Environmental carcinogens play a critical role in inducing DNA damage and triggering the initiation of cancer pathways through complex biochemical and molecular mechanisms. These carcinogens—such as polycyclic aromatic hydrocarbons (PAHs), heavy metals, tobacco smoke, aflatoxins, and certain industrial chemicals—interact directly or indirectly with the DNA, leading to the formation of adducts, strand breaks, and oxidative lesions. This genotoxic stress compromises genomic integrity by interfering with replication and transcription processes. If not effectively repaired by cellular mechanisms like nucleotide excision repair or base excision repair, the accumulated DNA damage can result in mutations in critical genes, including oncogenes and tumor suppressor genes. This mutational burden sets the stage for the activation of oncogenic signaling pathways, disruption of normal cell cycle checkpoints, and evasion of apoptosis, which collectively promote the transformation of normal cells into malignant ones. Furthermore, chronic exposure to environmental carcinogens often leads to sustained inflammation and epigenetic alterations, such as DNA methylation and histone modifications, that further exacerbate cancer risk. Understanding the role of these environmental factors in cancer initiation is vital for developing targeted prevention strategies and improving early detection and intervention methods.
