title: Traffic air pollution and oxidized LDL.
abstract: BACKGROUND
  Epidemiologic studies indirectly suggest that air pollution accelerates atherosclerosis. We hypothesized that individual exposure to particulate matter (PM) derived from fossil fuel would correlate with plasma concentrations of oxidized low-density lipoprotein (LDL), taken as a marker of atherosclerosis. We tested this hypothesis in patients with diabetes, who are at high risk for atherosclerosis.
  
  
  RESULTS
  In a cross-sectional study of non-smoking adult outpatients with diabetes we assessed individual chronic exposure to PM by measuring the area occupied by carbon in airway macrophages, collected by sputum induction and by determining the distance from the patient's residence to a major road, through geocoding. These exposure indices were regressed against plasma concentrations of oxidized LDL, von Willebrand factor and plasminogen activator inhibitor 1 (PAI-1). We could assess the carbon load of airway macrophages in 79 subjects (58 percent). Each doubling in the distance of residence from major roads was associated with a 0.027 µm(2) decrease (95% confidence interval (CI): -0.048 to -0.0051) in the carbon load of airway macrophages. Independently from other covariates, we found that each increase of 0.25 µm(2) [interquartile range (IQR)] in carbon load was associated with an increase of 7.3 U/L (95% CI: 1.3 to 13.3) in plasma oxidized LDL. Each doubling in distance of residence from major roads was associated with a decrease of -2.9 U/L (95% CI: -5.2 to -0.72) in oxidized LDL. Neither the carbon load of macrophages nor the distance from residence to major roads, were associated with plasma von Willebrand factor or PAI-1.
  
  
  CONCLUSIONS
  The observed positive association, in a susceptible group of the general population, between plasma oxidized LDL levels and either the carbon load of airway macrophages or the proximity of the subject's residence to busy roads suggests a proatherogenic effect of traffic air pollution.
authors.affiliation: Occupational and Environmental Medicine, Unit of Lung Toxicology, Katholieke Universiteit Leuven, Leuven, Belgium.
authors.forename: Lotte
authors.initials: L
authors.lastname: Jacobs
authors.forename: Jan
authors.initials: J
authors.lastname: Emmerechts
authors.forename: Marc F
authors.initials: MF
authors.lastname: Hoylaerts
authors.forename: Chantal
authors.initials: C
authors.lastname: Mathieu
authors.forename: Peter H
authors.initials: PH
authors.lastname: Hoet
authors.forename: Benoit
authors.initials: B
authors.lastname: Nemery
authors.forename: Tim S
authors.initials: TS
authors.lastname: Nawrot
mesh_terms: D000328:Adult; D000368:Aged; D000397:Air Pollution / Q000009:adverse effects*; D050197:Atherosclerosis / Q000209:etiology; D015415:Biomarkers / Q000097:blood; D003430:Cross-Sectional Studies; D048909:Diabetes Complications; D003920:Diabetes Mellitus; D004781:Environmental Exposure / Q000009:adverse effects; D005260:Female; D006801:Humans; D008077:Lipoproteins, LDL / Q000097:blood*; D016676:Macrophages, Alveolar / Q000737:chemistry; D008297:Male; D008875:Middle Aged; D012306:Risk; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D015415:Biomarkers; D008077:Lipoproteins, LDL; D001335:Vehicle Emissions; C099252:oxidized low density lipoprotein