Lung cancer is the leading cause of cancer death in both men and women. Smoking causes 80-90% of cases of lung cancer. In this study, an attempt was made to assess the impact of cigarette smoking on the risk of lung cancer by the so-called threshold-specific energy model. This model allows to analyse the biological effects of radon daughter products on the lung tissue, and is based on the assumption that the biological effect (i.e. cell inactivation) will manifest itself after the threshold-specific energy z0 deposited in the sensitive volume of the cell is exceeded. Cigarette smoking causes, among others, an increase in the synthesis of the survivin protein that protects cells from apoptosis and thereby reduces their radiosensitivity. Based on these facts, an attempt was made to estimate the shape of the curves describing the increase in the oncological effect of radiation as a function of daily cigarette consumption.
Exposure to radon and radon decay products in some residential areas and at workplaces constitutes one of the greatest risks from natural sources of ionising radiation. Recently, increasing attention has been paid to the precise estimations of this health risk by numerous models. The compartmental model published in ICRP Publication 66 (HRTM) has been used for calculating alpha activity concentration in human lung. Energy deposition in the tissue was calculated by the Bethe-Bloch equation. The aim of this study was to check the performance and to compare the reliability of the microdosimetric models. In this work different thicknesses of mucus in the cases of non-smokers and smokers has been considered. Transformed cells were considered as the radiation risk parameters. The radiation risk evaluation for different exposure levels was based on homogeneous and heterogeneous distributions of target cells. The results of application of these procedures were compared with the epidemiological study of Czechoslovakian uranium miners.
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