Summary
Introduction:
This text presents the results of a study investigating the carcinogenic effects of electronic-cigarette smoke (ECS) in mice. The study exposes mice to ECS for an extended period and examines the development of lung and bladder lesions. The study also explores the role of nicotine and nitrosamines in ECS-induced carcinogenesis.
Key Points:
* The study exposed mice to ECS, vehicle control, or filtered air for 54 weeks.
* Mice exposed to ECS developed lung adenocarcinomas (22.5%) and bladder urothelial hyperplasia (57.5%).
* These lesions were extremely rare in mice exposed to vehicle control or filtered air.
* The study also found that nicotine and its nitrosation product, nicotine-derived nitrosamine ketone, cause similar deleterious effects in human lung epithelial and bladder urothelial cells.
* The authors propose that ECS, as well as nicotine, may induce lung and bladder cancer.
* The study addresses the controversy surrounding nicotine carcinogenicity in animal models.
* The authors suggest that the small size of ECS aerosol allows nicotine to penetrate deeply into lung tissues, inducing DNa damage, whereas stream air vapors are mainly deposited in the upper aerodigestive linings and tissues, which are rich in antioxidants.
Main Message:
The study suggests that ECS, as well as nicotine and NNK, is a lung carcinogen and a 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 study emphasizes the need for in-depth research to determine the potential risks associated with ECS use in humans.
Citation
Tang MS, Wu XR, Lee hW, et al. Electronic-cigarette smoke induces lung adenocarcinoma and bladder urothelial hyperplasia in mice. Proceedings of the National academy of Sciences of the United States of america. 2019;116(43):21727-21731. doi:10.1073/pnas.1911321116
