Radon-222, a naturally occurring radioactive gas, is the second leading cause of lung cancer globally, after tobacco use. When inhaled, its decay products, especially polonium-218 and polonium-214, emit high-energy alpha particles that induce dense DNA damage in the bronchial epithelium. Because ambient radon measurements often vary significantly over time and across locations, they provide limited insight into individual exposure levels. This suggests the urgent need for biological markers that can accurately indicate internal dose and early signs of lung cancer development. This review offers an extensive overview of biomarkers associated with radon exposure, from internal dosimetry to early biological responses. It covers internal dose markers (e.g., radon progeny in air and 210Po/210Pb in bones and teeth), molecular and cytogenetic indicators of effective dose (such as chromosomal aberrations, γ-H2AX foci, and DNA adducts), and early effect markers (including somatic mutations, epigenetic changes, miRNA profiles, and autoantibody signatures). The review highlights translocations detected via FISH, discussing those that are stable over time versus those that are transient. It also evaluates the reliability and practicality of these biomarkers in occupational and residential settings, noting how smoking complicates causal inference due to overlapping mutation pathways. Finally, it suggests that integrating multi-omics technologies could improve the precision of biomarker panels.
Rathebe et al. (Thu,) studied this question.