Vaping additives cannabinoid oil and vitamin E acetate adhere to and damage the human airway epithelium.
E-cigarette
airway toxicity
cannabinoids
vaping
vitamin E acetate
Journal
Journal of applied toxicology : JAT
ISSN: 1099-1263
Titre abrégé: J Appl Toxicol
Pays: England
ID NLM: 8109495
Informations de publication
Date de publication:
05 2023
05 2023
Historique:
revised:
25
10
2022
received:
17
07
2022
accepted:
11
11
2022
pmc-release:
01
05
2024
medline:
14
4
2023
pubmed:
15
11
2022
entrez:
14
11
2022
Statut:
ppublish
Résumé
E-cigarette, or vaping product use-associated lung injury (EVALI), is a severe respiratory disorder that caused a sudden outbreak of hospitalized young people in 2019. Using cannabis oil containing vaping products, including vitamin E acetate contaminants, was found to be strongly associated with EVALI. However, the underlying tissue impacts of the condition are still largely unknown. Here, we focused on the vehicle cannabinoid oil (CBD oil) and contaminant vitamin E acetate (VEA) effects on airway epithelial cells. Primary human bronchial epithelial (HBE) cultures were exposed to e-liquid aerosols that contained CBD oil and VEA in combination or the common e-liquid components PG/VG with and without nicotine. Cell viability analysis indicated dramatically increased cell death counts after 3 days of CBD exposure, and this effect was even higher after CBD + VEA exposure. Microscopic examination of the cultures revealed cannabinoid and VEA depositions on the epithelial surfaces and cannabinoid accumulation in exposed cells, followed by cell death. These observations were supported by proteomic analysis of the cell secretions that exhibited increases in known markers of airway epithelial toxicity, such as xenobiotic enzymes, factors related to oxidative stress response, and cell death indicators. Overall, our study provides insights into the association between cannabinoid oil and vitamin E acetate vaping and lung injury. Collectively, our results suggest that the adherent accumulation of CBD oil on airway surfaces and the cellular uptake of both CBD oil- and VEA-containing condensates cause elevated metabolic stress, leading to increased cell death rates in human airway epithelial cultures.
Identifiants
pubmed: 36372912
doi: 10.1002/jat.4415
pmc: PMC10101868
mid: NIHMS1850425
doi:
Substances chimiques
Cannabinoids
0
Dronabinol
7J8897W37S
Vitamin E
1406-18-4
Acetates
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
680-693Subventions
Organisme : NHLBI NIH HHS
ID : R03 HL140402
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL135642
Pays : United States
Organisme : NHLBI NIH HHS
ID : P50 HL120100
Pays : United States
Informations de copyright
© 2022 John Wiley & Sons Ltd.
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