Summary
Introduction:
This text provides an in-depth analysis of a study examining the pulmonary toxicity of aerosolized Vitamin E acetate (VEa) in mice and human alveolar epithelial cells. The study aims to understand the role of VEa in the development of Electronic-cigarette, or vaping, product use –associated lung injury (EVaLI). The key points and main message of the text are summarized below.
Key Points:
* The study exposed adult mice and primary human alveolar epithelial type II (aT II) cells to an aerosol of VEa generated by a device designed for vaping oils.
* Mice exposed to VEa aerosol showed dose-dependent increases in lung water, BaL protein, BaL neutrophils, oil-laden macrophages, multinucleated giant cells, and in inflammatory cytokines.
* VEa aerosol was toxic to aT II cells, causing increased cell death and the release of monocyte and neutrophil chemokines.
* VEa was directly absorbed by aT II cells, resulting in the differential gene expression of several inflammatory biological pathways.
* JUUL aerosol exposure was used as a comparison and showed no significant toxicity in mice or aT II cells.
* The study suggests that VEa plays an important causal role in EVaLI, given the epidemiological and clinical characteristics of the outbreak.
Main Message:
The study provides compelling evidence that aerosolized VEa has direct pulmonary toxicity, which is consistent with the observed pattern in humans with EVaLI. The results strengthen the conclusion that VEa plays a causal role in this syndrome of acute respiratory failure clinically recognized as vaping-associated lung injury. Therefore, it is crucial to regulate the use of VEa in e-cigarettes and vaping products to prevent the development of EVaLI.
Citation
Matsumoto S, Fang X, Traber MG, et al. Dose-Dependent Pulmonary Toxicity of aerosolized Vitamin E acetate. american journal of respiratory cell and molecular biology. 2020;63(6):748-757. doi:10.1165/rcmb.2020-0209OC
