Secondary organic aerosol from biomass burning intermediates induced significant oxidative stress in human lung epithelial cells

Phenol and methoxyphenols are key semi-volatile compounds released from biomass burning with great potential in forming secondary organic aerosol (SOA), threatening global climate and public health. However, the underlying toxicity mechanisms of SOA from biomass burning (BBSOA) remain poorly understood. A detailed examination of the chemical composition and in vitro exposure were performed to comprehensively understand the oxidative stress effects of BBSOA on human bronchial epithelial (BEAS-2B) cells. Oxidative damage and inflammatory responses of the cells following exposure to SOA from phenol (PSOA), guaiacol (GSOA), and syringol (SSOA) were evaluated. Exposure to BBSOA resulted in a noticeable reduction in cell viability, marked by a significantly increased apoptosis in BEAS-2B cells. Flow cytometry and confocal image analysis revealed significant increases in reactive oxygen species (ROS), indicating mitochondrial stress in vitro . The oxidative stress effect from PSOA was observed to be the most significant among all the three types of BBSOA. Using PSOA as a model system, RT-qPCR and RNA-sequencing confirmed that BBSOA induces the upregulation of typical oxidative stress genes, such as NQO1, HOMX1, and ALDH1A3, resulting in inflammation and cell death. From acellular oxidative potential to cellular transcriptomic level, our work provided direct evidence on the oxidative stress effects from BBSOA, highlighting the health impacts of secondary biomass burning aerosol during regional transportation. • SOA from typical biomass burning emission, guaiacol, syringol, and phenol were produced. • Exposing human lung BEAS-2B cells to BBSOA induced significant cell death. • Expression of IL-8, Nrf-2, and NQO1were significantly enhanced upon BBSOA exposure. • Phenol SOA resulted in the most pronounced oxidative stress effects in human lung cells. • Exposure to phenol SOA enhances the expression of 141 oxidative stress-related genes.