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Genotoxic, Cytotoxic, and Inflammatory Alterations of the Oral Mucosa Caused by the Use of Electronic Cigarettes: Literature Systematic Review

Jul 2026 · Revista Brasileira de Cancerologia · Vol 72, pp. e115536 · 0 citations · 29 references

TL;DR

It is demonstrated that vapes are capable of activating carcinogenic pathways in head and neck cells and oral mucosa, creating a microenvironment favorable to neoplastic initiation, promotion, and progression.

Abstract

Introduction: The increased use of electronic cigarettes (vapes) has been identified as a new public health problem. Objective: To find evidence on the effects of vaping on the establishment of cellular and tissue damage and to identify carcinogenic pathways related to head and neck cancer and oral cancer. Method: Systematic review research in the PubMed, LILACS, SciELO, and Cochrane databases, with a ten-year time frame (2014-2024). Descriptors: e-cigarettes, vaping, oral cancer, squamous carcinoma, and head & neck cancer. Fourteen original in vitro and in vivo studies that investigated alterations at the molecular and clinical level resulting from exposure to and consumption of vapes were included and analyzed. The studies were classified according to the risk of bias using the OHAT and ROBINS-E tools. Results: Findings were grouped by the predominance of genotoxic and cytotoxic effects, as well as alterations in inflammatory pathways and cell progression and tissue lesions in the oral mucosa. In vitro and in vivo results showed DNA damage, micronucleus formation, reduced cell viability, increased LDH and ROS, activation of oncogenic pathways such as NF-κB and STAT3, and inflammatory pathways (increased interleukins) and progression pathways (epithelial-mesenchymal transition phenotype). Conclusion: Together, the findings demonstrate that vapes are capable of activating carcinogenic pathways in head and neck cells and oral mucosa. In addition, we consider activating and accelerating inflammatory processes, creating a microenvironment favorable to neoplastic initiation, promotion, and progression. These findings highlight the need for more robust clinical studies and mechanistic investigations focused on agent-speciftradic pathways.

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