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 (NO₂), oxides of nitrogen (NO _x ), particulate matter with a 50% cut-off aerodynamic diameter of <2.5 μm (PM_2.5) 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_CT). Peripheral TPVV_CT was 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.

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·m^-3 black carbon, 14.6 ppb NO₂ and 11.0 μg·m^-3 ambient PM_2.5. Mean±sd peripheral TPVV_CT was 79.2±18.2 cm³ and TPVV_CT was 129.3±35.1 cm³. Greater black carbon exposure was associated with a larger peripheral TPVV_CT, including after adjustment for city (mean difference 0.41 (95% CI 0.03-0.79) cm³ per interquartile range; p=0.036). Associations for peripheral TPVV_CT with NO₂ were similar but nonsignificant after city adjustment, while those for PM_2.5 were of similar magnitude but nonsignificant after full adjustment. There were no associations for NO _x or ozone, or between any pollutant and TPVV_CT.

Conclusions

Long-term black carbon exposure was associated with a larger peripheral TPVV_CT, suggesting diesel exhaust may contribute to remodelling of small pulmonary vessels in the general population.