title: Air pollution and markers of inflammation and coagulation in patients with coronary heart disease.
abstract: BACKGROUND
  Ambient air pollution has been shown to be associated with cardiovascular morbidity and mortality.
  
  
  OBJECTIVE
  A prospective panel study was conducted to study the early physiologic reactions characterized by blood biomarkers of inflammation, endothelial dysfunction, and coagulation in response to daily changes in air pollution in Erfurt, Germany.
  
  
  METHODS
  Blood parameters were repeatedly measured in 57 male patients with coronary heart disease during the winter of 2000/2001. Fixed-effects linear and logistic regression models were applied, adjusting for trend, weekday, and meteorologic parameters.
  
  
  METHODS
  Hourly data on ultrafine particles (UFPs; number concentration of particles from 0.01 to 0.1 microm), mass concentration of particles less than 10 (PM(10)) and 2.5 microm in diameter, elemental and organic carbon, gaseous pollutants, and meteorologic data were collected at central monitoring sites.
  
  
  RESULTS
  Increased levels of C-reactive protein above the 90th percentile were observed for an increase in air pollution concentrations of one interquartile range. The effect was strongest for accumulation mode particles, with a delay of 2 d (odds ratio [OR], 3.2; confidence interval [CI], 1.7, 6.0). Results were consistent for UFPs and PM(10), which also showed a 2-d delayed response (OR, 2.3; CI, 1.3, 3.8; and OR, 2.2; CI, 1.2, 3.8, respectively). However, not all of the blood markers of endothelial dysfunction and coagulation increased consistently in association with air pollutants.
  
  
  CONCLUSIONS
  These results suggest that inflammation as well as parts of the coagulation pathway may contribute to the association between particulate air pollution and coronary events.
authors.affiliation: GSF-National Research Center for Environment and Health, Institute of Epidemiology, Ingolstaedter Landstrasse 1, 85764 Neuherberg, Germany. rueckerl@gsf.de
authors.forename: Regina
authors.initials: R
authors.lastname: Rückerl
authors.forename: Angela
authors.initials: A
authors.lastname: Ibald-Mulli
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Koenig
authors.forename: Alexandra
authors.initials: A
authors.lastname: Schneider
authors.forename: Gabriele
authors.initials: G
authors.lastname: Woelke
authors.forename: Josef
authors.initials: J
authors.lastname: Cyrys
authors.forename: Joachim
authors.initials: J
authors.lastname: Heinrich
authors.forename: Victor
authors.initials: V
authors.lastname: Marder
authors.forename: Mark
authors.initials: M
authors.lastname: Frampton
authors.forename: H Erich
authors.initials: HE
authors.lastname: Wichmann
authors.forename: Annette
authors.initials: A
authors.lastname: Peters
mesh_terms: D000368:Aged; D000397:Air Pollution / Q000009:adverse effects*; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation; D002097:C-Reactive Protein / Q000032:analysis*; D003327:Coronary Disease / Q000097:blood* / Q000276:immunology*; D006801:Humans; D007249:Inflammation / Q000209:etiology; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012044:Regression Analysis
chemical_list: D015415:Biomarkers; D002097:C-Reactive Protein