Relationships of cotinine and self-reported cigarette smoking with hemoglobin A1c in the U.S.: results from the National Health and Nutrition Examination Survey, 1999-2008.

Abstract

Whether nicotine leads to a persistent increase in blood glucose levels is not clear. Our objective was to assess the relationship between cotinine, a nicotine metabolite, and glycated hemoglobin (HbA(1c)), an index of recent glycemia. We used cross-sectional data from the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2008. We limited our analysis to 17,287 adults without diabetes. We created three cotinine categories: <0.05 ng/mL, 0.05-2.99 ng/mL, and ≥3 ng/mL. Using self-report, 25% of the sample were current smokers, 24% were former smokers, and 51% were nonsmokers. Smokers had a higher mean HbA(1c) (5.36% ± 0.01 SE) compared with never smokers (5.31% ± 0.01) and former smokers (5.31% ± 0.01). In a similar manner, mean HbA(1c) was higher among participants with cotinine ≥3 ng/mL (5.35% ± 0.01) and participants with cotinine 0.05-2.99 ng/mL (5.34% ± 0.01) compared with participants with cotinine <0.05 ng/mL (5.29% ± 0.01). In multivariable-adjusted analysis, we found that both a cotinine ≥3 ng/mL and self-reported smoking were associated with higher HbA(1c) compared with a cotinine <0.05 ng/mL or not smoking. People with a cotinine level ≥3 ng/mL had a relative 5% increase in HbA(1c) compared with people with a cotinine level <0.05 ng/mL, and smokers had a relative 7% increase in HbA(1c) compared with never smokers. Our study suggests that cotinine is associated with increased HbA(1c) in a representative sample of the U.S. population without diabetes.