On the toxicity of e-cigarettes consumption: Focus on pathological cellular mechanisms.

Recent studies suggest that exposure to e-cigarettes may enhance breast cancer progression and pulmonary metastasis in cellular and in vivo models. E-cigarette exposure increases the expression of the tumor proliferator factor Ki-67 and reduces the level of pro-apoptotic caspase-3, leading to significant tumor growth. In vitro studies have shown that human bronchial epithelial cells exposed to e-cig aerosol have changes in gene expression pathways similar to those seen in tobacco smoking models. These findings were supported by the observation of malignant transformation features in airway epithelial cells exposed to e-cig emission. E-cigarette exposure has also been linked to the increase of DNa damage markers, such as ano-deoxyguanosines, and a reduction in the activity of DNa repair enzymes, thereby increasing the risk of new cancer occurrence. additionally, e-cigarette exposure has been shown to increase reactive oxygen species (ROS) production, inflammatory response, and reduce glutathione (GSh) levels in human bronchial epithelial cells and lung fibroblasts which can lead to cytotoxicity, dysfunction of bronchial epithelial barrier function and stress signs and morphological changes.

Vivarelli F, Granata S, Rullo L, et al. On the toxicity of e-cigarettes consumption: Focus on pathological cellular mechanisms. Pharmacological research. 2022;182:106315. doi:10.1016/j.phrs.2022.106315