While studies suggest impacts of individual environmental exposures on type 2 diabetes (T2D) risk, mechanisms remain poorly characterized. Glycated hemoglobin (HbA1c) is a biomarker of glycemia and diagnostic criterion for prediabetes and T2D. We explored associations between multiple environmental exposures and HbA1c in non-diabetic adults.
HbA1c was assessed once in 12,315 women and men in three U.S.-based prospective cohorts: the Nurses' Health Study (NHS), Nurses' Health Study II (NHSII), and Health Professionals Follow-up Study (HPFS). Residential greenness within 270 m and 1,230 m (normalized difference vegetation index, NDVI) was obtained from Landsat. Fine particulate matter (PM) and nitrogen dioxide (NO) were estimated from nationwide spatiotemporal models. Three-month and one-year averages prior to blood draw were assigned to participants' addresses. We assessed associations between single exposure, multi-exposure, and component scores from Principal Components Analysis (PCA) and HbA1c. Fully-adjusted models built on basic models of age and year at blood draw, BMI, alcohol use, and neighborhood socioeconomic status (nSES) to include diet quality, race, family history, smoking status, postmenopausal hormone use, population density, and season. We assessed interactions between environmental exposures, and effect modification by population density, nSES, and sex.
Based on HbA1c, 19% of participants had prediabetes. In single exposure fully-adjusted models, an IQR (0.14) higher 1-year 1,230 m NDVI was associated with a 0.27% (95% CI: 0.05%, 0.49%) lower HbA1c. In basic component score models, a SD increase in Component 1 (high loadings for 1-year NDVI) was associated with a 0.19% (95% CI: 0.04%, 0.34%) lower HbA1c. CI's crossed the null in multi-exposure and fully-adjusted component score models. There was little evidence of associations between air pollution and HbA1c, and no evidence of effect modification.
Among non-diabetic adults, environmental exposures were not consistently associated with HbA1c. More work is needed to elucidate biological pathways between the environment and prediabetes.