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Background. Many children in low- and middle-income countries face enhanced risks of exposure to contaminants via the environment, parental occupation, and other routes. While mercury (Hg) is a global pollutant whose transport properties allow it to have an impact even in pristine areas, the presence of significant Hg sources in the developing world can cause localized effects that are more severe than those observed in other areas. Objectives. This paper provides a narrative review of sources of Hg exposure to people in the developing world with a particular focus on children, and presents an overview of key aspects to this important issue. Methods. We searched Web of Knowledge and Google Scholar using keywords including combinations of “mercury” and one or more of the following: “children,” “exposure,” “breast milk,” “artisanal mining,” “prenatal,” “religion,” “medicine,” “dental amalgam,” “chlor-alkali,” “VCM,” “vaccine,” “e-waste,” “industry,” “beauty,” “cosmetics,” “strategies,” “child labor,” “costs,” and “developing countries” to find peer-reviewed articles pertaining to Hg exposure in the developing world. Results. Sources of Hg exposure include mining, consumption, industrial operations, religious practices, traditional medicines, beauty products, vaccines, dental amalgams, and waste scavenging and recycling. Conclusion. Children in the developing world are often subject to higher levels of Hg exposure than those living in developed countries due to the higher prevalence of Hg-intensive industrial processes and consumer products, lack of environmental regulation, and limits in mobility and food choices, among other factors. This issue can be addressed through additional research to fill in data gaps on exposure sources, establish sound and enforceable policies, and increase education and participation in affected communities. Challenges to addressing this problem include limited resources for needed equipment, training, and manpower to implement solutions. Competing Interests. The authors declare no competing financial interests.

Biofilms can methylate mercury (Hg) at higher rates than unattached bacteria and are increasingly recognized as important Hg methylation sites in the environment. Our previous study showed that methylation rates in biofilm cultures were up to 1 order of magnitude greater than those in planktonic cultures of a sulfate-reducing bacterium. To probe whether the differential Hg methylation rates resulted from metabolic differences between these two cultures, Hg methylation assays following molybdate or chloroform inhibition (a specific inhibitor of the acetyl-CoA pathway) were conducted on biofilm and planktonic cultures of Desulfovibrio desulfuricans strains M8 and ND132. Molybdate was as effective in inhibiting Hg methylation as well as growth in both planktonic and biofilm cultures. The addition of chloroform only impacted Hg methylation in biofilm cultures, suggesting that different pathways are used for methylation in biofilm compared to planktonic cultures. To investigate this further, expression of the cooS gene, which encodes for carbon monoxide dehydrogenase, a key enzyme in the acetyl-CoA pathway, was compared in biofilm and planktonic cultures of ND132. Biofilm cultures showed up to 4 times higher expression of cooS than planktonic cultures. On the basis of these results, the acetyl-CoA pathway appears to play an important role in methylation in biofilm cultures of this organism, possibly by supplying the methyl group to Hg methylating enzymes; methylation in planktonic cultures appears to be independent of this pathway. This observation has important implications, particularly in developing reliable models to predict Hg methylation rates in different environments and perhaps eventually in being able to control this undesirable chemical transformation.

The speciation of mercury (Hg) is a major determinant of its methylation rate by sulfate-reducing bacteria (SRB), considered the primary methylators. Under anoxic conditions, sulfur (S) cycling may have a significant influence on Hg complexation and methylation, by influencing both SRB activity and the pool of available reduced S ligands, as the presence of zero-valent sulfur (S(0)) in sulfidic water results in the formation of polysulfides. While SRB frequently coexist with S-oxidizing bacteria in natural environments, the effect that these organisms may have on methylation by SRB is not understood. In this study, we investigate the role of S(0) in methylation by SRB monocultures and cocultures with phototrophic green or purple S-oxidizing bacteria. In the coculture experiments, the presence of S-oxidizers was found to increase Hg methylation rates, apparently by maintaining favorable chemical speciation in the environment. The measured Hg methylation rates were in accord with predictions based on geochemical modeling of speciation. In SRB monoculture experiments conducted in the presence and absence of S(0), the data showed that at limited total Hg, the presence of polysulfides resulted in decreased Hg methylation, presumably by causing a decrease in the most bioavailable Hg–sulfide complexes. These results indicate that models of Hg speciation and methylation in the environment should include a detailed investigation of S redox speciation.