title: Fine particulate matter air pollution and atherosclerosis: Mechanistic insights.
abstract: Atherosclerosis is a progressive disease characterized by the accumulation of lipids and fibrous plaque in the arteries. Its etiology is very complicated and its risk factors primarily include genetic defects, smoking, hyperlipidemia, hypertension, lack of exercise, and infection. Recent studies suggest that fine particulate matter (PM2.5) air pollution may also contribute to the development of atherosclerosis.
  
  
  
  The present review integrates current experimental evidence with mechanistic pathways whereby PM2.5 exposure can promote the development of atherosclerosis.
  
  
  
  PM2.5-mediated enhancement of atherosclerosis is likely due to its pro-oxidant and pro-inflammatory effects, involving multiple organs, different cell types, and various molecular mediators.
  
  
  
  Studies about the effects of PM2.5inhalation on atherosclerosis may yield a better understanding of the link between air pollution and major cardiovascular diseases, and provide useful information for policy makers to determine acceptable levels of PM2.5 air quality. This article is part of a Special Issue entitled Air Pollution, edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu.
authors.affiliation: Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, United States; Division of Environmental Health Sciences, College of Public Health, The Ohio State University, United States.
authors.forename: Yuntao
authors.initials: Y
authors.lastname: Bai
authors.affiliation: Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, United States; Division of Environmental Health Sciences, College of Public Health, The Ohio State University, United States; State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China. Electronic address: sun.224@osu.edu.
authors.forename: Qinghua
authors.initials: Q
authors.lastname: Sun
mesh_terms: D000397:Air Pollution / Q000009:adverse effects*; D050197:Atherosclerosis / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D005487:Foam Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D006801:Humans; D006949:Hyperlipidemias / Q000503:physiopathology; D006973:Hypertension / Q000503:physiopathology; D019570:Inhalation Exposure / Q000009:adverse effects*; D008077:Lipoproteins, LDL / Q000819:agonists / Q000096:biosynthesis; D018384:Oxidative Stress; D010316:Particle Size; D052638:Particulate Matter / Q000633:toxicity*; D058226:Plaque, Atherosclerotic / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D017382:Reactive Oxygen Species / Q000819:agonists* / Q000378:metabolism; D012307:Risk Factors; D057185:Sedentary Behavior; D012907:Smoking / Q000503:physiopathology
chemical_list: D008077:Lipoproteins, LDL; D052638:Particulate Matter; D017382:Reactive Oxygen Species; C099252:oxidized low density lipoprotein
keywords: Air pollution; Atherosclerosis; Fine particulate matter; Inflammation; Oxidative stress