Citation:

Ghio, A., D. Gonzalez, S. Paulson, J. Soukup, L. Dailey, M. Madden, B. Mahler, S. Elmore, Mette C. Schladweiler, AND U. Kodavanti. Ozone reacts with carbon black to produce a fulvic acid-like substance and increase an inflammatory effect. TOXICOLOGIC PATHOLOGY. Society of Toxicology, RESTON, VA, 48(7):887-898, (2020). https://doi.org/10.1177/0192623320961017

Impact/Purpose:

Ozone exposure can introduce oxygen-containing functional groups in particulate matter effecting a greater capacity of the particle for metal complexation. We tested the postulate that 1) a fulvic acid-like substance can be produced through a reaction of a carbonaceous particle with high concentrations of ozone and 2) such a fulvic acid-like substance can initiate biological effects, including inflammation, following exposure of respiratory epithelial cells and animals.

Description:

Exposure to ambient ozone has been associated with increased human mortality. Ozone exposure can introduce oxygen-containing functional groups in particulate matter (PM) effecting a greater capacity of the particle for metal complexation and inflammatory effect. We tested the postulate that (1) a fulvic acid-like substance can be produced through a reaction of a carbonaceous particle with high concentrations of ozone and (2) such a fulvic acid-like substance included in the PM can initiate inflammatory effects following exposure of respiratory epithelial (BEAS-2B) cells and an animal model (male Wistar Kyoto rats). Carbon black (CB) was exposed for 72 hours to either filtered air (CB-Air) or approximately 100 ppm ozone (CB-O3). Carbon black exposure to high levels of ozone produced water-soluble, fluorescent organic material. Iron import by BEAS-2B cells at 4 and 24 hours was not induced by incubations with CB-Air but was increased following coexposures of CB-O3 with ferric ammonium citrate. In contrast to CB-Air, exposure of BEAS-2B cells and rats to CB-O3 for 24 hours increased expression of pro-inflammatory cytokines and lung injury, respectively. It is concluded that inflammatory effects of carbonaceous particles on cells can potentially result from (1) an inclusion of a fulvic acid-like substance after reaction with ozone and (2) changes in iron homeostasis following such exposure.

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