Anthropogenic Hg in the ocean: Trajectories of change and implications for exposure in the United States

Abstract:

Humans have been releasing mercury (Hg) to the environment for millenia through activities such as mining and fuel combustion. The result has been an enrichment of the ocean, atmosphere, and terrestrial ecosystems. Consumption of marine fish contaminated with methylmercury (MeHg) is the primary route of exposure in many populations globally. We present an updated analysis of sources of MeHg exposures in the United States that shows the majority (>70%) is from oceanic fish rather than coastal species. Using a fully coupled biogeochemical box model we also estimate Hg accumulation across major ocean basins and show anthropogenic enrichment is highest in the North Atlantic Ocean and lowest in the deep Pacific Ocean. Our results for contemporary ocean concentrations are consistent with recent data from the Pacific, Atlantic, Indian and Southern Oceans measured as part of the CLIVAR repeat hydrography program. Our estimates of natural (i.e., pre-anthropogenic) seawater Hg concentrations are lower than suggested by other studies, implying a greater anthropogenic perturbation in the ocean. Our work suggests total accumulation of anthropogenic Hg in the global oceans is greater than recently derived based on anthropogenic CO₂. We compare modeled seawater concentrations since 1980 to observations over this period to evaluate evidence for changes in recent decades and then investigate potential impacts of changing global emissions. To do this, we use a range of historical and future anthropogenic Hg emission inventories. Our previous work using the box model indicates burial of Hg at ocean margins is the single largest global sink of anthropogenic Hg. We will discuss how the magnitude and permanence of this sink affects estimates of enrichment and time scales of recovery in all geochemical Hg reservoirs. Governing time scales of response in each ocean basin are diagnosed using eigenanalysis and discussed in the context of changes in human MeHg exposure resulting from regulation of human Hg sources.