Vaping additives cannabinoid oil and vitamin E acetate adhere to and damage the human airway epithelium.


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
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

680-693

Subventions

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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Auteurs

Boris Reidel (B)

Marsico Lung Institute, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Department of Pathology and Laboratory Medicine, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

Sabri Abdelwahab (S)

Marsico Lung Institute, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Department of Cell Biology and Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

Joe Alexander Wrennall (JA)

Marsico Lung Institute, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Department of Cell Biology and Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

Phillip W Clapp (PW)

Department of Pediatrics, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

Jessica L Beers (JL)

Division of Pharmacotherapy and Experimental Therapeutics, Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

Klarissa D Jackson (KD)

Division of Pharmacotherapy and Experimental Therapeutics, Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

Robert Tarran (R)

Marsico Lung Institute, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Department of Cell Biology and Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

Mehmet Kesimer (M)

Marsico Lung Institute, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Department of Pathology and Laboratory Medicine, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

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Classifications MeSH