Methylmercury (MeHg) is the most biologically available and toxic form of mercury, and can act as a powerful teratogen, neurotoxin and endocrine disruptor in vertebrates. However, mechanisms of endocrine impairment and net effects on demography of biota are poorly understood. Here, we report that experimental exposure of an aquatic bird over 3 years to environmentally relevant dietary MeHg concentrations (0.05–0.3 ppm wet weight) resulted in dose-related increases in male–male pairing behaviour (to 55% of males), and decreases in egg productivity (to 30%). Dosed males showed decreased rates of key courtship behaviours, and were approached less by courting females in comparison to control males. Within dosed groups, homosexual males showed a similar reduction when compared with dosed heterosexual males. We found an average 35 per cent decrease in fledgling production in high-dose birds over the study duration. These results are of interest because (i) MeHg exposure is experimentally tied to demographically important reproductive deficits, (ii) these effects were found at low, chronic exposure levels commonly experienced by wildlife, and (iii) effects on reproductive behaviour and sexual preference mediated by endocrine disruption represent a novel and probably under-reported mechanism by which contaminants may influence wild populations of birds.

To test the hypothesis that fledging wading birds would be more at risk from mercury toxicosis than younger nestlings, captive great egret nestlings were maintained as controls or were dosed from 1- to 14-wk-old with 0.5 or 5 mg methylmercury chloride/kg wet weight in fish. Birds dosed with 5 mg/kg suffered from subacute toxicosis at wk 10-12. Growing feather concentrations were the most closely correlated with cumulative mercury consumed per weight. Blood concentrations of mercury increased more rapidly after 9 wk in all groups when feathers stopped growing. Total mercury accumulated in tissues in concentrations in the following order: growing scapular feathers > powderdown > mature scapular feathers > liver > kidney > blood > muscle > pancreas > brain > bile > fat > eye. The proportion of total mercury that was methylated depended upon tissue type and dose group. Selenium accumulated in liver in direct proportion to liver mercury concentrations. After wk 9, appetite and weight index (weight/bill length) declined significantly in both dosed groups. At current exposure levels in the Everglades (Florida, USA) mercury deposited in rapidly growing feathers may protect nestlings from adverse effects on growth until feathers cease growing.

Captive great egret (Ardea albus) nestlings were maintained as controls or were dosed with methylmercury chloride at low (0.5), and high doses (5 mg/kg, wet weight) in fish. Low dosed birds were given methylmercury at concentrations comparable to current exposure of wild birds in the Everglades (Florida, USA). When compared with controls, low dosed birds had lower packed cell volumes, dingy feathers, increased lymphocytic cuffing in a skin test, increased bone marrow cellularity, decreased bursal wall thickness, decreased thymic lobule size, fewer lymphoid aggregates in lung, increased perivascular edema in lung, and decreased phagocytized carbon in lung. High dosed birds became severely ataxic and had severe hematologic, neurologic, and histologic changes. The most severe lesions were in immune and nervous system tissues. By comparing responses in captive and wild birds, we found that sublethal effects of mercury were detected at lower levels in captive than in wild birds, probably due to the reduced sources of variation characteristic of the highly controlled laboratory study. Conversely, thresholds for more severe changes (death, disease) occurred at lower concentrations in wild birds than in captive birds, probably because wild birds were exposed to multiple stressors. Thus caution should be used in applying lowest observed effect levels between captive and wild studies.