(165h) Pulmonary Functionality Changes Following Titanium Dioxide Particulate Exposure and Antioxidant Protection

Fine particulate matter (PM2.5) is a major health concern, impacting the respiratory system through impaired lung function, infection, cancer, and contributing to 48,000 deaths in the United States every year. Exposure to PM2.5 causes oxidative stress through the direct introduction of exogenous ROS and compounds that drive free radical reactions, or indirectly through the recruitment and activation of inflammatory cells which release free radicals. The large surface area of the lungs and direct contact with inhaled air make the respiratory system highly susceptible to oxidative stress related injury. Individuals with immunodeficiencies and pulmonary diseases including asthma and COP are especially susceptible as these conditions have been correlated with decreased antioxidant status in lung lining fluids and tissues.

Titanium dioxide nanoparticles are widely used in industrial and consumer products including paints, plastics, pharmaceuticals, cosmetics, and food products. Large production of this nanoparticle and other engineered nanoparticles are a cause for concern of occupational exposure through inhalation and dermal contact. TiO₂ nanoparticle toxicity has been studied extensively in dermal models, however, respiratory effects and oxidative damage pathways remain a concern.

This study aims to characterize oxidative stress response in human pulmonary cell line A549 following isolated and repeated exposures to titanium dioxide nanoparticles. Size, charge, and morphology of TiO₂ nanoparticles were characterized using DLS, zeta potential, and SEM prior to exposure. Post-exposure investigation included cell viability by MTT assay and physiological response parameters including IL-8 secretion, apoptosis execution determined by caspase 3 activation, ratio of reduced and oxidized glutathione, and quantification of reactive oxygen species. Further, antioxidant pretreatment is investigated to supplement decreased antioxidant capacity and reduce extent of functionality impairment.