Published online Sep 20, 2025. doi: 10.5493/wjem.v15.i3.108025
Revised: May 16, 2025
Accepted: July 16, 2025
Published online: September 20, 2025
Processing time: 131 Days and 17.9 Hours
Smoking is a leading cause of carcinogenesis in the head and neck region, representing a critical public health issue. Identifying genotoxic damage in smokers can provide valuable insights for developing preventive interventions.
To assess genotoxic damage through the micronucleus assay in exfoliated buccal mucosa cells from users of conventional tobacco, reverse smoking, cannabis, electronic cigarettes, and non-smokers.
A cross-sectional study was conducted with 100 participants divided into five groups: 20 conventional tobacco smokers, 20 reverse smokers, 20 electronic cigarette users, 20 cannabis users, and 20 non-smokers. Exfoliated buccal mucosa cells were analyzed using Giemsa and Papanicolaou staining to identify micronuclei (MN) as markers of genotoxic damage.
MN were present in 86% of the samples. Statistically significant differences were observed in the median micronucleus count between conventional, reverse, and electronic cigarette smokers compared to non-smokers (P < 0.001), while no significant difference was found for cannabis smokers (P = 0.89). A significant correlation was identified between the presence of oral lesions and micronucleus count (P = 0.03). Regression analysis ruled out alcohol as a confounding factor.
This study identified genotoxic damage associated with various smoking habits, except for cannabis use, highlighting the need for public health interventions to reduce smoking and mitigate its genotoxic effects. These findings provide a foundation for future research and the implementation of preventive policies.
Core Tip: This study reveals significant genotoxic damage in buccal mucosa cells among conventional, reverse, and electronic cigarette smokers, but not cannabis users, using the micronucleus assay. A strong correlation was found between smoking-related oral lesions and micronucleus frequency, independent of alcohol use. These findings underscore the urgent need for targeted public health strategies to reduce smoking-induced DNA damage and prevent oral carcinogenesis. The results provide critical evidence for policymakers and future research on tobacco-related harm.