Key Points
Air pollution exposure is common, and may increase risk of developing blood clots.
Greater long-term exposure to air pollution (i.e., PM2.5, NOxNO2) was associated with higher risk of developing venous thromboembolism.
Air pollution exposure may induce procoagulant effects, and chronic exposure may be linked to greater risk of venous thromboembolism (VTE). We tested the hypothesis that air pollution is associated with increased VTE risk in the prospective Multi-Ethnic Study of Atherosclerosis (MESA), which has well-characterized air pollution measures and information on potential confounding factors. We included 6,651 participants recruited in 2000-2002 (baseline age range: 45-84 yrs; 53% female). Air pollution was assessed with a validated spatio-temporal model that incorporates cohort-specific monitoring. Four indices of air pollution updated each fortnight over follow-up were averaged to estimate participant-level chronic exposure: fine particulate matter ≤2.5 micrometers in aerodynamic diameter (PM2.5), oxides of nitrogen (NOx), nitrogen dioxide (NO2), and ozone (O3). Mean±SD PM2.5 was 13.5±3.0 µg/m3, NO2 17.9±8.2 ppb, NOx 36.1±19.6 ppb, and O3 22.2±3.7 ppb. Incident VTE was identified using hospitalization discharge codes through 2018. A total of 248 VTE events accrued over a median follow-up of 16.7 years. After adjustment for baseline demographics, health behaviors and body mass index, the hazard ratio (95% CI) for incident VTE associated per 3.6 µg/m3 higher PM2.5 was 1.39 (1.04-1.86); per 13.3 ppb higher NO2 concentration was 2.74 (1.57-4.77); and per 30 ppb higher NOx was 2.21 (1.42-3.44). O3 was not related. In this prospective community-based cohort with individual-level estimation of chronic air pollution exposure, higher average ambient concentrations of PM2.5, NO2 and NOX were associated with greater risk of developing VTE. Findings add to accumulating evidence of adverse health effects attributed to air pollution exposure.
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