Abstract
The primary mechanisms controlling the accumulation of methylmercury and inorganic mercury in aquatic food chains are not sufficiently understood. Differences in lipid solubility alone cannot account for the predominance of methylmercury in fish because inorganic mercury complexes (e.g., HgCl2), which are not bioaccumulated in fish, are as lipid soluble as their methylmercury analogs (e.g., CH3HgCl). Mercury concentrations in fish are ultimately determined by methylmercury accumulation at the base of the food chain, which is governed by water chemistry, primarily pH and chloride concentration. Our studies of mercury speciation, toxicity, and phytoplankton uptake demonstrate that passive uptake of uncharged, lipophilic chloride complexes is the principal accumulation route of both methylmercury and inorganic mercury in phytoplankton. The predominance of methylmercury in fish, however, is a consequence of the greater trophic transfer efficiency of methyl- mercury than inorganic mercury. In particular, methylmercury in phytoplankton, which accumulates in the cell cytoplasm, is assimilated by zooplankton four times more efficiently than inorganic mercury, which is principally bound in phytoplankton membranes. On the basis of these results, we constructed a simple model of mercury accumulation in fish as a function of the overall octanol−water partition coefficient of methylmercury. Our model can explain the variability of mercury concentrations in fish within, but not among, different lake regions.