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AWARDS | Innovation Grant


Biomarkers of exposure and health risk among fish consumers in Amazonian Brazil
Jennifer Nyland, PhD, Research Associate, Department of Environmental Health Science, JHSPH 

The overall goal of this innovation project is to demonstrate associations between methyl mercury (MeHg) exposure, via fish consumption, and biomarkers of immunotoxicity. To accomplish this goal, we will utilize a unique population-based study (in which we are collaborators), conducted in Amazonian Brazil, involving persons exposed to MeHg through fish consumption. The results will have significant implications for the health of other fish consumers, and will provide us with tools for investigating the risks of subsistence and recreational fish consumption in populations in Maryland and elsewhere. Because of the rich database on diet and biomarkers in this study, we will also be able to test the hypothesis that selenium intake may modulate the immunotoxic effects of mercury.

There is considerable debate about the risks and benefits of fish consumption in the context of the nutritional value of omega-3-fatty acids and the presence of MeHg in many fish species (Guallar et al. 2002; Yoshizawa et al. 2002). This debate has focused on the neurodevelopmental and cardiovascular risks of exposures to MeHg; no consideration has been given to the immunotoxic effects of mercury compounds. We and others have reported on associations between mercury exposures and immune suppression as well as increased risks of autoimmune diseases. In this study, we will test the hypothesis that MeHg exposure, via fish consumption, increases the odds of elevations in specific biomarkers, indicative of autoimmune dysfunction in a dose-related manner. Autoimmune diseases are among the most devastating chronic diseases in the US, affecting nearly 50 million people. While autoimmune diseases are generally recognized to involve both heritable and acquired risk factors, relatively little is known about the latter risks for human disease aside from exposure to infectious agents, such as viruses and bacteria. These infectious agents are believed to trigger the development of autoimmune diseases, but the expression and severity of disease may be a reflection of pre-existing genetic susceptibility. Our research to date has indicated that Hg exposure may also play an important role in this complex causal pathway, either by modifying host response to the triggering event or by exacerbating the autoimmune process subsequent to infection (Silbergeld et al. 2005).

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