TY - JOUR
T1 - Ambient air pollution and pulmonary vascular volume on computed tomography
T2 - The MESA Air Pollution and Lung cohort studies
AU - Aaron, Carrie P.
AU - Hoffman, Eric A.
AU - Kawut, Steven M.
AU - Austin, John H.M.
AU - Budoff, Matthew
AU - Michos, Erin D.
AU - Stukovsky, Karen Hinckley
AU - Sack, Coralynn
AU - Szpiro, Adam A.
AU - Watson, Karol D.
AU - Kaufman, Joel D.
AU - Barr, R. Graham
N1 - Funding Information:
Acknowledgements: The authors thank the other investigators, staff and participants of the MESA (Multi-Ethnic Study of Atherosclerosis) study for their valuable contributions. A full list of participating MESA investigators and institutions can be found at www.mesa-nhlbi.org. The MESA study is conducted and supported by the US National Heart, Blood, and Lung Institute, National Institutes of Health and by the US Environmental Protection Agency (EPA) and MESA investigators. This publication was also developed under a STAR research assistance agreement, number RD831697 (MESA Air), awarded by the EPA. This publication has not been formally reviewed by the EPA. The views expressed in this document are solely those of the authors and the EPA does not endorse any products or commercial services mentioned in this publication.
Funding Information:
Conflict of interest: C.P. Aaron reports grants from NIH, during the conduct of the study; grants from Alpha1 Foundation and Stony Wold-Herbert Fund, outside the submitted work. E.A. Hoffman reports grants from NIH, during the conduct of the study; grants from NIH, outside the submitted work; and is a founder and shareholder of VIDA Diagnostics, from whom software was utilised for the data analysis. S.M. Kawut reports grants from NIH, during the conduct of the study; grants from NIH, Actelion, United Therapeutic, Gilead, Lung Biotech, Pfizer, Ikaria, Merck, Bayer, Pulmonary Hypertension Association and GeNO, travel reimbursement from American College of Chest Physicians and American Thoracic Society, and personal fees from European Respiratory Journal, outside the submitted work. J.H.M. Austin reports grants from NIH, during the conduct of the study; personal fees from PulmonX, outside the submitted work. M. Budoff reports grants from NIH, during the conduct of the study; grants from GE, outside the submitted work. E.D. Michos reports personal fees from Siemens Healthcare Diagnostics, outside the submitted work. K. Hinckley Stukovsky reports salary support from Cystic Fibrosis Foundation, outside the submitted work. C. Sack has nothing to disclose. A.A. Szpiro has nothing to disclose. K.D. Watson reports grants from NIH, during the conduct of the study. J.D. Kaufman reports grants from US EPA, during the conduct of the study. R.G. Barr reports grants from NIH, during the conduct of the study; grants from NIH, Alpha1 Foundation and COPD Foundation, outside the submitted work.
Publisher Copyright:
© ERS 2019.
PY - 2019/6/1
Y1 - 2019/6/1
N2 - Background: Air pollution alters small pulmonary vessels in animal models. We hypothesised that longterm 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 longterm exposures to ambient black carbon, nitrogen dioxide (NO2), oxides of nitrogen (NOx), particulate matter with a 50% cut-off aerodynamic diameter of <2.5 μm (PM2.5) 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 (TPVVCT). Peripheral TPVVCT 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 PM2.5. Mean±SD peripheral TPVVCT was 79.2±18.2 cm3 and TPVVCT was 129.3±35.1 cm3. Greater black carbon exposure was associated with a larger peripheral TPVVCT, 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 TPVVCT with NO2 were similar but nonsignificant after city adjustment, while those for PM2.5 were of similar magnitude but nonsignificant after full adjustment. There were no associations for NOx or ozone, or between any pollutant and TPVVCT. Conclusions: Long-term black carbon exposure was associated with a larger peripheral TPVVCT, suggesting diesel exhaust may contribute to remodelling of small pulmonary vessels in the general population.
AB - Background: Air pollution alters small pulmonary vessels in animal models. We hypothesised that longterm 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 longterm exposures to ambient black carbon, nitrogen dioxide (NO2), oxides of nitrogen (NOx), particulate matter with a 50% cut-off aerodynamic diameter of <2.5 μm (PM2.5) 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 (TPVVCT). Peripheral TPVVCT 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 PM2.5. Mean±SD peripheral TPVVCT was 79.2±18.2 cm3 and TPVVCT was 129.3±35.1 cm3. Greater black carbon exposure was associated with a larger peripheral TPVVCT, 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 TPVVCT with NO2 were similar but nonsignificant after city adjustment, while those for PM2.5 were of similar magnitude but nonsignificant after full adjustment. There were no associations for NOx or ozone, or between any pollutant and TPVVCT. Conclusions: Long-term black carbon exposure was associated with a larger peripheral TPVVCT, suggesting diesel exhaust may contribute to remodelling of small pulmonary vessels in the general population.
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U2 - 10.1183/13993003.02116-2018
DO - 10.1183/13993003.02116-2018
M3 - Article
C2 - 31167881
AN - SCOPUS:85067436026
VL - 53
JO - European Respiratory Journal, Supplement
JF - European Respiratory Journal, Supplement
SN - 0903-1936
IS - 6
M1 - 1802116
ER -