Epigenetic changes driven by environmental pollutants in lung carcinogenesis: a comprehensive review.

Lung cancer remains the leading cause of cancer-related mortality globally, with environmental pollutants identified as significant risk factors, especially for nonsmokers. The intersection of these pollutants with epigenetic mechanisms has emerged as a critical area of interest for understanding the etiology and progression of lung cancer. Epigenetic changes, including DNA methylation, histone modifications, and non-coding RNAs, can induce alterations in gene expression without affecting the DNA sequence and are influenced by environmental factors, contributing to the transformation of normal cells into malignant cells. This review assessed the literature on the influence of environmental pollutants on lung cancer epigenetics. A comprehensive search across databases such as PubMed, Web of Science, Cochrane Library, and Embase yielded 3,254 publications, with 22 high-quality papers included for in-depth analysis. These studies demonstrated the role of epigenetic markers, such as DNA methylation patterns of genes like F2RL3 and AHRR and alterations in the miRNA expression profiles, as potential biomarkers for lung cancer diagnosis and treatment. The review highlights the need to expand research beyond homogenous adult male groups typically found in high-risk occupational environments to broader population demographics. Such diversification can reduce biases and enhance the relevance of findings to various clinical contexts, fostering the development of personalized preventive and therapeutic measures. In conclusion, our findings underscore the potential of innovative epigenetic therapies, such as DNA demethylating drugs and histone modification agents, to counter environmental toxins' carcinogenic effects. The growing interest in miRNA therapies and studies aiming to correct aberrant methylation patterns indicate significant strides toward better lung cancer management and a healthier future for global communities.