Atmospheric aging increases the cytotoxicity of bare soot particles in BEAS-2B lung cells
Michal Pardo, Hendryk Czech, Svenja Offer, Martin Sklorz, Sebastiano Di Bucchianico, Elena Hartner, Jana Pantzke, Evelyn M. Kuhn, Andreas Paul, Till Ziehm, Zhihui Zhang, Gert Jakobi, Stefanie Bauer, Anja Huber, Elias J. Zimmermann, Narges Rastak, Stephanie Binder, Ramona Brejcha, Eric Schneider, Jürgen Orasche, Christopher P. Rüger, Thomas Gröger, Sebastian Oeder, Jürgen Schnelle‐Kreis, Thorsten Hohaus, Markus Kalberer, Olli Sippula, Astrid Kiendler‐Scharr, Ralf Zimmermann, Yinon Rudich
Abstract
Soot particles (SP) are ubiquitous components of atmospheric particulate matter and have been shown to cause various adverse health effects. In the atmosphere, freshly emitted SP can be coated by condensed low-volatility secondary organic and inorganic species. In addition, gas-phase oxidants may react with the surface of SP. Due to the chemical and physical resemblance of SP carbon backbone with polyaromatic hydrocarbon species and their potent oxidation products, we investigated the biological responses of BEAS-2B lung epithelial cells following exposure to fresh- and photochemically aged-SP at the air–liquid interface. A comprehensive physical and chemical aerosol characterization was performed to depict the atmospheric transformations of SP, showing that photochemical aging increased the organic carbon fraction and the oxidation state of the SP. RNA-sequencing and qPCR analysis showed varying gene expression profiles for fresh- and aged-SP. Exposure to aged-SP increased DNA damage, oxidative damage, and upregulation of NRF2-mediated oxidative stress response genes compared to fresh-SP. Furthermore, aged-SP augmented inflammatory cytokine secretion and activated AhR-response, as evidenced by increased expression of AhR-responsive genes. These results indicate that oxidative stress, inflammation, and DNA damage play a key role in the cytotoxicity of SP in BEAS-2B cells, where aging leads to higher toxic responses. Collectively, our results suggest that photochemical aging may increase SP toxicity through surface modifications that lead to an increased toxic response by activating different molecular pathways.