Benzo[a]pyrene (B[α]P) is a common environmental carcinogen, mainly from the smoke generated by the incomplete combustion of coal, oil and natural gas in the industrial production and living process, which undergoes a series of metabolic reactions in vivo, and ultimately generates the active metabolite, benzopyrene dihydroxy epoxide (B[α]PDE) to exert a strong carcinogenic effect. In this paper, we provide an overview of the mechanisms involved in the malignant transformation of bronchial epithelial cells induced by B[α]PDE in terms of DNA base mutations, DNA repair function, related signaling pathways and epigenetic variations. B[α]PDE covalently binds to DNA bases to form B[α]PDE-DNA adducts, which cause DNA base mutations, inducing malignant transformation of bronchial epithelial cells and ultimate tumor formation. Interestingly, it was found that B[α]PDE-DNA adducts showed a high GC-dependent distribution and the single-nucleotide resolution profile of DNA damage profile was highly similar to that of mutations previously identified in the lung cancer genomes of smokers. B[α]PDE can also regulate the expression or silencing of proto-oncogenes and oncogenes by activating the classical AhR signaling pathway, as well as the PI3K/AKT/mTOR and NF-κB signaling pathways, inducing epithelial-mesenchymal transition (EMT) in bronchial epithelial cells, and interfering with cellular metabolism and the cell cycle, thereby inducing the development of lung cancer. The genes mutated in B[α]PDE-induced malignant transformation of bronchial epithelial cells include the proto-oncogenes RAS, KIF11, and PPP1R13L as well as the oncogenes PHLPP2 and p53. B[α]PDE exposure leads to single nucleotide polymorphisms in the 3"-UTR of the DNA repair enzyme gene, which inhibits the transcription of genes encoding proteins related to DNA damage repair, and subsequently affects the cell cycle, proliferation, and apoptosis of tumor cells. B[α]PDE exposure can induce lung carcinogenesis and progression by inducing hypomethylation of specific gene promoter regions to activate proto-oncogenes and hypermethylation to silence oncogenes. The aberrantly expressed miRNAs or lncRNAs may regulate the expression and signaling of lung cancer-related genes, thereby affecting lung cancer-related biological functions, including cell proliferation, apoptosis, migration and invasion. poly (ADP-ribose) glycohydrolase (PARG) regulates DNA damage repair and maintains genomic stability, whereas silencing PARG inhibits B[α]PDE-induced deterioration of bronchial epithelial cells. B[α]PDE exposure induces metabolic reprogramming in cancer cells, which provides energy to cancer cells rapidly proliferation by increasing glucose uptake and glycolysis, and also regulates cancer cell growth and survival by affecting lipid and nucleic acid metabolism. In conclusion, in B[α]PDE-induced lung cancer, epigenetic changes such as DNA methylation, miRNAs, lncRNAs, metabolic reprogramming, and PARG work together to form a complex regulatory network that affects gene expression, cellular metabolism, and genomic stability. An in-depth study of the mechanism of B[α]PDE-induced malignant transformation of bronchial epithelial cells can provide a theoretical basis for the study of potential targets for the development of anti-tumor drugs, which will help to guide the prevention and treatment of lung cancer in polluted environments and exposure to smoky environments, and also provide theoretical support for the Healthy China measures of tobacco control and smoking ban.