Cytotoxicity of PM2.5 vehicular emissions in the Shing Mun Tunnel, Hong Kong

Associations between human exposures to vehicular emissions (VE) and cardiopulmonary diseases have been found, with a dearth of information on particle cytotoxicity. This study exposes human lung alveolar epithelial (A549) cells to PM2.5 (particulate matter with aerodynamic diameter < 2.5 mu m) samples collected in a tunnel and investigates the oxidative and inflammatory responses. The cytotoxicity factor (CF) is used to normalize the VE cytotoxicity. The emission factors (EFs) were 27.2 +/- 12.0 mg vehicle(-1) km(-1) for PM2.5 and 4.93 +/- 1.67 mu g vehicle(-1) km(-1) for measured polycyclic aromatic hydrocarbons (PAHs). Higher EFs were found for high (4-6 rings) than low (2-3 rings) molecular-weight particulate PAHs. PM2.5 VE caused oxidative stress and inflammation of human lung cells. Organic carbon (OC), element carbon (EC), and several PAHs were significantly (p < 0.05) correlated with bioreactivity. Higher CFs were found when diesel vehicle counts were highest during the morning rush hour, implying that diesel-fueled VE were major contributors to cytotoxic effects. This study provides a broader understanding of the toxicity in an engine-exhaust dominated environment. (c) 2020 Elsevier Ltd. All rights reserved.