<p>Air pollution increases mortality and the risk of atrial arrhythmias through electrical and structural remodeling, including fibrosis, although the underlying mechanisms remain unclear. In this study, a human-based multiscale in silico framework was applied, integrating a human atrial myocyte model in two- and three-dimensional (2D and 3D) atrial models with varying degrees of fibrosis, to evaluate the impact of main atmospheric pollutants at different concentrations on atrial electrophysiology and arrhythmia generation. Pollutant-specific modulation of ionic currents was implemented to represent pollutant exposure. Electrogram signals were recorded using a virtual basket catheter. Pollutant exposure altered ionic currents, shortening the action potential plateau and duration in a concentration-dependent manner by up to 62% in the left atrium and 61% in the right atrium. In 2D models, vulnerability to reentry increased with pollutant concentration. In 3D models, pollutants promoted reentrant activity, producing more reentries and chaotic propagation as pollutant levels and fibrosis rose. Electrogram analysis revealed higher activation rates of up to 115% in the left atrium and 125% in the right atrium, particularly under structurally vulnerable conditions, accompanied by marked disorganization in the left atrium, which reinforces its dominant role in maintaining the rapid, irregular conduction characteristic of atrial fibrillation. Overall, air pollution can destabilize atrial electrical activity, enhancing susceptibility to reentry and irregular rhythms, particularly with fibrosis. These findings suggest that air pollutants may act as silent proarrhythmic modifiers, facilitating the initiation and maintenance of reentrant and irregular atrial rhythms, particularly in fibrotic atria.</p>