With the development of the times, electronic cigarettes (e-cigarettes) are being received by more and more people. We compared the different effects of e-cigarettes and tobacco cigarettes on human umbilical vein endothelial cells (HUVECs) treated with the typical e-cigarette aerosol extracts (ECA) and cigarette smoking extracts (CS) sourced from commercial retail stores. HUVECs were treated with different kinds of ECA or CS with different nicotinic concentrations (0.03125, 0.125, 0.5, 2, 8, or 32 μg/mL). Cell viability was examined by the MTT assay. The cell apoptosis was investigated by acridine orange (AO) and Hoechst 33258 staining. The RT-PCR and western blot assays were used to analyze the adhesion molecules and inflammation cytokines released by HUVECs. Furthermore, the intracellular reactive oxygen species (ROS) was observed by fluorescence microscopy. Our data showed that the CS (nicotine concentration at 0.125 μg/mL could decrease the viability of HUVECs by 71%, but not the four kinds of ECA. The apoptotic ratio was about 32.5% in the CS group. No matter the levels of adhesion molecules, inflammation cytokines or ROS, they were higher in CS groups than in ECA groups. Overall, the four kinds of e-cigarettes induced significantly less cytotoxicity than the commercially available tobacco cigarettes in HUVECs. The CS showed the most severe impact on HUVECs. ECA might provide a harm reduction measure, especially in cardiovascular risk, after people switch from tobacco cigarettes to e-cigarettes.

Use of electronic cigarettes (e‐cigarettes) has increased significantly over the past decade due to consumer perception that these products represent a less risky alternative to combustible cigarettes. E‐liquids generally contain a simple mix of vegetable glycerin, propylene glycerol, nicotine, organic acids, and flavourings. Regulators require that harmful and potentially harmful constituents (HPHCs) that might cause harm to the consumer must be monitored in the aerosol generated by e‐cigarettes and in cigarette smoke (CS). To quantify HPHCs in aerosols from commercial flavoured e‐cigarettes in Chinese market, this study has systematically compared levels of HPHCs, including eight carbonyls, five volatile organic compounds, four tobacco‐specific nitrosamines, 16 polycyclic aromatic hydrocarbons, and seven heavy metals, in the aerosols of four market‐leading flavoured e‐cigarettes and mainstream CS, alongside in vitro cytotoxicity and mutagenicity assays. The vast majority of HPHCs were either undetected or significantly lower in the e‐cigarette aerosols than in commercial CS or reference CS (3R4F). Where HPHCs were detected, there were small variations among the different flavoured e‐cigarettes. In the neutral red uptake and Ames assays, aqueous extracts of the e‐cigarette aerosols did not induce obvious cytotoxicity or mutagenicity, whereas CS aqueous extract showed dose‐related cytotoxicity and mutagenicity. Collectively, these results indicate that use of e‐cigarettes might potentially lead to a significant reduction in exposure to harmful substances, with fewer cytotoxic and mutagenic effects, as compared with conventional smoking. Further studies based on human puffing conditions and longer evaluation periods will be needed to substantiate this potential.

Smoking increases the risk of a number of diseases, including cardiovascular, oral, and lung diseases. E-cigarettes are gaining popularity among young people as an alternative to cigarettes, but there is debate over whether they are less harmful to the mouth than e-cigarettes. In this study, human gingival epithelial cells (HGECs) were treated with four commercially available e-cigarette aerosol condensates (ECAC) or commercially available generic cigarette smoke condensates (CSC) with different nicotine concentrations. Cell viability was determined by MTT assay. Cell apoptosis was observed by acridine orange (AO) and Hoechst33258 staining. The levels of type I collagen, matrix metalloproteinase (MMP-1, MMP-3), cyclooxygenase 2, and inflammatory factors were detected by ELISA and RT-PCR. Finally, ROS levels were analyzed by ROS staining. The different effects of CSC and ECAC on HGECs were compared. The results showed that higher nicotine concentration of CS significantly reduced the activity of HGECs. By contrast, all ECAC had no significant effect. The levels of matrix metalloproteinase, COX-2, and inflammatory factors were higher in HGECs treated with CSC than those treated with ECAC. In contrast, the level of type I collagen was higher in HGECs treated with ECAC than those treated with CSC. In conclusion, all four flavors of e-cigarettes were less toxic to HGE cells than tobacco, but further clinical studies are needed to determine whether e-cigarettes are less harmful to oral health than conventional cigarettes.

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