Environ. Sci. Technol. 2009, 43, 2661–2662
Response to Comment on “Elevated House Dust and Serum Concentrations of PBDEs in California: Unintended Consequences of Furniture Flammability Standards?”
200 mg/day, and a body weight of 10 kg. The result was a daily intake of 6200 ng/kg-days60 times higher than the EPA RfD of 100 ng/kg-day (8, 9) and close to the short-term ATSDR reference level of 7000 ng/kg-day based on liver toxicity (10). In addition, exposure estimates based on dust ingestion alone underrepresent total PBDE exposure because they do not consider inhalation, dermal contact, or diet.
We appreciate Banasik and colleague’s interest in our recent article (1) reporting elevated concentrations of penta-BDEs in California house dust and serum, and providing evidence that California’s unique furniture flammability standard has resulted in significantly higher human exposure to pentaBDEs compared to other regions in the U.S.
The NHANES PBDE serum levels in Californians reported in our study are the highest population levels observed to date. However, these levels likely underestimate population exposures in California since NHANES did not measure PBDEs in children under the age of 12. Other studies indicate that young children are a highly exposed subpopulation with up to three times the body burden of their parents (11).
Banasik et al. (2) suggest that the PBDE levels we reported in house dust do not pose a health risk based on their exposure calculations and comparisons with health-based guidance values. They also question whether our dust collection method is relevant for exposure assessment and raise concerns about EPA’s Reference Dose (RfD) for PBDEs. Their comments are tangential to the main thrust of our article, and do not represent mainstream scientific views regarding risks of PBDEs, which have been banned in the European Union and 11 U.S. States. Moreover, their risk estimates are inadequate because they omit important exposure pathways and likely underestimate exposure and risk at the upper end of the distribution. Banasik et al. suggest that our dust collection protocol would have collected deep dust and thus is not relevant to exposure. In fact, as described in Rudel 2003 (3), dust was collected by “slowly and lightly drawing the crevice tool just above the surface” being sampled, in order to collect surface dust rather than deep dust. Dust collection protocols employing the Eureka Mighty-Mite vacuum have been used in numerous studies for evaluation of exposures to PBDEs, pesticides, and allergens (3-5). This method has been compared with other well-established dust collection methods such as the Cyclone vacuum and showed similar precision (4). Also, Lorber (6) found good agreement between predicted PBDE body burdens derived from house dust concentrations (and PBDEs in other media) and those observed in blood and breast milk. Lastly, Wu’s study (5), which employed a dust sampling method similar to ours found a strong correlation (r ) 0.76) between participants’ PBDE breast milk concentrations and levels in their house dust. House dust is a direct exposure pathway through incidental ingestion, inhalation of resuspended dust, and dermal absorption. Dust measures are also a proxy for exposures occurring in the home through inhalation and direct contact with furnishings. Banasik et al. estimated exposures based on our reported PBDE dust concentrations, but these likely underestimate the full distribution of exposures. Specifically, Banasik et al. use a soil ingestion rate of 60 mg/day, which is substantially lower than values used in other assessments which use an average of 100 mg/day (6) and a maximum of 200 mg/day (7) for young children. Banasik et al. also chose to compare the exposure estimates calculated from our maximum dust concentrations with short-term (
