Chemico-Biological Interactions 166 (2007) 163–169 Atmospheric photochemical transformations enhance 1,3-butadiene-induced inflammatory responses in human epithelial cells: The role of ozone and other photochemical degradation products  Melanie Doyle a,∗ , Kenneth G. Sexton a , Harvey Jeffries a , Ilona Jaspers b a Department of Environmental Sciences and Engineering, University of North Carolina-Chapel Hill, CB #7431, Chapel Hill, NC 27599, USA b CEMLAB, University of North Carolina, Chapel Hill, NC, USA Available online 3 June 2006 Abstract Chemistry of hazardous air pollutants has been studied for many years, yet little is known about how these chemicals, once reacted within urban atmospheres, affect healthy and susceptible individuals. Once released into the atmosphere, 1,3-butadiene (BD) reacts with hydroxyl radicals and ozone (created by photochemical processes), to produce many identified and unidentified products. Once this transformation has occurred, the toxic potential of atmospheric pollutants such as BD in the ambient environment is currently unclear. During this study, environmental irradiation chambers (also called smog chambers), utilizing natural sunlight, were used to create photochemical transformations of BD. The smog chamber/in vitro exposure system was designed to investigate the toxicity of chemicals before and after photochemical reactions and to investigate interactions with the urban atmosphere using representative in vitro samples. In this study, we determined the relative toxicity and inflammatory gene expression induced by coupling smog chamber atmo- spheres with an in vitro system to expose human respiratory epithelial cells to BD, BDs photochemical degradation products, or the equivalent ozone generated within the photochemical mixture. Exposure to the photochemically generated products of BD (primarily acrolein, acetaldehyde, formaldehyde, furan and ozone) induced significant increases in cytotoxicity, IL-8, and IL-6 gene expression compared to a synthetic mixture of primary products that was created by injecting the correct concentrations of the detected products from the irradiation experiments. Interestingly, exposure to the equivalent levels of ozone generated during the photochemical transformation of BD did not induce the same level of inflammatory cytokine release for either exposure protocol, suggesting that the effects from ozone alone do not account for the entire response in the irradiation experiments. These results indicate that BDs full photochemical product generation and interactions, rather than ozone alone, must be carefully evaluated when investigating the possible adverse health effects to BD exposures. The research presented here takes into account that photochemical  This publication has not been formally reviewed by the American Chemistry Council. The views expressed in this document are solely those of Melanie Doyle, Dr. Kenneth Sexton, Dr. Harvey Jeffries, and Dr. Ilona Jaspers. Although the research described in this article has been funded wholly or in part by the United States Environmental Protection Agency through cooperative agreements CR829522 with the Center for Environmental Medicine, Asthma, and Lung Biology and R829762 with the Department of Environmental Science and Engineering at the University of North Carolina at Chapel Hill, it has not been subjected to the Agency’s required peer and policy review, and therefore does not necessarily reflect the views of the Agency and no official endorsement should be inferred. Mention of trade names or commercial products does not constitute endorsement or recommendation for use. ∗ Corresponding author. Tel.: +1 919 966 1372; fax: +1 919 966 7911. E-mail address: doylem@email.unc.edu (M. Doyle). 0009-2797/$ – see front matter © 2006 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.cbi.2006.05.016