title: Exposure to Fine Particulate Air Pollution Is Associated With Endothelial Injury and Systemic Inflammation.
abstract: BACKGROUND
  Epidemiological evidence indicates that exposures to fine particulate matter air pollution (PM2.5) contribute to global burden of disease, primarily as a result of increased risk of cardiovascular morbidity and mortality. However, mechanisms by which PM2.5exposure induces cardiovascular injury remain unclear. PM2.5-induced endothelial dysfunction and systemic inflammation have been implicated, but direct evidence is lacking.
  
  
  OBJECTIVE
  To examine whether acute exposure to PM2.5is associated with endothelial injury and systemic inflammation.
  
  
  RESULTS
  Blood was collected from healthy, nonsmoking, young adults during 3 study periods that included episodes of elevated PM2.5levels. Microparticles and immune cells in blood were measured by flow cytometry, and plasma cytokine/growth factors were measured using multiplexing laser beads. PM2.5exposure was associated with the elevated levels of endothelial microparticles (annexin V+/CD41-/CD31+), including subtypes expressing arterial-, venous-, and lung-specific markers, but not microparticles expressing CD62+. These changes were accompanied by suppressed circulating levels of proangiogenic growth factors (EGF [epidermal growth factor], sCD40L [soluble CD40 ligand], PDGF [platelet-derived growth factor], RANTES [regulated on activation, normal T-cell-expressed and secreted], GROα [growth-regulated protein α], and VEGF [vascular endothelial growth factor]), and an increase in the levels of antiangiogenic (TNFα [tumor necrosis factor α], IP-10 [interferon γ-induced protein 10]), and proinflammatory cytokines (MCP-1 [monocyte chemoattractant protein 1], MIP-1α/β [macrophage inflammatory protein 1α/β], IL-6 [interleukin 6], and IL-1β [interleukin 1β]), and markers of endothelial adhesion (sICAM-1 [soluble intercellular adhesion molecule 1] and sVCAM-1 [soluble vascular cellular adhesion molecule 1]). PM2.5exposure was also associated with an inflammatory response characterized by elevated levels of circulating CD14+, CD16+, CD4+, and CD8+, but not CD19+cells.
  
  
  CONCLUSIONS
  Episodic PM2.5exposures are associated with increased endothelial cell apoptosis, an antiangiogenic plasma profile, and elevated levels of circulating monocytes and T, but not B, lymphocytes. These changes could contribute to the pathogenic sequelae of atherogenesis and acute coronary events.
authors: From the Department of Economics, Brigham Young University, Provo, UT (C.A.P.); and Diabetes and Obesity Center, Division of Cardiovascular Medicine, Department of Medicine, University of Louisville, KY (A.B., J.P.M., W.A., D.J.C., T.O.). cap3@byu.edu.
authors: C Arden
authors: CA
authors: Pope
authors: From the Department of Economics, Brigham Young University, Provo, UT (C.A.P.); and Diabetes and Obesity Center, Division of Cardiovascular Medicine, Department of Medicine, University of Louisville, KY (A.B., J.P.M., W.A., D.J.C., T.O.).
authors: Aruni
authors: A
authors: Bhatnagar
authors: From the Department of Economics, Brigham Young University, Provo, UT (C.A.P.); and Diabetes and Obesity Center, Division of Cardiovascular Medicine, Department of Medicine, University of Louisville, KY (A.B., J.P.M., W.A., D.J.C., T.O.).
authors: James P
authors: JP
authors: McCracken
authors: From the Department of Economics, Brigham Young University, Provo, UT (C.A.P.); and Diabetes and Obesity Center, Division of Cardiovascular Medicine, Department of Medicine, University of Louisville, KY (A.B., J.P.M., W.A., D.J.C., T.O.).
authors: Wesley
authors: W
authors: Abplanalp
authors: From the Department of Economics, Brigham Young University, Provo, UT (C.A.P.); and Diabetes and Obesity Center, Division of Cardiovascular Medicine, Department of Medicine, University of Louisville, KY (A.B., J.P.M., W.A., D.J.C., T.O.).
authors: Daniel J
authors: DJ
authors: Conklin
authors: From the Department of Economics, Brigham Young University, Provo, UT (C.A.P.); and Diabetes and Obesity Center, Division of Cardiovascular Medicine, Department of Medicine, University of Louisville, KY (A.B., J.P.M., W.A., D.J.C., T.O.).
authors: Timothy
authors: T
authors: O'Toole
mesh_terms: D000328:Adult; D000397:Air Pollution / Q000009:adverse effects*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism*; D004781:Environmental Exposure / Q000009:adverse effects*; D015525:Fatty Acids, Omega-3 / Q000008:administration & dosage; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000139:chemically induced; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors / Q000097:blood*; D008297:Male; D010316:Particle Size; D052638:Particulate Matter / Q000009:adverse effects*; D011897:Random Allocation; D055815:Young Adult
chemical_list: D015525:Fatty Acids, Omega-3; D018836:Inflammation Mediators; D052638:Particulate Matter
keywords: air pollution; cardiovascular disease; inflammation; particulate matter; vascular disease