In Silico Study of Gaseous Air Pollutants Effects on Human Atrial Tissue

Exposure to gaseous air pollutants such as carbon monoxide (CO), nitric oxide (NO) and sulfur dioxide (SO
2
) promotes the occurrence of cardiac diseases. Investigations have shown that CO and SO
2
block the calcium channel (I
CaL
) of myocytes. The SO
2
also increases the sodium channel (I
Na
), the transient outward (I
to
) and inward rectifying (I
K1
) potassium currents. The NO blocks I
Na
and increases I
CaL
. 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 action potential duration (APD) was measured. S1-S2 cross-field protocol was applied to initiate a rotor. The CO and SO
2
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). The gaseous air pollutants caused an APD shortening and loss of plateau phase of the action potential in a fraction that increases as the pollutant concentration increases. When the highest concentration was applied, the APD decreased by 81%. In the 2D model, from case 4 conditions it was possible to generate rotor, propagating with high stability. These results show pro-arrhythmic effects of gaseous air pollutants.