Is Indoor Air Pollution the Missing Link Between Radon and Lung Cancer? Rethinking Epidemiological Support for the LNT Model

The validity of the linear-no-threshold (LNT) model in radiation regulation remains contested. Although extensive experimental evidence challenges it, epidemiological studies-especially cohort and case-control designs-are still used to justify its application. This article focuses on a key methodological limitation of individual-level epidemiological studies, particularly the reported link between residential radon and lung cancer. Pooled case-control analyses suggest a linear dose-response relationship consistent with the LNT model, while ecological studies show mixed results. Case-control data are often deemed more reliable than ecological studies, but their validity requires reexamination. A central issue is the neglect of radon's role within the broader context of indoor air pollution. Because more than 90% of radon decay products adhere to airborne particles, measured radon levels can effectively serve as a proxy for indoor particulate matter (PM), which is a complex mixture of harmful compounds. Since PM2.5 is a well-established lung carcinogen, the observed radon-lung cancer association may reflect PM2.5 effects rather than radon itself. This confounding is weaker in ecological studies, which use regional averages less directly tied to individual homes. When experimental evidence, evolutionary reasoning, and ecological findings contradict individual-level studies, it is possible that the latter are inherently flawed by design. Continued reliance on epidemiological studies to uphold the LNT model should therefore be critically reconsidered.