Open AccessOzone Reacts With Carbon Black to Produce a Fulvic Acid-Like Substance and Increase an Inflammatory Effect
Author(s) -
Andrew J. Ghio,
David H. Gonzalez,
Suzanne E. Paulson,
Joleen M. Soukup,
Lisa A. Dailey,
Michael C. Madden,
Beth Mahler,
Susan A. Elmore,
Mette C. Schladweiler,
Urmila P. Kodavanti
Publication year - 2020
Publication title -
toxicologic pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.613
H-Index - 108
eISSN - 1533-1601
pISSN - 0192-6233
DOI - 10.1177/0192623320961017
Subject(s) - ozone , chemistry , carbon black , environmental chemistry , particulates , nuclear chemistry , organic chemistry , natural rubber
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-O 3 ). 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-O 3 with ferric ammonium citrate. In contrast to CB-Air, exposure of BEAS-2B cells and rats to CB-O 3 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.