期刊
TOXICOLOGIC PATHOLOGY
卷 48, 期 7, 页码 887-898出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/0192623320961017
关键词
ozone; fulvic acid; air pollution; iron; lung diseases; carbon black; fulvic acid-like substance; inflammation; rats
资金
- NIH
- Environmental Protection Agency
- National Institute of Environmental Health Sciences
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [ZICES103319] Funding Source: NIH RePORTER
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.
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