A patient-specific model of reactive air pollutant uptake in proximal airways of the lung: Effect of tracheal deviation

We present a three-dimensional dosimetry model to examine the influence of proximal airway deformations such as the tracheal deviation that often occur in the setting of fibrotic lung disease, on transport and uptake of inhaled reactive air pollutants in the human lung. Anatomically-accurate models of proximal airways are reconstructed from high-resolution multidimensional computer tomography (MDCT) scans of healthy and fibrotic adult male lungs. Numerical simulation of pollutant transport and reaction within the virtual airways is then performed to determine the toxicant flux distribution at the airway wall. For quasi-steady inspiratory flow under rest conditions, the flow structure and toxicant concentration distribution in the fibrotic lung are qualitatively different from those in the healthy lung, thereby leading to significantly different patterns of elevated toxicant flux at the airway walls. In contrast to the healthy lung where regions of elevated wall flux are primarily confined to the carina and subsequent bifurcations, hotspots of flux in the disease-modified lung are more widely distributed in the distal trachea and the main bronchi where secondary flow generated by the tracheal deviation persists. This leads to much larger fractional uptake of toxicant in the trachea and main bronchi of the fibrotic lung.