PMID- 27780829 OWN - NLM STAT- MEDLINE DCOM- 20170503 LR - 20220318 IS - 1524-4571 (Electronic) IS - 0009-7330 (Print) IS - 0009-7330 (Linking) VI - 119 IP - 11 DP - 2016 Nov 11 TI - Exposure to Fine Particulate Air Pollution Is Associated With Endothelial Injury and Systemic Inflammation. PG - 1204-1214 LID - 10.1161/CIRCRESAHA.116.309279 [doi] AB - RATIONALE: Epidemiological evidence indicates that exposures to fine particulate matter air pollution (PM(2.5)) contribute to global burden of disease, primarily as a result of increased risk of cardiovascular morbidity and mortality. However, mechanisms by which PM(2.5) exposure induces cardiovascular injury remain unclear. PM(2.5)-induced endothelial dysfunction and systemic inflammation have been implicated, but direct evidence is lacking. OBJECTIVE: To examine whether acute exposure to PM(2.5) is associated with endothelial injury and systemic inflammation. METHODS AND RESULTS: Blood was collected from healthy, nonsmoking, young adults during 3 study periods that included episodes of elevated PM(2.5) levels. Microparticles and immune cells in blood were measured by flow cytometry, and plasma cytokine/growth factors were measured using multiplexing laser beads. PM(2.5) exposure 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], GROalpha [growth-regulated protein alpha], and VEGF [vascular endothelial growth factor]), and an increase in the levels of antiangiogenic (TNFalpha [tumor necrosis factor alpha], IP-10 [interferon gamma-induced protein 10]), and proinflammatory cytokines (MCP-1 [monocyte chemoattractant protein 1], MIP-1alpha/beta [macrophage inflammatory protein 1alpha/beta], IL-6 [interleukin 6], and IL-1beta [interleukin 1beta]), and markers of endothelial adhesion (sICAM-1 [soluble intercellular adhesion molecule 1] and sVCAM-1 [soluble vascular cellular adhesion molecule 1]). PM(2.5) exposure was also associated with an inflammatory response characterized by elevated levels of circulating CD14(+), CD16(+), CD4(+), and CD8(+), but not CD19(+) cells. CONCLUSIONS: Episodic PM(2.5) exposures 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. CI - (c) 2016 American Heart Association, Inc. FAU - Pope, C Arden 3rd AU - Pope CA 3rd AD - 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. FAU - Bhatnagar, Aruni AU - Bhatnagar A AD - 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.). FAU - McCracken, James P AU - McCracken JP AD - 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.). FAU - Abplanalp, Wesley AU - Abplanalp W AD - 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.). FAU - Conklin, Daniel J AU - Conklin DJ AD - 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.). FAU - O'Toole, Timothy AU - O'Toole T AD - 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.). LA - eng GR - P20 GM103492/GM/NIGMS NIH HHS/United States GR - R01 ES019217/ES/NIEHS NIH HHS/United States PT - Journal Article DEP - 20161025 PL - United States TA - Circ Res JT - Circulation research JID - 0047103 RN - 0 (Fatty Acids, Omega-3) RN - 0 (Inflammation Mediators) RN - 0 (Particulate Matter) SB - IM MH - Adult MH - Air Pollution/*adverse effects MH - Endothelium, Vascular/drug effects/*metabolism MH - Environmental Exposure/*adverse effects MH - Fatty Acids, Omega-3/administration & dosage MH - Female MH - Humans MH - Inflammation/blood/chemically induced MH - Inflammation Mediators/antagonists & inhibitors/*blood MH - Male MH - Particle Size MH - Particulate Matter/*adverse effects MH - Random Allocation MH - Young Adult PMC - PMC5215745 MID - NIHMS822009 OTO - NOTNLM OT - air pollution OT - cardiovascular disease OT - inflammation OT - particulate matter OT - vascular disease EDAT- 2016/10/27 06:00 MHDA- 2017/05/04 06:00 PMCR- 2017/11/11 CRDT- 2016/10/27 06:00 PHST- 2016/09/13 00:00 [received] PHST- 2016/10/03 00:00 [revised] PHST- 2016/10/04 00:00 [accepted] PHST- 2016/10/27 06:00 [pubmed] PHST- 2017/05/04 06:00 [medline] PHST- 2016/10/27 06:00 [entrez] PHST- 2017/11/11 00:00 [pmc-release] AID - CIRCRESAHA.116.309279 [pii] AID - 10.1161/CIRCRESAHA.116.309279 [doi] PST - ppublish SO - Circ Res. 2016 Nov 11;119(11):1204-1214. doi: 10.1161/CIRCRESAHA.116.309279. Epub 2016 Oct 25.