Abstract

BackgroundElectronic cigarette use is on the rise despite a number of reports linking electronic cigarettes with adverse health outcomes. Recent studies have suggested that alterations in lipid signaling may be one mechanism by which electronic cigarettes contribute to lung pulmonary function. Vitamin E acetate, for example, is synthetic form of Vitamin E transported via lipids, found to be associated with electronic cigarette associated lung injury. Lipids are absolutely critical for normal lung physiology and perturbations in a number of lipid pathways have been associated with respiratory illness. Is it conceivable that electronic cigarette use even in seemingly healthy cohorts are associated with alterations in lipid pathways?MethodsTo investigate quantitative alterations in the plasma lipidome associated with electronic cigarette use in healthy we obtained plasma samples from 119 male and female participants with who were either: (1) chronic tobacco cigarette (TC) smokers (> 12 months of self-reported TC use), (2) chronic Electronic cigarette (EC) users (> 12 months of self-reported EC use), or (3) non-users. We measured quantitative lipid species across different lipid sub-classes from plasma samples using the Sciex Lipidyzer.ResultsWe found that male and female tobacco and electronic cigarette users had distinct lipidome signatures across a number of lipid species although the vast majority of lipids were unchanged when compared to non-users. Intriguingly, we found that female but not male electronic cigarette users had lower levels of plasmalogens, critical glycerophospholipids secreted by alveoli and required for normal surfactant function.ConclusionsIn summary, our study does not reveal striking changes associated with electronic cigarette use but we observed sex-specific changes in lipids known to be critical for lung function.

Highlights

  • Electronic cigarette use is on the rise despite a number of reports linking electronic cigarettes with adverse health outcomes

  • Liquid components of Electronic cigarettes (ECIGS) such as propylene glycol and glycerol can theoretically interfere with critical lipid metabolic reactions but whether ECIG use in humans is associated with perturbations in lipid homeostasis and how ECIG use compare with TCIG use remains unexplored

  • Principal component analysis (PCA), a technique that summarizes the variation in samples and strong patterns in datasets, showed significant overlap between samples across groups for both males (Fig. 1b) and females (Fig. 1c) consistent with the notion that TCIG or ECIG use do not globally alter lipid composition

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Summary

Introduction

Electronic cigarette use is on the rise despite a number of reports linking electronic cigarettes with adverse health outcomes. Recent studies have suggested that alterations in lipid signaling may be one mechanism by which electronic cigarettes contribute to lung pulmonary function. Lipids are absolutely critical for normal lung physiology and perturbations in a number of lipid pathways have been associated with respiratory illness. Is it conceivable that electronic cigarette use even in seemingly healthy cohorts are associated with alterations in lipid pathways?. A subset of vaping associated pulmonary diseases have been associated with lipid overload of immune cells and more recent evidence suggested that changes in specific lipids such as the isoprenoid Vitamin E acetate is associated with acute lung injury [8, 10]. Liquid components of ECIGS such as propylene glycol and glycerol can theoretically interfere with critical lipid metabolic reactions but whether ECIG use in humans is associated with perturbations in lipid homeostasis and how ECIG use compare with TCIG use remains unexplored

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