Microdosimetric energy depositions have been suggested as a key variable for the modeling of the relative biological effectiveness (RBE) in proton and ion radiation therapy. However, microdosimetry has been underutilized in radiation therapy. Recent advances in detector technology allow the design of new mico- and nano-dosimeters. At the same time Monte Carlo (MC) simulations have become more widely used in radiation therapy. In order to address the growing interest in the field, a microdosimetric extension was developed in TOPAS. The extension provides users with the functionality to simulate microdosimetric spectra as well as the contribution of secondary particles to the spectra, calculate microdosimetric parameters, and determine RBE with a biological weighting function approach or with the microdosimetric kinetic (MK) model. Simulations were conducted with the extension and the results were compared with published experimental data and other simulation results for three types of microdosimeters, a spherical tissue equivalent proportional counter (TEPC), a cylindrical TEPC and a solid state microdosimeter. The corresponding microdosimetric spectra obtained with TOPAS from the plateau region to the distal tail of the Bragg curve generally show good agreement with the published data.
13 September 2021 in Physics in Medicine & Biology
Purpose. Recent studies suggest ultra-high dose rate (FLASH) irradiation can spare normal tissues from radiotoxicity, while efficiently controlling the tumor, and this is known as the ‘FLASH effect’. This study performed theoretical analyses about the impact of radiolytic oxygen depletion (ROD) on the cellular responses after FLASH irradiation. Methods. Monte Carlo simulation was used to model the ROD process, determine the DNA damage, and calculate the amount of oxygen depleted ( LROD ) during FLASH exposure. A mathematical model was applied to analyze oxygen tension (pO 2 ) distribution in human tissues and the recovery of pO 2 after FLASH irradiation. DNA damage and cell survival fractions (SFs) after FLASH irradiation were calculated. The impact of initial cellular pO 2 , FLASH pulse number, pulse interval, and radiation quality of the source particles on ROD and subsequent cellular responses were systematically evaluated. Results. The simulated electron LROD range was 0.38–0.43 μ M Gy −1 when pO 2 ranged from 7.5 to 160 mmHg. The calculated DNA damage and SFs show that the radioprotective effect is only evident in cells with a low pO 2 . Different irradiation setups alter the cellular responses by modifying the pO 2 . Single pulse delivery or multi-pulse delivery with pulse intervals shorter than 10–50 ms resulted in fewer DNA damages and higher SFs. Source particles with a low linear energy transfer (LET) have a higher capacity to deplete oxygen, and thus, lead to a more conspicuous radioprotective effect. Conclusions . A systematic analysis of the cellular response following FLASH irradiation was performed to provided suggestions for future FLASH applications. The FLASH radioprotective effect due to ROD may only be observed in cells with a low pO 2 . Single pulse delivery or multi-pulse delivery with short pulse intervals are suggested for FLASH irradiation to avoid oxygen tension recovery during pulse intervals. Source particles with low LET are preferred for their conspicuous radioprotective effects.
Monte Carlo (MC) track structure simulation tools are commonly used for predicting radiation induced DNA damage by modeling the physical and chemical reactions at the nanometer scale. However, the outcome of these MC simulations is particularly sensitive to the adopted parameters which vary significantly across studies. In this study, a previously developed full model of nuclear DNA was used to describe the DNA geometry. The TOPAS-nBio MC toolkit was used to investigate the impact of physics and chemistry models as well as three key parameters (the energy threshold for direct damage, the chemical stage time length, and the probability of damage between hydroxyl radical reactions with DNA) on the induction of DNA damage. Our results show that the difference in physics and chemistry models alone can cause differences up to 34% and 16% in the DNA double strand break (DSB) yield, respectively. Additionally, changing the direct damage threshold, chemical stage length, and hydroxyl damage probability can cause differences of up to 28%, 51%, and 71% in predicted DSB yields, respectively, for the configurations in this study.
21 June 2018 in Journal of Radiological Protection
As radon is one of the most important natural radiation sources, its radiation hazard has always been a concern. α and β particles emitted by short-lived radioactive radon progeny nuclides could result in a high local dose and induce radiation damage to the respiratory tract. A detailed respiratory tract model needs to be built and dose distribution in the respiratory tract should be studied to reflect the characteristics of energy deposition caused by radon and its progeny. Therefore, in the present work, a dosimetric study was conducted on the respiratory tract and non-uniform dose distribution in the bronchial region was studied. First, a detailed voxel respiratory tract model was established based on the anatomic bronchial parameters of an adult Chinese male. The dimensional parameters of the tracheo-bronchial tree of an adult male adopted in ICRP Publication 66 (ICRP 1994 Human Respiratory Tract Model for Radiological Protection ICRP Publication 66 (Oxford: Pergamon)), featured by consecutive 16 generations of bronchi structures to express the irregular structure of the respiratory tract and the radiosensitive tissues in the bronchial region, were also built for dosimetric study. Then the deposition and clearance models recommended by ICRP were used to analyse the regional deposition and transfer in the respiratory tract, and a fluid dynamic simulation was used to obtain 3D distribution of radon progeny aerosol particles in the bronchial region. The result showed that the highest deposition fraction density occurs at the first and second generations of bronchi. Furthermore, the detailed voxel respiratory tract model along with the Monte Carlo method were used to obtain dose distribution in the BB region. It was found that the dose distribution in the respiratory tract is very non-uniform and the maximum voxel dose is about 30 times higher than the average voxel dose. The dose conversion factor (DCF) for lung in the home environment derived with the dosimetry method in the present work is 9.86 mSv·WLM −1 . Sensitivity analysis was performed for the parameters involved in the DCF calculation and it was found that the unattached fraction and breathing rate influence the DCF the most.