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Applying the two-stage clonal expansion model to epidemiology of lung canceramong uranium miners, it has been revealed that radon acts as a promoting agentfacilitating the clonal expansion of already mutated cells. Clonal expansionrate increases non-linearly by radon concentration showing a plateau above agiven exposure rate. The underlying mechanisms remain unclear. Earlier weproposed that progenitor cell hyperplasia may be induced upon chronic radonexposure. The objective of the present study is to test whether the inductionof hyperplasia may provide a quantitative explanation for the plateau in clonalexpansion rate. For this purpose, numerical epithelium models were preparedwith different number of basal cells. Cell nucleus hits were computed by anown-developed Monte-Carlo code. Surviving fractions were estimated based on thenumber of cell nucleus hits. Cell division rate was computed supposingequilibrium between cell death and cell division. It was also supposed thatclonal expansion rate is proportional to cell division rate, and therefore therelative increase in cell division rate and clonal expansion rate are the samefunctions of exposure rate. While the simulation results highly depend on modelparameters with high uncertainty, a parameter set has been found resulting in acell division rate exposure rate relationship corresponding to the plateau inclonal expansion rate. Due to the high uncertainty of the applied parameters,however, further studies are required to decide whether the induction ofhyperplasia is responsible for the non-linear increase in clonal expansion rateor not. Nevertheless the present study exemplifies how computational modellingcan contribute to the integration of observational and experimental radiationprotection research.

Quantitative analysis of the potential role of basal cell hyperplasia in the relationship between clonal expansion and radon concentration