3D-modelling of radon-induced cellular radiobiological effects in bronchial airway bifurcations: direct versus bystander effects.
ABSTRACT The primary objective of this paper was to investigate the distribution of radiation doses and the related biological responses in cells of a central airway bifurcation of the human lung of a hypothetical worker of the New Mexico uranium mines during approximately 12 hours of exposure to short-lived radon progenies.
State-of-the-art computational modelling techniques were applied to simulate the relevant biophysical and biological processes in a central human airway bifurcation.
The non-uniform deposition pattern of inhaled radon daughters caused a non-uniform distribution of energy deposition among cells, and of related cell inactivation and cell transformation probabilities. When damage propagation via bystander signalling was assessed, it produced more cell killing and cell transformation events than did direct effects. If bystander signalling was considered, variations of the average probabilities of cell killing and cell transformation were supra-linear over time.
Our results are very sensitive to the radiobiological parameters, derived from in vitro experiments (e.g., range of bystander signalling), applied in this work and suggest that these parameters may not be directly applicable to realistic three-dimensional (3D) epithelium models.
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ABSTRACT: Radiation carcinogenesis is one of the major biological effects considered to be important in risk assessment of radioactive exposures. The purpose of this work is to calculate the probability of cell transformation effect per mSv induced by α-particle radiation, from radon progeny, on sensitive cells of human lung. Probability was calculated by applying the analytical model cylindrical bifurcation (Jovanović et al., J Radioanal Nucl Chem 290(3):607–613, 2011) which was created to simulate the geometry of human airways with the geometric distribution of cell nuclei in the airway wall of the tracheobronchial tree. Cell transformation can change form or structure DNA, and this change cause that a normal cell undergoes as it becomes malignant. It is possible that radon is the number one cause of lung cancer among people who do not smoke. This analytical model of the human traheobronchial tree represent the extension of the ICRP66 (ICRP Human Respiratory Tract Model for Radiological Protection, 1994) model. Propagation of α-particle was simulated by Monte Carlo method. Reported probabilities are calculated for various targets and alpha particle energies. The sources included fast and slow mucus in BB and bb region. The targets are basal and secretory cells in BB region, and secretory cells in bb region. Results obtained in this work are unique.Journal of Radioanalytical and Nuclear Chemistry 11/2013; DOI:10.1007/s10967-013-2620-x · 1.42 Impact Factor