********************************************************** The following document, titled "DIOXIN REASSESSED: A GENERAL OVERVIEW" was prepared for COPA by Environmental Compliance Organization (ECO), COPA's technical assistance grant (TAG) contractor. Paper copies are available upon request, or you may download this file from the "main" file library on this bulletin board. *********************************************************** DIOXIN REASSESSED: A GENERAL OVERVIEW OUTLINE I. Introduction II. What is Dioxin? III. Health Risks Posed by Dioxin and Dioxin-like Chemicals IV. Views of Some Scientists in the Public Interest Community V. Media Reports on the Dioxin Issue VI. Recommendations for Community Awareness This document is printed on recycled paper utilizing non-toxic vegetable based inks. ********************************************************* I. Introduction This overview is designed to provide current information from health experts, scientific literature, and government reports regarding the likely human health impacts from exposure to dioxin and dioxin-like chemicals. Dioxin and/or dioxin-like chemicals are likely to exist in areas contaminated by pesticides and pesticide by-products. Moreover, additional dioxin may be created by the use of cleanup technologies employing burning or excessive heat to destroy or free chemical contaminants from soils and other contaminated materials. The information below is presented in summary form to give the reader a general overview of the impacts of dioxin. II. What is Dioxin? In 1989 the U.S. Agency for Toxic Substances and Disease Registry(ATSDR) described dioxin as follows: The chlorinated dibenzo-p-dioxins are a class of compounds that are loosely referred to as dioxins. There are 73 possible dioxins. The one with four chlorine atoms at positions 2, 3, 7, and 8 of the dibenzo-p-dioxin chemical structure is called 2,3,7,8-tetrachlorinated dibenzo-p-dioxin (2,3,7,8-TCDD). It is a colorless solid with no known odor ... It can be inadvertently produced in very small amounts as an impurity during the manufacture of certain herbicides and germicides and has been detected in products of incineration of municipal and industrial wastes. The ATSDR toxicological profile also described some of the potential sources of dioxin. The main environmental sources of 2,3,7,8- TCDD are: * Use of herbicides containing 2,4,5- trichlorophenoxy acids (2,4,3-T) * Production and use of 2,4,5- trichlorophenol in wood preservatives * Production and use of hexachlorophene as a germicide * Improper disposal of certain chlorinated chemical wastes Although 2,4,5-T, 2,4,S-trichlorophenol, and hexachlorophene are no longer produced commercially ... disposal sites of past production wastes are still sources of present exposure. 2,3,7,8-TCDD has been found in at least 28 of 1,177 hazardous waste sites on the [[Superfund] National Priorities List (NPL).1 (1) Of the members of the dioxin family referred to by ATSDR, 2,3,7,8- TCDD is viewed as the most potent. In September 1994, in its most recent reassessment effort, the U.S. Environmental Protection Agency (EPA) described dioxin in a similar manner. Chlorinated dibenzo-p-dioxins and related compounds (commonly known simply as dioxins) are contaminants present in a variety of environmental media. This class of compounds has caused great concern in the general public as well as intense interest in the scientific community. Much of the public concern revolves around the characterization of these compounds as among the most potent man-made" toxicants ever studied. 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. (2) Beyond the 73 member dioxin family referred to by ATSDR there are dioxin-like chemicals. These chemicals have structures similar to dioxin and may pose comparable health concerns. There are literally thousands of chemicals that have a dioxin-like chemical structure. In general, the differences may be that they are chlorinated, brominated, or a combination of chlorinated and brominated. EPA described the family of dioxin-like chemicals as follows. There are 73 individual compounds comprising the CDDs, depending on the positioning of the chlorine(s), and 133 different CDFs. These are called individual congeners. Likewise, there are 73 different positional congeners of BDDs and 133 different congeners of BDFs ... There are 209 PCB congeners ... Mixed chlorinated and brominated congeners also exist increasing the number of compounds considered dioxin-like. (3) Thus, particularly where dioxin is present, the presence of dioxin-like chemicals must also be considered. III. Health Risks Posed by Dioxin and Dioxin-Like Chemicals A. EPA's 1994 Reassessment EPA has been involved in The assessment of dioxin and dioxin-like chemicals for more than five years. The effort to assess the health effects of dioxin has been coupled with an analysis of how best to estimate the exposures (e.g. sources of exposure, routes of ingestion into the body, expected health effects, etc.) to dioxin-like chemicals.(4) EPA described the history of the dioxin assessment work as follows: In 1983 and 1988; the Agency prepared assessments of the human health risks from environmental exposures to dioxin. Also, in 1988, a draft exposure document was prepared that presented procedures for conducting site-specific exposure assessments to dioxin-like compounds. These assessments were reviewed by the Agency's Science Advisory Board (SAB). At the time of the 1988 assessments, there was general agreement within the scientific community that there could be a substantial improvement over the consensus as to a more biologically defensible methodology. The Agency was asked to explore the development of such a method. The Agency's [[September 19941 reassessment activities are in response to this request. (5) EPA's description of the dioxin reassessment effort is rather bland. In the view of many in the environmental community, dioxin health risk issues were "reassessed" at the insistence of industry. Fortunately, a number of impartial scientists have been involved in the EPA's reassessment effort, making the analysis at least somewhat beneficial. Over the last few months EPA took comments on the 1994 reassessment documents and hopes to finalize them within about one year. What follows are important excerpts from EPA's current draft reassessment volumes. This summary is designed to give the reader a significant sampling of EPA's analysis regarding dioxin. 1. Effects on the Immune System Extensive evidence has accumulated over the past 20 years to demonstrate that the immune system is a target for toxicity of... TCDD ... and structurally related halogenated aromatic hydrocarbons (HAHs), including the polychlorinated dibenzofurans(PCDFs), polychlorinated biphenyls (PCBs), and polybrominated biphenyls (PBBs). This evidence was derived from numerous studies in various animal species, primarily rodents, but also guinea pigs, rabbits, monkeys, marmosets, and cattle. Epidemiological studies also provide evidence for the immunotoxicity of HAHs in humans. EPA 1994 at 4-1. 2. Reproductive Effects The potential for dioxins and related compounds to cause reproductive and developmental toxicity has been recognized for many years. Recent laboratory studies have broadened our [EPA's] knowledge in this area and suggest that altered development may be among the most sensitive TCDD endpoints.(6) EPA 1994 at 5-1. 3. Cancer Effects There have been several long-term studies designed to determine if TCDD is a carcinogen in experimental animals. All of these studies have been positive and demonstrate that TCDD is a multi-site carcinogen, is a carcinogen in both sexes and in several species including the Syrian hamster, is a carcinogen in sites remote from the site of treatment, and increases cancer incidence at doses well below the MTD. EPA 1994 at 638. The mechanistic basis for inter-individual variation is unclear, and this lack of knowledge complicates approaches to estimate human risks from experimental animal data. However, several studies indicate that, for the most part, humans appear to respond like experimental animals for biochemical and carcinogenic effects. EPA 1994 at 6-39 - 6-40. ...although there are uncertainties associated with the epidemiological evidence that could have influenced risk estimates, the overall weight of the evidence from the epidemiologic studies suggests that the generally increased risk of cancer is more than likely due to exposure to TCDD. The consistency of this finding in the four major cohort studies is corroborated by animal studies that show TCDD to be a multi-site, multisex, and multispecies carcinogen. EPA 1994 at 7J7. 4. Other Effects TCDD alters a number of other pathways involved in the regulation of cell differentiation and proliferation. The specific relationships of these effects to multistage carcinogenesis are not known, but the broad array of effects on hormone systems, growth factor pathways, cytokines, and signal transduction components is consistent with the notion that TCDD is a powerful growth dysregulator. EPA 1994 at 6-38. Human exposure to ... TCDD ... has been associated with non-cancer effects in most systems. The majority of effects have been reported among occupationally exposed groups, such as chemical production workers, pesticide users, and individuals who handled or were exposed to materials treated with ... TCDD-contaminated pesticides, and among residents of communities contaminated with tainted waste oil (Missouri, USA) -and industrial effluent (Seveso, Italy). EPA 1994 at 7-87. 5. Overall Conclusions EPA's September 1994 reassessment draft makes the following overall conclusions regarding the impact of dioxin and related chemicals on human health. a. Exposure sources and background levels The principal identified sources of environmental release of CDDs and CDFs may be grouped into four major types: combustion and incineration sources; chemical manufacturing processing sources; industrial/ municipal processes; and reservoir sources EPA 1994 at 9-73 - 9-76. Exposure levels to ... TCDD in industrialized nations are estimated to be about 0.3-0.6 pg [[picograms] TCDD/ kg body weight/ day. EPA 1994 at 9-77. Estimates of exposure to dioxin-like CDDs and CDFs based on dietary intake are in the range of 1-3 pg TEQ/kg body weight/ day. Estimates based on the contribution of dioxin-like PCBs to toxicity equivalents raise the total to 3-6 pg TEQ/kg body weight/day. This range is used throughout this characterization [[EPA reassessment] as an estimate-of average background exposure to dioxin-like CDbs, CDFs, and PCBs. This average background exposure leads to body burdens in the human population that average 40-60 pg TEQ/ g lipid (40-60 ppt [[parts per trillion]) when all dioxins, furans, and PCBs are included. High-end estimates of body burden of individuals in the general population (approximately the top 10% of the general population) may be greater than three times higher. EPA 1994 at 9-77 - 9-78. With regard to average intake, humans are currently exposed to background levels on dioxin-like compounds on the order of 3-6 pg-TEQ/kg body weight/day, including dioxin like PCBs. This is more than 500 fold higher than EPA's 1983 risk-specific dose associated with a plausible upper bound, ... and several hundred fold higher than revised risk specific dose estimates ... Plausible upper-bound risk estimates for general population exposures to dioxin and related compounds, therefore, may be as high as ... one in ten thousand to one in a thousand ... EPA 1994 at 9-86. b. Toxicity and non-cancer effects TCDD is the most potent form of a broad family of xenobiotics that bind to an intracellular protein known as the Ah receptor. Other members of this family include halogenated hydrocarbon such as the PCBs, naphthalenes, and dibenzofurans, as well as nonhalogenated species such as 3-methyleholanthrene and B-naphthaflavone. The biological properties of dioxins have been investigated extensively in over 3,000 publications and abstracts since the identification of TCDD as a chloracnegen ... [[in 1957]. EPA 1994 at 8-1. From the complex picture that evolves from the ... data, it is amply evident that TCDD elicits a plethora of toxic responses, both after short term and long term exposure. EPA 1994 at 3-34 ...based on the results of two or more studies, recent evidence suggests that chloracne, elevated GGT (7) levels, an increased risk of diabetes, and altered reproductive hormone levels (luteinizing hormone, follicle-stimulating hormone, and testosterone) appear to be long term consequences of exposure to ... TCDD ... EPA 1994 at 7-238. Based on all of the data reviewed in this reassessment and scientific inference, a picture emerges of TCDD and related compounds as potent toxicants in animals with the potential to produce a spectrum of effects. Some of these effects may be occurring in humans at very low levels and some may be resulting in adverse impacts on human health. [[emphasis in original] EPA 1994 at 9-87. c. Cancer effects With regard to carcinogenicity, a weight of the evidence evaluation suggests that dioxin and related compounds (CDDs, CDFs, and dioxin-like PCBs) are likely to present a cancer hazard to humans. [emphasis in original] EPA 1994 at 9-83. V. VIEWS OF SOME SCIENTISTS IN THE PUBLIC INTEREST COMMUNITY Several scientists in the fields of public health, toxicology, chemistry, and risk assessment have provided somewhat stronger or more direct comments on the impacts and concerns related to human exposure to dioxin-like chemicals. For example, public health expert Dr. Richard Clapp has testified that there is no safe level of exposure to dioxin.(8) Dr. Clapp added that in his opinion there was ample evidence to establish that dioxin causes cancer in humans.(9) Dr. Peter Kahn (10) has noted that dioxin causes immunosuppressive and reproductive effects.(11) Recently, Dr. Kahn wrote a paper with other scientists examining the potential long term impacts of TCDD on children born to mothers who lived in a dioxin-contaminated environment. The conclusion of the paper was stated as follows: The results appear to demonstrate that immune deficiencies caused by in utero and post-natal exposure to TCDD may persist for 10 years or more.(12) In a second and related study similar conclusions were reached regarding other long-term effects of dioxin exposure. The TCDD exposed children exhibited neurophysiological dysfunction principally in the bilateral frontal lobe regions relative to unexposed children, with females exhibiting more dysfunction than males.(13) The work of Dr. Kahn and others is important to consider when evaluating current and future exposures to dioxin-like chemicals. Dr. Peter Montague has been a frequent analyst and chronicler of the impacts of dioxin and dioxin-like chemicals.(14) Dr. Montague has noted that there is a growing body of disturbing research indicating that dioxin- like chemicals (e.g. dioxins, furans, PCBs, pesticides) may be seriously impacting male reproductive systems. What follows are condensed reports taken from Rachel's Environment & Health Weekly. * Research during the past decade has shown that there are two basic ways that chemicals can affect male reproduction [[footnotes omitted]. Chemicals can directly affect the testes, where sperm originates. The number of sperm can be diminished, or some sperm can be damaged, or sperm may eventually carry toxins directly to the egg. Alternatively, toxins can attack The male nervous system, or endocrine system, affecting the flow of hormones that act as messengers regulating the complex chemical processes that must all work well for conception to occur. No matter what the mechanism of damage may be, there is a growing body of evidence showing that male exposures to toxins can produce defective children. (15) [emphases added] A recent study in the British Medical Journal concludes that men in western countries today have sperm counts less than half as high as their grandfathers had at the same age [[footnote omitted]. In addition, the occurrence of cancer in the testicles has increased 3-fold to 4-fold during the past 40 years; and various birth defects of the male reproductive system have increased 2-fold to 4-fold during the same period, including undescended testicles (a condition called cryptorchidism) and a birth defect called hypospadias in which the male urinary canal is open for a variable distance on the underside of the penis. * An article in ...The Lancet... asks whether these phenomena can all be traced to the same cause, namely exposure of males very early in life to female sex hormones (estrogens) or to environmental chemicals that act like estrogens [[footnote omitted]. These findings and hypotheses add to the growing body- of medical knowledge indicating that many chemicals -- especially chlorinated hydrocarbons -- mimic hormones and interfere with the endocrine systems of fish, birds, wildlife and humans. Earlier studies have linked chlorinated hydrocarbons to female breast cancer ... and it is worth pointing out that breast cancer in women is associated with an increased likelihood of testicular cancer in their sons (footnote omitted). Thus breast cancer, testicular cancer, and defects of the male reproductive system, including diminished sperm count, all seem linked. (16) (emphasis added] Sharing the views and concerns of Dr. Montague is Dr. Barry Commoner. Dr. Commoner is considered by many to be one of the key scientific figures responsible for stimulating the environmental movement in the United States. Dr. Commoner is well versed in the disciplines of risk assessment, environmental science and public health. Regarding dioxin, Dr. Commoner extensively studied the environmental and human health impacts of the chemical for many years. He has carefully studied the dioxin contamination impacts of the industrial accident in Seveso, Italy. The Seveso incident is one of the most well known dioxin contamination incidents in the world. As an expert witness in the case challenging the operation of the Waste Technologies Industries (WTI) hazardous waste incinerator, Dr. Commoner testified that dioxin causes immune system defects and acts as a kind of environmental hormone. (17) He went on to testify that exposure to any level of dioxin will have an effect, noting further that if there is little or no benefit from an action that releases dioxin then public health principles dictate that the action should not be taken. (18) Most recently, as the keynote speaker at the Second Citizens' Dioxin Conference, Dr. Commoner provided a further warning to citizens and government regulators about the impacts of dioxin. The general spread of dioxin and dioxin-like chemicals in the U.S. environment has already exposed the entire population to levels of these extremely toxic substances that are expected to cause a number of serious health effects. These include an average risk of cancer of 100 or more per million in the entire U.S. population 100 times greater than the risk standard that has triggered EPA remedial action, for example at Times Beach in Missouri Superfund site].(19) In evaluating the results of EPA's current dioxin reassessment effort The Environmental Defense Fund (EDF) and Physicians for Social Responsibility(PSR), in part, reached the following conclusions: The only way to reduce contaminants of food is for the federal government to take comprehensive action to protect the food supply. This is the best way to safeguard the public at large, particularly young children and developing fetuses, who are the most sensitive to dioxin's effects. The proper response to EPA's report [[September 1994 dioxin reassessment] is to recognize that dioxin exposure is now a threat to public health. Many Americans arc ingesting levels of dioxin that could adversely affect their health. That's why we must reduce the sources of exposure to dioxin and to all of the related chemicals that have similar toxicities. For ourselves and for future generations, we must take preventative action by strictly controlling emissions and keeping these toxic chemicals out of the environment. (20) In reviewing an early draft of EPA's 1994 Dioxin Reassessment, Dr. Montague and his colleagues reached similar conclusions. ...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. ...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 ... 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. 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 ... Another way to estimate the size of the cancer hazard is to note that .... dioxin in food and air may be causing somewhere between 75,000 and 150,000 cancers each year. (21) How much dioxin is "safe"? EPA's answers: For cancer hazards? Three hundred to 600 times less than we all now intake every day ... For non-cancer hazards? Ten to 100 times less than we all now take in every day .(22) V. MEDIA REPORTS ON THE DIOXIN ISSUE The media, particularly non-mainstream press and technical publications, have not missed the dioxin issue and its effects on a variety of industries. however, aside form the occasional local news coverage abut a particular site or facility, the television and radio networks seem to have missed the story almost entirely. The general public knows little of the scientific and political controversies surrounding dioxin. a small sample of some print media stories gives an anecdotal account of dioxin coverage. In 1991, chemistry & Industry magazine reported on the interests of certain industries in the "reassessment" of dioxin. ...scientists are challenging the very basis of EPA's approach to risk assessment for dioxin. The Chloralkli industry, which has come under pressure as environmentalists target paper bleaching as a source of dioxin, has taken an active interest in the course of the scientific debate. Concern about the environmental blacklisting of its products has been serious enough to prompt a "public outreach program" coordinated by the Chlorine Institute. (23) The political controversy surrounding the assessment of dioxin was well described in an article in the Multinational Monitor. In the face of mounting public concern over toxic chemical pollution, several industries and their allies in government have launched a full scale campaign to reverse the long-held belief that dioxin is the most toxic chemical known to science. If the government, the courts and the public accept what many scientists believe the evidence [[about the effects of dioxin] has already demonstrated ... the chlorine, waste incineration and pulp and paper industries stand to lose billions of dollars through lawsuits and lost contracts. (24) Other stories have also published the bad news about dioxin-like chemicals (like PCBs) and some pesticides and their effects on reproductive systems. These articles stress the concern about impacts on fertility and breast cancer. (25) VI. RECOMMENDATIONS FOR COMMUNITY AWARENESS As noted in previous comments to EPA, thorough testing of dioxin and dioxin-like chemicals in water and soil in and around the Bloomington sites is imperative. PCBs which has been subjected to incomplete burning, as is the case here, frequently results in residues of dioxin and/or dioxin-like chemicals. The public health implications and environmental impacts from exposures to contaminated air, water, and soil from the Bloomington sites prior to remediation is possibly significant. This problem is exacerbated by the current dangerous levels of dioxins already contained in our bodies. Moreover, the community must be seriously concerned about the additional exposures that will occur during remediation. As noted in this review, ingestion of certain pesticides, dioxin, and/or dioxin-like chemicals in unimaginably small quantities can cause 1) birth defects by damaging male or female reproductive systems, 2) immune system dysfunction, 3) endocrine system damage, and 4) cancer. Pregnant women, women of childbearing age, children, persons with illnesses, and elderly persons are particularly susceptible to the impacts of these ultra-toxic chemicals. Given the history of activities at the site, medical monitoring of longtime residents of the area is needed. In addition, the community must insist on no further exposure to dioxin or related chemicals coming from the Bloomington sites either before, or during remediation. (26) For these crucial health and safety reasons, all interested and affected persons must monitor EPA's remedial process at these sites and voice their concerns accordingly. REFERENCES (1) ATSDR. 1989. Toxicological Profile for 2,3,7 8- Tetrachlorodibenzo-P-Dioxin. Report # ATSDR/TP-88/23. p. 1. (2) Health Assessment Document for 2,3,7,8-Tetrachlorodibenzo- p-Dioxin (TCDD) and Related Compounds, EPA/600/BP-92/001?, U.S. EPA, August 1994 at 9-1. Hereafter this document will be referred to as "EPA 1994." (3) EPA 1994 at 9-6 to 9-7. (4) The current dioxin health assessment and estimating dioxin exposures documents can be referenced through EPA as follows. Health assessment documents: Volume I (chapters I - 6) (EPA/600/BP-92/OOla); Volume II (chapters 7 and 8) (EPA/600/BP-92/OO1b); Volume III (chapter 9) (EPA/600/BP-92/OO1c). Estimating exposures documents: Volume I (EPA/600/6-88/OO5ca); Volume II (EPA/600/6-88/OO5Cb); Volume III (EPA/600/6-88/OO5cc). (5) Gerber: "Reassessment of 2,3,7, 8-Tetrachlorodibenzo-p- dioxin (2,3,7,8-TCDD, dioxin)", August 30, 1994, at 5. Note: this document was handed out when EPA released the latest draft Documents on September 13, 1994. (6) Two tables that describe the effects of dioxin on animals and humans are Volume I, page 3-35, and Volume II, page 7-239. (7) Gamma glutamyl transpeptidase. (8) Greenpeace V. Waste Technologies Indus., No. 4: 93CVOOS3 (N.D. Ohio), Testimony of Dr. Richard Clapp, February 8, 1993, at 26 - 27. (9) Greenpeace v. Waste Technologies Indus., No. 4: 93CV00S3 (N.D. Ohio), Testimony of Dr. Richard Clapp, February 8, 1993, at 36. (10) Dr. Kahn was qualified before the Maryland Office of Administrative Hearings as an expert in biochemistry, toxicology of dioxins and related compounds in humans, animals, and the environment. In the Matter of the Montgomery County Resource Recovery Facility, No. 9l- MDE-AMA-0l3-2301, March 28, 1992, at 141. (11) In the Matter of the Montgomery County Resource Recovery Facility, No. 91-MDE-AMA-0l3-2301, March 28, 1992, at 146. (12) See, Kahn, Rodgers, Suffin, Moconnachie: "In Utero Postnatal Exposure to 2,3,7,8-TODD in Times Beach, Missouri: I. Immunological Effects: Lymphocyte Phenotype Frequencies" at 1. (13) Cantor, Holder, Cantor, Kahn, Rodgers, Smoger, Swain, Berger, and Suffin: " In Utero and Postnatal Exposure to 2,3,7,8-TCDD in Times Beach, Missouri: 2. Impact on Neurophysiological Functioning" at 1. (14) Dr. Montague is editor of the publication Rachel's Environment & Health Weekly (formerly Rachel's Hazardous Waste News. The work of Dr. Montague and his capable colleagues is published by the Environmental Research Foundation. (15) Environmental Research Foundation, Rachel's Hazardous Waste News # 321: "Male Reproductive System is Harmed by Toxic Exposures, Causing Birth Defects, Sterility," January 20, 1993 (16) Environmental Research Foundation, Rachel's Hazardous Waste News # 343: "Are Environmental Chemicals Causing Men to Lose Their Fundamental Masculinity?," June 24,-l993. See also Environmental Research Foundation, Rachel's Hazardous Waste News # 372: "PCBs Diminish Penis Size," January 13, 1994. (17) Greenpeace v. Waste Technologies Indus., No. 4: 93CV0083 (N.D. Ohio), Testimony of Dr. Barry Commoner, February 16, 1993, at 669. (18) Greenpeace v. Waste Technologies Indus., No. 4: 93CV0083 (N.D. Ohio), Testimony of Dr. Barry Commoner, February 16, 1993, at 672. (19) Reported by the Environmental Research Foundation, Rachel's Environment & Health Weekly # 405: "Turning Point for the Chemical Industry," September 1, 1994. (20) "Putting" the Lid on Dioxins- Protecting Public Health and the Environment," A joint report by Physicians for Social Responsibility and the Environmental Defense Fund, at 2. (21) Environmental Research Foundation, Rachel's Hazardous Waste News # 390: "Dioxin Reassessed -- Part 1, " May 19, 1994. (22) Environmental Research Foundation, Rachel's Hazardous Waste News # 390: "Dioxin Reassessed -- Part 2, " May 26, 1994. (23) Chemistry & Industry: "Scientists challenge EPA standards", February 18, 1991 at 112. (24) Multinational Monitor: "Defenders of Dioxin- The corporate campaign to Rehabilitate Dioxin", October 1991, at 8. (25) See, Chemical & Engineering News: "Environmental Estrogens Linked to Reproductive Abnormalities, cancer", January 31, 1994, at 19 - 23; Newsweek: "The Estrogen complex", March 21,1994, at 76 - 77; The Nation: "A Toxic Link to Breast cancer", June 20, 1994, at 866 - 869. (26) Combustion and/or thermal processes (like thermal desorption or incineration) will create additional dioxins. EPA has noted that the formation of dioxin and dioxin-like chemicals can occur at temperatures in the range of 250 - 450 C (482 - 842 F). Thermal desorption units typically heat contaminated soil to temperatures ranging from 600 - 950 F. *******************************************************************