Radiation dose models

Sundberg A L, Blomquist E, Carlsson J, et al. (2003). Cellular retention of radioactivity and increased radiation dose. Model experiments with EGF-dextran. Nucl. Med. Biol. 30 303-315. 

Nonetheless, these methods only estimate organ-averaged radiation dose. Any process which results in high concentrations of radioactivity in organs outside the MIRD tables or in very small volumes within an organ can result in significant error. In addition, the kinetic behavior of materials in the body can have a dramatic effect on radiation dose and models of material transport are constandy refined. Thus radiation dosimetry remains an area of significant research activity. 

The model has been used to establish the radiation dose (Sv) per unit of ingested241 Am activity (Bq) for ages 3 months to 70 years (ICRP 1989). 

The model is designed to calculate the 241 Am intake that would produce the maximum allowed occupational radiation dose to all major organs, including the bone surfaces, bone marrow, and liver, but the conversion factors for other tissues and organs are published in the same tables. 

The model is designed to calculate americium excretion and time courses for americium levels in the liver, skeleton, and gonads. This output could be used to predict radiation doses to these tissues. 

Dose Assessment—An estimate of the radiation dose to an individual or a population group usually by means of predictive modeling techniques, sometimes supplemented by the results of measurement. 

Current lung dosimetry models are based on the assumption that basal cells of the bronchial epithelium are the critical target cells for malignant transformation and that the alpha dose to these cells is the relevant radiation dose. 

Georgievsky V. Ecological and dose models in radiation accidents, 1994. - 236 p. 

Shell W.R., Linkov I., Belenkaja E. Radiation dose from Chernobyl forests Assessment using FORESTPATH model // Proc. of the 1-st international conference (Minsk, Belarus, 18-22 March, 1996). - Luxembourg, 1996.-P. 217-220. 

As anticipated, lower temperature increases the number of observations from an X-ray diffraction data collection (at constant radiation dose). This is however just one of the advantages that could improve a structure solution or a refinement. In fact, a reduced thermal motion usually implies a more reliable standard model, given that for smaller atomic displacements the harmonic approximation is more appropriate and less correlation is found between variables within a least squares refinement. This returns higher precision of the parameters calculated from those variables (for example bond distances, bond angles, etc.). 

Fig. 8.2 Dose-response curves for four different mathematical models relating cancer incidence to radiation dose (from BEIR III Report, NAS/NRC, 1980).

Conditions such as DjDj+l = DjHj — D HJ+i = 0 follow immediately from the model. Let kx be the rate constant of dimer formation. Then the probability rates of dimer formation per radiation dose, PUi(Sj), which depend upon the nature of the occupation of a set of sites, Sj, are given in Table I. The probability of the reverse reaction of the dimer (jj + 1),... 

The experimental kinetics of accumulation of the Frenkel defects - F centres in alkali-halide crystals at liquid-helium temperatures - was studied in [17] and [40] within the framework of a model that yields a logarithmic dependence of the concentration of defects on the irradiation dose - equation (6) of Table 7.6). Although we criticized this relationship above, at low radiation doses it can be represented as a polynomial in powers of uqVq resembling equations (3) to (5). At the same time cogent arguments exist favoring the... 

Estimation of this radiation dose is sometimes accomplished by modeling the sequence of events involved in the acquisition, deposition, clearance, and decay of radium within the body. While based on the current understanding of experimental data on radium toxicokinetics, different models make different assumptions about these processes, thereby resulting in different estimates of dose and risk. These models are described in numerous reports including BEIR IV (1988), ICRP (1979), and Raabe et al. (1983). In this section, the toxicokinetics of radium are described based on the available experimental data rather than on descriptions derived from models. 

Given the models for estimating external or internal radiation doses in specific organs or tissues, the following sections consider the responses resulting from a given dose by any route of exposure. As is the case with hazardous chemicals, both stochastic and deterministic radiation effects can occur. 

Figure 4.12 Cell survival fractions SF(D) as a function of absorbed radiation dose D in Gy (top panel). The bottom panel is the so-called reactivity R(D) given by product of the reciprocal dose D-1 and the negative natural logarithm of SF(D), as the ordinate versus D as the abscissa. Experiment (symbols) the mean clonogenic surviving fractions SF(D) (top panel) and R(D) = — (1/D) ln(SF) (bottom panel) for the Chinese hamster cells grown in culture and irradiated by 50 kV X-ray [73]. Theories solid curve - PLQ (Pads Linear Quadratic) model and dotted curve - LQ model (the straight line a + /SD on the bottom panel).

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