Rajendra Prasad Parajuli1, Jaclyn M Goodrich2, Hwai-Nan Chou3, Stephen E Gruninger4, Dana C Dolinoy5, Alfred Franzblau6, Niladri Basu7. 1. Faculty of Agricultural and Environmental Sciences, McGill University, Montreal, Quebec, Canada. Electronic address: rp.parajuli@mcgill.ca. 2. Department of Environmental Health Sciences, Unisiversity of Michigan School of Public Health, Ann Arbor, MI, USA. Electronic address: gaydojac@umich.edu. 3. American Dental Association, Chicago, IL, USA. Electronic address: chouh@ada.org. 4. American Dental Association, Chicago, IL, USA. Electronic address: gruningers@ada.org. 5. Department of Environmental Health Sciences, Unisiversity of Michigan School of Public Health, Ann Arbor, MI, USA; Department of Nutritional Sciences, University of Michigan School of Public Health, Ann Arbor, MI, USA. Electronic address: ddolinoy@umich.edu. 6. Department of Environmental Health Sciences, Unisiversity of Michigan School of Public Health, Ann Arbor, MI, USA. Electronic address: afranz@umich.edu. 7. Faculty of Agricultural and Environmental Sciences, McGill University, Montreal, Quebec, Canada; Department of Environmental Health Sciences, Unisiversity of Michigan School of Public Health, Ann Arbor, MI, USA. Electronic address: niladri.basu@mcgill.ca.
Abstract
BACKGROUND/AIMS: Mercury (Hg) is a potent toxicant of concern to the general public. Recent studies suggest that several genes that mediate Hg metabolism are polymorphic. We hypothesize that single nucleotide polymorphisms (SNPs) in such genes may underline inter-individual differences in exposure biomarker concentrations. METHODS: Dental professionals were recruited during the American Dental Association (ADA) 2012 Annual Meeting. Samples of hair, blood, and urine were collected for quantifying Hg levels and genotyping (88 SNPs in classes relevant to Hg toxicokinetics including glutathione metabolism, selenoproteins, metallothioneins, and xenobiotic transporters). Questionnaires were administrated to obtain information on demographics and sources of Hg exposure (e.g., fish consumption and use of dental amalgam). Here, we report results for 380 participants with complete genotype and Hg biomarker datasets. ANOVA and linear regressions were used for statistical analysis. RESULTS: Mean (geometric) Hg levels in hair (hHg), blood (bHg), urine (uHg), and the average estimated Hg intake from fish were 0.62µg/g, 3.75µg/L, 1.32µg/L, and 0.12µg/kg body weight/day, respectively. Out of 88 SNPs successfully genotyped, Hg biomarker levels differed by genotype for 25 SNPs, one of which remained significant following Bonferroni correction in ANOVA. When the associations between sources of Hg exposure and SNPs were analyzed with respect to Hg biomarker concentrations, 38 SNPs had significant main effects and/or gene-Hg exposure source interactions. Twenty-five, 23, and four SNPs showed significant main effects and/or interactions for hHg, bHg, and uHg levels, respectively (p<0.05), and six SNPs (in GCLC, MT1M, MT4, ATP7B, and BDNF) remained significant following Bonferroni correction. CONCLUSION: The findings suggest that polymorphisms in environmentally-responsive genes can influence Hg biomarker levels. Hence, consideration of such gene-environment factors may improve the ability to assess the health risks of Hg more precisely.
BACKGROUND/AIMS: Mercury (Hg) is a potent toxicant of concern to the general public. Recent studies suggest that several genes that mediate Hg metabolism are polymorphic. We hypothesize that single nucleotide polymorphisms (SNPs) in such genes may underline inter-individual differences in exposure biomarker concentrations. METHODS: Dental professionals were recruited during the American Dental Association (ADA) 2012 Annual Meeting. Samples of hair, blood, and urine were collected for quantifying Hg levels and genotyping (88 SNPs in classes relevant to Hg toxicokinetics including glutathione metabolism, selenoproteins, metallothioneins, and xenobiotic transporters). Questionnaires were administrated to obtain information on demographics and sources of Hg exposure (e.g., fish consumption and use of dental amalgam). Here, we report results for 380 participants with complete genotype and Hg biomarker datasets. ANOVA and linear regressions were used for statistical analysis. RESULTS: Mean (geometric) Hg levels in hair (hHg), blood (bHg), urine (uHg), and the average estimated Hg intake from fish were 0.62µg/g, 3.75µg/L, 1.32µg/L, and 0.12µg/kg body weight/day, respectively. Out of 88 SNPs successfully genotyped, Hg biomarker levels differed by genotype for 25 SNPs, one of which remained significant following Bonferroni correction in ANOVA. When the associations between sources of Hg exposure and SNPs were analyzed with respect to Hg biomarker concentrations, 38 SNPs had significant main effects and/or gene-Hg exposure source interactions. Twenty-five, 23, and four SNPs showed significant main effects and/or interactions for hHg, bHg, and uHg levels, respectively (p<0.05), and six SNPs (in GCLC, MT1M, MT4, ATP7B, and BDNF) remained significant following Bonferroni correction. CONCLUSION: The findings suggest that polymorphisms in environmentally-responsive genes can influence Hg biomarker levels. Hence, consideration of such gene-environment factors may improve the ability to assess the health risks of Hg more precisely.
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