Exposure to naphthalene and β-pinene-derived secondary organic aerosol induced divergent changes in transcript levels of BEAS-2B cells

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 beta-pinene SOA (SOA beta Pin-SP) and SP coated with naphthalene SOA (SOANap-SP) in a human bronchial epithelial cell line (BEAS-2B) residing at the air-liquid interface. SOA beta Pin-SP mostly contained oxygenated aliphatic compounds from beta-pinene photooxidation, whereas SOANap-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 SOANap-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 SOANap-SP. SOANap-SP also induced a stronger genotoxicity response than that of SOA beta Pin-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 cyto-toxic potential than that of the beta-pinene-derived SOA.

Automated summary

This study investigates the toxicities of secondary organic aerosols (SOAs) derived from different precursor compounds. It shows that SOAs derived from a typical anthropogenic precursor have higher toxicological potency and activate different cellular mechanisms compared to those derived from a typical biogenic precursor.