Simulated burn pit smoke condensates cause sustained impact on human airway epithelial cells

Arunava Ghosh; Keith L Rogers Jr; Samuel C Gallant; Stephanie A Brocke; Adam M Speen; Yong Ho Kim; M Ian Gilmour; Scott H Randell; Ilona Jaspers

doi:10.1093/toxsci/kfae161

Simulated burn pit smoke condensates cause sustained impact on human airway epithelial cells

Toxicol Sci. 2024 Dec 14:kfae161. doi: 10.1093/toxsci/kfae161. Online ahead of print.

Authors

Affiliations

¹ Center for Environmental Medicine, Asthma, and Lung Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA.
² Curriculum in Toxicology and Environmental Medicine, University of North Carolina at Chapel Hill, 116 Manning Drive, Chapel Hill, NC, 27599-7310, USA.
³ Marsico Lung Institute, University of North Carolina at Chapel Hill, Chapel Hill, USA.
⁴ Public Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment, U.S. Environmental Protection Agency, Research Triangle Park, NC, 27711, USA.
⁵ Department of Environmental Sciences and Engineering (ESE), Gillings School of Global Public Health, University of North Carolina at Chapel Hill.

PMID: 39673801
DOI: 10.1093/toxsci/kfae161

Abstract

Inhalation of smoke from burn pits during military deployment is associated with several adverse pulmonary outcomes. We exposed human airway epithelial cells to smoke condensates from burn pit waste materials. Single and repeated exposure of condensates triggered unique and common responses in terms of gene expression, that sustained through the recovery phase. Source material and combustion condition influenced the outcome. Intensified response in female donor cells indicated a determining role of biological sex. The observations indicate a lasting impact of burn pit smoke exposure on epithelial gene expression, potentially contributing to disease pathogenesis.

Keywords: Burn pit waste; RNA sequencing; human airway epithelial cells; sex differences.