Toxicological responses of A549 and HCE-T cells exposed to fine particulate matter at the air–liquid interface

Abstract

Fine particulate matter (PM 2.5 ) can enter the human body in various ways and have adverse effects on human health. Human lungs and eyes are exposed to the air for a long time and are the first to be exposed to PM 2.5 . The “liquid immersion exposure method” has some limitations that prevent it from fully reflecting the toxic effects of particulate matter on the human body. In this study, the collected PM 2.5 samples were chemically analyzed. An air–liquid interface (ALI) model with a high correlation to the in vivo environment was established based on human lung epithelial cells (A549) and immortalized human corneal epithelial cells (HCE-T). The VITROCELL Cloud 12 system was used to distribute PM 2.5 on the cells evenly. After exposure for 6 h and 24 h, cell viability, apoptosis rate, reactive oxygen species (ROS) level, expression of inflammatory factors, and deoxyribonucleic acid (DNA) damage were measured. The results demonstrated significant dose- and time-dependent effects of PM 2.5 on cell viability, cell apoptosis, ROS generation, and DNA damage at the ALI, while the inflammatory factors showed dose-dependent effects only. It should be noted that even short exposure to low doses of PM 2.5 can cause cell DNA double-strand breaks and increased expression of γ-H2AX, indicating significant genotoxicity of PM 2.5 . Increased abundance of ROS in cells plays a crucial role in the cytotoxicity induced by PM 2.5 exposure These findings emphasize the significant cellular damage and genotoxicity that may result from short-term exposure to low levels of PM 2.5 .

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