title: Particulate matter air pollution exposure promotes recruitment of monocytes into atherosclerotic plaques.
abstract: Epidemiologic studies have shown an association between exposure to ambient particulate air pollution <10 microm in diameter (PM(10)) and increased cardiovascular morbidity and mortality. We previously showed that PM(10) exposure causes progression of atherosclerosis in coronary arteries. We postulate that the recruitment of monocytes from the circulation into atherosclerotic lesions is a key step in this PM(10)-induced acceleration of atherosclerosis. The study objective was to quantify the recruitment of circulating monocytes into vessel walls and the progression of atherosclerotic plaques induced by exposure to PM(10). Female Watanabe heritable hyperlipidemic rabbits, which naturally develop systemic atherosclerosis, were exposed to PM(10) (EHC-93) or vehicle by intratracheal instillation twice a week for 4 wk. Monocytes, labeled with 5-bromo-2'-deoxyuridine (BrdU) in donors, were transfused to recipient rabbits as whole blood, and the recruitment of BrdU-labeled cells into vessel walls and plaques in recipients was measured by quantitative histological methodology. Exposure to PM(10) caused progression of atherosclerotic lesions in thoracic and abdominal aorta. It also decreased circulating monocyte counts, decreased circulating monocytes expressing high levels of CD31 (platelet endothelial cell adhesion molecule-1) and CD49d (very late antigen-4 alpha-chain), and increased expression of CD54 (ICAM-1) and CD106 (VCAM-1) in plaques. Exposure to PM(10) increased the number of BrdU-labeled monocytes adherent to endothelium over plaques and increased the migration of BrdU-labeled monocytes into plaques and smooth muscle underneath plaques. We conclude that exposure to ambient air pollution particles promotes the recruitment of circulating monocytes into atherosclerotic plaques and speculate that this is a critically important step in the PM(10)-induced progression of atherosclerosis.
authors: James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, University of British Columbia, Saint Paul's Hospital, Vancouver, British Columbia, Canada.
authors: Kazuhiro
authors: K
authors: Yatera
authors: Joanne
authors: J
authors: Hsieh
authors: James C
authors: JC
authors: Hogg
authors: Erin
authors: E
authors: Tranfield
authors: Hisashi
authors: H
authors: Suzuki
authors: Chih-Horng
authors: CH
authors: Shih
authors: Ali R
authors: AR
authors: Behzad
authors: Renaud
authors: R
authors: Vincent
authors: Stephan F
authors: SF
authors: van Eeden
mesh_terms: D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D000963:Antimetabolites; D001011:Aorta / Q000473:pathology; D050197:Atherosclerosis / Q000378:metabolism / Q000473:pathology*; D001973:Bromodeoxyuridine; D015815:Cell Adhesion Molecules / Q000096:biosynthesis; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects; D005260:Female; D005434:Flow Cytometry; D006207:Half-Life; D007150:Immunohistochemistry; D007958:Leukocyte Count; D008854:Microscopy, Electron; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D052638:Particulate Matter / Q000633:toxicity*; D011817:Rabbits
chemical_list: D000393:Air Pollutants; D000963:Antimetabolites; D015815:Cell Adhesion Molecules; D052638:Particulate Matter; D001973:Bromodeoxyuridine