Background: Exposure to gaseous air pollutants like carbon monoxide (CO), nitric oxide (NO) and sulfur dioxide (SO2) promotes the occurrence of cardiac diseases. Studies have shown that CO and SO2 block the calcium channel (ICaL) of myocytes. SO2 also increases the sodium channel (INa), the transient outward (Ito) and inward rectifying (IK1) potassium currents. NO blocks INa and increases ICaL. Aim: To assess the effects of the gaseous pollutants at different concentrations on human atrial tissue, using computational simulation. Methods: Based on experimental data, we developed concentration-dependent equations to simulate the gaseous pollutants effects on the ionic currents. They were incorporated in the Courtemanche model of human atrial cell and in a 2D tissue model. A train of 10 stimuli was applied. The APD90 was measured. S1-S2 cross-field protocol was applied to initiate a rotor. CO and SO2 concentrations from 0 to 1000 uM and NO concentration from 0 to 500 nM were implemented. Six concentration combinations were simulated (cases 1 to 6). Results: Our results in a human atrial cell model are in agreement with results from non-human in vitro and in vivo studies. The gaseous air pollutants cause the APD shortening and loss of plateau phase of the action potential in a fraction that increases as the concentration increases. When the highest concentrations was applied, the ICaL peak decreased by 95%, the INa, Ito and IK1 peaks increased by 43%, 96% and 61%, respectively, and the APD90 decreased by 81%. In the 2D model was possible to generate rotors from case 4, from 600 µm of CO, 100 µm of SO2 and 100 nM of NO. The rotors showed high stability. Conclusion: Our results show pro-arrhythmic effects of gaseous air pollutants on expressed through APD shortening and a rotor generation, during normal electrophysiological conditions.