Correspondence (letter to the editor): Tumor-Promoting Activities of Nicotine not Addressed

In their review (1), the authors have discussed the pros and cons of e-cigarettes from the perspectives of preventive and respiratory medicine. The authors arrive at the conclusion that e-cigarettes may to some extent be useful as an aid to smoking cessation and that the toxicological dangers are some orders of magnitude less than those of tobacco smoking. However, the tumor-triggering effects of nicotine is not mentioned at all (2). For about ten years it is known that almost all cells of the human body express nicotinic receptors (3). Nicotine and its metabolites cotinine and N-nitrosonornicotine activate these receptors and are thus capable of promoting tumor growth and even carcinogenicity. Nicotine may have a mutagenic effect on epithelial cells (2). In animal studies with mice, the administration of a dose of 2.1 mg nicotine/kg (5 days per week over a period of 24 months) resulted in the development of leiomyo- and rhabdomyosarcomas in 78% of the exposed animals (2). Abnormal cell growth, telomerase activation, apoptosis inhibition, and promotion of tumor cell spread were demonstrated (2); thus today various tumors are thought to be associated with nicotine consumption (non-small cell and small cell lung cancer, head and neck tumors, gallbladder tumors, urinary bladder, and stomach, as well as kidney, breast and colorectal cancers). These new insights should be taken into consideration when the use of e-cigarettes (as well as other carrier systems for the systemic administration of nicotine) is evaluated, especially since genetic-based differences seem to have an individual impact on the nicotine toxicity described above (2).