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Ambient air pollution has been associated with cardiovascular mortality (Forastiere et al. 2005; Peters et al. 2000; Schwartz and Dockery 1992) and hospital admissions for various cardiovascular diseases (Burnett et al. 1997; Schwartz 1999). Also, an elevated risk for acute myocardial infarction (MI) (Lanki et al. 2006; Peters et al. 2001a) and cardio-respiratory symptoms (de Hartog et al. 2003) has been reported in relation to air pollution. Some studies have suggested that patients with preexisting coronary heart disease (CHD) (Goldberger et al. 2001) might be a particularly susceptible population. The exact mechanisms linking the inhalation of ambient air particles to an acute exacerbation of cardiovascular disease are not completely understood (Brook et al. 2004). Alveolar inflammation induced by particles may either directly or via oxidative stress lead to systemic inflammation with increased levels of blood coagulability, progression of atherosclerosis, and destabilization or even rupture of vulnerable plaques, resulting in acute ischemic events (Brook et al. 2004; Seaton et al. 1995). So far, studies using repeated measures to assess the association between ambient air particles and inflammatory markers have had controversial results. In addition, they have been conducted only on a small scale, with samples sizes ranging from 9 to 112 (Riediker et al. 2004; Ruckerl et al. 2006; Seaton et al. 1999). In larger studies, however, associations have been based on single blood measurements (Zeka et al. 2006), and the examined populations have encompassed healthy and diseased subjects, covering a variety of diseases. All these differences might explain the conflicting results. For interleukin 6 (IL-6), hypothesized to play a central role in the triggering of the inflammatory process (Woods et al. 2000), associations with high levels of particulate matter (PM) < 10 μm in aerodynamic diameter (PM10) have been shown (van Eeden et al. 2001), although a study in elderly subjects in the United Kingdom (Seaton et al. 1999) did not reveal significant associations with ambient PM10. The present study was designed to address the responses of IL-6, fibrinogen, and C-reactive protein (CRP) to elevated air pollution levels in a large cohort of MI survivors across Europe. We were particularly interested in MI survivors because they are especially prone to a progression of atherosclerosis and adverse cardiovascular events.