This section briefly reviews alternative approaches to estimating lung-cancer risk associated at radon exposure levels typically found in homes and provides the rationale for the committee's selected approach. Figure 1-3 showed the alternative approaches considered and the related data sources.
The dosimetric approach applies the well-characterized radiation data from human exposures to γ rays, in particular data from the atomic-bomb survivors, to derive estimates of the risk associated with exposure to radon (ICRP 1990). This approach has the following steps:
Use physical dosimetric models of the lung to estimate alpha-particle dose to lung-airway epithelium for indoor radon exposure.
Convert the alpha-particle dose to an equivalent low-linear-energy-transfer (low-LET) dose for low-LET radiations, using an appropriate weighting factor for radon-progeny alpha particles in the bronchial epithelium.
Convert the equivalent dose to an effective dose, using the appropriate tissue-weighting factor for lung (ICRP 1990). (It is possible to omit step 3 and use lung-specific γ-ray-based risk estimates in step 4).
Use risk coefficients per unit of effective dose, based primarily on atomic-bomb survivor data, to estimate the risk per unit of cumulative exposure to radon.
One strength of this dosimetric approach is its use of the wealth of data from the continuing epidemiologic study of the atomic-bomb survivors in Hiroshima and Nagasaki. Lung-cancer risk has been well characterized in that cohort in relation to dose. However, the approach is weakened by the need for scaling factors to convert from the acute, whole-body, primarily γ-ray exposure to the chronic, localized, alpha-particle exposure of the lung from indoor radon. In addition, the data from Hiroshima and Nagasaki are subject to uncertainty owing to limitations of the dosimetry and the need to extrapolate from an exposed population in Japan to other population groups with differing background cancer rates.
Biologically motivated models are intended to provide realistic representation of the steps in radon carcinogenesis from energy deposition to the appearance of cancer. In this context, the parameters of the model have a direct biologic interpretation. One such model is the Moolgavkar-Venzon-Knudson 2-stage clonal expansion model, which incorporates both tissue growth and cell kinetics (Moolgavkar and Luebeck 1990). Such approaches to cancer risk estimation