conducted in Dallas, Texas (Schecter et al., 2004), the highest levels of total PBDEs were found in samples of salmon, catfish, and shark. It is notable that the congener pattern was highly variable across samples, even within types (e.g., catfish), perhaps reflecting site specificity in the magnitude and nature of the problem of PBDE contamination. Total PBDE levels were also greater in meats with relatively high fat content, such as pork sausage, hot dogs, and duck; and in dairy products with higher fat content, such as cheese and butter (Schecter et al., 2004). Similar findings were reported in a market basket survey of foods conducted in California (Luksemburg et al., 2004), in which the highest PBDE levels were found in swordfish, Alaskan halibut, and Atlantic salmon. PBDE levels were 15 times greater in Pacific farm-raised salmon than in Pacific wild salmon (Easton et al., 2002). PBDE levels are higher in salmon farmed in the United States and Europe than in Chile (Hites et al., 2004a). Limited data are available, however, on the association between seafood consumption and PBDE levels in human tissues. In a small study of 94 urban anglers in the New York–New Jersey area, greater consumption of locally caught fish was not significantly related to blood PBDE levels, suggesting that, at least at this time and in this study population, consumption of local fish is not a major route of exposure to PBDEs (Moreland et al., 2005).


Adverse Health Effects The data available on the toxicity of PBDEs are extremely limited. Experimental animal studies indicate that PBDEs affect the nervous (Viberg et al., 2003), endocrine (Stocker et al., 2004), and immune systems (Fowles et al., 1994), and that the potency of PBDEs might be comparable to that of PCBs, although considerable uncertainty remains (Kodavanti and Ward, 2005). No population-based epidemiological studies have evaluated the human health effects of environmental exposure to PBDEs. It is not known whether all PBDEs share a common mechanism of action, complicating any effort to characterize toxicity using a toxic equivalence factor approach. In light of the fact that in vitro studies with purified PBDE congeners do not show AhR activation, it is possible that the presence of trace amounts of DLCs have confounded these assessments of PBDE toxicity (FAO/WHO JECFA, 2006). The FAO/WHO Joint Expert Committee on Food Additives and Contaminants concluded that the toxicological data available on PBDEs were insufficient to establish a Provisional Tolerable Weekly Intake (FAO/WHO JECFA, 2005). The data, however, are not sufficient to identify “no observed adverse effect levels” (NOAELs) for congeners of greatest interest, and thus to draw inferences about the prevalence of exposures of concern in the US population.



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