Effects of chemical contaminant exposure may be contributing to the decline of spectacled eiders (Somateria fischeri) nesting in coastal areas of western Alaska. We evaluated chemical exposure and potential effects in 20 male eiders collected near St. Lawrence Island, Alaska. Analytes included metals, trace elements, chlorinated organics, and (137)Cesium ((137)Cs). Effects of contaminant exposure were evaluated using histopathology and biochemical measures of porphyrin profiles, cytochrome P450 activities, and metallothionein (MT) concentrations. Copper, cadmium, and selenium concentrations were elevated in spectacled eiders when compared to literature values for other marine birds. Only a few samples had trace concentrations of chlorinated organic compounds. Muscle (137)Cs levels were all below the average minimum quantifiable concentration of 0.079 Bq/g. No histopathological lesions were associated with elevated contaminant concentrations in liver, kidney, or testes. Protoporphyrin was found in highest concentration in both the liver and kidneys, followed by coproporphyrin and uroporphyrin, respectively. Hepatic uroporphyrin concentrations correlated significantly to hepatic arsenic concentrations. Mean activities of hepatic EROD, MROD, BROD, and PROD were consistent with other avian species. Comparisons of cadmium/MT ratios from this study to published literature ratios in seven marine avian species suggest that, although adult male spectacled eiders have elevated liver concentrations of certain MT-inducing metals, their MT concentrations are not as strongly induced as would be predicted based on literature values. Despite elevated metal concentrations, the apparent good health of the St. Lawrence Island birds suggests that should these contaminants be a factor in population declines, they likely act by decreasing fecundity or survival of young rather than via direct health impacts on adult male spectacled eiders.

Changes in urinary porphyrin excretion patterns (porphyrin profiles) during prolonged mercury exposure are attributable to mercury accumulation in the kidney and to consequent effects of Hg2+ on renal porphyrin metabolism. In the present study, we evaluated the quantitative relationship of urinary porphyrin concentrations to mobilizable renal mercury content, using the metal chelator 2,3-dimercapto-1-propanesulfonic acid (DMPS) to modulate kidney mercury levels. Rats exposed to methylmercury hydroxide (MMH) at 10 ppm in drinking water for 6 weeks were treated with up to 3 consecutive doses of DMPS (100mg/kg, ip) at 72-h intervals. Consistent with previous findings, the concentrations of pentacarboxyl- (5-) and copro- (4-) porphyrins and of an atypical porphyrin specific to mercury exposure, precoproporphyrin, were significantly elevated in urine of MMH-exposed rats, compared with that of rats exposed to distilled water (dH2O) for the same period. Consecutive DMPS treatments of MMH-exposed rats significantly decreased kidney concentrations of total, as well as Hg2+ and CH3Hg+ species, and promoted increased urinary mercury excretion. Concomitantly, DMPS treatment decreased both kidney and urinary porphyrin concentrations, consistent with depletion of renal mercury levels. Regression analyses demonstrated a high correlation (r approximately 0.9) between prechelation urinary porphyrins and postchelation urinary mercury levels and also between prechelation urinary porphyrins and prechelation kidney mercury concentrations. These findings demonstrate that urinary porphyrin concentrations relate quantitatively to DMPS-mobilizable mercury in the kidney and, therefore, serve as a biochemical measure of renal mercury content.

Methylmercury cation (MeHg) and divalent mercury (Hg++) accumulation in liver, kidney, and brain were quantified in prairie voles (Microtus ochrogaster) at 0, 3, 6, and 12 weeks during chronic exposure to aqueous MeHg. Dose groups received deionized water or aqueous solutions containing 9, 103, or 920 ng MeHg/ml. Our study presents temporal patterns of Hg++ and MeHg concentrations in organ tissues and makes inter-tissue comparisons at each time point to illustrate the accumulation and distribution of Hg species during the study. MeHg was accumulated in tissues for 3 weeks and then concentrations plateaued. Mercury accumulated in brain, liver, and kidney to average concentrations of 510 ng/g, 180 ng/g, and 3400 ng/g, respectively. MeHg and Hg++ concentrations were roughly equivalent in liver, kidney, and urine. MeHg concentrations in brain tissue were 2 to 20 times the concentrations of Hg++. Regression analysis was also used to demonstrate the utility of urinalysis as an indicator of Hg++ and MeHg concentrations in organ tissue (p< 0.001).

Methyl mercury cation (MeHg(+)) and divalent mercury (Hg(2+)) were quantified in urine, liver, kidney, and brain of prairie voles (Microtus ochrogaster) during a 12 week exposure to aqueous MeHg(+) at concentrations of 10, 100, and 1000 ng MeHg(+)/mL. Aqueous MeHg(+) exposures increased mercury accumulation in tissues of voles from each exposure group. Accumulation was greater within the higher two exposure groups. Similar [Hg(2+)] and [MeHg(+)] were determined within a given organ type before and after 2,3-dimercapto-1-propane sulfonate (DMPS) chelation. Similar correlations were seen for Hg(2+) and MeHg(+) concentrations in pre and post chelation urine. Post chelation urine more reliably predicted mercury species concentrations in tissues than did urine collected before chelation. These data demonstrate the utility of DMPS in noninvasive assessment of wildlife exposure to mercury, which may have utility in evaluating meta-population level exposure to hazardous wastes.