title: Anti-oxidative and inflammatory responses induced by fly ash particles and carbon black in lung epithelial cells.
abstract: Combustion-derived nanoparticles as constituents of ambient particulate matter have been shown to induce adverse health effects due to inhalation. However, the components inducing these effects as well as the biological mechanisms are still not fully understood. The fine fraction of fly ash particles collected from the electrostatic precipitator of a municipal solid waste incinerator was taken as an example for real particles with complex composition released into the atmosphere to study the mechanism of early biological responses of BEAS-2B human lung epithelial cells. The studies include the effects of the water-soluble and -insoluble fractions of the fly ash and the well-studied carbon black nanoparticles were used as a reference. Fly ash induced reactive oxygen species (ROS) and increased the total cellular glutathione (tGSH) content. Carbon black also induced ROS generation; however, in contrast to the fly ash, it decreased the intracellular tGSH. The fly ash-induced oxidative stress was correlated with induction of the anti-oxidant enzyme heme oxygenase-1 and increase of the redox-sensitive transcription factor Nrf2. Carbon black was not able to induce HO-1. ROS generation, tGSH increase and HO-1 induction were only induced by the insoluble fraction of the fly ash, not by the water-soluble fraction. ROS generation and HO-1 induction were markedly inhibited by pre-incubation of the cells with the anti-oxidant N-acetyl cysteine which confirmed the involvement of oxidative stress. Both effects were also reduced by the metal chelator deferoxamine indicating a contribution of bioavailable transition metals. In summary, both fly ash and carbon black induce ROS but only fly ash induced an increase of intracellular tGSH and HO-1 production. Bioavailable transition metals in the solid water-insoluble matrix of the fly ash mostly contribute to the effects.
authors.affiliation: Institute of Toxicology and Genetics, Karlsruhe Institute of Technology, Eggenstein-Leopoldshafen, Germany. silvia.diabate@kit.edu
authors.forename: Silvia
authors.initials: S
authors.lastname: Diabaté
authors.forename: Britta
authors.initials: B
authors.lastname: Bergfeldt
authors.forename: Diana
authors.initials: D
authors.lastname: Plaumann
authors.forename: Caroline
authors.initials: C
authors.lastname: Ubel
authors.forename: Carsten
authors.initials: C
authors.lastname: Weiss
mesh_terms: D000393:Air Pollutants / Q000032:analysis / Q000633:toxicity*; D002460:Cell Line; D060729:Coal Ash / Q000032:analysis / Q000633:toxicity*; D004847:Epithelial Cells / Q000187:drug effects* / Q000201:enzymology / Q000276:immunology / Q000378:metabolism*; D005978:Glutathione / Q000378:metabolism; D051547:Heme Oxygenase-1 / Q000378:metabolism*; D006801:Humans; D017745:Incineration; D018384:Oxidative Stress / Q000187:drug effects; D052638:Particulate Matter / Q000032:analysis / Q000633:toxicity*; D017382:Reactive Oxygen Species / Q000378:metabolism; D053260:Soot / Q000032:analysis / Q000633:toxicity*
chemical_list: D000393:Air Pollutants; D060729:Coal Ash; D052638:Particulate Matter; D017382:Reactive Oxygen Species; D053260:Soot; D051547:Heme Oxygenase-1; D005978:Glutathione