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Gene Expression Profiling in Human Lung Cells Exposed to Isoprene-Derived Secondary Organic Aerosol Ying-Hsuan Lin, Maiko Arashiro, Phillip W. Clapp, Tianqu Cui, Kenneth G. Sexton, William Vizuete, Avram Gold, Ilona Jaspers, Rebecca C Fry, and Jason Douglas Surratt Environ. Sci. Technol., Just Accepted Manuscript • DOI: 10.1021/acs.est.7b01967 • Publication Date (Web): 21 Jun 2017 Downloaded from http://pubs.acs.org on June 25, 2017
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Environmental Science & Technology
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Gene Expression Profiling in Human Lung Cells Exposed to Isoprene-Derived
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Secondary Organic Aerosol
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Ying-Hsuan Lin,1,a,* Maiko Arashiro,1,b Phillip W. Clapp,2 Tianqu Cui,1 Kenneth G. Sexton,1
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William Vizuete,1 Avram Gold,1 Ilona Jaspers,1,2,3 Rebecca C. Fry,1 and Jason D. Surratt1, *
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Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, United States 2 Center for Environmental Medicine, Asthma and Lung Biology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, United States 3 Department of Pediatrics, School of Medicine, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, United States a Current address: Department of Environmental Sciences, Environmental Toxicology Graduate Program, University of California, Riverside, California 92521, United States b Current address: Department of Environmental Studies, Dickinson College, Carlisle, Philadelphia 17013, United States *
To whom correspondence should be addressed. Tel.: (951)-827-3785. Fax: (951)-827-4652. Email:
[email protected] (Y.-H. L) Tel.: (919)-966-0470. Fax: (919)-966-7911. Email:
[email protected] (J.D.S.)
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Abstract
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Secondary organic aerosol (SOA) derived from the photochemical oxidation of isoprene
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contributes a substantial mass fraction to atmospheric fine particulate matter (PM2.5). The
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formation of isoprene SOA is influenced largely by anthropogenic emissions through multiphase
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chemistry of its multi-generational oxidation products. Considering the abundance of isoprene
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SOA in the troposphere, understanding mechanisms of adverse health effects through inhalation
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exposure is critical to mitigating its potential impact on public health. In this study, we assessed
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the effects of isoprene SOA on gene expression in human airway epithelial cells (BEAS-2B)
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through an air-liquid interface exposure. Gene expression profiling of 84 oxidative stress and 249
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inflammation-associated human genes was performed. Our results show that the expression
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levels of 29 genes were significantly altered upon isoprene SOA exposure under non-cytotoxic
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conditions (p