bone] in 48 of 189 workers." [Largent, 1961]

Isopropyl acetate:

EFFECT.

"The limit, 250 ppm,... is considered adequate to prevent significant irritation of the eyes and respiratory passages." [ACGIH, 1976]

VALIDATION?

"We found that at 200 ppm, the majority of... twelve subjects of both sexes... experienced some degree of eye irritation." [Silverman and others, 1946]

Magnesium oxide fume:

EFFECT.

"The limit, 10 mg/m**3, is recommended on the basis that this value represents a maximal desirable limit for dusts of relatively minor hazard." [ACGIH, 1976]

VALIDATION?

In 1 of 4 subjects exposed to an average concentration of magnesium oxide at 5.8 mg/m**3 and in 2 of 4 subjects exposed to an average concentration of magnesium oxide of 4.1 mg/m**3 "was found... a leukocytosis [an abnormally large number of white blood cells] and a fever resembling those caused by the heavy metals." [Drinker and others, 1927]

Mercury:

EFFECT.

"Following a study of the chlorine industry it was concluded in general that exposure at 0.1 mg/m**3 [100 micrograms/m**3] produced no significant incidence of mercury poisoning but contained little or no margin of safety." [ACGIH, 1976]

VALIDATION?

"Symptoms or signs of chronic mercury poisoning were found in 1 of 9 and in none of 3 men... engaged in repairing D.C. meters... where the concentration of mercury in the atmosphere averaged 19 and 40 micrograms/m**3, respectively." [Bidstrup and others, 1951]

Mica:

EFFECT.

"The limit of 20 mppcf [million particles per cubic foot of air]... should prevent disabling pneumoconiosis, but may not be sufficiently low to eliminate positive chest x-ray findings in workers with many years' exposure." [ACGIH, 1976]

VALIDATION?

"In mica factories... the exposure to dust is limited to muscovite mica only... which contains less than 1% free silica. When the dust concentrations to which most workers were exposed ranged from 2 to 21 mppcf, with an average of 10 mppcf,... 27 of 61 workers examined had ground-glass 2 readings of their chest x-rays." [Heimann and others, 1953]

Selenium:

EFFECT.

"The limit of 0.2 mg/m**3 for elementary selenium and its common inorganic compounds is believed low enough to prevent systemic toxicity and to minimize irritation of eyes and respiratory passages." [ACGIH 1976]

VALIDATION?

In the "manufacture of rectifiers... conjunctivitis and slight tracheo-bronchitis were present in 9 of 62 workers... The atmospheric concentrations at different stages of the process varied from 0.007 to 0.05 mg/m**3, nowhere reaching the recommended MAC [maximum allowable concentration] of 0.1 mg/m**3." [Note: 0.007 to 0.5 is 4 to 28 times smaller than 0.2, the TLV.] [Kinningkeit, 1962]

Turpentine:

EFFECT.

"A TLV of 100 ppm is... recommended to prevent chiefly irritative effects." [ACGIH, 1976]

VALIDATION?

"Turpentine at 75 ppm caused nose and throat irritation in several of 10 volunteers." [Nelson and others, 1943]

[To be continued.]

--Peter Montague

===============

[1] Philip J. Landrigan, "Commentary: Environmental Disease--A Preventable Epidemic," AMERICAN JOURNAL OF PUBLIC HEALTH Vol. 82 (July 1992), pgs. 941-943.

[2] Barry I. Castleman and Grace E. Ziem, "Editorial: Toxic Pollutants, Science, and Corporate Influence," ARCHIVES OF ENVIRONMENTAL HEALTH Vol. 44, No. 2 (March/April, 1989), pgs. 68, 127.

[3] Barry I. Castleman and Grace E. Ziem, "Corporate Influence on Threshold Limit Values," AMERICAN JOURNAL OF INDUSTRIAL MEDICINE Vol. 13, No. 5 (1988), pgs. 531-559.

[4] S.A. Roach and S.M. Rappaport, "But They Are Not Thresholds: A Critical Analysis of the Documentation of Threshold Limit Values," AMERICAN JOURNAL OF INDUSTRIAL MEDICINE Vol. 17, No. 6 (1990), pgs. 727-753.

Descriptor terms: apha; american public health association; osha; occupational safety and health act; acgih; american conference of governmental industrial hygienists; committee on threshold limits; tlvs; Belgium; West Germany; Austria; Italy; the Netherlands; Portugal; Denmark; Sweden; Finland; Norway; Spain; Switzerland; England; Japan; great britain; united kingdom; air quality standards; clean air act; caa; indoor air pollution; superfund remediation; groundwater; standards; reagan; acetaldehyde; benzene; butyl alcohol; chlorine dioxide; chlorodiphenyl; ethyl ether; fluoride; fluorine; isopropyl acetate; magnesium oxide fume; mercury; mica; selenium; turpentine;