title: Proposed pathophysiologic framework to explain some excess cardiovascular death associated with ambient air particle pollution: Insights for public health translation.
abstract: The paper proposes a pathophysiologic framework to explain the well-established epidemiological association between exposure to ambient air particle pollution and premature cardiovascular mortality, and offers insights into public health solutions that extend beyond regulatory environmental protections to actions that can be taken by individuals, public health officials, healthcare professionals, city and regional planners, local and state governmental officials and all those who possess the capacity to improve cardiovascular health within the population. The foundation of the framework rests on the contribution of traditional cardiovascular risk factors acting alone and in concert with long-term exposures to air pollutants to create a conditional susceptibility for clinical vascular events, such as myocardial ischemia and infarction; stroke and lethal ventricular arrhythmias. The conceptual framework focuses on the fact that short-term exposures to ambient air particulate matter (PM) are associated with vascular thrombosis (acute coronary syndrome, stroke, deep venous thrombosis, and pulmonary embolism) and electrical dysfunction (ventricular arrhythmia); and that individuals having prevalent heart disease are at greatest risk. Moreover, exposure is concomitant with changes in autonomic nervous system balance, systemic inflammation, and prothrombotic/anti-thrombotic and profibrinolytic-antifibrinolytic balance. Thus, a comprehensive solution to the problem of premature mortality triggered by air pollutant exposure will require compliance with regulations to control ambient air particle pollution levels, minimize exposures to air pollutants, as well as a concerted effort to decrease the number of people at-risk for serious clinical cardiovascular events triggered by air pollutant exposure by improving the overall state of cardiovascular health in the population. This article is part of a Special Issue entitled Air Pollution, edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu.
authors.affiliation: Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Chapel Hill, NC, USA. Electronic address: cascio.wayne@epa.gov.
authors.forename: Wayne E
authors.initials: WE
authors.lastname: Cascio
mesh_terms: D000397:Air Pollution / Q000009:adverse effects*; D001145:Arrhythmias, Cardiac / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D016757:Death, Sudden, Cardiac / Q000209:etiology* / Q000473:pathology; D004198:Disease Susceptibility; D005487:Foam Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007249:Inflammation; D008077:Lipoproteins, LDL / Q000819:agonists / Q000096:biosynthesis; D017202:Myocardial Ischemia / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress; D052638:Particulate Matter / Q000633:toxicity*; D011634:Public Health; D017382:Reactive Oxygen Species / Q000819:agonists / Q000378:metabolism; D012307:Risk Factors; D013927:Thrombosis / Q000209:etiology* / Q000378:metabolism / Q000473:pathology
chemical_list: D008077:Lipoproteins, LDL; D052638:Particulate Matter; D017382:Reactive Oxygen Species; C099252:oxidized low density lipoprotein
keywords: Air pollution; Cardiovascular mortality; Particulate matter; Pathophysiological mechanisms; Sudden death; Susceptible populations