Background The incidence of arrhythmia increases by air pollution. However, the arrhythmogenic mechanism of air pollution is still poorly understood. Recent studies suggest that the intracellular sources of reactive oxygen species (ROS) can be related with the arrhythmia. This study investigated whether the air pollution can induce arrhythmia and is related with oxidative stress. Methods The cell viability and ROS generation were evaluated after treatment with diesel emission product (DEP). Using optical mapping technique, arrhythmic events and mechanism were evaluated in Langendorff-perfused Adult Sprague-Dawley rat heart (n=25) after DEP. To remove the effect of agglomeration, the DEP was sonificated for 20 minutes, and confirmed the particle size less than 100 nm with electronic microscope. Results In cell viablity test, DEP provoked cell death in dose dependant manner, showing 40% cell death at 400���/ml. DEP induced ROS generation in time and dose dependant manner, showing that 67% myocyte generated ROS at 400���/ml after 6hr exposure. In Langendorff-perfused rate hears, DEP infusion of 12.5 mg/L for 10-15 minutes significantly prolonged APD90 at pacing cycle length (CL) of 300 ms (from 125 짹 29 to 232 짹 45 ms, p=0.003) (n=10). The spontaneous early afterdepolarization (EAD), ventricular arrhythmia were frequently observed after DEP, while they were not observed at baseline. After DEP infusion, the APD alternans were easily observed at longer CL (117 짹 81 ms) compared with baseline (99 짹 7 ms, p=0.04), suggesting enhanced dispersion of repolarization. The pretreatment with N-acetylcystein of 5 mmol/L successfully prevented DEP induced APD prolongation, alternans, EAD and ventricular arrhythmias (n=5). DEP induced EAD was prevented by nifedipine (10 關mol/L, n=5), but not by the combined infusion of thapsigargin (200 nmol/L) and ryanodine (10 關mol/L, n=5). Active calcium calmoduline kinase II (CaMKII) blockade, KN 93 (1 關mol/L, n=5), prevented DEP induced APD prolongation and arrhythmia. However, inactive CaMKII blockade, KN 92 (n=5) failed to prevent it. Conclusion DEP induced APD prolongation, APD alternans, spontaneous EAD and ventricular arrhythmia were completely prevented by the antioxidant, nifedipine, and KN93. Our results suggest that the arrhythmogenesis by air pollution is mediated by the oxidative stress and CaMKII activation, which provokes EAD.