Anticipating chronic effects of contaminant exposure on amphibian species is complicated both by toxicological and ecological uncertainty. Data for both chemical exposures and amphibian vital rates, including altered growth, are sparse. Developmental plasticity in amphibians further complicates evaluation of chemical impacts as metamorphosis is also influenced by other biotic and abiotic stressors, such as temperature, hydroperiod, predation, and conspecific density. Determining the effect of delayed tadpole development on survival through metamorphosis and subsequent recruitment must include possible effects of pond drying accelerating metamorphosis near the end of the larval stage. This model considers the combined influence of delayed onset of metamorphosis in a cohort as well as accelerated metamorphosis toward the end of the hydroperiod and determines the net influence of counteracting forces on tadpole development and survival.
Amphibian populations with greater initial density dependence have less capacity for developmental plasticity and are therefore more vulnerable to delayed development and reduced hydroperiod. The consequential reduction in larval survival has a relatively greater impact on species with a shorter lifespan, allowing for fewer breeding seasons during which to successfully produce offspring. In response to risk assessment approaches that consider only survival and reproductive endpoints in population evaluation, we calculate contaminant-related growth effects in terms of reduced survival and present these altered vital rates in the larger context of long-term population consequences for different species.