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

Abstract

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 μm) 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 μg 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.