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Transcriptomic and Functional Responses of Human Airway Cells to Vaped ∆8-THC and its Oxidation Product ∆8-THCQ

ABSTRACT: Δ8-tetrahydrocannabinol (Δ8-THC) vaping products rapidly expanded following the 2018 Farm Bill, yet remain largely unregulated despite high cannabinoid concentrations, additives and contaminants, and growing links to adverse respiratory outcomes. Here we show that the reactive electrophile Δ8-THC quinone (Δ8-THCQ, HU-336) is present in significant quantities in commercial Δ8-THC distillate and disposable products and increases after vaping. Across high concentration products, Δ8-THCQ rose an average of 3.67-fold, reaching millimolar levels. While Δ8-THC itself produced no measurable transcriptomic response in a bronchial epithelial cell line, Δ8-THCQ markedly altered gene expression, prominently upregulating cilia and stress related programs alongside xenobiotic metabolism and inflammatory pathways. Using primary differentiated human bronchial epithelial cells exposed with the UNC Vaping Product Exposure System (VaPES), we demonstrate that vaped commercial Δ8-THC mixtures induce immediate early stress genes, suppress ribosome and mitochondrial pathways, and trigger fibrosis associated signaling, while juices caused comparatively modest effects, primarily limited to upregulation of cell-cycle and proliferation-associated genes. Computational analysis further mechanistically linked coordinated chemical features of Δ8-THC aerosols to the airway transcriptional programs they induced, identifying clusters of chemicals that drive specific biological responses. Functionally, distillate and disposable aerosols rapidly impaired motile cilia activity. Together, these data identify Δ8-THCQ as a major vaping-generated reactive product in Δ8-THC aerosols and suggest that repeated inhalation may disrupt mucociliary defense and promote chronic airway injury.

ORGANISM(S): Homo sapiens

PROVIDER: GSE320065 | GEO | 2026/02/21

REPOSITORIES: GEO

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Project description:Study Smoking and COPD are associated with decreased mucociliary clearance and healthy smokers have shorter cilia in the large airway than nonsmokers. Intraflagellar transport (IFT) is the process by which cilia are produced and maintained. We assessed expression of IFT-related genes in smokers and nonsmokers and evaluated cilia length in the large and small airway of nonsmokers, healthy smokers, and smokers with COPD. Methods Airway epithelium was obtained via bronchoscopic brushing. Affymetrix microarrays were used to evaluate IFT gene expression in 2 independent data sets from large and small airway. Cilia length was assessed by measuring 100 cilia (10 cilia on each of 10 cells) per subject. Results All 40 IFT genes were expressed in the human large and small airway epithelium. In the large airway, 10 IFT genes were down-regulated and 1 up-regulated in smokers. In the small airway, 11 genes were down-regulated and 3 up-regulated in smokers. A set of 8 IFT genes was down-regulated in both data sets. In the large and small airway epithelium, cilia were significantly shorter in healthy smokers than nonsmokers, and significantly shorter in COPD smokers than in both healthy smokers and nonsmokers. Answer to the Question These results support the concept that loss of cilia length contributes to defective mucociliary clearance in COPD, and that smoking-induced changes in expression of IFT genes may be one mechanism of abnormally short cilia in smokers. Strategies to normalize cilia length may be an important avenue for novel COPD therapies. Gene expression was assessed for 40 intraflagellar transport related genes in the LAE of nonsmokers (n=21) and healthy smokers (n=31) and the SAE of an independent group of nonsmokers (n=28) and healthy smokers (n=69). Cilia length was assessed in a total of 228 airway epithelium samples, including 120 LAE samples and 108 SAE samples; a subset of the 228 samples is represented among the 149 samples in this Series.

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Transcriptomic and Functional Responses of Human Airway Cells to Vaped ∆8-THC and its Oxidation Product ∆8-THCQ

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