E-cigarette smoke damages DNA and reduces repair activity in mouse lung, heart, and bladder as well as in human lung and bladder cells.
Level 5 - mechanism / opinion, no new human data
Preclinical animal and in vitro laboratory study without clinical human outcome data
PubMed 29378943 · doi:10.1073/pnas.1718185115
What was done
Mice were exposed to e-cigarette smoke (aerosol) to directly measure nitrosamine-induced DNA damage in the lung, bladder, and heart, as well as DNA-repair activity and repair proteins (XPC and OGG1/2) in the lung. Cultured human bronchial epithelial and urothelial cells were exposed to nicotine and its metabolite, nicotine-derived nitrosamine ketone, to assess mutational susceptibility and tumorigenic transformation.
What was found
The abstract reports no numerical values. Mutagenic O6-methyldeoxyguanosines and γ-hydroxy-1,N2-propano-deoxyguanosines were found in the lung, bladder, and heart of exposed mice. DNA-repair activity and repair proteins XPC and OGG1/2 were significantly reduced in the murine lung. Nicotine and its metabolite induced the same DNA-damaging effects and enhanced mutational susceptibility and tumorigenic transformation in cultured human bronchial epithelial and urothelial cells.
Why it matters
This study demonstrates in vivo nicotine nitrosation and mechanistic pathways for DNA damage and impaired DNA repair following e-cigarette aerosol exposure. It suggests plausible biological mechanisms by which e-cigarette use might contribute to lung and bladder cancer and heart disease.
Limits
The study was conducted entirely in mice and in vitro human cell cultures, precluding direct clinical conclusions for humans. The abstract does not report animal sample sizes, aerosol dosing levels, exposure durations, or quantitative effect sizes.
Cited by
- supports Smoking, especially nicotine, damages DNA, increases inflammation, and shortens lifespan.