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  • 标题:Ambient Coarse Particulate Matter and the Right Ventricle: The Multi-Ethnic Study of Atherosclerosis
  • 本地全文:下载
  • 作者:Jennifer C. D’Souza ; Steven M. Kawut ; Laura R. Elkayam
  • 期刊名称:Environmental Health Perspectives
  • 印刷版ISSN:0091-6765
  • 电子版ISSN:1552-9924
  • 出版年度:2017
  • 卷号:125
  • 期号:7
  • 页码:077019
  • DOI:10.1289/EHP658
  • 语种:English
  • 出版社:OCR Subscription Services Inc
  • 摘要: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. https://doi.org/10.1289/EHP658
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