UPTAKE, TOXICITY, AND TROPHIC TRANSFER OF MERCURY IN A COASTAL DIATOM

The primary mechanisms controlling the accumulation of methylmercury a nd inorganic mercury in aquatic food chains are not sufficiently under stood. Differences in lipid solubility alone cannot account for the pr edominance of methylmercury in fish because inorganic mercury complexe s (e.g., HgCl2), which are not bioaccumulated in fish, are as lipid so luble as their methylmercury analogs (e.g., CH3HgCl). Mercury concentr ations 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 specia tion, toxicity, and phytoplankton uptake demonstrate that passive upta ke of uncharged, lipophilic chloride complexes is the principal accumu lation route of both methylmercury and inorganic mercury in phytoplank ton. The predominance of methylmercury in fish, however, is a conseque nce of the greater trophic transfer efficiency of methylmercury than i norganic 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 b ound in phytoplankton membranes. On the basis of these results, we con structed a simple model of mercury accumulation in fish as a function of the overall octanol-water partition coefficient of methylmercury. O ur model can explain the variability of mercury concentrations in fish within, but not among, different lake regions.