Airborne Disease Transmission via Bioaerosols: Formation Mechanisms and the Influence of Viscoelasticity
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CitationThomas, Matthew K. 2012. Airborne Disease Transmission via Bioaerosols: Formation Mechanisms and the Influence of Viscoelasticity. Doctoral dissertation, Harvard University.
AbstractAirborne disease transmission is a prominent problem facing an increasingly mobilized world. It involves small droplets (bioaerosols) containing pathogens which form in the lungs and are expelled to the environment, where they may persist in the air until inhaled by others. Conceptually, there are two basic approaches to preventing transmission: protect the potential target, or eliminate the source. To this end, the effectiveness of modifying mucus viscoelasticity, through cation exposure, to prevent pathogen transport via bioaerosols was investigated. In vitro models were developed to explore the proposed mechanisms for droplet formation: shear-induced surface-wave instabilities in the airway lining fluid (ALF) of the upper airways; and film formation during the re-opening of collapsed bronchioles in the lower airways. Droplet formation during tidal breathing was shown to be an inhalation process for both upper and lower airway models, and the bifurcation angle of the first bronchi was relevant to the upper airway model. A simulated cough system was also developed and produced the largest number of droplets. COPD sputum viscoelasticity was characterized and its response to cation presence measured: low concentrations of calcium resulted in increased complex modulus and decreased loss tangent (indicating increased fluid stiffness resulting from higher elasticity). Higher concentrations of calcium had the reverse effect. Using the cough system, calcium treated (low concentration) and untreated sputum were compared: treated sputum produced fewer droplets. Droplet concentration (number per liter of air) correlated well with the magnitude of the complex modulus. Once the reduction in total droplets was established, pathogen transport experiments, in which human rhinovirus (HRV) was added to calcium-treated and untreated COPD sputum, were performed. Cell culture media was exposed to cough-air from the samples and then placed on HRV-sensitized HeLa cells, which were then monitored for cell death. Cell death was observed for untreated sputum samples, but not for cation-treated samples, indicating that reducing bioaerosol formation (through cationic modification of mucus viscoelasticity) prevented airborne transport of the virus.
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