ArticleInhalation toxicology2026
Exposure to electronic cigarette aerosols triggers alterations in genomic DNA methylation that impacts cancer pathways in mice.
Article in Inhalation toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveThe aim of this laboratory study was to characterize the effects of sub-chronic electronic cigarette (E-cig) aerosol exposures on genome-wide DNA methylation in mice to begin to elucidate the pathophysiology of E-cig-related pulmonary diseases and cancer. MATERIALS AND
methodsMale C57BL/6 and FVBN mice were randomly assigned to one of two treatment groups (n = 6 per group) and exposed daily to either filtered air or a 50:50 mixture of propylene glycol and vegetable glycerol containing 24 mg/mL nicotine (+Nic). Whole-body inhalation exposures were conducted for 3 h/d, 5 d/week, for a total of 1-month. Sequences for ∼285 000 CpG probes were aligned to the mouse genome, and mixed linear models were used to model DNA methylation levels (β values). These evaluations were followed by ingenuity pathway analysis (IPA), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Ontology (GO) analysis. RESULTS AND DISCUSSION: E-cig inhalation exposure induced significant DNA methylation changes in adult male mice, with a notable impact on cancer-related pathways. A total of 2300 genes in C57BL/6 mice and 6732 genes in FVBN mice were hypomethylated, while 1673 and 5529 genes were hypermethylated, respectively. KEGG and GO analyses highlighted key pathways such as Wnt/β-catenin signaling and proteoglycans in cancer, suggesting that E-cig aerosol exposure could disrupt critical genomic regulation and potentially promote carcinogenesis. These in vivo findings underscore the potential cancer-promoting effects of E-cig aerosols through epigenetic modifications.
conclusionsFindings from this study provide compelling evidence that sub-chronic E-cig exposure induces genomic DNA methylation changes linked to cancer pathways in two strains of adult male mice, highlighting the serious adverse consequences of E-cig use and strain-specific response differences.
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