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Mercury (Hg) is a neurotoxicant known to cause developmental and behavioral abnormalities in vertebrates. Increasing evidence suggests that Hg can also disrupt endocrine functions and endocrine-dependent processes. For example, dietary Hg has been shown to delay tail resorption during metamorphic climax in amphibians, a process mediated by thyroid hormones. However, a direct link between Hg, hormone disruption, and developmental delays in amphibians has not been explored. Therefore, we examined the effects of dietary Hg (0.01, 2.5, and 10 μg/g total Hg, dry wt) on thyroid hormone concentrations, development, growth, performance, and survival of wood frogs (Rana sylvatica). Tadpoles accumulated Hg in a concentration-dependent manner; total Hg concentrations in tadpoles at the beginning of metamorphic climax (Gosner stage 42) were 0.03, 1.06, 3.54 μg/g, dry wt, for control, low, and high Hg diets, respectively. During metamorphic climax, tadpoles eliminated 35% of the inorganic Hg from their tissues but retained most of their accumulated methylmercury. Contrary to our predictions, we found no effect of Hg on the duration of tadpole development, size at metamorphosis, tail resorption time, or hopping performance. Consistent with the lack of effects on development, we also detected no differences in whole-body thyroid hormone concentrations among our dietary treatments. Our results, when compared with the effects of Hg on other amphibians, suggest that amphibian species may differ substantially in their sensitivity to dietary Hg, emphasizing the need for data on multiple species when establishing toxicity benchmarks.

Organisms born into the same contaminated environment as their parents can be exposed both maternally and environmentally to contaminants, potentially placing them at greater risk of adverse effects than when exposed via either of the two pathways independently. We examined whether embryonic exposure to maternally derived mercury (Hg) interacts with dietary exposure to negatively influence larval development in American toads ( Bufo americanus ). We collected eggs from breeding pairs at reference and Hg-contaminated sites and monitored performance, development, and survival of larvae fed three experimental Hg diets (total Hg, 0.01, 2.5, and 10 μg/g). The negative sublethal effects of maternal and/or dietary Hg manifested differently, but maternal Hg exposure had a greater overall influence on offspring health than dietary exposure. However, the combination of sublethal effects of the two exposure routes interacted with lethal consequences; larvae exposed to maternal Hg and high dietary Hg experienced 50% greater mortality compared to larvae from reference mothers fed the control diet. This study is the first to demonstrate that the latent effects of maternally transferred contaminants may be exacerbated by further exposure later in ontogeny, findings that may have important implications for both wildlife and human health.