Ambient air pollution in Massachusetts: inequality trends, residential infiltration, and childhood weight growth trajectories
Rosofsky, Anna Stillman
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Exposure to pollutants of ambient origin contributes significantly to the global disease burden (Cohen et al., 2017). Mounting evidence has demonstrated disproportionately high ambient PM2.5 and NO2 concentrations in the U.S. among nonwhite and low-income populations, potentially contributing to environmental health disparities (Bell and Ebisu, 2012; Clark et al., 2014; Morello-Frosch and Lopez, 2006). There is limited understanding of temporal trends and underlying causes of exposure inequalities (EIs), and whether residential building characteristics modify observed EIs. Further, while ambient pollutants have been linked to cardiometabolic disease in adulthood, few studies have documented the link between early-life ambient air pollution exposure and weight growth trajectories in early childhood- an informative step on the causal pathway between early life exposures and chronic outcomes. Using 1 km2 PM2.5 and NO2 predictions in Massachusetts and Census data, we quantify longitudinal EI between sociodemographic groups over a decade. We estimate AER for all Massachusetts residential parcels using publicly available data and assess whether accounting for AER exacerbates or ameliorates PM2.5 inequalities. We examine associations of weight growth trajectories in early childhood with residential prenatal and postnatal PM2.5 and distance to road (traffic) exposure in the Boston-based Children’s HealthWatch cohort. PM2.5 and NO2 inequalities increased across the study period in urban areas, and EIs were more pronounced for NO2 than PM2.5 and among racial/ethnic groups compared to other population subgroups. Analyzing EI longitudinally revealed that spatio-temporal shifts in air pollution, and not demographic distributions, contributed to exposure disparities. We found substantial variability in estimated AER across the state, and that PM2.5 EIs were magnified when AER was considered. Prenatal PM2.5 >9.5 µg/m3 predicted higher weight growth rates among females, but with an opposite direction of effect in males. This association was modified by birth weight and AER, with a stronger magnitude of effect in low-birthweight and higher-AER females. These findings underscore the importance of considering vulnerable communities and residential characteristics in ambient air pollution reduction strategies. This dissertation provides an opportunity to understand susceptible phenotypes and periods of potential intervention to reduce ambient air pollution impacts on cardiometabolic outcomes.