Inflammation and thrombosis play crucial roles in the pathogenesis of athero-thrombotic vascular disease. Amassing evidence points to a cross-link between these two systems. For instance, while some studies have shown that inflammation can activate coagulation, others demonstrate that coagulation can induce inflammation [1]. Seasonal variations in cardiovascular disease risk have previously been observed and are postulated to be explained, at least in part, by elevated wintertime fibrinogen levels [2]. However, details pertaining to the causeof seasonalvariations infibrinogen levelshaveyet tobeelucidated. C-reactive protein (CRP) is proposed to be an emerging, but reliable cardiovascular risk factor [3, 4]. In a study of healthy middleaged women, the highest CVD risk was found among those with elevated levels of both fibrinogen and CRP [3]. Further, a recent review identified both fibrinogen and CRP as important and evidence-based markers of CVD risk [4]. Exposure to particulate matter (PM) air pollution is also associated with increased levels of blood inflammation markers and coagulation parameters [5, 6]. In addition, the cause of elevated mortality rates in winter season has been attributed to virus infections, especially influenza [7]. However, there exists limited information of the prospective effects of environmental factors (including antibody titer of influenza and PM) on seasonal variations of plasma fibrinogen levels and its determinants. From July to September 2002, 155 office employees whoworked in a petrochemical company based in the Taipei and who participated in a cardiovascular health promotion program were recruited for a second blood sampling for CRP and fibrinogen during the wintertime (January–February 2003). Overnight fasting blood samples for lipids and glucose levels were assayed in the central laboratory. Serum highsensitivity CRP (hs-CRP) was measured using a chemiluminescent enzyme-labeled immunometric assay (Diagnostic Products Co., Los Angeles). Plasma fibrinogen was measured using the clotting method of Clauss (Diagnostica Stago, France). Antibody titer of influenza A and B was measured via a commercial anti-influenza A and B virus ELISA IgG kit (EUROIMMUN, Lubeck, Germany). A Particulate Matter Supersite monitoring station (Supersite), located in the center of the Taipei metropolitan area monitored the environmental conditions. Concentrations of PM10, temperature and humidity level were measured on an hourly basis [5, 6]. The participants had a mean age of 56.26±5.00 years and were predominantly male (85.53%). Analysis of seasonal variations in levels of plasma fibrinogen, serum hs-CRP and other covariates are illustrated in Table 1. The mean summer plasma fibrinogen level was 9.45±2.36 μmol/L and increased significantly to 9.89±1.58 μmol/L during the winter. A similar wintertime increase in PM10 was also noted. However, mean hs-CRP levels did not differ according to season. After controlling for potential confounders, multiple linear regression analyses revealed serumhs-CRP levels tobe thebest correlate of summer andwinter plasma fibrinogen levels. One day prior exposure to PM10 levels in summer and winter–summer difference were also significantly associatedwith the correspondingplasmafibrinogen levels (Table 2). The positive correlation of seasonal differences between each participant's hs-CRP and fibrinogen levels is demonstrated in Fig. 1. This study in middle-aged office workers demonstrates a clear seasonal variation of fibrinogen levels that is strongly correlated with hs-CRP levels. This finding suggests a major role of inflammation in association with the seasonal variation of fibrinogen levels. In addition, PM air pollution was identified as another independent determinant of plasma fibrinogen during the summer, as well as its seasonal variation. Indeed, numerous studies have consistently reported that ambient air pollution, especially PM, is associated with cardiovascular morbidity and mortality [8, 9]. This study also supports the notion that CRP levels are stable across different seasons and are thus suitable for assessment in epidemiological and clinical applications [10]. A prior study suggested that the cause of the winter increase in US mortality was likely explained solely by increased rates of influenza [7]. However, we found no relationship between influenza A and B and fibrinogen levels in our study. This indicates that the relationship between fibrinogen levels and mild subclinical inflammation, as represented by CRP levels, was independent of influenza A and B. Plasma fibrinogen levels are correlated with the basal subclinical inflammation, implying that the activation of coagulation is determined by the basal inflammation status. Thus, therapies aimed at reducing inflammatory status, such as HMG-Co A reductase inhibitors (statins) and aspirin, may readily reduce cardiovascular events, even among patients without overt hyperlipidemia [11]. In conclusion, our findings support the hypothesis that the seasonal rhythm of fibrinogen is correlated with the basal