How vitamin E acetate might injure vapers’ lungs 维生素E醋酸盐如何伤害Vapers的肺


News Release 16-Sep-2020

American Chemical Society

Research News

E-cigarette, or vaping, associated lung injury (EVALI) has sickened thousands of people, most under the age of 35. Studies have linked vitamin E acetate, an oily substance in some vaping liquids, to the disorder. Now, researchers reporting in ACS’ Chemical Research in Toxicology have uncovered a possible mechanism: Vitamin E acetate could increase the fluidity of lung surfactant, causing the surfactant layer to collapse, contributing to symptoms such as shortness of breath and lung inflammation.

电子烟(或电子烟)引起的肺部疾病(EVALI)使成千上万的人患病,其中大多数年龄在35岁以下。研究已将维生素E乙酸酯(某些电子烟液中的一种油性物质)与该疾病联系在一起。 现在,在ACS毒理学化学研究中报告的研究人员发现了一种可能的机制:醋酸维生素E可以增加肺表面活性剂的流动性,导致表面活性剂层塌陷,导致呼吸急促和肺部炎症等症状。

The lungs are made up of alveoli, which are tiny cavities where gas exchange takes place. Oxygen that is breathed in diffuses across the alveolar membrane and into the capillaries, while carbon dioxide passes in the opposite direction to be exhaled. Lung surfactant, a fluid made up of lipids and proteins, coats the inner surface of the alveoli, reducing the surface tension so that the alveoli can easily inflate when someone inhales. Scientists still don’t know exactly how the surfactant layer expands and contracts when a person breathes in and out, but one hypothesis is that certain lipids get “squeezed out” or expelled when the alveoli contract, and then spread across the surface again when the alveoli expand. Drew Marquardt and colleagues wondered how vitamin E acetate, which has been found in the lungs of most EVALI patients but not in healthy controls, could influence this process.

To find out, the researchers added increasing amounts of vitamin E acetate to two model lung surfactants in the lab: one containing only the lipid DPPC (the primary component of lung surfactant), and the other containing a mixture of the four major lipids in the fluid. Using a combination of neutron spin echo and small-angle neutron scattering, the team found that increasing vitamin E acetate concentration increased membrane fluidity and compressibility for both model surfactants, up to a plateau. These findings suggest that, in the presence of the vaping additive, the lung surfactant monolayer could “squeeze out” lipids prematurely during exhalation, thereby becoming unstable. However, the researchers note that these experiments were conducted in a model system without protein components or alveoli, so more work still needs to be done.

The authors acknowledge funding from the Natural Sciences and Engineering Research Council of Canada, the Ontario Graduate Scholarship program, the National Institute of Standards and Technology, the Center for High Resolution Neutron Scattering, the National Science Foundation, the WE-SPARK Health Institute and the University of Windsor.

The abstract that accompanies this paper is available here.

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