Weekly prenatal PM2.5 and NO2 exposures in preterm, early term, and full term infants: Decrements in birth weight and critical windows of susceptibility.

BACKGROUND: Previous studies have observed associations between birth weight and prenatal air pollution exposure, but there is not consensus on timing of critical windows of susceptibility. OBJECTIVE: We estimated the difference in birth weight among preterm, early term and full term births associated with weekly exposure to PM2.5 and NO2 throughout gestation. METHODS: We included all singleton live births in the Lower Peninsula of Michigan (United States) between 2007 and 2012 occurring at or after 32 weeks gestational age (n = 497,897). Weekly ambient PM2.5 and NO2 concentrations were estimated at maternal residences using 1-km gridded data from ensemble-based models. We utilized a distributed lag nonlinear model to estimate the difference in birth weight associated with weekly exposures from the last menstrual period (week 0) through 31 weeks gestation for preterm births; through 36 weeks gestation for early term births; and through 38 weeks gestation for full term births. RESULTS: In single-pollutant models, a 5 µg/m3 increase in PM2.5 exposure was associated with a reduction in birth weight among preterm births (-37.1 g [95% confidence interval [CI]: 60.8 g, -13.5 g]); early term births (-13.5 g [95% CI: 26.2 g, -0.67 g]); and full term births (-8.23 g [95% CI: 15.8 g, -0.68 g])]. In single-pollutant models, a 10 ppb increase in NO2 exposure was associated with a -11.7 g (95% CI: 14.46 g, -8.92 g) decrement in birth weight among full term births only. In models co-adjusted for PM2.5 and NO2, PM2.5 exposure was associated with reduced birth weight among preterm births (-36.9 g [95% CI: 61.9 g, -11.8 g]) and NO2 exposure was associated with reduced birth weight among full term births (-11.8 g [95% CI: 14.7 g, -8.94 g]). The largest decrements in birth weight were associated with PM2.5 exposure between approximately 10 and 26 weeks of pregnancy; for NO2 exposure, the largest decrements in birth weight in full term births were associated with exposure between weeks 6-18. CONCLUSION: We observed the largest and most persistent adverse associations between PM2.5 exposure and birth weight in preterm infants, and between NO2 exposure and birth weight in full term infants. Exposure during the first half of pregnancy had a greater impact on birthweight.

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

BACKGROUND: 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. METHODS: 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 (PM2.5) and nitrogen dioxide (NO2) 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. RESULTS: 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. CONCLUSIONS: 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.

Impacts of long-term ambient particulate matter and gaseous pollutants on circulating biomarkers of inflammation in male and female health professionals.

BACKGROUND: Systemic inflammation may serve as a biological mechanism linking air pollution to poor health but supporting evidence from studies of long-term pollutant exposure and inflammatory cytokines is inconsistent. OBJECTIVE: We studied associations between multiple particulate matter (PM) and gaseous air pollutants and pro- and anti-inflammatory cytokines within two nationwide cohorts of men and women. METHODS: Data were obtained from 16,151 women in the Nurses' Health Study and 7,930 men in the Health Professionals' Follow-up Study with at least one measure of circulating adiponectin, C-Reactive Protein (CRP), Interleukin-6 (IL-6) or soluble tumor necrosis-factor receptor-2 (sTNFR-2). Exposure to PM with aerodynamic diameter ≤2.5, 2.5-10, and ≤10 µm (PM2.5, PM2.5-10, PM10) and nitrogen dioxide (NO2) was estimated using spatio-temporal models and were linked to participants' addresses at the time of blood draw. Averages of the 1-, 3-, and 12-months prior to blood draw were examined. Associations between each biomarker and pollutant were estimated from linear regression models adjusted for individual and contextual covariates. RESULTS: In adjusted models, we observed a 2.72% (95% CI: 0.43%, 5.95%), 3.11% (-0.12%, 6.45%), and 3.67% (0.19%, 7.26%) increase in CRP associated with a 10 µg/m3 increase in 1-, 3-, and 12- month averaged NO2 in women. Among men, there was a statistically significant 5.96% (95% CI: 0.07%, 12.20%), 6.99% (95% CI: 0.29%, 14.15%), and 8.33% (95% CI: 0.35%, 16.94%) increase in CRP associated with a 10 µg/m3 increase in 1-, 3-, and 12-month averaged PM2.5-10, respectively. Increasing PM2.5-10 was associated with increasing IL-6 and sTNFR-2 among men over shorter exposure durations. There were no associations with exposures to PM2.5 or PM10, or with adiponectin. Findings were robust to sensitivity analyses restricting to disease-free controls and non-movers. CONCLUSIONS: Across multiple long-term pollutant exposures and inflammatory markers, associations were generally weak. Focusing on specific pollutant-inflammatory mechanisms may clarify pathways.