page_title: Safety of electronic cigarettes
section_title: Carcinogenicity
hierarchical_section_title: Safety of electronic cigarettes / Toxicology / Carcinogenicity
caption_attribution_description: English: The cancer risk from vaping is 0.5% of the risk from smoking
context_page_description: The use of electronic cigarettes carries health risks compared to not using any inhaled recreational drugs, especially for children, young adults, and pregnant women. The risk depends on the composition of electronic cigarette aerosol, which varies according to the contents of the liquid, the physical and electrical design of the device, and user behavior. As of 2019, the long-term risks of vaping are somewhat uncertain because studies have yet to be performed on the relatively new technology, though the long-term risks of some individual substances in vaping aerosols and tobacco smoke have been studied.
  When used to deliver nicotine, vaping avoids several carcinogens usually found in tobacco smoke produced by cigarettes and cigars, such as ash, tar, and carbon monoxide. E-cigarettes reduce lung function, reduce cardiac muscle function, and increase inflammation, but to a much lower extent than with traditional cigarettes. Some hazards occur with vaping but not with smoking.
context_section_description: Concerns about the carcinogenicity of e-cigarettes arise from both nicotine and from other chemicals that may be in the vapor. As regards nicotine, there is evidence from in vitro and animal research that nicotine may have a role as a tumor promoter, but carcinogenicity has not been demonstrated in vivo. A 2014 Surgeon General of the United States report stated that the single relevant randomized trial "does not indicate a strong role for nicotine in promoting carcinogenesis in humans". They concluded that "There is insufficient data to conclude that nicotine causes or contributes to cancer in humans, but there is evidence showing possible oral, esophageal, or pancreatic cancer risks". Nicotine in the form of nicotine replacement products is less of a cancer risk than with smoking, and they have not been shown to be associated with cancer in the real world. Nicotine promotes metastasis by causing cell cycle progression, epithelial-to-mesenchymal transition, migration, invasion, angiogenesis, and avoidance of apoptosis in a number of systems. Nicotine does promote the growth of blood vessels that supply tumors and it speeds tumor growth. Whether long-term vaping can raise the chance for malignancy in individuals with a susceptibility for tumor growth is unknown. The effects of nicotine on the sympathoadrenal system could stimulate the advancement of cancer in people who have cancer.
  Nicotine has been shown to induce DNA damage in the Escherichia colipol A+/pol− test. Low concentrations of nicotine stimulate cell proliferation, while high concentrations are cytotoxic. Nicotine decreases the tumor suppressor Chk2, which is activated by DNA damage. The decrease in Chk2 in cells exposed to nicotine suggests that nicotine may be capable of overriding DNA damage checkpoint activation, disrupting genetic surveillance, and increasing the risk of oncogenesis. There is strong evidence that some substances found in e-cigarette vapors such as formaldehyde and acrolein can induce DNA damage and mutagenesis.
  Nicotine promotes endothelial cell migration, proliferation, survival, tube formation, and nitric oxide (NO) production in vitro, mimicking the effect of other angiogenic growth factors. In 2001, it was found that nicotine was a potent angiogenic agent at tissue and plasma concentrations similar to those induced by light to moderate smoking. Effects of nicotine on angiogenesis have been demonstrated for a number of tumor cells, such as breast, colon, and lung. Similar results have also been demonstrated in in vivo mouse models of lung cancer, where nicotine significantly increased the size and number of tumors in the lung, and enhanced metastasis.
  A 2014 study suggested that e-cigarette use may be a risk factor for lung cancer. In several in vitro experiments, it has been found that nicotine in concentrations as low as 1 μM decreased the anti-proliferative and pro-apoptotic effects exerted by chemotherapeutics on several different malignant cell lines. These effects were partially reverted by exposure to α-bungarotoxin (α-BTX), an inhibitor of α7-nAChR. In the case of radiotherapy (RT), nicotine administration increased survival of H460 and A549 lung cancer cells. This effect was likewise reduced by addition of α-BTX prior to nicotine addition and radiation. On this basis, it is expected that use of nicotine products during cancer treatment may reduce the effects due to reactions following interaction of nicotine with α7-nAChR.
  Evidence from experimental in vitro studies on cell cultures, in vivo studies on rodents as well as studies on humans inclusive of epidemiological studies indicate that nicotine may contribute in cancer development by stimulating a number of important processes. Nicotine acts primarily by activation of nicotine acetylcholine receptors and nicotine binds to these receptors with a higher affinity than acetylcholine. Furthermore, the tobacco-specific nitrosamines (TSNAs) NNN (N′-nitrosonornicotine) and NNK (4-(metylnitrosamino)-1-(3-pyridyl)-1-butanon) may be formed from nicotine after oral administration. E-ci
caption: The cancer risk from vaping is 0.5% of the risk from smoking
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