America's Choice
Children's Health or Corporate Profit
The American People's Dioxin Report
Technical Support Document
November 1999
 Center for Health, Environment and Justice
 Falls Church, VA

The Center For Health, Environment and Justice's Science Director, Stephen Lester, deserves special thanks and recognition for his tireless hours of collecting data and the most recent scientific reports on dioxin and human health which went into this report. He also coordinated and worked with the writers, researchers, and scientific peer review group.

Special thanks also goes to editor Patty Lovera, in recognition for hours of editing, researching and fact-checking this document. CHEJ also extends our thanks to Joe Mullins for the cover design, Barbara Sullivan for the layout, Ray Lambert for technical editing, and to Kathleen Schuler and Cecelia Deloach for their contributions. CHEJ's Charlotte Brody also deserves a special thanks for her role in the development of the American People's Dioxin Report.

We want to thank the following scientists who contributed to the writing of the Technical Support Document.

Dr. Richard Clapp, Boston University School of Public Health
Pat Costner, Greenpeace
Dr. Beverly Paigen, Jackson Laboratories
Dr. Arnold Schecter, University of Texas School of Public Health-Dallas
Dr. Ted Schettler, Physicians for Social Responsibility
Dr. Allen Silverstone, State University of New York Health Science Center
Tom Webster, Boston University School of Public Health

We also want to thank the scientists who reviewed the Technical Support Document and provided us with comments. This peer review group had no role in defining or reviewing the policy recommendations found in the American People's Dioxin Report. Their affiliations are included only for identification purposes.

Peer Reviewers:

Dr. Linda Birnbaum, US Environmental Protection Agency
Dr. Mark Cohen, National Oceanographic and Atmospheric Administration
Dr. Barry Commoner, Queens College
Dr. Lynn Goldman, John Hopkins University School of Public Health
Dr. Philip Landrigan, Mt. Sinai School of Medicine
Dr. George Lucier, National Institute for Environmental Health Sciences
Dr. David Ozonoff, Boston University School of Public Health
Dr. David Rall, retired, former Director, National Toxicology Program.
 
 
 

This Technical Support Document (TSD) is the third and final section of America's Choice: Children's Health or Corporate Profit - The American People's Dioxin Report. The first section is a summary of the newest scientific research on the health effects of dioxin, detailing how American families are being silently poisoned by dioxin. The second section of the report provides a set of policy recommendations developed by a diverse group of more than 50 people, including grassroots activists who live near dioxin-contaminated sites or dioxin-producing facilities, activists who work on policy development, and scientific researchers. These policy recommendations provide clear workable solutions to eliminating dioxin sources without devastating our economy. The first two sections of the report can be found together in a separate document.

This Technical Support Document provides the scientific basis and support for the conclusions and recommendations made in the report. This document describes where dioxin comes from, how it moves through the environment and gets into our food, how it builds up in our bodies, and how it is affects our health and our children. Particular emphasis is given to how dioxin affects the immune, reproductive, and developmental systems of the human body and how it causes cancer. This Technical Support Document provides the reader with a scientific discussion and analysis of the latest research on dioxin, including extensive references and an overall characterization of the risk of dioxin to public health.

The American People's Dioxin Report is intended to accomplish three goals:

• Provide up-to-date scientific information and research on the effects of dioxin on human health;

 
• Provide the American people with suggested protective policies which they can ask their elected officials to enact to prevent this life-threatening chemical from harming our families; and

• Engage the American people in a national debate, community by community, on the nature of government in our society--how people became powerless as the corporations became powerful--and why our government protects the right to pollute more than it protects the American people's health.

This new effort to eliminate dioxin exposures is part of CHEJ's Stop Dioxin Exposure Campaign, which began in 1995. This report builds upon the still valid scientific information found in Dying From Dioxin. Dying From Dioxin contains organizing ideas and non-technical explanations of dioxin and its impacts. The information in the book is still very useful for non-scientific audiences. To obtain a copy contact CHEJ's offices.

--- Lois Marie Gibbs
Executive Director
Center For Health, Environment and Justice
November, 1999
 
 
 
 

This Technical Support Document (TSD) to America's Choice: Children's Health or Corporate Profit - The American People's Dioxin Report discusses the latest scientific research on the toxic effects caused by or associated with exposure to dioxin. This document is intended to inform the public and their representatives in government so appropriate action can be taken to safeguard the health of the American people. It is clear that there is an extensive body of high quality scientific information describing the toxic effects of dioxin in people. This data indicates that dioxin is a potent chemical that produces a wide variety of toxic effects in animals and that some of these effects are occurring in people.

The TSD's overall conclusion is that the American people are at serious risk from their daily intake of dioxin in food. This exposure appears to be affecting the growth and development of children, notably the development of the immune, reproductive and nervous systems, in particular, cognitive and learning abilities. While exposure of the general population occurs through ingestion of many common foods, children exposed in utero during critical periods of development appear to be the most sensitive and vulnerable to the toxic effects of dioxin.

The newest studies on dioxin's effects on human health lead to the following conclusions:

• All American children are born with dioxin in their bodies. The greatest impact of this exposure appears to be to the growth and development of children. Disrupted sexual development, birth defects and damage to the immune system may result.

 
• Dioxin exposure has been associated with IQ deficits, increased prevalence of withdrawn/depressed behavior, adverse effects on attentional processes, and an increase in hyperactive behavior in children. These effects have been documented in 42-month old Dutch children whose exposure to dioxins and PCBs came primarily before birth. The children's mothers were exposed to "background" levels of dioxins and PCBs as a result of the daily ingestion of dioxin in food.

• Dioxin exposure has been associated with alterations in immune function including increased susceptibility to infections and changes in T-cell lymphocyte populations. These effects have been reported in 42-month old Dutch children exposed to dioxins and PCBs primarily before birth. Altered immune function, reported at birth, 3, and 18 months of age, persists to 42 months of age in these children. Reported immune effects included an increase in middle ear infections and chicken pox, and a decrease in allergic reactions.

 
• There is evidence of both developmental and reproductive effects in children exposed to dioxin. These effects include defects in permanent teeth, adverse effects on thyroid hormones, altered sex ratio (more females than males), and increased respiratory infections.

 
• Hormonal effects associated with dioxin exposures in humans include a decrease in testosterone in dioxin-exposed workers and a decrease in thyroid hormones following prenatal exposure to background levels of dioxin in infants.

• Dioxin interferes with the hormone insulin and alters glucose tolerance which leads to diabetes. New studies of soldiers exposed to Agent Orange and residents of Seveso, Italy add to the existing evidence from studies of workers that exposure to dioxin increases the risk of developing diabetes.

 
• The average daily intake of dioxin in food poses a substantial cancer risk to the general American population. The lifetime risk of getting cancer from exposure to dioxin is 1 in 10,000 for the general American population and 1 in 1,000 for highly exposed members of the population. These risks are 100 and 1,000 times higher, respectively, than the generally "acceptable" one-in-a-million cancer risk for carcinogens.

• Updates of ongoing studies of cancer rates in dioxin-exposed workers in the U.S. and Germany, and in residents of Seveso, Italy all indicate increasing cancer rates in the highest exposure groups. These studies provide strong support for the decision by the World Health Organization's International Agency for Research on Cancer (IARC) to define dioxin (TCDD) as a "known human carcinogen." This decision is further supported by evidence from animal studies and data on dioxin's mechanisms of action in the body.

• Nearly all Americans are exposed to dioxin through ingestion of common foods, especially meat and dairy products. Dairy cows and beef cattle absorb dioxin by eating dioxin contaminated feed crops. The crops become contaminated by airborne dioxins that settle onto soil and plants. Dioxins enter the air from thousands of sources including incinerators that burn medical, municipal, and hazardous waste, chemical processing facilities that use chlorine to make products such as pesticides and PVC plastic, and metal refining and smelting operations.

• The average daily intake of the American people is already well above two federal guidelines for "safe" exposure. The American average daily intake is more than 200 times higher than the Environmental Protection Agency's cancer risk guideline and over twice the Agency for Toxic Substances and Disease Registry's lowest adverse effect level.

• Some groups of people are at higher risk of exposure to dioxin. These groups include children, nursing infants, some workers, people who eat fish as a main staple of their diet, such as some indigenous peoples and fishermen, and people who live near dioxin release sites. These groups of people are likely exposed to at least 10 times as much dioxin as the general population.

 
• The average daily exposure of dioxin and dioxin-like chemicals in the U.S. is approximately 3-6 pg TEQ/kg body weight per day. Nursing infants ingest about 50 times this much each day.

• Dioxin accumulates in biological tissue. The average tissue or "body burden" level of Americans ranges from 36 to 58 ng TEQ/kg lipid (36-58 ppt). Approximately 10% of the population may have tissue levels as much as three times higher than this level.

• There is a small difference between the body burdens of dioxins that cause adverse non-cancer effects in animals and average levels in the general human population. Some people who have above average levels are already suffering from the adverse effects of exposure to dioxin.

• While TCDD is the most toxic form of dioxin, 90% of the total toxicity resulting from exposure to dioxins is due to dioxin-like compounds other than TCDD.

• There is an extensive body of high quality, published information on the toxicity of dioxin. This body of data indicates that dioxin is a potent toxin which produces a wide variety of adverse effects in animals and that some of these effects are likely already occurring in people.

We know that the daily intake of Americans is already too high, and exceeds two federal risk guidelines. We also know that some members of the general population are particularly sensitive and that others are exposed to dioxins at greater than the average daily levels. These are infants and children, people who live near contaminated sites, fishermen and indigenous people who rely on fish as a main staple of their diet, some workers, and others with high exposures. These groups have suffered a disproportionate share of dioxin exposure and many already suffer the adverse health effects caused by these exposures.

We agree with the World Health Organization who recommended that "every effort should be made to limit environmental releases of dioxin and related compounds to the extent feasible in order to reduce their presence in the food chains, thereby resulting in continued reductions in human body burdens..." (WHO, 1998). Americans have a choice: take action to protect public health by eliminating dioxin creation or continue to allow dioxin to be created and not burden industry with the short term transition costs of eliminating dioxin and related compounds.
 
 

Dioxin has been the subject of government study for more than twenty years. The history of its progress through the regulatory system is full of controversy, industry pressure, politics, and delays. This chapter outlines that history - from the time dioxin's toxicity was first discovered to the most recent delays in the United States Environmental Protection Agency's (EPA) release of a comprehensive assessment of dioxin's health effects.

Adverse health effects caused by exposure to dioxins were first reported in chemical workers at plants manufacturing chlorinated phenols in Michigan in the 1930s (Butler, 1937); in Nitro, West Virginia in the 1940s (Ashe, 1949; Suskind, 1984); and in western Germany in the 1950s (Goldman, 1972; Suskind, 1977). The most pronounced effect observed in these workers was chloracne, a severe skin disease. Effects on the liver, and the nervous, endocrine, cardiovascular, gastrointestinal, and immune systems were also reported (Moses, 1984). It was not until 1957 that a German chemist discovered that the compound responsible for these toxic effects was 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (Kimming, 1957).

One of the earliest findings of dioxin's toxicity in animals was that it caused birth defects in mice at very low levels (Courtney, 1971). This finding led to dioxin being characterized as "one of the most potent teratogenic environmental agents" (Pratt, 1984). The first evidence that dioxin causes cancer came from several animal studies completed in the late 1970's (Van Miller, 1977; Kociba, 1978). The most important of these, published in 1978 by a team of scientists from Dow Chemical Company, led by Richard Kociba, found liver cancer in rats exposed to very low levels of dioxin (Kociba, 1978). This study helped establish dioxin as one of the most potent animal carcinogens ever tested and, together with the finding of birth defects in mice, led to the general statement that dioxin is the "most toxic synthetic chemical known to man."

In 1982, the National Toxicology Program (NTP), a program of the U.S. Department of Health and Human Services, completed a major study of the carcinogenocity of dioxin and found cancer in both mice and rats exposed to levels of dioxin similar to those in the Kociba study (NTP, 1982, 1982a). In 1985, the EPA published a scientific review of the health effects of dioxin. This review served as the scientific basis for the dioxin risk assessments used for all EPA programs and established an "acceptable daily dose" for dioxin of 0.006 picograms per kilogram of body weight per day (pg/kg/day) (USEPA, 1985). At the time, this risk estimate was the lowest of any risk estimate defined by other state and federal agencies as well as by other countries. Industry protested that this estimate was too low (Webster, 1994).

By 1987, the EPA's National Dioxin Study had found dioxin in the effluent of paper mills across the country (USEPA, 1987), and the paper industry was pressuring the EPA to reconsider its risk estimate. Shortly afterwards, the agency set up an internal workgroup of EPA staff to reassess the 1985 document. Most of this reassessment dealt with the different models of how chemicals like dioxin might cause cancer. Since the EPA workgroup could not agree on the best model, they averaged the acceptable risk values predicted by the various models and obtained a new risk value that was 16 times higher than EPA's original estimate. The EPA's Science Advisory Board (SAB), a group of non-government scientists, chastised the EPA workgroup for its unusual approach. Several of the models used to calculate the average risk value contradicted each other, and it did not make sense to average them to find one value. Since the SAB found no scientific basis for revising EPA's original 1985 risk value for dioxin, it was not changed (Commoner, 1994).

In October, 1990, the EPA and the Chlorine Institute, which represents companies that use or manufacture chlorine, co-sponsored a scientific meeting at the Banbury Center on Long Island, New York (Roberts, 1991). The purpose of the meeting was to review the latest data related to how dioxin might cause cancer. Most of the meeting focused on the role the "Ah" receptor (see Chapter Five) plays in mediating dioxin's toxic effects. The participants generally agreed that most, if not all, of dioxin's effects were mediated by binding to the Ah receptor. A few industry participants felt that the effects of a chemical operating through a receptor must have threshold, a dose below which there would be no effect (Commoner, 1994).

In April 1991, EPA Administrator William Reilly announced that the EPA would undertake a second reassessment of dioxin. He was responding to internal pressure from staff scientists who attended the Banbury meeting and felt that the 1985 report needed to be updated. The Chlorine Institute also pressured the agency to reassess the health effects of dioxin because they felt that the findings from the Banbury meeting meant that dioxin was much less toxic than previously thought.

According to Reilly, the primary focus of the second reassessment was the idea of a threshold, or "safe" level of dioxin exposure, a concept advanced by industry (Roberts, 1991). News of the reassessment, including the notion that dioxin was much less toxic than previously thought, was widely reported in the lay press (Gorman, 1991; Schneider, 1991).

Barely five months into the EPA's second reassessment, new research by George Lucier and Chris Portier of the National Institute for Environmental Health Sciences suggested that there was no threshold for some of dioxin's effects (Roberts, 1991a). These findings, presented at the Eleventh International Symposium on Chlorinated Dioxins and Related Compounds in September 1991, seriously weakened the threshold theory. In addition, new research presented at this meeting suggested that dioxin acted like a hormone, disrupting many systems of the body.

Much of the research that came out of the 1991 Symposium on Dioxin supported the findings of EPA's 1995 health assessment on dioxin. It also provided the basis for EPA's third assessment of dioxin, which was released by the agency as a "public review draft" in September 1994 (USEPA, 1994). In this report, the EPA incorporated all of the latest scientific evidence on the health effects, methods of exposure, and fate after entry into the body of all dioxin and dioxin-like chemicals. The report also emphasized that: dioxin can cause health problems other than, and possibly more injurious than, cancer; dioxin accumulates in biological tissues; the average level of dioxin in Americans' bodies is at or just below levels that cause some adverse health effects; and humans are exposed to dioxin primarily by eating a wide variety of common foods which contain small amounts of dioxin (USEPA, 1994a).

In 1995, the EPA's SAB endorsed all of the exposure document and most of the chapters of the health assessment document. The SAB made it clear that the scientific basis of the draft report was sound. It made only minor comments on the exposure document and suggested some changes in Chapter 8, Dose-Response Modeling, and Chapter 9, Risk Characterization, of the health assessment document (USEPA, 1995). After the SAB's review in 1995, the EPA announced that it would release the final health and exposure documents in the fall of 1995. This was the first of numerous missed deadlines and broken promises by EPA about the release of the final assessment document. In March 1997, the agency did submit a revised draft of Chapter 8 to a peer review committee, and the draft was approved with minor revisions (USEPA, 1997). However, the final version of Chapter 8 has still not been released to the public. Similarly, in April 1998, the EPA released an "external review draft" of the dioxin sources inventory, which updated the 1994 draft exposure document (USEPA, 1998). Though this document was also peer reviewed (ERG, 1998), the final version has not been released to the public. As of the fall of 1999, four years after the date given to the SAB for the release of the reassessment, there is still no final version of EPA's reassessment of the health effects of dioxin.

Although the EPA has failed to finalize its 1994 reassessment of dioxin, it has made new rules for dioxin-producing industries such as municipal waste incinerators (GPO, 1995), medical incinerators (GPO, 1997), and pulp and paper mills (GPO, 1998). These new rules, however, are all technology based, and not health-risk based.

In the past 20 years, a great deal of information, based on sound scientific research, has been discovered about dioxin's health effects on humans. Much of this work was summarized very well by the EPA in their draft reassessment document (USEPA, 1994). Since that time, however, there have been many delays which have prevented EPA from finalizing their assessment and providing decision-makers at all levels of government with the scientific basis and understanding needed to make decisions to protect the American people from exposures to dioxin. Without this information, exposures to dioxin that could be avoided, reduced, or eliminated will continue. This report is intended to make the latest information on dioxin available so that an informed public and their representatives in government can take action to safeguard the health of the American people.
 
 

Chemistry
 

Dioxins, furans, and polychlorinated biphenyls (PCBs) are a family of chemicals with related properties and toxicity. Dioxin and dioxin-like chemicals are composed of two benzene rings hooked together in one of three different ways (Figure 2-1). If they are hooked together by a six-member ring containing two oxygens, they belong to the family of dibenzo-p-dioxins. If they are hooked together by a five-member ring containing one oxygen, they belong to the family of dibenzofurans. If they are hooked together directly, they are called biphenyls. The dioxins and furans have three rings in their structure, but the biphenyls have only two.
 

Figure 2-1: Diagrams of Dioxin, Furan, and Biphenyl
 
 

Each of the hydrogen atoms in the benzene rings can be chemically replaced by chlorine atoms. To keep track of where the chorines are, the molecules are numbered as shown in Figure 2-1, and the name of the molecule gives both the number of chlorines (by the prefix tetra, penta, hexa, etc.) and the location of the chlorines. For example, 2,3,7,8-tetrachlorodibenzodioxin has 4 chlorines at positions 2, 3, 7 and 8. Table 2-1 shows the number of possible molecules that can be formed, depending on the number and arrangement of chlorines. For example, two chlorines can arrange on the dioxin molecule in 10 different ways, so there are ten different dichloro-p-dioxins. All together, there are 75 different dioxins, or polychlorinated dibenzodioxins (PCDDs), 135 different furans, or polychlorinated dibenzofurans (PCDFs), and 209 different polychlorinated biphenyls (PCBs). Bromine, an element closely related to chlorine, can also replace the hydrogens and form similar compounds. Chloro- and bromo- congeners can exist together. Both chlorinated and brominated chemicals are toxic, but the chlorinated ones are more common. Very little is known about the brominated congeners.

Not all of these chemicals have dioxin-like toxicity, and the toxic ones are not equally toxic. Only 7 of the 75 dioxins, 10 of the 135 furans, and 12 of the 209 PCBs have dioxin-like toxicity. These 29 different dioxins, furans, and PCBs all exhibit similar toxic effects caused by a common mechanism: binding to a complex molecule known as the aryl hydrocarbon or "Ah" receptor (see Chapter Five). It is believed that the tighter the binding to the Ah receptor, the more toxic the chemical. The most potent member of this family is 2,3,7,8-tetrachlorodibenzo-p-dioxin or TCDD, which also has the greatest affinity for the Ah receptor. One key factor in toxicity is the number of chlorines in the molecule: those with three or fewer chlorines lack dioxin-like toxicity. Another key factor is where the chlorines are attached. In dioxins and furans, it is critical that chlorines be at the 2, 3, 7, and 8 positions. In PCBs, it is critical that the corresponding positions, which are 3, 3', 4, and 4', have chlorines. The chlorine number and position probably affects the toxicity of the molecules by changing their shapes, which in turn determines binding to the Ah receptor. For simplicity, the terms "dioxin" and "dioxins" are used in this report to refer to any of the dioxin family members that act as Ah receptor ligands and elicit dioxin like effects.
 

Toxic Equivalents (TEQs)

Because this family of related chemicals contains so many different members, assessing the risk
of an environmental sample contaminated with them is difficult. Initially, a contaminated
sample's risk was measured according to the concentration of 2,3,7,8-TCDD, the most toxic of the chemical family members, present in the mixture. However, laboratory tests showed that this approach greatly underestimated the toxicity of the sample. The current approach uses Toxic Equivalency Factors or TEFs to estimate Toxic Equivalents, or TEQs. This approach was first used in the late 1970s (Eadon, 1986) when a transformer fire contaminated an office building with dioxins, furans and PCBs, and it was critical to determine when the building was safe for reoccupation. In this approach, each form of dioxin or dioxin-like chemical is assigned a toxicity factor, which is then multiplied by its concentration in a complex mixture to obtain its TEQ. The TEQs of each chemical are summed to give a total TEQ for the sample. The most toxic form of dioxin, 2,3,7,8-TCDD, is assigned a toxic equivalency factor (TEF) of 1. Each of the 17 toxic dioxins/furans and 12 PCBs is then assigned a "toxicity factor" that estimates its toxicity relative to TCDD. For example, a dioxin or dioxin-like substance that is half as toxic as TCDD is assigned a toxic equivalency factor of 0.5 and so on down to 0.00001. The toxicity factor for each dioxin and furan is shown in Table 2-1, and for PCBs in Table 2-2.
 
 

The use of TEQ to estimate the toxicity of a complex mixture of dioxins is based on several assumptions (Van den Berg, 1998). The first assumption is that chemicals with dioxin-like toxicity share a common mechanism of toxicity that begins by binding to the Ah receptor. Only those dioxins, furans and PCBs that bind to the Ah receptor are considered to have dioxin-like activity. Some non dioxin-like PCBs can produce toxic effects that act by another mechanism, and these toxicities are not accounted for by the TEQ. A second assumption is that the toxicity of chemicals is additive. Should chemicals interact in a synergistic or antagonistic manner, then the practice of adding the TEQs would not be valid. The third assumption or convention, adopted to harmonize many different studies, is the estimation of toxicity factors in orders of magnitude; i.e. 1, 0.1, 0.01, and 0.001 and so on.

The concept of TEQs has evolved considerably since the late 1970s when they were first used. At the first consensus meeting on TEQs held by the World Health Organization in 1993, it was agreed that TEQs were a useful, but interim, measure which should be re-evaluated every five years. At the second consensus meeting in 1998, the database of literature was updated and the scientific basis for each toxicity factor reviewed (Van den Berg, 1998). Consensus was reached on toxicity factors (TEFs) for PCBs. The second important result was the development of toxicity factors for fish and birds. Separate toxicity factors were developed because of an understanding that absorption, metabolism, and excretion for specific chemicals are different among species, and because of the possible differences in binding to the Ah receptor (see Tables 2-1 and 2-2). Third, a few of the toxicity factors from 1993 were revised: 1,2,3,7,8-pentachloro-dibenzodioxin was revised from 0.5 to 1.0 and octachlorodibenzo-p-dioxin and furan were both revised from 0.001 to 0.0001 (Van den Berg, 1998).

TEQs assume that the toxicity of chemicals in a complex mixture is additive, but that assumption is not always true. Examples of synergism, where the presence of one chemical enhances the toxicity of a second (Safe 1990; Van Birgelen, 1996, 1996a), and antagonism, where the presence of one chemical reduces the toxicity of a second, are known (Safe, 1990; Morrisey, 1992; Smialowicz, 1997). Based on many studies, it is estimated that these antagonistic and synergistic interactions are not common and that the assumption of additivity is a reasonable approximation that is unlikely to lead to errors more than two-fold, especially at levels typically found in the environment.

Certain dioxin-like chemicals account for most of the family's toxicity. For example, PCBs account for approximately 50% and TCDD accounts for 10% of the toxicity of dioxin in cow and human milk (Ahlborg, 1994). Most of the toxicity of dioxin in human samples is attributed to TCDD, PCDD, 4-pentachlorodibenzofuran, and PCB 126.

Just how valid is the TEQ concept and how valid are the assumptions that underlie the setting of the toxicity factors? One way to determine if the concept is valid is to measure the toxicity of a mixture and to compare this to the calculated toxicity using the TEQ. This has been done for several mixtures and the use of TEQ was found to be reasonable. For example, when evaluated with TEQ, a contaminated sample of leachate from the Love Canal chemical waste site had an estimated 5-10 micrograms (ug) of TCDD, whereas measured toxicity was 3 ug TCDD (Silkworth, 1989). The TEQ of soot from a PCB transformer fire correlated well with the measured toxicity (Eadon, 1986). And, TEQ methods reasonably predict toxicity of mixtures in the laboratory (Viluksila, 1998, 1998a).

TEQs based on an analysis of soil or sediment are not very useful for estimating toxicity to wildlife or humans, because the various dioxin-like chemicals are absorbed, metabolized, and excreted differently by different animals. For dioxins, the 2,3,7,8 forms are preferentially enriched in mammals, birds, and fish. Thus, it is best to use an analysis of the animal's food source or the animal itself to estimate toxicity rather than an environmental sample such as sediment or soil.
 

Physical Properties and Environmental Fate

Dioxin-like chemicals share many physical properties that affect how they behave in the environment. They dissolve poorly in water, but very well in oils, fats, and organic solvents. They adhere strongly to organic components of soil and water and therefore do not wash out easily. They have a low vapor pressure which means they do not evaporate readily. Since they do not react with oxygen or water and are not broken down by bacteria, they persist in the environment for long periods of time. They can be broken down very slowly by sunlight, but only under certain conditions. The most stable members of the group have four or more chlorines (Zook, 1994; IARC, 1997; ATSDR, 1998).

Because PCBs are somewhat more reactive than dioxin, they are more easily broken down by sunlight, air, and bacteria. PCBs will volatilize and, depending on the congener and the air temperature, can be found in the vapor phase as much as 90% of the time (Murray, 1992; Cohen, 1997). They will gradually settle out (dry deposition) or be washed out by rainfall (wet deposition) and may slowly evaporate back into air (Baker, 1990). Furans, dioxins, and PCBs eventually settle on terrestrial plants where they enter the food chain. Dioxins fall out onto crops that are fed to dairy cows and beef cattle where they accumulate in the milk and meat of these animals. Dioxins are not well metabolized in the body and thus are not eliminated in urine or feces. Rather, they dissolve and accumulate in the body fat of these animals. People who consume the contaminated meat and dairy products ingest substantial amounts of dioxins. Generally, plants do not absorb dioxins through their roots, although there appear to be a few exceptions. Studies have shown that some plants (zucchini, pumpkin, and perhaps carrots) seem to absorb dioxin through their roots (Schroll, 1993; Hulster, 1994; Muller, 1994).

Dioxins and furans are not manufactured intentionally. Instead, they form as an unintended contaminant or byproduct during combustion or during the manufacture of certain chlorinated chemicals. Most dioxins and furans escape into the environment from incinerator stacks, pulp and paper industry discharges, and the manufacture of polyvinyl chloride (PVC) plastic, chlorinated solvents, and chlorinated pesticides (USEPA, 1998) (see Chapter Three). Some also escape into the environment from the burning of toxic chemicals in cement kilns and from metal smelting and refining (USEPA, 1998). PCBs were once produced intentionally in large quantities, and, though their manufacture is now banned, existing products containing PCBs are still used and discarded. Once released into the atmosphere, dioxins and furans stay suspended a long time and may travel all over the world before settling (IARC, 1997). In the air, dioxins are usually bound to particles such as incinerator ash and are shielded from photodegradation. Eventually, they settle to earth. On surface soil, it may take from 9 to 15 years to degrade half of the dioxin in the top 0.1 centimeters (cm) and 25 to 100 years to degrade half the dioxin in the subsurface soil below 0.1 cm (Paustenbach, 1992). In Times Beach, Missouri, it took 16 months before half of the dioxin in the top eighth of an inch of contaminated soil was photodegraded (Freeman, 1987). Dioxin below that level did not wash out with rain, nor did it evaporate. Whether it settles directly on water or ends up there due to soil erosion, dioxins end up in the bottom muds and sediments of rivers, lakes and ocean. These chemicals are taken up by aquatic organisms and are concentrated as they move up the food chain to fish and eventually to humans.

Dioxins can easily re-enter the environment when muds and sediments are disturbed, such as in the dredging of a harbor. When buried in landfills or trapped in soil, this chemical family tends to stay in place unless carried away by oily substances or organic solvents such as benzene and toluene, which are often present in landfills. At Love Canal, New York, dioxin moved long distances from the canal into storm sewers and a creek in exactly this manner (DOH, 1981).
 

Dioxin Formation

Dioxins and furans form whenever chlorine-containing compounds are exposed to high heat or catalysts in the presence of organic material (Pennise, 1996). They form at temperatures as high as 1,000^o Celsius (C) (Hunsinger, 1997) and as low as 20^o C in the gas, liquid, or even solid phase (Klimm, 1998). In incinerators, dioxins form at temperatures from 200^o C to 1,000^o C (Hunsinger, 1997), with optimum formation temperatures varying from 300^o to 600^o C (Yasuhara, 1988; Huang, 1995). At 800^o C, pure dioxins decompose almost completely, but dioxins bound to particles remain intact even at 1,150^o C (Esposito, 1980). They form primarily when incinerator gases cool as they flow toward the stack. Trace metals, especially copper and zinc, may act as catalysts (Acharya, 1991).

Whatever the mechanism, chlorine is essential. Apparently any form of it, whether organic (such as found in PVC plastic, pentachlorophenol, or PCBs) or inorganic (such as potassium chloride, sodium chloride, cuprous or cupric chloride, or ferric chloride), can participate in the reactions (Addink, 1995; Danish EPA, 1997). A better understanding of mechanism is important to reducing dioxin emissions. If organic chlorinated precursors are important, then dioxin emissions can be prevented by removing PVC, polychlorinated benzenes, and polychlorinated phenols from wastes. Alternately, if even simple forms of chlorine lead to significant dioxin formation, then prevention will depend on following chlorine through its cycle of use in industrial processes, keeping track of every product and waste that are potential dioxin carriers, and perhaps even sharply curtailing chlorine use.
 
 

"[I]t can be concluded that dioxins were largely anthropogenic and associated with events taking place around 1935-40. What were these events? The explanation is likely to be the introduction of chlorinated organic compounds (polyvinyl chloride and chlorinated pesticides are but two examples) in the 1935-40 time-frame...[T]he introduction of these chlorinated products into wastes that were combusted appears to be the most likely cause of the increased dioxin deposition measured in sediments."

U.S. Environmental Protection Agency
Science Advisory Board, 1995.
 
 

Dioxins are found everywhere in the world - in water, air, soil, and sediment - even in places where dioxin or dioxin-containing products have never been used. This broad distribution is evidence that the sources are multiple and that dioxins can travel long distances. Dioxins get into the environment from industrial air emissions, wastewater discharges, disposal activities, and from burning material containing chlorine. Airborne dioxin eventually settles onto soil, plants, and water. It then moves up the food chains and may end up in people's bodies. In this chapter, we will examine how and where dioxins are released into the environment. Most of the estimates in this chapter are from the United States Environmental Protection Agency's (EPA) The Inventory of Sources of Dioxin in the United States (USEPA, 1998). The EPA acknowledges that there are many limitations with its estimates, and they are discussed later in this chapter. The most serious limitation is the lack of sufficient data to make accurate estimates of the amount of dioxin released into the environment by different sources.
 

Background

The EPA assembled one of the first listings of U.S. dioxin sources in 1980. The list identifies 25 commercial chemicals whose manufacture have a "high probability" of forming dioxin. Of these 25 chemicals, 15 are chlorinated compounds whose manufacture is expected to form polychlorinated dioxin and furan by-products. The remainder are brominated, fluorinated or iodinated compounds whose manufacture is expected to form polyhalogenated dioxins other than the chlorinated species.

The list also identifies 55 chemicals whose manufacture has the "possibility"of forming dioxin by-products. In addition, the list identifies 18 pesticides whose manufacture is "highly likely" to form dioxin by-products and another 20 whose manufacture has a "reasonable probability" of forming dioxin by-products. The EPA also identifies municipal waste incinerators, some industrial incinerators, and cigarettes as dioxin sources, and notes that combustion of naturally occurring compounds "in the presence of chlorine-containing compounds (e.g., DDT or polyvinyl chloride) can lead to the formation of chlorinated dioxins" (Esposito, 1980).

By 1985, the EPA concluded that the "primary sources of PCDD [dioxin] contamination in the environment result from the manufacture of chlorophenols and their derivatives and the subsequent disposal of wastes from these industries." Five categories of dioxin sources were identified: manufacturing processes, municipal incinerators, other combustion processes, chemical disposal sites, and photochemical processes (USEPA, 1985). In 1987, EPA released the results of a two-year nationwide study of contamination by the most potent of the dioxins, 2,3,7,8- tetrachlorodibenzo-p-dioxin (TCDD). The study lists sites where the pesticide 2,4,5-trichlorophenol was produced or used and sites for the disposal of the associated wastes. In addition, combustion sources and production sites of other chemicals where 2,3,7,8-TCDD may have been produced are examined, as are levels of 2,3,7,8-TCDD in fish and in urban and rural soils (USEPA, 1987).

U.S. Inventories of Dioxin Sources and Emissions

In 1994, the EPA released a review draft of its second dioxin "reassessment." This report contains the first detailed inventory of U.S. dioxin sources and their estimated releases. It identified 31 source categories (facilities or activities that are known or suspected to release dioxins into air, water, land, and products) and estimated that the amount of dioxin released to air, water, land and products totaled 11,660 grams of toxic equivalents per year (gm TEQ/yr) (see Table 3-1) (USEPA, 1994b). One year later, the EPA's Science Advisory Board (SAB) reviewed the 1994 dioxin inventory and recommended revisions (USEPA, 1995). The EPA released a revised inventory in 1998 in the a report, The Inventory of Sources of Dioxin in the United States. Though it describes at least 70 source categories for dioxin, EPA only considers the 54 in Table 2-2 of their report to be part of its inventory. Estimated dioxin releases for some of these 54 sources, though in the report's text, are either not in that table, are summarized in another table, Table 2-5 (of the EPA report), or are missing. Nevertheless, the inventory estimates that dioxins released from these 54 source categories in reference year 1995 totaled 28,023 gm TEQ/yr (Table 3-1) (USEPA, 1998).
 

Table 3-1 Estimated Dioxin Releases to the Environment in the U.S.

	1994 Draft Inventory	1998 Draft Inventory
Dioxin Releases	Total, gm TEQ/yr*	Total, gm TEQ/yr*
To Air	9,300	2,745 **
To Water	110	20
To Land	2,100	208
To Products	150	25,050
Total	11,660	28,023

Source: USEPA, 1994b, 1998
* The values presented here are central estimates.
** USEPA considers the national dioxin inventory to consist only of those source categories and emissions presented in Table 2-2 of the inventory document. If preliminary estimates presented in the document, but not included on Table 2-2 are included, then dioxin releases to air are 4,925 gm TEQ/yr and total releases are 30,203 gm TEQ/yr.
 
 

As Table 3-1 shows, most of the dioxin is released into the air. However, because dioxins released into the water easily end up in fish people eat, dioxin emissions to water are also significant to human health. Dioxins disposed on land, mostly in landfills and as sewage sludge that is spread on farmland, can also pose significant health risks because of movement of dioxin out of these disposal sites.
 

Overview of EPA's 1998 Inventory of Sources of Dioxin

The EPA estimated how much dioxin was released into air, water, land, and commercial products in the U.S. in 1995 (Table 3-2). These estimates include only the 54 source categories for which EPA has sufficient confidence in the available data (USEPA, 1998). For example, estimates for air releases are made for only 20 of the 54 source categories. Preliminary estimates for a number of source categories are not included in EPA's inventory. Estimates are considered preliminary because they lack direct emissions measurements or because there are large uncertainties in the activity level or applicability of available data from facilities in other countries. Dioxins released from negligible sources, or dioxins already present in the environment in "reservoir" sources are not included or are listed as having "no emissions." No estimates are made for some source categories for which there is evidence of emissions. Detailed summaries of many of these specific sources are included in Appendix A. EPA estimates of these same sources using data from 1987 are also shown in Table 3-2.
 
 

Table 3-2 Inventory of Sources of Dioxin in the United States (gm TEQ/year)
Reference Year 1995 Reference Year 1987
Air: lower central upper lower central upper
Municipal waste incineration	492	1,100	2,460		3,540	7915	17,698
Secondary copper smelting	171	541	1,710		96	304	960
Medical waste incineration	151	477	1,510		781	2,470	7,810
Forest, brush and straw fires	64.5	208	645		53.8	170	538
Cement kilns (hazardous waste burning)	48.4	153	484		37	117	370
Coal combustion	32.6	72.8	163		28	62.6	140
Wood combustion - residential	19.8	62.8	198		28.3	89.6	283
Wood combustion - industrial	13.0	29.1	65		12.3	27.5	61.5
Vehicle fuel combustion - diesel	10.6	33.5	106		8.3	26.3	83.2
Cement kilns (non hazardous waste burning)	5.6	17.8	56.3		4.3	13.7	43.3
Secondary aluminum smelting	5.4	17	53.8		3.0	9.5	30
Oil combustion - industrial/utility	2.9	9.3	29		4.9	15.5	49
Sewage sludge incineration	2.7	6	13.4		2.7	6	13.4
Hazardous waste incineration	2.6	5.7	12.8		2.2	5	11.2
Vehicle fuel combustion - unleaded	2	6.3	20		1.2	3.8	12
Kraft recovery boilers	1	2.3	5		0.9	2	4.5
Secondary lead smelters	0.73	1.63	3.65		0.55	1.22	2.73
Cigarette combustion	0.25	0.81	2.5		0.31	1	3.1
Boilers/industrial furnaces	0.12	0.38	1.2		0.24	0.77	2.4
Crematoria	0.07	0.24	0.75		0.05	0.16	0.51
Total	1,026	2,745	7,541		4,616	11,274	28,220
Products:
Pentachlorophenol-treated wood	17,700	25,000	35,400		25,500	36,000	51,957
Bleached chemical wood pulp and paper mills	17.0	24.1	34.0		375	505	714
Dioxazine dyes and pigments	0.11	0.36	1.1		20	64	200
2,4-Dichlorophenoxy acetic acid	13.0	18.4	26.0		15.1	21.3	30.2
Non-incinerated municipal sludge	4.0	7	12.5		4	7	12.5
Total	17,734	25,050	35,474		25,914	36,597	51,957
Land:
Non-incinerated municipal sludge	120	207	375		120	207	375
Bleached chemical wood pulp and paper mills	1	1.4	2		10	14.1	20
Total	121	208	377		130	221	395
Water:
Bleached chemical wood pulp and paper mills	13.8	19.5	27.6		252	356	504

Note: It is not known what fraction, if any, of the estimated emissions from forest fires represents a "reservoir" source.  Source: USEPA, 1994b, 1998

The estimates in Table 3-2 include an average or "best guess" estimate as the central value of a range of high and low estimates for each source (USEPA, 1998). Based on the quantity and quality of data available to EPA, the estimates are evaluated as follows: for high confidence estimates, the range between the high and low estimates is two fold; for medium confidence estimates, the range is about five fold; for low confidence estimates, the range is ten fold. For example, for municipal waste incineration, the difference between the lower and upper estimates is five fold. This means that EPA has medium confidence in the data used to make the estimates. Of the 20 source categories for which estimates for air emissions are made, EPA has low confidence in 13 of them and medium confidence in the remaining seven. EPA does not have high confidence in any of the air source categories. These confidence ratings are discussed in more detail below.

As seen in the Table 3-2, the major sources of dioxin can be found in two major categories: combustion and metal refineries. Combustion sources account for nearly 80% of the national inventory of dioxin released to air and includes burning of medical, municipal, and hazardous waste, sewage sludge, hazardous waste in cement kilns, fuels such as coal, wood and petroleum products to generate power or energy, and uncontrolled burning, such as forest and brush fires (see Appendix A, Tables A-1, A-2, and A-3 for summaries). It is unclear what portion of the emissions during forest and brush fires is actually resuspension from residues deposited on leaves rather than newly formed dioxins (Clement, 1991; McLachlan, 1998).

The second significant group of sources is metal smelting, refining, and processing which includes primary and secondary metals operations, iron ore sintering, steel production, and scrap metal recovery. This category accounts for about 20% of the national inventory of dioxin released to air. A summary of the metal smelting and processing sources is presented in Appendix A.

In the 1998 EPA inventory, dioxins released to the air and products are the most thoroughly characterized (Table 3-3). For approximately 85% of source categories, releases to air are either estimated, given preliminary estimates or classified as having negligible or no releases.* Preliminary estimates of emissions to air are made for 12 source categories including open burning of household waste, landfill fires, iron ore sintering plants, and coal combustion from residential homes. None of these preliminary estimates are included in EPA's final inventory.

These preliminary estimates add up to an additional 2,180 gm TEQ/year and potentially increase the total dioxins released to air to 4,925 gm TEQ/year (see Table 3-3). Eleven source categories are considered negligible, and no estimates are made for eight source categories for which there is evidence of dioxin emissions. Dioxins released in products are similarly characterized for 91%

* EPA concluded that some source categories do not have any releases to air. In such cases, EPA used the term "not applicable."
 

(49/54) of source categories. However, as EPA notes, only a few commercial chemicals are included in their inventory because only a limited number have been analyzed for dioxins (USEPA, 1998). Dioxins released to land and water are much less well characterized: only 37% (20/54) of the source categories for land and 44% (24/54) of the source categories for water for which evidence of dioxin releases exists are characterized.
 

* One source category for which no estimate was made is included in an estimate for another source category.   Source: USEPA, 1998
 

Confidence Ratings of Dioxin Emissions Estimates

EPA estimates emissions by multiplying activity levels (amount of waste burned, quantity of chemical produced, etc.) and emission factors (quantity of dioxin released per unit of activity). The strength of each estimate is based on the confidence ratings of the activity levels and emission factors. EPA's rating system is shown in Table 3-4.
 

Source: USEPA, 1998
 

As shown in Table 3-5, EPA presented no confidence ratings for activity levels, emission factors or other characterizations for 61% of the source categories identified as having potential dioxin emissions to the air; 97% of source categories with potential releases to water; 95% of source categories with potential releases to land; and 58% of source categories with potential releases in products. In summary, EPA's confidence in dioxin releases to air, water, land, and products is relatively poor.
 

Source: USEPA, 1998
 

Sources Not Included in the EPA's Inventory

The EPA only makes estimates of source categories for which they have sufficient confidence in the available data (USEPA, 1998). Preliminary estimates are made for some source categories (Table 3-6), but these estimates are not included in the national inventory. In addition, EPA makes judgements about some source categories that they feel contribute "negligible" emissions to the national inventory (Table 3-7). For other source categories, no estimates are made even though there is some evidence of emissions (Table 3-8). EPA notes that for most sources there are insufficient data to quantify the dioxins they release to air, water, or soil, yet there are apparently no efforts to collect such data. Some of these source categories, if included, would contribute substantially to the National Inventory.
 

Source: USEPA 1998
 

For example, there are at least three U.S. magnesium production facilities in Texas, Utah and Washington, which have produced approximately 117,000 metric tons of magnesium in 1998 (USGS, 1999). These facilities use an electrolytic process that relies on chlorine-based technology that is known to generate dioxins (Oehme, 1989). The dioxin emission factor derived for the Magnola/Noranda magnesium production facility in Asbestos, Canada, is 38,000 nanograms (ng) TEQ per kg of magnesium produced. Dioxin emissions to air are 2 ng TEQ/kg of magnesium produced, from stacks; and 30-140 ng TEQ/kg of magnesium produced, volatilized from land. Estimated dioxin emissions to land are 300-1,400 ng TEQ/kg of magnesium produced; and 8,000-29,000 ng TEQ/kg of magnesium produced are transferred off-site (Bramley, 1998). These data suggest that magnesium production is a potentially large, but as-yet undetermined, dioxin source in the U.S.

Another potentially significant source category not included in the EPA inventory is the production and use of elemental chlorine, sodium hypochlorite, or metal chlorides. In each instance, the EPA cited the lack of data from U.S. facilities as the reason for not including these sources in the inventory. However, data is available from European facilities (USEPA, 1998). The production of PVC is identified as a source by EPA, but is not included in the inventory for the same reason - the lack of data on U.S. facilities. Greenpeace estimated that dioxin emissions from PVC production range from 500 to 1,000 gm TEQ per year (Thornton, 1994). This estimate would place PVC production among the largest sources of dioxin emissions in the U.S. Industry estimates are much lower (See appendix A).

The production of dioxin from accidental fires in homes and buildings that contain PVC wiring, carpeting, flooring, siding, molded furniture and other chlorinated plastics is also omitted from the inventory. There were over 500,000 structural fires in the U.S. in 1995 (USDOC, 1997), and several studies document that burning PVC plastic results in dioxin formation (Thiesen, 1989; Christmann, 1989). Several estimates of dioxin releases from accidental/structural fires have been made. Thomas (1995) estimated that 20 gm of TEQ are released annually from structural fires in the U.S. and Lorenz (1996) estimated that from between 78 to 212 gm TEQ are released annually from structural fires in Germany. Others believe that dioxin emissions from accidental/structural fires may be even greater, rivaling annual emissions from medical or municipal waste incinerators (Thornton, 1995).

Perhaps the largest known sources of dioxin omitted from EPA's National Inventory are the reservoir sources, which include dioxin in the bottom sediments of water bodies, dioxin in landfills, and dioxin in the hundreds of contaminated industrial and hazardous waste sites around the country.

Most of these sites are not cleaned up and are a major threat to their surrounding communities.
Dioxins at the bottom of oceans, lakes, and rivers are covered by new sediments each year, but if they are stirred up by dredging, storms, or floods, substantial amounts may re-enter the environment.

Another reservoir of dioxin is created by the fallout of airborne dioxin onto soil and vegetation (Weiss, 1998). Soil and vegetative surfaces are continually covered by fallout. The amount of dioxin on these surfaces will vary mostly depending on the proximity to different sources. However, construction, erosion, and other earth-moving activities such as dredging, can cause dioxin near the surface to re-enter the environment. For example, dioxin deposited on forest leaves by airborne fallout re-enters the environment during forest fires and brush fires. The EPA estimates that reservoir sources contain between 15 to 36 times the amount of dioxin typically generated in one year (USEPA, 1994b). Thus, there is a great potential for future exposure from these sources even if all dioxin creation is stopped today.

For a number of the dioxin sources not included in the EPA inventory, estimates have been made for inventories of other countries or regions and/or identified in the scientific literature. These include estimates for:

• Waste oil disposal (Dyke, 1997)
• Run-off from roads (Dyke, 1997)
• Rubber vulcanization (Lexen, 1993)
• Electrolytic production of magnesium and aluminum (Danish EPA, 1997)
• Nickel refining (Danish EPA, 1997)
• Combustion of landfill gas (Fiedler, 1992; Koning, 1993; Bremmer, 1994;

• Asphalt mixing plants (Koning, 1993; Bremmer, 1994; Douben, 1995)
• Accidental fires (Wevers, 1995)
• Carbon reactivation furnaces (Douben, 1995, Eduljee, 1996)
• Lime production (Wevers, 1995; Douben, 1995; UKDE, 1995; Eduljee, 1996)
• Ceramics and glass manufacture (Douben, 1995; Eduljee, 1996)
• Emissions from pentachlorophenol-treated wood (Douben, 1995; Eduljee, 1996)

• Textile manufacturing
• Dry cleaning operations
• Phthalocyanine dyes and pigments (Huntzinger, 1991)
• Printing inks (Santl, 1994)
• Drinking water treatment
• Small commercial and industrial furnaces and boilers
• High-rise apartment incinerators (Laber, 1994)

 

EPA's estimated emissions of dioxin released into the air are lower in 1998 than in 1994. While this may appear to be good news, there are so many uncertainties in these estimates as well as significant sources not included in the 1998 inventory, that it is difficult to draw any meaningful conclusions about trends. There are several obvious differences between the two reference years. For one, the 1998 inventory adds the large release of 25,000 gm TEQ of pentachlorophenol. Also, since the 1994 report, dioxins released to the air have changed. Many municipal and medical waste incinerators, which were both significant source categories of air releases reported in the 1994 inventory, are closed due in large part to the efforts of grassroots community based organizations. The resulting reduction in estimated air releases is offset to a great degree by the identification of two new large source categories in the 1998 report, open burning of household waste and landfill fires. Although both of these newly identified sources have preliminary estimated releases greater than 1,000 gm TEQ/yr, neither are included in EPA's National Inventory shown in Table 3-2.

Releases to Water

Because of the impact of point source discharges of dioxins to water on anglers and Native Americans, the SAB specifically asked EPA to further investigate these discharges in its review of the 1994 report (USEPA, 1995). Nonetheless, in both the 1994 and 1998 inventories, EPA estimates releases to water from only one source category, pulp and paper mills. Dioxins released to water from these sources are estimated to be 110 gm TEQ/yr in 1994 and 19.5 gm TEQ/yr in the 1998 report. This change is attributed to "process changes of a pollution prevention nature" and the availability of new, more accurate data (USEPA, 1998). Municipal waste water treatment systems, or publicly owned treatment works (POTWs), are listed as dioxin sources in the 1994 inventory, but not in the 1998 inventory, even though EPA provides a preliminary estimate of 163 gm TEQ/yr (USEPA, 1998).

In the 1998 report, EPA notes that there are insufficient data for most industrial and commercial facilities to quantify the dioxins they release to water, yet there are apparently no efforts to collect such data. According to EPA, there is one program in which chemical manufacturers report the amount of dioxin in their products, but not in their waste discharges. And since most dioxins formed during chemical and pesticide manufacture end up in wastes and waste treatment residues, this program can only identify a few dioxin sources among chemical and pesticide manufacturers.

Releases to Land

Another major difference between the 1994 and 1998 inventories is the treatment of dioxins released to landfills. In the 1994 inventory, dioxins released to landfills are included with those released to land and are estimated to total 2,100 gm TEQ/yr. This dioxin contaminated waste comes mostly from municipal incinerators (ash), POTWs (sludge), and cement kilns (dust) (USEPA, 1994b). These releases are not included in the 1998 inventory.

In the 1998 report, EPA establishes a new policy that seems to serve no purpose other than to enable it to exclude dioxins released to landfills from the national dioxin inventory. It claims that "properly designed and operated landfills are considered to achieve long term isolation from the circulating environment" (USEPA, 1998). EPA's unsubstantiated assessment of landfill performance is contradicted by studies showing that dioxin-like chemicals evaporate from landfills and leach into groundwater from both existing and redundant landfills (USEPA, 1987; Bracewell, 1993; Hiraoka, 1993). A recent assessment of sustainable landfills concludes that "liner failure will occur ultimately, and that in the long term, the escape of waste materials and their products of degradation is inevitable" (Westlake, 1997).

EPA's recent decision to exclude dioxins that are taken to landfills from its inventory contradicts its earlier designation of incinerator ash disposal in landfills as a source category (USEPA, 1992). Moreover, this policy is highly inconsistent with those of other national inventories such as the European Union, the United Kingdom, and Denmark (Dyke, 1997; NRWSEA, 1997; Danish EPA, 1997). The U.K. inventory includes estimated dioxin releases to land/landfills from 23 source categories, with municipal incinerator ash being the largest contributor (Dyke, 1997). The European Union inventory estimates that dioxins released via residues and sent to landfills are of the same order of magnitude as those to air (NRWSEA, 1997). The U.K. inventory concludes: "Releases to land appear greater than those to air or water" (Dyke, 1997).

In its 1995 review, the SAB recommended that EPA evaluate more thoroughly the potential release of dioxins from reservoirs, including sediments, which SAB notes "might indeed be important" (USEPA, 1995). Nonetheless, EPA's new inventory lists only one source category, chlorophenol-treated wood, as a dioxin reservoir. The agency does, however, identify several
other reservoir sources - soils, sediments and vegetation - in its explanation of why these reservoirs are not included in its inventory (USEPA, 1998). EPA states that "no empirical evidence exists on the magnitude of reservoir emissions from soil to air." EPA presents no estimate of the quantity of dioxin-contaminated soils and sediments in the 1998 report. However, the U.S. Congress' Office of Technology Assessment estimated in 1991 that there were 500 million kilograms of dioxin-contaminated soil in the U.S. that require treatment (USOTA, 1991). If 1 part per billion (ppb) of 2,3,7,8-TCDD is the minimum level that requires treatment, this soil is a reservoir of at least 500 gm TEQ. It is also important to note that landfills, as described earlier, readily meet EPA's definition of a reservoir sources, as discussed above.

Other Inventories

The EPA's inventory of dioxin sources is one of only a few efforts to identify and estimate dioxin emissions from different sources. Other estimates exist in the U.S. (Travis, 1991; Thomas, 1995); Canada (Sheffield, 1985); Sweden (Rappe, 1991; Lexen, 1993); Germany (Fiedler, 1992); The Netherlands (Koning, 1993; Bremmer, 1994); Switzerland (Schatowitz, 1993); Austria (Riss, 1993); Belgium (Wevers, 1995); and Great Britain (Douben, 1995; UKDE, 1995). Also, the Center for the Biology of Natural Systems (CBNS) at Queens College in New York has collaborated with EPA to generate a separate estimate of dioxin emissions to air (Commoner, 1998). This study, headed by Dr. Barry Commoner, estimates total annual dioxin emissions for both the U.S. and Canada from 20 source categories to be 4,350 gm TEQ, of which 3,890 gm TEQ are generated in the U.S. and 460 gm TEQ are generated in Canada (Commoner, 1998). The survey found that 86% of the total dioxin emitted in the U.S. results from only five types of sources: municipal waste incinerators, medical waste incinerators, secondary copper smelters, cement kilns that burn hazardous waste, and iron sintering plants. Two of these, municipal and medical waste incinerators, account for 2,640 gm TEQ/year, nearly two-thirds of the total emissions in the U.S. This estimate agrees fairly well with EPA's total estimate of 2,745 gm TEQ/yr (4,925 gm TEQ/year if preliminary estimates are included) for these sources. CBNS comments that "given the uncertainties inherent in such estimate inventories ... the actual values may be several times greater or smaller than the mid-point" (Commoner, 1998).
 
 

Simply by eating, Americans have accumulated harmful or almost harmful levels of dioxin in their bodies. Some segments of the population, such as nursing babies and people who eat a diet high in animal fat or foods contaminated because of their proximity to dioxin release sites, have been exposed to higher than average levels of dioxin. Others, such as Vietnam veterans and some chemical plant workers, have accumulated additional dioxins because of their exposure to Agent Orange or chemicals in the workplace. Previous chapters in this report have discussed the chemistry of dioxin and its sources. This chapter discusses how exposure to dioxin is measured, how much dioxin exposure the average American and certain highly exposed groups have experienced, attempts by several government agencies to establish "safe" levels of dioxin exposure, and whether such safe levels exist.

Daily Intake in the U.S.

One way of assessing health risks from exposure to dioxin is to measure the average American's daily intake of dioxin. It is estimated that, simply by eating, the average American's daily dioxin intake ranges from 18 to 192 picograms (pg) TEQ per day. The EPA estimated that the average 150-pound adult ingests 120 pg of dioxin TEQ per day (Schaum, 1994). This is equivalent to a 75-kilogram adult ingesting 1.6 pg TEQ per kilogram of body weight (bw) per day. As discussed later, nursing infants ingest 35-118 pg/kg bw/day, far more than the average adult (Schecter, 1994a; Patandin, 1999).

In one of the few surveys of dioxin levels in food from U.S. supermarkets, Schecter (1994) estimated that the average American adult ingests 0.3 to 3 pg TEQ/kg bw daily. This is equivalent to a 65 kg (143 pound) adult ingesting 18 to 192 pg TEQ/day, a value that compares well with EPA's estimate of 120 pg TEQ/kg bw/day. The daily intake is less in strict vegetarians (Schecter, 1998). In a more recent survey of 100 food samples from supermarkets in Binghamton, New York; Chicago, Illinois; Louisville, Kentucky; Atlanta, Georgia; and San Diego, California, Schecter (1996) estimated that the average daily U.S. intake of dioxins for a 65 kg (143 pounds) adult ranges from 34 to 167 pg TEQ. This is equivalent to a daily adult intake of 0.52 to 2.57 pg TEQ/kg bw. If dioxin-like PCBs are also included, the daily adult intake increases to 1.16 to 3.57 pg TEQ/kg bw. These estimates agree with Schecter's original estimate and with EPA estimate.
 

Daily Intake in Other Countries

Studies conducted in other industrialized countries found estimates similar to U.S. values for the daily intake of dioxin. A survey of 100 food samples collected from commercial outlets in Canada reported a total daily dioxin intake of about 0.8 pg TEQ/kg body weight (Ryan, 1997). An earlier Canadian survey of different foods from the U.S. and Canada reported a total daily intake of 1.8 pg TEQ/kg body weight for a 60 kg adult (Birmingham, 1989). A German study of 22 samples of different foods estimated an average daily dioxin intake of 164 pg TEQ for a 70 kg (154 pounds) adult, equivalent to an average daily intake of 2.3 pg TEQ/kg body weight (Beck, 1989; Beck 1994). A second German study reported a daily intake of 85 pg TEQ (Furst, 1990). In the United Kingdom, it was estimated that the average daily intake of dioxin is 125 pg TEQ (Startin, 1994). The World Health Organization estimated that average daily intake of dioxin and dioxin-like PCBs in industrialized countries ranges from 3 to 6 pg/kg/day (WHO, 1998). Even people who live in remote places are affected by dioxin. The Inuit Eskimos of northern Canada have a high intake of dioxins and PCBs because their primary diet is fish, seal and whale, all animals high in the food chain and high in fat (Dewailly, 1994).
 

Dioxin Content in Foods
 

Approximately 90% (Schecter, 1994; Schaum, 1994; ATSDR, 1998), and perhaps as much as 98% (Hattemer-Frey, 1989), of the dioxin that Americans are exposed to comes from the foods they regularly eat. Though dioxin has been found in all organs of the body (Schecter, 1999), it accumulate mostly in the fats of meat, fish, and milk. Consequently, when people consume these foods, they also consume dioxins. As Table 4-1 indicates, ground beef has the highest dioxin content, 1.5 pg/gm (equivalent to 1.5 parts per trillion or ppt), of many common foods.

By multiplying the average dioxin content in a food by its average consumption rate (Schaum, 1994) (see Table 4-2), the total daily intake of dioxins from different food types by the average American (Figure 4-1) can be determined. As Figure 4-1 indicates, of the 119 pg/day taken in daily by the average American, about 97% (115.7 pg/day) comes from beef, chicken, pork, fish, and dairy products (cheese, milk, and eggs). However, the estimates in Figure 4-1 may not accurately reflect the dangers that consumption of some foods pose. For example, Figure 4-1 indicates that the average daily intake of dioxins through fish is low in the U.S., but that is because average fish consumption in the U.S. is low. If fish consumption were to increase, or if certain segments of the population who consume more fish than average were to be examined, measured daily intake of dioxins through fish would also increase. Also, as discussed below, certain segments of the population, either because of their diet or lifestyle, consume more dioxin in their food than the average American.
 

Note: The amount of dioxin ingested when certain foods are eaten can be estimated by multiplying the average level of dioxin in that food (Table 4-1) by its average consumption rate (Table 4-2).
   
Source: USEPA, 1994b

 
 
 
 
 

Table 4-2 Consumption Rate for Various Food Groups
Food Group	Consumption Rate (gm/day)			Low Range of  Dioxin in Food  (pg/gm) (ppt)			High Range of Dioxin in Food (pg/gm) (ppt)
Fruits and Vegetables		283		---			---
Milk		254		0.04			0.04
Beef		88		0.04			1.50
Other Dairy Products		55		0.04			0.70
Poultry		31		0.03			0.03
Pork		28		0.03			0.30
Fish		18		0.02			0.13

Source: Schecter, 1994
 

Body Burden Levels of Dioxin

In addition to measuring an organism's exposure to dioxin by its daily intake, its exposure can also be estimated by its "body burden." An organism's body burden not only estimates dioxins currently present in its body per kilogram of body weight, but it also reflects its total accumulation of dioxins. In contrast to daily intake, which is calculated in picograms (trillionths of a gram)/kg bw/day, body burdens are measured in nanograms (billionths of a gram)/kg bw. Two methods of estimating body burden may be used. The first one, the only option available until recently, estimates the body burden of dioxin in an organism by analyzing a sample of its fat, which is difficult to obtain and expensive to analyze.

he second method, a result of the discovery that dioxins are carried in the lipid part of the blood and that these lipids reflect the concentration of dioxins in fat tissue (Papke, 1989; Schecter, 1990), makes it possible to calculate body burdens from blood samples. Whichever of the two methods is used to calculate body burdens, the following assumptions are made (DeVito, 1995): dioxins are almost equally distributed in the body lipids (fat), and all tissues have the same lipid-adjusted concentrations of TCDD; lipid-adjusted serum levels are equivalent to lipid-adjusted adipose tissue levels; and approximately 22% of the body weight of the average adult is lipids. Given these assumptions, body burden levels are calculated by multiplying lipid-adjusted serum or fat tissue concentrations (expressed as ng TCDD/kg or ng TEQ/kg) by 0.22, the fraction of fat in the body.

The most extensive survey of dioxin body burdens in humans, the National Human Adipose Tissue Survey (NHATS), conducted by the EPA in 1982 to monitor the level of selected chemicals in the general U.S. population (USEPA, 1991), used the fat sample method. In that survey, fat tissue samples from 865 individuals from different regions of the country indicated a national average dioxin tissue concentration of 28 ng TEQ per kilogram lipid or 28 ppt (USEPA, 1991; Orband, 1994). These levels show an increase with age, but there are no differences between races, sexes, or geographical regions of the U.S. (USEPA 1994b). In 1987, the survey was repeated, and the results suggest some decrease in average dioxin concentrations, but the decrease may be due to improved analytical methods or to other issues involving methods of study. For most congeners, including TCDD, the differences between 1982 and 1987 dioxin levels are not statistically significant (USEPA, 1994b).

Studies using the newer blood sampling technique are less extensive. In a study of 100 Americans, Schecter (1991) reported an average lipid-adjusted dioxin concentration of 41 ng/kg whole blood (combined PCDDs and PCDFs) and a range of 28 to 41 ng TEQ/kg lipid (Schecter, 1994a). In addition, average lipid-adjusted dioxin-like PCB concentrations range from 8 to 17 ng TEQ/kg tissue (Patterson, 1994). If the average PCBs levels are added to the average dioxin levels, the average total tissue concentrations range from 36 to 58 ng TEQ/kg lipid (DeVito, 1995).

Using the average tissue concentrations from the studies above, the estimated national average body burden of dioxins is 6 to 9 ng TEQ/kg body weight. If dioxin-like PCBs are included, the average body burden of dioxins ranges from 8 to 13 ng TEQ/kg body weight. In these estimates, TCDD contributes approximately 15% of the total TEQ (DeVito, 1995). These estimates represent average body burdens for a middle-aged person. Individuals vary, but, in general, younger people have lower body burdens than older people.
 

Highly Exposed Groups

The reported levels of dioxin in meat, poultry, fish, and dairy products that most Americans are exposed to are averaged from food sources all over the U.S. However, people who eat a great deal of local food that is heavily contaminated with dioxin can accumulate higher than average dioxin concentrations. For example, though the uptake of dioxins by plant roots is very poor (Startin, 1994), if air emissions containing dioxins from large garbage incinerators, copper smelters, or similar dioxin sources settles on homegrown and farm crops, people who eat these plants may be exposed to higher than average levels of dioxins. Animals and animal products raised near a local dioxin source are more easily contaminated by dioxin than plants are. A subsistence farmer who lives near a large source of dioxin emissions and consumes the milk and beef produced on the farm risks a high exposure to dioxin.

People who fish for recreation and subsistence, or people who consume a great deal of freshwater, farm-grown or coastal fish or shellfish contaminated with dioxin also risk higher than average exposure to dioxin (USEPA, 1987; Hodson, 1992; USEPA 1992a). It has been demonstrated that levels of TCDD are higher in fish caught downstream from pulp and paper mills than fish caught where there are no paper mills (USEPA, 1987), and that concentrations of dioxin in sport fish and shellfish from dioxin-contaminated waters can be at least an order of magnitude higher than in commercial fish and shellfish purchased in a supermarket (ATSDR, 1998).

In EPA's 1987 National Dioxin Study, 38% of the fish caught downstream from paper mills have dioxin concentrations greater than 5 ppt, some as high as 85 ppt (Kuehl, 1989). These levels are higher than the average dioxin levels found in ground beef, which contains the highest levels of dioxin in food (see Table 4-1). Currently, 66 advisories in 21 states restrict consumption of dioxin-contaminated fish and shellfish. In addition, three states have statewide advisories for dioxins in their marine waters (USEPA 1998a). The level of concern is set in each individual state, but many states use the FDA tolerance level of greater than 25 ppt, but less than 50 ppt of dioxin in fish flesh to advise consumers to restrict consumption of dioxin contaminated fish and shellfish (ATSDR, 1998).
 

High Exposure from Accidents, the Workplace, and Agent Orange

People living in dioxin-contaminated communities such as Times Beach, Missouri; Jacksonville, Arkansas; and Pensacola, Florida have been, and in some cases still are, exposed to dioxins leaking from contaminated sites. These dioxins are in