The health effects of exposure to secondary organic aerosols (SOAs) are still limited. Here, we investigated and compared the toxicities of soot particles (SP) coated with β-pinene SOA (SOA-SP) and SP coated with naphthalene SOA (SOA-SP) in a human bronchial epithelial cell line (BEAS-2B) residing at the air-liquid interface. SOA-SP mostly contained oxygenated aliphatic compounds from β-pinene photooxidation, whereas SOA-SP contained a significant fraction of oxygenated aromatic products under similar conditions. Following exposure, genome-wide transcriptome responses showed an Nrf2 oxidative stress response, particularly for SOA-SP. Other signaling pathways, such as redox signaling, inflammatory signaling, and the involvement of matrix metalloproteinase, were identified to have a stronger impact following exposure to SOA-SP. SOA-SP also induced a stronger genotoxicity response than that of SOA-SP. This study elucidated the mechanisms that govern SOA toxicity and showed that, compared to SOAs derived from a typical biogenic precursor, SOAs from a typical anthropogenic precursor have higher toxicological potency, which was accompanied with the activation of varied cellular mechanisms, such as aryl hydrocarbon receptor. This can be attributed to the difference in chemical composition; specifically, the aromatic compounds in the naphthalene-derived SOA had higher cytotoxic potential than that of the β-pinene-derived SOA.
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| http://dx.doi.org/10.1016/j.envint.2022.107366 | DOI Listing |
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