Association between whole blood mercury and glucose intolerance among adult Inuit in Greenland.

Environ Res

Center for Health Research in Greenland, National Institute of Public Health, University of Southern Denmark, Øster Farimagsgade 5A, 2. Fl., 1353 Copenhagen C, Denmark; Steno Diabetes Center A/S, Niels Steensens Vej 2-4, DK-2820 Gentofte, Denmark.

Published: November 2015

Objectives: The Arctic diet is partly constituted by traditional food characterized by top predator animals such as whales, walrus, and seals with high mercury content. Mercury exposure has been associated with glucose intolerance in Western populations. We studied the association between whole blood mercury and glucose intolerance in a highly exposed non-Western population

Methods: Cross-sectional study of 2640 Inuit (18+ years) with information on ancestry, smoking, waist circumference, total energy intake, and physical activity. Mercury, fasting- and 2-h plasma glucose, insulin, and c-peptide were measured in blood. Fasting participants without diabetes were classified into normal glucose tolerance, impaired glucose tolerance, impaired fasting glycemia, or type 2 diabetes. We calculated hepatic insulin resistance with homoeostatic model assessment - insulin resistance index, peripheral insulin sensitivity by ISI0,120., and relative beta cell function by c-peptide/insulin ratio. We conducted adjusted linear- and logistic regression analyses.

Results: For an increase in whole blood mercury of 5 µg/L we found a positive association with fasting glucose [% change=0.25 (95% CI: 0.20; 0.30); p<0.001], and 2-h glucose [% change=0.23 (95% CI: 0.05; 0.40); p=0.01]. Mercury was weakly associated with impaired fasting glycemia [OR=1.03 (95% CI: 1.02; 1.05)], and type 2 diabetes [OR=1.02 (95% CI: 1.01; 1.04)].

Conclusion: While the study found a weak but statistically significant association between whole blood mercury and both impaired fasting glycemia and type 2 diabetes, no associations were found with measures of underlying disturbances in glucose homoeostasis.

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Source
http://dx.doi.org/10.1016/j.envres.2015.10.013DOI Listing

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