Abstract 14900: Association of Endothelial Microparticles and Mediators of Systemic Inflammation With Exposure to Fine Particulate Matter Air Pollution
Introduction: A growing body of evidence indicates that exposure to fine particulate matter air pollution (PM2.5) contributes to the risk of cardiovascular morbidity and mortality, but the mechanisms by which PM2.5 exposure induces cardiovascular injury remain unclear.
Hypothesis: We hypothesize that that acute exposure to elevated PM2.5 levels is associated with increased endothelial injury and systemic inflammation.
Methods: Blood was collected five or six times each from three groups of 24 healthy, non-smoking young adults recruited over three winter/spring study periods (January – March 2013, January – March 2014, and December 2014 – April 2015) in the Provo, Utah area. Using cell- and tissue-specific surface markers, levels of circulating microparticles were measured by flow cytometry. Bio-markers of systemic inflammation were measured in the same samples by multiplexing laser bead technology.
Results: Elevated levels of PM2.5 were associated with increased levels of endothelial microparticles (annexin V+/CD41-/CD31+) including subgroups expressing arterial (Ephrin B2), venous (EphB4), and lung (CD143) specific markers, but not with microparticles derived from the activated endothelium (CD62+). PM2.5 exposures were also associated with elevated markers of systemic inflammation and the soluble intercellular adhesion molecules ICAM-1 and VCAM-1.
Conclusions: Episodic PM2.5 exposures are associated with biomarkers of endothelial injury and systemic inflammation in young healthy adults. PM2.5 exposures likely induce endothelial cell apoptosis, endothelial dysfunction, and systemic inflammation contributing to pathogenic sequelae of atherosclerotic lesion formation and acute coronary events.
Author Disclosures: T. O’Toole: None. W. Abplanalp: None. D.J. Conklin: None. A. Bhatnagar: None. C.A. Pope: None.
- © 2016 by American Heart Association, Inc.