Electronic and Tobacco Cigarettes Alter Polyunsaturated Fatty Acids and Oxidative Biomarkers

Abstract

Rationale: Chronic electronic cigarette (EC) users exhibit a higher susceptibility of LDL (low-density lipoprotein) to undergo oxidation as compared with nonuser controls. However, there is a paucity of data regarding EC effects on lipid peroxidation in the blood and their relationship to cardiovascular risk. Objective: To test the hypothesis that chronic (≥1 year) EC use exerts intermediate effects on plasma lipid peroxidation and/or antioxidant defense compared with chronic tobacco cigarette (TC) smoking. Methods and Results: We enrolled EC-users (n=32), TC-smokers (n=29), and nonusers (n=45), with mean ages of 28.3, 27.8, and 27.4 years, respectively. Plasma concentrations of free polyunsaturated fatty acids and oxidized metabolites were assessed by mass spectrometry. Total antioxidant capacity, concentrations of glutathione, bilirubin, HO-1 (heme oxygenase-1), and functional activity of PON1 (paraoxonase1) were determined by colorimetric and enzymatic assays. Multivariable analysis was performed using classification models for segregating participants based on biomarker profiles. TC-smokers exhibited higher plasma arachidonic acid concentration. Instead, EC-users displayed lower plasma concentrations of both arachidonic acid and linoleic acid as compared to non-users and TC-smokers ( P <0.05). Oxidized linoleic acid metabolites (9- and 13-hydroxyoctadecadienoic acid) were lower in EC-users and TC-smokers as compared with nonusers ( P <0.001). Consistently, total antioxidant capacity and bilirubin were elevated in EC-users and TC-smokers as compared with nonusers ( P <0.05). Of interest, plasma HO-1 concentration was higher in TC-smokers as compared with nonusers ( P =0.01) with intermediate levels in EC-users. Multivariable analysis identified 5 biomarkers (13-hydroxyoctadecadienoic acid, linoleic acid, 9-hydroxyoctadecadienoic acid, 12-hydroxyeicosatetraenoic acid, arachidonic acid) that discriminated EC-users from TC-smokers and nonusers with an accuracy of 73.4%. Conclusions: Chronic use of EC induces common (ie, lower 9- and/or 13-hydroxyoctadecadienoic acids and higher total antioxidant capacity and bilirubin) as well as differential effects (ie, altered arachidonic acid and linoleic acid concentrations) to those induced by TC, along with intermediate plasma HO-1 concentration, suggesting that EC, likewise TC smoke, could impact cardiovascular risk.