PBDE concentration ranges in dust and serum in the present study were similar to concentrations found in other studies conducted among North Americans (21
), and therefore the PBDE exposures among individuals in this study are likely representative of exposures of the general US population. There were strong correlations between dust concentrations of PBDE congener groups with the same or close degree of bromination. These relationships resemble the congener mixtures (PentaBDE, OctaBDE, or DecaBDE) in commercial products and suggest that the congeners originated from the same sources within the home. Because BDE 202 is not present at detectable levels in commercial formulations, its detection in dust samples may be indicative of environmental debromination of BDE 209 (27
). BDE 209 was measured at the highest concentrations in dust, followed by BDE 99 and BDE 47. In contrast, BDE 47 and BDE 153 were measured at the highest concentrations in serum. BDE 47 may dominate serum samples due to dietary intake, as it was often found as the dominant congener in food items analyzed as part of a market basket survey (28
). The predominance of BDE 47 in serum samples may also be due in part to gaseous inhalation, as BDE 47 has been found to be a dominant congener in indoor air (13
). However, it is not possible to evaluate contributions to exposure from diet or inhalation of volatile gases in the present study. Our observation of a strong correlation between dust and serum BDE 47 concentrations supports the argument that dust is a major exposure pathway for BDE 47.
Several congeners, including BDE 209, had low detection rates in serum and therefore conclusions regarding dust-serum or within-couple relationships for these congeners were not possible. Several congeners (BDE 28, 47, 99, 100, 153) had high detection rates, and therefore associations with PBDE concentrations in dust could be evaluated. There were strong correlations between dust and serum concentrations of the major Penta formulation BDE congeners 47, 99 and 100, which suggests that dust is a good measure of exposure to these congeners. Serum concentrations of these congeners were also strongly correlated between males and females of couples (), which supports the use of a serum or dust measurement from one member of a couple living together to represent their partner's exposure to these congeners. This estimate of exposure may not apply to children living in the same household, as a child's exposure to dust is expected to be greater (30
). Dust and serum levels of BDE 153 were not correlated, which may be due to differences in exposure sources (e.g. diet or exposures outside the home), transformation, distribution or metabolism of this congener. BDE 153 has a long half-life as compared to the other congeners (31
). Serum concentrations of BDE 153 were also not correlated between males and females within couples. Conversely, BDE 153 in dust was correlated to lower brominated congeners in serum, which may support the argument that transformation is occurring. As observed by Qiu, et al. (33
), different PBDE congeners may have different rates of hydroxylation, and this may be an explanation why human serum may exhibit different congener profiles than dust or commercial product mixtures. Huwe et al. (34
) demonstrated that PBDE congeners have different degrees of bioconcentration in rats, possibly due to metabolism differences between congeners. The lack of BDE 209 measured in serum may be due to higher detection limits and/or to its short biological half-life. Stapleton et al. (6
) demonstrated that when carp were fed BDE 209, only lower-brominated congeners, and not BDE 209, bioaccumulated in the fish. Further research into the transformation processes of individual PBDE congeners is needed to understand patterns in the biomarker profiles of these compounds.
A recent study utilizing the National Health and Nutrition Examination Survey (NHANES) dietary questionnaire responses and serum PBDE data concluded that intake of poultry and red meat is a source of PBDE exposure in the US population (35
). In particular, BDE 153 was the only congener associated with total fat intake, and although vegetarians had lower total PBDE serum levels, they did not have significantly reduced levels of BDE 153. Higher levels of dietary exposure to BDE 153 may explain higher BDE 153 levels in serum in the present study population. However, US market basket surveys (28
) do not indicate that certain foods have higher concentrations of BDE 153. Fraser et al. (35
) also found similar results to the present study in terms of serum congener correlations, with the Penta formulation congeners (BDE 28, 47, 99, 100 and 153) being strongly correlated with one another. However, the authors reported that BDE 153 had a weaker association than the other congeners. In the present study, the Penta formulation congeners were also strongly correlated, but BDE 153 was not associated with the other congeners in serum.
Limited studies have assessed relationships between dus t and serum concentrations of PBDEs. A study of only five Swedish homes reported a correlation between researcher-collected house dust and plasma levels of PBDEs, although the association was dependent on one of the five households (37
). A recent study of 19 Belgian students found no correlation between PBDE concentrations in the students’ serum and dust concentrations in their dormitories (38
). Another study conducted on 34 German homes found no significant correlation between dust and serum concentrations of PBDEs, and the authors concluded that diet is the main exposure pathway (39
). However, although European food samples were reported to have the same level of PBDE contamination as US samples, (10
), dust levels in European countries are orders of magnitude lower than US levels (24
), and therefore these data may not be comparable to the data in the present study. Based on pharmacokinetic modeling, Lorber (10
) concluded that dietary and inhalation exposures could not explain US body burdens of PBDEs, and that exposure to indoor dust is the primary pathway.
Various studies on indoor environmental contaminants employ different methods in the collection of house dust as a measure of exposure. Specifically, researcher-collected dust has been compared to vacuum bag dust (26
). The studies by Colt et al concluded that there was a high level of agreement between researcher-collected dust (high-volume surface sampler, HVS3) and vacuum bag dust for pesticides and other organic contaminants, including polychlorinated biphenyls (PCBs). The study by Allen et al (26
) found that researcher-collected dust had varying degrees of correlation with vacuum bag dust concentrations of PBDEs (r = 0.39–0.77), depending on the room in the home and the sampling round. Furthermore, PBDE concentrations in researcher-collected dust were significantly different between rooms of the same home. Future studies on dust collection methods should focus on the validation of these methods and include biomarkers as evidence of biological relevance. It is possible that the use of vacuum bag dust in exposure assessment may be a superior method of dust collection, provided that the dust collected is a measure of longer term integrative exposure representative of the total home environment, and thus total exposure, and not limited to a specific area or time. The use of vacuum bags may also provide a much more time- and cost-efficient method for measuring dust contamination in large-scale epidemiological studies. On the other hand, researcher-collected dust samples would likely have more utility in studies aiming to define specific PBDE exposure sources in the home or other microenvironments.
This study is the first to provide empirical evidence of the association between house dust and serum concentrations of PBDEs in the US. For PBDE congeners that do not show strong correlation between dust and serum, such as BDE 153, dust may not be a good indicator of body burden. However, for other PBDE congeners such as the major Penta formulation BDEs, which were strongly correlated between dust and serum concentrations, house dust may be a good measure of exposure. This observation serves to further validate our recent finding of significant relationships between dust concentrations of PentaBDEs and circulating hormone levels in men (20
). Furthermore, house dust may provide a satisfactory estimate of human exposure to BDE 209 due to its high concentrations in dust and current limitations of measuring BDE 209 in serum. The relatively short biological half-life of BDE 209 may prevent reliable measurement in serum, but because BDE 209 concentrations in dust are high, people are likely continuously exposed. Thus, dust concentrations may currently be the best marker of exposure to BDE 209 in the absence of other biomarkers.