ABSTRACT
Wetlands are widely regarded as biogeochemical hotspots of highly toxic methylmercury (MeHg), mainly mediated by sulfate-reducing bacteria. In low-lying coastal wetlands, sea level rise, a phenomenon caused by global climate change, is slowly degrading numerous healthy freshwater forested wetlands into salt-degraded counterparts with a nickname "ghost forests", and eventually converting them to saltmarshes. However, little is known about the changes of mercury (Hg) methylation, bioaccumulation, and biomagnification along the forest-to-saltmarsh gradient. Here, we conducted extensive field sampling in three wetland states (healthy forested wetlands, salt-degraded forested wetlands, and saltmarsh) along a salinity gradient (from 0 to 9.4 ppt) in Winyah Bay, South Carolina, USA. We found that in our study wetland systems the saltmarshes had the lowest levels of both total Hg and MeHg in sediments and biota, as compared to healthy forested wetlands and saltwater-degraded ghost forests. Our results suggest that the slow conversion of forested wetland to saltmarsh could reduce net MeHg production in our study wetland systems, which we hypothesized that could be attributed to increased sulfate reduction and excessive buildup of sulfide in sediment that inhibits microbial Hg methylation, and/or reduced canopy density and increased photodegradation of MeHg. However, it should be noted that biogeochemical MeHg responses to salinity changes may be site-specific and we urge more similar studies in other wetland systems along a salinity gradient. Therefore, long-term salinization of coastal wetlands and the slow conversion of forests to marshes could decrease long-term exposure of toxic MeHg levels in coastal food webs that are similar to our system, and ultimately reduce human exposure to this neurotoxin.
