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_βPin-SP) and SP coated with naphthalene SOA (SOA_Nap-SP) in a human bronchial epithelial cell line (BEAS-2B) residing at the air–liquid interface. SOA_βPin-SP mostly contained oxygenated aliphatic compounds from β-pinene photooxidation, whereas SOA_Nap-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_Nap-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_Nap-SP. SOA_Nap-SP also induced a stronger genotoxicity response than that of SOA_βPin-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.

接触二次有机气溶胶 (SOA) 对健康的影响仍然有限。_{在这里，我们研究并比较了β-蒎烯 SOA 包被的烟灰颗粒 (SP) (SOA βPin} -SP) 和萘 SOA 包被的 SP (SOA _Nap -SP) 在人支气管上皮细胞系 (BEAS-2B) 中的毒性位于气液界面。SOA _βPin -SP 主要含有来自 β-蒎烯光氧化的氧化脂肪族化合物，而 SOA _Nap -SP 在类似条件下含有很大一部分氧化芳香族产物。暴露后，全基因组转录组反应显示出 Nrf2 氧化应激反应，特别是 SOA _Nap -SP。_{其他信号传导途径，如氧化还原信号传导、炎症信号传导和基质金属蛋白酶的参与，被认为在暴露于 SOA Nap} -SP后具有更强的影响。SOA _{Nap -SP 还诱导了比 SOA βPin} -SP更强的遗传毒性反应。这项研究阐明了控制 SOA 毒性的机制，并表明，与源自典型生物前体的 SOA 相比，源自典型人为前体的 SOA 具有更高的毒理学效力，并伴随着多种细胞机制的激活，例如芳烃受体。这可以归因于化学成分的差异；具体来说，萘衍生的 SOA 中的芳香族化合物比 β-蒎烯衍生的 SOA 具有更高的细胞毒性潜力。