BACKGROUND: Coarse particulate matter (PM10–2.5) is primarily mechanically generated and includes crustal material, brake and tire wear, and biological particles. PM10–2.5 is associated with pulmonary disease, which can lead to right ventricular (RV) dysfunction. Although RV characteristics have been associated with combustion-related pollutants, relationships with PM10–2.5 remain unknown. OBJECTIVES: To quantify cross-sectional associations between RV dysfunction and PM10–2.5 mass and components among older adults and susceptible populations. METHODS: We used baseline cardiac magnetic resonance images from 1,490 participants (45–84 y old) from the Multi-Ethnic Study of Atherosclerosis and assigned 5-y residential concentrations of PM10–2.5 mass, copper, zinc, phosphorus, silicon, and endotoxin, using land-use regression models. We quantified associations with RV mass, end-diastolic volume, and ejection fraction after control for risk factors and copollutants using linear regression. We further examined personal susceptibility. RESULTS: We found positive associations of RV mass and, to a lesser extent, end diastolic volume with PM10–2.5 mass among susceptible populations including smokers and persons with emphysema. After adjustment for copollutants, an interquartile range increase in PM10–2.5 mass (2:2 μg/m3) was associated with 0:5 g (95% CI: 0.0, 1.0), 0:9 g (95% CI: 0.1, 1.7), and 1:4 g (95% CI: 0.4, 2.5) larger RV mass among former smokers, current smokers, and persons with emphysema, respectively. No associations were found with healthy individuals or with ejection fraction. CONCLUSIONS: Alterations to RV structure may represent a mechanism by which long-term PM10–2.5 exposure increases risks for adverse respiratory and cardiovascular outcomes, especially among certain susceptible populations.
Bibliographical noteFunding Information:
This work was supported by supported by grants RD 833741010 and RD 83169701 from the U.S. Environmental Protection Agency (EPA) and the National Institutes of Health (NIH) (R01 HL086719). MESA was further supported by contracts HHSN268201500003I, N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168 and N01-HC-95169 from the National Heart, Lung, and Blood Institute and by grants UL1-TR-000040 and UL1-RR-025005 from NCRR. MESA RV was funded by NIH R01-HL086719. MESA Lung was supported by NIH-R01-HL077612 and RC1 HL100543. MESA Neighborhood was supported by 2R01 HL071759. One author (P.S.T.) was supported by NIH P30 ES005605 and another (J.D.K.) by P30 ES07033 and K24 ES013195. Although funded by the U.S. EPA, this publication has not been formally reviewed by the U.S. EPA, and the views expressed in this document are solely the views of the authors. The U.S. EPA also does not endorse any products or commercial services mentioned in this publication.
S.M.K. receives nonfinancial support from the American College of Clinical Pharmacology and the American Thoracic Society; personal fees from the European Respiratory Journal; and grants from Actelion, Gilead, GeNO, and Bayer that are unrelated to the submitted work.
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