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Arch Toxicol

Title:		Electronic cigarette aerosols induce oxidative stress-dependent cell death and NF-kappaB mediated acute lung inflammation in mice
Author(s):		Ma T; Wang X; Li L; Sun B; Zhu Y; Xia T;
Address:		"Division of Nanomedicine, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, 90095-1772, USA. Department of Environmental Health Sciences, Jonathan and Karin Fielding School of Public Health, University of California, Los Angeles, CA, 90095-1772, USA. State Key Laboratory of Fine Chemicals, School of Chemical Engineering, Dalian University of Technology, 2 Linggong Road, Dalian, 116024, China. Department of Environmental Health Sciences, Jonathan and Karin Fielding School of Public Health, University of California, Los Angeles, CA, 90095-1772, USA. Yifang@ucla.edu. Division of Nanomedicine, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, 90095-1772, USA. txia@ucla.edu"
Journal Title:		Arch Toxicol
Year:		2021
Volume:		20201107
Issue:		1
Page Number:		195 - 205
DOI:		10.1007/s00204-020-02920-1
ISSN/ISBN:		1432-0738 (Electronic) 0340-5761 (Print) 0340-5761 (Linking)
Abstract:		"Electronic cigarette (e-cigarette) use has been linked to recent acute lung injury case clusters in over 2000 patients and dozens of deaths in the United States, however, the mechanism leading to lung injury is not certain although ultrafine particles, heavy metals, volatile organic compounds, and other harmful ingredients have been implicated. To systematically evaluate e-cigarette toxicity, we generated e-cigarette aerosols by varying the puff numbers (20-480), nicotine contents (0-24 mg/mL), and collected e-cigarette samples through an impinger system for biological assays. The calculated samples' concentration ranged from 1.96 to 47.06 mg/mL. THP-1 monocyte-differentiated macrophages, BEAS-2B bronchial epithelial cells, wild-type C57BL/6 mice, and NF-kappaB-luc transgenic mice were used to test the effects of these samples. E-cigarette samples showed cytotoxicity to THP-1 cells and BEAS-2B in vitro, leading to increased oxidative stress, inflammatory cytokine production with or without nicotine, and cell death. Furthermore, aerosol generated from PG is more toxic than VG. The toxicity of e-cigarette samples is at least partially due to the reactive oxygen species and aldehydes, which are generated during the aerosolization processes by the e-cigarette device. After NF-kappaB-luc mice exposed with e-cigarette samples by oropharyngeal aspiration, NF-kappaB expressions were observed in a dose-response fashion with or without nicotine. In addition, the e-cigarette samples induced neutrophil infiltration, IL-1beta production, oxidative stress marker heme oxygenase-1 expression in wild-type C57BL/6 mice. These results suggested that oxidative stress, pro-inflammatory NF-kappaB pathway activation, and cell death are involved in e-cigarette aerosol-induced acute lung inflammation"
Keywords:		"Aerosols Aldehydes/metabolism Animals Cell Death/drug effects Cytokines/metabolism E-Cigarette Vapor/*toxicity Humans Inhalation Exposure Lung/*drug effects/immunology/metabolism/pathology Macrophages/drug effects/immunology/metabolism Mice, Inbred C57BL;"
Notes:		"MedlineMa, Tiancong Wang, Xiang Li, Liqiao Sun, Bingbing Zhu, Yifang Xia, Tian eng R01 HL139379/HL/NHLBI NIH HHS/ NHLBI R01 HL139379/HL/NHLBI NIH HHS/ Research Support, N.I.H., Extramural Germany 2020/11/08 Arch Toxicol. 2021 Jan; 95(1):195-205. doi: 10.1007/s00204-020-02920-1. Epub 2020 Nov 7"