Wednesday, January 14, 2009

Stochastic aspects of primary cellular consequences of radon inhalation.

Stochastic aspects of primary cellular consequences of radon inhalation.
Radiat Res. 2009 Jan;171(1):96-106.

The present calculations with our composite microdosimetric model confirm the assumption that the strong inhomogeneity of radon progeny deposition within the central respiratory passages results in non-uniform local distributions of radiation dose along the epithelium of the bronchi. The “hot spots” of nuclide deposition close to the carinal ridges are transformed into more widely dispersed high radiation dose areas around the bifurcation units of the airways, but dose is still distributed inhomogeneously among the cell nuclei of the epithelium. On a log-log scale, the number of hit cell nuclei decreases linearly as a function of the number of hits per cell nucleus. In the case of the exposure lengths analyzed in this study, the cell nuclei receiving multiple hits are located mainly in the neighborhoods of the carinas. In spite of the fact that maximum cell nucleus doses were found among these nuclei, the cells possessing high transformation probabilities were not restricted to the cells whose nuclei were hit more than once. This phenomenon can be explained with the help of our results obtained for cell inactivation probabilities, according to which a considerable number of the hit cells have high inactivation probabilities, independent of the number of hits. Only a very small percentage of the cell nuclei of our tracheobronchial geometry model were actually hit by α particles. As a consequence, orders of magnitude increases were observed in the mean nuclear dose and cell transformation probabilities if only the exposed cell nuclei were considered instead of all the cell nuclei. The maximum doses and transformation probabilities were close to the mean values if only the exposed cells were considered. On a log-log scale, the maximum dose increases as a function of the number of inhalations. The maximum transformation probability asymptotically approaches its maximum of 10−3. This phenomenon can be elucidated by the fact that high doses yield high inactivation probabilities that prevent cell transformation by killing the cell. The sum of the nuclear doses, the number of the killed cells and the number of the cell transformations vary in linear fashion as a function of the number of inhalations. Thus, based on the model applied in this work, an LNT relationship exists between the number of cell transformations and the length of exposure in case of radon inhalation.


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