Assessing abalone growth inhibition risk to cadmium and silver by linking toxicokinetics/toxicodynamics and subcellular partitioning.

The purpose of this study was to link toxicokinetics/toxicodynamics and subcellular partitioning for assessing the susceptibility and the growth inhibition risks of abalone Haliotis diversicolor supertexta exposed to waterborne and foodborne cadmium (Cd) and silver (Ag). We reanalyzed published data on growth inhibition and subcellular partitioning associated with the present mechanistic model to explore the correlations among elimination (k (e)), detoxification (k (d)), and recovery (k (r)) rate constants and to assess the growth inhibition risk. We found a positive correlation among k (e), k (d), and k (r) in abalone exposed to Ag. We also employed a life-stage based probabilistic assessment model to estimate the growth inhibition risk of abalone to environmentally relevant Cd (5-995 μg l(-1)) and Ag (0.05-9.95 μg l(-1)) concentrations in Taiwan. The results showed that abalone had a minimum 20% probability of the growth inhibition risk exposed to Cd, whereas Ag exposure was not likely to pose the risk. The maximum biomasses were estimated to be 0.0039 and 0.0038, 61.61 and 43.87, and 98.88 and 62.97 g for larvae, juveniles, and adults of abalone exposed to the same levels of Cd and Ag, respectively. Our study provides a useful tool to detect potential growth biomass of abalone populations subjected to Cd and Ag stresses and mechanistic implications for a long-term ecotoxicological risk assessment in realistic situations.