October 20, 2019

Stanton A. Glantz, PhD

Direct evidence that e-cigs cause cancer

The fact that e-cigarettes deliver substantially lower levels of tobacco specific nitrosamines that cigarettes has been the basis for the assumption that e-cigarettes pose much lower cancer risk.  A new mouse study shows that, despite delivering lower levels of TSNAs, e-cigarettes still cause cancer. 

Moon-shong Tang and colleagues at NYU exposed mice to e-cigarette aerosol for 4 hours per day 5 days a week for 54 weeks and found lung cancers in 22.5% and bladder hyperplasia in 57.5% of the mice.  Exposing the mice to nicotine-free aerosol (i.e., PG/VG alone) did not increase cancer incidence.

They note, “In contrast to the results showing that stream air-vaporized nicotine is not lung carcinogenic in rats, our results showed that E-cig nicotine induces lung adenocarcinoma in mice. The sources of this discrepancy are unclear. It has been found that the aerosol size of [e-cigarette aerosol] is smaller than the aerosols generated in [tobacco smoke]. It is likely that the small size of E-cig aerosol allows the [nicotine in the e-cigarette aerosol] to penetrate deeply into lung tissues, inducing DNA damage in bronchioloalveolar cells, whereas the stream air vapors are mainly deposited in the upper aerodigestive linings and tissues, which are rich in antioxidants such as glutathione, glutathione peroxidase, and superoxide dismutase and can effectively neutralize the metabolites of nitrosamines.”

It could also be that other components of the e-cigarette (the PG/VG, flavorings, etc) could also be interacting with the nicotine and other compounds to case the effect.

Here is the abstract:

Electronic-cigarettes (E-cigs) are marketed as a safe alternative to tobacco to deliver the stimulant nicotine, and their use is gaining in popularity, particularly among the younger population. We recently showed that mice exposed to short-term (12 wk) E-cig smoke (ECS) sustained extensive DNA damage in lungs, heart, and bladder mucosa and diminished DNA repair in lungs. Nicotine and its nitrosation product, nicotine-derived nitrosamine ketone, cause the same deleterious effects in human lung epithelial and bladder urothelial cells. These findings raise the possibility that ECS is a lung and bladder carcinogen in addition to nicotine. Given the fact that E-cig use has become popular in the past decade, epidemiological data on the relationship between ECS and human cancer may not be known for a decade to come. In this study, the carcinogenicity of ECS was tested in mice. We found that mice exposed to ECS for 54 wk developed lung adenocarcinomas (9 of 40 mice, 22.5%) and bladder urothelial hyperplasia (23 of 40 mice, 57.5%). These lesions were extremely rare in mice exposed to vehicle control or filtered air. Current observations that ECS induces lung adenocarcinomas and bladder urothelial hyperplasia, combined with our previous findings that ECS induces DNA damage in the lungs and bladder and inhibits DNA repair in lung tissues, implicate ECS as a lung and potential bladder carcinogen in mice. While it is well established that tobacco smoke poses a huge threat to human health, whether ECS poses any threat to humans is not yet known and warrants careful investigation.

The full citation is: Tang MS, Wu XR, Lee HW, Xia Y, Deng FM, Moreira AL, Chen LC, Huang WC, Lepor H. Electronic-cigarette smoke induces lung adenocarcinoma and bladder urothelial hyperplasia in mice.  Proc Natl Acad Sci U S A. 2019 Oct 7. pii: 201911321. doi: 10.1073/pnas.1911321116. [Epub ahead of print].  It is available here.

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