#462: Killing Science

=======================Electronic Edition========================
RACHEL'S ENVIRONMENT & HEALTH WEEKLY #462
---October 5, 1995---
News and resources for environmental justice.
==========
Environmental Research Foundation
P.O. Box 5036, Annapolis, MD 21403
Fax (410) 263-8944; Internet: erf@rachel.clark.net
==========
RACHEL-4CM = DIOXIN FOCUSED DIRECTORY Remote Access Chemical Hazards Electronic Library. Dioxinnz.com
========================Original Source========================

Last week Congress permanently closed down its scientific research arm, the Office of Technology Assessment (OTA). Although we did not agree with the recommendations of every report that OTA produced during its 23 years of policy analysis, we know that the death of OTA will be an immeasurably great loss to the nation's ability to get the facts straight. The so-called conservatives in this Congress claim to favor public policies based on "good science," yet they are hacking away the infrastructure of laboratories and institutes that, for decades, has done the nation's scientific work. Next on the chopping block is the National Institute of Standards and Technology (NIST, formerly the National Bureau of Standards), which designs standardized testing and measurement protocols that are relied upon by scientists and engineers throughout the world. This Congress is moving us steadily back toward the dark ages.

On the chopping block as we go to press is the university-based program of basic research within the National Institute of Environmental Health Sciences (NIEHS), part of the National Institutes of Health (NIH). The NIEHS Superfund Basic Research Program, now in its ninth year, provides funding to 17 programs at 60 universities and institutions around the country, studying the human health effects of hazardous chemicals in the environment, especially those found at leaking waste dumps.

Congress has already reduced the appropriation for this program, which makes up barely 1% of the Superfund toxic waste cleanup effort. But now the House Subcommittee on Commerce, Trade and Hazardous Materials, chaired by Rep. Michael Oxley of Ohio's 4th District, is refusing to reauthorize the program entirely, thus killing it dead. Mr. Oxley's position is that Superfund money should only be used for cleanup, not for any "extraneous" uses like determining how clean our cleanups need to be, and why. Like other so-called "conservatives" who claim they want policies based on "good science," Mr. Oxley reveals his true intentions as he prevents any "good science" from being funded and carried out.

Looking at some of last year's research highlights produced by the Superfund research program, one can appreciate Mr. Oxley's fear of what good science will reveal: [1]

** Researchers determined the dose-response relationship for benzene down to doses as low as those received by ordinary people. Millions of Americans are exposed to small amounts of benzene when, for example, they pump their own gasoline. These benzene experiments strongly suggest that a cancer risk from benzene is present even at very low doses. With millions of people exposed to benzene every day, it seems important to know that benzene really does cause cancer.

** Other investigations demonstrated for the first time in laboratory animals that benzene exposure, which has been associated with leukemia and aplastic anemia in humans and animals, is also mutagenic; that is, it causes inheritable genetic changes which can affect the next generation, the next after that, and so on.

** Researchers showed that several biological markers (subtle observable changes in a person) can be used to detect probable chromium exposure in humans living near places where chromium wastes have been dumped. Researchers studied Jersey City, N.J., and surrounding Hudson County where corporate polluters dumped chromium wastes on the ground for decades. Such research should make it easier to sue corporate polluters for exposure to toxics.

** Researchers developed a test to detect a single molecule of a cancer-associated chromosomal rearrangement in the presence of DNA from a million normal human cells. This work offers the possibility of very sensitive detection of the ability of chemicals to cause chromosomal rearrangements as an indicator of their cancer-causing potential.

** Researchers are studying the neurological and immune-system effects of drinking water containing mercury compounds. Early results indicate that even a small dose of methyl-mercury, such as 5 ppm [parts per million] in drinking water, impairs neurological, endocrine (hormone), and immune-system functions in animals. This corresponds to a daily consumption of 0.3 milligrams per kilogram (mg/kg) of body weight which is smaller than the "safe" dose of 0.48 mg/kg body weight indicated by the World Health Organization. In other words, mercury is even more dangerous than formerly believed.

** A large epidemiologic study examined the respiratory disease hazards of susceptible individuals living near toxic waste sites and industrial facilities. Analysis of interim data has provided important information on the association between asthma status (active or inactive) and exposure to irritants --active asthmatics have been found to suffer an adverse effect on lung function resulting from irritant chemical exposure (after adjustment for smoking). Asthma is increasing each year in the U.S. population, and annual production of toxic chemicals is increasing as well. Could these two trends be related? It would be important to know.

** Researchers demonstrated a high degree of correspondence between laboratory and field-test results of immune-system toxicity in dogs exposed to industrial PCBs [polychlorinated biphenyls]. Not only have these studies clarified effects of PCBs on the immune system, but they have sparked a number of spin-off studies involving the thyroid, lymphocyte (white blood cell) development, and brain function. These studies help clarify how PCBs affect behavior, physiology, and response to infectious disease, in addition to environmentally-induced threats such as cancer. Efforts to date have provided a key step in validating laboratory immune-system toxicity observations with field studies of animal health.

** In a study comparing effects of perinatal (near the time of birth) vs. adult exposure to PCBs, researchers have found that toxic effects on the brain occur in completely opposite ways. In adults, ortho-PCBs reduce brain dopamine levels while dioxin-like coplanar-PCBs have no such effect. (Dopamine is an important natural chemical in the brain.) However, following perinatal exposure, dioxin-like PCBs elevate brain dopamine concentrations and alter the behavior of exposed female offspring while ortho-PCBs reduce brain dopamine concentrations. Thus, PCB exposures have opposite effects, depending on the age at exposure and the type of PCBs to which the organism is exposed. These results suggest that PCBs may not only directly affect nerve function, but may also alter steroid hormone function during a baby's development.

** Some of the most interesting and important Superfund research involves the role of estrogens and estrogen-like chemicals that seem to interfere with the reproductive system of fish, birds, and mammals, probably including humans. Estrogens are female sex hormones.

A study of sea gulls on Santa Barbara Island, not far from Los Angeles, in 1977 revealed bizarre gull behavior: female gulls were pairing up and sharing nests. In 1981, bird toxicologist Michael Fry published a study showing that, by injecting a small amount of DDT into bird eggs, he could produce hermaphroditic male birds --that is, male birds with the sex organs of both a male and a female. Fry's work met with skepticism back in 1981, but in the subsequent decade wildlife experts worldwide reported declining birth rates, hermaphroditic offspring, lowered sperm counts, and deformities of the testicles of fish, panthers, alligators, and other animals in polluted habitats. [2]Timothy Gross, a wildlife endocrinologist (hormone specialist) at the University of Florida in Gainesville, says, "If you look at people, the same pollutants are in our bodies. What is a safe level? We don't know. But I'd be a pretty naive scientist to conclude there couldn't be the same effects in humans." [3]

The possible effects of estrogen-like chemicals on humans are now thought to include prostate cancer and testicular cancer [4]in men, and perhaps breast cancer in women. [5] Prostate cancer has been steadily increasing in the U.S. in recent years, especially among older men; it strikes 244,000 men each year in the U.S., and kills about 40,000. Breast cancer strikes 183,000 American women each year and kills about 46,240. One out of every 8 women gets breast cancer, and one out of every 7 men gets prostate cancer. Because men with undeveloped testes, and castrated men, rarely develop prostate cancer, researchers began to suspect that sex hormones circulating in the blood might affect prostate cancer. "The evidence has since been stacking up to form an alarming picture that paints estrogen [female sex hormone] and testosterone [male sex hormone] as cancer culprits," says a recent issue of ENVIRONMENTAL HEALTH PERSPECTIVES, [4]published by the National Institute of Environmental Health Sciences [NIEHS], a staid scientific organization that does not use the word "alarming" lightly. Estrogens and estrogen-mimicking industrial chemicals in the environment have now been shown to alter testosterone levels in men. Thus the wildlife research supported by Superfund money has begun to pay off with a better understanding of major killer diseases. "We're relying on Superfund money for research," says wildlife-and-hormone specialist Timothy Gross at University of Florida. "And who knows what will happen to that? Congress now has a vendetta against lots of this environmental research," he says. [3]

Indeed, people calling themselves "conservatives" in Congress are determined to cut off the funding for this line of research. In their mind, the only good science is no science. Without federal funding, this research will cease because the private sector has no interest in showing how industrial discharges may be contributing to the nation's steadily-rising burden of cancer, diabetes, birth defects, endometriosis, and infertility.

Now a Congressman from Ohio is leading the charge to kill this important health research program. Mr. Oxley might change his mind if he received letters or phone calls from people in his district, who hold the power to end his political career. In addition, calls from outside his district might help, too. Mr. Oxley represents 11 counties (Allen, Auglaize, Crawford, Hancock, Hardin, Knox, Logan, Marion, Morrow, Richland and Wyandot), with the district's four most populous cities being Lima, Mansfield, Marion, and Findlay (Mr. Oxley's home town). His phone number in D.C. is: (202) 225-2676; fax: (202) 226-1160. Mail: 2233 Rayburn Building, Washington, D.C. 20515.

 --Peter Montague

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

[1] Highlights of Superfund research can be found on the World Wide Web at http://www.niehs.nih.gov/sbrp/1994-hig.htm.

[2] Recent work on estrogen-like chemicals and wildlife appears in "Wildlife Development," ENVIRONMENTAL HEALTH PERSPECTIVES Vol. 103, Supplement 4 (May, 1995).

[3] Gross quoted in Amanda Spake, "Is the modern world giving us cancer?" HEALTH (October, 1995), pg. 55.

[4] Renee Twombly, "Assault on the Male," ENVIRONMENTAL HEALTH PERSPECTIVES Vol. 103, No. 9 (September, 1995), pgs. 802-805.

[5] Devra Lee Davis and H. Leon Bradlow, "Can Environmental Estrogens Cause Breast Cancer?" SCIENTIFIC AMERICAN Vol. 273, No. 4 (October, 1995), pgs. 166-172.

Descriptor terms: research funding; superfund; congress; science; ota; benzene; chromium; congressman michael oxley; cancer; mercury; asthma; hazardous wastes; pcbs; dogs; estrogens; hormones; immune system; nervous system; endocrine system; endocrine disruptors; wildlife; hermaphroditism; fish; gulls; birds; panthers; alligators; prostate cancer; testicular cancer; breast cancer; morbidity statistics; mortality statistics; testosterone; niehs

#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;

#092: New Study Shows Incinerator Ash More Dangerous Than We Realized.

=======================Electronic Edition========================

RACHEL'S HAZARDOUS WASTE NEWS #92
---August 29, 1988---
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========================

A new study by a team of engineers at Rutgers, the state university of New Jersey, shows that municipal incinerator ash is more dangerous than previously realized.

When household garbage burns, the resulting ash has two parts: fly ash, most of which is captured from the smoke stack by an air pollution control system, and the heavier "bottom ash" which falls through the grate of the combustion chamber into an ash pit; both types of ash must be carted away. Both types of ash contain toxic heavy metals (chromium, cadmium, lead, arsenic, zinc, and other metals) as well as organic compounds (PCBs, dioxins, benzene, and other cancer-causing organics). Here we will discuss only the metals.

When the ash is thrown away, the metals in the ash become available to the environment. Currently, such ash is typically heaped on the ground somewhere, or is dumped in a municipal landfill. Then rainwater seeps into the ash and begins to dissolve the metals and carry them into the general environment.

Chemical engineers at Rutgers have released a new study showing that toxic metals in municipal incinerator ash are more abundant and more soluble, and therefore more dangerous, than previously thought.

The Rutgers team took samples of household solid waste from three locales (Pennsauken, NJ, Magnolia, NJ, and Somerset County, NJ) and burned them in a small (50 ton per day) solid waste incinerator. They captured the fly ash and the bottom ash. The solid waste samples did not include substantial quantities of industrial trash but were restricted to household wastes.

The actual composition of the ash is shown in Table 1. There were, of course, other elements and compounds in the ash, but the Rutgers team did not measure these because they are not regulated under federal law. As is obvious from these numbers (which are all given as parts per million, or ppm) there are large quantities of metals in the ash.

Table 2 shows how many pounds of metal are found in each ton of ash, using the "average" values given at the bottom of Table 1. (We, not the Rutgers group, did the averaging in Table 1.)

The numbers are quite astonishing. Take lead, for example. If a 2000 ton-per day incinerator produces 500 tons of ash per day, and if 10% is fly ash and 90% is bottom ash, the total daily ash will contain 2935 pounds of lead. That's a ton and a half of lead per day. The same arithmetic tells us that one day's ash will contain 48 pounds of chromium, 61 pounds of cadmium, and 97 pounds of arsenic. In a year's time (operating 5 days a week, 52 weeks a year), such an incinerator will put out 12,610 pounds of chromium, 15,990 pounds of cadmium, 25,246 pounds of arsenic, and three quarters of a million pounds of lead (763,256, actually). These are all metals that are toxic in microgram quantities (there are 454 million micrograms in one pound).

ALL of this metal will most likely leach into the environment sooner or later. But the law does not view it that way. The law requires that the ash be tested for toxicity using something called the "extraction procedure" toxicity test (EP Tox Test for short). The EP tox test asks, "If we mix the ash with a dilute solution of acetic acid and then test the dilute solution, how much metal do we find has dissolved into the solution?" If we find more than 100 times as much metal as is allowed in drinking water, then the ash is declared a "hazardous waste." If the metals are not present at levels 100 times the drinking water standard, the ash is declared "nonhazardous" no matter how many tons of dangerous metals it may contain. (This system clearly does not protect the public, but it's what the EPA [U.S. Environmental Protection Agency] has set, so it's what we've got.)

Many scientists have criticized the EP Tox Test for a variety of reasons. So the EPA has proposed a new test, which will soon replace the EP Tox test. The new one is called the TCLP extraction test (short for Toxicity Characteristic Leaching Procedure). The details of the TCLP are different from the EP Tox test, but the basic idea is the same.

The Rutgers team tested the ash from the three locales with the EP Tox Test, and the Pennsauken sample was given the TCLP test. All the fly ash samples were deemed "hazardous" for both lead and cadmium by the EP Tox test. The TCLP results showed that THE TCLP LEACHED EVEN MORE METALS THAN 

THE EP TOX TEST. Lessons from the work at Rutgers: 

(1) The amount of metal in solid waste ash varies from place to place with socio-economic status, geographic location, season, collection patterns, and recycling practices. Your local waste stream should be sampled every 2 weeks for a year to see what it really contains; some consulting firm's "estimate" of what's in your local waste is most likely off; 

(2) the quantity of toxic metals in your waste may be very high and the toxicity will endure forever; ask how long the landfill liners are guaranteed. 

(3) The EP tox test may show that the ash is legally "hazardous" but the TCLP test is even more likely to show that the ash is legally hazardous. Get T.L. Clapp and others, "Municipal Solid Waste Composition and the Behavior of Metals in Incinerator Ashes," ENVIRONMENTAL PROGRESS, Vol. 7 (Feb., 1988), pgs. 22-30. Dr. Clapp 's address is: Department of Chemical and Biochemical Engineering, College of Engineering, Rutgers, P.O. 909, Piscataway, NJ 08854; phone (201) 932-3047 or 932-2213.

TABLE 1-- Metals in ash resulting from combustion of household wastes
============================================

Waste Source	Metal	Fly ash (ppm)	Bottom ash (ppm)
Pennsauken	Chromium	30	40
	Cadmium	490	100
	Lead	4990	6970
	Arsenic	47	118
	Zinc	4700	4400
Magnolia	Chromium	50	73
	Cadmium	130	5
	Lead	2838	650
	Arsenic	80	71
Somerset	Chromium	52	35
	Cadmium	227	8
	Lead	3993	852
	Arsenic	87	112
Average	Chromium	44	49
	Cadmium	282	37
	Lead	3940	2824
	Arsenic	71	100

============================================
============================================
TABLE 2 -- Pounds of metal in each ton of ash

Metal	Fly ash (lbs.)	Bottom ash (lbs.)
Chromium	0.09	0.1
Cadmium	0.56	0.07
Lead	7.9	5.6
Arsenic	0.14	0.2

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

--Peter Montague, Ph.D.

Descriptor terms: incineration; ash; studies; findings; rutgers; ep toxicity; msw; landfilling; heavy metals; cancer; disease statistics; risk assessment; leachate; groundwater; nj; lead; chromium; cadmium; arsenic; monitoring; drinking water; hazardous waste industry; epa; tclp extraction test; t.l. clapp;

#295: As The Story Of PCBs Unfolds...

=======================Electronic Edition========================

RACHEL'S HAZARDOUS WASTE NEWS #295
---July 22, 1992---
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 ==================

As the scientific reassessment of dioxin unfolds inside EPA [U.S. Environmental Protection Agency], one of the stickiest issues is how to deal with PCBs (polychlorinated biphenyls). PCBs are a family of 209 separate chemicals, some of which have the same unpleasant characteristics as dioxins--they interfere in growth and reproduction, they damage the immune system, they cause cancer, and they cause these effects in fish, birds, mice, rats, mink, seals, sea lions, whales, humans and other forms of life. One key difference between PCBs and dioxins is that there are much larger quantities of PCBs in the environment, compared to dioxins. And many major industrial firms have a long track record of exposing their workers and their neighbors to PCBs. Therefore, the potential for PCB-related lawsuits and liability is large. And therefore the political visibility of PCBs inside EPA is also large.

There is now considerable evidence that humans WITHOUT OCCUPATIONAL EXPOSURES are being adversely affected by PCBs. Humans are exposed mainly through food, especially meat and most especially fish. Two groups of U.S. children have been studied from birth to age four, looking for effects from the PCBs we all carry in our bodies. In Michigan, 313 newborns have been studied; 242 of their mothers had eaten PCB-contaminated sportfish from Lake Michigan. Higher PCB levels in umbilical cords have been correlated with smaller birth size (including reduced head size, diminished girth in the chest) and shorter gestation, an effect also seen in children whose mothers had occupational exposure.[1] On standardized tests for infant development, higher PCB levels in the Michigan children were correlated with abnormally weak reflexes, less responsiveness to stimulation, more jerky, unbalanced movement, and more startles.

In North Carolina, 912 infants have been followed from birth. Their mothers had no unusual PCB exposures but, like all Americans, they carry PCBs in their body tissues. Among 866 North Carolina infants tested, higher PCBs in mother's milk was correlated with hypotonicity [loss of muscle tone] and more abnormally weak reflexes. Subsequent studies of 802 of the North Carolina children at ages 6 months and 12 months revealed those with higher levels of PCBs had poorer performance in tests requiring fine motor coordination. At seven months, a test of 123 of the Michigan children showed higher PCB levels were related to poorer visual memory. Researchers reviewing the history of these children conclude, "There is thus consistent evidence that prenatal exposure to levels of PCBs commonly encountered in the U.S. produce detectable effects on motor maturation and some evidence of impaired infant learning."[2] In North Carolina, about 5% of the children have so far shown measurable effects related to PCB exposure, and in Michigan somewhat more than 5% of the children are showing effects.

At age 4, children in the Michigan group with higher PCBs levels weighed 10% (4 pounds) less than children with lower PCB levels. The effect was particularly significant in girls. In addition, the Michigan children were ranked according to an "activity" index, and higher PCB levels were correlated with children who were unusually "quiet and inactive." These effects on growth and behavior were specifically correlated with exposure to PCBs before birth and not with exposure after birth. This leads researchers to conclude that PCBs attack the central nervous system more successfully during its earlier developmental stages.[3]

The Agency for Toxic Substances and Disease Registry (ATSDR) has identified human populations with potentially high exposures as: individuals exposed in the workplace, breast-fed infants of mothers who consume more than 6 pounds (12 meals) of fish per year, and "people who live in the vicinity of incinerators and PCB disposal facilities."[4]

How did this situation develop? The Westinghouse story helps us understand how we got where we are today.

In 1957 Westinghouse began operating a large transformer factory in Bloomington, Indiana, processing large quantities of PCBs, which they purchased from Monsanto, the inventor of PCBs. PCBs don't conduct electricity, but they conduct heat well, and they are very stable (they don't break down readily) so they make a nearly ideal fluid for insulating electrical transformers and capacitors.

PCBs came to the attention of the scientific world in 1966 when a Swedish scientist revealed that damage to birds that he had attributed to DDT was actually being caused by PCBs.

In 1968, PCBs came to public attention when it was reported that 1300 Japanese people had become ill from eating PCB-contaminated rice oil. Many of the PCB-exposed women subsequently gave birth to children with birth defects. Workers at the Westinghouse plant in Bloomington say they were never told of any health hazards from PCBs. On the contrary, when they began to ask questions after the mass poisoning in Japan, they say, Westinghouse officials led them to believe PCBs were entirely safe. Jason Morrow, a former union local president at the plant, recalls employee meetings in which then-plant manager Donald M. Sauter "washed his hands and face in what he told workers was liquid PCBs to convince them not to worry." A Westinghouse spokesman, Christopher C. Newton, confirmed for BUSINESS WEEK magazine that Sauter "dipped his hands" into PCBs at a meeting.

Westinghouse and Monsanto insist that they have always told the world what they knew about PCB toxicity as soon as they knew it. However, in a letter dated September 15, 1947, E.C. Barnes of Westinghouse's medical department wrote that long-term exposure to PCBs "may produce bodily injury which may be disabling or could be fatal." According to workers now suing Westinghouse for injuries they say are PCB-related, this information was never passed along to the people Westinghouse exposed to PCBs day in and day out for 25 years.

In 1971, fearing lawsuits, Monsanto began requiring its customers like Westinghouse to sign a waiver relieving it of financial liability for improper uses of the chemical, thus putting buyers on notice of possible dangers. That same year a Westinghouse biochemist named Thomas O. Munson says he received instructions directly from then-chief executive officer Donald C. Burnham to study PCB contamination around four Westinghouse plants. In 1972 Munson submitted his report to Westinghouse officials, urging them to tell the local communities of the massive contamination he had found and to take remedial action. Instead Westinghouse kept the Munson report secret and continued to dump liquid PCBs directly into the local environments, Munson says.[5]

What does the future hold?

Between 1929 and today, Monsanto made, or licensed someone else to make, a total of 1.2 million tons of PCBs.[6] Of this total, 31% (370,000 tons) has so far escaped into the general environment. An estimated 4% of original production has been fed into incinerators, in hopes of destroying it. However, 780,000 tons of PCBs are still in use in transformers and capacitors, or have been sent to landfills where they are waiting patiently to escape. Thus the amount waiting to be released into the environment is approximately twice as large as the amount that has already been released.

Almost all PCBs released into the environment end up in the oceans eventually. Because PCBs are not water-soluble but are fat soluble, they have a marked tendency to accumulate in living organisms. Marine mammals at the top of the oceanic food chain are likely to have up to 10 million times more PCBs in their fat, compared to the concentration of PCBs in the water they live in.

Once they enter the oceans, PCBs build up in the bodies of fish and then in fish-eating birds and mam-mals. Fish-eating birds and mammals (seals, sea lions, some whales, and dolphins) have a distinct inability to metabolize PCBs--they lack certain enzyme systems that land-based mammals (such as humans) have that speed the breakdown of PCBs. As a consequence, ocean birds and mammals accumulate unusually high levels of PCBs in their bodies and pass the PCBs to their offspring via eggs (birds) and milk (mammals). Since PCBs released into the environment move into the oceans readily, in coming decades ocean birds and mammals seem likely to experience a continuing buildup of PCBs in their flesh. There is good evidence that PCBs in marine mammals and birds are already causing major reproductive failure.[7] Therefore, it seems likely that ocean mammals (whales, seals, sea lions, and dolphins) will experience increasing reproductive failure and will become extinct unless substantial efforts are made to prevent the release of PCBs that are still in use or are stored in landfills. (See RHWN #144.) At present, no such efforts are under way or even under discussion.

--Peter Montague, Ph.D.

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

[2] Tilson, cited above, pg. 245. Some of the human data are also reviewed on pgs. 53-54 of Syracuse Research Corporation, DRAFT TOXICOLOGICAL PROFILE FOR POLYCHLORINATED BIPHENYLS (Atlanta, GA: Division of Toxicology, Agency for Toxic Substances and Disease Registry, Public Health Service, U.S. Department of Health and Human Services, October, 1991.) See also, Anthony B. Miller and others, ENVIRONMENTAL EPIDEMIOLOGY. VOL. 1. PUBLIC HEALTH AND HAZARDOUS WASTES (Washington, DC: National Academy Press, 1991). pgs. 204-205, [207,] 208-210; and see 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.

[3] 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.]319-326.

[4] Syracuse Research Corporation, cited above, pg. 140.

[5] Michael Schroeder, "Did Westinghouse Keep Mum on PCBs?" BUSINESS WEEK August 12, 1991, pgs. 68-70.

[6] Shinsuke Tanabe, "PCB Problems in the Future: Foresight from Current Knowledge," ENVIRONMENTAL POLLUTION Vol. 50 (1988), pgs. 5-28.

[7] See, for example, Robert L. DeLong and others, "Premature Births in California Sea Lions: Association With High Organochlorine Pollutant Residue Levels," SCIENCE Vol. 181 (Sept. 21, 1973), pgs. 1168-1170; and Peter J. H. Reijnders, "Reproductive failure in common seals feeding on fish from polluted coastal waters," NATURE Vol. 304 (Dec. 4, 1986), pgs. [456-457.]456-457.

Descriptor terms: pcbs; epa; lake michigan; nc; prenatal exposure; atsdr; westinghouse; donald suater; monsanto; munson report; ocean mammals; bioaccumulation; mi; health; studies;

#193: Human Breast Milk Is Contaminated.

=======================Electronic Edition========================

RACHEL'S HAZARDOUS WASTE NEWS #193
---August 8, 1990---
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========================

If breast milk from American women were bottled and sold commercially, it would be subject to ban by the U.S. Food and Drug Administration (FDA) because it is contaminated with more than 100 industrial chemicals, including pesticides. [1] FDA has set limits on contamination of commercial milk by pesticides, and human milk routinely exceeds those limits by a wide margin. (For example, see Table 1.)

We do not want to discourage breast feeding. Breast feeding is a highly desirable practice, despite the presence of toxic chemicals in human milk. Breast feeding gives an infant immunity against gastrointestinal diseases and respiratory infections; it may also offer protection against food allergies. The emotional bonding that takes place between mother and child can be exceedingly important as well. [2] Furthermore, the alternatives (prepared formulas) are all less healthy.

Still, it is important for Americans to recognize the consequences of allowing the chemical industry (and, more recently, the incineration industry) to expand unchecked, and contamination of breast milk is one well-established consequence. The problem is not widely acknowledged or often discussed, perhaps because it forces us to ask ourselves, what kind of people allow their infant children to ingest low concentrations of a hundred industrial poisons with every mouthful of their mother's milk?

Scientists first discovered that human breast milk was contaminated with DDT in 1951. [3] DDT, like many other chlorinated organic chemicals, is soluble in fat but not very soluble in water, so when it enters the body it is not easily excreted and it builds up in fatty (adipose) tissue. The main way that females excrete such chemicals is through their breast milk. Breast milk contains about 3% fat (average) and fat-soluble chemicals collect there. Unfortunately, this contaminates infant children who breast feed.

(When examining data on milk contamination, be aware that concentrations are sometimes given as ppm [parts per million] for fat, or ppb [parts per billion] for whole milk; fat concentrations are about 30 times higher than whole milk concentrations, so, for example, 2.5 ppm in fat is approximately equivalent to 75 ppb whole milk.)

The most extensive survey of the milk of American women was conducted by U.S. Environmental Protection Agency in 1975. They took samples from more than 1000 women, but analyzed them for only a few pesticides. They found DDT in 100% of samples; PCBs in 99% of samples; dieldrin in 83% of samples. EPA says DDT, dieldrin and PCBs are all "probable carcinogens" in humans.

There has been only one study of non-pesticide organic chemicals in the milk of American women. [1] It found 192 organic compounds, many of them well-known industrial poisons like carbon tetrachloride and benzene (both known human carcinogens). We list the 192 compounds in footnote 1. From reading the scant literature on this topic, one draws the unmistakable impression that further study would reveal more contamination.

Table 1 shows how grossly contaminated the milk of American women is, based on just four pesticides. The first column names the pesticide; column 2 gives typical levels of contamination reported in scientific studies; column 3 gives the FDA's "action level" for each pesticide; this is the level at which the FDA can (if it chooses to) take commercial cows' milk off the shelves because of excessive contamination; column 4 shows the allowable daily intake of each pesticide for an adult (expressed in micrograms of pesticide per kilogram of body weight). [There are 28 grams in one ounce; a kilogram is about 2.2 pounds.] The last column shows the actual daily intake for a nursing infant in America. It is clear that the actual daily intake by an infant exceeds an adults's allowable daily intake by anywhere from a factor of 6 to a factor of 14.

No allowable daily intakes have been calculated for infants, but it is known that infants are much more susceptible to toxic chemicals than are adults because an infant's kidneys, liver, enzyme systems, and blood-brain barrier are not fully developed. Furthermore, a newborn has very little body fat available for storage; consequently, the fat soluble chemicals are circulated in the blood throughout the body for a longer period and may interfere more intensely with normal enzyme activity.

These disturbing data are one more reason why the U.S. should begin now to institute a policy of "zero discharge" for all industrial chemicals (see RHWN #154, #155 and #187).

--Peter Montague, Ph.D.

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

[1] Edo D. Pellizzari and others, "Purgeable Organic Compounds in Mother's Milk." BULLETIN OF ENVIRONMENTAL CONTAMINATION AND TOXICOLOGY Vol. 28 (1982), pgs. 322-328, analyzed 12 samples of human milk from New Jersey, Pennsylvania and Louisiana; the following chemicals were identified (the percentage in parentheses indicates what percent of the 12 samples contained each chemical):

• Halogenated compounds: Chlorodifluoromethane (8%); chlorotrifluoromethane (33%); dichlorodifluoromethane (16%); chloromethane (16%); chloroethane (16%); trichlorofluoromethane (58%); dichloroethylene (8%); Freon 113 (75%); methylene chloride (75%); chloroform (58%); 1,1,1-trichloroethane (75%); carbon tetrachloride (42%); trichloroethylene (75%); chloropentane (16%); dibromochloromethane (8%); tetrachloroethylene (58%); dichloropropene (8%); chlorobenzene (42%); chlorohexane (33%); iodopentane (8%); 3-methyl-1-iodobutane (16%); chloroethylbenzene (8%); dibromodichloromethane (8%); dichlorobenzene (75%); chlorodecane (8%); trichlorobenzene (8%). Aldehydes: acetaldehyde (33%); methyl propanal (16%); n-butanal (50%); methyl butanal (16%); crotonaldehyde (8%); n-pentanal (58%); n-hexanal (75%); furaldehyde (16%); n-heptanal (58%); benzaldehyde (75%); n-octanal (25%); phenyl acetaldehyde (8%); n-nonanal (50%); methyl furaldehyde (8%); n-decanal (16%); n-undecanal (16%); n-dodecanal (8%).
• Ketones: acetone (75%); methyl ethyl ketone (42%); methyl propyl ketone (16%); methyl vinyl ketone (8%); ethyl vinyl ketone (33%); 2-pentanone (33%); methyl pentanone (16%); methyl hydrofuranone (8%); 2-methyl-3-hexanone (8%); 4-heptanone (8%); 3-heptanone (33%); 2-heptanone (50%); methyl heptanone (16%); furyl methyl ketone (8%); octanone (16%); acetophenone (75%); 2-nonanone (33%); 2-decanone (8%); alkylated lactone (8%); phthalide (8%).
• Other oxygenated isomers: C4H6O (8%); C4H8O (16%); C5H10O (42%); C6H8O (8%); C6H10O (16%); C4H6O2 (8%); C6H12O (16%); C7H12O (33%); C7H10O (16%); C7H14O (16%); C6H6O2 (8%); C8H14O2 (8%); C8H16O (16%); C7H8O2 (16%); C7H10O2 (8%); C9H18O (25%); C8H6O2 (8%); C10H12O2 (8%); C10H14O (8%); C10H16O (16%); C10H18O (25%); C10H20O (16%); C10H22O (8%); C9H8O2 (8%); C11H20O (8%); C10H10O2 (8%).
• Alcohols: methanol (8%); isopropanol (75%); 2-methyl-2-propanol (8%); n-propanol (8%); 1-butanol (25%); 1-pentanol (33%); à-furfuryl alcohol (16%); 2-ethyl-1-hexanol phenol (8%); 2,2,4-trimethylpenta-1,3-diol (8%); à-terpineol (8%).
• Acids: acetic acid (16%); decanoic acid (8%). 
• Sulfur compounds: sulfur dioxide (8%); carbon disulfide (75%); dimethyl disulfide (50%); carbonyl sulfide (8%). 
• Nitrogen compounds: nitromethane (8%); C5H6N2 (8%); C5H8N2 (8%); C4H4N2O (8%); methyl acetamide (8%); benzonitrile (25%); methyl cinnoline (8%).
• Esters: vinyl propionate (25%); ethyl acetate (8%); ethyl-n-caproate (8%); isoamyl formate (8%); methyl decanoate (8%); ethyl decanoate (8%).
• Ethers: dimethyl ether (8%); dihydropyran (16%).
• Epoxides: 1,8-cineole (8%).
• Furans: furan (8%); tetrahydrofuran (8%); methyl furan (16%); methyl tetrahydrofuran (8%); ethylfuran (16%); dimethylfuran (8%); 2-vinylfuran (8%); furaldehyde (16%); 2-n-butylfuran (8%); 2-pentylfuran (58%); methylfuraldehyde (8%); furyl methyl ketone (8%); à-furfuryl alcohol (16%); benzofuran (25%).
• Alkanes: C3H8 (8%); C4H10 (50%); C5H12 (75%); C6H14 (75%); C7H16 (58%); C8H18 (58%); C9H20 (75%); C10H22 (58%); C11H24 (58%); C12H26 (58%); C13H28 (25%); C14H30 (25%); C15H32 (16%). ALKENES: C3H6 (16%); C4H8 (42%); C5H10 (25%); C6H12 (75%); C7H14 (75%); C8H16 (75%); C9H18 (58%); C10H20 (50%); C11H22 (50%); C12H24 (8%); C13H26 (8%); isoprene (8%).
• Alkynes: C5H8 (16%); C6H10 (8%); C7H12 (25%); C8H14 (25%); C9H16 (33%); C10H18 (16%); C12H22 (8%).
• Cyclic: cyclopentane (50%); methyl cyclopentane (50%); cyclohexane (42%); ethyl methyl cyclohexane (8%); C10h14 isomers (8%); C10h16 isomers (other) (33%); limonene (75%); methyl decalin (8%); à-pinene (8%); camphene (8%); camphor (8%).
• Aromatics: benzene (75%); toluene (75%); ethylbenzene (75%); xylene (75%); phenyl acetylene (8%); styrene (75%); benzaldehyde (75%); C3-alkylbenzene isomers (75%); C4-alkylbenzene isomers (50%); methyl styrene (16%); dimethyl styrene (42%); C5-alkylbenzene isomers (16%); naphthalene (50%); C6-alkylbenzene isomers (8%).

[2] D.B. Jelliffe and E.F.P. Jelliffe, HUMAN MILK IN THE MODERN WORLD: PSYCHOSOCIAL, NUTRITIONAL AND ECONOMIC SIGNIFICANCE (NY: Oxford University Press, 1978).

[3] E.P. Laug and others, "Occurrence of DDT in Human Milk." ARCHIVES OF INDUSTRIAL HYGIENE Vol. 3 (1951), pgs. 245-246.

TABLE I: Typical levels of pesticides and PCBs in human milk in the U.S., FDA Action Levels, Allowable Daily Intake, and Actual Daily Intake of Breast-Fed Infants.

-------------------------- parts per billion --------------------------

Pesticide	Typical Levels (whole milk)	FDA Action Levels for whole milk (cows')	Allowable Daily Intake (Adult)	Actual Daily Intake (Infant)	Actual Daily Intake by Infants over the Allowable Daily Intake for Adults
Dieldrin	1-6	9	0.1	0.8	8 times higher
Heptachlor Expoxide	8-30	0.3	0.5	4.0	8 times higher
PCBs	40-100	63	1.0	14	14 times higher
Total DDT	50-200	38	5.0	28	5.6 times higher

Source: Walter J. Rogan and others. "Pollutants in Breast Milk," NEW ENGLAND JOURNAL OF MEDICINE Vol. 302 (June 26, 1980), pg. 1451, Table 3.

Descriptor terms: ddt; dde; pesticides; tolerance levels; risk assessment; human breast milk; lactation; food safety; infants; children; pcbs; heptachlor epoxide; allowable daily intake; adi; zero discharge; heptachlor; carcinogens; dieldrin; surveys; statistics; studies;

#490: Our Stolen Future, Part 3: Flying Blind

=======================Electronic Edition========================

RACHEL'S ENVIRONMENT & HEALTH WEEKLY #490
---April 19, 1996---
News and resources for environmental justice.
==========
Environmental Research Foundation
P.O. Box 5036, Annapolis, MD 21403
Fax (410) 263-8944; Internet: erf@rachel.clark.net
==========
RACHEL-4CM = DIOXIN FOCUSED DIRECTORY Remote Access Chemical Hazards Electronic Library. Dioxinnz.com ========================Original Source========================

OUR STOLEN FUTURE, the new book on hormone-disrupting chemicals, [1] provides many lessons about our use of chemicals, and about our reliance on science as a guide for public policy.

Here is a short discussion of the main lessons we find in the book (numbers inside parentheses are page numbers from the book):

** Genes are not destiny. Many people seem to think that we may be able to explain everything from cancer to homosexuality by locating the responsible genes. But in a series of scientific papers starting in 1980, Frederick vom Saal at University of Missouri demonstrated that there are other powerful forces shaping individuals--both females and males--before birth. Genes are not the whole story. Before birth, levels of both male and female sex hormones in the womb can affect the physical characteristics and the behavior of mice, giving rise to great variation in offspring that are genetically identical. By examining human twins, scientists have now revealed similar effects in humans. [2]Thus we now know that hormones are a way that nature provides variation within a species. Profound variation among individuals can be caused by miniscule hormone differences in the womb, differences of a few parts per trillion. (One part per trillion is a million times lower than one part per million.) This is a degree of sensitivity to hormones that approaches the unfathomable, a sensitivity, vom Saal says, "beyond people's wildest imagination." This exquisite sensitivity provides rich opportunities for creating varied offspring from the same genetic stock. However, the dark side is that this same sensitivity also makes the reproductive system vulnerable to serious disruption if something interferes with normal hormone levels. (pgs. 39-41)

** The exposure of a million American women to the drug, DES, in the 1960s and 1970s showed that the human body could mistake a synthetic (human-created) chemical for a natural hormone. (pg. 66)

** Another lesson from the work of vom Saal and others is that hormones in the womb permanently program (and organize) cells, organs, the brain, and behavior prior to birth, in many ways determining an individual's course for life. (pgs. 39-40)

** The dose of hormones that an embryo receives is not the only thing that matters; the TIMING of the dose --WHEN it occurs during development in the womb --can be as important as the dose itself. (pgs. 50-51)

** Birth defects may not be noticeable at birth. Serious effects of hormones on the unborn and on the newborn may not be recognizable for decades. (pg. 66)

** In fact, birth defects may never become visible at all, but may involve cellular damage that undermines an organism's ability to survive. For example, exposure to the drug DES, a synthetic hormone, gave rise to a rare form of cancer in female children of DES-exposed women. (pg. 66)

** Mice and humans share a common fate. To an astonishing degree, evolution has retained through hundreds of millions of years a basic strategy for embryonic development in vertebrates [creatures with a backbone] which depends on hormones. Regardless of whether the offspring is a human or a mouse, a whale or a bat, a turtle or an alligator, hormones regulate its development in fundamentally the same way. In the field of cancer research, scientists argue that data gathered from experiments on mice may not reveal anything useful about humans. This uncertainty occurs because the underlying causes of cancer are poorly understood. On the other hand, the working of hormones is better understood, and knowledge gained from experiments on non-humans CAN reveal useful information about humans. "It is important to take the effects we see in animals seriously," says Dr. Earl Gray, a senior research biologist with U.S. Environmental Protection Agency [EPA]. (pg. 66)

** Industrial chemicals at exceedingly low levels can combine together to produce additive effects. Dr. Ana Soto at Tufts University combined 10 hormone disrupters, each at one-tenth of the dose required to produce a minimal response; she found that the combination produced a response. [3] Thus combinations of chemicals must be taken into account when we try to learn how much "effective exposure" we are getting to hormone-disrupting chemicals.

** Testing hormones at high doses may reveal no effects whereas testing the same hormones at low doses may reveal dramatic effects. This is contrary to the traditional assumptions of toxicology [study of poisons]. The dose-response curve for many hormones is U-shaped: at low doses, the hormones cause effects but at high doses the system becomes overwhelmed and shuts down. This has profound implications for testing. Traditionally, chemicals have been tested on laboratory animals at high doses; now we know that tests must be conducted at low doses as well. (pgs. 169-170)

** Up to now our concept of injury from toxic chemicals had focused on two things: (a) whether a chemical attacks the DNA inside cells, possibly causing cancer; or, (b) whether a chemical damages and kills cells, the way poisons do. However, hormone-disrupting chemicals may not kill or damage cells, and they may not damage DNA. Thus they do not fit the definition of "poisons" or "carcinogens" yet they may cause great harm by disrupting normal growth and development of many organs and tissues, including sex organs, the brain, the nervous system, and the immune system. The key concept in thinking about this kind of toxic assault is the disruption of chemical messages. (pgs. 203-204)

** The traditional approach to toxic chemicals is to look for disease as a result of exposure. However, hormone-disrupting chemicals may not cause "disease" at all: they may cause diminished function --reduced IQ, poorer short-term memory, diminished ability to pay attention, reduced sperm count. These are not signs of "disease" yet they are toxic effects that can be caused in some species by some hormone-disrupting chemicals. (pgs. 205-206)

** To screen for chemicals that cause diminished function, it will be necessary to look for developmental effects across three generations. The first generation (the generation that gets the initial exposures) may not be affected at all. The second generation may have diminished function (for example, diminished ability to reproduce) but the actual effects may not be apparent until the third generation (the grandchildren of the exposed generation). (pg. 207)

** We are flying blind. (pgs. 243, 246) We cannot know whether the ominous shape looming into view is a cloud bank or a mountain. If anything is certain, it is that we must expect more unpleasant surprises. We are flying blind; we can never know that new chemicals are safe (though, if we chose to, we could do a much more thorough job of testing them than we've done in the past).

To show that we are flying blind, OUR STOLEN FUTURE relies on the evidence of hormone-disrupting chemicals and of depletion of the earth's ozone shield by human-created chemicals (see REHW #246, #259, #259).     But there is much additional evidence that could have been cited as well. For example, during just the past 25 years, we have been surprised by:

** Global warming brought on by combustion of fossil fuels (REHW #467, #466);   

** Mercury build-up to toxic levels in the bodies of fish (chiefly from burning coal, oil, and municipal solid waste) (REHW #291);

** Increasing birth defects in American children. Of 38 kinds of birth defects for which the Centers for Disease Control maintains records, 29 have increased during the past 20 years (REHW #410, #411);  

** Steadily increasing cancers, particularly of the reproductive system (prostate; testicles; female breast) and nervous system (brain) (REHW #412, #447, #462);    

** The astonishing toxicity of a family of chemicals called dioxins and furans (including some PCBs, or polychlorinated biphenyls), which now contaminate the entire planet from the depths of the oceans to the polar ice caps (REHW #390 , #391, #414);

** The accelerated loss of species, which, according to the fossil record, is now occurring at rates 10 to 1000 times as fast as natural background rates that were occurring before humans appeared on the scene (REHW #441);

** Acid rain damaging lakes, killing trees, stunting forests, and washing nutrients from soils across much of the northeastern U.S., southern Canada, and northern Europe (REHW #476); ** Rapidly increasing immune system disorders such as asthma (REHW #374) and diabetes (REHW #417);

** Epidemics of disease among marine mammals (seals, dolphins, etc.), apparently related to chemical contamination and to blooms of toxic algae caused by excesses of nutrients (chiefly nitrogen and phosphorus) in near-shore marine ecosystems (REHW #466);

** Diminished IQ and reduced ability to concentrate among 1.7 million American children and 300 to 400 thousand fetuses (at any given moment in time), as a result of exposures to the toxic metal, lead (REHW #369);

** Disappearance or decline of some frog and other amphibian populations worldwide (REHW #380, #441);

** Steep declines or near-total depletion of fish stocks at 13 of the world's 17 major fisheries (REHW #399).

** Decline of 50% in sperm among men in industrial countries (REHW #432, #446 , #448a), and a significant loss of sperm quality during the same period.

** A 60% increase in the rate of migraine headaches among Americans during the period 1980 to 1990. 

Most (71%) of the increase occurred among people aged less than 45 years. [4]

This does not exhaust the evidence, but represents a fair sample of the kinds of problems that have suddenly loomed into view since 1970. Have we encountered the last of such unsuspected and unlooked-for problems? Certainly not. No, there doesn't seem to be any doubt about it: we are rushing forward at high speed with no sure way to learn what hazards lie ahead. We really are flying blind. To us, this seems the most important lesson of OUR STOLEN FUTURE.

Under such circumstances, can science provide us with adequate guidance? 

Next week.#491

--Peter Montague

=============== 

[1] See REHW #485 and #486, reviewing Theo Colborn, Dianne Dumanoski and John Peterson Myers, OUR STOLEN FUTURE (N.Y.: Dutton, 1996).

[2] F. vom Saal and F. Bronson, "Sexual Characteristics of Adult Female Mice Are Correlated with Their Blood Testosterone Levels During Prenatal Development," SCIENCE Vol. 208 (1980), pgs. 597-599. And see: M. Clark and others, "Hormonally Mediated Inheritance of Acquired Characteristics in Mongolian Gerbils," NATURE Vol. 364 (1993), pg. 712. Hormones have also been shown to affect humans exposed in the womb: D. McFadden, "A Masculinizing Effect on the Auditory Systems of Human Females Having Male Co-Twins," PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCE Vol. 90 (1993), pgs. 11900-11904.

[3] Reported in Ana M. Soto and others, "The Pesticides Endosulfan, Toxaphene, and Dieldrin Have Estrogenic Effects on Human Estrogen-Sensitive Cells," ENVIRONMENTAL HEALTH PERSPECTIVES Vol. 102, No. 4 (April 1994), pgs. 380-383.

[4] "Prevalence of chronic migraine headaches -United States, 1980-1989," MORBIDITY AND MORTALITY WEEKLY REPORT Vol. 40, No. 20 (May 24, 1991), pgs. 331-333.

Descriptor terms: endocrine disrupters; hormones; our stolen future; des; diethylstilbestrol; frederick vom saal; ana soto; science; oceans; marine mammals; global warming; mercury; fish; wildlife; birth defects; cancer; dioxins; furans; pcbs; species loss; acid rain; lead; migraine headaches; theo colborn; john peterson myers; dianne dumanoski;