@article{3058285,
    title = "Air pollution and inflammation (Interleukin-6, C-reactive protein, fibrinogen) in myocardial infarction survivors",
    author = "Rückerl, R. and Greven, S. and Ljungman, P. and Aalto, P. and Antoniades, C. and Bellander, T. and Berglind, N. and Chrysohoou, C. and Forastiere, F. and Jacquemin, B. and von Klot, S. and Koenig, W. and Küchenhoff, H. and Lanki, T. and Pekkanen, J. and Perucci, C.A. and Schneider, A. and Sunyer, J. and Peters, A.",
    journal = "Environmental Health Perspectives",
    year = "2007",
    volume = "115",
    number = "7",
    pages = "1072-1080",
    issn = "0091-6765, 1552-9924",
    doi = "10.1289/ehp.10021",
    keywords = "acute phase protein;  C reactive protein;  fibrinogen;  interleukin 6, adult;  aged;  air pollution;  ambient air;  article;  cigarette smoking;  confidence interval;  controlled study;  diabetes mellitus;  disease association;  disease exacerbation;  exhaust gas;  female;  fibrinogen blood level;  Finland;  Germany;  Greece;  heart failure;  heart infarction;  human;  hypothesis;  inflammation;  Italy;  longitudinal study;  major clinical study;  male;  meteorological phenomena;  particulate matter;  pollution monitoring;  priority journal;  protein blood level;  Spain;  survivor;  Sweden;  time series analysis, Air Pollution;  C-Reactive Protein;  Fibrinogen;  Humans;  Inflammation;  Interleukin-6;  Myocardial Infarction",
    abstract = "Background: Numerous studies have found that ambient air pollution has been associated with cardiovascular disease exacerbation. Objectives: Given previous findings, we hypothesized that particulate air pollution might induce systemic inflammation in myocardial infarction (MI) survivors, contributing to an increased vulnerability to elevated concentrations of ambient particles. Methods: A prospective longitudinal study of 1,003 MI survivors was performed in six European cities between May 2003 and July 2004. We compared repeated measurements of interleukin 6 (IL-6), fibrinogen, and C-reactive protein (CRP) with concurrent levels of air pollution. We collected hourly data on particle number concentrations (PNC), mass concentrations of particulate matter (PM) < 10 μm (PM10) and < 2.5 μm (PM2.5), gaseous pollutants, and meteorologic data at central monitoring sites in each city. City-specific confounder models were built for each blood marker separately, adjusting for meteorology and time varying and time invariant covariates. Data were analaysed with mixed-effects models. Results: Pooled rsults show an increase in IL-6 when cncentrations of PNC were elevated 12-17 hr before blood withdrawal [percent change of geometric mean, 2.7; 95% cionfidence interval (CI), 1.0-4.6). Five day cumulative exposure to PM10 was associated with increasded fibrinogen concentrations (percent change of arithmentic mean, 0.6; 95% CI, 0.1-1). Results remained stable for smokers, diabetics, and patients with heart failure. No consistent associations were found for CRP. Conclusions: Results indicate an immediate respnse to PNC on the IL-6 level, possibly leading to the production of acute-phase proteins, as seen in increased fibrinogen levels. This might provide a link between air pollution and adverse cardiac events."
}