Serum levels of the dioxin-like chemicals reflect accumulated exposure because these chemicals are stored in body fat and only slowly eliminated. Observed differences in the levels of these chemicals in people are due in part to differences in environmental exposure.For instance, people who ate dioxin-like chemical contaminated fish from the Great Lakes region had mean lipid adjusted serum concentrations of these chemicals that were several times higher than background values in the U.S. population (Anderson et al., 1998; Falk et al., 1999; Hanrahan et al., 1999; Turyk et al., 2006). Observed differences between people may also be due to longer periods of accumulation of these persistent chemicals. Several studies have shown that levels of the more highly chlorinated dioxins, furans, and PCBs in serum or fat will increase with the age of the population studied (Falk et al., 1999; Geyer et al., 2002; Kang et al., 1997; Luotamo et al., 1991; Patterson et al., 1986). Many of the dioxins, furans, and PCBs measured pooled serum samples obtained from a representative New Zealand population showed that levels trended upward with age (Bates et al., 2004). In a U.S. representative sample from NHANES 1999-2000, participants aged 20 years and older had higher levels than participants aged 12-19 years when levels at the higher percentiles of the more highly chlorinated congeners were compared (CDC, 2013). Similarly, the TEQ increased with age in an analysis of the NHANES 2003-2004 subsample (Patterson et al., 2009). Other factors also explain differences in levels observed between people. In a TEQ analysis of the NHANES 2001-2002 subsample, the total TEQ increased with age, was lower for Mexican Americans than non-Hispanic whites or blacks, and was higher in smokers than nonsmokers older than 60 years of age (Ferriby et al., 2007). Body mass is also a factor directly associated with increasing levels of some polychlorinated dibenzo-p-dioxins (Collins et al., 2007; Michalek et al., 1999). Gender is another predictor of levels of some dioxin-like chemicals. Compared with Japanese men, women had higher levelsof octachlorodibenzo-p-dioxin, 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin, and 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin, but men had higher levels of PCBs 169, 156, and 189 (Arisawa et al., 2003). In the NHANES 2001-2002 subsample, females had higher adjusted geometric mean levels than males for 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin, and 3,3',4,4',5-pentachlorobiphenyl (PCB 126). However, males had higher levels than females for 3,3',4,4',5,5'-hexachlorobiphenyl (PCB 169) (CDC, 2013).
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The generally low lipid-adjusted levels observed in the U.S. representative NHANES subsamples of 1999-2000, 2001-2002, and 2003-2004 support the observation that human serum levels of polychlorinated dibenzo-p-dioxins, dibenzofurans, and PCBs have decreased by more than 80% since the 1980s (Aylward and Hays, 2002; Lorber, 2002; Patterson et al., 2009). Levels of some dioxin-like chemicals, such as the hexachlordibenzo-p-dioxins, were shown to decrease gradually from 1993 to 2003 in pooled samples from children in selected regions of Germany, whereas the hexachlordibenzofuran levels showed little change (Link et al., 2005). The levels of polychlorinated dibenzo-p-dioxins, dibenzofurans, and coplanar and mono-ortho-substituted biphenyls seen in the U.S. population were generally well below the levels associated with occupational or unintentional exposures that have produced health effects. There are no firmly established relationships between concentrations (mainly considering TCDD) and health effects in people. Observations following industrial and accidental exposures have suggested that acute exposures resulting in serum concentrations of about 800 pg/g of lipid might be necessary to induce clinical effects such as chloracne, although levels in the thousands of pg/g of lipid do not always produce this effect (Mocarelli et al., 1991). Such studies of clinical effects in people after large unintentional exposures have measured concentrations ranging from several hundred to the tens of thousands of pg/g of lipid of TCDD or equivalent (Eskenazi et al., 2004; Masuda, 2001; Masuda et al., 1998; Mocarelli et al., 1991). However, it has been suggested that background total TEQ for the general population are about 10-100 times the TEQ levels associated with a possible risk for adaptive or subclinical adverse effects (e.g., endocrine changes) (U.S.EPA, 2004).
Of the dioxins and furans measured in the U.S. representative subsamples of NHANES 1999-2000, 2001-2002, and 2003-2004, octachlorodibenzo-p-dioxin typically was present in the highest concentration, but contributed little to the TEQ, with the other commonly detected dioxin and furan congeners being more than eight-fold lower in concentration. Levels of octachlorodibenzo-p-dioxin that were similar to slightly higher than those in these NHANES subsamples were seen in a representative pooled sampling New Zealander residents aged 15 years and older obtained during 1997-1998 and also in a small convenience sample of German residents aged 18-71 years in 1996 (Bates et al., 2004; Papke et al., 1998; CDC, 2013). Similar levels were also found in 232 Belgian blood donors in 2000 (Debacker et al., 2007).
Of the polychlorinated dibenzofurans, the following could be characterized at the 95th percentiles (or lower) in the NHANES 1999-2000, 2001-2002 and 2003-2004 subsamples:1,2,3,4,6,7,8-heptachlorodibenzofuran, 1,2,3,4,7,8-hexachlorodibenzofuran, 1,2,3,6,7,8-hexachlorodibenzofuran, and 2,3,4,7,8-pentachlorodibenzofuran. Generally, these levels are similar to other large population studies.In 237 workers with past exposure to trichlorophenol, where little polychlorinated dibenzofuran exposure would be expected, higher percentiles values were similar to a referent population and to the NHANES 1999-2000 and 2001-2002 subsamples (Collins et al., 2007; CDC, 2013). In 232 Belgian blood donors from the year 2000, the geometric mean level of 1,2,3,4,6,7,8-heptachlorodibenzofuran was several times lower than the geometric mean value in the NHANES 2001-2002 subsample of adults and the other dibenzofurans examined in the Belgian donors were lower than the limits of detection in NHANES 2000-2001 (CDC, 2013; Debacker et al., 2007). In Yucheng rice oil contamination victims when examined 15 years after their exposure, levels of the polychlorinated dibenzofurans were still hundreds of times higher than in levels for the U.S. population observed in the NHANES subsamples (Hsu et al., 2005).
Of the mono-ortho-substituted PCB congeners, the most frequently detected in general population studies are PCBs 118 and 156. Of these, PCB 118 levels were higher than levels of PCB 156 in the NHANES 1999-2000, 2001-2002, and 2003-2004 subsamples, although PCB 156 contributes more to the TEQ because its TEF is five-fold greater than the TEF of PCB 118. Although these PCBs are relatively less potent (i.e., lower TEFs), their contribution to the total TEQ in the U.S. population is about 25% (Ferriby et al., 2007) since they are present in much higher concentrations than are the coplanar PCBs, dioxins, and furans. In a convenience sample of the U.S. population in 1988 (Patterson et al., 1994), levels of PCB 118 were five-fold higher than in the NHANES 1999-2002 subsamples (CDC, 2013). Comparable levels of PCB 156 levels in NHANES 1999-2000 were slightly lower than those reported for a Canadian population study in 1994 (Longnecker et al., 2000). In a referent population of 311 residents in northern Italy during 2001-2003, the 95th percentile levels of PCB 156 and PCB 118 were two to three times higher than for the NHANES 1999-2002 subsamples (Apostoli et al., 2005; CDC, 2013). Levels of PCB 156 and PCB 118 were slightly higher in a Swedish study of 150 men than in the NHANES 1999-2000 subsample, possibly due to higher fish intake in the Swedish population (Glynn et al., 2000; CDC, 2013). However, in fish-consuming Japanese men and women studied during 1996-1997, PCB 118 levels at the 75th percentile were similar to levels in the NHANES 2001-2002 subsample (Arisawa et al., 2003).
Longnecker MP, Ryan JJ, Gladen BC, Schecter AJ. Correlations among human plasma levels of dioxin-like compounds and polychlorinated biphenyls (PCBs) and implications for epidemiologic studies. Arch Environ Health 2000;55(3):195-200.
The U.S. EPA has established the safe daily intake of BPA to be 50 μg/kg body weight/d based on the assumption that the main source of exposure is oral through food ingestion. However, recent publications suggest that food is not the only relevant source of exposure and that the half-life of BPA in humans is longer than expected (6). Numerous publications addressing fetal exposures to BPA have used parenteral administration. This practice was based on one hand on the fact that the fetus is exposed to BPA through the internal milieu of the mother, and on the other hand that parenteral administration via an osmotic minipump allows for a precise and constant level of exposure. Using this route of administration, exposure of a pregnant mouse dam to 25 and 250 ng BPA/kg body weight/d (namely, 2000 and 200 times lower than the safe dose) for 14 d beginning on d 8 gestation has been shown to impact certain aspects of development in their female offspring. When examined on gestational d 18, fetuses of mothers exposed to the higher dose of BPA exhibited altered growth parameters of the mammary gland anlagen. Changes in the appearance of the mammary epithelium were observed, such as decreased cell size and delayed lumen formation, as well as increased ductal area. In the stroma, BPA exposure promoted advanced maturation of the fat pad and altered localization of fibrous collagen (128). Because maturation of the fat pad is the driving event for ductal growth and branching, it is likely that the increased ductal area in BPA-exposed animals is due to the accelerated formation of their fat pads. By postnatal d 10, in the offspring born to mothers exposed to either dose of BPA, the percentage of proliferating epithelial cells was significantly decreased relative to those not exposed. At 30 d of age, the area and number of terminal end buds relative to the gland ductal area increased, whereas cell death in these structures decreased in BPA-exposed offspring compared with controls. It is likely that the reduced cell death in the terminal end buds of BPA-exposed females may be the cause of the observed ductal growth delay because cell death is essential for both the hollowing and the outward growth of the subtending duct. Collectively, these effects observed at puberty may be attributed to an increased sensitivity to estradiol that has been observed in the BPA-exposed animals (145). Because of the new epidemiological data cited above and the effects found in the low-dose animal studies using parenteral exposure, the EPA recommendations need to be reevaluated. 2ff7e9595c
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