Diffusion in Replica Healthy and Emphysematous Alveolar Models Using Computational Fluid Dynamics

Deposition of nanosized particles in the pulmonary region has the potential of crossing the blood-gas barrier. Experimental in vivo studies have used micron-sized particles, and therefore nanoparticle deposition in the pulmonary region is not well understood. Furthermore, little attention has been paid to the emphysematous lungs, which have characteristics quite different from the healthy lung. Healthy and emphysematous replica acinus models were created from healthy and diseased human lung casts using three-dimensional reconstruction. Particle concentration and deposition were determined by solving the convective-diffusion equation numerically for steady and unsteady cases. Results showed decreased deposition efficiencies for emphysema compared to healthy lungs, consistent with the literature and attributed to significant airway remodeling in the diseased lung. Particle diffusion was found to be six times slower in emphysema compared to healthy model. The unsteady state simulation predicted deposition efficiencies of 96% in the healthy model for the 1？nm and 3？nm particles and 94% and 93% in the emphysema model for the 1？nm and 3？nm particles, respectively. Steady state was achieved in less than one second for both models. Comparisons between steady and unsteady predictions indicate that a steady-state simulation is reasonable for predicting particle transport under similar conditions. 1. Introduction Emphysema is a chronic obstructive pulmonary disease characterized by irreversible damage to alveolar sacs in the pulmonary region of the lung [1, 2]. Specifically, the septa separating the individual acini are destroyed so that the tiny acini merge together to create one large air sac. The effect of emphysema-related lung remodeling on airflow and particle deposition is currently unknown. Understanding how deposition changes in the pulmonary region due to emphysema will help to improve differential risk assessment for those suffering from the disease as well as increase the accuracy of delivering inhaled medication used to treat disease. Studies that model pulmonary airflow and deposition, both experimentally and numerically, are summarized in Table 1, including model characteristics and deposition mechanisms addressed in each study. Deposition in the pulmonary region is governed primarily by diffusion and sedimentation. Whole lung models, such as MPPD, Trumpet, and NCRP [3–5], use analytical deposition equations derived by Ingham [6–8] for straight tube geometries, whereas alveolar models have been published that account for the presence of individual