379 16 Exposure to Dioxin and Dioxin-Like Compounds 1 Daniel J. Stralka U.S. Environmental Protection Agency Harold A. Ball U.S. Environmental Protection Agency CONTENTS 16.1 Synopsis 379 16.2 Dioxin Toxicity 380 16.3 Toxicity Factors and Equivalence 382 16.4 Sources, Emissions, and Environmental Fate 384 16.5 Media and Food Levels 387 16.6 Sources and Pathways to Human Exposure 389 16.7 Summary and Future Directions 391 16.8 Questions for Review 391 References 392 16.1 SYNOPSIS Dioxin and dioxin-like compounds (DLC) are a family of natural and human-made chemicals that are ubiquitous and biologically persistent. They are associated with a broad spectrum of adverse biological effects, both cancer and non-cancer. Dioxin entered the public lexicon as a result of a number of high-profile news stories over the past several decades. Although never intentionally produced, dioxins were later found to be significant chemical by-products in the synthesis of a range of chemical products. For example, dioxin was a common contaminant in products produced from chlorophenol, including Agent Orange, a chemical defoliant used in Vietnam, and a bactericide used for disinfection. Inappropriate disposal of waste from the manufacture of hexachlorophene led to significant exposure of residents of Times Beach, MO, to dioxin. The area was subsequently cleaned up by the U.S. Environmental Protection Agency (USEPA) under Superfund legislation. However, the major source of environmental dioxin release today is as a by-product of almost every combustion process. Dioxins then move through the environment where they bioconcentrate in animals and fish, which become a source of low-level exposure to the population. There are a number of PBTs, or persistent, bioaccumulative and toxic compounds, that are receiving international attention. The focus of this chapter is the occurrence and fate of dioxin in the environment, dioxin toxicity and current exposure to the population, and strategies to manage the general population risks associated with dioxin. 1 The contents of this chapter do not necessarily reflect the views or policies of the U.S. Environmental Protection Agency. © 2007 by Taylor & Francis Group, LLC 380 Exposure Analysis 16.2 DIOXIN TOXICITY Dioxins are a class of compounds that have a wide range of toxic effects at very low doses. This group of compounds is defined by a similar physical structure, their affinity for an extracellular membrane protein, and is thought to express some of its effects through a common mechanism of action. This group of about 30 or so active compounds is defined by its binding to an extracellular receptor called the aryl hydrocarbon (Ah) receptor (Whitlock 1993). All of these compounds have a planar configuration, 2 or 3 rings and their binding is potentiated by being halogenated in the lateral positions (Figure 16.1). Congeners are specific compounds within each family of compounds that differ by the degree and extent of halogenation. These physical properties also make them resistant to enzymatic action and fat soluble, which leads to persistence and bioaccumulation or biomagnification in the environment. A model for this class of compounds is 2,3,7,8-tetrachlorod- ibenzo-p-dioxin (2,3,7,8-TCDD), which is the most studied of this group. While all these com- pounds express similar toxic responses, they differ in the doses necessary to elicit the same level of response (USEPA 2000b). This attribute of variable binding affinity for the Ah receptor is used to construct a relative ranking of all the compounds in this class. In the environment, exposure is usually to a complex mixture of these active dioxins, depending on the source of the exposure (USEPA 2000a). Almost any environmental soil and water sample will have trace amounts of dioxins when advanced analytical procedures are employed. There is a wide range of possible toxic outcomes from exposure to dioxins (USEPA 2000b). These effects are usually delayed from exposure. The delay supports the receptor-mediated response model. Frank effects at high doses are gonadal and lymphoid tissue atrophy, wasting syndrome, and death. Lower doses can be expressed in humans as chloracne, a severe skin disease with acne- like lesions. Altered pigmentation, hyperplasia, and hyperkeratosis have also been reported. Car- cinogenesis has been evaluated by both the International Agency for Research on Cancer (IARC 1997) and the USEPA (2000c), which rank 2,3,7,8-TCDD as a human carcinogen. Further studies evaluating the carcinogenic mechanism of action demonstrate that 2,3,7,8-TCDD is itself a weak mutagen but a very potent cancer promoter (USEPA 2000b). This is further evidence that TCDD is not genotoxic but is operating through a receptor-mediated response. Other effects that are seen at still lower doses can range from biochemical effects like oxidative stress, enzyme induction, changes in hormone and growth factors, immunosuppression, and altered glucose tolerance, ultimately leading to diabetes. Organism life stage at exposure is also critical to the type and extent of effect expressed. For example, in utero exposures can lead to congenital FIGURE 16.1 Example structures of polychlorinated dibenzo-p-dioxins, dibenzofurans and biphenyls. O O Cl Cl Cl Cl O Cl Cl Cl Cl Cl Cl Cl Cl Cl Cl 2,3,7,8-Tetrachlorobenzo-p-Dioxin (TCDD) 2,3,7,9-Tetrachlorodibenzofuran (TCDF) 3,3 ´,4,4´,5,5´-Hexachlorobiphenyl (PCB-169) © 2007 by Taylor & Francis Group, LLC Exposure to Dioxin and Dioxin-Like Compounds 381 malformations and subsequent developmental effects whereas similar exposures to an adult organ- ism may or may not show effects. There is a wide variation between species for any one specific effect, if expressed in the particular species at all, but the overall type and magnitude of effects is similar across species. There is also difference in magnitude of any response within species that can range as much as 10,000 times. Thus the ultimate disease outcome may be different within any population (USEPA 2000b). For humans, the World Health Organization (WHO) has derived a tolerable daily intake (TDI), a daily average intake that would not present adverse effects, as 1–4 pg/kg-day (JECFA 2001) reduced from 10 pg/kg-day in 1998. This is based on no adverse effect levels (NOEAL) in animals with a safety factor of 100 (10× for extrapolating from animals to humans and 10× for response sensitivity within the human population). The USEPA in its recent dioxin exposure reassessment (USEPA 2000a) has estimated that our primary source of dioxin exposure is from food (meat, dairy, and fish) and at levels of about 1 pg/kg-day. In order to prioritize risks and the uncertainties of the various inputs into both the toxicity evaluation and the exposure assumptions, it is useful to look at the margin of exposure (MOE). The MOE is the simple ratio of a safe dose divided by the actual dose to a compound of interest. Generally, the higher the MOE the less the concern, and MOEs greater than 100 are not of great concern because there is a 100-fold margin of safety. For dioxins, the MOE is less than 10 suggesting that there may be effects being expressed in the human population. However, these effects may not be adverse in that there could be adaptability to some of the initial effects, which would be interpreted as variability within the human population. Regardless, the low MOE suggests that exposure should be minimized to increase the margin of safety. The initial steps that define the receptor response are the agonist binding to the Ah receptor on the cell surface, being internalized, moving into the nucleus and binding to DNA and regulating gene expression (Birnbaum 1994) (Figure 16.2). Multiple genes may be affected, both up- and down-regulated. This multiple gene response is a similar cascade of events initiated by hormones with relatively small concentrations having an effect that is greatly multiplied through gene regu- lation. One protein in particular that seems to be the most sensitive indicator of dioxin exposure is the expression of mixed function oxidases called cytochrome P-450 in the endoplasmic reticulum. In particular, isoforms of cytochrome P-450 are expressed (1A1 in lung and skin, and 1A2 in liver). These enzymes play a critical role in a number of cellular processes from hormone synthesis to cellular homeostasis. A function of these enzymes is to insert an active oxygen species into a typically lipid soluble compound. This oxygen molecule, once inserted into the compound, can act as a point of attachment for the detoxifying enzyme systems to chemically add compounds that increase water solubility, thus enhancing partitioning in the body and ultimately the body’s ability to clear it. Unfortunately, the process of inserting the active oxygen species into the lipophilic compound can also result in a more reactive species that can then react with other cellular components and possibly lead to changes that ultimately could be expressed as cancer. The variability seen within a species and between species may be due to the effects later in the chain of events caused by the receptor binding or due to the structural affinity of the Ah receptor. Whatever the cause of this variability, the binding affinity for the Ah receptor is proportional to the level of response. It is this attribute that has been used to extrapolate the wealth of information specific to 2,3,7,8-TCDD to the other active dioxin compounds. In balancing all the different endpoints or effects measured in various species, several groups have derived numerous schemes for describing the potency of the individual dioxins. The most recent consensus group sponsored by the WHO has derived a set of toxicity equivalent factors (TEFs) for mammals, birds, and fish (Van den Berg et al. 1998). © 2007 by Taylor & Francis Group, LLC 382 Exposure Analysis 16.3 TOXICITY FACTORS AND EQUIVALENCE Polychlorinated dibenzo-p-dioxins (CDDs) are a family of tricyclic aromatic compounds consisting of chlorinated benzene rings joined by an oxygenated ring. CDDs along with some polychlorinated dibenzofurans (CDFs) and certain polychlorinated biphenyls (PCBs) make up a group of chemicals that are termed dioxin-like compounds (DLC). There are a total of 75 different CDD congeners, 135 CDF congeners, and 209 different PCB congeners. The subsets of this class of compounds that are considered “dioxin-like” are those congeners that are characterized by similar structure, physical-chemical properties, and toxic response. The dioxin-like CDDs and CDFs are characterized by chlorine substitution at the 2,3,7,8 positions on the benzene rings. Some of the PCBs have FIGURE 16.2 Mechanism of dioxin uptake into the cell. (From USEPA 2002b, modified by Willa AuYeung.) Cell membrane N u c l e u s m e m b r a n e 2. TCDD binds to AhR protein 3. TCDD-AhR complex enters nucleus and binds to Arnt protein 5. Overexpression of cytochrome P-450 mRNA 6. mRNA exits nucleus 7. Overexpression of cytochrome P-450 protein mRNA mRNA P-450 PRO TCDD 1. TCDD enters cell DNA 2,3,7,8-Tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) Aryl hydrocarbon (Ah) receptor protein Ah receptor nuclear translocator protein DNA Dioxin responsive elements Cytochrome P-450 gene mRNA Cytochrome P-450 protein Endoplasmic reticulum DREs P-450 Legend P-450 PRO P-450 PRO AhR DREs P-450 Arnt 4. TCDD – AhR – Arnt complex binds to DNA Endoplasmic reticulum TCDD TCDD TCDD TCDD AhR TCDD AhR Arnt TCDD AhR Arnt TCDD AhR Arnt P-450 PRO © 2007 by Taylor & Francis Group, LLC Exposure to Dioxin and Dioxin-Like Compounds 383 dioxin-like character when chlorine is substituted at four or more of the lateral positions and no more than one of the ortho positions (USEPA 2000c). In the environment, the dioxin-like compounds are typically found as a mixture of congeners. Consequently, an approach was developed in 1989 to estimate the risks associated with exposure to mixtures of CDDs and CDFs (USEPA 1989). Here, toxic equivalency factors (TEFs) were determined for the various congeners based upon relative toxicity when compared to the well- studied 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the most toxic member of the group. TEFs reflect the differing potencies of compounds that all initiate a similar cascade of events, compared to TCDD, which is assigned a TEF of 1.0. Adopted internationally, this approach is not exact but is thought to have an uncertainty within a factor of 10. The current WHO consensus dioxin TEFs are presented in Table 16.1 (Van den Berg et al. 1998). In a complex mixture, the Toxic Equivalency concentration (TEQ) is determined by multiplying the concentration of each congener in the mixture by its corresponding TEF, and summing all the products to give a single 2,3,7,8-TCDD equivalent as follows: Total Toxic Equivalency (TEQ) = ΣC i TEF i where C i equals the concentration of the individual congener (i) in the complex mixture. The accepted nomenclature for this TEQ scheme is TEQ DFP -WHO 98 , where TEQ represents the toxic equivalency of the mixture as 2,3,7,8-TCDD. The subscripts DFP indicate that dioxins (D), furans (F), and dioxin-like PCBs (P) are included in the scheme. The subscript 98 following WHO displays the year changes made to the TEF scheme were published. The currently accepted TEFs presented in Table 16.1 include 7 dioxin congeners, 10 furan congeners, and 12 dioxin-like PCB congeners. However, in human tissue samples and food products, only five of these congeners, TCDD, 1,2,3,7,8-PCDD, 1,2,3,6,7,8-HxCDD, 2,3,4,7,8-PeCDF, and PCB 126, account for over 70% of the total TEQ (USEPA 2000b). TABLE 16.1 Toxic Equivalency Factors (TEF-WHO 98 ) for Dioxins and Dioxin-Like Compounds Dioxin (D) Congener TEF Furan (F) Congener TEF Dioxin-Like PCB (P) TEF 2,3,7,8-TCDD 1,2,3,7,8-PeCDD 1,2,3,4,7,8-HxCDD 1,2,3,6,7,8-HxCDD 1,2,3,7,8,9-HxCDD 1,2,3,4,6,7,8-HpCDD 1,2,3,4,6,7,8,9-OCDD 1.0 1.0 0.1 0.1 0.1 0.01 0.0001 2,3,7,8-TCDF 1,2,3,7,8-PeCDF 2,3,4,7,8-PeCDF 1,2,3,4,7,8-HxCDF 1,2,3,6,7,8-HxCDF 1,2,3,7,8,9-HxCDF 2,3,4,6,7,8-HxCDF 1,2,3,4,6,7,8-HpCDF 1,2,3,4,7,8,9-HpCDF 1,2,3,4,6,7,8,9-OCDF 0.1 0.05 0.5 0.1 0.1 0.1 0.1 0.01 0.01 0.0001 3,3′,4,4′-TCB (77) 3,4,4′,5-TCB (81) 2,3,3′,4,4′-PeCB (105) 2,3,4,4′,5-PeCB (114) 2,3′,4,4′,5 -PeCB (118) 2′,3,4,4′,5-PeCB (123) 3,3′,4,4′,5-PeCB (126) 2,3,3′,4,4′,5-HxCB (156) 2,3,3′,4,4′,5′-HxCB (157) 2,3′,4,4′,5,5′-HxCB (167) 3,3′,4,4′,5,5′-HxCB (169) 2,3,3′,4,4′,5,5′-HpCB (189) 0.0001 0.0001 0.0001 0.0005 0.0001 0.0001 0.1 0.0005 0.0005 0.00001 0.01 0.0001 CDD — chlorodibenzo-p-dioxin; CDF — chlorodibenzo-p-furan; CB — chlorobiphenyl; T — tetra; Pe — penta; Hx — hexa; Hp — hepta; O — octa. Source: Van den Berg et al. 1998. © 2007 by Taylor & Francis Group, LLC 384 Exposure Analysis 16.4 SOURCES, EMISSIONS, AND ENVIRONMENTAL FATE Dioxin and dioxin-like compounds are inadvertently formed by natural processes (including forest fires) and a number of human activities. Dioxin can be a product of industrial processes in such industries as paper, metal smelting, and chemical manufacturing. PCBs are no longer manufactured in the United States but they were once widely used and are present in the environment. The major sources of dioxin formation today, however, are combustion related. Several mechanisms have been proposed to explain the appearance of DLC in combustion emissions (Lustenhouwer, Olie, and Hutzinger 1980) including: (1) the DLC can be a contaminant in the material being burned but is not destroyed; (2) the DLC can be a breakdown product of larger, complex organic molecules reacting in the presence of chlorine and heat; and (3) de novo synthesis of the DLC from unrelated precursor molecules involving “heterogeneous, surface- catalyzed reactions between carbonaceous particulates and an organic or inorganic chlorine donor” (USEPA 2001b). Such surface-catalyzed reactions are thought to be the dominant mechanism for DLC formation. These reactions typically occur as combustion gases are cooling and take place in a temperature range between 200°C and 400°C (Kilgroe et al. 1990). The reaction is promoted by the presence of molecular chlorine, which chlorinates DLC precursors through substitution reac- tions. Chloride ions from the fuel or from atmospheric sources can participate if condensed to chlorine through the Deacon reaction catalyzed by copper (Griffin 1986; Gullett, Bruce, and Beach 1990). Copper also acts to catalyze the condensation reactions of chlorinated aromatic rings to form the DLC backbone molecular structure (Gullett et al. 1992). If present, sulfur acts as an inhibitor to the reaction, apparently by reacting with and depleting the chlorine present and by poisoning the copper catalyst (Griffen 1986; Raghunathan and Gullet 1996). Recently, the USEPA updated its inventory of sources of DLC release to the environment in the United States (USEPA 2001a). Here, the most reliable data on source emission rate and dioxin concentration was used to estimate total dioxin releases for the years 1987 and 1995. A summary of the emissions data is presented in Table 16.2. Due to data limitations in the study, only the dioxin and furans were considered and TEQs were determined using the TEQ DF -WHO 98 scheme. The year 1987 was selected because prior to that time little CDD/CDF emissions data were available, and it was a time period before there was widespread installation of controls to limit CDD/CDF emissions. The year 1995 was selected as the most recent year for which reliable activity-level data were available for many source categories and also a year prior to which numerous regulatory and non-regulatory efforts to reduce formation and release of dioxin-like compounds had been imple- mented. In 1987 all known human source activity (for which reliable estimates could be made) in the United States contributed 13,998 grams TEQ DF -WHO 98 to the environment. By 1995, these same sources contributed 3,253 grams TEQ DF -WHO 98 to the environment, a reduction of approx- imately 80%. Since 1995, the USEPA has adopted a number of regulations that should reduce the DLC emissions from various sources, including: municipal waste combustors, medical waste incinerators, hazardous waste incinerators, cement kilns burning hazardous waste, and pulp and paper facilities using chlorine bleached processes (USEPA 1998, 2002). Although only recently identified as a significant source, uncontrolled backyard burning of household trash is and will continue to be a significant contributor to the national DLC budget (Lemieux et al. 2000). In 1995, the environmental releases of DLC were 96% to the atmosphere, about 3% to land, and about 1% to water (Figure 16.3). A schematic of the transport of DLC through the environment is presented in Figure 16.4 (USEPA 2000a). As discussed above, DLC are primarily released to the atmosphere from combustion sources and transported. DLC are then deposited and adsorbed into plant matter, or adsorbed onto soils. Where plant matter is used as feed for farm animals, the animals consume the feed and take up associated DLC. DLC in soils are washed into sediments and bioaccumulate through the food chain to fish. In animals and fish, dioxins tend to accumulate in fatty tissues. Dioxin has very low solubility in groundwater and is preferentially associated with soils and sediments. © 2007 by Taylor & Francis Group, LLC Exposure to Dioxin and Dioxin-Like Compounds 385 DLC compounds are extremely stable in the environment. The only environmentally significant transformation processes for these congeners are believed to be atmospheric photooxidation and photolysis of nonsorbed species in the gaseous phase or at the soil or water-air interface (USEPA 2000a). Consequently, in media where photodegradation is not possible, the ultimate sink for DLC TABLE 16.2 Inventory of Sources of Dioxin-Like Compounds in the United States (TEQ DF -WHO 98 ) 1987 and 1995 Inventory Source 1987 Emissions gTEQ DF /yr 1995 Emissions gTEQ DF /yr Percent Reduction 1987–1995 Municipal Solid Waste Incineration, air 8877.0 1250.0 86 Backyard Refuse Barrel Burning, air 604.0 628.0 –4 Medical Waste Incineration, air 2590.0 488.0 81 Secondary Copper Smelting, air 983.0 271.0 72 Cement Kilns (hazardous waste burning), air 117.8 156.1 –33 Sewage Sludge (land applied), land 76.6 76.6 0 Residential Wood Burning, air 89.6 62.8 30 Coal-Fired Utilities, air 50.8 60.1 –18 Diesel Trucks, air 27.8 33.5 –21 Secondary Aluminum Smelting, air 16.3 29.1 –79 2,4-D, land 33.4 28.9 13 Iron Ore Sintering, air 32.7 28.0 14 Industrial Wood Burning, air 26.4 27.6 –5 Bleached Pulp and Paper Mills, water 356.0 19.5 95 Cement Kiln (nonhazardous waste burning), air 13.7 17.8 –30 Sewage Sludge Incineration, air 6.1 14.8 –143 Ethylene Dichloride/Vinyl Chloride, air NA 11.2 NA Oil-Fired Utilities, air 17.8 10.7 40 Crematoria, air 5.5 9.1 –65 Unleaded Gas, air 3.6 5.6 –56 Hazardous Waste Incineration, air 5.0 5.8 –16 Lightweight Ag Kilns (hazardous waste), air 2.4 3.3 –38 Commercially Marketed Sewage Sludge, land 2.6 2.6 0 Kraft Recovery Boilers, air 2.0 2.3 –15 Petroleum Refining Catalyst Regeneration, air 2.24 2.21 1 Leaded Gasoline, air 37.5 2.0 95 Secondary Lead Smelting, air 1.29 1.72 –33 Bleached Pulp and Paper Mill Sludge, land 14.1 1.4 90 Cigarette Smoke, air 1.0 0.8 20 Ethylene Dichloride/Vinyl Chloride, land NA 0.73 NA Primary Copper, air 0.5 0.5 0 Ethylene Dichloride/Vinyl Chloride, water NA 0.43 NA Boilers and Industrial Furnaces, air 0.78 0.39 50 Tire Combustion, air 0.11 0.11 0 Drum Reclamation, air 0.08 0.08 0 Carbon Reactivation Furnace, air 0.08 0.06 25 Totals 13,998 3,253 77 NA = not available Source: USEPA 2001a. © 2007 by Taylor & Francis Group, LLC 386 Exposure Analysis FIGURE 16.3 Environmental releases of dioxins and furans in the U.S. 1995 (TEQDF-WHO98). (From USEPA 2001a.) FIGURE 16.4 Pathways for entry of dioxin-like compounds into the terrestrial and aquatic food chains. (From USEPA 2000a.) TABLE 16.3 Mean Background Concentrations of Dioxin-Like Compounds in the U.S. (TEQ DF -WHO 98 ) Environmental Media Background Concentration (TEQ DF -WHO 98 ) Environmental Screening Level Urban Soil (ppt, pg/g) 9.3 3.9 Rural Soil (ppt, pg/g) 2.7 3.9 Urban Air (pg/m 3 ) 0.12 0.045 Rural Air (pg/m 3 ) 0.013 0.045 Sediment (ppt, pg/g) 5.3 5.8* Water (ppq, pg/L) 0.00056 0.45 * Upper effects threshold for freshwater sediments. Source: Buchman 1999; USEPA, 2003, 2004b. Water – 20 g TEQ (1%) Air – 3125 g TEQ (96%) Land – 110 g TEQ (3%) SOURCES TRANSPORT DEPOSITION FOOD SUPPLY Reentrainment Runoff Erosion Discharge © 2007 by Taylor & Francis Group, LLC Exposure to Dioxin and Dioxin-Like Compounds 387 is deep soil or sediments. In 2000, the USEPA reported estimates for background levels of DLC in environmental media based on data from a variety of studies conducted at different locations in North America (USEPA 2000a). These estimates are reported in Table 16.3. For this estimate, the USEPA utilized available data from locations described as “background” and not from areas impacted by local sources of contamination. Due to the limited available data, the USEPA indicated that these data cannot be considered to be definitive national means. Nonetheless, the “environ- mental media concentrations found in the United States were consistent across the various studies, and were consistent with similar studies in Europe.…The limited data on dioxin-like PCBs in environmental media are summarized in the document, but were not deemed adequate for estimating background levels. Because of the limited number of locations examined, however, it is not known if these ranges adequately capture the full national variability, if significant regional variability exists making national means of limited utility, or if elevated levels above this range could still be the result of background contamination processes” (USEPA 2000a). Table 16.3 also presents environmental screening levels for air, water, and soil (USEPA 2004b) that are used by the USEPA to screen contaminated sites for potential risk from direct contact to the individual media and, in the case of sediments, by the National Oceanic and Atmospheric Administration (Buchman 1999) to identify potential impacts of contaminated sites on coastal resources and habitats. As is clear from Table 16.3, the background concentration of DLC in air, soil, and sediments is within an order of magnitude of current environmental screening levels. However, in 2000, the USEPA found that environmental levels of DLC appear to be declining. The USEPA indicated that “Concentrations of CDD/CDFs in the environment were consistently low for centuries until the 1930s. Then, concentrations rose steadily until about the 1960s, at which point concentrations began to drop. Evidence suggests that the drop in concentrations is continuing to the present” (USEPA 2000a). This finding is based on several lines of evidence, including sampling of sediment cores in North America, and a review of trends in environmental loading. Further monitoring of environmental levels will be needed to reduce the uncertainty in these projections and confirm this trend. 16.5 MEDIA AND FOOD LEVELS DLCs are transported in the atmosphere and deposited onto vegetation and soils. Since DLCs are quite persistent, they bioconcentrate in both the terrestrial and aquatic food chains. As discussed below, the primary route of population exposure to DLCs in the environment is through the consumption of food with small concentrations of this contaminant. In the past 20 years, significant effort has gone into determining the concentration of DLC in the food supply of both the United States and Europe. Schecter et al. (1997) reported data on the concentrations of TEQ DFP in common food groups obtained from supermarkets in the United States in 1995. Their findings are shown in Figure 16.5. It is interesting to note that the dioxin-like PCBs contribute a significant portion of the total TEQ in much of the food tested. In 2000, the USEPA summarized the data available for concentration of DLCs in North American food (USEPA 2000a). Using current data on food consumption rates, and data on typical inhalation, water consumption, and soil exposure rates, combined with the data on DLC concentration in food and environmental media, the USEPA calculated DLC intake rates for a typical adult in the United States (USEPA 2000c). This data is presented in Table 16.4. In summary, an individual with a typical diet in the United States would ingest approximately 0.9 pg TEQ DFP -WHO 98 /kg-d. The primary source (96%) of individual exposure to DLC is through food consumption, with 3% from inhalation and 1% from soil (Figure 16.6). The USEPA’s review of available congener-specific data indicated that 65% of the total TEQ was from the dioxin and furans, while 35% was from the dioxin-like PCBs. © 2007 by Taylor & Francis Group, LLC 388 Exposure Analysis FIGURE 16.5 DLC levels in North American foods in 1995. (From Shecter et al. 1997. With permission.) TABLE 16.4 Typical Adult Intake of DLC in the U.S. (TEQ DFP -WHO 98 ) Source Concentration (TEQ) Contact Rate Intake (pg TEQ/kg-d) Intake (%) Beef 0.264 pg/g 0.67 g/kg-d 0.19 20 Fish/shellfish — freshwater 2.2 pg/g 5.9 g/d 0.184 20 Dairy 0.178 pg/g 55 g/d 0.14 15 Other meats 0.221 pg/g 0.35 g/kg-d 0.076 8 Milk 0.027 pg/g 175 g/d 0.067 7 Fish/shellfish — marine 0.51 pg/g 9.6 g/d 0.07 7 Pork 0.292 pg/g 0.22 g/kg-d 0.065 7 Poultry 0.094 pg/g 0.5 g/kg-d 0.047 5 Eggs 0.181 pg/g 0.24 g/kg-d 0.043 5 Inhalation 0.12 pg/m 3 13.3 m 3 /d 0.023 2 Vegetable fat 0.093 pg/g 17 g/d 0.023 2 Soil ingestion 11.6 pg/g 50 mg/d 0.0082 0.9 Soil dermal contact 11.6 pg/g 12 g/d 0.002 0.2 Water 0.0005 pg/L 1.4 L/d 1.1E-5 0.001 Total 0.94 Source: USEPA, 2003. 0 0.2 0.4 0.6 0.8 1 1.2 1.4 1.6 Beef Chicken Pork Hot Dog/Bologna Eggs Fish (ocean) Fish (freshwater) Vegan Butter Cheese Milk Ice Cream TEQ (pg/g, ppt) PCDD PCDF PCB © 2007 by Taylor & Francis Group, LLC [...].. .Exposure to Dioxin and Dioxin-Like Compounds 389 Food 96% Soil 1% Water 0.001% Inhalation 2% FIGURE 16. 6 Sources of average adult DLC exposure (From USEPA 2000b.) 16. 6 SOURCES AND PATHWAYS TO HUMAN EXPOSURE In order to address how and to what extent people are exposed to dioxins, let us first look at environmental concentrations As shown in Table 16. 3, concentrations in soil,... more than 95% of human exposure is from diet, primarily dairy and meat products (USEPA 2000b) (Figure 16. 5 and Figure 16. 6) These estimates are for the general population, but there are certain segments of the population that may be of concern for higher exposure Those that are in close proximity to point sources and also produce their food near those sources could be at increased exposure Also certain... Francis Group, LLC 390 Exposure Analysis 60 TEQ, pg/g lipid 50 40 30 20 10 0 20 30 40 50 60 70 Age FIGURE 16. 7 DLC serum levels with age (From ATSDR 1999.) is relatively short However, with compounds with long half-lives, a rather short exposure can lead to a significant body concentration over a long period This is the concept of a body burden that is recommended for evaluating dioxin exposure (USEPA 2000c)... source of dioxin exposure is from food, types and total amount consumed change over a lifetime, and dioxin exposure can be quite variable But since the half-life is long the body burden should reflect exposure over the long term Figure 16. 7 illustrates the body burden increase seen with age This change is reflective of the overall temporal trend of dioxins measured in sediment cores Analysis of sediment... safe and national trends in the overall exposure and body burden of dioxins are decreasing with the further control of sources Nonetheless, the margin of exposure is small (USEPA 2000c) There are additional measures individuals can do to reduce their exposure, such as following the National Dietary Guidelines (USDA 2000), which © 2007 by Taylor & Francis Group, LLC Exposure to Dioxin and Dioxin-Like Compounds... 63(72): 18503–18751 USEPA (2000a) Exposure and Human Health Reassessment of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds, Part I: Estimating Exposure to Dioxin-Like Compounds, Vol 3: Properties, Environmental Levels, and Background Exposures, Draft, Report No EPA/600/P-00/001Bc, U.S Environmental Protection Agency, Washington, DC USEPA (2000b) Exposure and Human Health Reassessment... the upper-bound risk to the general population from current dioxin exposure may exceed a 1 in 1000 increased chance of experiencing cancer Given that the current national cancer rate is 1 in 3, is dioxin a significant problem? 6 Should backyard barrel burning of household trash be banned? © 2007 by Taylor & Francis Group, LLC 392 Exposure Analysis REFERENCES American Academy of Pediatrics (AAP) (1997)... Guidelines for Americans, Home and Garden Bulletin 232 © 2007 by Taylor & Francis Group, LLC Exposure to Dioxin and Dioxin-Like Compounds 393 USEPA (1989) Interim Procedures for Estimating Risks Associated with Exposures to Mixtures of Chlorinated Dibenzo-p-Dioxins and -Dibenzofurans (CDDs and CDFs), Report No EPA/625/3-89. 016, U.S Environmental Protection Agency, Risk Assessment Forum, Washington, DC USEPA... DLC in the environment and in foods to increase our confidence in current exposure models; and (4) understanding developing methods to interrupt the cycle of DLC through the food supply These efforts constitute the current direction in the overall development of a strategy to reduce risk associated with environmental dioxin exposure 16. 8 QUESTIONS FOR REVIEW 1 Discuss the ways that environmental dioxin... of Pediatrics (AAP) (1997) Breast-Feeding and the Use of Human Milk, Pediatrics, 100(6): 1035–1039 ATSDR (1999) Health Consultation (Exposure Investigation) Calcasieu Estuary (aka Mossville) Lake Charles, Calcasieu Parish, Louisiana, Cerclis No, LA0002368173, prepared by Exposure Investigation and Consultation Branch, Division of Health Assessment and Consultation, Agency for Toxic Substances and Disease . Toxicity 380 16. 3 Toxicity Factors and Equivalence 382 16. 4 Sources, Emissions, and Environmental Fate 384 16. 5 Media and Food Levels 387 16. 6 Sources and Pathways to Human Exposure 389 16. 7 Summary. 379 16 Exposure to Dioxin and Dioxin-Like Compounds 1 Daniel J. Stralka U.S. Environmental Protection Agency Harold A. Ball U.S. Environmental Protection Agency CONTENTS 16. 1 Synopsis 379 16. 2. & Francis Group, LLC 386 Exposure Analysis FIGURE 16. 3 Environmental releases of dioxins and furans in the U.S. 1995 (TEQDF-WHO98). (From USEPA 2001a.) FIGURE 16. 4 Pathways for entry of dioxin-like