Abstract
Background: Long-term exposure to ambient air pollution, including fine particulate matter (PM2.5), has been associated with cardiovascular morbidity and mortality. Impaired vascular responses may in part explain these findings, but few studies have examined chronic effects of long-term exposures incorporating measures of both conduit artery and microvascular function in a large population-based study. Aims: We evaluated the impact of residential proximity to primary or secondary highway (<100m, 100-200m, 200-400m, >400m) and long term exposure to PM2.5 (1-year average) on brachial artery flow mediated dilation (FMD) and reactive hyperemia in the Framingham Offspring and Third Generation Cohorts. Methods: FMD (%) and hyperemic flow velocity (cm/s) were assessed in the Offspring 7th (1998-2001) and Third Generation 1st (2001-2005) exams (n=5,133). We evaluated associations between residential proximity to major roads and spatially resolved estimated PM2.5 from land use and satellite images with FMD and hyperemic flow using linear regression. Results: Compared to living further than 400m from a major road, living within 100m was associated with -0.31% (95% CI: -0.53, -0.09) lower FMD and -1.49 cm/s (95% CI: -2.9,- 0.09) lower hyperemic flow velocity in models adjusted for age, sex, body mass index, smoking status, long-term time trends, season, cohort, and indicators of socioeconomic position. A 1 µg/m3 higher average PM2.5 was associated with -0.09% (95% CI: -0.24, 0.06) lower FMD, and -1.07 cm/s (95% CI: -2.0, -0.12) lower hyperemic flow. Results were not materially altered after further adjustment for potential mediators. The magnitude of estimates for hyperemic flow became stronger when we excluded smokers and participants using antihypertensive or lipid-lowering medications. Conclusions: In a large, community-based cohort, measures of long-term exposure to air pollution were associated with impaired conduit and microvascular function.
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