Air pollution and inflammation (Interleukin-6, C-reactive protein, fibrinogen) in myocardial infarction survivors

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.