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Gene Expression Profiling in Human Lung Cells Exposed to Isoprene-Derived Secondary Organic Aerosol.
Environ Sci Technol. 2017 Jul 18; 51(14):8166-8175.ES

Abstract

Secondary organic aerosol (SOA) derived from the photochemical oxidation of isoprene contributes a substantial mass fraction to atmospheric fine particulate matter (PM2.5). The formation of isoprene SOA is influenced largely by anthropogenic emissions through multiphase chemistry of its multigenerational oxidation products. Considering the abundance of isoprene SOA in the troposphere, understanding mechanisms of adverse health effects through inhalation exposure is critical to mitigating its potential impact on public health. In this study, we assessed the effects of isoprene SOA on gene expression in human airway epithelial cells (BEAS-2B) through an air-liquid interface exposure. Gene expression profiling of 84 oxidative stress and 249 inflammation-associated human genes was performed. Our results show that the expression levels of 29 genes were significantly altered upon isoprene SOA exposure under noncytotoxic conditions (p < 0.05), with the majority (22/29) of genes passing a false discovery rate threshold of 0.3. The most significantly affected genes belong to the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) transcription factor network. The Nrf2 function is confirmed through a reporter cell line. Together with detailed characterization of SOA constituents, this study reveals the impact of isoprene SOA exposure on lung responses and highlights the importance of further understanding its potential health outcomes.

Authors+Show Affiliations

Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, ‡Center for Environmental Medicine, Asthma and Lung Biology, School of Medicine, and §Department of Pediatrics, School of Medicine, The University of North Carolina , Chapel Hill, North Carolina 27599, United States.Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, ‡Center for Environmental Medicine, Asthma and Lung Biology, School of Medicine, and §Department of Pediatrics, School of Medicine, The University of North Carolina , Chapel Hill, North Carolina 27599, United States.Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, ‡Center for Environmental Medicine, Asthma and Lung Biology, School of Medicine, and §Department of Pediatrics, School of Medicine, The University of North Carolina , Chapel Hill, North Carolina 27599, United States.Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, ‡Center for Environmental Medicine, Asthma and Lung Biology, School of Medicine, and §Department of Pediatrics, School of Medicine, The University of North Carolina , Chapel Hill, North Carolina 27599, United States.Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, ‡Center for Environmental Medicine, Asthma and Lung Biology, School of Medicine, and §Department of Pediatrics, School of Medicine, The University of North Carolina , Chapel Hill, North Carolina 27599, United States.Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, ‡Center for Environmental Medicine, Asthma and Lung Biology, School of Medicine, and §Department of Pediatrics, School of Medicine, The University of North Carolina , Chapel Hill, North Carolina 27599, United States.Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, ‡Center for Environmental Medicine, Asthma and Lung Biology, School of Medicine, and §Department of Pediatrics, School of Medicine, The University of North Carolina , Chapel Hill, North Carolina 27599, United States.Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, ‡Center for Environmental Medicine, Asthma and Lung Biology, School of Medicine, and §Department of Pediatrics, School of Medicine, The University of North Carolina , Chapel Hill, North Carolina 27599, United States.Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, ‡Center for Environmental Medicine, Asthma and Lung Biology, School of Medicine, and §Department of Pediatrics, School of Medicine, The University of North Carolina , Chapel Hill, North Carolina 27599, United States.Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, ‡Center for Environmental Medicine, Asthma and Lung Biology, School of Medicine, and §Department of Pediatrics, School of Medicine, The University of North Carolina , Chapel Hill, North Carolina 27599, United States.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28636383

Citation

Lin, Ying-Hsuan, et al. "Gene Expression Profiling in Human Lung Cells Exposed to Isoprene-Derived Secondary Organic Aerosol." Environmental Science & Technology, vol. 51, no. 14, 2017, pp. 8166-8175.
Lin YH, Arashiro M, Clapp PW, et al. Gene Expression Profiling in Human Lung Cells Exposed to Isoprene-Derived Secondary Organic Aerosol. Environ Sci Technol. 2017;51(14):8166-8175.
Lin, Y. H., Arashiro, M., Clapp, P. W., Cui, T., Sexton, K. G., Vizuete, W., Gold, A., Jaspers, I., Fry, R. C., & Surratt, J. D. (2017). Gene Expression Profiling in Human Lung Cells Exposed to Isoprene-Derived Secondary Organic Aerosol. Environmental Science & Technology, 51(14), 8166-8175. https://doi.org/10.1021/acs.est.7b01967
Lin YH, et al. Gene Expression Profiling in Human Lung Cells Exposed to Isoprene-Derived Secondary Organic Aerosol. Environ Sci Technol. 2017 Jul 18;51(14):8166-8175. PubMed PMID: 28636383.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Gene Expression Profiling in Human Lung Cells Exposed to Isoprene-Derived Secondary Organic Aerosol. AU - Lin,Ying-Hsuan, AU - Arashiro,Maiko, AU - Clapp,Phillip W, AU - Cui,Tianqu, AU - Sexton,Kenneth G, AU - Vizuete,William, AU - Gold,Avram, AU - Jaspers,Ilona, AU - Fry,Rebecca C, AU - Surratt,Jason D, Y1 - 2017/07/05/ PY - 2017/6/22/pubmed PY - 2018/1/13/medline PY - 2017/6/22/entrez SP - 8166 EP - 8175 JF - Environmental science & technology JO - Environ Sci Technol VL - 51 IS - 14 N2 - Secondary organic aerosol (SOA) derived from the photochemical oxidation of isoprene contributes a substantial mass fraction to atmospheric fine particulate matter (PM2.5). The formation of isoprene SOA is influenced largely by anthropogenic emissions through multiphase chemistry of its multigenerational oxidation products. Considering the abundance of isoprene SOA in the troposphere, understanding mechanisms of adverse health effects through inhalation exposure is critical to mitigating its potential impact on public health. In this study, we assessed the effects of isoprene SOA on gene expression in human airway epithelial cells (BEAS-2B) through an air-liquid interface exposure. Gene expression profiling of 84 oxidative stress and 249 inflammation-associated human genes was performed. Our results show that the expression levels of 29 genes were significantly altered upon isoprene SOA exposure under noncytotoxic conditions (p < 0.05), with the majority (22/29) of genes passing a false discovery rate threshold of 0.3. The most significantly affected genes belong to the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) transcription factor network. The Nrf2 function is confirmed through a reporter cell line. Together with detailed characterization of SOA constituents, this study reveals the impact of isoprene SOA exposure on lung responses and highlights the importance of further understanding its potential health outcomes. SN - 1520-5851 UR - https://www.unboundmedicine.com/medline/citation/28636383/Gene_Expression_Profiling_in_Human_Lung_Cells_Exposed_to_Isoprene_Derived_Secondary_Organic_Aerosol_ L2 - https://doi.org/10.1021/acs.est.7b01967 DB - PRIME DP - Unbound Medicine ER -