Electronic cigarette users show lower levels of biomarkers of exposure (NNK, nicotine, acrolein, and carbon monoxide) and biomarkers of potential harm (platelet activation, oxidative stress, and endothelial function) than cigarette smokers
Electronic cigarette can induce cardiovascular disease similar to conventional cigarette smoking. The severity of toxicity increases with exposure duration and nicotine content.
Electronic cigarette with nicotine induce an abnormal increase in ROS levels and mitochondrial DNA mutations associated with cardiac dysfunction and atherogenesis. Electronic cigarette without nicotine did not produce significant effect.
Electronic cigarette vapor increases vascular, cerebral, and pulmonary oxidative stress via a NOX-2-dependent mechanism. The adverse effect is more pronounced with nicotine than without nicotine.
Electronic cigarette vapor shows small or completely absent effects on systolic and diastolic functions of the heart, atherosclerotic progression, altered lipid profiles, and alteration of the heart ventricle and aorta transcriptomes compare to 3R4F conventional cigarette smoke.
Notes: () The SYRCLE’s RoB for animal intervention does not provide overall risk of bias.