INTRODUCTION:Electronic cigarettes (E-cigs) are in a controversial state. Although E-cig aerosol generally contains fewer harmful substances than smoke from burned traditional cigarettes, aerosol along with other compounds of the E-cigs may also affect lung functions and promote the development of lung-related diseases. We investigated the effects of E-cig on the pulmonary functions of male C57BL/6 mice and reveal the potential underlying mechanisms. METHODS:A total of 60 male C57BL/6 mice were randomly divided into four groups. They were exposed to fresh-air, traditional cigarette smoke, E-cig vapor with 12 mg/mL of nicotine, and E-cig with no nicotine for 8 weeks. Lung functions were evaluated by using quantitative analysis of the whole body plethysmograph, FlexiVent system, lung tissue histological and morphometric analysis, and RT-PCR analysis of mRNA expression of inflammation-related genes. In addition, the effects of nicotine and acrolein on the survival rate and DNA damage were investigated using cultured human alveolar basal epithelial cells. RESULTS:Exposure to E-cig vapor led to significant changes in lung functions and structures including the rupture of the alveolar cavity and enlarged alveolar space. The pathological changes were also accompanied by increased expression of interleukin-6 and tumor necrosis factor-α. CONCLUSIONS:The findings of the present study indicate that the safety of E-cig should be further evaluated. IMPLICATIONS:Some people currently believe that using nicotine-free E-cigs is a safe way to smoke. However, our research shows that E-cigs can cause lung damage regardless of whether they contain nicotine.

目的 探讨电子烟代谢产物及其溶剂对去内皮Sprague-Dawley(SD)大鼠肠系膜上动脉(SMA)环收缩反应的影响.方法 将溶剂(DMSO)、电子烟气溶胶提取物(ECAEs)、烟油溶剂[丙二醇(PG)和甘油(VG)]、烟碱体内主要代谢产物[N-亚硝基降烟碱(NNN)和亚硝胺酮(NNK)]、以及电子烟副产物丙烯醛(Acr)分别加入培养基孵育去内皮SD的SMA环24 h,观察不同浓度5-羟色胺(5-HT,10-10～10-4 mol/L)和苯肾上腺素(PE,10-10～10-4 mol/L)诱导的收缩反应.结果 DMSO、ECAEs对SMA环收缩反应无影响;丙二醇使5-HT诱导收缩的pD2值(SMA环收缩效应达到50％的时候所对应的收缩剂的浓度值)与对照组比较,差异有统计学意义(P<0.05),甘油使PE(10-9～10-7 mol/L)浓度区间的收缩反应减弱(P<0.05);NNN和NNK在100μmol/L浓度下均可增强5-HT和PE诱导收缩反应的最大效应值Emax(P<0.05),且PE在10-5～10-4 mol/L剂量范围内可明显诱导SMA的收缩;丙烯醛培养的SMA环Emax值与对照组之间均有差异(P<0.01),5-HT和PE在10-5.5～10-4 mol/L剂量范围内诱导的收缩曲线均显著左移.结论 电子烟各类潜在危害因子24 h短期急性暴露可不同程度的增强去内皮SD大鼠肠系膜上动脉环的收缩反应,增强血管平滑肌的收缩反应.