Dietary exposure of American kestrels (Falco sparverius) to decabromodiphenyl ether (BDE-209) flame retardant: Uptake, distribution, debromination and cytochrome P450 enzyme induction 机翻标题: 暂无翻译,请尝试点击翻译按钮。

Environment international
2014 / 63 / Feb.
Environment Canada, National Wildlife Research Centre, Carleton University (Raven Road), Ottawa, Ontario K1A 0H3, Canada;Avian Science and Conservation Centre, Department of Natural Resource Sciences, McGill University, Ste-Anne-de-Bellevue, Quebec, Canada;Avian Science and Conservation Centre, Department of Natural Resource Sciences, McGill University, Ste-Anne-de-Bellevue, Quebec, Canada,Ecotoxicology & Wildlife Health Division, Science & Technology Branch, Environment Canada, Burlington, Ontario, Canada;
Robert J. Letcher;Sarah C. Marteinson;Kim J. Fernie;
Accumulation and evidence of debromination of the flame retardant 2,2',3,3',4,4',5,5',6,6'-decabromodiphenyl ether (BDE-209) have been reported for biota, including raptorial birds, based on PBDE congener residues in tissues and eggs. However, in vivo studies with BDE-209-exposed birds are rare and unknown for a raptorial species. In the present study, males (n = 22) of raptorial American kestrels (Falco sparverius) were exposed to 116,000 ng of BDE-209 (high purity, >98%; in safflower oil) per day for 21 days (~2,436,000 ng total BDE-209 exposure over this uptake period), followed by a 25-day depuration period. Control males (n = 11) received the safflower vehicle only. In the exposed birds, BDE-209 was quantifiable in all plasma (end of uptake and depuration period) as well as liver and fat (end of depuration only) samples. The mean (±SE) BDE-209 level in plasma was 1474 ± 1145 ng/g wet weight (ww) at the end of the uptake period, and was significantly (p < 0.001) lower (88%) at 174 ± 148 ng/g ww after the 25 day depuration period. This equates to a mean reduction rate of 52 ng/g ww per day and a rough estimation of the BDE-209 half-life in plasma of approximately 14 days. The mean (±SE) BDE-209 levels were 4668 ± 6192 ng/g ww in the fat, and 338 ± 311 ng/g wwin the liver, of exposed individuals, which were significantly (p ≤ 0.001) greater than mean concentrations (25 ± 20 in fat and 2.6 ± 0.9 ng/g ww in liver) in the control birds. In addition to BDE-209, lower brominated PBDE congeners, and mainly meta- and para-debromination products of BDE-209 were also quantified in plasma, liver and/or fat. We estimated based on the dose that at least 80% of the non-BDE-209 concentration in the kestrel tissues and plasma must be derived from BDE-209 debromination by the kestrels. Where quantifiable, lower brominated PBDE concentrations were significantly (0.023 > p > 0.001) higher in the exposed relative to the control bird samples (except for BDE-154 and -153 in fat). Additional PBDE congeners found in plasma included nona-BDEs (208,207 and 206), followed by octa-BDEs (197,196,201 and 203), and in liver and/or fat, the hepta-BDEs 180 and 183 and BDE-153. Higher hepatic EROD activity (cytochrome P450 1A1 monooxygenase-mediation) in the exposed birds compared to control birds was strongly suggested to be PBDE-induced, and was consistent with BDE-209 and congener metabolism in the exposed kestrels. The mean EROD activity rate was 36.1 pmol/min/mg protein relative to the (n = 4) control birds whose activity was just above the detection limit (10.3 pmol/min/mg protein). Overall, the results demonstrated that following diet exposure of kestrels to high purity BDE-209, uptake occurred as well as BDE-209 degradation via debromination to lower brominated PBDE congeners.
Polybrominated diphenyl ether (PBDE);Decabromodiphenyl ether (BDE-209);American kestrel;Accumulation;Debromination;Enzyme activity;