Metals and Organohalogen Contaminants in Bald Eagles (Haliaeetus leucocephalus) from Ontario, 1991-2008.

We examined the degree of exposure of lead (Pb), mercury (Hg), and several organohalogen contaminants and its potential impact on survival of bald eagles in Ontario from 1991 to 2008. Overall, results for 43 dead or dying bald eagles collected in the province indicate that 23% (10/43) of birds died of Pb poisoning and 9% (4/43) died of suspected Hg poisoning. Pb poisoning was diagnosed based on exceedances of toxicity thresholds in liver and kidney and supported by clinical observations, necropsy results, and histology findings when available. Evidence for Hg poisoning in eagles was limited; however, Hg concentrations exceeded the toxicity threshold in kidney. Pb concentrations ranged widely in liver and kidney. Total Hg concentrations were relatively higher in kidney compared with liver and were significantly correlated with selenium (Se) concentrations in both tissues. Concentrations of p,p'-DDE and sum PCBs in livers of 12 bald eagles collected from 2001 to 2004 were likely below concentrations associated with adverse effects. Hepatic concentrations of total polybrominated diphenyl ethers were generally higher in birds collected from southern Ontario compared with northern Ontario. Potential impacts of exposure to these flame retardants and others are not known. Elevated metal exposure appears to influence survivorship and may affect the recovery of bald eagles in the province, particularly in southern Ontario and along the Great Lakes where a disproportionate number of poisoned eagles were collected. Increased efforts are needed to identify sources of exposure and develop measures to reduce metal exposure in this top predator.

Effects of dose, administration route, and/or vehicle on decabromodiphenyl ether concentrations in plasma of maternal, fetal, and neonatal rats and in milk of maternal rats.

The effects of route and vehicle on blood and milk levels of decabromodiphenyl ether (DecaBDE; CASRN 1163-19-5) were investigated in the rat to assist in the design and conduct of a developmental neurotoxicity study. Blood plasma and/or milk concentrations were determined in dams, fetuses, and/or nursing pups after repeated DecaBDE administration by gavage throughout gestation or gestation and lactation using corn oil (CO) or soyaphospholipon/Lutrol F 127-water (SPL) as the vehicle. The impact of vehicle on plasma levels was also investigated in pups derived from naive dams after a single postnatal dose. This study reports for the first time fetal and neonatal plasma concentrations concurrent with those of maternal plasma and/or milk. Higher concentrations of DecaBDE were achieved in plasma and in milk with CO than with SPL. Furthermore, pups derived from dams treated with only SPL were lower in body weight, compared with those from dams treated with either CO, CO and DecaBDE, or SPL and DecaBDE. The study further shows that exposure to DecaBDE is relatively consistent across the dose range of 100 to 1000 mg/(kg · day) when administered in CO.