Volume II Chapter 5.0 Pages 2 of 2 page    
      • 5.4.1. Human Adipose Tissue and Blood Data 5-18
      • 5.4.2. Dermal Exposure 5-27
      • 5.5.1. Nursing Infants 5-29
      • 5.5.2 Subsistence Fishers 5-33
      • 5.5.3. Subsistence Farmers 5-34


5.4.1. Human Adipose Tissue and Blood Data

Examination of body burden data provides another, potentially more accurate, way to estimate exposures of humans to CDD/CDFs. However, these data may not represent only background exposure to CDD/CDFs as defined here because the sampled individuals may have lived in areas where dioxin sources were present.

The most extensive U.S. study of CDD/F body burdens is the National Human Adipose Tissue Survey (NHATS) (EPA, 1991b). This survey analyzed for CDD/Fs in 48 human tissue samples that were composited from 865 samples. Each composite contained an average of 18 specimens. These samples were collected during 1987 from autopsied cadavers and surgical patients. 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:

. National Averages - The national averages for all TEQ congeners were estimated as listed in Table 5-8. Nondetects were treated as half the detection limit for averaging purposes. As shown in this table, all congeners except some of the CDFs had a very low frequency of nondetects. Thus, the overall TEQ estimate is not sensitive to how nondetects were treated in the averaging.

· 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. Only one TEQ congener was found to have a significant difference among geographic regions of the country. This compound, 2,3,4,7,8-PeCDF, was found at the lowest level in the West (4.49 pg/g) and the highest in the Northeast (13.7 pg/g).

· Race Effects - No significant difference in CDD/F tissue concentrations was found on the basis of race.

· Sex Effects - No significant difference in CDD/F tissue concentrations was 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). Human adipose from 28 individuals was collected. The individuals studied were ones that died suddenly in the Atlanta area during 1984 or 1986. Their ages ranged from 19 to 78 yr and averaged 49 yr. The tissue data are summarized in Table 5-9.

This table shows that the mean PCB levels generally exceeded the mean 2,3,7,8-TCDD level and PCB-126 exceeded the 2,3,7,8-TCDD level by over an order of magnitude. The mean TEQ levels for these coplanar PCBs summed to about 17 ppt (using the toxic equivalency factors proposed by Safe, 1990). A complete CDD/F congener analysis was conducted on tissues of five of the individuals, resulting in an average of 25 ppt on a TEQ basis.

These tissue samples were also analyzed for PCBs 77, 126 and 169. The TEQ levels for these coplanar PCBs summed to 8.2 ppt (using the toxic equivalency factors proposed by Safe, 1990). Thus, 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.

table Table 5-8 NHATS Mean Adipose Tissue Data. table Table 5-9 Human Adipose Tissue Data.
expand table Table V2 5-8 expand table Table V2 5-9

These samples were pooled from over 200 donors. The average levels for 2,3,7,8-TCDD and PCBs are summarized in Table 5-10. 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.

Schecter et al. (1993) reported on the comparison of the congener-specific measurement of CDDs, CDFs, and dioxin-like PCBs in whole blood samples of four individuals with known exposures to that of the general population. In this comparison, the analytical results of separate 450 ml blood samples collected from 50 Michigan residents, and a pooled blood sample from 5 donors at a blood bank in Missouri were used as the control group.

Two of the exposed individuals were pulp and paper plant workers with potential exposure to dioxins, and the other two were Michigan residents who had elevated blood PCB levels from consuming contaminated fish. It was found that the control group and the pulp and paper mill workers who had no known exposures to PCBs had relatively high levels of coplanar, mono-ortho and di-ortho PCBs in their whole blood.

On average, the Michigan and Missouri control samples showed a mean CDD/CDF TEQ concentration of 27 ppt and 25 ppt, respectively. These same samples showed PCB-TEQ (based on Safe, 1990) mean concentrations of 66 ppt for the Michigan controls, and 45 ppt for Missouri controls.

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. pooled samples from 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. In a later report, Schecter et al. (1994a) reported human blood levels for the general population from various countries.

These data are presented in Table 5-11. Schecter (1991) reports adipose tissue levels in various countries, as summarized in Table 5-12.

table Table 5-10 Mean Levels in Human Serum (ppt). table Table 5-11 CDD/CDF Levels in Human Blood from Various Countries.
expand table Table V2 5-10 expand table Table V2 5-11
table Table 5-12 Dioxin Levels in Human Adipose Tissues from Various Countries.
The adipose tissue data show more variation between countries but also involved much fewer samples, reducing confidence in the accuracy of the mean. Beck et al. (1994) reported on levels of CDD/CDFs in adipose tissue from 20 males (mean age-50 years) from Germany.

TEQs ranged from 18 ppt to 122 ppt with a mean of 56 ppt, on a fat weight basis. Beck et al. (1994) also observed that CDD/CDF levels were found to be dependent on the age of the individual. 2,3,7,8-TCDD was found to increase at a rate of 0.12 pg/g fat per year, and TEQs increased at a rate of 0.77 pg/g fat per year.

Beck et al. (1994a) also reported on CDD/CDF levels in various organs of the body.
expand table Table V2 5-12

In comparison to adipose tissue, the concentrations of CDD/CDFs in brain and placental tissue were found to be low. Accumulation of CDD/CDFs was not found to occur in the thymus, spleen, and liver, based on whole weight concentrations. Schecter et al. (1994a) also reported on TEQ levels in organs of two autopsy patients from New York.

The highest concentrations of CDD/CDFs were found in adipose tissue (28 ppt TEQ), adrenal tissue (14 ppt TEQ), and liver (12 ppt TEQ), on a whole weight basis. Lower concentrations were observed in spleen (4.6 ppt TEQ), muscle (2.4 ppt TEQ), and kidney (0.8 ppt TEQ). Schecter et al. (1994b) reported PCB levels for these two autopsy potients. Total PCBs in adipose tissue were 280.7 ppb on a wet weight basis and 344.2 ppb on a lipid weight basis.

In Chapter 6, the level of 2,3,7,8-TCDD found in human adipose tissue is assumed to average about 5.0 to 6.7 ppt in the United States based on data from a variety of studies. These adipose tissue data were used to estimate the associated exposure levels using a simple pharmacokinetic model that back calculates the dose needed to achieve the observed adipose tissue levels under the assumption of steady state exposure/dose. This model requires an estimate of the elimination rate constant.

Based on available data, this elimination rate constant was assumed to be about 5 to 7 years which yielded a background dose rate of about 10 to 31 pg/day. This estimate agrees very well with the background exposure estimates (to 2,3,7,8-TCDD only) of 35 pg/day by Travis and Hattemer-Frey (1991), 25 pg/day by Fürst et al. (1991) and 12 pg/day from this assessment, all derived using typical media levels and contact rates. Further discussion of body burden data and associated exposures is presented in Chapter 6.

Chapter 6 presents biologically-based pharmacokinetic models to estimate body burden levels. Some less sophisticated approaches have also been presented in the literature. For example, Travis and Hattemer-Frey (1988) developed linear relationships between the bioaccumulation of organic chemicals in human tissues and the octanol-water partition coefficients (Kow) of the chemicals.

The biotransfer factors (BTFs) that can be calculated using this relationship can be used to estimate adipose tissue and breast milk concentrations of organics. The BTF for human adipose tissue (Bf) is defined as the concentration of an organic in adipose tissue (mg/kg) divided by the average daily intake of that organic (mg/day). The human breast milk BTF (Bm) is defined as the concentration of an organic in breast milk (mg/kg) divided by the average daily intake of that organic (mg/day). Adipose tissue and milk concentrations are assumed to be equilibrium concentrations resulting from long-term, consistent daily intake of an organic.

Measured tissue concentrations and either measured or estimated daily chemical intakes were used to estimate the BTFs (12 chemicals for Bf and 6 chemicals for Bm). Geometric mean regression analysis was used to ascertain the correlation between Kow values and the calculated BTFs. The results of the analyses are as follows:

Diagram V2 5-1

The high correlation coefficients demonstrate that the BTFs for human adipose tissue and breast milk are strongly, positively correlated with the octanol-water coefficient. While the data upon which these correlations are based are limited both in terms of number of chemicals and the extent of measured vs. estimated intakes, the results are consistent with results reported by Travis and Hattemer-Frey (1988) for beef and dairy cattle.

5.4.2. Dermal Exposure

Horstman and McLachlan (1994) measured CDD/F levels in human skin using an adhesive tape stripping method. Skin samples of the stratum corneum were collected from the backs of eight volunteers of varying age and sex. Two additional layers of increasing depth were collected from 5 people. All showed a decrease in CDD/F levels with depth.

The concentration in the first layer ranged from 1,000 to 7,800 pg/g on a total CDD/F basis. The second layer was an average of 43 percent lower and the third layer was an average of 33 percent lower. OCDD was the dominant congener in all three layers. Also, non-2,3,7,8 substituted congeners were identified, congeners which are not normally present in human tissue.

In addition, samples of the epidermis and subcutis were analyzed. These analyses indicated that levels of the non-2,3,7,8 substituted congeners were much higher in the stratum corneum than in the epidermis and none were identified in the subcutis. The authors argue that because these congeners could not be transported from inside the body to the stratum corneum, the CDD/F in the stratum corneum must originate from external sources.

Horstman and McLachlan (1994) hypothesized that textiles could be the source of skin contamination. Thirdy-five new textiles, primarily cotton products, were analyzed and found to have a total CDD/F level that was generally less than 50 ng/kg, but several colored T-shirts had high levels, with concentration up to 290,000 pg/g. The homolog patterns in the textiles were similar to the patterns found in the skin. Experiments were then conducted measuring the CDD/F levels in human skin before and after wearing T-shirts. Significant increases in CDD/F levels in the skin occurred after wearing the highly contaminated shirts for 1-2 weeks and significant decreases in CDD/F levels in the skin occurred after wearing the uncontaminated shirts for 1-2 weeks.

Thus, this work strongly suggests that dermal exposure to textiles may be contributing to background exposures to CDD/Fs. Horstman and McLachlan (1994) comment that although the levels of most CDD/F congeners in humans can be explained on the basis of diet, the origins of OCDD in humans is less clear. Since OCDD was found to be the dominant congener in textiles and skin, they speculate that the human body burden of this congener may result from dermal absorption. Horstman and McLachlan (1994) further discuss that human scale (stratum corneum) contributes to house dust and could lead to exposure via inhalation.


Certain groups of people may have higher exposures to the dioxin-like compounds than the general population. The following sections discuss the potential for higher exposures that result from dietary habits. Other population segments can be highly exposed due to occupational conditions or industrial accidents.

For example, several epidemiological studies have evaluated whether elevated dioxin exposure has occurred to certain workers in the chemical industry, members of the Air Force who worked with Agent Orange, and residents of Seveso, Italy who were exposed as a result of a pesticide plant explosion. These epidemiological studies are fully discussed in the Epidemiology Chapter of the Dioxin Health Reassessment Document (EPA, 1994) and should be consulted if further details are desired.

Although certain subpopulations 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 particular group by simply adding the dioxin intake from the highly consumed food to the typical background exposure levels. 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 the dioxin-like compounds. The following points should be considered:

. Ingestion Rates - A subpopulation who has a high consumption rate of one particular food type is likely to eat less of other food types. For example, a subsistence fisher may ingest much more fish than the typical individual, but is also likely to ingest less meat of other types. Lacking case-specific data, it may be reasonable to assume that most people generally consume the same total amount of meats. The background exposure estimate assumes ingestion of 230 g/d of meat and eggs. Thus, as a first approximation, if a subsistence fisher consumes 140 g/d of fish, then he may consume 90 g/d of other meats and eggs.

. Concentrations in Foods - The levels of dioxin-like compounds in all major food types should be established on a case-specific basis. This is particularly important for the food groups which are consumed at unusually high rates.

. Estimating Intake - Finally the ingestion rates and concentrations are multiplied to get intake of dioxin-like compounds for each food category and then summed. This total can be compared to the typical intake of 119 pg of TEQ/d to determine if the subpopulation is truly exposed over background levels.

5.5.1. 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 (Fürst et al., 1994). Bates et al. (1994) analyzed breast milk samples from 38 women in New Zealand and reported mean lipid-based TEQs of 16.5 ppt for urban women and 18.1 ppt for rural women.

The age of the mother was found to be positively correlated with the concentration of CDD/CDFs in breast milk. Beck et al. (1994) reported a mean TEQ of 30 ppt in the milk fat based on 112 human milk samples from Germany. The congeners that contributed the most to the total TEQ were 2,3,4,7,8-PeCDF (35 percent), total HxCDD (22 percent), and 1,2,3,7,8-PeCDD (21 percent).

Beck et al. (1994) observed that CDD/CDFs levels decreased with the number of children and the duration of breast feeding, but increased with the age of the mother. Beck et al. (1994) also compared the adipose tissue levels of breast-fed and bottle-fed infants who had died of sudden infant death syndrome. The breast-fed infants had higher tissue levels (5.4 to 22 pg/g fat; n=4) than the bottle-fed infants (2.1 to 4.4 pg/g fat; n=2).

The levels 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 also presented in Chapter 6. The approach by Smith assumes that the concentration in breast milk fat is the same as in maternal fat and can be calculated as:

Formula V2 5-1

This steady-state model assumes that the contaminant levels in maternal fat remain constant. Though not described here, Smith (1987) also presents more complex approaches that account for changes in maternal fat levels during breast feeding. The model developed by Sullivan et al. (1991) is a variation of the models proposed by Smith (1987). The Sullivan model considers changes in maternal fat levels and predicts chemical concentrations in milk fat as a function of time after breast feeding begins. The model proposed by Smith assumes that infant fat concentration at birth is zero, whereas Sullivan assumes that the infant fat concentration at birth is equal to the mother's fat concentration.

As discussed in Chapter 6, the half-life of 2,3,7,8-TCDD in humans is estimated to be 5 to 7 years. For the purpose of this preliminary analysis, it is assumed that a 7-year half-life applies to all of the dioxin-like compounds. Smith (1987) suggests values of 0.9 for f1 and 0.3 for f2. Using these assumptions and a background exposure level of 1 to 3 pg of TEQ/kg-d (derived from diet analysis, see Section 5.3), the concentration in breast milk fat is predicted to be about 10 to 30 ppt of TEQ, which agrees well with the measured values.

Using the estimated dioxin concentration in breast milk, the dose to the infant can be estimated as follows:

Formula V2 5-2

This approach assumes that the contaminant concentration in milk represents the average over the breast feeding time period. If the dynamic models mentioned above are used, the dose can be estimated using an integration approach to account for the changes in concentration over time.

Smith (1987) reports that a study in Britain found that the breast milk ingestion rate for 7 to 8-month old infants ranged from 677 to 922 ml/d and that a study in Houston measured the mean production of lactating women to range from 723 to 751 g/d. Smith (1987) also reports that breast milk ingestion rates remain relatively constant over an infant's life, that the milk can be assumed to have a 4 percent fat content, and that 90 percent of the ingested contaminant are absorbed. The National Center for Health Statistics (1987) reports the following mean body weights for infants:

6-11 months: 9.1 kg

1 year: 11.3 kg

2 year: 13.3 kg

Using Equation 5.2 and assuming that an infant breast feeds for 1 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 ADD to the infant over this period (i.e., AT = 1 yr) 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 year averaging time is used, then the LADD (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 LADD as the basis for evaluating cancer risk and the ADD (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 Chapter 6 and in the companion document on dioxin health effects.

The simplified procedure described above contains a number of uncertainties. A tendency toward overestimates of the dose to the infant is caused by the assumption that reductions do not occur in maternal fat levels during breast feeding. Sullivan et al. (1991) estimates that the steady-state assumption may lead to overestimates of 20 percent.

Uncertainty is also introduced by the assumption that the assumed half-life rate and partitioning factors apply to all the dioxin related compounds. Although these properties are likely to be similar among the various congeners, some variation is expected. It is unknown whether the net effect of these uncertainties would lead to over or under estimates of dose.

However, the simple model appears to provide reasonable predictions of background levels found in breast milk and was judged adequate for purposes of a preliminary analysis. For detailed assessments, readers should consider using the more complex models and developing chemical-specific property estimates.

Travis and Hattemer-Frey (1988) presented an alternative approach to estimating breast milk contaminant levels. They proposed a biotransfer approach:

Formula V2 5-3

They also argue that the biotransfer factor is primarily a function of the octanol-water partition coefficient (Kow ) and developed the following geometric mean regression:

Formula V2 5-4

This regression was derived from data on 6 lipophilic compounds (log Kow range: 5.16 to 6.5), but did not include any dioxins or furans. Assuming a log Kow of 6.6 for 2378-TCDD, a Bm of 3700 kg/d is predicted.

Combing this value with a maternal intake of 10 pg/d (or 10-7 mg/d), a breast milk concentration of 37 ppt is predicted. This prediction is about 10 times higher than what has been measured in the U.S. Thus, this approach does not appear to work as well as the earlier approach suggested by Smith et al (1987).

5.5.2 Subsistence Fishers

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

Svensson et al. (1991) found elevated blood levels of CDDs and CDFs in high fish consumers living near the Baltic Sea in Sweden. Three groups were studied: nonconsumers (n=9), moderate consumers (n=9, 220 to 500 g/wk) and high consumers (n=11, 700-1750 g/wk). The high consumer group was composed of fishermen or workers in the fish industry who consumed primarily salmon (30 - 90 pg TEQ/g) and herring (8-18 pg TEQ/g) from the Baltic Sea. The TEQ blood level was found to average about 60 pg TEQ/g lipid among the high consumers and 20 pg TEQ/g lipid for the nonconsumers. This difference was particularly apparent for the PeCDFs.

Studies are underway to evaluate whether native Americans living on the Columbia River in Washington have high dixoin 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 and a 95th percentile rate of 170 g/day. Currently studies are underway to measure dioxin levels in fish from this region.

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. Of the 185 study samples, the 10 samples with the highest total PCB levels were analyzed for coplanar PCBs.

Samples from Red Cross blood donors in Ontario served as controls. Coplanar PCB levels were 20 times higher among the 10 highly exposed fishermen than among the controls. Based on these results of the 10 highest samples, Dewailly et al. (1994) estimated that for the entire fishing population studied, coplanar PCB levels would be eight to ten times higher than the control group.

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. Breast milk samples were collected from 109 Inuit women within the first three days after delivery and analyzed for di-ortho-coplanar PCBs during 1989 and 1990. Subsets of 35 and 40 randomly selected samples were analyzed for mono-ortho coplanar and non-ortho coplanar PCBs, respectively.

Samples from 96 caucasian women from Quebec served as controls. The levels of non-ortho coplanar PCBs for Inuit women ranged from 24.7 to 220.9 ppt. These values were 3 to 7 times higher than those observed in the control group. For mono-ortho and di-ortho coplanar PCBS, the levels among the Inuit women were three to ten times higher than in the control group.

5.5.3. Subsistence Farmers

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 they are not likely to have unusually high exposures. However, individuals who raise their own livestock for purposes of basic subsistence have the potential for elevated exposures. No epidemiological studies were found in the literature that evaluated this issue. However, Volume III of this document presents methods for evaluating this type of exposure on a site-specific basis.


  • Bates, M.N.; Hannah, D.J.; Buckland, S.J.; Taucher, J.A.; Van Maanen, T. (1994) Chlorinated organic contaminants in breast milk of New Zealand women. Environmental Health Perspectives. Vol. 102, Suppl. 1:211-217.
  • Beck, H.; Dross, A.; Mathar, W. (1994) PCDD and PCDF exposure and levels in humans in Germany. Environmental Health Perspectives. Vol. 102, Suppl. 1:173-185.
  • Columbia River Intertribal Fish Commission (1993) A fish consumption survey of the Umtilla, Nez Perce, Yakima, and Warm Springs tribes of the Columbia River basin. Peer Review Draft Report.
  • Dewailly, E.; Ryan, J.J.; Laliberte, C.; Bruneau, S.; Weber, J.P.; Gingras, S.; Carrier, G. (1994) Exposure of remote maritime populations to coplanar PCBs. Environmental Health Perspectives. Vol. 102, Suppl. 1:205-209.
  • Fürst, P.; Fürst, C.; Groebel, W. (1990) Levels of PCDDs and PCDFs in food stuffs from the Federal Republic of Germany. Chemosphere 20(7-9): 787-792.
  • Fürst, P.; Fürst, C.; Wilmers, K. (1991) Body burden with PCDD and PCDF from food. In: Gallo, M.; Scheuplein, R.; Van der Heijden, K. eds. Biological basis for risk assessment of dioxins and related compounds. Banbury Report #35. Plainview, NY: Cold Spring Harbor Laboratory Press.
  • Fürst, P.; Fürst, C.; Wilmers, K. (1994) Human milk as a bioindicator for body burden of PCDDs, PCDFs, organochlorine pesticides, and PCBs. Environmental Health Perspectives. Vol. 102, Suppl. 1:187-193.
  • Gilman, A.; Newhook, R. (1991) An updated assessment of the exposure of Canadians to dioxins and furans. Chemosphere 23(11-12): 1661-1667.
  • Henry, S.; Cramer, G.; Bolger, M.; Springer, J.; Scheuplein, R. (1992) Exposures and risks of dioxin in the U.S. food supply. Chemosphere 25(1-2):235-238.
  • Hites, R.A. (1991) Atmospheric transport and deposition of polychlorinated dibenzo-p-dioxins and dibenzofurans. Prepared for the U.S. Environmental Protection Agency, Methods Research Branch, Atmospheric Research and Exposure Assessment Laboratory, Office of Research and Development, Research Triangle Park, NC. EPA/600/3-91/002.
  • Horstmann, M.; McLachlan, M.S. (1994) Textiles as a source of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/F) in human skin and sewage sludge. Environ. Sci. and Pollut. Res. 1(1):15-20.
  • Koester, C.J.; Hites, R.A. (1992) Wet and dry deposition of chlorinated dioxins and furans. Environ. Sci. Technol. 26:1375-1382.
  • McCrady, J.K.; McFarlane, C.; Gander, L.K. (1990) The transport and fate of 2,3,7,8-TCDD in soybean and corn. Chemosphere 21:359-376.
  • Patterson, D.G.; Todd, G.D.; Turner, W.E.; Maggio, V.; Alexander, L.R.; Needham, L.L. (1994) Levels of nonortho-substituted polychlorinated biphenyls, dibenzo-p-dioxins, and dibenzofurans in human serum and adipose tissue. Environmental Health Perspectives. Vol. 101, Suppl. 1:195-204.
  • Safe, S. (1990) Polychlorinated biphenyl, dibenzo-p-dioxins, dibenzofurans, and related compounds: environmental and mechanistic consideratins which support the development of toxic equivalency factors. CRC Crit. Rev. Toxicol. 21:51-88.
  • Schecter, A. (1991) Dioxins and related chemicals in humans and in the environment. In: Gallo, M.; Scheuplein, R.; Van der Heijden, K. eds. Biological basis for risk assessment of dioxins and related compounds. Banbury Report #35. Plainview, NY: Cold Spring Harbor Laboratory Press.
  • Schecter, A.; di Domenico, A.; Tirrio-Baldassarri, L.; Ryan, J. (1992) Dioxin and dibenzofuran levels in milk of women from four geographical regions in Italy as compared to levels in other countries. Presented at: Dioxin '92, 12th International symposium on Chlorinated Dioxins and Related Compounds; Tampere, Finland; August 1992.
  • Schecter, A.; DeVito, M.J.; Stanely, J.; Boggess, K. (1993) Dioxins, dibenzofurans and dioxin-like PCBs in blood of Americans. Presented at: Dioxin '93, 13th International Symposium on Chlorinated Dioxins and Related Compounds; Vienna, Austria; September, 1993.
  • Schecter, A.; Fürst, P.; Fürst, C.; Päpke, O.; Ball, M.; Ryan, J.; Cau, H.D.; Dai, L.C.; Quynh, H.T.; Cuong, H.Q.; Phuong, N.T.N.; Phiet, P.H., Biem, A.; Constable, J.; Startin, J.; Samedy, M.; Seng, Y.K. (1994a) Chlorinated dioxins and dibenzofurans in human tissue from general populations; a selective review. Environmental Health Perspectives Vol. 102, Suppl. 1:159-171.
  • Schecter, A.; Stanley, J.; Boggess, K.; Masuda, Y.; Mes J.; Wolff, M.; Fürst, P.; Fürst, C.; Wilson-Yang, K.; Chisholm, B. (1994b) Polychlorinated biphenyl levels in the tissues of exposed and nonexposed humans. Environmental Health Perspectives. Vol. 102, Suppl. 1:149-158.
  • Smith, A.H. (1987) Infant exposure assessment for breast milk dioxins and furans derived from waste incineration emissions. Risk Analysis. 7(3):347-353.
  • Smith, R.M.; O'Keefe P.; Briggs, R.; Hilker, D.; Connor, S. (1992) Measurement of PCDFs and PCDDs in air samples and lake sediments at several locations in upstate New York. Chemosphere 25:1-2, pp. 95-98.
  • Svensson, B.G.; Nelsson, A.; Hansson, M.; Rappe, C.; Akesson, B.; Skerfving, S. (1991) Exposure to dioxins and dibenzofurans through the consumption of fish. New England Journal of Medicine. 324(1):8-12.
  • Sullivan, M.J.; Custance, S.R.; Miller, C.J. (1991) Infant exposure to dioxin in mother's milk resulting from maternal ingestion of contaminated fish. Chemosphere 23(8-10):1387-1396.
  • Theelen, R.M.C. (1991) Modeling of human exposure to TCDD and I-TEQ in the Netherlands: background and occupational. In: Gallo, M.; Scheuplein, R.; Van der Heijden, K. eds. Biological basis for risk assessment of dioxins and related compounds. Banbury Report #35. Plainview, NY: Cold Spring Harbor Laboratory Press.
  • Theelen, R.M.C.; Liem, A.K.D.; Slob, W.; Van Wijnen, J.H. (1993) Intake of 2,3,7,8 chlorine substituted dioxins, furans, and planar PCBs from foods in the Netherlands, median and distribution. Chemosphere. 27(9):1625-1635.
  • Travis, C.C.; Hattemer-Frey, H.A. (1987) Human exposure to 2,3,7,8-TCDD. Chemosphere 16:2331-2342.
  • Travis, C.C.; Hattemer-Frey, H.A. (1988) Relationship between dietary intake of organic chemicals and their concentrations in human adipose tissue and breast milk. Arch. Environ. Contam. Toxicol. 17:473-478.
  • Travis, C.C.; Hattemer-Frey, H.A. (1991) Human exposure to dioxin. Sci. Total Environ. 104: 97-127.
  • U.S. Department of Agriculture (1992) Food and nutrient intakes by individuals in the United States, 1 day, 1987-88: Nationwide Food Consumption Survey 1987-88. Washington, DC: USDA Human Nutrition Information Service. NFCS Rpt. No. 87-I-1 in preparation.
  • U.S. Department of Agriculture (1993) Food consumption, prices, and expenditures, 1970-1992. Washington, DC: USDA Economic Research Service. Statistical Bulletin 867.
  • U.S. Environmental Protection Agency (1989) Exposure factors handbook. Washington, DC: Office of Health and Environmental Assessment. EPA/600/8-89/043.
  • U.S. Environmental Protection Agency (1990a) Background document to the integrated risk assessment for dioxins and furans from chlorine bleaching in pulp and paper mills. Washington, DC: Office of Toxic Substances. EPA 560/5-90-014.
  • U.S. Environmental Protection Agency (1990b) Chlorinated dioxins and furans in the general U.S. population: NHATS FY1987 results. Washington, DC: Office of Toxic Substances. EPA 560/5-91-003.
  • U.S. Environmental Protection Agency (1991a) Feasibility of environmental monitoring and exposure assessment for a municipal waste combustion: Rutland Vermont Pilot Study. Washington, DC: Office of Research and Development. EPA-600/8-91/007.
  • U.S. Environmental Protection Agency (1991b) Chlorinated dioxins and furans in the general U.S. population: NHATS FY87 results, Washington, DC: Office of Toxic Substances. EPA-560/5-91-003.
  • U.S. Environmental Protection Agency. (1994) Health Assessment for 2,3,7,8-TCDD and related compounds, Washington, DC: Office of Research and Development. EPA 600/BP-92/001.
  • Welge, P.; Wittsiepe, J.; Schrey, P.; Ewers, U.; Exner, M.; Sclenka, F. (1993) PCDD/F-levels in human blood of vegetarians compared to those of non-vegetarians. Presented at: Dioxin '93, 13th International Symposium on Chlorinated Dioxins and Related Compounds; Vienna, Austria; September 1993.
  • Wolfe, R.J.; Walker, R.J. (1987) Subsistence Economics in Alaska: Productivity, Geography and Developmental Impacts. Arctic Anthropology 24(2):56-81.
  • Yang, Y-Y.; Nelson, C.R. (1986) An estimation of daily food usage factors for assessing radionuclide intake in the U.S. population. Health Phys. 50(2):245-257.