In Vitro Biological Effects of E-Cigarette on the Cardiovascular System-Pro-Inflammatory Response Enhanced by the Presence of the Cinnamon Flavor.
Marine MichonClément MercierClaudie PetitLara LeclercLaurent BertolettiJérémie PourchezValérie ForestPublished in: Toxics (2022)
The potential cardiovascular effects of e-cigarettes remain largely unidentified and poorly understood. E-liquids contain numerous chemical compounds and can induce exposure to potentially toxic ingredients (e.g., nicotine, flavorings, etc.). Moreover, the heating process can also lead to the formation of new thermal decomposition compounds that may be also hazardous. Clinical as well as in vitro and in vivo studies on e-cigarette toxicity have reported potential cardiovascular damages; however, results remain conflicting. The aim of this study was to assess, in vitro, the toxicity of e-liquids and e-cigarette aerosols on human aortic smooth muscle cells. To that purpose, cells were exposed either to e-liquids or to aerosol condensates obtained using an e-cigarette device at different power levels (8 W or 25 W) to assess the impact of the presence of: (i) nicotine, (ii) cinnamon flavor, and (iii) thermal degradation products. We observed that while no cytotoxicity and no ROS production was induced, a pro-inflammatory response was reported. In particular, the production of IL-8 was significantly enhanced at a high power level of the e-cigarette device and in the presence of the cinnamon flavor (confirming the suspected toxic effect of this additive). Further investigations are required, but this study contributes to shedding light on the biological effects of vaping on the cardiovascular system.
Keyphrases
- smoking cessation
- inflammatory response
- replacement therapy
- endothelial cells
- aortic valve
- high glucose
- left ventricular
- dna damage
- cell proliferation
- human health
- risk assessment
- pulmonary artery
- lipopolysaccharide induced
- coronary artery
- atrial fibrillation
- induced pluripotent stem cells
- drug induced
- reactive oxygen species
- endoplasmic reticulum stress