Environmental Epimutagens and Molecular Mechanisms Linking Pollution to Cancer

Background: Environmental pollution is an increasingly important contributor to cancer risk, yet its carcinogenic effects cannot be explained solely by direct DNA damage. Emerging evidence indicates that many pollutants act as environmental epimutagens, inducing persistent changes in gene regulation without altering the underlying DNA sequence. These epigenetic alterations may influence cancer susceptibility by disrupting molecular pathways involved in genomic stability, inflammation, apoptosis, cell-cycle control, and tissue-specific developmental programming. Objective: This narrative review synthesizes current evidence on the molecular mechanisms through which environmental epimutagens link pollution exposure to cancer development, with emphasis on DNA methylation, histone modifications, chromatin remodeling, non-coding RNA dysregulation, developmental vulnerability, and public health implications. Methods: A narrative literature synthesis was conducted using peer-reviewed studies retrieved from PubMed, Scopus, Web of Science, ScienceDirect, and Google Scholar. The main search period covered 2014–2024, with older landmark studies included when they provided foundational mechanistic evidence. Eligible studies addressed environmental pollutants, epigenetic alterations, and cancer-related molecular pathways. Evidence was organized thematically by pollutant class and epigenetic mechanism rather than statistically pooled. Results: The synthesized evidence indicates that particulate matter, heavy metals, polycyclic aromatic hydrocarbons, endocrine-disrupting chemicals, pesticides, and industrial contaminants converge on four major epigenetic regulatory systems: DNA methylation, histone modification, chromatin remodeling, and non-coding RNA expression. Global DNA hypomethylation, promoter-specific hypermethylation of tumor suppressor and DNA repair genes, altered histone acetylation or methylation, and dysregulated microRNAs were repeatedly linked with genomic instability, impaired DNA repair, apoptosis resistance, chronic inflammation, and proliferative signaling. Developmental exposures during embryonic, fetal, childhood, pubertal, and germline-sensitive periods may produce durable epigenetic programming that increases later-life cancer susceptibility. Conclusion: Environmental epimutagens provide a biologically plausible framework for understanding pollution-associated carcinogenesis through mechanisms that complement classical genotoxic pathways. Incorporating epigenetic biomarkers, developmental exposure prevention, and non-genotoxic endpoints into environmental health policy may strengthen cancer prevention strategies.