Dietary exposure of American kestrels (Falco sparverius) to decabromodiphenyl ether (BDE-209) flame retardant: Uptake, distribution, debromination and cytochrome P450 enzyme induction

•Dietary uptake and depuration of BDE-209 flame retardant occurred in American kestrels.•The mean reduction rate of BDE-209 in plasma was estimated to be 52 ng/g ww per day.•The estimated BDE-209 half-life in plasma of kestrels was 14 days.•BDE-209 debromination to lower brominated PBDE congeners occurred.

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 ww in 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.