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.

Mercury exposure and neurochemical impacts in bald eagles across several Great Lakes states.

In this study, we assessed mercury (Hg) exposure in several tissues (brain, liver, and breast and primary feathers) in bald eagles (Haliaeetus leucocephalus) collected from across five Great Lakes states (Iowa, Michigan, Minnesota, Ohio, and Wisconsin) between 2002-2010, and assessed relationships between brain Hg and neurochemical receptors (NMDA and GABA(A)) and enzymes (glutamine synthetase (GS) and glutamic acid decarboxylase (GAD)). Brain total Hg (THg) levels (dry weight basis) averaged 2.80 µg/g (range: 0.2-34.01), and levels were highest in Michigan birds. THg levels in liver (r(p) = 0.805) and breast feathers (r(p) = 0.611) significantly correlated with those in brain. Brain Hg was not associated with binding to the GABA(A) receptor. Brain THg and inorganic Hg (IHg) were significantly positively correlated with GS activity (THg r(p) = 0.190; IHg r(p) = 0.188) and negatively correlated with NMDA receptor levels (THg r(p) = -0245; IHg r(p) = -0.282), and IHg was negatively correlated with GAD activity (r(s) = -0.196). We also report upon Hg demethylation and relationships between Hg and Se in brain and liver. These results suggest that bald eagles in the Great Lakes region are exposed to Hg at levels capable of causing subclinical neurological damage, and that when tissue burdens are related to proposed avian thresholds approximately 14-27% of eagles studied here may be at risk.