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DEVELOPMENTAL AGE EFFECTS ON TISSUE DISPOSITION OF BDE 47 IN MICE
Citation:
DILIBERTO, J. J., D. STASKAL, AND L. S. BIRNBAUM. DEVELOPMENTAL AGE EFFECTS ON TISSUE DISPOSITION OF BDE 47 IN MICE . Presented at 45th Annual Society of Toxicology Meeting 2006, San Diego, CA, March 05 - 09, 2006.
Description:
Public health concern for polybrominated diphenyl ethers (PBDEs) has focused on potential hazardous effects resulting from exposure to infants and young children because of previous studies reporting adverse developmental effects in rodent studies. This study investigated distribution and excretion of BDE 47, most dominant PBDE congener found in USA biotic samples, at different times during development in mice. C57BL/6 mice were orally exposed to 1 mg/kg [14C]BDE 47 on postnatal day (PND) 22, 28 or 40. Tissue and urine samples were collected 24 hr following exposure; carcass analyses were used as an indirect measure of excretion. In all age groups, BDE 47 distributed to lipophilic tissues; most tissue concentrations of BDE 47 were highest in PND 22 mice, and by PND 40 closely mimicked adult tissue concentrations, except in blood and liver. Developmental changes were seen in ratios of blood:brain (0.24, PND 22 to 0.04, adult) and liver:fat (0.06, PND 22 to 0.63, adult). Previous toxicokinetic studies in adult mice have shown a rapid urinary excretion of BDE 47 in mice. Results of this study suggest that young, developing mice have an impaired ability to excrete BDE 47 based on lower concentrations of BDE 47 in urine as compared to adults and a larger % dose remaining in the body 24 hr following exposure in younger mice. The carcass residual % dose decreased from 59%, PND 22 to 34%, PND 40. Because active renal transport has been suggested to be involved with rapid excretion of BDE 47, excretion patterns in mice of increasing age (PND 22 to 40) were compared to ontological expression of renal transport proteins in this species in an attempt to further identify the mechanism(s) responsible for rapid urinary excretion. These developmental differences led to higher concentrations of BDE 47 at target tissues during critical windows of development, which may ultimately explain the sensitivity of developing systems to adverse effects of BDE 47. This abstract does not reflect EPA policy. Work partially funded by EPA DESE CT 826513.