title: Particulate air pollution induces progression of atherosclerosis.
abstract: OBJECTIVE
  We sought to determine the effect of exposure to air pollution particulate matter <10 microm (PM(10)) on the progression of atherosclerosis in rabbits.
  
  
  BACKGROUND
  Epidemiologic studies have associated exposure to ambient PM(10) with increased cardiovascular morbidity and mortality. We have previously shown that PM(10) exposure induces a systemic inflammatory response that includes marrow stimulation, and we hypothesized that this response accelerates atherosclerosis.
  
  
  METHODS
  Watanabe heritable hyperlipidemic rabbits were exposed to PM(10) (n = 10) or vehicle (n = 6) for four weeks, and bone marrow stimulation was measured. Quantitative histologic methods were used to determine the morphologic features of the atherosclerotic lesions.
  
  
  RESULTS
  Exposure to PM(10) caused an increase in circulating polymorphonuclear leukocytes (PMN) band cell counts (day 15: 24.6 +/- 3.0 vs. 11.5 +/- 2.7 x 10(7)/l [PM(10) vs. vehicle], p < 0.01) and an increase in the size of the bone marrow mitotic pool of PMNs. Exposure to PM(10) also caused progression of atherosclerotic lesions toward a more advanced phenotype. The volume fraction (vol/vol) of the coronary atherosclerotic lesions was increased by PM(10) exposure (33.3 +/- 4.6% vs. 19.5 +/- 3.1% [PM(10) vs. vehicle], p < 0.05). The vol/vol of atherosclerotic lesions correlated with the number of alveolar macrophages that phagocytosed PM(10) (coronary arteries: r = 0.53, p < 0.05; aorta: r = 0.51, p < 0.05). Exposure to PM(10) also caused an increase in plaque cell turnover and extracellular lipid pools in coronary and aortic lesions, as well as in the total amount of lipids in aortic lesions.
  
  
  CONCLUSIONS
  Progression of atherosclerosis and increased vulnerability to plaque rupture may underlie the relationship between particulate air pollution and excess cardiovascular death.
authors.affiliation: McDonald Research Laboratory and iCAPTURE Centre, University of British Columbia, St. Paul's Hospital, Vancouver, British Columbia, Canada.
authors.forename: Tatsushi
authors.initials: T
authors.lastname: Suwa
authors.forename: James C
authors.initials: JC
authors.lastname: Hogg
authors.forename: Kevin B
authors.initials: KB
authors.lastname: Quinlan
authors.forename: Akira
authors.initials: A
authors.lastname: Ohgami
authors.forename: Renaud
authors.initials: R
authors.lastname: Vincent
authors.forename: Stephan F
authors.initials: SF
authors.lastname: van Eeden
mesh_terms: D000393:Air Pollutants / Q000009:adverse effects*; D000818:Animals; D001011:Aorta / Q000503:physiopathology; D001775:Blood Circulation / Q000502:physiology; D001853:Bone Marrow / Q000098:blood supply / Q000737:chemistry; D001854:Bone Marrow Cells / Q000378:metabolism; D002170:Canada / Q000453:epidemiology; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003324:Coronary Artery Disease / Q000097:blood / Q000139:chemically induced* / Q000503:physiopathology; D003331:Coronary Vessels / Q000737:chemistry / Q000503:physiopathology; D004195:Disease Models, Animal; D018450:Disease Progression; D005260:Female; D008168:Lung / Q000098:blood supply / Q000737:chemistry / Q000166:cytology; D016676:Macrophages, Alveolar / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism; D010316:Particle Size; D011817:Rabbits; D012307:Risk Factors; D012720:Severity of Illness Index; D014481:United States / Q000453:epidemiology; D014504:Urban Health
chemical_list: D000393:Air Pollutants; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL