(174c) Oxidative Stress Response in Human Pulmonary Cells Following Titanium Dioxide Particulate Exposure

Fine particulate matter (PM2.5) is a major health concern, impacting the respiratory system through impaired lung function, infection, cancer, and contributing to 4.2 million deaths globally in 2016 [1]. Exposure to particulate matter 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. Titanium dioxide nanoparticles are widely used in industrial and consumer products including paints, plastics, pharmaceuticals, cosmetics, and food products. Large production of this nanoparticle is a cause for concern of occupational exposure through dermal contact and inhalation. TiO₂ nanoparticle toxicity has been studied extensively in in vitro and in vivo dermal models and acute pulmonary exposures, however, there is a need for further characterization of oxidative stress response in respiratory cells following acute and chronic exposure.

The goal of this work was to characterize oxidative stress response of human pulmonary cell line A549 following isolated and repeated exposures to titanium dioxide nanoparticles. Size and charge 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 by western blotting, and ratio of reduced and oxidized glutathione quantified by HPLC.

[1] https://www.who.int/gho/phe/outdoor_air_pollution/en/