ArticleHeart rhythm2026
Oxidative stress mediates cardiac electrophysiological injury in inhalation exposure to flavored vaping products.
Article in Heart rhythm, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundElectronic nicotine delivery systems (ENDS) use "E-liquids" to generate "E-vapor," an inhalable aerosolized mixture containing nicotine and flavors. Flavored ENDS are very popular among teens who vape, however, the possible cardiac electrophysiological harm of inhalation exposure to flavored ENDS are not fully understood.
objectiveTo test if inhalation exposure to flavoring carbonyls in E-liquids compromises mitochondrial integrity, increases oxidative stress, and leads to cardiac electrophysiological toxicity.
methodsGas chromatography mass spectrometry (GC/MS), and flow cytometry, oxygen consumption rate measurement, in vivo programmed electrical stimulation (PES), and multielectrode array (MEA) were used in atrial like HL-1 myocytes, human induced pluripotent stem cells-derived cardiomyocytes, and in mice overexpressing the antioxidant mitochondrial catalase (mCAT) exposed to flavored E-vapor.
resultsWe compared the toxicity of E-vapor exposure from 30 differently flavored E-liquids (70% vegetable glycerin, 30% propylene glycol, with 6 mg/mL nicotine) in HL-1 cells using apoptotic annexin V flow cytometry. The toxicity of most E-liquids was significantly higher than air control. We subsequently determined the composition and quantified the concentrations of major flavoring carbonyls (cinnamaldehyde, vanillin, ethyl vanillin, maltol, and ethyl maltol) in the E-liquids using GC/MS. Linear regression analysis showed that toxicity correlated with carbonyl concentration. We then measured in HL-1 cells exposed to vanilla flavored E-vapor reactive oxygen species (ROS) and mitochondrial membrane potential (ΔΨ) with flow cytometry, respectively. ROS increased in exposed cells, but this was prevented by N-acetylcysteine antioxidant pretreatment, and ΔΨ was depolarized in exposed cells. In vivo inhalation exposure to vanilla flavored E-vapor increased the duration of PES-induced ventricular tachycardia in wild type but not in mCAT mice, compared with air controls. Finally, MEA recordings in hiPSC-derived cardiomyocytes monolayers exposed to vanilla flavored E-vapor, with or without nicotine, resulted in decreased activation time, and increased corrected field potential duration.
conclusionInhalation exposure to flavored ENDS negatively affects ventricular electrophysiology, in part via adverse mitochondrial remodeling, and increased oxidative stress.
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