Nicotine Is Not a Proinflammatory Component of E-cigarette Vapor

Cigarette smoking is causally associated with a number of chronic diseases in which inflammation plays an important pathogenic role including pulmonary carcinoma, chronic bronchitis, emphysema, atherosclerosis, and thrombosis. In addition, cigarette smoking can exacerbate Crohn's disease and rheumatoid arthritis. In both the particulate and vapor phases, cigarette smoke contains a number of chemicals with proinflammatory or cytotoxic potential. In contrast with cigarette smoking, nicotine has been shown to ameliorate several inflammatory conditions via activation of α7- and α9-nicotinic cholinergic receptors. The chemistry of electronic cigarette (e-cigarette) vaping aerosols is comprised mainly of glycerol, propylene glycol, nicotine, and flavors. The nicotine can be found in either the free base or salt forms depending on the particular product design. E-cigarettes containing nicotine salts have the potential for nicotine exposure levels higher than cigarettes as the sensory cues associated with tobacco smoke nicotine (containing a mixture of free base nicotine and nicotine salts) have been dampened. In this review and analysis, the role of nicotine in inducing inflammation in the absence of other main-stream cigarette smoke constituents is examined. Established and putative mechanisms by which nicotine influences inflammatory pathways in users of nicotine-containing products are described toward better understanding nicotine's potential contribution to the risk profile. For the majority of diseases with an inflammatory component induced by cigarette smoking, evidence suggests that nicotine is not the causative agent. E-cigarette aerosols should limit the diversity of chemical constituents and minimize exposure to proinflammatory chemicals, e.g., acrolein, acetaldehyde, formaldehyde, and heavy metals.