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Studies evaluating possible associations between long-term exposure to air pollution and inflammatory and thrombotic markers are limited.From 2009 to 2011, we monitored hematologic parameters and thrombotic markers in 402 volunteers 35–65 years of age who were recruited as the non-coronary heart disease (CHD) controls in a study of work-related factors and CHD in Taipei. We applied land-use regression models developed by the European Study of Cohorts for Air Pollution Effects to estimate the mean annual exposure of each participant to five air pollutants at their residence in Taipei, namely particulate matter (PM) of diameter <10 μm (PM10) and 2.5 μm (PM2.5), the absorbance of PM2.5 (PM2.5 abs), nitrogen dioxide (NO2), and nitrogen oxide (NOx).The mean annual exposures were 47.82 ± 4.78 µg/m3 for PM10, 29.08 ± 5.10 µg/m3 for PM2.5, and 2.04 ± 0.37 (10−5 m−1) for PM2.5 abs. Multivariate linear regression analyses showed that the mean percentage (95% confidence interval) of blood monocyte counts increased by 9.08% (1.61%, 16.54%) per 10 µg/m3 increase in PM10, by 16.28% (6.66%, 25.89%) per 1.0 × 10−5 m−1 increase in PM2.5 abs, by 8.28% (2.08%, 14.48%) per 20 µg/m3 increase in NO2, and by 2.84% (1.22%, 4.46%) per 10 µg/m3 increase in NOx. In addition, each 5 μg/m3 increase in PM2.5 was associated with 1.97% (0.02%, 3.92%) increases in fibrinogen.Long-term exposure to traffic-related air pollution is positively associated with subclinical inflammatory and thrombotic markers in middle-aged workers in Taipei.