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      Association of Low-Moderate Arsenic Exposure and Arsenic Metabolism with Incident Diabetes and Insulin Resistance in the Strong Heart Family Study

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          Abstract

          Background:

          High arsenic exposure has been related to diabetes, but at low-moderate levels the evidence is mixed. Arsenic metabolism, which is partly genetically controlled and may rely on certain B vitamins, plays a role in arsenic toxicity.

          Objective:

          We evaluated the prospective association of arsenic exposure and metabolism with type 2 diabetes and insulin resistance.

          Methods:

          We included 1,838 American Indian men and women free of diabetes (median age, 36 y). Arsenic exposure was assessed as the sum of inorganic arsenic (iAs), monomethylarsonate (MMA), and dimethylarsinate (DMA) urine concentrations ( Σ As ). Arsenic metabolism was evaluated by the proportions of iAs, MMA, and DMA over their sum (iAs%, MMA%, and DMA%). Homeostasis model assessment for insulin resistance (HOMA2-IR) was measured at baseline and follow-up visits. Incident diabetes was evaluated at follow-up.

          Results:

          Median Σ As , iAs%, MMA%, and DMA% was 4.4 μ g / g creatinine, 9.5%, 14.4%, and 75.6%, respectively. Over 10,327 person-years of follow-up, 252 participants developed diabetes. Median HOMA2-IR at baseline was 1.5. The fully adjusted hazard ratio [95% confidence interval (CI)] for incident diabetes per an interquartile range increase in Σ As was 1.57 (95% CI: 1.18, 2.08) in participants without prediabetes at baseline. Arsenic metabolism was not associated with incident diabetes. Σ As was positively associated with HOMA2-IR at baseline but negatively with HOMA2-IR at follow-up. Increased MMA% was associated with lower HOMA2-IR when either iAs% or DMA% decreased. The association of arsenic metabolism with HOMA2-IR differed by B-vitamin intake and AS3MT genetics variants.

          Conclusions:

          Among participants without baseline prediabetes, arsenic exposure was associated with incident diabetes. Low MMA% was cross-sectional and prospectively associated with higher HOMA2-IR. Research is needed to confirm possible interactions of arsenic metabolism with B vitamins and AS3MT variants on diabetes risk. https://doi.org/10.1289/EHP2566

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          Scientific Opinion on Arsenic in Food

          (2009)
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            Mechanisms of arsenic biotransformation.

            Marie Vahter (2002)
            Inorganic arsenic, a documented human carcinogen, is methylated in the body by alternating reduction of pentavalent arsenic to trivalent and addition of a methyl group from S-adenosylmethionine. Glutathione, and possibly other thiols, serve as reducing agents. The liver is the most important site of arsenic methylation, but most organs show arsenic methylating activity. The end metabolites are methylarsonic acid (MMA) and dimethylarsinic acid (DMA). These are less reactive with tissue constituents than inorganic arsenic and readily excreted in the urine. However, reactive intermediates may be formed. Absorbed arsenate (As(V)) is fairly rapidly reduced in blood to As(III), which implies increased toxicity. Also, intermediate reduced forms of the methylated metabolites, MMA(III) and DMA(III), have been detected in human urine. In particular MMA(III) is highly toxic. To what extent MMA(III) and DMA(III) contribute to the observed toxicity following exposure to inorganic arsenic remains to be elucidated. There are marked differences in the metabolism of arsenic between mammalian species, population groups and individuals. There are indications that subjects with low MMA in urine have faster elimination of ingested arsenic, compared to those with more MMA in urine.
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              Arsenic exposure and prevalence of type 2 diabetes in US adults.

              Eliseo Guallar, Ana Navas-Acien, Roberto Pastor-Barriuso … (2008)
              High chronic exposure to inorganic arsenic in drinking water has been related to diabetes development, but the effect of exposure to low to moderate levels of inorganic arsenic on diabetes risk is unknown. In contrast, arsenobetaine, an organic arsenic compound derived from seafood intake, is considered nontoxic. To investigate the association of arsenic exposure, as measured in urine, with the prevalence of type 2 diabetes in a representative sample of US adults. Cross-sectional study in 788 adults aged 20 years or older who participated in the 2003-2004 National Health and Nutrition Examination Survey (NHANES) and had urine arsenic determinations. Prevalence of type 2 diabetes across intake of arsenic. The median urine levels of total arsenic, dimethylarsinate, and arsenobetaine were 7.1, 3.0, and 0.9 mug/L, respectively. The prevalence of type 2 diabetes was 7.7%. After adjustment for diabetes risk factors and markers of seafood intake, participants with type 2 diabetes had a 26% higher level of total arsenic (95% confidence interval [CI], 2.0%-56.0%) and a nonsignificant 10% higher level of dimethylarsinate (95% CI, -8.0% to 33.0%) than participants without type 2 diabetes, and levels of arsenobetaine were similar to those of participants without type 2 diabetes. After similar adjustment, the odds ratios for type 2 diabetes comparing participants at the 80th vs the 20th percentiles were 3.58 for the level of total arsenic (95% CI, 1.18-10.83), 1.57 for dimethylarsinate (95% CI, 0.89-2.76), and 0.69 for arsenobetaine (95% CI, 0.33-1.48). After adjustment for biomarkers of seafood intake, total urine arsenic was associated with increased prevalence of type 2 diabetes. This finding supports the hypothesis that low levels of exposure to inorganic arsenic in drinking water, a widespread exposure worldwide, may play a role in diabetes prevalence. Prospective studies in populations exposed to a range of inorganic arsenic levels are needed to establish whether this association is causal.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Environ Health Perspect
                Journal ID (iso-abbrev): Environ. Health Perspect
                Journal ID (publisher-id): EHP
                Title: Environmental Health Perspectives
                Publisher: Environmental Health Perspectives
                ISSN (Print): 0091-6765
                ISSN (Electronic): 1552-9924
                Publication date (Electronic): 20 December 2017
                Publication date Collection: December 2017
                Volume: 125
                Issue: 12
                Electronic Location Identifier: 127004
                Affiliations
                [ 1 ]Department of Environmental Health and Engineering, Johns Hopkins Bloomberg School of Public Health , Baltimore, Maryland, USA
                [ 2 ]Department of Environmental Health Sciences, Columbia University Mailman School of Public Health , New York City, New York, USA
                [ 3 ]Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health , Baltimore, Maryland, USA
                [ 4 ]Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins Bloomberg School of Public Health , Baltimore, Maryland, USA
                [ 5 ]Kidney Institute and Division of Nephrology, Department of Internal Medicine, China Medical University Hospital , Taichung, Taiwan
                [ 6 ]Big Data Center, China Medical University Hospital , China Medical University , Taichung, Taiwan
                [ 7 ]School of Medicine, College of Medicine, China Medical University , Taichung, Taiwan
                [ 8 ]Department of Environmental Health, Rollins School of Public Health, Emory University , Atlanta, Georgia, USA
                [ 9 ]Division of General Internal Medicine, Department of Medicine, Johns Hopkins School of Medicine , Baltimore, Maryland, USA
                [ 10 ]Institute of Chemistry, University of Graz , Graz, Austria
                [ 11 ]Department of Medicine, Johns Hopkins School of Medicine , Baltimore, Maryland, USA
                [ 12 ]Georgetown-Howard Universities Center for Clinical and Translational Science , Washington, DC, USA
                [ 13 ]MedStar Health Research Institute , Hyattsville, Maryland, USA
                [ 14 ]Department of Epidemiology, Missouri Breaks Industries Research, Inc. , Eagle Butte, South Dakota, USA
                [ 15 ]Center for American Indian Health Research, College of Public Health, University of Oklahoma Health Sciences Center , Oklahoma City, Oklahoma, USA
                [ 16 ]Department of Genetics, Texas Biomedical Research Institute , San Antonio, Texas, USA
                Author notes
                Address correspondence to M. Grau-Perez, Columbia University Mailman School of Public Health, 722 W. 168th St., Room 1105, New York, NY 10032. Telephone: 212-342-4712. Email: mg3749@ 123456cumc.columbia.edu , or A. Navas-Acien, Columbia University Mailman School of Public Health, 722 W. 168th St., Room 1105, New York, NY 10032. Telephone: 212-342-4712. Email: an2737@ 123456cumc.columbia.edu
                Article
                Publisher ID: EHP2566
                DOI: 10.1289/EHP2566
                PMC ID: 5963590
                PubMed ID: 29373862
                SO-VID: f101076c-625d-49f3-b02a-46b77cbbfbcb
                License:

                EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted.

                History
                Date received : 23 July 2017
                Date revision received : 30 October 2017
                Date accepted : 07 November 2017
                Categories
                Subject: Research

                ScienceOpen disciplines: Public health
                Data availability:
                ScienceOpen disciplines: Public health

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