Alpha particle dosimetry in bronchial target cells for inhaled radon progeny

The application of the ICRP human respiratory tract model [1] to the inhalation of short-lived radon progeny yields a dose-exposure conversion factor for indoor exposures which is roughly a factor of 3 higher than that derived from epidemiological studies. Although other lung dosimetry models predict dose-conversion factor which are lower by about a factor of 2 than the ICRP-value, any further reduction down to the epidemiology-derived estimate seems to be most unlikely. Thus the discrepancy between dosimetry-based and epidemiology-derived estimates of the dose-exposure conversion factor can only be reconciled by reducing the present value of the radiation weighting factor for alpha particles of 20 by about a factor of 2-3. Indeed, such a smaller value would be consistent with maximum RBE-values for in vitro oncogenic transformation, which range from 3 to 10. Alternative explanations are that the intra-and inter-subject variabilities of biological parameters involved in lung dosimetry and the non-uniform radon progeny activity distributions on bronchial airway surfaces may affect lung cancer incidence. Indeed, stochastic dose calculations indicate that the inherent variability of morphological and physiological parameters, affecting deposition, clearance and dosimetry, can cause significant fluctuations of cellular doses. This raises the question, whether lung cancer risk is better correlated with the average dose received by a group of individuals, as is current practice, or with the higher doses received by a small fraction of individuals for the same exposure conditions. Furthermore, radon progeny accumulations at carinal ridges in bronchial airway bifurcations lead to highly non-uniform exposure conditions. Thus cells located at carinal ridges receive significantly more cellular hits and thus higher cellular doses than those along the cylindrical airway portions, leading to correspondingly higher transformation frequencies at these sites. This suggests that lung cancers may originate primarily at bronchial bifurcation sites. (orig.)