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Dietary accumulation, disposition, and metabolism of technical pentabrominated diphenyl ether (DE‐71) in pregnant mink ( Mustela vison ) and their offspring
Author(s) -
Zhang Si,
Bursian Steve,
Martin Pamela A.,
Chan Hing Man,
Martin Jonathan W.
Publication year - 2008
Publication title -
environmental toxicology and chemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.1
H-Index - 171
eISSN - 1552-8618
pISSN - 0730-7268
DOI - 10.1897/07-487.1
Subject(s) - mink , biomagnification , polybrominated diphenyl ethers , bioaccumulation , weaning , biology , offspring , transplacental , diphenyl ether , bioconcentration , chemistry , zoology , environmental chemistry , ecology , pregnancy , pollutant , fetus , genetics , placenta , organic chemistry
Concentrations of polybrominated diphenyl ethers (PBDEs) in humans and wildlife suggest significant bioaccumulation potential in mammals, but no quantitative biomagnification data from controlled experiments are currently available. As part of a larger study examining the effects of PBDEs on mink ( Mustela vison ) reproduction and development, we examined congener‐specific tissue distribution, maternal transfer, biotransformation, and biomagnification of the technical penta‐BDE mixture, DE‐71, in farmed mink. Adult female mink were fed one of four concentrations of DE‐71 (0‐2.5 μg/g) in the diet from breeding through gestation and until weaning at 6 weeks postparturition. Parent PBDEs were measured in tissues and excreta of adult mink, kits, and juveniles, whereas hydroxylated PBDEs (OH‐PBDEs) were measured in juveniles only. Similar lipid‐normalized concentrations of PBDEs were detected in most tissues of adult mink with the exception of brain, in which concentrations were significantly lower. Kits, however, had a higher proportion of PBDEs in brain compared with adults, presumably because of incomplete development of the blood‐brain barrier. Maternal transfer favored lower‐brominated PBDE congeners, and the bulk of the body burden in kits at weaning resulted from lactational rather than transplacental transfer. Lipid‐normalized, whole‐body biomagnification factors ranged from 0.5 to 5.2 for the major congeners and were highest for BDEs 47 and 153. Metabolism clearly limited the biomagnification of some PBDEs, and OH‐PBDEs were detectable in plasma, liver, and feces. On a mass basis, OH‐PBDEs accounted for 28 to 32% of the excreted fraction, indicating metabolism was an important elimination pathway. Further studies are required to understand the mechanisms of PBDE biotransformation.