title: Role of metal-induced reactive oxygen species generation in lung responses caused by residual oil fly ash.
abstract: Inhalation of residual oil fly ash (ROFA) increases pulmonary morbidity in exposed workers. We examined the role of reactive oxygen species (ROS) in ROFA-induced lung injury. ROFA was collected from a precipitator at Boston Edison Co., Everett, MA, USA. ROFA (ROFA-total) was suspended in saline, incubated for 24 h at 37 degrees C, centrifuged, and separated into its soluble (ROFA-sol.) and insoluble (ROFA-insol.) fractions. Sprague-Dawley rats were intratracheally instilled with saline or ROFA-total or ROFA-sol. or ROFA-insol. (1 mg/100 g body wt.). Lung tissue and bronchoalveolar lavage cells were harvested at 4, 24, and 72 h after instillation. Chemiluminescence (CL) of recovered cells was measured as an index of ROS production, and tissue-lipid-peroxidation was assessed to determine oxidative injury. Significant amounts of Al, Fe, and Ni were present in ROFA-sol., whereas ROFA-insol. contained Fe, V, and Al. Using electron spin resonance (ESR), significantly more hydroxyl radicals were measured in ROFA-sol. as compared to ROFA-insol. None of the ROFA samples had an effect on CL or lipid peroxidation at 4 h. Treatment with ROFA-total and ROFA-insol. caused significant increases in both CL (at 24 h) and lipid peroxidation (at 24 and 72 h) when compared to saline control value. ROFA-sol. significantly reduced CL production at 72 h after treatment and had no effect on lipid peroxidation at any time point. In summary, ROFA, particularly its soluble fraction, generated a metal-dependent hydroxyl radical as measured by a cell-free ESR assay. However, cellular oxidant production and tissue injury were observed mostly with the ROFA-total and ROFA-insol. particulate forms. ROS generated by ROFA-sol. as measured by ESR appear not to play a major role in the lung injury caused after ROFA exposure.
authors.affiliation: Department of Safety and Environmental Management, College of Engineering and Mineral Resources, Morgantown, WV 26506, USA.
authors.forename: Anthony B
authors.initials: AB
authors.lastname: Lewis
authors.forename: Michael D
authors.initials: MD
authors.lastname: Taylor
authors.forename: Jenny R
authors.initials: JR
authors.lastname: Roberts
authors.forename: Stephen S
authors.initials: SS
authors.lastname: Leonard
authors.forename: Xianglin
authors.initials: X
authors.lastname: Shi
authors.forename: James M
authors.initials: JM
authors.lastname: Antonini
mesh_terms: D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D002244:Carbon / Q000008:administration & dosage / Q000633:toxicity*; D060729:Coal Ash; D004195:Disease Models, Animal; D004578:Electron Spin Resonance Spectroscopy; D015227:Lipid Peroxidation; D008163:Luminescent Measurements; D008171:Lung Diseases / Q000139:chemically induced* / Q000473:pathology; D008297:Male; D008670:Metals / Q000737:chemistry / Q000633:toxicity*; D052638:Particulate Matter; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism*; D012995:Solubility; D013997:Time Factors
chemical_list: D000393:Air Pollutants; D060729:Coal Ash; D008670:Metals; D052638:Particulate Matter; D017382:Reactive Oxygen Species; D002244:Carbon