Associations between air pollution, residential greenness, and glycated hemoglobin (HbA1c) in the three prospective cohorts of U.S. adults

Abstract

Background and Aim: While studies suggest impacts of individual environmental exposures on type 2 diabetes (T2D) risk, the biological mechanisms remain poorly characterized. Glycated hemoglobin (HbA1c) is an important biomarker for diagnosing prediabetes and predicting T2D risk. We explored associations between multiple environmental exposures and HbA1c. Methods: HbA1c was assessed in 12,698 non-diabetic women and men in three U.S.-based prospective cohorts: the Nurses’ Health Study (NHS) in 1990, the Nurses’ Health Study II (NHSII) in 1998, and the Health Professionals Follow-up Study (HPFS) in 1993. Residential greenness data within 270m and 1,230m (normalized difference vegetation index, NDVI) was obtained from Landsat. Fine particulate matter (PM₂.₅) and nitrogen dioxide (NO₂) were estimated from nationwide spatiotemporal models. Three-month and one-year average exposures prior to blood draw were assigned to participants’ addresses. We used single and multi-exposure linear regression models, as well as mixture methods such as models with component scores from Principal Components Analysis (PCA), to assess associations with HbA1c. We first applied basic models adjusted for age and year at blood draw, BMI, alcohol use, and neighborhood socioeconomic status (nSES). In fully-adjusted models, we included overall diet quality, race, family history, smoking status, postmenopausal hormone use, population density, and season. We assessed potential modification via stratification. Results: Based on HbA1c thresholds, 19% of participants had prediabetes. In basic models, we observed a small negative association between PM₂.₅ and HbA1c: an IQR increase was associated with a 0.28% (95% CI: 0.54%, 0.02%) lower HbA1c. In fully-adjusted models, we did not find any associations between the individual exposures or the component scores and HbA1c. There was no evidence of differing associations by sex, nSES, or population density. Conclusions: In this study of adults, environmental exposures were not associated with HbA1c. More work is needed to elucidate biological pathways between the environment and prediabetes.