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Accelerated Longitudinal Glycemic Changes in Relation to Urinary Toxic/Essential Metals and Metal Mixtures among Mexican Americans Living in Starr County, Texas

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posted on 2024-09-15, 00:10 authored by Margaret C. Weiss, Jiehuan Sun, Brian P. Jackson, Mary E. Turyk, Luyu Wang, Eric L. Brown, David Aguilar, Sharon A. Brown, Craig L. Hanis, Maria Argos, Robert M. Sargis

Objective: Metal and metalloid exposures (hereafter “metals”) are associated with adverse health outcomes, including type 2 diabetes mellitus (T2DM); however, previous studies were largely cross-sectional or under-powered. Furthermore, underserved racial/ethnic groups are underrepresented in environmental health research despite having higher rates of T2DM and greater risk of metal exposures. Consequently, we evaluated continuous glycemic traits in relation to baseline urinary toxic metal, essential metal, and metal mixtures in a cohort of Mexican American adults.

Research Design and Methods: 510 subjects were selected based upon self-reported diabetes status and followed over 3 years. Urinary metals were assessed at baseline. Linear mixed effects models were used to estimate per month changes in hemoglobin A1c, fasting plasma glucose, and post-load glucose in relation to urinary metal levels. Multiple statistical approaches were used to assess the associations between glycemic traits and metal mixtures.

Results: After adjustment, higher urinary levels of arsenic, selenium, copper, molybdenum, nickel, and tin were associated with faster increases in measures of glycemia. The toxic metal mixture composed of arsenic, lead, cadmium, nickel, and tin was associated with faster increases in post-load glucose. Using post-load glucose criteria, highest versus lowest arsenic was predicted to accelerate conversion of normoglycemia to prediabetes and diabetes by 23 and 65 months, respectively.

Conclusions: In this underrepresented, high-risk Mexican American population, exposure to toxic metals and alterations in essential metal homeostasis were associated with faster increases in glycemia over time that may accelerate T2DM development.

Funding

This work was supported by the National Institutes of Health (R01 ES028879 and R21 ES030884 supporting RMS; P30 ES027792 supporting MA, MT, and RMS; UL1 TR002003 supporting MA and RMS via the UIC Center for Clinical and Translational Science; F30 ES033510 supporting MW; the University of Illinois at Chicago’s Medical-Scientist Training Program (T32 GM079086) supporting MS and LW; P30 CA023108 supporting BPJ via the Dartmouth Cancer Center NCI Cancer Center Support Grant; R01 DK109920 supporting SAB; and R01 HL102830, R01 DK116378, and R01 DK118631 supporting ELB, DA, SAB, and CLH). RMS is also supported by the Department of Veterans Affairs (I01 BX006108) and the Department of Defense Toxic Exposures Research Program (TX220140).

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