Mechanistic Models for Radon-induced Lung Cancer Risk Based on Cellular Radiation Effects

Mechanistic models for radon progeny induced lung cancer risk have been developed, based on radiation mechanisms at the cellular level. The cellular effects relevant to radiation-induced carcinogenesis are transformation, cell killing, stimulated cell division, and removal from contact inhibition. Depending upon the 115 ©Naturwissenschaftlich-Medizinischen Vereinigung in Salzburg; download unter www.biologiezentrum.at initiation and/or promotion properties of ionizing radiation, we distinguish between (i) an initiation-promotion-survival model, (ii) a promotion-survival model, and (iii) a survival model. Cigarette smoke or other carcinogenic substances may also act as initiators and/or promotors. Predictions of the relative lung cancer risk in each model are compared herein to published epidemiological data. Each risk model may be most efficient at a different exposure level. A composite risk model, representing combined exposures to radon progeny and other carcinogenic factors, suggests that the relative lung cancer risk for environmental exposures is significantly smaller than that derived from linear extrapolation.