Genetic polymorphisms are associated with hair, blood, and urine mercury levels in the American Dental Association (ADA) study participants

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.

Autism spectrum disorder and mercury toxicity: use of genomic and epigenetic methods to solve the etiologic puzzle

“…The incorporation of newer genetic (or genomic) and epigenetic insights into theories of causation of neurodevelopmental disease constitutes an important means to more fully understand the fundamental etiologies of these conditions. A number of genetic factors influencing mercury toxicity and risk of ASD have been, and continue to be, reported (Spalletta et al, 2007;Goodrich et al, 2011;Austin et al, 2014;Drescher et al, 2014;Engstrom et al, 2016;Parajuli et al, 2016;Spencer et al, 2018). ASD risk has a strong genetic component.…”

Non-Essential Trace Elements Dietary Exposure in French Polynesia: Intake Assessment, Nail Bio Monitoring and Thyroid Cancer Risk

“…Polynesians had the lower Hg fingernail concentration; however, they were the most exposed. This could be explained by the effect of genetic polymorphism on Hg levels in the blood and hair, as suggested by other studies (Wang et al, 2012;Barcelos et al, 2013;Barcelos et al, 2015;Parajuli et al, 2016 ).…”

Calls to Florida Poison Control Centers about mercury: Trends over 2003–2013

“…For the purposes of describing the overall temporal trends in calls about mercury, there is a substantive rationale for simplifying all kinds of mercury exposure as “mercury”: mercury in the environment can gain or lose a methyl group (Celo et al, 2006; Choi and Bartha, 1994; Li and Cai, 2013) and mercury can also change methylation state in the gut and body (Parajuli et al, 2016; Rothenberg et al, 2016; Sherman et al, 2013). Furthermore, on a practical level, there may be inconsistencies in how calls about specific mercury species were recorded by poison control center specialists, so collapsing into a single category of mercury should reduce misclassification of the number of calls.…”