BACKGROUND: Air pollution alters small pulmonary vessels in animal models. We hypothesised that long-term ambient air pollution exposure would be associated with differences in pulmonary vascular volumes in a population-based study.
METHODS: The Multi-Ethnic Study of Atherosclerosis recruited adults in six US cities. Personalised long-term exposures to ambient black carbon, nitrogen dioxide (NO), oxides of nitrogen (NO), particulate matter with a 50% cut-off aerodynamic diameter of <2.5 μm (PM) and ozone were estimated using spatiotemporal models. In 2010-2012, total pulmonary vascular volume was measured as the volume of detectable pulmonary arteries and veins, including vessel walls and luminal blood volume, on noncontrast chest computed tomography (TPVV). Peripheral TPVVwas limited to the peripheral 2 cm to isolate smaller vessels. Linear regression adjusted for demographics, anthropometrics, smoking, second-hand smoke, renal function and scanner manufacturer. 2 2.5CT CT x
RESULTS: The mean±sd age of the 3023 participants was 69.3±9.3 years; 46% were never-smokers. Mean exposures were 0.80 μg·mblack carbon, 14.6 ppb NOand 11.0 μg·mambient PM. Mean±sd peripheral TPVVwas 79.2±18.2 cmand TPVVwas 129.3±35.1 cm. Greater black carbon exposure was associated with a larger peripheral TPVV, including after adjustment for city (mean difference 0.41 (95% CI 0.03-0.79) cmper interquartile range; p=0.036). Associations for peripheral TPVVwith NOwere similar but nonsignificant after city adjustment, while those for PMwere of similar magnitude but nonsignificant after full adjustment. There were no associations for NOor ozone, or between any pollutant and TPVV. -3 -3 3 3 3 2 2.5CT CT CT CT2 2.5CT x
CONCLUSIONS: Long-term black carbon exposure was associated with a larger peripheral TPVV, suggesting diesel exhaust may contribute to remodelling of small pulmonary vessels in the general population. CT
