II.3.3.Conclusions for Mechanisms of Impact to Food Chain

CDD/F can enter aquatic systems by either direct effluent discharges or atmospheric deposition. CDD/Fs in the atmosphere can deposit directly onto water bodies or onto watersheds and run off into the water system. The mechanism of impact which dominates in aquatic systems will depend on site specific conditions. This assessment proposes the hypothesis that the primary mechanism by which dioxin-like compounds enter the terrestrial food chain is via atmospheric deposition.

Deposition can occur directly onto plant surfaces or onto soil. Soil deposits can enter the food chain via direct ingestion (i.e. earth worms, fur preening by burrowing animals, incidental ingestion by grazing animals, etc). CDD/F in soil can become available to plants by volatilization and vapor absorption or particle resuspension and adherence to plant surfaces. In addition, CDD/F in soil can adsorb directly to underground portions of plants, but uptake from soil via the roots into above ground portions of plants is thought to be insignificant (McCrady, et al. 1990).

Support for this air-to-food hypothesis is provided by Hites (1991) who concluded that "background environmental levels of PCD/F are caused by PCD/F 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 argument supporting this hypothesis is offered below:§ Numerous studies have shown that CDD/Fs are emitted into the air from a wide variety of sources (see Chapter 3 of Volume II).§ Studies have shown that CDD/Fs can be measured in wet and dry deposition in most locations including remote areas (Koester and Hites, 1993; Rappe, 1991).§ Numerous studies have shown that CDD/Fs are commonly found in soils throughout the world (see Chapter 4 of Volume II).

Atmospheric transport and deposition is the only plausible mechanism that could lead to this widespread distribution.§ Models of the air-to-plant-to-animal food chain have been constructed. Exercises with these models show that measured deposition rates and air concentrations can be used to predict measured food levels (Travis and Hattemer-Frey, 1991; also see Chapter 7 of Volume III).Alternative mechanisms to the air-to-food hypothesis seem less likely:

- Uptake from water into food crops and livestock is minimal due to the hydrophobic nature of these compounds. Travis and Hattemer-Frey (1987, 1991) estimate water intake accounts for less than 0.01% of the total daily intake of 2,3,7,8-TCDD in cattle. Experiments by McCrady, et al. (1990) show very little uptake in plants from aqueous solutions.

- Relatively little uptake is expected in food from soil residues that originate from sources other than atmospheric dispersion, i.e. pesticides, sewage sludge, and waste disposal operations. Pesticides are discussed below. Sewage sludge application onto agricultural fields is not a widespread practice and the amount of CDD/F in this material is quite low compared to the amount emitted to the atmosphere (See Chapter 3 of Volume II).

Waste disposal operations can be the dominant source of CDD/F in soils at isolated locations such as Times Beach, but are not sufficiently widespread to explain the ubiquitous nature of these compounds.

- The contribution of CDD/Fs to the environment via pesticides has been reduced in recent years but remains somewhat uncertain. In the past, CDD/Fs have been associated with certain phenoxy herbicides. Many of these compounds are no longer produced and EPA has sponsored data call-ins requiring certain pesticide manufacturers to test their products for dioxin content. The responses, so far, indicate that levels in these products are below or near the limit of quantitation (see Chapter 3 of Volume II).

- Uptake into food from paper products also appears to be minimal. In the early 1980s, testing showed that CDD/Fs could migrate from paper containers into food. Current levels in paper products are now much lower, and food testing in products such as milk and beef have shown detectable levels prior to packaging, suggesting packaging is not the major source (see Chapter 4 of Volume II).

A related issue is whether the CDD/F in food results more from current or past emissions. Sediment core sampling indicates that CDD/F levels in the environment began increasing around the beginning of the twentieth century and have been declining since about 1980 (Smith et al, 1992).

Thus, CDD/Fs have been accumulating for many years and may have created a reservoir that continues to impact the food chain. As discussed in Chapter 3 of Volume II, researchers in several countries have attempted to compare known emissions with deposition rates. These studies may suggest that annual deposits exceed annual emissions.

One explanation may be that the reservoir sources cause deposition through volatilization/atmospheric scavenging or particle resuspension. These mass balance studies are highly uncertain and it remains unknown how much of the food chain impact is due to current versus past emissions.


Small amounts of dioxin-like compounds may be formed during natural fires suggesting that these compounds may have always been present in the environment. However, it is generally believed that much more of these compounds have been produced and released into the environment in association with man's industrial and combustion practices, and as a result, environmental levels are likely to be higher in modern times than they were in prior times. However, the trend may now be reversing (i.e., releases and environmental levels may be gradually decreasing) due to changes in industrial practices (Rappe, 1992).

As discussed earlier, the potential for environmental 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, improved emission controls for incinerators, and reductions in the manufacture and use of chlorinated phenolic intermediates and products.

Studies that may be used to assess temporal trends in human exposure to dioxins and furans are extremely limited. Analysis of sediment core layers has shown increases in CDD/CDF concentrations beginning in the 1920's and continuing until the late 1970's (Smith et al, 1992). Another useful study for evaluating changes in human exposure over time is EPA's National Human Adipose Tissue Survey or NHATS. The purpose of NHATS is to monitor the human body burden of selected chemicals in the general U.S. population (EPA, 1991a).

The results of this study indicate that exposure to certain dioxins and furan congeners may have decreased over this 5-year time period. However, further studies are needed to verify that these changes are not a result of protocol changes, but actual reductions in exposures. A recent study by Patterson et al. (1994) found decreases in PCB body burdens from 1982 to 1988/89 based on human tissue and blood testing.


Table II-6 illustrates the derivation of a background exposure level to CDD/F for the United States on the basis of diet. This estimate was derived using the upper-range background concentrations (i.e., those calculated using one-half the detection limit for the non-detects) and central estimates of ingestion rates. This approach yields a total background exposure estimate for CDD/Fs of 119 pg TEQ/d. The exposures by pathway are diagrammed in Figure II-5.

The background exposure estimates are intended to be representative of the general population. They do not account for individuals with higher consumption rates of a specific food group (e.g., subsistence fishermen, nursing infants, and subsistence farmers--these are discussed Section II-6). The fish concentration used to estimate background exposures, represents the average value found in fish from fresh and estuarine waters (see Section 4.5 of Volume II).

Correspondingly, the ingestion rate used here reflects the per capita average ingestion rate of fresh/estuarine fish (EPA, 1989). Many individuals are likely to have higher ingestion rates of marine fish. However, the limited data on marine species indicates that the dioxin levels may be one to two orders of magnitude lower than fresh/estuarine water fish (also see Section 4.5 of V. II).

table Table II-6. Estimated TEQ background exposures in the United States.
The contact rates for ingestion of fish, soil, and water, and inhalation were derived from the Exposure Factors Handbook (EPA, 1989). For food products such as milk, dairy, eggs, beef, pork, and poultry, a different approach was taken because there is evidence that consumption rates have changed since the data for the Exposure Factors Handbook were collected. Contact rates for these food groups were derived from commodity disappearance data from the United States Department of Agricultures's (USDA) report on Food Consumption, Prices, and Expenditures between 1970 and 1992 (USDA, 1993), and intake data from USDA's Nationwide Food Consumption Survey (NFCS) (USDA, 1992). USDA (1993) estimated per capita consumption rates using disappearance data (i.e., the quantity of marketable food commodities utilized in the United States over a specified time period) divided by the total population.
expand table Table VX X-X

The average of USDA disappearance and NFCS intake rates were used in this study to represent the most current estimates of typical ingestion rates in the United States.

These background exposure estimates for the United States are comparable to analogous estimates for European countries, as displayed in Figure II-6. These include estimates for Germany, which range from 79 pg TEQ/day based on Fürst, et al. (1990) to 158 pg TEQ/day based on Fürst, 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. Over 90 percent of human exposure is estimated to occur through the diet, with foods from animal origins being the predominant sources.Background exposures can also be estimated on the basis of body burdens through the use of pharmacokinetic models. Pharmacokinetic compartmental models are presented in Chapter 6 of Volume II which can be used to estimate daily dose intake of 2,3,7,8-TCDD from adipose tissue or blood lipid concentrations.

Using this approach, exposure levels to 2,3,7,8-TCDD are estimated to be about 10 to 30 pg/day which is consistent with the estimates derived using diet-based approaches. The model can also be applied to other dioxin congeners with knowledge of their biophysical properties.

The most extensive United States study of CDD/F body burdens is the National Human Adipose Tissue Survey (NHATS) (EPA, 1991a). This survey 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. The sample compositing prevents use of this data to examine the distribution of CDD/F levels in tissue among individuals. However, it did allow conclusions in the following areas:

. National Averages:
The national averages for all TEQ congeners were estimated and totaled to 28 pg of TEQ/g.

table Figure II-5 Background TEQ exposures for North America by pathway. table Figure II-6 Comparison of background TEQ exposures for North America, Germany, and the Netherlands.
expand table Figure VX X-X expand table Figure VX X-X
. Age Effects:
Tissue concentrations of CDD/Fs were found to increase with age.

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

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

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

. 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 percent reductions among individual congeners varied from 9 percent to 96 percent.

New information on levels of dioxin-like compounds in human tissue/blood has recently been published (Patterson et al., 1994). The adipose tissue samples (collected from 28 individuals) were analyzed for PCBs 77, 81, 126 and 169. The TEQ levels for these coplanar PCBs summed to 17 ppt (using the toxic equivalency factors proposed by Safe, 1990).

The PCB levels generally exceeded the mean 2,3,7,8-TCDD level (10.4 ppt) and PCB-126 exceeded the 2,3,7,8-TCDD level by over an order of magnitude. The authors found that the PCBs contributed 24% of the total TEQs. Patterson et al. (1994) also studied serum collected by the CDC blood bank in Atlanta during 1982, 1988 and 1989. These samples were pooled from over 200 donors. The serum data appears to indicate a decrease in exposure to PCBs from 1982 to 1988/1989.

In general, the Patterson et al. (1994) data suggests that the coplanar PCBs can contribute significantly to body burdens of dioxin-like compounds. The data suggest that the coplanar PCBs can increase the total background body burden to over 40 ppt of TEQ. This conclusion is uncertain because the people studied by Patterson et al. (1994) may not be representative of the overall U.S. population, and the toxic equivalency factors proposed by Safe (1990) have been acknowledged to be conservative.

Levels of these 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. (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 ppt in the German subjects and was 41 ppt in the pooled U.S. samples.


Certain groups of people may have higher exposures to the dioxin-like compounds than the general population. This section discusses such exposures which result from dietary habits. Other population segments can be highly exposed due to occupational conditions or industrial accidents and are discussed in the Epidemiology Chapter if the Dioxin Health Reassessment Document (EPA, 1994) and should be consulted if further details are desired.

Although the subpopulations discussed below have the potential for high exposure to dioxin-like compounds, a careful evaluation is needed to confirm this possibility. It would generally be inappropriate to compute the total background exposure for a certain group by simply adding the dioxin intake from the highly consumed food to the background exposure levels.

The background exposure estimate assumes a typical pattern of food ingestion, whereas persons in a subpopulation who have a high consumption rate of one particular food type are likely to eat less of other food types. Ideally, the assessor should base this evaluation on the entire diet of the subpopulation and use case-specific values for food ingestion rates and concentrations of dioxin-like compounds.One group of potentially highly exposed individuals is nursing infants. Schecter et al. (1992) reports that a study of 42 U.S. women found an average of 16 ppt of TEQ (3.3 ppt of 2,3,7,8-TCDD) in the lipid portion of breast milk.

A much larger study in Germany (n = 526) found an average of 29 ppt of TEQ in lipid portion of breast milk. The level in human breast milk can be predicted on the basis of the estimated dioxin intake by the mother. Such procedures have been developed by Smith (1987) and Sullivan et al. (1991) and are presented in Chapters 5 and 6 of Volume II.

Using these procedures and assuming that an infant breast feeds for one year, has an average weight during this period of 10 kg, ingests 0.8 kg/d of breast milk and that the dioxin concentration in milk fat is 20 ppt of TEQ, the average daily dose to the infant over this period is predicted to be about 60 pg of TEQ/kg-d. This value is much higher than the estimated range for background exposure to adults (i.e., 1-3 pg of TEQ/kg-d). However, if a 70 yr averaging time is used, then the lifetime average daily dose is estimated to be 0.8 pg of TEQ/kg-d which is near the lower end of the adult background exposure range.

On a mass basis, the cumulative dose to the infant under this scenario is about 210 ng compared to a lifetime background dose of about 1700 to 5100 ng (suggesting that 4 to 12 percent of the lifetime dose may occur as a result of breast feeding). Traditionally, EPA has used the lifetime average daily dose as the basis for evaluating 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 noncancer endpoints. This issue is discussed further in the companion document on dioxin health effects.

The possibility of high exposure to dioxin as a result of fish consumption is most likely to occur in situations where individuals consume a large quantity of fish from one location where the dioxin level in the fish are elevated above background levels. Most people eat fish from multiple sources and even if large quantities are consumed are not likely to have unusually high exposures. However, individuals who fish regularly for purposes of basic subsistence are likely to obtain their fish from one source and have the potential for elevated exposures.

Such individuals may consume quite large quantities of fish. EPA (1989) presents studies that indicate that recreational anglers near large water bodies consume 30 g/d (as a mean) and 140 g/d (as an upper estimate). Wolfe and Walker (1987) found subsistence fish ingestion rates up to 300 g/d in a study conducted in Alaska.

Several studies have identified potentially highly exposed populations as a result of fish consumption:

Svensson et al. (1991)
found elevated blood levels of CDDs and CDFs in high fish consumers living near the Baltic Sea in Sweden.

• 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 the controls. Dewailly et al. (1994) also observed 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

• Studies are underway to evaluate whether native Americans living on the Columbia River in Washington have high dioxin exposures as a result of fish consumption. These tribes consume large quantities of salmon from the river. A recent study (Columbia River Intertribal Fish Commission, 1993) suggests that these individuals have an average fish consumption rate of 30 g/day. Currently studies are underway to measure dioxin levels in fish from this region.

The possibility of high exposure to dioxin as a result of consuming meat and dairy products is most likely to occur in situations where individuals consume a large quantity of these foods from one location where the dioxin level is elevated above background levels. Most people eat meat and diary products from multiple sources and even if large quantities are consumed are not likely to have unusually high exposures.

Individuals who raise their own livestock for purposes of basic subsistence, however, have the potential for elevated exposures. No epidemiological studies were found in the literature evaluating this issue. Volume III of this document, however, presents methods for evaluating this type of exposure on a site-specific basis.

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