#353: EPA: Dioxin Does Cause Cancer In Humans

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

RACHEL'S HAZARDOUS WASTE NEWS #353
---September 2, 1993---
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========================

An explosion at a Hoffman-LaRoche chemical plant in Seveso, Italy, in 1976 sent a cloud of the herbicide 2,4,5-T over the surrounding countryside, contaminating several thousand people. Dioxin is created as an unwanted by-product during the manufacture of 2,4,5-T, so the Seveso population was exposed to dioxin. For years, optimists have been pointing to Seveso saying, "Dioxin doesn't cause cancer in humans--look at Seveso." Now a new study in the journal EPIDEMIOLOGY reveals that people exposed to dioxin during the Seveso explosion have begun to exhibit excessive numbers of cancers.[1]

Dr. Linda Birnbaum, director of environmental toxicology for U.S. EPA [Environmental Protection Agency], told the Associated Press that the new study "is one more nail in the coffin" for dioxin.[2] Birnbaum, who is coordinating EPA's multi-year "scientific reassessment" of dioxin said, "This, together with other studies, clearly supports that dioxin has the potential to cause cancer in people, just as it does in every animal it's been tested in. The weight of the evidence is becoming overwhelming," she told AP reporter Paul Raeburn.

The area around Seveso has been divided into three zones, called A, B and R. The small A zone was most heavily contaminated, but its 724 residents were evacuated. ("Heavy" contamination means that each square yard of land contained 13 to 494 micrograms of dioxin; a microgram is a millionth of a gram and there are 28 grams in an ounce.) The B zone was less heavily contaminated but its 4824 residents were not evacuated; zone B contained 43 micrograms of dioxin per square yard of soil, or less. The R zone was even less contaminated (average contamination being 4.3 micrograms per square yard), so its 31,647 residents were probably exposed to low levels. Another 181,579 people living beyond zone R serve as a control group living in "noncontaminated" areas.

The greatest cancer increase has occurred in zone B. In zone A the numbers are small and no significant cancer increases have occurred. In zone R one kind of cancer has increased: soft tissue sarcoma. Previous studies have linked dioxin exposure to soft tissue sarcoma in humans.

In zone B, among women there has been an observable increase in cancers of the gall bladder and biliary tract (the system that delivers bile from the liver to the small intestine), and in cancers related to the blood-forming system (multiple myeloma and myeloid leukemia).

Among men in zone B, there were observable increases in cancers of the blood-forming system, and in one kind of non-Hodgkin's lymphoma (a cancer of the lymph system called lymphoreticulosarcoma).

This new study only covers the period 1976 through 1986--10 years after the Seveso accident. Since most cancers take longer than 10 years to develop, the cancers reported in this study may represent only the earliest signs of more trouble to come.

This Seveso study is not the first to indicate that dioxin causes cancer in humans. [3-10,14,15] Swedish researchers in the late 1970s began reporting that exposure to phenoxy herbicides (2,4-D and 2,4,5-T) caused a 3-fold to 6-fold increase in the risk of soft tissue sarcomas and lymphomas. Phenoxy herbicides are contaminated with dioxin during manufacture.

Monsanto Corporation, a major manufacturer of phenoxy herbicides, in the late 1970s and early 1980s sponsored studies of workers that the company had exposed to dioxin, and these studies showed no increased cancer deaths among exposed workers. However, the Monsanto studies have been criticized by a report from the National Research Council, [11] which says Monsanto's studies were "plagued with errors in classification of exposed and unexposed groups, according to some reports, and hence have been biased toward a finding of no effect." A 1990 analysis of Monsanto workers, conducted by the National Institute for 

Occupational Safety and Health, reported a statistically-significant increase in soft tissue sarcomas. [12]

As part of its multi-year scientific reassessment of dioxin, EPA recently published a draft review of all scientific data linking dioxin to cancer and other health effects in humans. [13] The EPA's draft document concludes that four separate studies[8,9,14,15] of workers exposed to dioxin have revealed an "overall increased mortality from all malignancies combined." EPA speculates that dioxin's ability to mimic hormones gives dioxin the capacity to cause cancer in many different organs and bodily systems in humans. [13, pg. 7-7]

There seems to be little room left for doubt: As the EPA's "scientific reassessment team" told then-chief of EPA, William Reilly, January 27, 1992: "Dioxin does cause cancer in humans." (See RHWN #283.)

It therefore seems that EPA now has little choice but to declare dioxin a class A carcinogen, i.e., one known to cause cancer in humans. This would have far-reaching implications for public health policy. (A public hearing to discuss the new EPA document, and its implications, is scheduled for 9-to-5 September 7 and 8, 1993, at the Ritz-Carlton Hotel in Pentagon City, Arlington, Va. If you want to reserve time to speak, contact Helen Murray of Eastern Research Group: (617) 674-7374. The meeting will be full and space is limited, so we suggest you arrive by 8 a.m. if you want a seat.)

An editorial in the September issue of EPIDEMIOLOGY points out some of the public policy implications of the conclusion that dioxin causes cancer in humans. [16] The author of the editorial, Swedish dioxin researcher Olav Axelson, says that the "biological effects of TCDD [dioxin]" are "a first order public health concern." Axelson says "there seems to be an urgent and costly need to change or improve industrial and other processes so as not to produce dioxins (and the toxicologically similar chlorinated dibenzo-furans). For example, there is a need to restrict the use of chlorine in paper bleaching. Incineration of waste material at too low temperature should be avoided as well as the 'combustion' of organochlorine compounds in general," Axelson says.

Dioxin is produced by every municipal solid waste incinerator ever tested; it is produced by all hazardous waste incinerators, cement kilns and BIFs [boilers and industrial furnaces] that burn chlorinated wastes. It is produced by the manufacture of many pesticides (85% of which involve chlorine). It is produced by metal smelters, and paper mills, and probably by other common industrial processes. Although there is now little doubt that dioxin causes cancer in humans, translating that into public policies that genuinely protect public health will create a political firestorm. Once again, EPA chief Carol Browner faces a series of decisions that will define clearly and unmistakably which side she and Bill Clinton are on.

--Peter Montague, Ph.D.

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

[1] Pier Alberto Bertazzi and others, "Cancer Incidence in a Population Accidentally Exposed to 2,3,7,8-Tetrachlorodibenzo-PARA-dioxin," EPIDEMIOLOGY Vol. 4 (September, 1993), pgs. 398-406.

[2] Paul Raeburn, "Dioxin Dangers," a story on the Associated Press news wire datelined New York, August 29, 1993.

[3] Lennart Hardell and others, "Case-control study: soft-tissue sarcomas and exposure to phenoxyacetic acids or chlorophenols," BRITISH JOURNAL OF CANCER Vol. 39 (1979), pgs. 711-717.

[4] Lennart Hardell and others, "Malignant lymphomas and exposure to chemicals, especially organic solvents, chlorophenols, and phenoxy acids: a case-control study," BRITISH JOURNAL OF CANCER Vol. 43 (1981), pgs. 169-176.

[5] Mikael Eriksson and others, "Soft tissue sarcomas and exposure to chemical substances: a case-referent study," BRITISH JOURNAL OF INDUSTRIAL MEDICINE Vol. 38 (1981), pgs. 27-33.

[6] Sheila Hoar and others, "Agricultural herbicide use and risk of lymphoma and soft-tissue sarcoma," JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION Vol. 256 (1986), pgs. 1141-1147.

[7] Sheila Hoar Zahm and others, "A case-control study of non-Hodgkin's lymphoma and the herbicide 2,4-dichloro phenoxyacetic acid (2,4-D) in Eastern Nebraska," EPIDEMIOLOGY Vol. 1 (1990), pgs. 349-356.

[8] Marilyn Fingerhut and others, "Cancer Mortality in Workers Exposed to 2,3,7,8-tetrachloro-dibenzo-P-dioxin," NEW ENGLAND JOURNAL OF MEDICINE Vol. 324 (1991), pgs. 212-218.

[9] R. Saracci and others, "Cancer Mortality in Workers Exposed to Chlorophenoxy Herbicides and Chlorophenols," LANCET Vol. 338 (1991), pgs. 1027-1032.

[10] Pier Alberto Bertazzi and others, "Ten-year Mortality Study of the Population Involved in the Seveso Incident in 1976," AMERICAN JOURNAL OF EPIDEMIOLOGY Vol. 129 (1989), pgs. 1187-1200.

[11] Anthony B. Miller and others, ENVIRONMENTAL EPIDEMIOLOGY VOLUME 1 PUBLIC HEALTH AND HAZARDOUS WASTES (Washington, D.C.: National Academy Press, 1991), pg. 207.

[12] Marilyn A. Fingerhut and others, MORTALITY AMONG U.S. WORKERS EMPLOYED IN THE PRODUCTION OF CHEMICALS CONTAMINATED WITH 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (TCDD) FINAL REPORT [PB91-125971] (Springfield, Va.: National Technical Information Service, 1991).

[13] David Bayliss, Marie Sweeney and others, CHAPTER 7. EPIDEMIOLOGY/HUMAN DATA [EPA/600/AP-92/001g; Revised June 1993; Workshop Review Draft] (Cincinnati, Ohio: U.S. Environmental Protection Agency, Center for Environmental Research Information, 1993). For a free copy while supplies last, phone EPA in Cincinnati: (513) 569-7562.

[14] A. Manz and others, "Cancer mortality among workers in chemical plant contaminated with dioxin," LANCET Vol. 338 (1991), pgs. 959-964.

[15] A. Zober and others, "Thirty-four-year mortality follow-up of BASF employees exposed to 2,3,7,8-TCDD after the 1953 accident," INTERNATIONAL ARCHIVES OF OCCUPATIONAL AND ENVIRONMENTAL HEALTH Vol. 62 (1990), pgs. 139-157.

[16] Olav Axelson, "Seveso: Disentangling the Dioxin Enigma?" EPIDEMIOLOGY Vol. 4 (September, 1993), pgs. 389-391.

Descriptor terms: explosions; accidents; spills; hoffman-laroche; seveso; italy; 2,4,5-t; herbicides; pesticides; studies; linda birnbaum; epa; dioxin; carcinogens; cancer; soil contamination; soft tissue sarcoma; sts; gall bladder cancer; biliary tract cancer; liver cancer; multiple myeloma; myeloid leukemia; hematopoeitic system cancers; blood; lymphomas; non-hodgkin's lymphomas; phenoxy herbicides; 2,4-d; monsanto; william gaffey; w r gaffey; judith zack; j a zack; occupational safety and health; nrc; national research council; niosh; marilyn fingerhut; chlorine; chlorinated solvents; incineration; cement kilns; bifs; boilers; industrial furnaces; carol browner; bill clinton;

#375: Cancer Down On the Farm

=======================Electronic Edition========================
RACHEL'S HAZARDOUS WASTE NEWS #375 
---February 3, 1994---
News and resources for environmental justice.
==========
Environmental Research Foundation
P.O. Box 5036, Annapolis, MD 21403
Fax (410) 263-8944; Internet: erf@igc.apc.org ==========
RACHEL-4CM = DIOXIN FOCUSED DIRECTORY Remote Access Chemical Hazards Electronic Library. Dioxinnz.com =======================Original Source========================

The 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;

#436: The Dogs of War

=======================Electronic Edition========================
RACHEL'S ENVIRONMENT & HEALTH WEEKLY #436
---April 6, 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========================

Somewhere between 2.6 and 3.8 million American men and women served in Vietnam during the years 1965 through 1971, the years when chemical herbicides were being used to denude the jungle and destroy enemy crops. Military records do not allow a more accurate determination of the true number who served. [1]

Alongside the humans serving in Vietnam, there were 3895 military working dogs, almost all of them purebred German shepherds. [2] (Among the 3895, there were 64 Labrador or golden retrievers used as trackers; the other 98.3 percent were German shepherds.) These dogs served as scouts, sentries, trackers, mine detectors, and tunnel explorers. About 91% of these dogs were "intact" (uncastrated) males.

When a military working dog dies, regardless of the circumstances of death or the duty location, an autopsy is performed by a veterinarian, and a standardized set of tissue specimens and organs are sent to the Armed Forces Institute of Pathology in Washington, D.C.

During the late 1980s, researchers compared autopsy records of 1167 military working dogs with Vietnam service against autopsy records of 791 military working dogs who served in the continental U.S. and saw no Vietnam service. In a separate study, the stateside dogs were also compared to 437 dogs that died in Okinawa, because many dogs that served in Vietnam were sent to Okinawa after the war. [3]

These studies showed that dogs who served in Vietnam were about twice as likely (1.8 times as likely) to have cancer of the testicles, compared to military working dogs who served only in the states. Likewise, military dogs that died in Okinawa were about twice as likely (2.2 times as likely) to have testicular cancer as dogs who served only in the states. A separate study was then conducted, excluding the dogs who had testicular cancer. Among the non-cancer dogs, there was clear evidence of significant deterioration of the testicles in those dogs who served in Vietnam (compared to dogs who served only in the U.S.): degeneration of the testicles, atrophy (shrinking) of the testicles, and evidence of a below-normal ability to produce sperm.

Dogs have often served as sentinels of human disease. Back in 1938, the well-known researcher W.C. Hueper showed that beta-naphthylamine caused bladder cancer in dogs. [4] In 1954, researchers showed that another industrial chemical, 4-aminodiphenyl, produced bladder cancer in dogs. [5] In 1980, a study of 8760 pet dogs showed that bladder cancer in dogs correlated with residence in industrialized counties in the U.S. and Canada; this same study showed that bladder cancer in men and women was similarly correlated with residence in industrialized areas. "The findings of this study suggest that the bladder cancer experience of pet dogs resembles that of human beings living in the same general locale," the study concluded. [6]

Pet dogs are particular relevant in such studies because 40 million pet dogs share their owner's domestic environment yet do not indulge in behavior that could confuse or confound the interpretation of epidemiologic studies: dogs don't smoke, and they usually don't work. In 1983, a study of pet dogs with the asbestos-related lung disease, mesothelioma, showed that their disease correlated with household members who (a) worked in an asbestos-related job, or (b) had an asbestos-related hobby or (c) applied flea powder to their dog. [7]

For these reasons, the finding of testicular cancer and testicular dysfunction in dogs who served in Vietnam was an eye-opener, and it soon led to a comparison of 271 human veterans with testicular cancer to 259 veterans without testicular cancer, to see whether Vietnam service was related to testicular cancer. This study revealed that, like dogs, human veterans of Vietnam were about twice as likely (2.5 times as likely), to have testicular cancer compared to veterans who did not serve in Vietnam. [8]

Naturally, the question occurs, what aspects of military service in Vietnam caused testicular cancer in men, and testicular cancer and dysfunction in military working dogs?

An obvious suspect is Agent Orange, which was sprayed in large quantities (11.2 million gallons, or 42.4 million liters) over 3.6 million acres (1.5 million hectares) of Vietnam. Agent Orange, named for the orange stripe on its 55-gallon storage containers, was a 50-50 mixture of two herbicides: 2,4,5-T and 2,4-D. One of these, 2,4,5-T, was banned in the U.S. about 1980 because evidence indicated that it could cause birth defects in humans; the other half of Agent Orange, 2,4-D, remains in wide use throughout the U.S. where it is popular for killing dandelions and other broad-leaf plants in lawns, and as an agricultural weed killer.

During manufacture, the herbicide 2,4,5-T becomes contaminated with dioxin unavoidably. According to the National Academy of Sciences, the average dioxin contamination in Agent Orange in Vietnam was 2 parts per million (ppm). An estimated total of 368 pounds of dioxin was sprayed onto Vietnam's land and people during the 7-year spray program. [9]

However, a recent study of Vietnam veterans that tried to estimate 2,4,5-T exposure and link it to testicular cancer found that only Navy men had elevated levels of testicular cancer associated with 2,4,5-T exposure; men in the other services showed no such effect of exposure to 2,4,5-T. [10] The authors of that study speculated that Navy men might also have been exposed to fuels (oil and gasoline), which previous studies have linked to testicular cancer.

The other half of Agent Orange, herbicide 2,4-D, is also a suspect. Although the manufacturers of 2,4-D claimed for years that their products were not contaminated with dioxin, this claim has now been shown to be false, using the manufacturers' own data. [11]

Dioxin has been shown to damage the reproductive organs and systems of many animal species, including men and women. [12]

A study of pet dogs in the U.S. found excess cancers (lymphomas) associated with 2,4,-D lawn spraying. [13] And a study of 32 farmers who sprayed 2,4-D, compared to a control group of 25 unexposed farmers, revealed significant effects on the exposed farmers: diminished sperm count, increased number of sperm with poor motility (swimming ability); increased numbers of dead sperm; and increased numbers of malformed sperm. [14]

No federal agency keeps close track of pesticide use in the U.S.; however U.S. Environmental Protection Agency (EPA) estimates that farmers apply 25 to 30 million pounds (11.3 to 13.6 million kilograms) of "active ingredient" of 2,4-D each year in the U.S. Non-agricultural use of 2,4-D in the U.S. is estimated to total another 12 to 15 million pounds (5.4 to 6.8 million kilograms) of "active ingredient" per year. [15] The "active ingredient" of a pesticide is only 0.5% to 5% of the total formulation so these "active ingredient" amounts must be multiplied by anywhere from 20 to 200 to get the total 2,4-D formulation used each year. The bulk of the formulation is secret ingredients (called "inerts") which are, themselves, often toxic solvents. [16]

Other chemicals suspected of causing testicular cancer and dysfunction in dogs and humans who served in Vietnam are the antibiotic tetracycline and the pesticide malathion. Many military dogs in Vietnam suffered from ear infections and other diseases. [17]Therefore, many received one or more doses of tetracycline during their tour of duty. Tetracycline is strongly absorbed by sperm in mammals, and is known to cause testicular atrophy (shrinkage), and diminished sperm quality in humans and dogs.

The other suspicious candidate is malathion. The same military unit that sprayed Agent Orange also sprayed DDT and malathion extensively in the vicinity of U.S. troops, to reduce the dangers of malaria carried by mosquitoes. It has been reported that 44% of the land of southeast Asia, mainly Vietnam, was sprayed with malathion during the war. [18]Furthermore, military working dogs in Vietnam were dipped in a 0.5% solution of malathion to kill disease-carrying ticks. Malathion is known to cause testicular atrophy and damage to the sperm-generating cells of laboratory animals. [19]

Malathion is widely use throughout the U.S. today for mosquito control though not for fear of malaria. Mosquitoes are simply a nuisance. EPA estimates that 4 to 6 million pounds (1.8 to 2.7 million kilograms) of "active ingredient" of malathion are sprayed in the U.S. each year. The yearly total of malathion formulation sprayed is, again, 20 to 200 times this amount.

Sperm count in men throughout the industrialized world appears to be dropping. (See RHWN #343.) Testicular cancer is the most prevalent cancer among white males between the ages of 25 and 34 years and the second most common in the 35-to-39 age group. The causes of testicular cancer are thought to be environmental because the rates vary widely from one location to another. During the last 15 years, the rates have increased rapidly (2.3% to 3.4% per year) in many industrialized countries. [20]

It may take scientists many decades to tell us all we would like to know about a complex chemical like dioxin, or malathion. However, we already know enough to act: To guide our personal choices, and new public policies, to minimize the danger to ourselves, our families, and our communities, we need only to remember that chemicals not used cannot cause harm. This we can learn from the dogs of war.

 --Peter Montague

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

[1] Harold Fallon and others, VETERANS AND AGENT ORANGE: HEALTH EFFECTS OF HERBICIDES USED IN VIETNAM (Washington, D.C.: National Academy Press, 1993), pg. 3-1.

[2] Howard M. Hayes and others, "U.S. Military Working Dogs with Vietnam Service: Definition and Characteristics of the Cohort," MILITARY MEDICINE Vol. 159, No. 11 (November 1994), pgs. 669-675.

[3] H. M. Hayes and others, "Excess of Seminomas Observed in Vietnam Service U.S. Military Working Dogs," JOURNAL OF THE NATIONAL CANCER INSTITUTE Vol. 82, No. 12 (June 20, 1990), pgs. 1042-1046.

[4] W.C. Hueper and others, "Experimental Production of Bladder Tumors in Dogs by Administration of Beta-Naphthylamine," The JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY Vol. 20, No. 1 (January 1938), pgs. 46-84.

[5] A.L. Walpole and others, "Tumours of the Urinary Bladder in Dogs After Ingestion of 4-aminodiphenyl," BRITISH JOURNAL OF INDUSTRIAL MEDICINE Vol. 11 (1954), pgs. 105-109.

[6] Howard M. Hayes and others, "Bladder Cancer in Pet Dogs: A Sentinel for Environmental Cancer?" AMERICAN JOURNAL OF EPIDEMIOLOGY Vol. 114, No. 2 (1981), pgs. 229-233.

[7] Lawrence T. Glickman and others, "Mesothelioma in Pet Dogs Associated with Exposure of Their Owners to Asbestos," ENVIRONMENTAL RESEARCH Vol. 32, No. 2 (December 1983), pgs. 305-313.

[8] Robert E. Tarone, and others, "Service in Vietnam and Risk of Testicular Cancer," JOURNAL OF THE NATIONAL CANCER INSTITUTE Vol. 83, No. 20 (October 16, 1991), pgs. 1497-1499.

[9] Fallon, cited above, pg. 2-4.

[10] Tim A. Bullman and others, "Risk of Testicular Cancer Associated with Surrogate Measures of Agent Orange Exposure among Vietnam Veterans on the Agency Orange Registry," ANNALS OF EPIDEMIOLOGY Vol. 4, No. 1 (January 1994), pgs. 11-16.

[11] U.S. Environmental Protection Agency, ESTIMATING EXPOSURE TO DIOXIN-LIKE COMPOUNDS VOL. II PROPERTIES, SOURCES, OCCURRENCE AND BACKGROUND EXPOSURES [EPA/600/6-88/005Cb June 1994 External Review Draft] (Washington, D.C.: U.S. Environmental Protection Agency, 1994), Table 3-18 on pg. 3-58.

[12] Arnold Schecter, editor. DIOXINS AND HEALTH (New York: Plenum Press, 1994); see, for example, pgs. 26, 145, 318, and 332, among others.

[13] Howard M. Hayes and others, "Case-Control Study of Canine Malignant Lymphoma: Positive Association With Dog Owner's Use of 2,4-Dichlorophenoxyacetic Acid Herbicides," JOURNAL OF THE NATIONAL CANCER INSTITUTE Vol. 83, No. 17 (September 4, 1991), pgs. 1226-1231.

[14] D. Lerda and R. Rizzi, "Study of reproductive function in persons occupationally exposed to 2,4-dichlorophenoxyacetic acid (2,4-D)" MUTATION RESEARCH Vol. 262 (1991), pgs. 47-50.

[15] Arnold L. Aspelin, PESTICIDES INDUSTRY SALES AND USAGE; 1992 AND 1993 MARKET ESTIMATES [733-K-94-001] (Washington, D.C.: U.S. Environmental Protection Agency, June 1994), pg. 19.

[16] John H. Bukowski and Leroy W. Meyer, "Simulated Air Levels of Volatile Organic Compounds Following Different Methods of Indoor Insecticide Application," ENVIRONMENTAL SCIENCE & TECHNOLOGY Vol. 29, No. 3 (1995), pgs. 673-676.

[17] Paul B. Jennings and others, "A Survey of Diseases of Military Dogs in the Republic of Vietnam," JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION Vol. 159, No. 4 (August 15, 1971), pgs. 434-440.

[18] Fallon, cited above, pg. 3-14.

[19] K. Balasubramanian and others, "Effect of malathion on the testis of male albino rats," MEDICAL SCIENCE RESEARCH Vol.15 (1987), pgs. 229-230.

[20] Hans-Olav Adami and others, "Testicular Cancer in Nine Northern European Countries," INTERNATIONAL JOURNAL OF CANCER Vol. 59 (1994), pgs. 33-38.

Descriptor terms: vietnam war; military; army; navy; marines; air force; herbicides; veterans; dogs; german shepherds; labrador retrievers; golden retrievers; okinawa; testicular cancer; sperm count; testicular atrophy; 4-aminodiphenyl; beta-naphthylamine; bladder cancer; asbestos; mesothelioma; flea powder; agent orange; 2,4,5-t; 2,4-d; birth defects; agriculture; farming; dioxin; fuel; oil; gasoline; lymphoma; pesticide use data; inert ingredients; secret ingredients; antibiotics; tetracycline; malathion; mosquito control;

#438: Warning on Male Reproductive Health

=======================Electronic Edition========================
RACHEL'S ENVIRONMENT & HEALTH WEEKLY #438
---April 20, 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========================

The Danish Environmental Protection Agency in Copenhagen, Denmark released a report April 18th entitled MALE REPRODUCTIVE HEALTH AND ENVIRONMENTAL CHEMICALS WITH ESTROGENIC EFFECTS. The 175-page English-language report, which we have obtained, says male reproductive health is deteriorating in many countries, and that the most likely cause is exposure to low levels of industrial chemicals that contaminate food, water, and many consumer products.

The Danish report says many industrial chemicals mimic sex hormones (chiefly the female hormone, estrogen) and thus interfere with the normal development of creatures (including humans) that become exposed before, or shortly after, birth. The report identifies many consumer products as sources of such hormone-like chemicals: pesticides, detergents, cosmetics, paints, and packaging materials, including plastic containers and food wraps. [1] The report calls for an aggressive, coordinated international research effort to describe the extent of the problem, and to design programs of "prevention and intervention."

Meanwhile in the U.S., the Chemical Manufacturers Association (CMA) has funded a report by a scientist who says these problems are not real. "The suggestion that industrial estrogenic chemicals contribute to an increased incidence of breast cancer in women and male reproductive problems is not plausible," the CMA's 6-page study concludes. [2]

In contrast, the Danish report says, "It is now evident that several aspects of male reproductive health have changed dramatically for the worse over the past 30-50 years. The most fundamental change has been the striking decline in sperm counts in the ejaculate of normal men; recent evidence from Paris indicates that this decrease amounts to about two percent per year over the last two decades. The result is that many, otherwise normal, men now have sperm counts so low that their fertility is likely to be impaired. Over the last half-century, the incidence of testicular cancer has increased progressively in many countries to become now the most common cancer in young men. Other disorders of the male reproductive tract may also be increasing in incidence, with several European countries reporting a progressive rise in hypospadias (a malformation of the external genitalia) and an apparently emerging trend towards an increasing incidence of testicular maldescent [undescended testicles]....

"While the etiologies [causes] underlying these apparent changes are currently not clear, both clinical and laboratory research suggest that all of the described changes in male reproductive health appear inter-related and may have a common origin in fetal life or childhood. This means that the increase in some of the disorders seen today originated 20-40 years ago and that the prevalence of such defects in male babies born today will not become manifest for another 20-40 years or more," the report says.

The Danish report was prepared by 19 scientists and physicians, including 13 from Denmark, two from France, one from England, one from Scotland, and two from the U.S.

The report says that declining reproductive health has also been widely observed in wildlife: "Trends in the reproductive health of species other than man also raise the possibility of environmental factors as partial etiologic [causal] contributions in a decline noted in the male reproductive health of wildlife. For example, wild panthers in the United States have been reported to have an increase in undescended testes and a decrease in semen quality, whereas male alligators in some lakes in Florida have been shown to have abnormalities in their sex hormone levels (tending towards femaleness) and to have smaller than normal genitalia. Male fish in some parts of the United Kingdom have been shown to express a 'female-like response' when studied in a relatively natural setting. Earlier studies of fish eating birds in the United States demonstrated nests containing male hatchlings that were apparently feminized. A recent report of lactating [milk-producing] male fruit bats suggested that the males were, in some way, exposed to a female sex hormone. Recent laboratory studies showed that when estrogenic forms of polychlorinated biphenyls (PCBs) were painted on turtle eggs, the male hatchlings were sex-reversed to females. Taken together, this growing body of evidence suggests that environmental factors that resemble female sex hormones may be having an adverse effect on the reproductive capacity and wellbeing of diverse species," the report says.

The report summarizes evidence indicating that all of these problems have a common origin: the exposure of male fetuses to estrogen-like chemicals before birth. "The wealth of experimental [laboratory animal] results and associated clinical [human] reports suggests strongly that prenatal exposure to exogenous [external] estrogens may play an etiologic role in the trends observed in male reproductive health," the report says.

The report lists many ways in which humans become exposed to chemicals that mimic hormones: "Estrogen effects are not restricted to a small group of therapeutic agents but appear in several groups of compounds that are in daily use in industry, agriculture or in the home," the report says. "A major problem is determining which chemicals are estrogenic... At present, tens of thousands [of] man-made chemicals are used, yet the effects on the endocrine [hormone] system have been studied for only a few of these. The estrogenic activity of most chemicals (e.g., alkylphenols, phthalate esters, bisphenol-A) has been detected by accident, not by intent; that is, no systematic screening, even on individual groups of chemicals, has been attempted. Hence it is highly possible that other estrogenic chemicals remain unidentified... Thus, the present situation is that man and wildlife are exposed to a very wide range of chemicals, and for the majority of them we do not know whether these chemicals are, or are not, estrogenic, whether their effects are additive, or even what the true exposure to these chemicals is."

The report points out that even weakly estrogenic chemicals may be of concern if they remain in the bodies of humans and wildlife for long periods. Natural hormones are created by the body, circulate in the blood stream very briefly to carry out a particular task, and are then destroyed by natural mechanisms. In contrast, many industrial chemicals that enter the body are not readily broken down so they circulate in the blood for long periods --in some cases many years --mimicking natural hormones.

The Danish report lists the following chemicals and classes of chemicals as known to have estrogenic activity:

Organochlorine pesticides: DDT, DDD, DDE, dicofol, perthane, methoxychlor, chlordane, oxychlordane, trans-nonachlor, heptachlor, heptachlorepoxide, aldrin, dieldrin, hexachlorobenzene, hexachlorocyclohexanes, lindane (gamma HCH), mirex, and toxaphene. Although these chemicals have been banned in several industrial countries, including the U.S., some of them are still manufactured [in the U.S. or overseas, by U.S. corporations--PM] and sold in developing countries where they are "widely used" today, the Danish report says.

Other known estrogenic chemicals include:

** Many of the 109 types of PCBs (polychlorinated biphenyls); 

** Dioxins and furans (unwanted by-products of all incinerators; paper-making mills; metal smelters; and the manufacture of some chemicals and pesticides); 

** Alkylphenols, the breakdown products of alkylphenol polyethoxylates (APEs) which are widely used in detergents, paints, herbicides and cosmetics. Some 300 million kilograms (660 million pounds) of APEs are produced each year and ultimately released into the environment. 

** Phytoestrogens, or plant-produced estrogens, including isoflavones and coumestans found in rye, wheat, cabbage, sprouts, spinach and soybeans. "Soybean is far and away the richest source of plant estrogens and is used ubiquitously [everywhere] in the food industry as a protein source including the production of infant milk formula substitutes," the Danish report says. Depending upon the dose, phytoestrogens have an estrogenic, or an anti-estrogenic, effect, the Danish report says. Unlike many of the other estrogenic chemicals identified in the Danish report, phytoestrogens do not bioaccumulate or biomagnify, but are readily metabolized and excreted. 

** Many common chemicals found in plastics, in-cluding bisphenol-A, phthalate esters (butylbenzyl phthalate and di-n-butylphthalate): "Phthalates are the most abundant man-made environmental pollutants, and human intake per day via various routes, especially via the diet, is measured in tens of milligrams," says the Danish report. Some plastics contain up to 40% phthalate esters (by weight). These esters leach out of, or volatilize out of, the plastics as time passes. Many foods in the U.S. and elsewhere are packaged in phthalate-containing plastics. Even blood for transfusions is sometimes packaged in phthalate-containing plastics. 

** Herbicides, such as the popular crab-grass and dandelion killer, 2,4-D, and the now-banned 2,4,5-T, both of which were widely used by U.S. forces in Vietnam. (See REHW #436.) Other herbicides with estrogenic effects include: alachlor; amitrole; atrazine; metribuzin; and trifluralin. 

** Fungicides: benomyl and its principal breakdown product, carbendazim, used on apples and bananas, among other food crops; and ethylene bis dithiocarbamates (EBDCs, including mancozeb, maneb, metiram, and zineb). 

** Hexachlorobenzene. Although this pesticide was banned in many countries in the 1970s, it "continues to be released to the environment as a byproduct and contaminant in many other chlorinated chemicals including chlorinated solvents," the Danish report says. 

** Tributyltin compounds. Tributyltin compounds, until very recently, were used in large quantities as antifouling paints on ships, boats, and mariculture pen nets. Now banned in many countries. 

** Malathion, heavily sprayed around residential areas of the U.S. to kill nuisance mosquitoes.

And finally the Danish report warns that exposure to low levels of many chemicals may be harming the reproductive health of humans and wildlife by mechanisms that have nothing to do with estrogen: "Although not the subject of this report, in considering and evaluating the possible role of estrogenic chemicals in male reproductive disorders, it should not be forgotten that many chemicals may have a detrimental effect on male reproductive health through other mechanisms than an estrogenic effect," the Danish report says.

 --Peter Montague

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

[1] Our thanks to Lisa Finaldi of Greenpeace International for helping us obtain a copy of the Danish EPA report.

[2] Stephen H. Safe, "Environment and Dietary Estrogens and Human Health: Is There a Problem?" ENVIRONMENTAL HEALTH PERSPECTIVES Vol. 103, No. 4 (April, 1995), pgs. 346-351.

Descriptor terms: endocrine disrupters; strogen; hormones; reproductive system; pesticides; detergents; cosmetics; paints; packaging materials; plastics; packaging; cma; chemical manufacturers association; denmark; sperm count; hypospadias; undescended testicles; testicular cancer; cryptorchidism; wildlife; panthers; alligators; penis size; fish; birds; bats; turtles; pcbs; chlorine; organochlorine compounds; pesticides; DDT; DDD; DDE; dicofol; perthane; methoxychlor; chlordane; oxychlordane; trans-nonachlor; heptachlor; heptachlorepoxide; aldrin; dieldrin; hexachlorobenzene; hexachlorocyclohexanes; lindane (gamma HCH); mirex; toxaphene; dioxin; furans; alkylphenols; alkylphenol polyethoxylates; apes; metal smelting; paper mills; incineration; phytoestrogens; bisphenol-A; phthalate esters; herbicides; 2,4-d; 2,4,5-t; agent orange; vietnam veterans; alachlor; amitrole; atrazine; metribuzin; trifluralin; benomyl; carbendazim; ethylene bis dithiocarbamates; ebdcs; mancozeb; maneb; metiram; zineb; hexachlorobenzene; tributyltin; malathion;


Next issue

#479: Nationwide Dioxin Campaign

=======================Electronic Edition========================
RACHEL'S ENVIRONMENT & HEALTH WEEKLY #479
---February 1, 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========================

New evidence of dioxin's ability to cause cancer in humans has come to light [1] just as environmental justice activists across the U.S. are planning a major campaign to attack dioxin at its sources. The campaign is holding a 3-day strategy session in Baton Rouge, Louisiana, March 15-17. (All citizen activists are welcome; to register, phone Jim Warren in North Carolina: (919) 774-9566; THE LAST DAY TO REGISTER IS MARCH 5.) The dioxin campaign puts the grass-roots environmental community squarely "in the face" of the biggest polluters in the nation, and it creates a "line in the sand"--a challenge to the old conservative wing of the environmental community, which to some extent has made its peace with the dioxin polluters. [2]

"We know that we are up against huge corporate power, but tackling the misuse of corporate power is what the 21st century is going to be about," says Ellen Connett, one of the leaders of the new grass-roots campaign, and editor of the indispensable weekly, WASTE NOT [phone: (315) 379-9200].

The well-know grass-roots leader, Lois Gibbs of the Citizens Clearinghouse for Hazardous Waste [phone (703) 237-2249], has just published an excellent book on dioxin [3]--the best we've ever seen on the subject --which describes the dioxin problem in the first half, and then lays out various campaign techniques that citizens could use to end the poisoning. Gibbs's books is technically sound, yet easily understandable by non-experts. It describes dioxin, where it comes from, and how it poisons people and wildlife. It tells the whole complicated dioxin story, yet is very readable. Furthermore, it is the best "organizing manual" for citizens we have ever seen. Gibbs's book seems likely to become the "bible" for dioxin campaigners.

Gibbs sees the dioxin problem as a failure of self-government, a failure of people to control corporations: "We can't shut down the sources of dioxin without finding the courage to change the way government works," she says. "We have to explore how people became powerless as the corporations became powerful. We have to figure out how to speak honestly and act collectively to rebuild our democracy."

The rebuilding of democracy is what separates the grass-roots environmental movement from the old conservative "enviros." The old-style enviros don't see democracy as an important issue--perhaps because to do so implies a direct challenge to corporate influence over our media, our elections, our courts, our schools, and our legislatures. For example, the Environmental Defense Fund (EDF) has refused to endorse campaign finance reform to get the corrupting influence of private money out of our elections. The grass-roots movement, on the other hand, believes democracy is THE fundamental environmental issue. "Without democracy there can be no justice, and without justice there is no way to protect human health or the environment," says Connie Tucker, of the Southern Organizing Committee in Atlanta [(404) 755-2855], another important participant among many in the Baton Rouge conference.

New Evidence of Dioxin's Toxicity to Humans

A new study published in December found a dose-dependent increase in risk of cancer and heart disease among a group of 1189 workers at a pesticide manufacturing plant in Hamburg, Germany who were exposed to dioxins during the period 1952 to 1984.4 The study group included every worker employed for three months or longer at the plant from 1952 until it shut down in 1984. The workers were followed through the end of 1992.

Exposure to dioxins was evaluated to see if dioxins were related to particular causes of death. Deaths among the pesticide workers were compared to deaths among a control group consisting of 2528 non-dioxin-exposed workers at a gas supply company located in the same region of Germany.

The pesticide workers had produced phenoxy herbicides [examples: 2,4-D, 2,4,5-T, and silvex], chlorophenols, and other herbicides and insecticides known to be contaminated with dioxins and furans. [Dioxins and furans are a family of 210 unwanted byproducts (75 dioxins, and 135 furans) from certain chemical reactions in the production of phenoxy herbicides. Dioxins may be produced by other chemical reactions as well, including metal smelting, and the incineration of solid and medical wastes. TCDD, or 2,3,7,8-tetrachlorodibenzo-P-dioxin, is the most toxic of the dioxin family.]

The study found, among dioxin-exposed workers, an increase in all deaths, an increase in cancer deaths, and an increase in deaths due to ischemic heart disease, compared to same-aged individuals in the control group. [Ischemic heart disease refers to a narrowing of the arteries with consequent reduction of blood flow. If blood flow to the heart muscle is reduced, a heart attack can result.] The disease-related deaths increased with the dose of dioxin to which the workers were exposed: greater dioxin exposure was related to higher death rates.

The study found that pesticide workers with the highest dioxin exposures faced more than three times the risk of dying from cancer, and 2.5 times the risk of dying from ischemic heart disease, compared to workers of similar ages from a nearby gas plant.

The study examined the mortality [death] experience of workers during the 40-year period from 1952 to 1992.

The study grouped the 1189 workers according to their degree of dioxin exposure. Dioxin exposure was calculated by measuring dioxin in the blood of 190 workers, or 16% of the exposed group. As the authors themselves say, "The major strength of the present study is the availability of a quantitative measure of exposure, which allows a direct estimate of dose-response relations."

The study evaluated several factors that could have biased the results. For example, they ruled out possible bias due to smoking because the group of pesticide workers and the control group both contained about the same proportion of smokers.

They evaluated and discussed possible effects due to exposures to chemicals besides dioxins. They could not rule out possible bias from exposure of the pesticide workers to cancer-causing chemicals besides dioxins.

The authors conclude that the results of this study "support the hypothesis of a dose-related effect of PCDD/F [dioxins and furans] on cancer and ischemic heart disease mortality."

The finding of elevated cancer deaths among dioxin-exposed workers is not a new finding. Three previous studies[4,5,6] have reported cancer increases among dioxin-exposed workers.

However, this new study is particularly interesting because it is based on actual measurements of dioxin levels in the blood of a sample of workers. Previous studies have estimated dioxin exposures instead of measuring them. The measurement of dioxin exposures allowed this study to look for a dose-response relationship, and such a relationship was found. Most people are familiar with the concept of dose-response; think of the effects from drinking one, two, or three glasses of wine. In general, greater dose leads to greater response. Finding greater numbers of cancers associated with larger doses of dioxin provides strong evidence of a cause-and-effect relationship between dioxin exposure and cancer in humans.

The finding of increased heart disease among dioxin-exposed workers is somewhat more surprising. Previous studies of this effect have been inconclusive; some studies of dioxin-exposed populations have reported increased heart disease, and other studies have reported no such increases. However, these previous studies have not been able to establish a dose-response relationship, as the present study has done.

In the present study, the dose-response relationship was clear. Because dioxin exposures were measured, and not merely estimated, in this study, these results should be given more weight than previous studies.

In studies of people exposed to dioxin after a chemical accident at a Hoffman-LaRoche pesticide factory in Seveso, Italy in 1976, it was noted that excessive numbers of people died of heart attacks. The authors of the Seveso study attributed these deaths to "stress from the accident." Now there is reason to ask whether these Seveso deaths were possibly caused, not by stress, but by exposure to dioxins released during the accident.

In sum, this is an important study that makes a unique contribution to our understanding of the relationship of dioxins to human health.

The strategy conference in Baton Rouge will focus on 9 distinct targets and strategies for getting dioxin out of the environment:

(1) the paper and pulp industry; (2) getting organochlorines out of manufacturing and cleaning; (3) stopping all forms of incineration; (4) phasing out all uses of PVC (polyvinyl chloride); (5) creating scientific swat teams to help communities; (6) linking dioxin to health; (7) getting dioxin out of our food; (8) developing tools to help poisoned communities; and (9) communicating dioxin issues to the public and the media.

See you in Baton Rouge March 15.
                                                                          --Peter Montague
===============
[1] Dieter Flesch-Janys and others, "Exposure to Polychlorinated Dioxins and Furans (PCDD/F) and Mortality in a Cohort of Workers from a Herbicide-producing Plant in Hamburg, Federal Republic of Germany." AMERICAN JOURNAL OF EPIDEMIOLOGY Vol. 142, No. 11 (December 1, 1995), pgs. 1165-1175.

[2] See, for example, the recent report by the Environmental Defense Fund (EDF) and its corporate partners, Johnson & Johnson, McDonald's, the Prudential Insurance Company, and Time, Inc.: PAPER TASK FORCE RECOMMENDATIONS FOR PURCHASING AND USING ENVIRONMENTALLY PREFERABLE PAPER, available for $25.00 from EDF; telephone (212) 505-2100.

[3] Lois Gibbs, DYING FROM DIOXIN (Boston: South End Press, 1995); $20.00 from South End Press: (617) 266-0629. Those wanting even more technical detail about the consequences of dioxin production will need to get Arnold Schecter, editor, DIOXINS AND HEALTH (New York: Plenum Press, 1994).

[4] Marilyn Fingerhut, W.E. Halperin, D.A. Marlow, and others. "Cancer Mortality in Workers Exposed to 2,3,7,8-tetrachlorodibenzo-P-dioxin." NEW ENGLAND JOURNAL OF MEDICINE Vol. 199 (1991), pgs. 212-218.

[5] A. Zober and others. "Thirty-Four year mortality follow-up of BASF employees exposed to 2,3,7,8-tetrachlorodibenzo-P-dioxin after the 1953 accident." INTERNATIONAL ARCHIVES OF OCCUPATIONAL AND ENVIRONMENTAL HEALTH Vol. 62 (1990), pgs. 139-157.

[6] A. Manz, J. Berger, J.H. Dwyer, and others. "Cancer mortality among workers in a chemical plant contaminated with dioxin." THE LANCET Vol. 338 (1991), pgs. 959-964.

Descriptor terms: dioxin; meetings; conferences; campaigns; strategy; corporations; lois gibbs; jim warren; nc warn; edf; soc; connie tucker; germany; occupational safety and health; cancer; heart disease; chlorophenols; pesticides; 2,4,5-t; 2,4-d; silvex; furans; seveso; italy; hoffman-laroche; baton rouge; la;

#47: Chemwaste Stashes Dioxin Wastes in A Public Storage Cubicle, Then Ships Them To Emelle Illegally As Federal EPA Looks The Other Way

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

RACHEL'S HAZARDOUS WASTE NEWS #47
---October 19, 1987---
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========================

Officials of Chemical Waste Management, Inc., are "either grossly negligent... or they don't know what's going on [in their own company]," says Buddy Cox, chief of the hazardous waste branch of the Alabama Department of Environmental Management (ADEM). Chemical Waste Management (ChemWaste), a subsidiary of Waste Management, Inc., runs America's largest chemical waste dump, at Emelle, in Sumter County, Alabama.

According to the Birmingham News (Sept. 27, 1987, pg. 1), Mr. Cox is asking himself, "If ChemWaste officials in Baton Rouge could so badly mishandle one of the most toxic of all chemicals [dioxin], then how much confidence should the public place in the company's other operations, including Emelle?"

This story begins in 1972 when surplus herbicide was shipped from Kelly Air Force Base in Texas to a federal surplus property outlet in Baton Rouge, LA. From there, it was sold to Louisiana hospitals, schools, and other public facilities.

A teacher at Capitol High School in Baton Rouge noticed that plants in the school's greenhouse were deformed with elongated leaves--a sign of exposure to 2,4,5-T, a weed-killer typically contam-inated with dioxin. According to H.F. Calhoun, director of pesticide and environmental programs for the Louisiana Department of Agriculture and Forestry (LDAF), samples from a ruptured barrel of herbicide outside the greenhouse revealed 2,4,5-T, including "levels of dioxin that we would have expected of military-vintage 2,4,5-T at that time." The herbicide 2,4,5-T was widely used to defoliate jungles in Vietnam; thousands of American GIs are now suing the U.S. government and several chemical companies for exposing them to the hazardous, dioxin-containing herbicide. Because of the dioxin risk, all use of 2,4,5-T was banned in the U.S. in 1986.

During 1983, Mr. Calhoun's department traced and recalled 14 additional barrels of 2,4,5-T that had originated with that shipment from Kelly Air Force Base back in 1972. Not knowing what else to do with the dangerous wastes, LDAF asked their manufacturer to take them back. The manufacturer hired Chemical Waste Management, Inc. (ChemWaste) to take the drums away. Chemwaste hauled them away alright, but not to a proper waste disposal facility. Instead Chemwaste rented a mini-warehouse--a rental storage space intended for consumers to store household articles. A typical cubicle in David Min-U-Storage, where Chemwaste stashed the herbicide, rents for $35 per month. Mr. Calhoun's records of the event include phone message slips, one of which reveals that ChemWaste officials told the manufacturer of the herbicide that they had found "secure storage" for the dangerous chemicals.

According to an official of LDAF, when ChemWaste arrived September 23, 1985 to pick up the chemicals, he asked them for a manifest. A manifest is an official paper that declares where hazardous wastes are being taken. The officials says he was told by ChemWaste that no manifest was needed--a statement the official now recognizes was false.

Chemwaste hauled the 14 drums of poison to their rented consumer cubicle, where it remained for two years. Storing chemicals in such a place is a violation of federal law and state law, and it also violated the rental contract on the space, which prohibited storage of chemicals and other "inherently dangerous materials."

As luck would have it, thieves or vandals broke into several of David Min-U-Storage's rental spaces, one of them ChemWaste's, and the jig was up. Manager of the rental spaces, Kerrie Lemieux, told reporters she entered ChemWaste's cubicle and smelled a "weird" odor. She saw all the drums, called ChemWaste and asked if the chemicals were toxic and, she says, "They told me no." Naturally, a flap ensued.

ChemWaste then shipped the wastes from the security of David Min-U-Storage in Louisiana to their landfill at Emelle, Alabama, where the wastes presently reside. Chemwaste's Emelle site is not authorized to store or dispose of dioxin wastes, so acceptance of the waste at the Emelle site was a further violation of federal law. The Alabama Department of Environmental Management (ADEM) has ordered ChemWaste to remove the wastes from the Emelle site and to pay a $20,000 fine. ADEM is also holding up issuance of a permanent license for the Emelle site, which has been operating under a temporary license since 1980. According to the Birmingham News, the U.S. Environmental Protection Agency has ruled that Chem-waste violated its federal permit when it accepted dioxin-contaminated herbicides at Emelle; however, EPA has imposed no penalty on the company. EPA has a long, consistent record of ignoring this particular company's infractions of the law, and of fining the company amounts that are less than the profits the company has earned by breaking the law. One whistle-blowing EPA official has been widely quoted saying that it looks to him as if the EPA is a wholly-owned subsidiary of Waste Management, Inc.

ChemWaste has fired the man chiefly responsible for arranging the storage of hazardous chemicals in a flimsy public storage cubicle. They have brought charges him, claiming he was acting as an individual and not on behalf of Chemwaste the corporation. However, Mr. Calhoun's telephone slips dating back to September, 1985, show that at least three separate Chemwaste officials negotiated with Louisiana Department of Agriculture over removal of the wastes and that Chemwaste, the corporation, not an individual, rented the cubicle at David Min-U-Storage. And by the time the federal permit at Emelle was violated by acceptance of the dioxin-contaminated wastes, the ousted Chemwaste official was long gone.

It looks as if Chemwaste is up to its old high jinx once again. It also looks as if the U.S. EPA is winking at the continued violation of the permit at Emelle, proving once again that where this particular company and this particular federal agency are concerned, crime pays.

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[Our thanks to Linda Wallace Campbell of Alabamians for a Clean Environment, P.O. Drawer 1526, Livingston, AL 35470, for alerting us to the facts in this matter. ChemWaste is Waste Management, Inc.'s hazardous waste subsidiary. They are expanding aggressively throughout the world. If you have a story about them, please contact us.]

--Peter Montague, Ph.D.

Descriptor terms: cwmi; al; adem; herbicides; dioxin; pesticides; hazardous waste treatment technologies; hazardous waste disposal techologies; emelle; la; epa; wmi;