(416d) Surface Chemistry Toxicity Parameters Associated with Combustion Produced PM2.5 by in Vitro Assays
AIChE Annual Meeting
Topical Conference: Environmental Aspects, Applications, and Implications of Nanomaterials and Nanotechnology
Tuesday, October 30, 2018 - 4:30pm to 4:50pm
Methods: An epithelial cell line (BEAS-2B) was incubated with lab-generated carbon (nascent, nitric acid-treated, and ozone-treated carbon) for 6 hr. and 24 hr. incubation times, at different concentrations (0-100 Î¼g/mL). After incubation, we measured cell viability using the MultiTox-Fluor Multiplex Assay. In addition, we extracted RNA and protein from cells to evaluate expression of inflammatory cytokines (IL-1b, IL-6, IL-8) and genes related to the inflammatory response and oxidative stress (TLR4, CCL2, MMP1, and NRF2).
Results: Treatment of carbon particles with nitric acid and ozone resulted in differential oxygen and carboxylic acid content in the PM2.5 surface. In BEAS-2B cells, an inverse relationship of cell viability and PM2.5 treatment concentration was observed at both time points assessed. Of the three PM2.5 preparations, BEAS-2B cells exposed to nitric acid-treated carbon resulted in the largest decrease (89% and 96%) of cell viability after 6 hr. and 24 hr., respectively, indicating that both carboxylic acid and oxygen content of the particle surface strongly contribute to PM2.5 toxicity. Additional results showed an increase in gene expression of the inflammatory cytokines IL-1b, and IL-6, and the oxidative stress markers TLR4 and NRF2 at higher concentrations of PM2.5 exposure (25-100 Î¼g/mL).
Conclusion: In summary, exposure of different types of particulate matter to lung epithelial cells increases inflammatory responses, with different effects associated with soot components such as particle surface chemistry. Future experiments will determine how functional groups in the PM2.5 surface chemistry affect the activation of the observed inflammatory response, and decrease in cell viability of lung epithelial cells.