Tissue distribution of decabrominated diphenyl ether (BDE-209) and its metabolites in sucking rat pups after prenatal and/or postnatal exposure.

Growing evidence has shown that decabromodiphenyl ether (BDE-209) can disrupt thyroid hormones and induce neurological and developmental effects, especially for the fetuses and neonates after prenatal or postnatal exposure. The present study was carried out to examine the effects of in utero and lactational exposure to BDE-209 on the absorption and tissue distribution of BDE-209 and its metabolites in offspring. Pregnant Sprague-Dawley rats were given daily oral doses of 5μmol/kg b.w. BDE-209 in peanut oil during gestational and lactational period or during lactational period only. BDE-209 and its debrominated congeners were analyzed in several maternal tissues, offspring carcass and neonatal tissues. The occurrence of polybrominated diphenyl ethers (PBDEs) and their time profiles in maternal blood, placenta and fetuses/sucking pups indicated that BDE-209 and its debrominated products can be transferred from mother to offspring via in utero or lactational exposure. Nona-BDEs were the predominant congeners in the analyzed pup tissues, and BDE-206 was the most abundant congener while BDE-197/204 was the major congener of octa-BDE. Then the contributions of transplacental and lactational transfer were compared for BDE-209 and its debrominated congeners. The levels of PBDEs in tissues of sucking pups of the in utero and lactational exposure group were much higher than those of only lactationally exposed group. BDE-197/204 was the debrominated congener with the most significant difference between these two groups and the pup brain was the tissue with the most significant difference of the levels of debrominated congeners. The results provide a basis for understanding the possible adverse effects caused by maternal transfer of BDE-209 during the critical periods of development of fetuses and sucking neonates.