Abstract

P-427 Abstract: Experimental studies have found that selenium (Se) may decrease methylmercury (MeHg) toxicity under certain exposure regimens. However, little is known about the potential protective effect of dietary Se against MeHg neurotoxicity in humans. We assessed the potential interaction between Hg and Se in two birth cohorts in the Faroe Islands. The first cohort consisted of singleton term birth from 1986–1987 (N = 1,022), the second included similar births in 1994–1995 (N = 182). In this fishing population, frequent seafood meals also included occasional consumption of whale meat, which is high in mercury. Hg and Se were measured in whole blood from the umbilical cord. For cohort 1, neurodevelopmental outcomes of the children were evaluated at 7 years, and assessments were carried out on several occasions of cohort 2 children up to age 7 years. We modeled each outcome as a function of Hg-Se concentrations (with adjustments for potential predictors) and considered their potential interactions in several ways: 1) Hg-Se ratio (both expressed in nmol/L); 2) Hg exposure by low and high Hg-Se ratio (defined as below and above the median ratio); and 3) Hg exposure by low and high Se levels (defined as below and above the median Se level). On the average, Se was present in cord blood in a molar excess of about 10-fold, and the Se concentrations suggested that all children were Se sufficient. The correlation coefficient between Hg and Se was 0.29 (p=0.0005). Overall, we found no evidence that Se was a significant protective factor against MeHg neurotoxicity. Preventive efforts therefore are needed to address MeHg exposures, rather than selenium intakes.

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