#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;

#391: Dioxin Reassessed--Part 2

=======================Electronic Edition========================
RACHEL'S HAZARDOUS WASTE NEWS #391
---May 26, 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========================

After three years of study, U.S. Environmental Protection Agency [EPA] is about to publish a 9-volume draft "scientific reassessment" of dioxin and other dioxin-like chemicals, including dibenzofurans and some PCBs [polychlorinated biphenyls]. PCBs are industrial poisons now banned in the U.S. because of widespread environmental damage. Dioxins and furans are highly toxic byproducts of certain industrial operations including incineration, tire burning, combustion of coal and oil, manufacture of paper and some pesticides, metal smelting, and perhaps diesel engine exhausts [pgs. 6-9]. There are probably other sources as well. Dioxins and furans are created when chlorine combines with other chemicals at high temperatures.

A copy of EPA's summary volume (Chapter 9) was leaked to the press in mid-May. We obtained a copy and reported some of its findings and conclusions last week, focusing on the cancer hazard. This week, we bring you more, stressing non-cancer effects. [Page numbers inside square brackets refer to EPA's draft of Chapter 9, dated May 2, 1994.]

According to EPA, nature produces only small amounts of dioxin. The vast majority of dioxin is created by human economic activities. Since about 1920, industrial emissions, and inattention to the potent toxic effects of dioxin-like chemicals, have allowed the environment to become widely contaminated with significant quantities of dioxins, furans and PCBs. As a result, all Americans eat and breathe small but important amounts of dioxin every day.

Human exposure to dioxin begins early in life. A human fetus lives in the womb enclosed inside a fluid-filled sac called the placenta, which provides a barrier to many poisons that the mother might ingest. Unlike many other poisons, dioxin crosses the placenta and begins affecting the fetus [pg. 23]. The human body retains dioxin, so a "body burden" begins accumulating in each of us during our early months in the womb. [1]

In humans and other species, it is the growing embryo or fetus that is most sensitive to the toxic effects of dioxin-like chemicals. 

EPA: "A general finding in fish, bird, and mammalian species is that the embryo or fetus is more sensitive to TCDD-induced mortality than the adult. [TCDD is a shorthand name for dioxin.] Thus the timing of TCDD exposure during the life history of an animal can greatly influence its susceptibility to overt dioxin toxicity." [pg. 36]

Growth occurs in two ways: cells multiply, and cells of one type turn into cells of another type (a process called differentiation). Thus some cells become eyes and other cells become fingers by differentiation. Dioxin-like chemicals can disrupt both cell multiplication and cell differentiation.

"Of particular interest to the risk assessment process is the fact that a wide variety of developmental events, crossing three vertebrate classes and several species within each class, can be perturbed, suggesting that dioxin has the potential to disrupt a large number of critical developmental events at specific developmental stages. Not only can these changes lead to increases in embryo/fetal mortality, but they can disrupt organ system structure and irreversibly impair organ function." [pgs. 34-35]. In other words, damage that occurs in the womb can last a lifetime.

After a baby (or animal) is born, rapid growth continues, so sensitivity to the toxic effects of dioxin continues as well. Human infants who breast feed get a particularly high dose of dioxins. EPA's report calculates that an infant who breast feeds for a year will receive 4% to 12% of his or her full lifetime dose of dioxin during that one year [pgs. 15, 21]. (Despite the presence of dioxin-like chemicals in human milk, breast feeding is still the best way to nourish an infant; all of the alternatives are worse. [2])

Although dioxin can presumably interfere with every bodily system in the growing infant, there is evidence that the developing immune system is one of the most sensitive to disruption by low-level exposure to dioxin-like chemicals. EPA says, "Furthermore, since TCDD [dioxin] alters the normal differentiation of immune system cells, the human embryo may be very susceptible to long-term impairment of immune function from in utero [in the womb] effects of TCDD on developing immune tissue." [pg. 39]

EPA points out that, "Impairment of the immune system can be considered an adverse outcome in its own right, being responsible for induced pathologies." [pg. 51] And: "Concern over the potential toxic effects of chemicals on the immune system arises from the critical role that the immune system plays in maintaining health. It is well recognized that suppressed immunological function can result in increased incidence and severity of infectious diseases as well as some types of cancer. Conversely, the inappropriate enhancement of immune function or the generation of misdirected immune responses can precipitate or exacerbate the development of allergic and autoimmune diseases." [pg. 37] In other words, there are two ways your immune system can malfunction: it can be depressed and fail to protect you against bacteria, parasites, viruses and cancer. Or it can become too active and start to attack you; this creates autoimmune diseases like asthma, diabetes, and lupus.

EPA clearly considers these immune system hazards important; the report spends considerable time discussing them: "Animal host resistance models that mimic human disease are available and have been used to assess the effect of TCDD on altered host resistance [to disease]. Results from host resistance studies provide evidence that exposure to TCDD results in increased susceptibility to bacterial, viral, parasitic, and neoplastic [cancer] disease. These effects are observed at relatively low doses and likely result from TCDD-induced suppression of immunological function." [pg. 38]

The immune system is as complex as the brain and central nervous system. [3] Scientists speak of two basic parts of the immune system: those that work via cells (called "cell-mediated") and those that work in the blood stream without entering cells (called "humoral").

EPA: "Both cell-mediated and humoral immune responses are suppressed following TCDD exposure, suggesting that there are multiple cellular targets within the immune system that are altered by TCDD. Evidence also suggests that the immune system is indirectly targeted by TCDD-induced changes in nonlymphoid tissues." [pg. 38]

EPA goes on: "One potentially important indirect mechanism is via effects on the endocrine system. Several endocrine hormones have been shown to regulate immune responses, including glucocorticoids, sex steroids, thyroxine, growth hormone, and prolactin. Importantly, TCDD and other related compounds have been shown to alter the activity of all of these hormones." [pg. 38]

The EPA's draft report speaks of "a window of sensitivity of biological processes." [pg. 48] In other words, there are certain times during the life of an animal (or human) when it is more sensitive to dioxin's effects than at other times. The perinatal period (shortly before or shortly after birth) is one such "window of sensitivity." But there are evidently other such "windows." EPA suggests that any time the immune system begins to respond to a challenge, disruption by dioxin can have far-reaching effects: "It is important to consider, however, that if an acute exposure to TCDD even temporarily raises the TCDD body burden at the time when an immune response is initiated, there may be a risk of adverse impacts even though the total body burden may indicate a relatively low average TCDD level." [pgs. 38-39] Thus even a short-term exposure to dioxin at the wrong time might cause disease in a person by suppressing the immune system, even though the person's average lifetime body burden of dioxin may not be greatly increased.

Dioxin may also cause inheritable genetic changes: "While dioxin and related compounds are not generally considered to be 'genotoxic' in traditional terms, both empirical data and the results of modeling efforts suggest that they may be functioning indirectly to produce irreversible genetic changes in exposed cells." [pg. 33]

EPA's draft report emphasizes that most people get their daily dose of dioxin from their food (about 90% from meat, fish and dairy products) [pg. 12]. However, people who live near sources of dioxin emissions (listed in our first paragraph, above), should consider that inhalation may be an important hazard for them. 

EPA says, "The use of incineration as a means of solid and hazardous waste management results in the emission of contaminated particles that may contain TCDD and related compounds into the environment. Thus, exposure to TCDD and related compounds may result from inhalation of contaminated fly ash, dust and soil. Systemic effects occur in animals after pulmonary exposure to TCDD, suggesting that transpulmonary [lung] absorption of 2,3,7,8-TCDD does occur. Further results suggest that the transpulmonary absorption of 2,3,7,8-TCDD and 2,3,7,8-TBDD was similar to that observed following oral exposure.... these data provide support for the inference that efficient absorption will occur when particles containing dioxin and related compounds are inhaled by humans." [pgs. 17-18]

How much dioxin is "safe"? 

EPA: "The USEPA has frequently defined a reference dose (RfD) for toxic chemicals to represent a scientific estimate of the dose below which no appreciable risk of non-cancer effects is likely to occur following chronic exposures. In the case of dioxin and related compounds, calculation of an RfD based on human and animal data and including standard uncertainty factors to account for species differences and sensitive subpopulations would result in a reference intake levels on the order of 10-100 times below the current estimates of daily intake in the general population." [pg. 51]

How much dioxin is "safe"? 

EPA's answers: For cancer hazards? Three hundred to 600 times less than we all now take in every day. (See RHWN #390.) For non-cancer hazards? Ten to 100 times less than we all now take in every day.

EPA's "dioxin reasessment" raises one key public policy question: How much additional dioxin is acceptable in the environment? To us, the answer seems clear: zero. To protect public health, no new sources can be allowed, and present sources must be sharply reduced.

--Peter Montague, Ph.D.

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

[1] The "half-life" of dioxins in humans is somewhere between 5.8 years and 7 years [pgs. 13, 20]. (The half-life is the time it takes for half of today's dioxin intake to be excreted.) Therefore, dioxin builds up in our bodies as we age.

[2] See, for example, Natalie Angier, "Mother's Milk Found to Be Potent Cocktail of Hormones," N.Y. TIMES May 24, 1994, pgs. C1, C10.

[3] Lydia Woods Schindler, UNDERSTANDING THE IMMUNE SYSTEM [NIH Publication No. 88-529] (Bethesda, Md.: National Institutes of Health, July, 1988).

Descriptor terms: epa; dioxin reassessment; studies; dibenzofurans; furans; pcbs; tire burning; coal; oil; fossil fuels; paper; pesticides; metal smelting; smelters; diesel; chlorine; infants; fetuses; immune system; immunotoxicity; asthma; lupus; diabetes; incineration; msw; hazardous waste; inhalation; air pollution;

#390: Dioxin Reassessed--Part 1

=======================Electronic Edition========================
RACHEL'S HAZARDOUS WASTE NEWS #390 
---May 19, 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========================

For three years, U.S. Environmental Protection Agency [EPA] has been reassessing the toxicity of dioxin and other dioxin-like chemicals, including dibenzofurans and some PCBs [polychlorinated biphenyls]. PCBs are industrial chemicals now banned in the U.S. because of widespread environmental damage. Dioxins and furans are unwanted byproducts of many industrial operations including incineration, tire burning, combustion of coal and oil, manufacture of paper and some pesticides, and metal smelting. Dioxins and furans are created when chlorine combines with other chemicals at high temperatures.

In 1990, the paper and chlorine industries campaigned to force EPA to undertake a thorough review of dioxin science (RHWN #275). It is now abundantly clear that the reassessment has not turned out the way those industries hoped it would. We have obtained two drafts of the EPA's summary report of its dioxin reassessment titled, "Chapter 9. Risk Characterization of Dioxin and Related Compounds," dated March 7, and May 2, 1994. Some conclusions of the May 2 draft were reported in the NEW YORK TIMES May 11, 1994. [1] What follows here is based entirely on the EPA's May 2 draft. Page numbers inside square brackets refer to that draft.

EPA has identified 30 dioxin-like chemicals (7 true dioxins, 10 furans, and 13 PCBs) that have dioxin-like characteristics. EPA's draft report describes the toxicity of all these 30 chemicals taken together; in this discussion we refer to them as simply dioxin.

EPA has concluded that:

** For non-cancer effects, such as damage to the reproductive, endocrine, and immune systems, in birds, fish and mammals, including humans, dioxin is much more toxic than previously believed [pg. 35].

The agency says, "Indeed, these compounds are extremely potent in producing a variety of effects in experimental animals based on traditional toxicology studies at levels hundreds or thousands of times lower than most chemicals of environmental interest." [pg. 1] And: "There is adequate evidence from studies in human populations as well as in laboratory animals and from ancillary experimental data to support the inference that humans are likely to respond with a plethora [an abundance] of effects from exposure to dioxin and related compounds." [pg. 49]

Dioxin's most powerful effects are seen in the reproductive system, the endocrine (hormone) system, and the immune system. Most sensitive of all are newborn infants and fetuses exposed while in the womb. "In mammals, postnatal functional alterations involving learning behavior and the developing reproductive system appear to be the developmental events most sensitive to perinatal dioxin exposure. The developing immune system may also be highly sensitive." [pg. 36] In other words, dioxin exposure of mammals (including humans) shortly before or shortly after birth ("perinatal") are most likely to impair intellectual development and the immune system. The immune system protects against bacterial and viral disease, and cancer, so damage to the immune system can invite other serious diseases.

** Some of dioxin's powerful effects are observable in humans at dioxin exposure levels already occurring in the U.S. population. [pgs. 34, 37, and Table 9-3 following pg. 43] EPA says, "Some of the effects of dioxin and related compounds have been observed in laboratory animals and humans at or near levels to which people in the general population are exposed." [pg. 47] And: "In humans, subtle changes in enzyme activity indicating liver changes, in levels of circulating reproductive hormones in males, in reduced glucose tolerance, and in cellular changes related to immune function suggest the potential for adverse impacts on human metabolism, reproductive biology, and immune competence at or within one order of magnitude of average background body burden levels." [pgs. 49-50] In other words, average levels of dioxin already present in the bodies of average Americans --or levels not more than 10 times as high as average levels --seem to be capable of damaging the immune system, reducing sex hormones in the blood stream of men, interfering with glucose metabolism (a condition suggestive of diabetes), and causing other negative changes in health and well being.

Table 9-3 shows that the average amount of dioxin in Americans is 9 nanograms per kilogram (ng/kg) of body weight; a nanogram is a billionth of a gram and there are 28 grams in an ounce. Table 9-3 also shows that sex hormones are diminished in men with 13 ng/kg; altered glucose tolerance has been observed in humans with 14 ng/kg; decreased growth is observable in humans having 47 ng/kg; endometriosis is produced in monkeys having 27 ng/kg.

Within the general public, some people are receiving lower-than-average doses of dioxin and others are receiving higher-than-average doses because of their diets, living near facilities emitting dioxin, exposures at work, and so forth. EPA says, "Some more highly exposed members of the population may be at risk for a number of adverse effects including developmental toxicity, reduced reproductive capacity in males based on decreased sperm counts, higher probability of experiencing endometriosis in women, reduced ability to withstand immunological challenge, and others." [pg. 50]

** Dioxin's cancer effects are worse than previously thought. EPA now says flatly, dioxin is "likely to present a cancer hazard to humans" [pg. 52]. And dioxin "probably increases cancer mortality of several types" in humans, EPA says. [pg. 31]

EPA shows numerically that existing levels of dioxin may be a significant cancer hazard: "Modeling estimates suggest that, if dioxin and related compounds are adding to human cancer burden, current background exposure may result in upper bound population cancer risk estimates in the range of one in ten thousand (10**-4) to one in a thousand (10**-3) attributable to exposure to dioxin and related compounds." [pgs. 43-44] In other words, EPA's best estimate is that existing levels of dioxin in the U.S. population may be sufficient to cause cancer in somewhere between one-in-every-thousand people and one-in-every-ten-thousand people each year. Since there are 250 million Americans, EPA is saying that existing dioxin levels may be causing somewhere between 25,000 and 250,000 new cancers each year. There are about one million new cancers diagnosed each year in the U.S. [see RHWN #385], so EPA's best estimate is that dioxin now present in the American people may be responsible for somewhere between 2.5% and 25% of all cancers.

[[The following is a rewording of this article from a greenleft publication:

"EPA's best estimate is that existing levels of dioxin in the US population may be sufficient to cause cancer in somewhere between one in 10,000 people and one in 1000 people during a lifetime (70 years). Since there are 250 million Americans, EPA is saying that existing dioxin levels may be causing somewhere between 25,000 and 250,000 cancers in a lifetime (70 years), or 350 to 3500 new cancers each year.

If EPA's estimate of the dioxin cancer hazard is correct, an individual's lifetime probability of getting cancer from dioxin in the US falls in the range of 1 in 1700 to 1 in 3300. This is the same risk you would get from 300 to 600 chest x-rays."]]

Another way to estimate the size of the cancer hazard is to note that EPA says the amount of dioxins sufficient to create a one-in-a-million cancer hazard is daily intake of 0.01 picograms of dioxin per kilogram of body weight [pg. 43]. (A picogram is a trillionth of a gram.) Average daily intake of total dioxins among Americans is 3 to 6 picograms per kilogram of body weight [pg. 50], or 300 to 600 times the one-in-a-million hazard level. This means that, in the U.S. population of 250 million, our average daily dose of dioxin in food and air may be causing somewhere between 75,000 and 150,000 cancers each year. Thus both ways of estimating the cancer hazard force the conclusion that dioxins may already be a major cancer hazard for Americans.

Dioxins are produced in very small quantities, if at all, by nature. EPA says, "...the presence of dioxin-like compounds in the environment occurs primarily as a result of industrial practices." [pg. 6]

EPA identifies 4 major sources of dioxin in the environment:

(1) COMBUSTION AND INCINERATION SOURCES. 

This category includes incineration of municipal solid waste, sewage sludge, hospital wastes and hazardous wastes; metallurgical operations, such as high-temperature steel production, smelting operations, and scrap metal recovery furnaces; and the burning of coal, wood, petroleum products and used tires for power or energy generation. Cigarette smoke, crematories, volcanoes and forest fires are "minor sources," says EPA. [pg. 7] (Forest fires release dioxins that have been discharged by industrial smoke stacks and have fallen onto the leaves of trees; by similar means, leaf compost can be contaminated by dioxins [pg. 8].)

(2) CHEMICAL MANUFACTURING/PROCESSING SOURCES. 

Dioxins and dioxin-like compounds are created by the manufacture of chlorine and such chlorinated compounds as chlorinated phenols, PCBs, phenoxy herbi-cides (e.g., 2,4,5-T, 2,4-D and 11 others), chlorinated benzenes, chlorinated aliphatic compounds, chlorinated catalysts, and halogenated diphenyl ethers. [pg. 7] Although manufacture of many chlorinated phenols, and PCBs, ceased in the U.S. around 1980, use and disposal are continuing both inside and outside the U.S. Large quantities of PCBs are in "storage" in leaking landfills; another billion pounds of PCBs (about 1/3 of all PCBs ever manufactured) simply cannot be accounted for (see RHWN #327).

(3) INDUSTRIAL/MUNICIPAL PROCESSES: 

Dioxin-like compounds are created during chlorination of naturally-occurring phenolic compounds, such as those in wood pulp. Chlorine bleaching in the manufacture of bleached pulp and paper has resulted in dioxins in paper products as well as in liquid and solid wastes from this industry. [pg. 7]

(4) RESERVOIR SOURCES: 

Dioxin degrades very slowly once it is released into the environment. Therefore past releases of dioxin have accumulated in various "reservoirs," such as soils, sediments, organic matter, and waste disposal sites. (The Hyde Park Landfill on the edge of the Niagara River bordering New York and Canada has been estimated to contain as much as a ton of dioxins. See RHWN #188.) When dioxins move from these reservoirs they can become "new sources" of dioxin for a particular locale. All together, these sources emit some 14,000 grams (30.9 pounds) of total dioxins each year in the U.S. [pg. 8] But the amount of dioxins falling on the surface of the U.S. each year is estimated to be between 20,000 and 50,000 grams (44.1 to 110.2 pounds) [pg. 9]. Obviously some important sources of dioxin have not yet been identified. Dioxins may be arriving from other countries, carried on the wind. EPA simply doesn't know.

Dioxins fall out of the atmosphere onto the land and water and are then incorporated into the food chain, or they are discharged directly into waterways and incorporated into food chains. They tend to concentrate as they move upward in the food chain; over 90% of the dioxins in our bodies enter with our food. The major sources of dioxin to humans are meat, fish and dairy products, though inhalation may be important near some emission sources, such as some incinerators.

[To be continued.] #391

  --Peter Montague, Ph.D.

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

[1] Keith Schneider, "Fetal Harm, Not Cancer, Is Called The Primary Threat From Dioxin," NEW YORK TIMES May 11, 1994, pgs. A1, A20.

Descriptor terms: dioxin; tcdd; 2,3,7,8-tetrachlorodibenzo-p-dioxin; dibenzofurans; furans; dioxins; pcbs; polychlorinated biphenyls; epa reassessment; studies; risk characterization; risk assessment; reprodctive disorders; endocrine disrupters; endocrine system; immune system; immune disorders; immunotoxicity; toxins; poisons; hormones; sex hormones; endometriosis; cancer; diabetes; glucose intolerance; sperm counts; incineration; smelters; smelting; fossil fuels; coal; oil; wood; tires; rubber tires; forest fires; leaf composting; medical wastes; infectious wastes; hospital wastes; sewage sludge; hazardous waste; municipal solid waste; msw; cigarettes; tobacco; volcanoes; cremation; crematories; chlorine; phenoxy herbicides; pesticides; paper; pulp; bleaching; landfilling; hyde park; niagara river; new york; canada; ny; cn; inhalation; food; meat; fish; dairy products; milk; cheese; food safety;

#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;

#314a: Cement and Kiln Dust Contain Dioxins

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

RACHEL'S HAZARDOUS WASTE NEWS #314
---December 2, 1992---
News and resources for environmental justice.
------
Environmental Research Foundation
P.O. Box 5036, Annapolis, MD 21403
Fax (410) 263-8944; Internet: erf@igc.apc.org ==========
RACHEL-4CM = DIOXIN FOCUSED DIRECTORY Remote Access Chemical Hazards Electronic Library. Dioxinnz.com =================================Original Source========================

During routine preparation of a REPORT TO CONGRESS ON CEMENT KILNS, the U.S.

Environmental Protection Agency (EPA) has learned that cement and cement kiln dust contain dioxins and furans (both of which are powerful poisons in animals and humans), according to a briefing document dated October 8, 1992, prepared by EPA staff for EPA's Director of Solid Waste, Sylvia Lowrance. The October briefing document also says 20 percent of the cement kiln dust that EPA tested contains the non-natural radioactive elements plutonium-238, plutonium-239 and cesium-137. Dioxins are the most powerful carcinogens (cancer-causing agents) ever tested in laboratory animals; plutonium is the most potent carcinogen in humans ever discovered.

Cement is a principal component of pipe often used to distribute drinking water in many American cities. Cement kiln dust is a byproduct of cement manufacture and is routinely given or sold to farmers as a soil treatment, or is discarded into pits or is piled on the ground near cement kilns in an uncontrolled fashion. According to Bill Schoenborn, an EPA staff member working on the REPORT TO CONGRESS, about 6 million tons of kiln dust is disposed of each year by cement kilns, 5.1 million tons of it buried on-site, and 900,000 tons of it shipped off-site for use in stabilizing other wastes (such as sewage sludge) or as a soil additive on farms. Cement kiln dust has previously been reported to contaminate groundwater with the toxic metals lead and chromium,[1] but until now no one has reported dioxins, furans, plutonium or cesium-137 in cement or cement kiln dust.

The REPORT TO CONGRESS is required by the federal Resource Conservation and Recovery Act (RCRA), the nation's basic hazardous waste law. Like mine wastes, cement kiln dust was initially exempt from RCRA because it is a high-volume waste presumed to be low in toxicity. Cement clinker (that is to say, cement itself) is exempt from RCRA because it is a product, not a waste. Section 8002(o) of RCRA required EPA to study cement kiln dust and to write a report for Congress on its findings. For several years, EPA dragged its feet preparing the report. Then Environmental Defense Fund (EDF) brought a lawsuit, and now EPA is under a court order to finish the report by April, 1993.

In the course of preparing the REPORT TO CONGRESS, EPA randomly selected 15 cement manufacturing plants (called kilns) for sampling, out of the 114 such plants presently operating in the U.S. Of the 15 plants sampled, eight burn hazardous waste as fuel and seven do not. In recent years, cement kiln operators have increasingly been using hazardous waste as fuel, to reduce fuel costs and thus increase profitability. The practice has proved controversial. (See RHWN #174 and #243.) Opponents of the practice say they fear cement will become contaminated with industrial poisons. Cement is a key raw material in concrete pipe for water delivery systems, and in concrete block and other concrete materials used in construction of private homes, commercial dwellings, public buildings, bridges and highways. Seventy to 80 million tons of cement are produced in the U.S. each year, depending on market demand.

Sampling Results

EPA took 15 samples of "clinker" (the product of a kiln, from which cement is made), plus 28 samples of dust (the unwanted byproduct of a kiln). All samples were analyzed for metals, chloride, cyanide, fluoride, total sulfate, total organic carbon, moisture content, and radioactive elements.

Samples from six kilns (4 burning hazardous waste, 2 not burning hazardous waste) were tested for dioxins and furans, volatile organic compounds, semivolatile organic compounds, and pesticides. All chemical analyses were completed by EPA's National Air and Radiation Environmental Laboratory (NAREL) in Alabama.

Dioxins and furans were detected in all samples of "clinker" and all samples of kiln dust analyzed for these compounds. The October briefing document says that the dioxin molecule known as 2,3,7,8-TCDD, the most potent poison in the dioxin family, was only identified in samples from kilns burning hazardous waste. Other dioxins were found in samples from kilns not burning hazardous waste, but no 2,3,7,8-TCDD. However, the October briefing document says it is not possible to generalize these differences to the entire 114 operating cement kilns.

Samples of cement kiln "clinker" did not contain pesticides or semivolatile organics. Clinker was not analyzed for volatile organics. On the other hand, cement kiln dust contained amounts of the volatile organics benzene and acetonitrile that exceeded RCRA limits "in a number of the samples of hazardous waste burners" but not in samples from kilns not burning hazardous wastes. The dust from one kiln not burning hazardous waste proved to be high in methylene chloride, according to the October briefing document.

These findings lend support to the view that burning hazardous waste in a cement kiln increases the amount and potency of toxins in the resulting cement kiln dust and perhaps in the cement itself.

At three kilns (2 burning hazardous waste, one not burning hazardous waste) levels of naturally-occurring radioactive radium-226 exceeded the cleanup standard for uranium mine and mill wastes (the standard being 5 picoCuries per gram). Cesium-137, a non-natural radioactive element, was present in the dust of 26 percent of the kilns tested (4 out of 15)--one hazardous waste burner and three non-hazardous waste burners. Plutonium-238 and plutonium-239 were detected in kiln dust samples from 3 of the 15 kilns tested. Each of these 3 facilities is "located near a DOE [U.S. Department of Energy] nuclear weapons production/testing facility," according to EPA's October briefing document. Plutonium and cesium-137 do not occur in nature but are created by nuclear bomb explosions and in nuclear power reactors.

A second EPA briefing document dated November 24, 1992, contains additional information about the problem of potent toxins being found in cement and in cement kiln dust. The document is titled "OSW Office Briefing on Cement Kiln Dust Risk Screening" and it contains a summary of a risk assessment that is being conducted by the EPA's Communications and Budget Division within the Regulatory Analysis Branch, Office of Solid Waste.

The November briefing document outlines two risk assessment scenarios: one in which cement dust blows off-site and affects a person living 750 feet from an active waste pile, and a second in which an individual is presumed to be living on top of an abandoned waste pile. No risk assessment was reported for the case of a farmer growing crops in soil to which cement kiln dust has been added.

Furthermore, no risk assessment is reported for the dioxins and furans measured in cement clinker, which it to say, in cement itself.

Based on the two risk assessment scenarios, the November briefing document describes amounts of toxins in cement kiln dust that appear to be acceptable, which is to say will only give cancer to one in 100,000 individuals so exposed. The November document lists 22 instances in which one or more EPA tests of cement kiln dust exceeded the criteria developed in the risk assessments. Criteria that are exceeded by one or more samples include: 2,3,7,8-TCDD, total dioxins, total dioxins and furans, total hexachloro dioxins, arsenic, beryllium, cadmium, chromium, lead, and thallium, plus the following radioactive elements: bismuth-214, cesium-137, potassium-40, lead-212, lead-214, radium-226, radium-228 and thorium-227.

The purpose of the risk assessments reported in the November document is to help EPA decide whether the agency needs to regulate cement kiln dust as a legally hazardous waste or not. Declaring cement kiln dust a legally hazardous waste would greatly increase the cost of waste disposal for some cement kilns, and thus might reduce the profitability of some kilns.

EPA employee Hugh Kaufman has previously charged that the agency has been "accommodating the regulated cement kiln hazardous waste incineration industry with nonexistent, or at best loose, regulation..."[2]

Now that EPA has found dioxins in cement clinker, and dioxins and radioactive elements in cement kiln dust, the agency will likely come under considerable pressure to regulate all cement kiln wastes as hazardous wastes.

For their part, citizens seem likely to start asking themselves anew whether kilns can be good neighbors.

--Peter Montague, Ph.D.

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

[1] Jeffrey D. Smith, "Cement Kilns 1991," EI DIGEST (August, [1991),] pgs. 20-32.

[2] Kaufman made his charge in a letter to EPA chief William Reilly dated Dec. 7, 1990; on February 21, 1991, cement kilns burning hazardous waste became regulated under the so-called "BIF" (boiler and industrial furnace) regulations, which can be found in the FEDERAL REGISTER February 21, 1991, pgs. 7134-[7240.] See also FEDERAL REGISTER July 17, 1991, pgs. 32688-[32692;] August 27, 1991, pgs. 42504-42517; September 5, 1991, pgs. 43874-43877; and August 25, 1992, pgs. 38558-38566.

Descriptor terms: cement kiln incineration; hazardous waste incineration; bif rules; sylvia lowrance; cement kiln dust; plutonium; cesium; dioxin; carcinogens; cancer; lead; chromium; metals; rcra; risk assessment; edf; concrete;

#264: The Wingspread Statement--Part 2: Major Challenge to 'Business as Usual'

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

RACHEL'S HAZARDOUS WASTE NEWS #264
---December 18, 1991---
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 international group of 21 scientists[1] met at Wingspread in Racine, Wisconsin in July, 1991 to discuss evidence that chemicals in the environment are causing changes in the sexual development of wildlife and conceivably in humans as well. (See RHWN #263.) The group produced a five-page "consensus statement."

Sexual development in wildlife, as in humans, is controlled by the endocrine system, a group of organs, tissues and cells that secrete hormones; the hormones interact with other cells, initiating chemical/biological reactions with far-reaching consequences. Male hormones are called androgens; female hormones are called estrogens.

It is now known that some chemicals disrupt the endocrine system. The Wingspread statement identifies the following: "Chemicals known to disrupt the endocrine system include: DDT and its degradation products [DDE and DDD], DEHP (di(2-ethylhexyl)phthalate), dicofol, HCB (hexachlorobenzene), kelthane, kepone, lindane and other hexachlorocyclohexane congeners [forms], methoxychlor, octachlorostyrene, synthetic pyrethroids, triazine herbicides, EBDC fungicides, certain PCB congeners [forms], 2,3,7,8-TCDD and other dioxins, 2,3,7,8-TCDF and other furans, cadmium, lead, mercury, tributyltin and other organo-tin compounds, alkyl phenols (non-biodegradable detergents and anti-oxidants present in modified polystyrene and PVCs), styrene dimers and trimers, soy products, and laboratory animal and pet food products."

In animals, and in humans, sexual characteristics are established at a particular point during development in the womb or egg. For example, Dr. Theodora Colborn of the World Wildlife Fund (Washington, DC) points out that a single dose of dioxin, administered to a pregnant rat at day 15 of the pregnancy--near the time when gender is established--results in demasculinization and feminization of male offspring.[2]

Samples of herring gulls from Lake Ontario collected in 1975 and 1976 showed cellular and anatomical changes in embryos and in newly hatched chicks that caused feminization of male chicks and overdevelopment of female reproductive organs. Elevated concentrations of DDE [a break down by product of DDT] and other residues were found in eggs from the same population. To test whether these sexual problems might be linked to the presence of the DDT, laboratory experiments were conducted in which Western gull eggs were injected with concentrations of DDT similar to those found in the Great Lakes environment. Male chicks became feminized, developing ovarian tissue and oviducts.[3]

What is becoming clear is that the older picture of chemical toxicity underestimates the number and kinds of effects that chemicals can have in fish, birds, and mammals. For decades, U.S. regulatory officials have focused their attention almost exclusively on cancer. Meanwhile, many of the chemicals that have been dumped into the environment, and are now coursing through food chains, cause many other detrimental effects besides cancer.

For example pesticides such as DDE, dieldrin, lindane, mirex, toxaphene, and PCBs, block communication between cells. Normal metabolism [energy use] and development of a cell may be disrupted because movement of nutrients, electrolytes, and hormones in and out of a cell is blocked by the presence of these poisons.[4]

Furans, benzo[a]pyrene, 2,3,7,8-TCDD [dioxin], DDE, dieldrin, HCB [hexachlorobenzene], lindane [beta-HCH], mirex, toxaphene, and PCBs induce enzyme activity. [Enzymes are large protein molecules that promote chemical activity in the body; the presence of particular enzymes makes possible particular chemical reactions that would not otherwise be possible.] When the enzyme activity is induced, normal products of the endocrine hormonal system can be released into the bloodstream. This can disrupt the role of steroid hormones, affecting growth and sexual maturation.[4]

The structure of DDT and DDE are, themselves, quite similar to estrogens and thus may mimic female hormones. In addition, DDE induces enzymes that break down male hormones. Under different circumstances, dioxin acts like an estrogen, or it may act as an anti-estrogen (what causes the same chemical to have opposite effects is not understood).[4]

At one Superfund site where data are available, humans are experiencing abnormalities of sexual development. At the Brio site south of Houston, Texas, where a housing development was built atop a chemical dump, girls 4 to 5 years old have developed pubic hair and enlarged breasts. One child (now four years old) was born without any genital organs; chromosome tests revealed that this is a male child, though he has a birth canal. This information, and other data about abnormal sexual development of children at the Brio site, is contained in a unique database of information that resulted from a health survey of the community by a local group (HELP) and by the Environmental Health Network (EHN) in Harvey, Louisiana.[5] Such surveys--providing an unusually valuable source of information about health problems near chemical dumps--are under way in several Superfund communities, looking for patterns of problems, including the kinds the Wingspread statement warns of.

The Wingspread statement presents a major new challenge to advocates of "business as usual." The participants in the conference represent 17 different fields of scientific inquiry. They have many thousands of data points on which they have based their conclusions. If they are right, we are all being exposed, on a daily basis, to chemicals that threaten out reproductive health, and the health of our offspring.

Because hormones and hormone disrupters do their work at extremely low concentrations, the only "safe" dose of an endocrine-system disrupter is zero. Thus any new sources of these chemicals should be aggressively discouraged while we figure out how to minimize exposure to the quantities of these chemicals already in the environment.

--Peter Montague, Ph.D.

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

[1] Participants in the Wingspread meeting included the following individuals (whose institutional affiliations are given for identification purposes only): Dr. Howard A. Bern, Professor of Integrative Biology (emeritus) and Research Endocrinologist, University of California-Berkeley; Dr. Phyllis Blair, Professor of Immunology, University of California-Berkeley; Sophie Brasseur, Marine Biologist, Research Institute for Nature Management, Texel, The Netherlands; Dr. Theo Colborn, Senior Fellow, World Wildlife Fund, Washington, DC; Dr. Gerald R. Cunha, Developmental Biologist, University of California-San Francisco; Dr. William Davis, Research Ecologist, Environmental Research Laboratory, U.S. Environmental Protection Agency, Sabine Island, FL; Dr. Klaus D. Dohler, Director, Research, Development & Production, Phar-ma Bissendorf Peptide GmbH, Hannover, Germany; Glen Fox, Contaminants Evaluator, National Wildlife Research Center, Environment Canada, Quebec, Canada; Dr. Michael Fry, Research Faculty, Department of Avian Sciences, University of California-Davis; Dr. Earl Gray, Section Chief, Developmental and Reproductive Toxicology Division, Health Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC; Dr. Richard Green, Professor of Psychiatry in Residence, School of Medicine, University of California-Los Angeles; Dr. Melissa Hines, Assistant Professor in Residence, School of Medicine, University of California-Los Angeles; Timothy J. Kubiak, U.S. Fish and Wildlife Service, East Lansing, MI; Dr. John McLachlan, Director, Division of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, NC; Dr. J.P. Myers, Director, W. Alton Jones Foundation, Charlottesville, VA; Dr. Richard E. Peterson, Professor of Toxicology and Pharmacology, School of Pharmacy, University of Wisconsin-Madison; Dr. P.J.H. Reijnders, Head, Section of Marine Mammology, Research Institute for Nature Management, Texel, The Netherlands; Dr. Ana Soto, Associate Professor, Tufts University School of Medicine, Boston, MA; Dr. Glen Van Der Kraak; Assistant Professor, University of Guelph, Ontario, Canada; Dr. Frederick vom Saal, Professor, Division of Biological Sciences, University of Missouri-Columbia; Dr. Pat Whitten, Assistant Professor, Department of Anthropology, Emory University, Atlanta, GA.

[2] David J. Hanson, "Dioxin Toxicity: New Studies Prompt Debate, Regulatory Action," C&EN [CHEMICAL & ENGINEERING NEWS] August 12, 1991, pg. 13.

[3] Theodora E. Colborn and others, GREAT LAKES GREAT LEGACY? (Washington, DC: Conservation Foundation, 1990), pg. 139.

[4] Theodora E. Colborn and others, cited above, pg. 142.

[5] For more information about the Brio site, contact HELP: 10904 Scarsdale Boulevard, M263, Houston, TX 77089; phone (713) 992-1867. For advice about health surveys, contact Linda King, Environmental Health Network, P.O. Box 1628, Harvey, LA 70058; phone (504) 362-6574.

Descriptor terms: endocrine disruptors; racine; wi; wildlife; sexual development; endocrine system; fish; birds; herring gulls; mammals; humans; reproductive hazards; reproductive disorders; ddt; des; pesticides; herbicides; insecticides; fungicides; theodora colborn; wwf; superfund; brio; ehn; environmental health network;

#290: Young Male Rats Are 'Demasculinized' and 'Feminized' By Low Doses of Dioxin

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

RACHEL'S HAZARDOUS WASTE NEWS #290
---June 17, 1992---
News and resources for environmental justice.
------
Environmental Research Foundation
P.O. Box 5036, Annapolis, MD 21403
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RACHEL-4CM = DIOXIN FOCUSED DIRECTORY Remote Access Chemical Hazards Electronic Library. Dioxinnz.com =======================Original Source========================

Three new studies by researchers at University of Wisconsin reveal that very low doses of dioxin alter the sexual development of young male rats, causing demasculinization and feminization. [1,2,3]

Dr. Linda S. Birnbaum, a scientist with U.S. EPA [Environmental Protection Agency] calls the new studies "highly significant."[4] Birnbaum is one of the chief scientists conducting the EPA's formal reassessment of the toxicity of dioxin (see RHWN #269, #270, #275). As we reported earlier (RHWN #279), many scientists, including Birnbaum, now consider dioxin an "environmental hormone." The new Wisconsin studies support that view.

The Wisconsin researchers, led by Dr. Richard E. Peterson, showed that dioxin interferes with the sexual development of male rats exposed to dioxin before, and shortly after, birth. Pregnant female rats were given a single oral dose of dioxin on the 15th day of pregnancy; their male offspring showed reduced levels of male hormones in their blood and a variety of sexual aberrations that stayed with them as they matured. The young males are demasculinized and feminized by doses of dioxin too low to cause any measurable toxicity in the mother rat. The sexual changes in the young males are both physiological and behavioral, and last into adulthood.

Dioxin passes through the placenta and enters the fetus, so the rat fetuses received part of the mother's dose almost immediately. After birth, the baby rats continued to receive a small dose of dioxin through their mother's milk. Peterson says the baby rats received the bulk of their dose through milk. In rats and humans both, females rid their bodies of dioxin chiefly by excreting it in their milk. Dioxin is soluble in fats and oils, and milk is high in fat.

Dioxin is the common name for a family of 75 toxins, the most potent of which is TCDD [2,3,7,8-tetrachlorodibenzo-P-dioxin]. The Wisconsin researchers used TCDD in their experiments.

Dioxin is not made intentionally for any industrial purpose, but is produced as a byproduct of the combustion of chlorine-containing wastes, the bleaching of paper, and the manufacture of some pesticides. The burning of municipal solid waste, and of many hazardous wastes, releases dioxin into the environment, as does paper manufacture. Government officials responsible for the quality of the environment in the Great Lakes have called for a phase-out of chlorine, to reduce dioxin levels in wildlife and humans around the Lakes. (See RHWN #284.)

In the Wisconsin experiments, young males whose mothers were given as little as 0.064 micrograms of dioxin per kilogram of body weight showed consistently reduced levels of male hormones, plus a variety of physical and behavioral changes, including:

--reduced testosterone levels and probably a reduced response to testosterone. Testosterone is a powerful hormone controlling various aspects of sexual development in males. 

--smaller accessory sex organs, including smaller testicles; 

--slower sexual maturation; 

--distinctly feminine-style regulation of one hormone related to testosterone production; 

--greater willingness to assume a receptive-female posture when approached by a sexually stimulated male.

These effects "strongly suggest, though do not conclusively prove, that TCDD impairs sexual differentiation in the CNS [central nervous system]," according to Peterson and co-workers. They go on to say that, "The present study provides the first evidence that TCDD impairs sexual differentiation of the CNS." Sexual differentiation--the full development of a female instead of a male, or vice versa--is affected by hormones circulating in the blood before and after birth.

Furthermore, these studies "strongly suggest" that "the demasculinization and feminization caused by IN UTERO and lactational TCDD exposure are irreversible," the Wisconsin researchers say. IN UTERO means "in the womb" and lactational means "from milk."

Other effects revealed by these studies include:

--Even the lowest dose tested (0.064 micrograms of dioxin per kilogram of the mother's body weight), yielded consistent reductions in a male offspring's daily sperm production. 

--The developing male reproductive system is more sensitive to the effects of this hormone-like toxicant [dioxin] that any other organ or organ-system studied. 

--the unborn or newborn is about 100 times more sensitive to dioxin than the sexually mature animal.

What do these studies mean for humans?

The Wisconsin researchers speculate, "Thus the findings from this study raise the possibility that TCDD could potentially affect sexually dimorphic behavior in man if exposure were to occur during fetal development." "Sexually dimorphic behavior" refers to the bodily and behavioral differences between men and women.

Peterson and co-workers point out that male rats typically inseminate a female rat with up to 10 times as many sperm as are typically needed to ensure impregnation. Humans, by contrast, typically release only about as many sperm as would be required for fertilization. "As a result," Peterson and his co-workers write, human reductions in sperm production "similar in magnitude to that in rats would be expected to reduce fertility in man." In other words, rats can continue to reproduce despite a reduction in sperm count because they produce an excess of sperm, but humans do not produce excess sperm so a reduction in human sperm count would likely reduce humans' ability to reproduce.[5]

"The real question is how general these effects are," Birnbaum says. Her EPA lab will repeat the Peterson studies with another strain of rats and eventually other species. And if these effects occur in another species? "I would get very concerned [about the potential human-health implications]," Birnbaum told SCIENCE 

NEWS reporter Janet Raloff.

At a public hearing on EPA's dioxin reassessment at EPA headquarters in Washington April 28, a representative of the American Paper Institute argued that only the study of humans can reveal anything meaningful about humans. Birnbaum responded somewhat testily, spelling out a dozen ways in which studies of rats and mice reveal useful information about dioxin's potential effects on humans.

June 10 at a Congressional hearing on dioxin in Washington, Assistant U.S. Surgeon General Barry L. Johnson, announced that a new study by the National Institute for Occupational Safety and Health (NIOSH) has found that workers exposed to high levels of dioxin have abnormally low levels of testosterone (male hormone) in their blood streams.[6] This finding is consistent with the rat studies of Peterson and co-workers. We have learned that this new NIOSH study was presented at a scientific meeting on June 10, but 

NIOSH sources have so far not released details of the new study to the general public.

At the Congressional hearing June 10, under questioning from Representative Ted Weiss (D-NY), Barry Johnson said that if it were faced with the Times Beach, Missouri, situation today, the U.S. Public Health Service would do exactly what it did 10 years ago, which is to evacuate people from their homes. He said the Times Beach evacuation was the appropriate response and would be repeated under similar circumstances today. Another official of U.S. Public Health Service, Vernon L. Houk, made headlines 14 months ago saying if he had the decision to make over again, he would not evacuate people from Times Beach. Times Beach is a town near St. Louis where an unscrupulous waste hauler spread dioxin-contaminated oil around as a dust suppressant in the 1970s. Horses and other animals became sick and died, and the Public Health Service evacuated the town in the early 1980s.

During the Congressional hearing Dr. Houk's views were further contradicted by the testimony of Dr. Marilyn Fingerhut of NIOSH, who studied the health of 5172 workers exposed to dioxin on the job. (See RHWN #219.) Dr. Houk made headlines a year ago when he said that, if dioxin causes cancer in humans at all, it is only "a weak carcinogen." (See RHWN #249.) Dr. Fingerhut contradicted this view, reporting that, among workers who had been exposed to dioxin for at least a year at least 20 years ago, there was 46% more cancer than among average U.S. males. During the hearing, Representative Weiss characterized Dr. Houk's views on dioxin as "quirky" and "cockamamie."

--Peter Montague, Ph.D.

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

[1] Thomas A. Mably and others, "IN UTERO and Lactational Exposure of Male Rats to 2,3,7,8-Tetrachlorodibenzo-P-dioxin. 1. Effects on Androgenic Status." TOXICOLOGY AND APPLIED PHARMACOLOGY Vol. 114 (May, 1992), pgs. 97-107.

[2] Thomas A. Mably and others, "IN UTERO and Lactational Exposure of Male Rats to 2,3,7,8-Tetrachlorodibenzo-P-dioxin. 2. Effects on Sexual Behavior and the Regulation of Luteinizing Hormone Secretion in Adulthood." TOXICOLOGY AND APPLIED PHARMACOLOGY Vol. 114 (May, 1992), pgs. 108-117.

[3] Thomas A. Mably and others, "IN UTERO and Lactational Exposure of Male Rats to 2,3,7,8-Tetrachlorodibenzo-P-dioxin. 3. Effects on Spermatogenesis and Reproductive Capability." TOXICOLOGY AND APPLIED PHARMACOLOGY Vol. 114 (May, 1992), pgs. [118-126.]118-126.

[4] J. Raloff, "Perinatal dioxin feminizes male rats," SCIENCE NEWS Vol. 141 (May 30, 1992), pg. 359.

[5] In unrelated studies, Congress's Office of Technology Assessment (OTA) reported several years ago that Americans in their prime reproductive years (ages 20 to 24) have experienced an increase in infertility in recent years. See "Reproductive Dysfunction in the Population," in U.S. Congress, Office of Technology Assessment, REPRODUCTIVE HEALTH HAZARDS IN THE WORKPLACE [OTA-BA-266] (Washington, DC: U.S. Government Printing Office, 1985), pgs. 341-364. At the time of this 1985 OTA report, low doses of dioxin were not known to interfere with reproductive systems of rats or humans.

[6] Barry L. Johnson, "Testimony... Before the Subcommittee on Human Resources and Intergovernmental Relations, Committee on Government Operations, House of Representatives, June 10, [1992,"] pg. 8. Johnson is Assistant U.S. Surgeon General with the U.S. Public Health Service.

Descriptor terms: dioxin; sexual development; linda s. birnbaum; epa; environmental hormone; richard e. peterson; mother's milk; tcdd; wisconsin; male hormones; sexual differentiation; sperm count; niosh;