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EFFECT OF AGE ON TISSUE DISTRIBUTION OF BDE 47 IN MICE
Citation:
STASKAL, D., J. J. DILIBERTO, AND L. S. BIRNBAUM. EFFECT OF AGE ON TISSUE DISTRIBUTION OF BDE 47 IN MICE. Presented at 45th Annual Society of Toxicology Meeting 2006, San Diego, CA, March 05 - 09, 2006.
Description:
Despite its minor contribution to global polybrominated diphenyl ether production and usage, 2,2',4,4'tetrabromodiphenyl ether (BDE 47) is the dominant congener found in most biotic samples in North America. The majority of public health concern 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 was designed to investigate the disposition of BDE 47 in young mice reported to be susceptible to the developmental neurotoxic effects of BDE 47. Infantile C57BL/6 mice pups were administered a single, oral 1.0 mg/kg dose of [14C]BDE 47 on postnatal day 10; tissue distribution was monitored 3, 8, 24 hours, 5, and 10 days following administration. Analyses of the carcass for total radioactivity were used as an indirect measure of excretion. The results show that the toxicokinetics of BDE 47 are different in developing mice than in adult mice (Staskal et al 2005). While patterns of tissue distribution were similar, concentrations of BDE 47 were consistently higher in pups. BDE 47 was found at the highest concentrations in lipophilic tissues (adipose, liver, and skin) 1-5 days following exposure. Brain concentrations were of particular interest; ten days following a single exposure, pups had an average concentration of 58 ng/g versus 4 ng/g in adults. The higher tissue concentrations in pups were likely due to a reduced capacity to eliminate BDE 47. In adults, only 6% of the dose remained in the carcass after ten days versus 34% in the pups. These differences lead to higher concentrations of BDE 47 at target tissues during critical windows of development, which may ultimately explain the sensitivity of developing systems to the adverse effects BDE 47. This abstract does not reflect EPA policy. Work partially funded by EPA DESE CT 826513.