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SYMPOSIUM #127 – ARE POLYBROMINATED DIPHENYL ETHERS FROM HOUSEHOLD DUST BIOAVAILABLE AND BIOLOGICALLY ACTIVE?
Citation:
HUWE, J. K., H. HAKK, J. J. DILIBERTO, V. RICHARDSON, H. M. STAPLETON, AND L. S. BIRNBAUM. SYMPOSIUM #127 – ARE POLYBROMINATED DIPHENYL ETHERS FROM HOUSEHOLD DUST BIOAVAILABLE AND BIOLOGICALLY ACTIVE? Presented at International Society of Exposure Analysis (ISEA) Meeting, Durham, NC, October 14 - 18, 2007.
Impact/Purpose:
research presentation
Description:
Recently, household dust has been implicated as a major source of polybrominated diphenyl ether (PBDE) exposure in humans. This finding may have important implications for young children, who are thought to ingest more dust than adults and may be more susceptible to some of the putative developmental effects of PBDEs. The bioavailability of PBDEs from ingested dust is not known; therefore, the objectives of this study were (1) to determine the absorption of PBDEs from dust using rats as a model system, (2) to observe any changes that may occur in hepatic enzymes, and (3) to compare these results with results from rats fed PBDEs dissolved in corn oil. Four groups of male Sprague-Dawley rats were fed for 21 days either a high or low dose of a PBDE-contaminated dust mixed into the feed or a PBDE formulation dissolved in oil and mixed with the feed. The low doses were representative of the highest levels reported in breast milk in the U.S. PBDEs bioconcentrated into rat tissues to the same degree when administered in either a dust or oil matrix. Typical bioconcentration factors in the adipose tissue were 10 – 20 for tri- to hexa-BDEs, 1 – 4 for hepta- to nona-BDEs, and <1 for deca-BDE. PBDEs in both dust and oil stimulated expression of Cyp2b1 and Cyp2b2 messenger RNA in the highest dosage groups. Therefore, the present study showed that PBDEs in dust were as bioavailable as those dissolved in an oil vehicle, that higher brominated congeners were less bioavailable than lower brominated congeners, and that PBDEs could induce certain enzyme systems at doses of 5 ug/kg body weight. The results support the hypothesis that, in addition to foods, ingested dust can be a source of PBDE exposure in humans. (This abstract does not reflect Agency policy.)