Patterns of air flow and particle deposition in the diseased human lung

In this work, we investigate particle deposition and air flow in the human lung. In particular we are interested in how the motion of particulate matter and air is affected by the presence of lung disease. Patients with compromised lung function are more sensitive to air pollution; understanding the extent of that sensitivity can lead to more effective air quality standards. Also, understanding of air flow and particle trajectories could lead to the development of better aerosol drugs to treat the lung diseases.; We focus our efforts on two diseases: chronic obstructive pulmonary disease (COPD) and bronchial tumors. Because COPD affects the majority of airways in a patient with the disease, we are able to take a more global approach to analyzing the effects of the disease. Using a FORTRAN cod which computes total deposition in the lung over the course of one breath, we modified the pre-existing code to account for the difference between healthy subjects and patients with COPD. Using the model, it was possible to isolate the different disease components of COPD and simulate their effects separately. It was determined that the chronic bronchitis component of COPD was responsible for the increased deposition seen in COPD patients.; While COPD affects the whole lung, tumors tend to be localized to one or several airways. This led us to investigate the effects of bronchial tumors in detail within these individual airways. Using a computational fluid dynamics package, FIDAP, we defined a Weibel type branching network of airways. In particular, we modeled the airways of a four-year-old child. In the work with the tumors, we ran numerous simulations with various initial velocities and tumor locations. It was determined that tumors located on the carinal ridge had the dominant effect on the flow. At higher initial velocities, areas of circulation developed downstream from the tumors. Extensive simulations were run with a 2-D model. The results from the 2-D model were then compared with some initial 3-D simulations.; In the development of the FIDAP model, we avoided the complications of flow past the larynx, by limiting the model to generations 2–5 of the Weibel lung. We developed a realistic inlet velocity profile to be used as the input into the model. The skewed nature of this inlet profile led to the question of boundary layer development and the determination of the entrance length needed to achieve fully developed parabolic flow. Simple scale analysis of the Navier-Stokes equations did not capture the results we were seeing with the CFD simulations. We turned to a more quantitative, energy correction analysis to determine the theoretical entrance length.; In conclusion, the presence of disease in the lung has a large effect both on global deposition patterns and on localized airflow patterns. This indicates the need for different protocols regarding susceptibility of people to airborne pollutants that take into account lung disease. It also suggests that treatment should account for changes in airflow in the diseased lung.