Inhalation Co-Exposure to Ultrafine Carbon and Ozone Leads to Significant Pulmonary and Systemic Oxidative Stress
Public Domain
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2020/03/01
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Details
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Personal Author:Erdely A ; Goldsmith WT ; Hubczak J ; Hussain S ; Kelly EE ; Kodali VK ; Majumder N ; Mark RA ; Nurkiewicz TR ; Williams XM
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Description:Particles and gases are integral components of ambient air pollution and both contribute significantly in adverse health outcomes. Recent epidemiologic data indicates that possible synergistic interactions between these components mediate the adverse phenotypes. Mechanistically, gaseous components can modify the particle surfaces and can reach distal portions of the lung, owing to the deeper penetrability of ultrafine particles. We hypothesize that ultrafine particles of carbon black (CB) and ozone (O3) co-exposure will lead to significantly greater oxidative stress response in the lungs, heart and liver compared with individual/single toxicant exposures. We performed rodent (C57Bl/6J mice) whole-body inhalation exposures (air, CB, O3 or CB+O3) and studied acellular and cellular bimolecular free radical production by immuno-spin trapping. Mice were exposed to 2.0 +/- 0.02 ppm O3 and/or 10 +/- 0.6 mg/m3 CB for 3 hours (16 microg particle deposited dose). Aerosol mobility (140 +/- 2 nm), and aerodynamic (84 +/- 1 nm) diameters were measured by scanning mobility particle analyzer (SMPS 3938) and an electrical low-pressure impactor (ELPI+). Fourier transformed infrared (FTIR) spectroscopy demonstrated significant alteration in particle surface functional group composition after interaction with O3. Ferric reducing ability of serum (FRAS) assay demonstrated significantly greater acellular oxidative potentials for co-exposure aerosol. A significantly greater increase in pulmonary and distal organ free radical production, xanthine oxidase activity and gene expression occurred after co-exposures compared with single exposures. In conclusion, our studies confirm interaction of gaseous and particle components of air pollution. By demonstrating distal organ oxidative stress response after pulmonary exposure, we describe a potential pathophysiologic mechanism for cardiovascular and hepatic dysfunction by air pollution exposure. Further mechanistic studies are underway to elaborate these findings using organoids and disease animal models. [Description provided by NIOSH]
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ISSN:1096-6080
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Volume:174
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Issue:1
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NIOSHTIC Number:nn:20058976
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Citation:Toxicologist 2020 Mar; 174(1):367
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Federal Fiscal Year:2020
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Peer Reviewed:False
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Source Full Name:The Toxicologist. Society of Toxicology 59th Annual Meeting and ToxExpo, March 15-19, 2020, Anaheim, California
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Main Document Checksum:urn:sha-512:12f6e425bfd7c1e79bee897249c39f44f0e50367ea5215a9021c8c529ee6e3233c6d5d0831f694515d4c248929e0c716e227041b15b2b4fe31559b5c0f862430
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