Numerical Simulation of Transport and Uptake of Reactive Air Pollutants in Healthy and Diseased Human Lungs

Open Access
- Author:
- Borhan, Shirin
- Graduate Program:
- Chemical Engineering
- Degree:
- Master of Science
- Document Type:
- Master Thesis
- Date of Defense:
- November 15, 2016
- Committee Members:
- Ali Borhan, Thesis Advisor/Co-Advisor
James Ultman, Committee Member
Rebecca Bascom, Committee Member - Keywords:
- respiratory tract
reactive inhalant
dosimetry - Abstract:
- Exposure to reactive air pollutants can initiate or exacerbate respiratory health problems, and absorption of inhaled toxicants can occur in all regions of the respiratory tract, from the nose to deep in the lung. It is believed that reactive gas-induced tissue injury depends on the local dose delivered to the airway walls. In order to determine whether individuals with disease-modified lung geometries are at higher risk of lung injury (compared to those with healthy lung geometries) as a result of exposure to harmful inhaled pollutants, numerical simulations of reactive gas transport and uptake were performed in anatomically-accurate human lung geometries reconstructed from high-resolution multidimensional computer tomography (MDCT) chest scans of two consenting adult males. The flow structures and toxicant concentration distributions within the proximal airways of the two lungs were determined via numerical solution of the governing equations, and hotspots of reactive gas flux on the airway walls were identified. For both quasi-steady inspiratory and quasi-steady expiratory flow, the flow structure and toxicant concentration distribution in the disease-modified lung were found to be qualitatively different from those in the healthy lung. The highly-deformed airway geometries in the disease-modified lung led to qualitatively different patterns of toxicant uptake and hotspot distributions on the airway walls. These differences were particularly prominent in the trachea and main bronchi, where development of complex secondary flow structures were observed in the disease-modified lung as a result of irregularities in the airway geometry.