9.4. SOURCES

The chlorinated and brominated dioxins and furans have never been intentionally produced other than on a laboratory-scale basis for use in chemical analyses. Rather, they are generated as by-products from various combustion and chemical processes. PCBs were produced in relatively large quantities for use in such commercial products as dielectrics, hydraulic fluids, plastics, and paints. They are no longer produced in the United States but continue to be released to the environment through the use and disposal of these products. A similar situation exists for the commercially produced PBBs, which were produced for a number of uses like flame retardants.

Dioxin-like compounds are released to the environment in a variety of ways and in varying quantities, depending on the source. Studies of sediment cores in lakes near industrial centers of the United States have shown that historical environmental deposition of dioxins and furans was quite low until about 1920, peaked around 1980, and has declined thereafter. This trend suggests that the presence of dioxin-like compounds in the environment has occurred primarily as a result of industrial practices and is likely to reflect changes in release over time. Further work to confirm declining trends in environmental samples and to relate these data to human exposures will be required.

Although these compounds are released from a variety of sources, the congener profiles of CDDs and CDFs found in sediments have been linked to combustion sources (Hites, 1991). Three theories have been suggested to explain formation of CDDs and CDFs during combustion: (1) CDDs and CDFs are present in the fuels or feed materials and pass through the combustor intact; (2) precursor chemicals are present in the fuels or feed material and undergo reactions catalyzed by particulates and other chemicals to form CDDs and CDFs; and (3) the CDDs and CDFs are formed de novo from organic and inorganic substrates bearing little resemblance in molecular structure.

The principal identified sources of environmental release of CDDs and CDFs may be grouped into four major types:

n Combustion and Incineration Sources: Dioxin-like compounds can be generated and released to the environment from various combustion processes when chlorine donor compounds are present. These sources can include incineration of wastes such as municipal solid waste, sewage sludge, hospital and hazardous wastes; metallurgical processes such as high-temperature steel production, smelting operations, and scrap metal recovery furnaces; and the burning of coal, wood, petroleum products, and used tires for power/energy generation.

n Chemical Manufacturing/Processing Sources: Dioxin-like compounds can be formed as by-products from the manufacture of chlorine and such chlorinated compounds as chlorinated phenols (e.g., pentachlorophenol), PCBs, phenoxy herbicides (e.g., 2,4,5-T), chlorinated benzenes, chlorinated aliphatic compounds, chlorinated catalysts, and halogenated diphenyl ethers. Although the manufacture of many chlorinated phenolic intermediates and products, as well as PCBs, was terminated in the late 1970s in the United States, production continued elsewhere around the world until 1990, and continued, limited use and disposal of these compounds can result in releases of CDDs, CDFs, and PCBs to the environment.

n Industrial/Municipal Processes: Dioxin-like compounds can be formed through the chlorination of naturally occurring phenolic compounds such as those present in wood pulp. The formation of CDDs and CDFs resulting from the use of chlorine bleaching processes in the manufacture of bleached pulp and paper has resulted in the presence of CDDs and CDFs in paper products as well as in liquid and solid wastes from this industry. Municipal sewage sludge has been found to occasionally contain CDDs and CDFs.

n Reservoir Sources: The persistent and hydrophobic nature of these compounds causes them to accumulate in soils, sediments, and organic matter and to persist in waste disposal sites. The dioxin-like compounds in these "reservoirs" can be redistributed by various processes such as dust or sediment resuspension and transport. Such releases are not original sources in a global sense, but can be on a local scale. For example, releases may occur naturally from sediments via volatilization or via operations that disturb them, such as dredging. Aerial deposition and accumulation on leaves can lead to releases during forest fires or leaf composting operations.

As awareness of these possible sources has grown in recent years, a number of changes have occurred in the United States, which should reduce the release rates. For example, releases of dioxin-like compounds have been reduced due to the switch to unleaded automobile fuels (and associated use of catalytic converters and reduction in halogenated scavenger fuel additives), process changes at pulp and paper mills, new emission standards and upgraded emission controls for incinerators, and reductions in the manufacture of chlorinated phenolic intermediates and products and the use of pesticides such as 2,4,5,-T and pentachlorophenol.

Although dioxins in the environment may arise from a number of sources as discussed above, the Exposure Document presents recent analyses of only air emissions of CDDs and CDFs for several European countries in terms of total toxic equivalents based on international TEFs for CDDs and CDFs. These studies assume that emissions to air make up the major portion of dioxins released to the environment. Estimates of total release in these countries range from approximately 100-1,000 g TEQ/year in West Germany and 100-200 g TEQ/year in Sweden to approximately 1,000 and 4,000 g TEQ/year maximum emissions in The Netherlands and United Kingdom, respectively. Similar nationwide estimates for the United States have not been compiled prior to this reassessment effort. The Exposure Document estimates the U.S. emissions to be in the range of 3,300-26,000 g TEQ/year, with a central estimate of 9,300 g TEQ/year. These estimates were derived from data from emission tests at relatively few facilities in each combustor class. These data were used to develop emission factors and then extrapolated to a nationwide basis using the total amount of waste feed material in each class. Variability of measured emissions from facilities within a class and the uncertainty in estimating the total amount of waste feed material in each class lead to the wide range presented above. Qualitatively speaking, major contributors to this total include medical waste incinerators, municipal waste incinerators, cement kilns, and industrial wood burning. Because of the limited number of measurements and the large number of potential sources for each of these emissions, total estimated emissions from these sources are considered highly uncertain. Municipal waste incineration has more measurement data than other air sources, but emissions are highly variable among facilities so that the overall estimate remains uncertain. Diesel-fueled vehicles, hazardous waste burning, forest fires, and metal smelting are more moderate contributors of dioxin-like compounds, but the magnitude of the contribution is also highly uncertain. Sewage waste incineration and residential wood burning as well as a few minor processes round out the current analysis and provide lower range estimates of medium to low certainty. Although still other sources are recognized and releases to land and water in addition to air are discussed in the Exposure Document, it is clear from this exercise that additional measurement data will be needed to gain an adequate appreciation for the nature and magnitude of major U.S. sources of CDD and CDF emissions.

Several investigators have attempted to conduct "mass balance" checks on the estimates of national dioxin releases to the environment. Basically, this procedure involves comparing estimates of the emissions to estimates of aerial deposition. Such studies in Sweden (Rappe, 1991) and Great Britain (Harrad and Jones, 1992) have suggested that the deposition exceeds the emissions by about tenfold. These studies are acknowledged to be quite speculative due to the strong potential for inaccuracies in emission and deposition estimates. In addition, the apparent discrepancies could be explained by long-range transport from outside the country, resuspension, and deposition of reservoir sources or unidentified sources. Bearing these limitations in mind, this procedure has been used in this reassessment to compare the estimated emissions and deposition in the United States.

Deposition measurements have been made at a number of locations in Europe and two places in the United States (see discussion of these studies in Volume II of the Exposure Document). These limited data suggest that a deposition rate of 1 ng TEQ/m²-yr is typical of remote areas and that 2-6 ng TEQ/m²-yr is more typical of populated areas. Applying these values, the total U.S. deposition can be estimated as 20,000 to 50,000 g TEQ/yr. This range can be compared to the range of emissions for the United States (3,300-26,000 g TEQ/yr) as presented in the Exposure Document. As noted above, interpreting such comparisons is highly speculative and supports the need to conduct further emissions testing into all media and deposition measurement, if we are to understand the total mass balance for these compounds.

While all of the above emission and deposition values are given in the form of TEQs, it should be noted that neither emission nor deposition is equivalent to exposure or intake. Significant changes in composition can occur to complex mixtures of CDDs, CDFs, and PCBs as they move through the environment. Measurements at or near the point of human contact provide the best estimates of human exposure. TEQs are most relevant to potential for hazard and risk when they represent intake values.

9.4.1. Levels in the Environment and in Food

CDDs, CDFs, and PCBs have been found throughout the world in practically all media, including air, soil, water, sediment, fish and shellfish, and agricultural food products such as meat and dairy products. The highest levels of these compounds are found in soils, sediments, and biota; very low levels are found in water and air. The widespread occurrence observed, particularly in industrialized countries, is not unexpected, considering the numerous sources that emit these compounds into the atmosphere and the overall resistance of these compounds to biotic and abiotic transformation.

The average levels of these compounds found in the various media in North America have been compiled in the Exposure Document. The levels shown for environmental media and for food in North America are based on few samples and must be considered uncertain. However, they seem reasonably consistent with levels measured in a number of studies in Western Europe and Canada. The consistency of these levels across industrialized countries adds some confidence to the limited data from the United States and provides some reassurance that the U.S. estimates are reasonable. A major concern raised regarding all of these data is that few if any of these studies had a statistical design that was satisfactory for generalization to national food supplies. This adds to the uncertainty of extrapolations using these findings and argues for additional data collection to evaluate national and regional differences of levels of dioxin-like compounds in the environment and in food.

This assessment proposes the hypothesis that the primary mechanism by which dioxin-like compounds enter the terrestrial food chain is via atmospheric deposition. Dioxin and related compounds enter the atmosphere directly through air emissions or indirectly, for example, through volatilization from land or water or from resuspension of particles. Deposition can occur directly onto soil or onto plant surfaces. Soil deposits can enter the food chain via direct ingestion (e.g., grazing animals, earth worms, fur preening by burrowing animals). Dioxin-like compounds in soil can become available to plants by volatilization and vapor absorption or particle resuspension and adherence to plant surfaces. In addition, dioxin-like compounds in soil can adsorb directly to underground portions of plants. Uptake from soil via the roots into above-ground portions of plants is thought to be insignificant.

Support for this air-to-food hypothesis is provided by Hites (1991) who concluded that "background environmental levels of dioxin-like compounds are caused by dioxin-like compounds entering the environment through the atmospheric pathway." His conclusion was based on demonstrations that the congener profiles in lake sediments could be linked to congener profiles of combustion sources. Further arguments supporting this hypothesis include: (1) numerous measurements show that emissions occur from multiple sources and deposition occurs in most areas, including remote locations; (2) atmospheric transport and deposition are the only mechanisms that could explain the widespread distribution of these compounds in soil; and (3) other mechanisms of uptake into food, for instance, from direct contamination or through packaging, are much less plausible. Direct uptake into food from soil or sediments is possible and could be important for "local" exposures. These routes are less likely to explain the general background level of dioxin and related compounds found in the diet of the general population.

At present, it is unclear whether atmospheric deposition represents primarily "new" contributions of dioxin and related compounds from all media reaching the atmosphere or whether it is "old" dioxin and related compounds that persist and recycle in the environment. Understanding the relationship between these two scenarios will be particularly important in understanding the relative contributions of individual point sources of these compounds to the food chain and assessing the effectiveness of control strategies focused on either "new" or "old" dioxins in attempting to reduce the levels in food.

9.4.2. Background Exposure Levels

The term "background" exposure has been used throughout this reassessment to describe exposure of the general population, who are not exposed to readily identifiable point sources of dioxin-like compounds, that results in widespread, low-level circulation of dioxin-like compounds in the environment. The primary route of this exposure is thought to be the food supply, and most of the dioxin-like compounds are thought to come from non-natural sources. For the purposes of estimating background exposures to dioxin-like compounds via dietary intake the upper-range background toxicity equivalent values (i.e., those calculated using one-half the detection limit for the nondetects) were used in the Exposure Document. Uncertainties associated with the use of TEQs have been described throughout this chapter. The estimates are based on intake of dioxin-like CDDs and CDFs and do not include estimates for dioxin-like PCBs or other dioxin-like compounds. Inclusion of dioxin-like PCBs could raise these estimates by 35-50%. The net effect of these calculations is that we may be overestimating background levels based on the use of one-half of the detection limit and underestimating background levels by not including the dioxin-like PCBs or other dioxin-like compounds.

A background exposure level of 120 pg TEQ/day for the United States was estimated. These estimates are comparable to analogous estimates for European countries. These include estimates for Germany, which range from 79 pg TEQ/day based on Furst et al. (1990) to 158 pg TEQ/day based on Furst et al. (1991), 118-126 pg TEQ/day exposure via numerous routes in The Netherlands (Theelen, 1991), and 140-290 pg TEQ/day for the typical Canadian exposed mainly through food ingestion (Gilman and Newhook, 1991). It is generally concluded by these researchers that dietary intake is the primary pathway of human exposure to CDDs and CDFs. These investigators among others suggest that greater than 90 percent of human exposure occurs through the diet, with foods from animal origins being the predominant pathway.

This conclusion, that food is the predominant pathway of exposure, remains to be validated in the United States. Although data are derived from multiple studies from around the world, the data represent limited numbers of samples. Use of one-half of the detection level for nondetects is a reasonable but conservative approach to estimating low levels in samples. For some data sets, use of zero values for nondetects would result in significantly lower estimates. Setting nondetects equal to zero, however, does not significantly change the average TEQ levels estimated for most categories of U.S. food. In the current assessment, similar estimates of TEQs derived from different data sets, developed by different investigators in several countries, strengthen the probability that this inference represents the exposure of the general population in industrialized countries to dioxin and related compounds.

Data on human tissue levels suggest that body-burden levels among industrialized nations are reasonably similar (Schecter, 1991). These data can also be used to estimate background exposure through the use of pharmacokinetic models. Using this approach, exposure levels to 2,3,7,8-TCDD in industrialized nations are estimated to be about 20 to 40 pg TCDD/day (0.3-0.6 pg TCDD/kg/day). This is generally consistent with the estimates derived using diet-based approaches to estimate total TCDD intake. Pharmacokinetic approaches have not been applied to estimate exposures to CDDs or CDFs other than TCDD, which contribute substantially to the body burden of dioxin-like compounds. Estimates of exposure to dioxin-like CDDs and CDFs based on dietary intake are in the range of 1-3 pg TEQ/kg/day. Estimates based on the contribution of dioxin-like PCBs to toxicity equivalents raise the total to 3-6 pg TEQ/kg/day. This range is used throughout this characterization as an estimate of average background exposure to dioxin-like CDDs, CDFs, and PCBs.

The U.S. study of CDD/F body burdens contained in the National Human Adipose Tissue Survey (NHATS) (U.S. EPA, 1991) analyzed for CDD/Fs in 48 human tissue samples which were composited from 865 samples. These samples were collected during 1987 from autopsied cadavers and surgical patients. While this was an important study of chemical residues occurring in human fat, numerous technical shortcomings of this study have been described. For instance, the sample compositing prevents use of these data to examine the distribution of CDD/F levels in tissue among individuals. However, it did allow conclusions in the following areas:

n National Averages: The national averages for all TEQ congeners (but excluding dioxin-like PCBs) were estimated and totaled to 28 pg TEQ/g lipid adjusted value (28 ppt).

n Age Effects: Tissue concentrations of CDD/Fs were found to increase with age.

n Geographic Effects: In general, the average CDD/F tissue concentrations appeared fairly uniform geographically.

n Race Effects: No significant differences in CDD/F tissue concentrations were found on the basis of race.

n Sex Effects: No significant differences in CDD/F tissue concentrations were found between males and females.

n Temporal Trends: The 1987 survey showed decreases in tissue concentrations relative to the 1982 survey for all congeners. However, it is not known whether these declines were due to improvements in the analytical methods or actual reductions in body-burden levels. The fact that areas surveyed in this study changed over time (due to drop-out of areas) also makes interpretation of time trends difficult. The percent reductions among individual congeners varied from 9% to 96%. The relationship of these data to an apparent declining trend of dioxin-like compounds in environmental samples, especially sediments, is currently unclear.

More recent data (Patterson et al., 1994) show similar decreasing trends with regard to levels of dioxin-like PCBs in blood and fat. In addition, these data showed a wide variability of PCB congeners in human adipose tissue samples as compared to concentrations of CDDs and CDFs, which were less variable.

Inclusion of dioxin-like PCBs in TEQ calculations raises the average body burden to 40-60 pg TEQ/g (40-60 ppt). Because available data from the two studies discussed above do not provide a representative population sample, these conclusions must be regarded as uncertain. Additional measurements will be necessary to confirm this hypothesis. Use of a protocol for sampling that allows an evaluation of age-adjusted population averages will be critical for understanding the current body-burden situation and evaluating impacts of future efforts to further reduce exposures to this class of compounds.

Levels of dioxin-like compounds found in human tissue/blood appear similar in Europe and North America. Schecter (1991) compared levels of dioxin-like compounds found in blood among people from U.S. pooled samples (100 subjects) and Germany (85 subjects). Although mean levels of individual congeners differed by as much as a factor of two between the two populations, the total TEQ averaged 42 pg TEQ/g (42 ppt) in the German subjects and was 41 pg TEQ/g (41 ppt) in the pooled U.S. samples. These values do not include TEQs for PCBs.

New information on levels of dioxin-like compounds in human adipose tissue and blood has recently been published (Patterson et al., 1994). This study reports measurements of dioxin-like PCB congeners as well as CDD and CDF levels in samples from 28 Atlanta residents. These measurements show that concentrations of dioxin-like PCBs can be more than an order of magnitude higher than concentrations of TCDD. Comparison with other published information suggests much higher levels of nondioxin-like congeners of PCBs and the possibility that concentrations of both types of congeners will depend heavily on previous human activities such as fish consumption. These data are consistent with the previous statement that dioxin-like PCBs may account for approximately one-third of the total TEQ in the general population. Values in Patterson’s study calculated TEQs for PCBs using the data of Safe (1990), which were acknowledged by the author as being conservative and, based on more recent data, overestimate the contribution of dioxin-like PCBs.

While, as described above, evaluation of the range of background population blood levels is difficult given existing data, the NHATS tissue data show that the maximum measured concentrations were about two times higher than the average for most congeners (U.S. EPA, 1991). These results are based on composite samples that each included approximately 20 individual samples. This high level of compositing will greatly reduce the individual variability of samples. Consequently, the range in body burdens in the entire population is expected to be larger than that found among the samples in this study. The Patterson et al. (1994) data show that the maximum 2,3,7,8-TCDD concentration was about three to four times higher than the average. Similar results were seen for PCB 126. These results are based on samples of 28 individuals. Again, the range of body burdens in the entire population will be greater than that found among these 28 individuals. Accordingly, it can be concluded that body burdens of dioxin-like compounds are likely to be at least three to four times higher than the average for some members of the population and, perhaps, even higher. While it is difficult to know the full extent of the range of body burdens, the Patterson data were found to fit reasonably well as a log-normal distribution. This observation has also been made for other data sets (Sielken, 1987). With such distributions in large populations, it is not unusual to see values that extend three standard deviations beyond the mean. The body burdens corresponding to three standard deviations beyond the mean (99th percentile) have been estimated (using a log-scale calculation) to be approximately seven times higher than the arithmetic mean. Whether individuals with background levels of dioxin-like compounds of this magnitude exist in the general population is unknown, but these calculations provide support for the inference that the general population may have a wide range of body burdens and, therefore, both average and high end values should be considered when evaluating potential for adverse impacts of background exposures.

9.4.3. Highly Exposed Populations

In addition to general population exposure, some individuals or groups of individuals may also be exposed to dioxin-like compounds from discrete sources or pathways locally within their environment. Examples of these "special" population exposures include occupational exposures, direct or indirect exposure to local populations from discrete local sources, exposure to nursing infants from mother’s milk, or exposures to subsistence or recreational fishers. These exposures have been discussed previously in terms of increased exposure due to dietary habits (see Exposure Document) or due to occupational conditions or industrial accidents (see Chapter 7). Although exposures to these populations may be significantly higher than to the general population, they usually represent relatively small numbers of individuals. Inclusion of their levels of exposure in the general population estimates would have little impact on average estimates and would obscure the potential significance of elevated exposures for these subpopulations.

For example, consumption of breast milk by nursing infants may lead to higher levels of exposure during the early postnatal period as compared to intake in the diet later in life. Schecter et al. (1992) report that a study of 42 U.S. women found an average of 16 pg TEQ/g (16 ppt), 3.3 ppt of which was 2,3,7,8-TCDD, in the lipid portion of breast milk. A much larger survey in Germany (n=728) found an average of 31 pg TEQ/g (31 ppt) with a range of 6 to 87 pg TEQ/g in the lipid portion of breast milk (Beck et al., 1991). These estimates do not include a contribution to total TEQ from dioxin-like PCBs. The level in human breast milk can be predicted on the basis of the estimated dioxin intake by the mother. Such procedures are presented in Volume II of the Exposure Document.

Elimination of 2,3,7,8-TCDD through mother's milk can result in higher exposure levels to the infant than for the general population. Assuming that an infant breast feeds for one year (a conservative assumption since, in the United States, 6 months of breast feeding is more typical), has an average weight during this period of 10 kg (which is on the high end [90-98th percentile] of the average weight distribution for the first year of life), ingests 0.8 kg/d of breast milk and that the dioxin concentration in milk fat is 20 pg/g (20 ppt) of TEQ, the average daily dose to the infant over this period is predicted to be about 60 pg TEQ/kg/d, not including dioxin-like PCBs. This value is 10 to 20 times higher than the estimated range for background exposure to adults (i.e., 3-6 pg TEQ including dioxin-like PCBs/kg/d) and would have been even higher if dioxin-like PCBs had been included in this sample analysis. A range of alternative assumptions could be made regarding the nursing time period, infant’s body weight, and milk ingestion rate. None of these factors is likely to vary individually by more than a factor of two and, when combined, will likely result in less than multiplicative variability in estimates of daily intake. WHO (1988) suggested that a reasonable average nursing scenario would be 6 months duration, 0.7 L/day ingestion rate, and a milk fat content of 3.5%. Using a milk ingestion rate of 120 mL/kg/day (compared to 80 mL/kg/day used above) and a milk concentration of 16.9 pg TEQ/g, WHO estimated a daily intake of 70 pg TEQ/kg/day.

If a 70-year averaging time is used to obtain an added increment of lifetime daily dose, then the increment of lifetime average daily dose attributable to the EPA nursing scenario is estimated to be 0.8 pg of TEQ/kg/d. On a mass basis, the cumulative dose to the infant under this scenario is about 210 ng compared to a lifetime background intake of about 1,700 to 5,100 ng (suggesting that 4% to 12% of the lifetime intake may occur as a result of breast feeding for the first year of life). WHO (1988) estimated that 4% of the lifetime intake would occur during the 6 months of nursing in their scenario. This percentage, as well as the daily intake rate, is nearly identical to the estimates presented in the Exposure Document although based on somewhat different assumptions. Traditionally, EPA has used the lifetime average daily dose as the basis for evaluating incremental cancer risk and the average daily dose (i.e., the daily exposure per unit body weight occurring during an exposure event) as the more appropriate indicator of risk for certain noncancer end points. The use of a lifetime average daily dose for high-level, early exposures may underestimate cancer risk if dose rate or perinatal sensitivity is important in the ultimate carcinogenic outcome. The average daily dose approach may be particularly important for the evaluation of noncancer end points if exposure is occurring during windows of sensitivity during prenatal and postnatal development. However, data are currently insufficient to verify this hypothesis.

In addition, consumption of unusually high levels of fish, meat, or dairy products containing elevated levels of dioxin and related compounds can lead to elevated blood levels in comparison to the general population. Most people eat fish from multiple sources, both fresh and salt water, where levels of dioxin-like compounds are likely to be low. Even if large quantities of fish are consumed, most people are not likely to have unusually high exposures to dioxin-like compounds. However, individuals who fish regularly for purposes of basic subsistence are likely to obtain their fish from a few sources and may have the potential for elevated exposures. Such individuals may also consume large quantities of fish. Although average consumers may eat a few fish meals a month (an average intake of approximately 6.5 grams of fish a day), many recreational anglers near large water bodies may consume, on average, four to five times as much (approximately 30 grams per day). Of course, these averages include some individuals who eat no fish at all. Some individuals at the high end of the consumption range may eat, on average, as much as 140 grams per day. Certain members of ethnic groups who are subsistence fishers may consume two to three times this high-end amount as an upper estimate (up to 400 grams or approximately 1 pound per day). If high-end consumers obtain their fish from areas where content of dioxin-like chemicals in the fish is high, they may constitute a highly exposed subpopulation. Svensson et al. (1991) found elevated blood levels of CDDs and CDFs in high fish consumers living near the Baltic Sea in Sweden. The highest consumers, fishermen or workers in the fish industry, had blood level TEQs that were approximately three times that of non-fish consumers (60 pg TEQ/g lipid versus 20 pg TEQ/g lipid). The difference in levels of dioxin-like compounds was particularly apparent for the CDFs. Dioxin-like PCBs were not accounted for in this study. Studies are currently under way to examine fish consumption patterns in several Native American groups. Recent results (Columbia River Intertribal Fish Commission, 1994) suggest that Native Americans living along the Columbia River may consume an average of 30 grams of fish a day; some individuals consume much higher levels. Studies are currently under way to determine levels of dioxin-like compounds in fish from this region. No measurements of dioxin-like chemicals in the blood of these Native American populations are currently available.

Dewailly et al. (1994) observed elevated levels of coplanar PCBs in the blood of fishermen on the north shore of the Gulf of the St. Lawrence River who consume large amounts of seafood. Coplanar PCB levels were 20 times higher among the 10 highly exposed fishermen than among controls. This study also reported elevated levels of coplanar PCBs in the breast milk of Inuit women of Arctic Quebec. The principal source of protein for the Inuit people is fish and sea mammal consumption.

The possibility of high exposures to dioxin-like chemicals as a result of consuming meat and dairy products is most likely to occur in situations where individuals consume large quantities of these foods from a locality where the level of these compounds is elevated. Most people eat meat and dairy products from multiple sources and, even if large quantities are consumed, are not likely to have unusually high exposures. However, individuals who raise their own livestock for basic subsistence have the potential for higher exposures if local levels of dioxin-like compounds are high. Volume III of the Exposure Document presents methods for evaluating this type of exposure scenario and concludes that indirect exposures via consumption of locally produced foods represent a major pathway for human exposure for a limited number of individuals in the population. In an example analysis contained in Volume III of the Exposure Document based on proximity to combustor emissions, the high end exposure estimates from food consumption were found to be about two orders of magnitude higher than inhalation exposures at the same location. However, it should be noted that no studies were found in the literature to demonstrate this potential increased exposure based on measurements of dioxin-like chemicals from source to livestock to humans.

Although the subpopulations discussed above have the potential for high exposure to dioxin-like compounds, a careful evaluation of dietary habits and proximity to sources of dioxin and related compounds is needed. It would generally be inappropriate to compute the total intake of dioxin-like compounds in a subpopulation by simply adding the dioxin intake from highly consumed food to the general population intake level. The general population background estimate assumes a typical pattern of food ingestion, whereas a subpopulation that has a high consumption rate of one particular food type is likely to eat less of other food types. Ideally, the evaluation should be based on the entire diet of the subpopulation and use case-specific values for food ingestion rates and concentrations of dioxin-like compounds.