#375: Cancer Down On the Farm

=======================Electronic Edition========================
RACHEL'S HAZARDOUS WASTE NEWS #375 
---February 3, 1994---
News and resources for environmental justice.
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The U.S. is losing its war on cancer, according to a long article in the January, 1994 SCIENTIFIC AMERICAN. [1] The basic measure of success or failure -- the age-adjusted cancer death rate -- continues to climb slowly year after year, despite $25 billion spent to find a cure since 1971 when Richard Nixon declared a national "war on cancer."

The cancer establishment--the largely male, largely white and largely elderly group of researchers who act as gatekeepers for cancer research dollars--try to put a good face on it. They point to reductions in deaths from childhood cancers, reductions in cancer deaths among young adults, and reductions in deaths from some specific cancers. Still the fact remains that the total age-adjusted death rate for cancer continues to climb year after year. The rise in the cancer death rate is particularly steep among people 65 and over.

The cancer establishment tends to blame cancer on individual lifestyles, such as diets high in fat and low in fiber. There is one major problem with this argument. Heart disease is known to be associated with cigarette smoking, heavy use of alcohol, and diets high in fat and low in fiber and low in antioxidants [beta-carotene, vitamin E and selenium, for example]. In several countries heart disease rates are decreasing. In the U.S., heart disease is down 40% from its peak in the 1960s. It therefore seems unlikely that recent increases in cancer are caused by the same factors that cause heart disease.

Now a group of younger cancer researchers is advocating a return to the fundamental principles of public health developed during the 19th century, based on prevention. Much of cancer is thought to be preventable because rates of occurrence and death vary substantially from one population to another. Environmental factors are likely to account for much of this variation.

Between 1969 and 1986, several cancers increased significantly among persons aged 64 to 84 in six industrial countries. [2] Multiple myeloma [cancer that starts in the bone marrow and spreads to various bones, especially the skull], melanoma of the skin, and cancers of the prostate, bladder, brain, lung and breast are increasing in the general population of several industrial countries. Except in the case of lung cancer, these increases remain largely unexplained.

In the last two years, cancer prevention researchers have focused new attention on environmental chemicals. Devra Lee Davis and others have developed a hypothesis about the cause of breast cancer in women. For a long time researchers have known that exposure to estrogen (the female hormone) increases a woman's risk of breast cancer. Now Davis has shown that many fat-soluble industrial chemicals, widely distributed in the environment, mimic or amplify the biological effects of estrogen. [3] [See RHWN #369.] The National Cancer Institute is now planning to establish a laboratory to study "hormonal carcinogenesis" (hormones as causes of cancer).

Now a second hypothesis has been developed by Devra Davis, Aaron Blair, Sheila Hoar Zahm, Neil Pearce, Joseph Fraumeni, and others at the National Cancer Institute, asking about the role of pesticides in certain cancers. The hypothesis begins by examining the health of farmers.

Two million farm workers, and three million farmers and their families, form a large occupational group exposed to toxic chemicals. [4] Farmers are a relatively healthy group. For any given age, farmers have a low overall mortality rate, indicating general good health. Compared to the general public, farmers have lower risk for ischemic heart disease [narrowing of the coronary arteries], and for all causes of cancer combined. [5] Farmers also have lower risks for cancers of the lung, esophagus, bladder, colon, liver, and kidney.

Low rates of cancer for lung, esophagus, and bladder, and low rates of heart disease, can be explained by low prevalence of smoking among farmers, which has been noted in numerous studies.

In addition, farmers have a low percentage of body fat, and a high measure of physical fitness, probably because they perform hard physical labor that keeps them in good shape. This good physical condition probably contributes to lower risks for heart disease and colon cancer, both of which are associated with a sedentary lifestyle.

Farmers also eat a relatively large amount of fruits and vegetables, compared to the average American, and relatively small amounts of processed foods. As a consequence, farmers' diets are most likely higher in fiber than the average diet. Furthermore, in general, farmers reside in areas with little air pollution.

However, despite their generally good health, farmers have higher-than-general-population risks for certain cancers: non-Hodgkin's lymphoma, skin melanomas, multiple myeloma, leukemia [cancer of the blood-forming organs], and cancers of the lip, stomach, prostate, and brain.

These high rates of a few select cancers among farmers, against a background of low risks for most cancers and for non-cancer diseases, suggests that work-related exposures may be causing specific cancers among farmers.

These patterns may have broad public health implications since several of the high-rate tumors among farmers are the same cancers that appear to be increasing in the general population of many developed countries: multiple myeloma, non-Hodgkin's lymphoma, melanoma of the skin, and cancers of the prostate and brain.

There are several factors that could be causing these cancers among farmers: farmers are out in the sun a lot, and ultraviolet sunlight is associated with melanoma and cancer of the lip. Exposure to phenoxy herbicides (2,4-D, 2,4,5-T, acilfluorfen, CNP, erbon, mecoprop, and others) has been linked to non-Hodgkin's lymphoma, and to soft tissue sarcoma. [6] Exposure to insecticides has been associated with leukemia, multiple myeloma, and brain cancer. It is possible that animal viruses may play a role in some farmers' cancers because elevated risks of leukemia, soft tissue sarcoma, and non-Hodgkin's lymphoma have been seen in slaughterhouse workers and veterinarians.

But there is also another possibility. Perhaps something in the environment damages the immune systems of farmers, who then fall prey to cancers that healthy immune systems would have been able to ward off.

It is noteworthy that the same cancers that affect farmers also affect people whose immune systems have been damaged by disease, or by medical intervention. Patients with AIDS (acquired immune deficiency syndrome) experience striking excesses in non-Hodgkin's lymphoma. (However, the AIDS epidemic does not provide a complete explanation for the increase in non-Hodgkin's lymphoma among the general population. The general increase started before the AIDS epidemic began. In the U.S., the greatest increases in non-Hodgkin's lymphoma, multiple myeloma, and leukemia have occurred in rural agricultural areas of the central region of the country.)

People who have organ transplants are given drugs to suppress their immune systems because the immune system would normally reject a foreign organ; these people, too, have high rates of non-Hodgkin's lymphoma. Brain and skin cancers occur among bone marrow transplant recipients; soft-tissue sarcomas, skin melanomas, and squamous cell carcinomas of the skin and lip occur in kidney transplant patients; leukemia and stomach cancers occur in people with immunodeficiency diseases.

This similarity between cancers associated with immunosuppression and cancers among farmers suggests that farmers' cancers may be caused by environmental factors that damage the immune system.

There is a large and convincing body of evidence showing that pesticides harm the immune systems of laboratory animals. [7] However, the number of human studies is very small. In humans, pesticide exposures have been linked to a variety of immune system effects including decreased host resistance to disease; suppressed T-cell activity; enhanced B-and T-cell immune response; and contact hypersensitivity. T-and B-cells are particular kinds of cells that circulate in the blood and protect the body by fighting off bacteria, viruses and cancer cells.

Increasingly, the general public is exposed to the same chemicals that farmers are exposed to. And, as we saw last week,#374 there is evidence that immune disorders are increasing in the general population. The hypothesis of Davis and her colleagues, that chemicals (or other factors) on farms are increasing the cancer rates among farmers, could have important consequences for us all. It represents a new kind of tough, creative thinking that has been missing from the war on cancer up until now.

--Peter Montague, Ph.D.

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

[1] Tim Beardsley, "A War Not Won--Trends in Cancer Epidemiology," SCIENTIFIC AMERICAN Vol. 270 (January 1994), pgs. 130-138.

[2] Devra Lee Davis, David Hoel, John Fox, and Alan Lopez, "International Trends in Cancer Mortality in France, West Germany, Italy, Japan, England and Wales, and the USA," THE LANCET Vol. 366, No. 8713 (August 25, 1990), pgs. 474-481.

[3] Devra Lee Davis and others, "Medical Hypothesis: Xenoestrogens As Preventable Causes of Breast Cancer," ENVIRONMENTAL HEALTH PERSPECTIVES Vol. 101 (October 1993), pgs. 372-377.

[4] Marion Moses, "Pesticide-Related Health Problems and Farmworkers," AAOHN [AMERICAN ASSOCIATION OF OCCUPATIONAL HEALTH NURSES] JOURNAL Vol. 37 (March 1989), pgs. 115-130.

[5] Devra Lee Davis and others, "Agricultural Exposures and Cancer Trends in Developed Countries," ENVIRONMENTAL HEALTH PERSPECTIVES Vol. 100 (1992), pgs. 39-44. And: Aaron Blair and others, "Clues to cancer etiology from studies of farmers," SCANDINAVIAN JOURNAL OF WORK, ENVIRONMENT AND HEALTH Vol. 18 (1992), pgs. 209-215.

[6] See studies of farmers and others reviewed in the Institute of Medicine's study, VETERANS AND AGENT ORANGE: HEALTH EFFECTS OF HERBICIDES USED IN VIETNAM (Washington, D.C.: National Academy Press, 1993).

[7] P.T. Thomas and others, "Immunologic Effects of Pesticides," in Scott R. Baker and Chris F. Wilkinson, editors, THE EFFECTS OF PESTICIDES ON HUMAN HEALTH (Princeton, N.J.: Princeton Scientific Publishing, 1990), pgs. 261-295.

Descriptor terms: cancer statistics; mortality; morbidity; diet; fat; fiber; antioxidants; heart disease; prevention; multiple myeloma; melanoma; skin cancer; prostate; bladder; brain; lung; breast; estrogen; agriculture; farm workers; farmers; smoking; air pollution; sunlight; phenoxy herbicides; viruses; soft tissue sarcoma; non-Hodgkin's lymphoma; aids; organ transplants; immune system; studies; hypotheses;

#377: Scientists Pretending

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RACHEL'S HAZARDOUS WASTE NEWS #377 
---February 17, 1994---
News and resources for environmental justice.
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For the past 3 or 4 years, evidence has been accumulating that many industrial chemicals (including many common plastics, pesticides, and by-products of combustion) mimic hormones. These hormone mimickers disrupt reproduction and development in humans and in many other species of mammals, birds, and fish. A growing body of evidence also indicates that these same chemicals may cause some of the most common and fastest-increasing cancers: breast cancer in women, and cancers of the testicles and prostate in men.

The American Chemical Society [ACS] recently affirmed the following phenomena: [1]

** Sperm count in men worldwide has dropped to 50% of what it was 50 years ago.** The incidence of testicular cancer has tripled in some countries in the last 50 years and prostate cancer has doubled.** Endometriosis--the growth outside the uterus of cells that normally line the uterus--which was "formerly a rare condition, now afflicts 5 million American women," the ACS said.** In 1960, a woman's chance of developing breast cancer during her lifetime was one in 20. Today the chances are one in nine.** Female common terns (sea birds) are sharing nests near a PCB-contaminated site in New Bedford Harbor, Mass., an unnatural female-female pairing.** Young male alligators in pesticide-contaminated lakes in Florida are growing up with penises so small that they are "sexually incompetent."

In January, the federal National Institute of Environmental Health Sciences [NIEHS] convened a meeting of 300 scientists who presented papers on estrogens and estrogen mimickers in the environment. Many of those scientists think there's probably a connection between diminished sperm counts, increasing endometriosis, female-to-female pairing in birds, sexually incompetent alligators, and breast cancer in women. The connection is poorly understood, they say, but the common link is probably chemicals dumped into the environment that mimic, or interfere with, hormones.

Slowly, mainstream scientific thinking has been coming to grips with this accumulating bad news. First the American Chemical Society began to write about it. [2] Then the National Institute of Environmental Health Sciences [NIEHS], a division of the U.S. National Institutes of Health, started writing about it. [3]And this month the JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION (JAMA) broke the story for its readers: "Estrogen and [chemical] agents that mimic it appear to be more pervasive and problematic then ever suspected," JAMA said February 9th. [4]

Estrogen is usually considered a female hormone, but males produce estrogen too, in small amounts. In the developing fetus, in both humans and animals, a specific ratio of estrogen to androgens (male hormones) must be maintained for proper sexual differentiation to occur; in other words, for a male to become a male and a female to become a female --regardless of the species --a certain balance of male and female hormones must be present in the mother between the time of fertilization and the time of birth or hatching.

If the hormone balance is disturbed, the offspring will be born with two sets of partially developed sex organs (intersex), or with a single set that is incompletely or improperly developed. Diminished sperm count, or future cancer, may be set at this early stage.

All plants and animals are composed of cells --tiny bags of fluid that work cooperatively together to carry out metabolism (extraction of energy from nutrients) to maintain life. The human body is composed of roughly 50 trillion individual cells that all cooperate and communicate with each other. Hormones are chemical messengers, essential to the body's healthy cooperation and internal communication. Hormones are present at very low levels (parts per billion or even parts per trillion), and often for only short periods of time, yet they have very powerful, long-lasting effects on growth, development, and metabolism.

The female hormone, estrogen, and chemicals that mimic estrogen, operate inside cells by fitting themselves into "estrogen receptors" (proteins) the way a key fits into a lock. Once the key is in the lock, the key-and-lock together can move into the nucleus of a cell and attach to the DNA, releasing messenger RNA which then causes a cascade of changes in cells, tissues, and organs throughout the body.

No, the story of estrogen mimickers is not simple. Some estrogen mimics fit into the lock wrong, filling up the space that the "correct" key would have used, thus interfering with natural estrogens; these are called estrogen antagonists. Some estrogen mimickers fit into locks that weren't ever intended to have an estrogen fitted into them. The amount of natural estrogen in the mother is usually much greater than the amount of estrogen mimickers. However most natural estrogens are bound up by sex-hormone-binding proteins in the blood stream, which are not able to bind estrogen mimickers. This increases the effective dose of the mimickers. The many ways estrogen mimickers can cause problems are just now beginning to be appreciated.

"The structural diversity of estrogenic chemicals is enormous," says John A. McLachlan, chief of the reproductive and developmental toxicology laboratory at NIEHS, according to JAMA.

In other words, you cannot simply observe a molecule and tell, by its chemical structure, whether it will act as an estrogen mimic or not.

"Compounds with widely different structure bind to estrogen receptors even though they bear no obvious structural resemblance" to estrogen, says John A. Katzenellenbogen, professor of chemistry at University of Illinois.

Examples of estrogen mimickers are DDT and its breakdown by-product DDE; Kepone; dieldrin; dicofol; methoxychlor; some PCBs; 3,9-dihydrooxybenz[a]anthracene; and alkyl phenols from penta-to nonylphenol, as well as bisphenol-A (the building block of polycarbonate plastics) which is used in many common detergents, toiletries, lubricants, and spermicides. Many estrogen mimickers are persistent (they resist breaking down in the environment) and highly soluble in fat (causing them to accumulate in the bodies of fish, birds, and mammals, including humans). Many of them cross the placental barrier and pass from the mother to the developing fetus.

It is not simple to distinguish estrogens from non-estrogens. "Historically, we think of the receptor as a switch," turning on or off the body's reactions. But it is not that simple, says George M. Stancel, head of the department of pharmacology at University of Texas Medical School. Estrogen-like chemicals can form "many molecular configurations" that can "act in differing ways," Stancel told JAMA. The same chemical can also act differently in different tissues, Stancel said.

To complicate the picture further, some cells appear to have estrogen receptors on their surface, rather than inside. So "even if compounds do not manage to get inside cells, they may still be estrogenic," says Cheryl Watson, associate professor of biological chemistry at the University of Texas Medical Branch at Galveston.

Finally, JAMA reported that estrogenic chemicals have a cumulative effect. David Feldman, professor of medicine and endocrinology at Stanford University, says, "The cumulative effect may be much greater than any individual molecule." Ana M. Soto at Tufts University combined 10 estrogen mimickers, each at one-tenth of the dose required to produce a minimal response; she found that the combination produced an estrogenic response.

This last bit of information has far-reaching implications for the regulation of chemicals. For 50 years the U.S. has regulated chemicals one by one, by conducting laboratory experiments on animals, and by experimenting on workers. If rats or workers get sick, then a particular chemical may be regulated to a level 10 times (or 100 times) lower than the lowest amount that caused an observable effect.

If chemicals at low ("safe") levels combine to produce an effect, this means that chemicals will have to be regulated in combination. "Testing mixtures is right on the mark" says George M. Stancel, at University of Texas Medical School. Kenneth Olden, head of NIEHS, agrees. "[W]e cannot ignore this milieu we live in that has all these estrogens. We have polluted our environment. It is polluted. Now we have to allocate resources to sort out the different effects of agents and learn whether they are synergistic, additive, inhibitory, or antagonistic. We don't know," Olden says, meaning we must try to learn whether chemicals in various combinations are weaker or stronger than each chemical alone.

But these are scientists pretending. Pretending that science can do something it cannot actually do. There is not sufficient money to study the full effects of individual chemicals, much less combinations of chemicals.

Scientists can pretend that they can discern "safe" levels of hundreds of different chemicals, all acting in combination. They can pretend that they can understand all the ill effects of multiple hormone mimickers on each type of cell, each tissue and each organ at every stage of development from conception to birth, through youth and puberty and into maturity, in each of the thousands of affected species. They can pretend to know these things, but they cannot ever actually know them. They are just pretending.

Scientists can pretend, but in so doing they perform a great disservice, preventing decision-makers from seeing what really needs to be done: we need to abandon the practice of chemical-by-chemical regulation. We need to regulate whole CLASSES of chemicals. And the dangerous classes need to be phased out and banned. Zero discharge. Pollution prevention. These are the keys to sustainability and survival.

 --Peter Montague, Ph.D.

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

[1] Bette Hileman, "Environmental Estrogens Linked to Reproductive Abnormalities, Cancer," C&EN [CHEMICAL & ENGINEERING NEWS] January 31, 1994, pgs. 19-23.

[2] Bette Hileman, "Concerns Broaden over Chlorine and Chlorinated Hydrocarbons," C&EN [CHEMICAL & ENGINEERING NEWS] April 19, 1993, pgs. 11-20.

[3] Theo Colborn, Frederick S. vom Saal, and Ana M. Soto, "Developmental Effects of Endocrine-Disrupting Chemicals in Wildlife and Humans," ENVIRONMENTAL HEALTH PERSPECTIVES Vol. 101 No. 5 (October 1993), pgs. 378-384.

[4] Paul Cotton, "Environmental Estrogenic Agents Area of Concern," JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION Vol. 271 (February 9, 1994), pgs. 414, 416.

Descriptor terms: endocrine disruptors; estrogen; androgens; hormones; wildlife; endocrine system; reproductive system; niehs; national institutes of health; national institute of environmental health sciences; nih; american medical association; ddt; dde; pesticides; plastics; dicofol; methoxychlor; pcbs; polychlorinated biphenyls; alkyl phenols; bisphenol-a; polycarbonate plastics; detergents; toiletries; lubricants; spermicides; pentaphenol; nonylphenol; 3,9-dihydrooxybenz[a]anthracene;

#398: the theories of Bruce Ames

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RACHEL'S HAZARDOUS WASTE NEWS #398
---July 14, 1994---
News and resources for environmental justice.
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Environmental Research Foundation
P.O. Box 5036, Annapolis, MD 21403
Fax (410) 263-8944; Internet: erf@igc.apc.org ==========
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The NEW YORK TIMES ran a long article July 5th explaining the theories of Bruce N. Ames, the controversial biochemist from Berkeley. [1] Ames's basic idea is that most of the poisons we ingest are natural toxins appearing in our food; from this, he concludes that money spent controlling industrial chemicals is largely wasted. The TIMES'S story occupied 87 column-inches and contained only one sentence that challenged Ames, thus suggesting that Ames's ideas are almost beyond question. [2] That is not the case. 

Here is an incomplete list of problems with the Ames hypothesis:

1) Production and use of synthetic pesticides (and other synthetic organic chemicals) emits large quantities of hazardous materials into the environment. Workers and neighbors at manufacturing and waste disposal facilities are exposed to toxins. THE NATIONAL CANCER INSTITUTE'S CANCER MAPS REVEAL CANCER CLUSTERS NEAR INDUSTRIAL FACILITIES. IT IS VERY UNLIKELY THAT SUCH CLUSTERS OCCUR BY RANDOM CHANCE. In the TIMES, Ames acknowledged this problem when he said, "Environmental pollutants are not an important cause of cancer. They account for a tiny percent of cancers in Americans but might be a problem in people like farm workers who apply pesticides if they are heavily exposed." Or in anyone else heavily exposed, he might have added.

2) Natural toxins and pesticides that occur in vegetation do not build up in the environment; nature has ways of reassimilating (decomposing) them. On the other hand, the concentration of synthetic (human-created) pesticides and other synthetic organic chemicals is increasing in the environment. Synthetic pesticides are now measurable in groundwater in many states, and the concentrations are growing as time passes. Many pesticides, and industrial poisons such as PCBs, are measurable in all the world's oceans, and even in the polar ice caps. There is compelling evidence that wildlife is being harmed (in some instances, driven to extinction) by this buildup of exotic chemicals throughout the global ecosystem. [3]

3) Ames presents himself as an expert on cancer, yet he makes sweeping generalizations that go far beyond his studies of cancer. In this, he has abandoned science and taken up politics. (Ames opposes government regulation on principle.) He says, for example, "We're shooting ourselves in the foot with environmental regulations that cost over 2 percent of the G.N.P., much of it to regulate trivia." Even if it were true that industrial chemicals cause only a small fraction of all cancers, cancer is not the only problem that we should consider when we examine the wisdom of dumping billions of pounds of pesticides and other industrial poisons into the environment each year. During the past decade, much new information has come to light indicating that many chemicals damage the nervous, immune and endocrine systems of wildlife (fish, birds, and mammals) and humans. According to these studies, one clear result is reproductive and developmental damage in the affected species, and an increased likelihood of succumbing to bacterial and viral infections as well as cancers. Ames ignores the non-cancer effects.

To cite but one example, the National Academy of Sciences acknowledged in a 1992 study, "In the general population, increasing numbers of people suffer from disorders of the immune system, such as allergies, asthma, and AIDS. The incidence of asthma has increased 58% since 1970, and it is well known that nitrogen dioxide and ozone, common air pollutants, interact with allergens to increase the frequency and severity of asthma attacks." [4] Ames ignores the evidence that pollution weakens the human immune system; he insists that we are wasting money curbing industrial discharges because industrial poisons do not cause many cancers, he says --as if cancer were the only problem created by industrial poisons. This is neither good science nor good public policy.

4) Chemical toxicity and exposures are poorly understood because current knowledge is based on:

(a) chemical tests that do not take into consideration children and the elderly, people who are already sick from something else, and populations that eat unusual quantities of one or more food items (e.g., native people who eat a lot of fish);

(b) chemical tests that omit the combined effects of multiple exposures because science has no affordable way of assessing combined and cumulative effects.

This is a point worth emphasizing because Ames makes sweeping generalizations based on data derived from testing one chemical at a time, as if combinations of chemicals don't occur in the real world.

A recent study focused on this problem. In June, three scientists from the National Institute for Occupational Safety and Health (NIOSH) in Cincinnati, Ohio announced an "inherent problem with the way workplace risks are characterized." [5] The "inherent problem" is that workers are usually exposed to many contaminants simultaneously, while "health standards are almost always designed to protect workers from a single exposure." In 25 percent of cases studied, the NIOSH researchers reported what they called an "alarming finding." They reported that, "when animals were exposed to several [chemical] agents at once, the animals (or their offspring) experienced a dramatically increased number of adverse health effects." "In fact," the NIOSH researchers said, "the reported health effects were many times greater than expected by simply adding the effects of each substance." (They also found, in 25% of cases, that combinations of chemicals produced FEWER effects than they would have expected.)

The NIOSH researchers reported that exposure of rats to the common plasticizer, di(2-ethylhexyl) phthalate (DEHP), produced prenatal death in 16 percent of the fetuses and congenital defects (birth defects) in 21 percent of the surviving fetuses. Exposure of rats to caffeine produced prenatal death in about 9 percent of fetuses and defects in 3 percent of the surviving fetuses. However, exposure to DEHP and caffeine simultaneously produced prenatal death in 80 percent of the fetuses and defects in 73 percent of the surviving fetuses.

The researchers point out that risk assessments should consider not only job-related chemical exposures but also prescription and non-prescription drugs. In addition, they say physical agents such as vibration, heat and noise must be considered as well. (And, if Ames is correct in his estimate of the potency of natural toxins in our food, natural toxins must be factored in too.)

The NIOSH team points out that, in nearly every work environment, there is a pervasive physical agent: non-ionizing electromagnetic radiation. One type of non-ionizing radiation, radio-frequency (RF) radiation, is used in a number of industries, including communications, electronics, medical and manufacturing. Many workers in these industries are exposed to RF energy at the same time they are exposed to exotic chemicals.

For years, RF exposures were assumed to be benevolent because they do not ionize (knock electrons off of) molecules or cells the way higher-energy radiation (ionizing radiation, such as x-ray energy) does. To test the hypothesis that RF might enhance the effects of chemicals, the NIOSH researchers exposed rats to a combination of 2-methoxyethanol (2ME) and RF energy. 2ME is a common glycol ether used in some degreasing solvents, and in some paints and varnishes. Alone, 2ME causes developmental toxicity in every species of animal tested to date, including non-human primates (monkeys). To test the interaction of RF energy and 2ME, rats were exposed to these substances on the 13th day of gestation, alone and in combination. RF radiation caused malformations in 30 percent of the rat fetuses, and 2ME produced malformations in 14 percent. Yet, combined exposure to 2ME and RF induced external malformations in 76 percent of the fetuses, "and these malformations were more severe than after single-agent exposure," the NIOSH researchers reported. Subsequent studies of different doses during various gestation times confirmed these findings, they said.

Another study reported by the NIOSH researchers indicates that noise and solvents combine to induce hearing loss in workers to a greater degree than either solvents or noise alone. They studied 200 workers (50 controls, 50 exposed to noise, 39 exposed to organic solvents alone, and 51 exposed to noise and toluene, a common organic solvent). The authors concluded that simultaneous occupational exposure to excessive levels of toluene and noise increased the probability of developing hearing loss. The NIOSH workers summarized, "The effect of combined exposure also suggested a synergistic [multiplier] interaction between noise and toluene on hearing loss. The level of hearing loss was much greater in workers exposed to both hazards than would be predicted by adding the effect of each agent."

Thus we can see that Bruce Ames --and others like him who belittle effects of chemicals on human and environmental health based on incomplete data and erroneous assumptions --may be underestimating the true hazards because they test only one substance at a time. Humans almost never encounter substances one at a time. Toxins in food, drugs (both pharmaceutical and "recreational"), air pollution, water pollution, noise, vibration, heat, electromagnetic radiation and ionizing radiation usually impact us simultaneously. They not only cause cancer but they affect the nervous, endocrine and immune systems in ways that are poorly understood. Risk assessment has no way to take into account such complex and cumulative interactions. The only approach that can consider all these effects together is prevention, the principle of precautionary action. (See RHWN #284, #319, and #378.) Bruce Ames represents solid 19th-century toxicological thinking, but a complex technological world requires that we adopt more modern and more prudent views, based on real-world exposures to combinations of natural and industrial hazards. For developing such a modern approach, many of Bruce Ames's sweeping generalizations are not only wrong and wrong-headed; they are also largely irrelevant.

--Peter Montague

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

[1] Jane E. Brody, "Strong Views on Origins of Cancer," NEW YORK TIMES July 5, 1994, pgs. C1, C10.

[2] In Brody, cited above, David Rall, former director of the National Institute of Environmental Health Sciences, says Ames's generalizations are based on "incomplete data" since "most of the chemicals we're exposed to haven't been tested for carcinogenicity."

[3] "Statement from the Work Session on Environmentally-Induced Alternations in Development: A Focus on Wildlife; Wingspread Conference Center, Racine, Wisconsin December 10-12, 1993." [A consensus statement from 23 scientists published, accompanied by a news release, April 20, 1994 by the World Wildlife Fund in Washington, D.C.; for a copy, phone: (202) 778-9510 or (202) 778-9536.]

[4] David W. Talmage and others, BIOLOGIC MARKERS IN IMMUNOTOXICOLOGY (Washington, D.C.: National Academy Press, 1992), pg. 1.

[5] B.K. Nelson, David L. Conover, and W. Gregory Lotz, "Combined Chemical, Physical Hazards Make Exposure Harder to Calculate," OCCUPATIONAL SAFETY AND HEALTH Vol. 63, No. 6 (June 1994), pgs. 50, 52-54.

Descriptor terms: bruce ames; cancer; carcinogens; policy; immunotoxicity; immune system; nervous system; endocrine system; niosh; occupational safety and health; standards; regulations; studies; teratogens; di(2-ethylhexyl phthalate); dehp; caffeine; electromagnet radiation; emf; rf; radio frequency radiation; non-ionizing radiation; 2-methuxyethanol; glycol ether; 2me; toluene; solvents; hearing loss; noise; synergism; multiplier effect; precautionary principle; principle of precautionary action; prevention;