GENETIC VARIABILITY IN SUSCEPTIBILITY AND RESPONSE TO MERCURY TOXICITY: SPECIAL CONSIDERATIONS

Notably, exposures to mercury continue to be significant health risks to both workers and non-occupational populations, with profound neurological, cardiovascular, hematological, pulmonary, renal, reproductive, and embryonic toxicological effects. Of course, children are recognized as having heightened susceptibility to the adverse effects of this heavy metal, compared to adults with similar exposures. In addition, all these effects on human health could be even greater than previously thought as result of variation in sources and levels of exposure that may contribute to the overall interindividual variation in mercury biomarker levels in humans. Traditionally, the knowledge of mechanisms of mercury uptake and distribution throughout the body, as well as the dynamic of different complexes in the various compartments inside cells, are of importance to resolve new health concerns. However, identify molecular markers for variation in susceptibility and pinpoint susceptible groups or life stages, who display very similar risk profiles, becomes crucial as well in terms of more accurate risk assessments and improved decision-making. Consequently, a general view is emerging that there are many genes now evaluated as potential mediators (i.e., in the biological causal pathway), moderators (i.e., risk modifiers), direct causes, or otherwise parts of complex causal pathways. For this reason, there is an increasing requirement in the quest to uncover responsive genes to mercury toxicity, their common biochemical pathways of action, and then expression, and pathogenetic roles of these potential candidate biomarkers of susceptibility. In conclusion, genetic polymorphisms may represent the direction of future work in the prognostic research area, of intense public health interest for reducing mercury exposures in the world's population.