title: Association between source-specific particulate matter air pollution and hs-CRP: local traffic and industrial emissions.
abstract: Long-term exposures to particulate matter air pollution (PM2.5 and PM10) and high traffic load have been associated with markers of systemic inflammation. Epidemiological investigations have focused primarily on total PM, which represents a mixture of pollutants originating from different sources.
  
  
  
  We investigated associations between source-specific PM and high-sensitive C-reactive protein (hs-CRP), an independent predictor of cardiovascular disease.
  
  
  
  We used data from the first (2000-2003) and second examination (2006-2008) of the Heinz Nixdorf Recall study, a prospective population-based German cohort of initially 4,814 participants (45-75 years of age). We estimated residential long-term exposure to local traffic- and industry-specific fine particulate matter (PM2.5) at participants' residences using a chemistry transport model. We used a linear mixed model with a random participant intercept to estimate associations of source-specific PM and natural log-transformed hs-CRP, controlling for age, sex, education, body mass index, low- and high-density lipoprotein cholesterol, smoking variables, physical activity, season, humidity, and city (8,204 total observations).
  
  
  
  A 1-μg/m3 increase in total PM2.5 was associated with a 4.53% increase in hs-CRP concentration (95% CI: 2.76, 6.33%). hs-CRP was 17.89% (95% CI: 7.66, 29.09%) and 7.96% (95% CI: 3.45, 12.67%) higher in association with 1-μg/m3 increases in traffic- and industry-specific PM2.5, respectively. RESULTS for PM10 were similar.
  
  
  
  Long-term exposure to local traffic-specific PM (PM2.5, PM10) was more strongly associated with systemic inflammation than total PM. Associations of local industry-specific PM were slightly stronger but not significantly different from associations with total PM.
authors.affiliation: IUF-Leibniz Research Institute for Environmental Medicine, Düsseldorf, Germany.
authors.forename: Frauke
authors.initials: F
authors.lastname: Hennig
authors.forename: Kateryna
authors.initials: K
authors.lastname: Fuks
authors.forename: Susanne
authors.initials: S
authors.lastname: Moebus
authors.forename: Gudrun
authors.initials: G
authors.lastname: Weinmayr
authors.forename: Michael
authors.initials: M
authors.lastname: Memmesheimer
authors.forename: Hermann
authors.initials: H
authors.lastname: Jakobs
authors.forename: Martina
authors.initials: M
authors.lastname: Bröcker-Preuss
authors.forename: Dagmar
authors.identifier: 0000-0003-0357-4192
authors.initials: D
authors.lastname: Führer-Sakel
authors.forename: Stefan
authors.initials: S
authors.lastname: Möhlenkamp
authors.forename: Raimund
authors.initials: R
authors.lastname: Erbel
authors.forename: Karl-Heinz
authors.initials: KH
authors.lastname: Jöckel
authors.forename: Barbara
authors.initials: B
authors.lastname: Hoffmann
mesh_terms: D000368:Aged; D000393:Air Pollutants / Q000633:toxicity*; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D015331:Cohort Studies; D004781:Environmental Exposure; D004784:Environmental Monitoring; D005260:Female; D005858:Germany; D006801:Humans; D007249:Inflammation; D008297:Male; D008875:Middle Aged; D008956:Models, Chemical; D052638:Particulate Matter / Q000633:toxicity*; D001335:Vehicle Emissions / Q000633:toxicity
chemical_list: D000393:Air Pollutants; D015415:Biomarkers; D052638:Particulate Matter; D001335:Vehicle Emissions; D002097:C-Reactive Protein
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