Atmospheric Aging Modifies the Toxicological Profile of Biomass Burning Particles in Epithelial Lung Cells

Wildfire activity and associated smoke emissions are increasing globally, leading to widespread exposure to biomass burning particulate matter (PM). Although people are mainly exposed to aged wildfire smoke rather than fresh emissions, the effects of atmospheric aging on wildfire particulate toxicity remain poorly understood. Here, we investigated how atmospheric processing ("aging") modifies biological effects of biomass burning particles (BBPs) generated under controlled flaming and smoldering combustion conditions. BB emissions were produced in the Photochemical Large Aerosol Chamber (PHOTO-LAC) and aged under alternating photochemical and dark conditions. Fresh and aged BBP extracts were subsequently sampled and tested in human bronchial epithelial cells (BEAS-2B). We assessed cytotoxicity, oxidative stress, oxidative DNA damage, genome-wide transcriptional responses, and inflammatory and extracellular matrix-related protein expression. Atmospheric aging substantially altered BBP toxicity in a combustion-dependent manner. Aged BBP enhanced intracellular reactive oxygen species formation and oxidative DNA damage, particularly for smoldering emissions, while cytotoxicity remained largely unchanged. In contrast, inflammatory and matrix-remodeling responses were attenuated with aging in smoldering particles but remained stable for flaming BBP. These findings demonstrate that atmospheric aging can simultaneously amplify oxidative and genotoxic stress while dampening inflammatory signaling, underscoring the need to incorporate aging state into health risk assessments of wildfire smoke exposure.