Ambient air pollution and pulmonary vascular volume on computed tomography: the MESA Air Pollution and Lung cohort studies

Abstract

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.

FIGURE 1

Map of estimated black carbon exposure derived from spatial averages over 2006–2008 in Chicago, IL. LAC: light absorption coefficient (0.5 per 100000 m LAC is approximately equivalent to 0.5 μg·m⁻³ black carbon).

FIGURE 2

Generalised additive model showing the estimated mean difference in peripheral total pulmonary vascular volume assessed on noncontrast computed tomography (TPVVct) over the range of black carbon exposure. Model adjusts for age, sex, race/ethnicity, height, weight, education, neighbourhood socioeconomic status index, smoking status, pack-years, second-hand smoke exposure, estimated glomerular filtration rate, scanner manufacturer and city. The dotted lines indicate 95% CI. Each spectral line indicates one observation, showing the distribution of black carbon measurements.

FIGURE 3

Sensitivity analyses showing estimated mean difference in peripheral total pulmonary vascular volume assessed on noncontrast computed tomography (TPVVct) for an interquartile range increase in black carbon exposure. Results are adjusted for age, sex, race/ethnicity, height, weight, education, neighbourhood socioeconomic status index, smoking status, pack-years, second-hand smoke exposure, estimated glomerular filtration rate, scanner manufacturer and city. p-values for interactions: sex 0.46, race/ethnicity 0.85, age 0.19, smoking status 0.84, airflow limitation 0.74 and scanner manufacturer 0.99. The size of the blue squares indicates the relative precision of the estimate, with larger squares reflecting more precision; 95% CIs are indicated. PM2.5: particulate matter with a 50% cut-off aerodynamic diameter of <2.5 μm; NO₂: nitrogen dioxide; FEV1 : forced expiratory volume in 1 s. ^#: airflow limitation indicates pre-bronchodilator FEV1/forced vital capacity <0.7; ^¶: cardiovascular risk factors included total cholesterol, triglycerides, hypertension, systolic blood pressure, diabetes and glucose intolerance.