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Institute of Medicine (US) Committee on the Implications of Dioxin in the Food Supply. Dioxins and Dioxin-like Compounds in the Food Supply: Strategies to Decrease Exposure. Washington (DC): National Academies Press (US); 2003.

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Dioxins and Dioxin-like Compounds in the Food Supply: Strategies to Decrease Exposure.

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2A Summary of Dioxin Reports, Assessments, and Regulatory Activity

This chapter begins with a brief summary of evaluations from several governmental bodies on the toxicity of chlorinated dibenzo-p-dioxins (CDDs) and related compounds, including chlorodibenzofurans (CDFs) and polychlorinated biphenyls (PCBs) with dioxin-like activity, and on the potential human health effects from exposure to these compounds. For brevity, these compounds will be referred to in this report collectively as “dioxin-like compounds” (DLCs), except when there is a need to refer to one of the specific compounds. This chapter also contains information on DLC-related regulations and guidelines that have been established in the United States, a number of European countries, Japan, and Australia for the environment, feeds, and foods. The chapter concludes with discussions on DLC monitoring and research programs and on methods of chemical analysis for DLCs in feeds and foods.


This section presents information about the toxicity of DLCs. For CDDs and CDFs, dioxin-like activity requires chlorination of the parent compounds at the 2, 3, 7, and 8 positions; for PCBs, this activity requires chlorination at four or more positions (with at most one ortho substitution). While there are 75, 135, and 209 different CDDs, CDFs, and PCBs, respectively, only 7, 10, and 12 of them are considered to have dioxin-like activity (Figure 2-1).

FIGURE 2-1. Chemical structures of representative congeners of (A) chlorinated dibenzo-p-dioxins, (B) chlorodibenzofurans, and (C) polychlorinated biphenyls.


Chemical structures of representative congeners of (A) chlorinated dibenzo-p-dioxins, (B) chlorodibenzofurans, and (C) polychlorinated biphenyls.

This section begins with a description of toxicity equivalency factors and toxic equivalencies, which are systems that have been developed to compare the potential toxicities of various dioxin congeners (i.e., compounds that have similar chemical structures or belong to closely related chemical families). Potential adverse human health effects (including cancer and noncancer effects) from exposures to DLCs are then summarized. Because this report focuses on general (i.e., background) exposures to DLCs through feed and food pathways, the discussion on adverse health effects focuses on general exposures, but a brief description of adverse health effects from high exposures to DLCs is also included. The final part of this section consists of a summary of body burden and intake data in the general population and certain vulnerable groups.

Review of Major Reports on DLCs

The body of literature on the toxicity of DLCs is voluminous, and the topic of potential human health effects from exposure to DLCs is highly controversial among scientists. It is beyond the scope of this report to provide a detailed critical analysis and evaluation of the DLC toxic effects data. However, to put some of the information presented in later chapters into context, the committee decided that it is appropriate to include a relatively brief description of the toxicity of DLCs. Several governmental bodies have recently compiled information about DLCs and evaluated their toxicity; the committee has drawn on these evaluations, which are listed below.

  • The Agency for Toxic Substances and Disease Registry's (ATSDR) Toxicological Profile for Chlorinated Dibenzo-p-dioxins (ATSDR, 1998). This report primarily covers the toxicity of CDDs. It alludes to CDFs and PCBs generally only in discussions of contaminant concentrations in environmental media and foods since these compounds (particularly CDDs and CDFs) are commonly analyzed simultaneously. (ATSDR has published separate toxicological profiles on CDFs and PCBs [ATSDR 1994, 2000].)
  • A report prepared for the European Commission DG Environment, Evaluation of the Occurrence of PCDD/PCDF and POPs in Wastes and Their Potential to Enter the Foodchain (Fiedler et al., 2000). This report provides a cursory discussion of toxicity, body burdens, and intakes and focuses on the occurrence of persistent organic pollutants (POPs) in environmental media, animal feeds, and pathways of contamination. It addresses only about a dozen POPs, but CDDs and CDFs are discussed thoroughly because of the relatively large databases for these compounds.
  • A report prepared for the European Commission DG Environment and the U.K. Department of the Environment and Transport and the Regions, Compilation of EU Dioxin Exposure and Health Data (AEA Technology, 1999). This report contains a thorough review of exposure and health effects data.
  • An initial report and an update from the Scientific Committee on Food of the European Commission, Health and Consumer Protection Directorate-General, Opinion of the Scientific Committee on Food on the Risk Assessment of Dioxins and Dioxin-like PCBs in Food (Scientific Committee on Food, 2000, 2001). The initial report focuses on dietary exposure and toxicity of DLCs; it does not address pathways of contamination. The update, based on scientific information made available after release of the initial report, includes new toxicity and tolerable intake information only.
  • The International Agency for Research on Cancer's (IARC) IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Volume 69: Polychlorinated Dibenzo-para-dioxins and Polychlorinated Dibenzofurans (IARC, 1997). The focus of this report is assessment of the potential human carcinogenicity of CDDs and CDFs, but other issues, such as other types of toxicity, environmental occurrence, and human exposure, are also covered.
  • The U.S. Environmental Protection Agency's (EPA) draft Exposure and Human Health Reassessment of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds (EPA, 2000). This draft reassessment is the most extensive compilation of data on the environmental occurrence and toxicity of DLCs and the consequent human exposures and risks.

Toxicity Equivalents and Toxicity Equivalency Factors

The biological activities of DLCs vary and, since humans are usually exposed to mixtures of DLCs, the toxicity of an exposure depends on the particular composition of the mixture. It is desirable to express the expected biological activity of mixtures using a common metric. The biological activities of the various dioxin congeners are compared to the activity of 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD). TCDD is the most biologically potent of the DLCs, and the greatest amount of toxicity information has been gathered for this dioxin congener. The toxic potency of a mixture of DLCs is therefore expressed in TCDD toxicity equivalents, or TEQs. As an example, exposure to a mixture of DLCs with a potency of 2 ng TEQ/kg means that the total mixture is expected to have the potency of an exposure equal to 2 ng TCDD/kg. The TEQ value for a mixture is calculated by multiplying the mass or concentration of each DLC by a toxicity equivalency factor (TEF) and summing across all DLCs present. TEFs are calculated as a way to express the activity of DLCs in relation to TCDD as determined by various biochemical or toxicological assays. A sample TEQ calculation is shown in Table 2-1. (For further discussion of the derivation and use of TEQs and TEFs see EPA, 2000.)

TABLE 2-1. Sample Toxicity Equivalents (TEQ) Calculation for a Mixture of Dioxin-like Compounds.


Sample Toxicity Equivalents (TEQ) Calculation for a Mixture of Dioxin-like Compounds.

Any mixture that yields a certain TEQ concentration is assumed to have the same toxic potential as another mixture with the same TEQ. Although the TEF system is useful for determining toxicity in mixtures of DLC congeners, it cannot be used to simplify environmental fate and transport analyses of DLCs because individual congeners differ in their physical and chemical properties, an important consideration in fate modeling. Several TEF schemes have been developed over the years; they differ regarding the inclusion of dioxin-like PCBs and TEFs for certain compounds. The biological activity of a mixture of DLCs may be estimated differently depending on the TEF system used and the particular compounds analyzed. Appendix Tables A-1 and A-2 present the common TEF systems.

Although the use of TEFs provides a convenient method for assessing the toxicity of mixtures of DLCs, there are limitations to this method. These limitations include uncertainties associated with the TEF values assigned to each DLC congener; whether TEF values are constant across all responses and ranges of dose; whether all effects of DLCs, including TCDD and PCB congeners, are mediated via the arylhydrocarbon receptor; whether a TEQ for a DLC mixture is the sum of the toxicity of each DLC present in mixture; and whether all mixtures with the same TEQ have the same toxicity.

Potential Human Health Effects from Exposure to DLCs

Chemical dose is typically measured as an intake in units of mass per unit of body weight, such as 2 mg of calcium/kg. However, for compounds that are cleared slowly from the body, such as DLCs, intakes are not very useful for understanding toxicity profiles, dose-response modeling, or interspecies comparisons. In the case of DLCs, a given intake can create very different internal concentrations in the species and target organs of interest, depending on the duration of dosing and toxicokinetic and toxicodynamic parameters (e.g., the fat content of the target tissue and the half-life of the specific dioxin congener in an organism). Reviews of DLC toxicity generally refer to an internal exposure metric, such as body burden, or to concentration in a particular tissue when such data are available. Different body burden definitions may be used, such as steady state, lifetime average, or peak concentrations. Because DLCs are preferentially associated with lipids, body burden concentrations are frequently given in units of mass per mass of lipid. Various reports cited in this chapter provide different measurement units. No conversions to other units were made for any of these values to ensure the accuracy of the values as presented by the study author.

Effects Observed in Humans at General Exposures

General exposure is defined here as that received through everyday life. The general population, breastfeeding infants, and consumers of contaminated fish are considered to have general exposures to DLCs. Occupationally exposed workers and victims of unintentional releases are not included. An exception is made for the Times Beach, Missouri investigations, since body burdens of TCDD in exposed subjects were similar to those of the general population, despite widespread soil contamination.

The reports cited earlier (AEA Technology, 1999; ATSDR, 1998; EPA, 2000; Fiedler et al., 2000; IARC, 1997; Scientific Committee on Food, 2000, 2001) consider all human data, regardless of dose, or focus on high-dose populations because of the greater probability of observing an effect. These reports describe certain populations as “poisoned” or “highly exposed,” including those in pesticide manufacturing studies, the Ranch Hand studies, the Seveso reports, and the Yusho and Yu-cheng investigations (see below). There are several studies of cancer in pesticide applicators, but they are confounded by lack of specific exposure information. Studies of Swedish (Axelson and Sundell, 1974, as cited in EPA, 2000) and Finnish (Riihimäki et al., 1982, 1983, as cited in EPA, 2000) applicators that used both 2,4-D (2,4-dichlorophenoxyacetic acid) and 2,4,5-T (2,4,5-trichlorophenoxyacetic acid) showed a slight increase in relative risk for cancer, but exposure to TCDD or other DLCs was not quantified.

A study of 1,261 Air Force veterans known as Ranch Hands, who were responsible for aerial herbicide spraying in Vietnam, showed that the men had a median TCDD blood serum level that was 12.4 ppt (range 0–618 ppt) compared with 4.2 ppt in controls (Air Force veterans engaged in cargo transport), with the greatest exposure in the nonflying ground personnel (median value 23.6 ppt) (Wolfe et al., 1990, as cited in EPA, 2000). Follow-up studies through the early 1990s suggested that this group did not have an increased risk of cancer death, although it was noted that in general the Ranch Hands did not have elevated TCDD levels significantly above background and were still a relatively young group, taking into account a 20-year cancer latency period (EPA, 2000).

In 1976, an unintended industrial release in Seveso, Italy, exposed a large population of people to TCDD. At the time of the release, serum levels of TCDD were as high as 56,000 ppt for the most highly exposed children, who developed severe chloracne (Mocarelli et al., 1991, as cited in EPA, 2000). Twenty years after the release, tissue plasma levels of TCDD were measured in randomly selected residents. Those from the area with the greatest initial exposure had geometric mean TCDD levels of 53.2 ppt (n = 7; range 1.2–89.9 ppt); those with the next greatest exposure had 11.0 ppt (n = 51); and those with the lowest exposure had 4.9 ppt (n = 52) (Landi et al., 1996, 1998, as cited in EPA, 2000). In a 15-year follow-up, the overall cancer mortality in the residents did not appear to be increased compared with a control group from outside the exposed area, although significant excess mortality risks occurred in the lowest exposure group for esophageal cancer in males and bone cancer in females (Bertazzi et al., 1997, 1998, as cited in EPA, 2000). EPA reports that the cancer data appear to be contradictory and are difficult to interpret because of the small number of cases, problems with exposure classification, and a 15-year rather than a 20-year follow-up (EPA, 2000).

Two significant occurrences of poisoning of food oils with PCBs and furans have been reported in Japan. The first occurred in 1968 in the Yusho incident, in which 1,900 people unintentionally consumed up to 2 g of rice oil that contained a 1:250 ratio of furans to PCBs. Tissue studies indicated that both the furans and the PCBs were retained for many years. There was a significantly increased risk of liver cancer in males 15 years after the incident, although determination of rice oil as the culprit was problematic (Kuratsune et al., 1988, as cited in EPA, 2000). Noncancer effects included acneform eruptions, hyperpigmentation, and hyperkeratosis and ocular lesions. The second incident (Yu-chen) was a contamination of cooking oil in Taiwan in 1979 that affected 2,000 people and resulted in similar noncancer effects. Six months after the incident, blood PCB levels ranged from 11 to 720 ppb with a mean value of 49 ppb and most values less than 100 ppb (Chen et al., 1980, as cited in EPA, 2000).

There have been few epidemiological investigations of the health effects of DLCs in populations with no extraordinary exposure circumstances. A large population of children from an industrial region in the Netherlands is currently being studied for a variety of health outcomes in relation to exposure to DLCs (Vreugdenhil et al., 2002), and Koopman-Esseboom and colleagues (1994a) examined DLC levels in blood and human milk in two cohorts, one industrial and one rural, in the Netherlands (see below).

Cancer. Epidemiological studies on carcinogenicity from general exposures to DLCs are sparse, but experimental animal studies provide strong support of carcinogenicity. The IARC monographs (1997) include no cancer epidemiology studies regarding general exposures to CDDs and express no opinion about the potential for carcinogenicity from such exposures. All of the investigations described in the monographs are cohort studies of workers with known, inferred, or presumed exposure to CDDs (usually TCDD); cohort studies of the Seveso population with unintentional TCDD exposure; or case-control studies in which subjects had known or expected contact, usually on the basis of occupation, with chlorophenoxy herbicides that likely contained TCDD. The monograph on CDFs describes a few studies of cancer in humans, including investigations that showed a moderate increase in cancer incidence and mortality in Swedish fishermen and consumers of Baltic Sea fish. Stomach cancer incidences in the Swedish consumers were 2.2 (1.3–3.5) and 1.6 (1.0–2.4) per thousand, compared with consumers of Atlantic Ocean fish and regional referents, respectively. Squamous-cell skin cancer rates were 1.9 (1.2–3.1) and 2.3 (1.5–3.5) per thousand compared with Atlantic Ocean fish consumers and the referent group, respectively (IARC, 1997).

EPA (2000) includes no cancer epidemiology studies regarding general exposures to DLCs, but it does provide dose-response data for populations that are highly exposed to DLCs. The relative risk for total cancer for the lowest-exposed stratum in the epidemiological studies cited by EPA ranged from 0.9 to 1.24 (see Appendix Table A-3). However, as reported by EPA (2000), in some exposed populations such as those in Seveso, Italy, the calculated relative risk for specific cancers was considerably higher (e.g., the relative risk for connective and soft tissue sarcoma in males was 2.8). In studies that have identified specific cancers arising after DLC exposure, the evidence is equivocal. However, the cumulative evidence of all studies is consistent with the possibility that DLC exposure is carcinogenic.

None of the evaluations reviewed by the committee (AEA Technology, 1999; ATSDR, 1998; EPA, 2000; Fiedler et al., 2000; IARC, 1997; Scientific Committee on Food, 2000, 2001) derives a conclusion about the carcinogenic potential of DLCs to humans solely from general exposures.

Noncancer Effects. Several potential noncancer health effects from general exposures to DLCs have been reported in recent evaluations of DLC toxicity (ATSDR, 1998; EPA, 2000; Fiedler et al., 2000; IARC, 1997). These evaluations indicate that there are possible adverse neurobehavioral effects and changes in the distribution of thyroid hormone concentrations in breastfed infants compared with formula-fed infants. Koopman-Esseboom and colleagues (1994b) found a negative correlation between extended DLC exposure and thyroid hormone levels in infants and mothers. The Scientific Committee on Food (2000, 2001) also reports neurobehavioral effects and changes in thyroid hormone status in breastfed infants, but stated that these adverse effects were “subtle, within the normal range, and considered without clinical relevance,” whereas Weisglas-Kuperus and coworkers (2000) and Patandin and coworkers (1998) concluded that DLCs have a negative effect on neurodevelopment, birth weight, and immunity. EPA (2000) identifies one study that found changes in the distribution of alanine aminotransferase and aspartate aminotransferase concentrations in breastfed infants.

Adverse effects on infant birth weight, neurodevelopment, neurobehavior, thyroid hormone status, and the immune system in children have been reported (AEA Technology, 1999). These observations were made in infants in the general population and in children whose mothers ate DLC-contaminated fish from Lake Michigan. Neurodevelopmental delays in breastfed infants in a Dutch study were also reported (Huisman et al., 1995). A negative correlation was found between neurodevelopment in infants and breast-milk concentrations of PCBs. At 42 months of age, the cognitive decrement remained (Patandin et al., 1999), although the psychomotor deficits seen at younger ages had disappeared (Lanting et al., 1998). A study of early learning in school-age Dutch children found that prenatal exposures to DLCs resulted in impaired cognitive and motor abilities, which could persist when the home environment was less than optimal, but no long-term impairment could be measured in children raised in more optimal environments (Vreugdenhil et al., 2002). One evaluation (AEA Technology, 1999) notes that people with exposure to TCDD from the Times Beach contamination showed reduced immune response and changes in T-lymphocyte differentiation, and people eating relatively large amounts of Baltic Sea fish showed changes in T-cell lymphocytes, but IARC (1997) reports contradictory findings about cell-mediated immunity in the Times Beach subjects. EPA (2000) considers the data about immunological effects from exposures to DLCs to be inconclusive.

Effects Observed in Humans at Higher Exposures

Cancer. The IARC (1997) evaluation discusses the body of epidemiological literature on CDDs, but it focuses on the high-exposure cohorts with documented TCDD exposure (all occupational exposures) in its evaluation of whether CDDs are carcinogenic to humans. It concludes that the overall standardized mortality rate for all cancer types combined was 1.4 per thousand (95 percent confidence interval, 1.2–1.6) for the most highly exposed subgroups in these occupational cohorts; statistically significant dose-response trends in two of the studies strengthen that opinion.

IARC also concludes, however, that the epidemiological data provide “limited evidence” of a carcinogenic effect of TCDD in humans, although the IARC monographs (1997) upgrade 2,3,7,8-TCDD from classification 2A, Probably Carcinogenic to Humans, to 1, Carcinogenic to Humans. In its monograph on the carcinogenicity of CDFs, IARC notes that male victims of the Yusho incident had a threefold excess of liver cancer mortality, but that no such excess occurred in victims of the Yu-cheng incident, and finds the evidence for the carcinogenicity of CDFs in humans to be inadequate.

The reports of the Scientific Committee on Food (2000, 2001) rely largely on the IARC (1997) evaluation and state that TCDD should be regarded as a human carcinogen, though not a direct-acting genotoxin. The report prepared by Fiedler and colleagues (2000) repeats the IARC (1997) evaluation of the carcinogenicity of CDDs. AEA Technology (1999) concludes that the epidemiological data suggest that TCDD exposure increases the rates of all cancers. On the basis of the epidemiological and animal studies, ATSDR (1998) concludes that TCDD may be a human carcinogen.

EPA (2000) considers TCDD to be a human carcinogen and that other DLCs are likely to be human carcinogens, based on a combination of epidemiological and animal cancer studies and mechanistic information. The epidemiological data alone do not demonstrate a causal association between exposure and cancer, but suggest that the compounds are multisite carcinogens, increasing cancer at all sites, lung cancer, and perhaps other particular cancers. EPA (2000) describes TCDD as a nongenotoxic carcinogen and a potent promoter.

Noncancer Effects. A number of noncancer human health effects have been associated with high exposures to DLCs. These effects are listed below.

  • Chloracne and other dermal effects (ATSDR, 1998; EPA, 2000; Fiedler et al., 2000; IARC, 1997).
  • Changes (AEA Technology, 1999; ATSDR, 1998; Fiedler et al., 2000; IARC, 1997) or possible changes (EPA, 2000; Scientific Committee on Food, 2000, 2001) in glucose metabolism and in diabetes risk.
  • Alterations (ATSDR, 1998) or possible alterations (EPA, 2000) in thyroid function.
  • Alterations in growth and development (AEA Technology, 1999; IARC, 1997; Scientific Committee on Food, 2000, 2001), neurodevelopment (AEA Technology, 1999; IARC, 1997), and neurobehavior (AEA Technology, 1999; IARC, 1997; Scientific Committee on Food, 2000, 2001). EPA (2000) considers postnatal developmental effects on neurobehavior to be possibly related to exposures to DLCs. Fiedler and colleagues (2000) note that there was an altered sex ratio among births after the Seveso unintended exposure.
  • Increased gamma-glutamyl transferase concentrations (EPA, 2000; Scientific Committee on Food, 2000, 2001).
  • Altered concentrations of reproductive hormones in men (EPA, 2000).
  • Alterations in liver function (Fiedler et al., 2000; IARC, 1997) and hepatic effects (ATSDR, 1998).
  • Possibly altered serum lipid (EPA, 2000; Scientific Committee on Food, 2000, 2001) and cholesterol concentrations (EPA, 2000).
  • Possibly altered alanine aminotransferase and aspartate aminotransferase concentrations (EPA, 2000).
  • Alterations in the immune system (Fiedler et al., 2000; IARC, 1997).
  • Possible ocular changes (ATSDR, 1998; IARC, 1997).
  • Increased mortality from cardiovascular disease (AEA Technology, 1999; Scientific Committee on Food, 2000, 2001).

Toxicity Benchmarks

Estimates of Tolerable Intakes

Several governmental bodies have derived or recommended acceptable daily intakes or similar parameters for TCDD or DLCs as a group (AEA Technology, 1999; ATSDR, 1998; EPA, 2000; Fiedler et al., 2000; Scientific Committee on Food, 2000, 2001). These guidance levels are summarized in Table 2-2.

TABLE 2-2. Estimates of Tolerable Intakes of Dioxins and Dioxin-like Compounds.


Estimates of Tolerable Intakes of Dioxins and Dioxin-like Compounds.

ATSDR (1997) defines a minimal risk level (MRL) for a hazardous substance (e.g., DLCs) as an estimate of daily human exposure that is likely to be without appreciable risk of adverse noncancer health effects over a specified duration and route of exposure. For 2,3,7,8-TCDD, ATSDR (1998) derives MRLs for oral exposure to over three intervals: acute (14 days or less), intermediate (15–364 days), and chronic (1 year or more). An MRL is “an estimate of the daily human exposure to a hazardous substance that is likely to be without appreciable risk of adverse non-cancer health effects over a specified duration of exposure” (ATSDR, 1998); the MRL does not pertain to cancer. The MRLs for TCDD are, respectively, 0.0002 μg/kg/d (200 pg/kg/d), 0.00002 μg/kg/d (20 pg/kg/d), and 0.000001 μg/kg/d (1 pg/kg/d). The acute MRL is based on immunological effects in female mice, the intermediate MRL on immunological effects in guinea pigs, and the chronic MRL on developmental effects in rhesus monkeys. In each case, uncertainty factors are applied to address animal-to-human extrapolation, interindividual variation in response, and (if necessary) a low-effect to no-effect dose extrapolation.

The report by Fiedler and colleagues (2000) reiterates the World Health Organization (WHO)-recommended tolerable daily intake (TDI) of DLCs of 1 to 4 pg TEQ/kg/d and also WHO's recommendation that exposures should be reduced as much as possible. Similarly, the AEA Technology (1999) report encourages member states of the European Union to adopt the recent WHO recommendation, and notes that PCBs contribute about half of dietary TEQ exposure. The Scientific Committee on Food (2000, 2001) derived a tolerable weekly intake (TWI) of DLCs based on TCDD body burdens associated with sensitive effects in experimental animals: developmental and reproductive effects in rats and monkeys and endometriosis in monkeys. Body burdens associated with the lowest-observed-adverse-effect levels in the relevant studies ranged from about 30 to 100 ng TCDD/kg. The estimated human dietary intakes needed to produce these body burdens were then calculated, and safety factors (ranging from 3 to 10) were applied. The lowest TDI thus calculated was 2 pg TCDD/kg, corresponding to a TWI of 14 pg TCDD/kg. The TWI is intended to apply to all DLCs expressed as TEQs using the WHO 1998 TEF system. Cancer is not considered one of the more important adverse effects of background DLC exposure; the Scientific Committee on Food (2000, 2001) believes that TCDD is a nongenotoxic carcinogen best evaluated with a threshold model, and that TCDD body burdens associated with cancer in laboratory animal bioassays and high-exposure human populations are “several orders of magnitude higher” than body burdens in the general population.

The IARC (1997) and EPA (2000) reports make no quantitative recommendations about intake or exposure to DLCs. EPA (2000) notes that if it were to develop reference doses or concentrations (life-long tolerable intakes for noncancer health effects), the values would be less than current exposures and, therefore, not useful for risk management. (Reference doses and concentrations are normally used to characterize the health risk posed by incremental exposures to compounds in the absence of significant background exposures.) IARC (1997) reports intake guidelines from several countries:

  • Canada, 10 pg I-TEQ/kg/d (CDDs and CDFs)
  • Nordic countries, 0 to 35 pg TCDD/kg/wk
  • Netherlands, 1 pg dioxin/kg/d
  • Sweden, 5 pg dioxin/kg/d
  • Japan, 10 pg/kg/d (CDDs and CDFs)

EPA (2000) derives quantitative upper-bound estimates of the excess lifetime cancer risk posed by exposure to DLCs. Cancer potencies (or slope factors) are derived from three occupational epidemiology investigations and range from 9 × 10–3 pg/kg/d TCDD (for all cancers) to 3 × 10–4 pg/kg/d TCDD (for lung cancer specifically).1 A meta-analysis of these studies yields a cancer potency of 1 × 10–3 pg/kg/d TCDD, which is EPA's preferred value based on human data. Potencies based on dose-response data from laboratory animal bioassays of TCDD range from 3 × 10–3 pg/kg/d to 1 × 10–4 pg/kg/d. EPA's preferred value based on animal data is 1 × 10–3 pg/kg/d TCDD. Overall, EPA (2000) believes a slope of 1 × 10–3 pg/kg/d (for all cancers) is most appropriate for TCDD. (This slope implies that a daily dose of 0.001 pg TCDD/kg poses an upper-bound excess lifetime cancer risk of 1 in 1 million.) In developing cancer potencies, EPA (2000) fitted linear models to study datasets to derive estimates of the 1 percent effective dose (ED01) and the lower 95 percent confidence limit on the ED01 (LED01) either for all cancers combined or for particular cancers (e.g., lung, liver). In that analysis, dose meant average excess body burden, and intakes corresponding to the ED01 and LED01 values were computed. A linear model was used because, in both the human and rodent datasets, there were too few dose levels to support more complicated models. The other reports that were examined (AEA Technology, 1999; ATSDR, 1998; Fiedler et al., 2000; IARC, 1997; Scientific Committee on Food, 2000, 2001) do not contain slope factors for TCDD or other DLCs.

Risk Estimates for Current Exposure

ATSDR (1998) does not comment on the degree of health risk posed by current exposures to DLCs. IARC (1997) does not comment on the issue with respect to CDFs and states only that its evaluation “[does] not permit conclusions to be drawn on the human health risks from background exposures to 2,3,7,8-TCDD.” Fiedler and colleagues (2000) repeat IARC's (1997) statement verbatim, and also states that “subtle effects” of DLC exposure may be occurring in the general population; however, no quantitative risk assessment is performed. AEA Technology (1999) also concludes that subtle health effects may be occurring, without giving quantitative risk estimates. The reports of the Scientific Committee on Food (2000, 2001) do not perform a quantitative risk assessment, but they note that (1) current body burdens of TCDD are much lower than those associated with cancer in experimental and epidemiology reports, and (2) “a considerable proportion of the European population [exceeds] the TWI derived by the Committee.”

Based on its estimate of the cancer potency of DLCs, 1 × 10–3 pg TEQ/kg/d, EPA (2000) concludes that intakes of about 3 pg TEQ/kg/d in the general population (three times the current intake level), pose an upper-bound, excess cancer risk greater than 1 in 1,000. If a small part of the population were to receive intakes two to three times higher than the upper-bound mean of 3 pg TEQ/kg/d, as EPA (2000) concludes, the excess cancer risk for those individuals would be proportionally higher as well.

EPA (2000) does not generate a specific number describing the risk of noncancer health effects posed by current exposures to, or body burdens of, DLCs. Rather, it calculates the margin of exposure between current intakes or body burdens and toxicological “points of departure.” A point of departure is a value near the low end of the dose-response curve for a sensitive health endpoint, such as a no-observed-adverse-effect level, a lowest-observed-adverse-effect level, or an ED01, based on human or laboratory animal data. If the margins of exposure are 100 to 1,000 or more, EPA considers it unlikely that significant human health effects would occur at background exposures or at incremental exposures plus background. EPA's (2000) calculated margins of exposure range from 1.2 to 238, with some values less than 10, based on several points of departure and a human body burden of 5 ng TEQ/kg. Most points of departure appear to be ED01 or LED01 estimated from laboratory animal experiments, derived by fitting certain models (which allowed for nonlinear forms) to the dose-response data.

Body Burdens and Intakes of DLCs

Data on body burdens of DLCs for the general population and for susceptible groups are presented below. There are several issues associated with the estimation and use of body burdens, including the validity of assumptions about the percent body fat (typically assumed to be 25 percent) for lipid-adjusted tissue concentrations, the uncertainty associated with intake rates and half-lives, and species extrapolations from short-term animal studies to steady-state human exposures (EPA, 2000).

General Population

Body Burdens. Recent body burden data (DLCs were measured in blood or adipose tissue) for persons living in Europe and North America are presented in several reports (AEA Technology, 1999; ATSDR, 1998; EPA, 2000; IARC, 1997). These data are summarized below.

  • The range of mean CDD/CDF body burdens for the general population in the United States is 8.5 pg I-TEQ/g of lipid to 50.0 pg TEQDF-WHO98/g of lipid.
  • EPA's (2000) preferred estimate of the mean body burden of CDD/CDF in the U. S. general population is 21.1 pg TEQDF-WHO98/g of lipid.
  • Dioxin-like PCBs have not been routinely assayed for in human tissues.
  • EPA's (2000) best estimate of the mean body burden of CDD, CDF, and PCBs in the U.S. general population is 25.4 pg TEQDFP-WHO98/g of lipid. PCBs contribute 5.3 pg TEQ/g of this body burden.
  • The range of mean CDD/CDF body burdens in the general populations of European and Scandinavian countries is 2.1 pg Nordic-TEQ/g of lipid to 57 pg I-TEQ/g of lipid.

Intake of DLCs. Dietary intake is widely believed to contribute up to 90 percent of human exposure to DLCs (see Chapter 5). Only the EPA (2000) document contains original estimates, and many of the other documents rely on the same published reports of intakes. The majority of intake estimates are based on a combination of contaminant concentrations in foods and food-consumption rates, but EPA (2000) also uses toxicokinetic modeling to estimate the average intakes that produce current body burdens of DLCs. The data are summarized below.

  • The best estimate of current CDD/CDF intake for adults from all sources in the United States is 41 pg TEQDF-WHO98/d, or 0.59 pg TEQDF-WHO98/kg/ d.
  • The best estimate of current dioxin-like PCB intake for adults from all sources in the United States is 25.2 pg TEQP-WHO98/d, or 0.36 pg TEQP-WHO98/kg/d.
  • Based on the two previous estimates, the best estimate of current CDD, CDF, and PCB intake for adults from all sources in the United States is about 65 pg TEQDFP-WHO98/d, or about 1 pg TEQDFP-WHO98/kg/d.
  • The preceding estimates are based on analysis of diet. Toxicokinetic modeling of the average past intake that would produce the current average adult body burden of 25.4 pg TEQDFP-WHO98/g of lipid gives 146 pg TEQDFP-WHO98/d. This suggests that (1) past intakes, on average, were considerably higher than current intakes, and (2) current body burdens are not at steady state given current intakes.
  • European estimates of mean adult dietary intakes of CDD/CDF range from about 0.4 to 1.5 pg I-TEQ/kg/d.
  • Intakes of CDD/CDF and PCBs among children are estimated to be higher than in adults on a body-weight basis, but decrease with age, both in the United States and the United Kingdom. In the United States, combined intakes are estimated to be 3.6 pg TEQDF-WHO98/kg/d (54 pg TEQDF-WHO98/d) at 1 to 5 years of age, 1.96 pg TEQDF-WHO98/kg/d (59 pg TEQDF-WHO98/d) at 6 to 11 years of age, and 1.00 pg TEQDF-WHO98/kg/d (64 pg TEQDF-WHO98/d) at 12 to 19 years of age; similar declines were seen in the United Kingdom.
  • EPA estimates that 70 percent of dietary TEQ comes from five compounds: TCDD, 14 pentachlorodibenzo-p-dioxins (1-PeCDD), 14 pentachlorodibenzo-p-furans (1-PeCDF), 10 hexachlorodibenzo-p-furans (1-HxCDF), and PCB 126; of these, PCB 126 contributes the most TEQ.

EPA estimates that the greatest contributors to adult dietary penta-p-chlorodioxin and pentachlorofuran exposure from foods are (in order of highest to lowest TEQ): beef, fish and shellfish, and dairy products and milk, and the greatest estimated contributors to adult PCB exposure are: fish and shellfish, beef, and dairy products and milk (EPA, 2000).

EPA (2000) estimates that intakes at the “upper end” (mean plus 3 standard deviations) of the general population are two to three times higher than mean intakes, based on measured variability in both fat consumption (assumed to be closely linked to DLC intake) and in consumption rates of specific foods. Estimates of intakes at the upper end of the distribution in a few European countries are also two to three times larger than mean intakes.

Contribution of PCBs to Intakes. The contribution of PCBs to total TEQ intakes is estimated as:

  • 37 percent for the U.K. mean total dietary exposure (AEA Technology, 1999; Fiedler et al., 2000),
  • 52 percent for the Netherlands median total dietary exposure (AEA Technology, 1999; Fiedler et al., 2000),
  • 49 to 57 percent for the Swedish mean total dietary exposure (AEA Technology, 1999; Fiedler et al., 2000),
  • 48 to 62 percent for dietary intake in Spain (AEA Technology, 1999),
  • approximately 50 percent in Finland, the Netherlands, Sweden, and the United Kingdom (Scientific Committee on Food, 2000),
  • approximately 80 percent in Norway (Scientific Committee on Food, 2000), and
  • approximately 37 percent for the mean and upper-percentile U.S. total dietary exposure (EPA, 2000).

Time Trends. Several of the reviewed reports describe data suggesting that a decrease in DLC body burdens and intakes has occurred over recent decades. Specifically, EPA (2000) applied nonsteady-state toxicokinetic modeling to a database of TCDD concentrations in body lipids collected since the 1970s, the results of which suggested that TCDD intakes increased from the 1940s through the 1970s and then began to drop. During the period of peak intake, daily exposure to TCDD may have reached 1.5 to 2.0 pg/kg/d, whereas EPA's best current estimate of TCDD intake is 5.6 pg/d, or 0.08 pg/kg/d for adults. EPA (2000) also argues, on the basis of body burden data from the 1980s through the present, that average DLC body burdens in the 1980s to the early 1990s were approximately 55 pg TEQDFP-WHO98/g of lipid, whereas the current average is about 25 TEQDFP-WHO98/g of lipid. EPA further reports that:

  • The estimate of dietary intake of DLCs in U.K. foods decreased from 240 pg I-TEQDF/d in 1982 to 69 pg I-TEQDF/d in 1992, with PCB intake dropping from 156 pg TEQP-WHO94 to 46 pg TEQP-WHO94.
  • Diet samples collected in the Netherlands in 1978, 1984 to 1985, and 1994 indicate that mean intakes were, respectively, 4.2 pg I-TEQDF/kg/d, 1.8 pg I-TEQDF/kg/d, and 0.5 pg I-TEQDF/kg/d, while mean PCB intakes were 11 pg TEQP-WHO94/kg/d, 4.2 pg TEQP-WHO94/kg/d, and 1.4 pg TEQP-WHO94/kg/d.
  • In Germany, the current mean intake of CDD/CDF is estimated at 69.6 pg I-TEQDF/d, compared with 127.3 pg I-TEQDF/d in 1990.
  • The mean total concentration of CDD/CDF in blood in Germany decreased from about 720 pg/g in 1991 to about 373 pg/g in 1996.
  • AEA Technology (1999) reports three time-trend analyses of DLC intake, from the Netherlands, Germany, and the United Kingdom. The Dutch data on DLCs in foods gathered in 1978, 1984 to 1985, and 1994 indicate a statistically significant decreasing trend in adult intake over time, with a 50 percent decrease in I-TEQ/kg/d over each 5.5-year interval in that period. Dietary studies conducted in Germany in 1989 and 1995 indicate a 45 percent decrease in I-TEQ intake. Dietary studies in the United Kingdom in 1982, 1988, and 1992 suggest a 45 percent decrease in intake at each time point compared with the preceding point. All of these estimates likely pertain to the average consumer. AEA Technology (1999) relates some body burden data indicating a decrease in the mean burden of DLCs: blood sampled in Germany between 1988 and 1996 shows a 64 percent decline in I-TEQ concentrations (presumably CDD/CDF) over the period, or 12 percent per year. Those same data are also cited by Fiedler and colleagues (2000).
  • Independent of changes over time in the DLC content of food and in dietary intake, it is generally recognized that body burdens of DLCs increase with age due to the long half-lives of these compounds.
  • There is evidence of decreasing concentrations of DLCs in human breast milk:
  • —There has been an approximately 25 percent decrease in I-TEQDF in cow and human milk fat between 1990 and 1994 in Germany.
  • —In Birmingham, England, breast-milk concentrations were 37 pg I-TEQDF/g of fat in 1987 to 1988 and 18 pg I-TEQDF/g of fat in 1993 to 1994, while concentrations at similar times in Glasgow, Scotland, were 29 pg I-TEQDF/g of fat and 15 pg I-TEQDF/g of fat, respectively.
  • —I-TEQDF concentrations in human breast milk in rural areas of Finland decreased from 20.1 pg/g of fat in 1987 to 13.6 pg/g in 1992 to 1994, and in urban areas from 26.3 pg/g to 19.9 pg/g.
  • A WHO-sponsored study in 11 countries suggested an annual decrease in CDD/CDF of 7.2 percent in human breast milk between 1977 to 1987 and 1992 to 1993.

Persistence of DLCs in the Body. Intakes and body burdens of DLCs are related through the half-lives of these compounds in the body. The Scientific Committee on Food (2000, 2001) notes that half-lives for TCDD range from 5 to 11 years. At least 20 to 30 years of exposure are needed to reach steady state if the half-life of TCDD is 7.5 years (the value the Scientific Committee on Food [2000, 2001] uses in its calculations of body burden or intake); half-lives also increase with age, perhaps due to changes in metabolism and fat burden. IARC (1997) describes several studies of CDD/CDF (mostly TCDD) half-lives in humans experiencing large exposures (e.g., Ranch Hand personnel) and reports that TCDD half-lives ranged from 5.1 to 11.3 years, increasing with increasing body fat, but not with age or changing proportion of body fat. Little information was available on the half-lives of other CDD congeners; CDFs have half-lives of 3.0 to 19.6 years.

EPA (2000) compiled half-life estimates for several CDDs and CDFs. The estimates range from 3.7 to 15.7 years for CDDs and from 3 to 19.6 years for CDFs. EPA estimates the half-life of TCDD in humans to be 7.1 years, based on a 25 percent fat volume for a 70-kg individual. There is no evidence to support that weight loss significantly reduces DLC body burdens.

Sensitive Groups

A subgroup of the general population that is more sensitive to the toxic effects of exposure to DLCs is developing fetuses. Infants and young children may be considered both sensitive (due to developmental immaturity) and more highly exposed (due to intake per body mass) subgroups.

Subgroups of the general population that are exposed to higher levels of DLCs through the food supply include indigenous populations in northern North America, subsistence and sports fishermen, small populations whose food supplies are affected by local contamination, and breastfed infants.

Body Burdens of Fetuses and Infants. Estimates of the total DLC body burden of the developing fetus have been made by comparing levels in maternal and cord plasma samples obtained at birth. This estimate is based on the assumption that the DLC level obtained would be representative of in utero exposure. Koopman-Esseboom and colleagues (1994a) determined that PCB concentrations, collected on a cohort in the Netherlands in 1990, were approximately 20 percent of maternal plasma values, expressed on a concentration basis. In contrast to these findings, Jacobson and colleagues (1984), in the Michigan Maternal/ Infant Cohort Study, found that PCB levels expressed on a lipid basis were equivalent between maternal plasma and cord serum samples.

A few measurements of body burdens of DLCs in infants are available in EPA's (2000) report; they are presented in Appendix Table A-4. EPA (2000) also modeled potential body burdens under four feeding scenarios for the first year of life: formula-feeding only and breast milk for 6 weeks, 6 months, or 1 year. After the first year, all models assumed the age-appropriate intake rates for the general population. In the third and fourth scenarios, the maximum body burden of DLCs in the first year, on a lipid basis, is 46 pg TEQDFP-WHO98/g, and all scenarios converge on a body burden of about 12 pg TEQDFP-WHO98/g (lipid) around age 10 years. The intake assumptions used to calculate the body burdens during infancy are described below.

Body Burdens of Fish Consumers. People who eat large quantities of fish or who eat contaminated fish might receive unusually large doses of DLCs. EPA (2000) notes that people who consume fish with typical CDD/CDF contaminant levels, but at very high rates of intake, could receive two to five times the mean intake for the general population.

EPA (2000) describes fish-eating populations whose body burdens of DLCs (on a TEQ basis) are considerably higher than in comparison populations, but the differences are no more than threefold. Possible exceptions are studies of dioxin-like PCBs in the blood of fishermen on the Gulf of the St. Lawrence River, in the blood of Swedish fishermen, and in breast milk of Inuit women in Arctic Quebec. In the first population, PCB TEQ concentrations were 20-fold higher in the fishermen than in blood donor controls; in the second, mass concentrations of individual PCBs were 1.5 to 8 times higher in men with high fish intake compared to none; and in the third, mass concentrations of PCB congeners were three- to tenfold higher. Finally, a group of sport-fish eaters in the United States had blood concentrations of total PCB (i.e., dioxin-like and nondioxin-like) more than three times higher than controls, but the specific difference in the dioxin-like PCBs was not described. These data are included in Appendix Table A-4.

ATSDR (1998) describes a study of CDD concentrations in the blood of three groups of Swedes: high-fish consumers, moderate-fish consumers, and nonfish consumers. TEQ blood levels were 3.6 times higher in the high-fish consumers (63.5 pg TEQ/g of lipid) than in the non-fish consumers (17.5 pg TEQ/g of lipid). ATSDR (1998) also reports an investigation of DLCs in the blood of Inuits in Canada, which found significantly higher concentrations of CDD, CDF, and PCB. These data are also shown in Appendix Table A-4.

Body Burdens of People Residing Near Local Sources of Contamination. EPA (2000) describes a number of investigations of DLC body burdens in people residing near local sources of contamination, such as wood preservative facilities, reclamation plants, and steel factories. These data are summarized in Appendix Table A-4.

DLC Intake of Infants. ATSDR estimates of DLC intake by breastfed infants are given in Appendix Table A-5. EPA (2000) models the intake of DLCs by infants during 12 months of nursing using a dosing equation that requires, among other inputs, the concentration in milk fat, milk ingestion rate, and infant body weight. The concentration of CDD/CDF/PCB in milk fat is assumed to be 25 pg TEQDFP-WHO98/g initially, EPA's best estimate of the mean body burden in the general population (per gram of lipid). Using this model, EPA estimates that DLC concentrations in breast milk decline by 30 to 50 percent after 1 year of breastfeeding. The infant's intakes at birth, 6 months, and 1 year of age are thus 242 pg TEQDFP-WHO98/kg/d, 55 pg TEQDFP-WHO98/kg/d, and 22 pg TEQDFP-WHO98/ kg/d, respectively; the average over the year is 92 pg TEQDFP-WHO98/kg/d (EPA, 2000). This model indicates that 1 year of breastfeeding contributes 12 percent of the lifetime dose of DLCs.

Although approximately 52 percent of women initiate breastfeeding, only about 20 percent are still breastfeeding after 6 months (IOM, 1991). Thus, the greatest number of infants exposed to DLCs through breastfeeding would likely be exposed during the first 6 months of life. In addition to its own model of DLC exposure in infants, the EPA (2000) report also reviews a previously published model for DLC exposure through breast milk over time. This model estimated that TCDD levels in breast milk declined by 20 percent every 3 months from initial exposure (Patandin et al., 1999), suggesting that the greatest exposure would occur in the first 12 weeks of breastfeeding.

Using data on concentrations of CDD/CDF in human milk from European countries, AEA Technology (1999) estimates that the average daily intake by infants in 1993 could have ranged from 106 pg I-TEQ/kg/d (rural areas) to 144 pg I-TEQ/kg/d (industrial areas). Estimates for the United Kingdom are 110 pg I-TEQ/kg/d at 2 months of age and 26 pg I-TEQ/kg/d at 10 months of age. Fiedler and colleagues (2000) and the Scientific Committee on Food (2000, 2001) state that intakes of DLCs by infants are one to two orders of magnitude greater than that for adults.

ATSDR (1998) reports estimates of CDD/CDF intakes in TEQ for breastfed infants of 83.1 pg TEQ/kg/d and 35 to 53 pg TEQ/kg/d.

DLC Intakes of Fish Consumers. AEA Technology (1999) reports Swedish data suggesting that Baltic Sea fishermen had 6.3 times the mean dietary intake of CDD/CDF in Nordic TEQ, at 11.7 to 12.5 pg N-TEQ/kg/d.

DLC Intakes of People Residing Near Local Sources of Contamination. Information on intakes of DLCs by people near local sources of contamination is presented in Appendix Table A-5.


As the toxic effects of DLCs were recognized, several countries, including the United States, implemented regulations designed to reduce or control exposure to DLCs. The main focus of DLC regulatory activity has been to reduce the release of DLCs into the environment, particularly through the control of stack emissions from waste incinerators. These efforts have yielded significant reductions in environmental emissions since the 1970s. Regulations have also been implemented that focus on DLC uptake rather than source reduction, limiting total human body burden levels. In recent years, as food has been identified as the primary route to human exposure, several new regulations and programs have been implemented to reduce DLC contamination in food. Within the United States, because of the complex pathway of DLC exposure (see Chapter 3), DLC regulation responsibilities can fall across a number of different federal and state agencies and departments for the environment, agriculture, public health, and food safety.

Tolerable Intakes

Total human exposures to DLCs in the forms of daily, weekly, and monthly tolerable intakes have been established by a number of countries and international organizations. These limits focus on exposure to DLCs and potential health effects, without regard to the source.

United States

ATSDR (1998) has established human MRLs for hazardous waste sites in the United States. These MRLs, which serve as a screening tool, may also be viewed as a mechanism to identify those hazardous waste sites that are not expected to cause adverse health effects. Three temporal exposure scenarios with three different health endpoints of concern were considered (see Table 2-3).

TABLE 2-3. Human Exposure Limits for Hazardous Waste Site Cleanup in the United States (Agency for Toxic Substances and Disease Registry Minimal Risk Levels).


Human Exposure Limits for Hazardous Waste Site Cleanup in the United States (Agency for Toxic Substances and Disease Registry Minimal Risk Levels).

Other Countries and Organizations

WHO, the WHO/Food and Agriculture Organization of the United Nations (FAO) Joint Expert Committee on Food Additives (JECFA), and the European Commission (EC) have established daily, weekly, and/or monthly tolerable intakes for DLCs. Australia and Japan have also adopted tolerable DLC intake levels (see Appendix Table A-6).

JECFA. In 2001, JECFA established a provisional tolerable monthly intake of 70 pg TEQ/kg of bodyweight/mo. Additionally, in 1998 it established a range of DLC TDIs of 1 to 4 pg WHO-TEQ/kg of bodyweight (Tran et al., 2002).

EC. The EC has established a TDI of 2 pg TEQ/kg/d (Tran et al., 2002).

Australia. The Australian Commonwealth Department of Health and Aging has supported a national health standard tolerable monthly intake of 70 pg TEQ/ kg of bodyweight for DLCs, which conforms to the JECFA tolerable intake and lies at the mid-point of the WHO guideline. The National Health and Medical Research Council released this proposal for public comment in late January 2002 (Tran et al., 2002).

Japan. Public concern in Japan led to the passing of the Law Concerning Special Measures Against Dioxin in July 1999. This law set the level of TDI of DLCs at 4 pg TEQ/kg/d, in addition to establishing environmental quality standards (Tran et al., 2002).

Environmental Regulations

DLCs are regulated in a number of countries through the establishment of DLC limits for specific environmental exposure media (e.g., air, water, soil/ sediment). In the following sections, more detailed summaries of existing DLC regulations in various countries are provided.

United States

U.S. federal regulations cover two basic areas with regard to DLCs: air emissions and water. There are a number of environmental acts that give EPA jurisdiction to create regulations regarding DLCs in the environment, including the Clean Air Act, the Clean Water Act, the Safe Drinking Water Act, and the Resource Conservation and Recovery Act. Appendix Table A-7 details the current federal regulations for DLCs.

In general, the air emissions regulations are promulgated under the Clean Air Act, and to some extent, the Resource Conservation and Recovery Act. Air emissions regulations are codified in Title 40 of the Code of Federal Regulations, Part 60. A variety of incinerators and combustors are regulated in 40 C.F.R. part 60, including municipal waste combustors, hospital/medical/infectious waste incinerators, and hazardous waste incinerators. Regulation of these sources of DLCs is fairly recent, with most of the laws coming into force in the late 1990s. Limits are set for both new and existing units and are usually given as a total amount of dioxins and furans.

DLC levels in water are regulated under the Safe Drinking Water Act, which was implemented in 1994. The maximum contaminant level, which is the legally enforceable limit, was set at 3 × 10–8 mg/L. A maximum contaminant level goal of zero was set as a voluntary health goal, but it is not legally enforceable.

In addition to federal regulations, some states have also established DLC regulations and guidelines. Regulations regarding the presence of DLCs in the air or water from California, Illinois, Massachusetts, Missouri, New Jersey, New York, and Wisconsin are provided in Appendix Table A-8. As with the federal regulations, many of the state laws regarding DLCs are recent, and some do not come into force for several more years. Because waste incinerators have been some of the largest contributors to DLC levels in the air, they have been the main focus of many state regulations.

Other Countries and Organizations

Many countries and multinational organizations also have established emission-reduction regulations. Air and water emissions from waste incineration, water quality, and risk management are the primary focus of these regulations. Many of these countries have programs that are newly established, so no data exist on their effectiveness.

EC. The EC has implemented several directives and regulations that are intended to control or reduce the release of DLCs into the environment, as presented in Appendix Table A-9. Member states are legally required to incorporate EC directives into their national legislation within a specified period of time. Some countries go beyond the requirements of the EC directive by (1) establishing target concentrations that are more stringent than those of the directives, (2) establishing target concentrations where none was set by the directives, or (3) addressing processes or media not regulated by existing directives. Appendix Table A-10 presents a detailed summary of each member state's DLC legislation and guidelines that go beyond the EC directives. Appendix Table A-11 presents existing limits in a summary form.

Australia. In its 2001–2002 Federal Budget, the Australian Commonwealth Government announced funding of $5 million over four years for a national program to reduce DLCs in the environment. The State and Territory Environment Ministers endorsed this National Dioxins Program in June 2001. The program is managed by Environment Australia, cooperatively with the states and other commonwealth agencies. The program consists of three stages: an initial-data gathering phase, assessment of the impact of DLCs on human health and the environment, and reduction or, where feasible, elimination of releases of DLCs in Australia. The first task of the National Dioxins Program will be to gather as much data as possible about DLCs in Australia, including levels occurring in food and people. Additionally, the program will develop an updated, comprehensive inventory of sources and emissions of DLCs.

Japan. The passing of the Law Concerning Special Measures Against Dioxin in July 1999 was in response to public concern about the levels of DLCs in Japan. This law states that “Businesses shall take necessary measures to prevent environmental pollution by DLCs that are generated in the course of conducting their business activities, as well as measures to remove such DLCs, and must also cooperate with measures taken by the federal and local governments for prevention of environmental pollutions by DLCs and for their removal.” Additionally, this law set the level of TDI of DLCs, established environmental quality standards for air, water, and soil, and set stricter standards to regulate emissions to air and water. These standards are summarized in Appendix Table A-12.

Feeds and Foods

As DLC exposure has been linked to food, many countries and multinational organizations have begun to consider ways to reduce this risk. They are working to develop or have established regulations and guidelines for acceptable contamination levels and management practices for animal feeds and foods.

United States

Currently, there are no U.S. legal standards (tolerances) for the presence of dioxins, as a class, in feeds or foods (Appendix Table A-13), although there are tolerances for PCBs in animal feeds and human foods (21 C.F.R. §109.30) and for an action level for PCBs in meat (FDA Compliance Policy Guide 565.200). The U.S. Food and Drug Administration (FDA), the U.S. Department of Agriculture (USDA), and EPA all conduct monitoring and studies on the incidence of DLCs in feeds and foods and are actively researching its sources and methods to limit human exposure through food. FDA (2000) has also issued revised guidance entitled “Guidelines for Industry: Dioxin in Anti-caking Agents Used in Animal Feed and Feed Ingredients.”

Other Countries and Organizations

Countries or entities other than the United States have established acceptable limits for various specific food types. Other regulations and guidelines are under consideration.

EC. In November 2001, EC adopted new regulations that set legally binding maximum limits for the presence of polychlorinated dibenzo-p-dioxins (PCDD) and polychlorinated dibenzofurans (PCDF) in terms of pg WHO-PCDD/F-TEQ/ g of fat or product for feeds and foods. This regulation took effect in July 2002. According to the EC's Community Strategy for Dioxins, Furans, and Polychlorinated Biphenyls, these maximum limits are set at a strict but feasible level in order to discard unacceptably contaminated products (Scientific Committee on Food, 2001). It is intended that these levels will be revised to include dioxin-like PCBs, and that the levels will decrease over time. EC also foresees establishing target levels that will reasonably ensure that a large majority of the European population will be within its TWI for DLCs. These target levels would be the driving force behind measures necessary to further reduce emissions of DLCs into the environment.

Additionally, in March 2002, EC recommended a series of action limits for the DLC content in feeds and foods. These levels are not legally binding, but if they are exceeded, it should trigger an investigation of possible contamination sources by EC member-state authorities. The levels are higher than the legally binding content limits adopted the previous year. EC recommended that authorities monitor food and take measures to reduce or eliminate contamination sources when DLC levels are found above the action threshold. These legally nonbinding action levels and legally binding levels are presented in Appendix Tables A-14, A-15, and A-16.

WHO/FAO. WHO, in collaboration with FAO through the joint WHO/FAO Codex Alimentarius Commission, is considering establishing guideline levels for DLCs in foods. Currently, there is no JECFA standard for DLCs in foods.

Monitoring and Research Programs

In order to determine the extent of and changes in DLC contamination and human exposures, it is necessary to establish actual levels of DLCs in food and the environment in which those foods are produced. In addition, basic and applied research on such topics as establishing pathways, the effectiveness of interventions, and mechanisms for the fate and transport of DLCs are very important to understanding the implication of DLCs in the food supply.

Many countries have established monitoring programs for DLCs or have incorporated DLC analysis into on-going monitoring programs. An understanding of the patterns and levels of DLC residues in foods, feeds, human tissues, and the environment can be used in contamination and exposure reduction efforts.

Monitoring in the United States

Most DLC monitoring programs in the United States are conducted at the federal level, although some are also conducted at the state level. At both levels, the majority of the ongoing programs are environmental sampling (air, soil, and sediment monitoring). It appears that at the present time, monitoring of feeds and foods are only being carried out by federal agencies, such as FDA, EPA, and USDA's Food Safety and Inspection Service. These are discussed below.

Wisconsin, New York, Illinois, and California have some form of environmental monitoring, either broad surveys or more targeted studies of identified locations or issues. A complete assessment, at the state level, of DLC monitoring and regulatory activities would necessitate a comprehensive 50-state survey. No monitoring of food takes place at the state level. The U.S. federal and state environmental and food monitoring programs are summarized in Appendix Tables A-17 and A-18, respectively.

Environmental, Feed, and Food Monitoring. FDA currently uses a subsample of between 200 and 300 food items from the Total Diet Study (TDS) to analyze for DLCs. This analysis is conducted separately from the analysis in the TDS (see Chapter 5). The sampling is conducted once per year and has been completed up to 2001. The food samples typically chosen are those that have not previously been analyzed for DLCs or those that may contain animal fats.

In addition to TDS sampling, FDA conducts a targeted sampling study aimed at foods that are potentially variable in contaminant levels, such as fish, vegetable oils, and dietary supplements. For example, a number of different fish varieties may be sampled rather than just one species in order to understand the sources of DLCs and the variability across species. This sampling is conducted on a yearly basis and generally includes 500 to 1,000 samples.

FDA also follows up on any unusually high values in any of their studies to determine sources of DLCs in the food supply. FDA does not target any specific imported foods, but it tries to create a representative sample of the diet of the general U.S. population, which may include imported foods. When FDA does investigate an imported food, it tends to look at imports from the top three countries for that product.

USDA and EPA conducted a joint program of three surveys for DLCs in beef, pork, and poultry, using 60 to 80 samples in each survey taken from federally inspected slaughterhouses in the United States. These studies were not repeated or continuous studies, but rather one-time events. Sixty-three beef samples were collected in May and June 1994 and examined for CDDs and CDFs. The sampling for the pork survey took place in August and September 1995 and yielded 78 final samples. It was the first survey for CDDs and CDFs in pork in the United States. Sampling was conducted in September and October 1996 for poultry, with a final sample size of 80. This poultry survey was also the first of its kind in the United States to survey for CDDs and CDFs (see later section, “Concentrations of DLCs in Foods”).

Human Biomonitoring. The Centers for Disease Control and Prevention's (CDC) National Health and Nutrition Examination Surveys (NHANES) are a series of studies that have collected data on the health and nutritional status of the U.S. population since the early 1960s. Between 1998 and 2001, the dietary component of NHANES and the USDA/Agricultural Research Service Continuing Survey of Food Intakes by Individuals merged; NHANES also became a continuous and annual survey. The sampling plan for each year follows a complex, stratified, multistage, probability cluster design to select a representative sample (approximately 5,000 individuals) of the noninstitutionalized, civilian U.S. population.

The NHANES protocol includes a home interview followed by a standardized physical examination in a mobile examination center. As part of the examination protocol, blood is obtained by venipuncture from participants aged 1 year and older, and urine specimens are collected from people aged 6 years and older. The venipuncture is performed to obtain laboratory results that provide prevalence estimates of disease, risk factors for examination components, and baseline information on the health and nutritional status of the population. Recently included among the NHANES laboratory measures are serum dioxins, furans, and coplanar PCBs.

CDC's National Center for Environmental Health, Division of Laboratory Sciences, performs the environmental chemical analysis of the blood or urine specimens collected in NHANES. The first National Report on Human Exposure to Environmental Chemicals (CDC, 2001) did not include DLC measurements. The second national report (NCEH, 2003), using data from the 1999–2000 NHANES survey, included DLC results, along with other environmental chemical analytes; data for people older than 12 years, including major demographic attributes (e.g., race and sex); and approximately 2,500 samples (from approximately 10,000 participants for the 2-year period, 5,000 participants per year). Unfortunately, none of these data were available in time for inclusion in this report. Human exposure data from the 2001–2002 NHANES survey on DLCs (and other environmental chemicals) is estimated to be released in fall 2003. It is anticipated that all four years of the NHANES data (1999–2002) will be combined for a more refined demographic analysis; it is not known when these data will be released.

Monitoring Programs of Other Countries and Organizations

EC. Appendix Table A-19 summarizes the nationally funded monitoring programs' research activities that were underway as of 1999 in each EC member state. Programs that were completed by 1999 are not included in this list.

Currently, there are several additional on-going DLC surveys in the United Kingdom, including cow's milk studies, wild and farmed fish studies, total diet studies, and a baby food study that is about to be launched (Personal communication, M. Gem, U.K. Food Standards Agency, May 3, 2002). Beginning in July 2002, EC member states are required to conduct food surveillance studies. In 2002, the United Kingdom will collect 62 food samples, concentrating on foods containing fat; the number of samples will be doubled in 2003 (Personal communication, M. Gem, U.K. Food Standards Agency, May 3, 2002). These results will be published in Food Safety Information Sheets. Several countries, including Austria, Belgium, Denmark, Finland, Germany, the Netherlands, Spain, Sweden, and the United Kingdom, have also participated in the WHO assessment of DLC concentrations in human breast milk.

WHO/FAO. WHO is involved in several monitoring studies of human breast milk and food. Through its European Center for Environment and Health in Bilthoven, the Netherlands, WHO conducts periodic studies on concentrations of DLCs in human breast milk, predominately in European countries.

Since 1976, WHO has been responsible for the Global Environment Monitoring System's Food Contamination Monitoring and Assessment Program. This program provides information on levels and trends of contaminants in food through its network of participating laboratories in over 70 countries around the world. The main objectives of the program are to collect data on levels of certain priority chemicals (including DLCs) in foods, to provide technical coordination with countries wanting to implement monitoring studies on foods, and to provide information to JECFA on contaminant levels to support its work on international standards on contaminants in foods.

Australia. DLCs are not routinely monitored in Australia, and there are very few data on the levels of DLCs in either the environment or in food. However, a survey of DLC levels in foods is currently being conducted by the Department of Health and Aging, the Australia New Zealand Food Authority, and the Australian Government Analytical Laboratories.

Japan. Japan's Law Concerning Special Measures Against Dioxins requires that businesses conduct surveillances of DLC concentrations in emission gas, effluent, ash, dust, and other compounds at least once a year. These results are to be submitted to prefectural governors. Beyond the regulatory requirements, it appears that there are not any ongoing surveillance programs in Japan (see Appendix Table A-20). However, several studies were conducted in 1998 and 1999 in order to identify DLC concentrations in blood, air/indoor air/soil, dust and soot/water, and food. These studies include:

  • The State of Dioxin Accumulation in the Human Body, Blood, Wildlife, and Food: Findings of the Fiscal 1998 Survey. Sponsored by the Ministry of the Environment: Environmental Health and Safety Division, Environmental Health Department, Environment Agency of Japan (cited in Tran et al., 2002).
  • Survey on the State of Dioxin Accumulation in Wildlife: Findings of the Fiscal 1999 Survey. Sponsored by the Ministry of the Environment: Environmental Risk Assessment Office, Environmental Health Department, Environment Agency of Japan (cited in Tran et al., 2002).
  • Detailed Study of Dioxin Exposure: Findings of the Fiscal 1999 Survey. Sponsored by the Ministry of the Environment: Environmental Risk Assessment Office, Environmental Health Department, Environment Agency of Japan (cited in Tran et al., 2002).

Canada. The Feed Program in the Canadian Food Inspection Agency (CFIA) routinely monitors for contaminants in livestock feeds as part of their National Feed Inspection Program. In a preliminary survey conducted by CFIA in 1998– 1999, 24 fishmeals and feeds and 9 fish oils were sampled across Canada and tested for dioxins, furans, and PCBs. The results are summarized in Appendix Table A-21. CFIA is currently utilizing these results to develop a continuing monitoring plan for dioxin, furans, and PCBs and future regulatory approaches.

Research Programs in the United States

While significant academic and industrial research on DLCs exists, many governmental organizations also have an active role in promoting and conducting research on DLCs. Much of this research is in complement to on-going monitoring and surveillance programs and includes a variety of modeling studies to evaluate the behavior of DLCs in the air, how they move through the environment, and how they become part of the food supply. The U.S. government has also been conducting research into the effects of exposure to DLCs on humans and examining historical data to determine how DLC levels change through time. Representative federal research programs are summarized in Appendix Table A-22.

Research Programs in Other Countries and Organizations

European Commission. Appendix Table A-23 summarizes the nationally funded research activities that were underway as of 1999 in each EC member state. Programs that were completed by 1999 are not included in this list.

WHO/FAO. WHO is involved in several research studies. The major research endeavor includes working with the United Nations Environmental Programme to provide risk assessments of POPs, including DLCs.

Chemical Methods for Analysis of DLCs in Feeds and Foods

Not all feeds or food products have been found to be at equal risk for DLC contamination. While commonly associated with feeds and foods containing animal fats, DLCs can, however, also be found in vegetables, fruits, and cereals. The need for detection of DLCs at these low levels makes the current quantitative methods of analysis expensive and challenging to perform, which limits the number of laboratories available to conduct these tests (Hass and Stevens, 2001). In order to efficiently develop a reliable picture of DLCs in the food supply, both screening methods (which can be used to analyze a large number and variety of feed and food samples), and trace analysis (which can quantify low levels of DLCs in follow-up to a positive screening result) can be useful.

Both current screening and trace analysis methods follow a two-part procedure: extraction/separation of the sample, where the compounds of interest are isolated from the matrix; and instrumental analysis, where DLCs are detected. The major challenge with regard to food samples is the extraction/separation of DLCs from other compounds in the food matrix. Techniques for DLC extraction from fruits, hard vegetables, soft vegetables, grains, dairy products, fish, and meats are very different, and composite foods and food additives are especially challenging.

Screening Methods

Because of their speed and cost efficiency, significant efforts have been made in recent years to develop screening assays for determining DLC and PCB contamination. However, screening assays provide speed and cost savings at the expense of specificity and a lower level of detection (Hass and Stevens, 2001). They do provide the sensitivity of conventional assays and, most importantly, minimize false negatives. Although to quantify contamination levels, trace analysis must follow a positive screening result, screening methods can be very useful in detecting a contamination event or identifying critical control points in a potential contamination pathway.

Two cost-effective approaches have been developed for screening purposes: instrumental methods and biotechnology approaches. Both approaches rely on the same basic extraction methods used in trace analysis, while reducing the cost of the analytical measurement.

Of the two screening methods, the development of the CALUX method was supported under a Small Business Innovation Research Grant from the National Institute of Environmental Health Sciences. FDA's Center for Veterinary Medicine, Arkansas Regional Laboratory, has a licensing agreement to use the CALUX method for its DLC research.

Instrumental Methods

Instrumental methods of screening for the presence of DLCs respond to the physical properties of the compounds. Interfering compounds that were not removed during the initial extraction procedure and may cause an overestimate of DLC contamination levels can be identified in an initial analysis. A secondary clean-up of the sample can be performed and the sample can be reanalyzed, reducing the number of false positives that this methodology produces.

Biotechnology Approach

The biotechnology approach is based on the chemical reactivity of compounds and uses immunoassay-type tests and arylhydrocarbon receptor-type tests. In comparison studies, the biotechnology approach has been found routinely to overestimate DLC content in the presence of interfering compounds, which results in false positives (Hass and Stevens, 2001). While some interfering compounds are removed during the extraction phase of the test, the residual presence of these compounds is not detectable during a biotechnology-based assay. Even more seriously, this approach also can have a problem with false negatives due to analyte loss during the extraction phase (Hass and Stevens, 2001). Assays of duplicate aliquots from a single sample can minimize this problem, but this doubles the cost of analysis.

Analytical Methods for Analysis of DLCs in Feeds and Foods

Trace Analysis

The analytical approach used most frequently to detect DLCs in feeds and foods relies on isotopic dilution. This method is isomer specific, very sensitive, and robust, although expensive and demanding. Following the extraction phase, a known amount of the isotope 13C is added to the sample, which creates a mixture of forms of the compound of interest that are chemically identical, yet distinguishable by mass spectrometry. Using a combination of gas chromatography and high-resolution mass spectrometry allows determination of the ratio between each analyte and its associated isotopically labeled standard, leading to accurate quantification of analyte concentration. The overall accuracy of the assay depends on the ability to spike the sample with the isotope accurately, weigh the sample, and measure the ratio. The effects of interfering compounds and minor sample losses due to handling are detectable and correctable. The analytical cost estimates associated with the standard analytical method for DLCs obtained from a number of sources are summarized in Appendix Table A-24.

EPA-Approved Method for Analysis of Dioxins and Furans in Wastewater

In 1997, to augment less sensitive methods approved earlier, EPA Method 1613: Tetra- Through Octa-Chlorinated Dioxins and Furans by Isotope Dilution High Resolution Gas Chromatography/High Resolution Mass Spectrometry (HRGC/HRMS), EPA 821-B-94-005, was approved. Method 1613 is the most sensitive analytical test procedure approved under the Clean Water Act for the analysis of CDDs and CDFs and was developed to meet the need for more stringent pollutant monitoring and control. Method 1613 also allows determination of the 17 tetra- through octa-chlorinated, 2,3,7,8-substituted CDDs and CDFs.

Method 1613 extends minimum levels of quantitation of CDDs and CDFs into the low parts-per-quadrillion range for aqueous matrices and the low parts-per-trillion range for solid matrices. Furthermore, the use of isotope dilution techniques, internal standard calibration, and the 1600 series method quality control protocol results in improved sensitivity, precision, and accuracy. These improvements have been validated through both intra- and interlaboratory validation studies. Method 1613 is also intended to encourage advances in technology and reductions in the cost of analysis by allowing the use of alternate extraction and clean-up techniques. The analyst is permitted to modify the method to overcome interferences or to lower the cost of measurements, provided that all method equivalency and performance criteria are met.

Concentrations of DLCs in Foods

This section presents recent data (1990 or later) regarding the concentrations of DLCs in European and North American foods, as provided by AEA Technology (1999), ATSDR (1998), EPA (2000), Fiedler and colleagues (2000), IARC (1997), and the Scientific Committee on Food (2000, 2001).

Recent Contamination Levels in Foods

Appendix Table A-25 provides DLC values for foods other than breast milk. The data are very heterogeneous with regard to collection date, the number of samples of a particular food, sampling method (individual versus composite samples), the compounds analyzed, the unit of analysis (e.g., fat, fresh weight, dry weight), and the state of the food (e.g., raw or cooked). Numbers in the table may represent means, ranges of means, or ranges of observations.

Temporal Trends

Evidence of temporal trends in the data on DLC contamination levels in foods is presented in some reviews, if only indirectly, in decreasing estimates of dietary intakes of DLCs. EPA (2000) reports, specifically that:

  • Concentrations of dioxins and furans in U.K. cows' milk declined from 1.1 to 3.3 pg I-TEQDF/g of lipid in 1990 to 0.67 to 1.4 pg I-TEQDF/g of lipid in 1995.
  • The mean pg I-TEQDF/g of lipid in German milk declined by about 25 percent between 1990 and 1994.
  • Examination of U.S. foods preserved over the last several decades suggests that dioxin and furan concentrations were two to three times higher in the 1950s to 1970s than at present, while PCB concentrations were ten times higher.

IARC (1997) states that PCDD/PCDF in milk, dairy products, eggs, poultry, and “fatty food composites” in the United Kingdom decreased markedly during the 1980s. Fiedler and colleagues (2000) cite a decrease in the level of contamination of German foods, most markedly for dairy products, meat, and fish.

In 1998, an EPA study compared the DLC concentration in historic samples to current DLC concentrations derived from post-1993 national food surveys for beef, pork, poultry, and milk (Winters et al., 1998). The surveys' principal objective was to determine the national average concentration of DLCs in the lipids of these animal-fat products. National mean TEQ concentrations from these surveys are shown in Appendix Table A-26.

Appendix Table A-27 presents the PCDD/PCDF and PCB TEQ concentrations of the 14 historical samples, as well as TEQ concentrations normalized and expressed as a percent of current concentrations for the most similar food type. For example, the 1908 beef ration percentage of 38 percent means that the 0.34 pg TEQ/g of lipid PCDD/PCDF (calculated at nondetects = ½ limit of detection) is 38 percent of the current beef concentration of 0.89 pg TEQ/g of lipid (at nondetects = ½ limit of detection), as determined by the recent national EPA beef survey.

Although not necessarily representative of these food types or their respective time period, it should be noted that all 10 samples from 1957 to 1982 were higher in PCDD/PCDF TEQ than the current mean concentrations (at nondetects = ½ limit of detection), and that 12 of the 13 samples taken from 1945 through 1983 were higher for PCB TEQ. If the samples are indicative of past concentrations of DLCs, normalized TEQ suggests a PCDD/PCDF concentration two to three times higher during the period of peak environmental loading, while PCB TEQ may have been over 10 times current concentrations. EPA plans to continue analyzing historic meat and dairy products as additional samples become available.

Contribution of Food Groups to DLC Exposure

According to the Scientific Committee on Food (2000), the major sources of dietary exposure to PCDD/PCDF intakes in Europe are milk and dairy products (16 to 39 percent), meat and meat products (6 to 32 percent), and fish and fish products (11 to 63 percent). Fish was a particularly large contributor in Finland and Sweden, fruits and vegetables in Spain, and cereals in the United Kingdom. In Germany, milk, meat, and fish contributed 31 percent, 23 percent, and 17 percent, respectively, of dietary I-TEQ from PCDD/PCDF (Scientific Committee on Food, 2000).

Temporal Trends

Several of the reviewed reports describe data that suggest a decrease in DLC intakes over recent decades. AEA Technology (1999) reports three time trend-analyses of DLC intake. Dutch data on DLC in foods gathered in 1978, 1984 to 1985, and 1994 indicate a statistically significant decreasing trend in adult intake over time, with a 50 percent decrease in I-TEQ/kg/d over each 5.5-year interval in that period. Dietary studies conducted in Germany in 1989 and 1995 indicate a 45 percent decrease in I-TEQ intake. Diet studies in the United Kingdom in 1982, 1988, and 1992 suggest a 45 percent decrease in intake at each time point compared to the preceding point. All of these estimates likely pertain to the average consumer. Independent of changes over time in the DLC content of food and in dietary intake, it is generally recognized that body burdens of DLCs increase with age due, in part, to the long half-lives of these compounds.


This chapter summarizes reports on the toxicity and risk of DLCs and on regulatory activity in the United States and other countries that are widely recognized to reflect current status and knowledge of these compounds (AEA Technology, 1999; ATSDR, 1998; EPA, 2000; Fiedler et al., 2000; IARC, 1997; Scientific Committee on Food, 2000, 2001). The risks from exposure to DLCs outlined in these documents are based on population groups that received exposures exceeding the daily exposures estimated for the general population, so risks to the general population are not known. Efforts to regulate DLCs range from exposure limits and environmental emission regulations to guidelines and recommendations to limit DLC levels in feed and food. Efforts in the United States and other countries to monitor DLCs and gather more current data are described. Research on DLC levels in human foods indicates that the greatest contribution to exposure from the food supply is from animal fats in meat, dairy products, and fish.


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A potency of 8.6 × 10–3 pg/kg/d TCDD implies an additional 8.6 extra cancer cases per 1,000 exposed people for every 1 pg/kg/d increase in TCDD exposure.

Copyright 2003 by the National Academy of Sciences. All rights reserved.
Bookshelf ID: NBK221715


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