TY - JOUR
TI - Air pollution and inflammation (Interleukin-6, C-reactive protein, fibrinogen) in myocardial infarction survivors
AU - Rückerl, R.
AU - Greven, S.
AU - Ljungman, P.
AU - Aalto, P.
AU - Antoniades, C.
AU - Bellander, T.
AU - Berglind, N.
AU - Chrysohoou, C.
AU - Forastiere, F.
AU - Jacquemin, B.
AU - von Klot, S.
AU - Koenig, W.
AU - Küchenhoff, H.
AU - Lanki, T.
AU - Pekkanen, J.
AU - Perucci, C.A.
AU - Schneider, A.
AU - Sunyer, J.
AU - Peters, A.
JO - Environmental Health Perspectives
PY - 2007
VL - 115
TODO - 7
SP - 1072-1080
PB - 
SN - 0091-6765, 1552-9924
TODO - 10.1289/ehp.10021
TODO - 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
TODO - 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.
ER -