ArticleAmerican journal of physiology. Lung cellular and molecular physiology2022
Aerosolized vitamin E acetate causes oxidative injury in mice and in alveolar macrophages.
Article in American journal of physiology. Lung cellular and molecular physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
- Vaping-related lung disease: a narrative review.Journal of thoracic disease · 2026Review
- Differential Regulatory Effects of Cannabinoids and Vitamin E Analogs on Cellular Lipid Homeostasis and Inflammation in Human Macrophages.Antioxidants (Basel, Switzerland) · 2026Article
- Biological sex modulates lung injury severity in adolescent mice exposed to short-term aerosolized vitamin E acetate.Physiological reports · 2025Article
- Gut Microbiota-Derived Lipopolysaccharides and Short-Chain Fatty Acids Regulate Immune Responses via FFAR2/FFAR3 in Lung Ischemia-Reperfusion Injury.Annals of the New York Academy of Sciences · 2025Article
- A mouse model of E-cigarette or vaping product use-associated lung injury (EVALI) induced by nose-only exposure to aerosolized vitamin E acetate and associated macrophage dysfunction.Respiratory research · 2025Article
- Chronic airway inflammatory diseases and e-cigarette use: a review of health risks and mechanisms.European journal of medical research · 2025Review
- E-cigarette or vaping product use-associated lung injury (EVALI). A case report of a 19-year-old male in Denmark.European clinical respiratory journal · 2025Article
- Vitamin E Acetate Is Associated with Select Proinflammatory Cytokines: An Analysis of a 2020-2022 Cohort of EVALI Patients.American journal of respiratory and critical care medicine · 2024Article
- Comparison of emissions across tobacco products: A slippery slope in tobacco control.Tobacco induced diseases · 2024Review
- Lipid from electronic cigarette-aerosol both with and without nicotine induced pro-inflammatory macrophage polarization and disrupted phagocytosis.Journal of inflammation (London, England) · 2023Article
- Multi-omic assessment shows dysregulation of pulmonary and systemic immunity to e-cigarette exposure.Respiratory research · 2023Article
- Pathogenesis of E-Cigarette Vaping Product Use-Associated Lung Injury (EVALI).Comprehensive Physiology · 2023Article
- External Factors Modulating Vaping-Induced Thermal Degradation of Vitamin E Acetate.Chemical research in toxicology · 2023Article
- Aerosolized nicotine from e-cigarettes alters gene expression, increases lung protein permeability, and impairs viral clearance in murine influenza infection.Frontiers in immunology · 2023Article
- E-cigarette vaping associated acute lung injury (EVALI): state of science and future research needs.Critical reviews in toxicology · 2022Review
- The implications of Vitamin E acetate in E-cigarette, or vaping, product use-associated lung injury.Annals of thoracic medicineReview
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Although vitamin E acetate (VEA) is suspected to play a causal role in the development of electronic-cigarette, or vaping, product use-associated lung injury (EVALI), the underlying biological mechanisms of pulmonary injury are yet to be determined. In addition, no study has replicated the systemic inflammation observed in humans in a murine EVALI model, nor investigated potential additive toxicity of viral infection in the setting of exposure to vaping products. To identify the mechanisms driving VEA-related lung injury and test the hypothesis that viral infection causes additive lung injury in the presence of aerosolized VEA, we exposed mice to aerosolized VEA for extended times, followed by influenza infection in some experiments. We used mass spectrometry to evaluate the composition of aerosolized VEA condensate and the VEA deposition in murine or human alveolar macrophages. Extended vaping for 28 days versus 15 days did not worsen lung injury but caused systemic inflammation in the murine EVALI model. Vaping plus influenza increased lung water compared with virus alone. Murine alveolar macrophages exposed to vaped VEA hydrolyzed the VEA to vitamin E with evidence of oxidative stress in the alveolar space and systemic circulation. Aerosolized VEA also induced cell death and chemokine release and reduced efferocytotic function in human alveolar macrophages in vitro. These findings provide new insights into the biological mechanisms of VEA toxicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.