Fig. 3.

A mediator role of oxidative stress in e-cigarette induced pathogenesis. The toxic components and vaporization products of e-cigarettes have been shown by recent studies to induce oxidative stress in human lung and branchial epithelial cells, and human vascular endothelial cells, resulting in inflammation, cytotoxicity and increased endothelial permeability. It also induces tissue infiltration of activated macrophages. Impairment in branchial epithelial cell autophagy induced by e-cigarette contained nicotine, and reduced bacterial and viral clearance in e-cigarette exposed mouse lung, represent potential mechanisms leading to development of COPD. Healthy human subjects responded to e-cigarette exposure with increased oxidative stress, reduced nitric oxide bioavailability, and impaired endothelial/vascular dysfunction that precede to cardiovascular diseases.