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The main sources of intersubject variations considered in the present study were: (1) size and structure of nasal and oral passages, affecting extrathoracic deposition and, in further consequence, the fraction of the inhaled activity reaching the bronchial region; (2) size and asymmetric branching of the human bronchial airway system, leading to variations of diameters, lengths, branching angles, etc.; (3) respiratory parameters, such as tidal volume, and breathing frequency; (4) mucociliary clearance rates; and (5) thickness of the bronchial epithelium and depth of target cells, related to airway diameters. For the calculation of deposition fractions, retained surface activities, and bronchial doses, parameter values were randomly selected from their corresponding probability density functions, derived from experimental data, by applying Monte Carlo methods. Bronchial doses, expressed in mGy WLM-1, were computed for specific mining conditions, i.e., for defined size distributions, unattached fractions, and physical activities. Resulting bronchial dose distributions could be approximated by lognormal distributions. Geometric standard deviations illustrating intersubject variations ranged from about 2 in the trachea to about 7 in peripheral bronchiolar airways. The major sources of the intersubject variability of bronchial doses for inhaled radon progeny are the asymmetry and variability of the linear airway dimensions, the filtering efficiency of the nasal passages, and the thickness of the bronchial epithelium, while fluctuations of the respiratory parameters and mucociliary clearance rates seem to compensate each other.

Deposition, mucociliary clearance, and dosimetry for the inhalation of radon progeny in the rat lung have been simulated for a variety of inhalation conditions. Computations indicate that the exposure-dose conversion factor for the rat lung is approximately twice as high as the corresponding value for the human lung for the same exposure conditions. However, if typical aerosol characteristics are used for animal inhalation experiments and human indoor exposures, the resulting exposure-dose conversion factors are comparable, thereby suggesting similar lung cancer risks per unit exposure. The predicted relative effects of radon progeny disequilibrium and unattached fractions on bronchial doses agree with results from inhalation experiments with laboratory rats.

The objective of the present study was to assess the lung cancer risk induced by exposures to radon progeny of people living in some areas of Transylvania, Romania. Indoor radon concentrations were measured in 667 dwellings of Stei area, Cluj, Bistrita-Nasaud, Sibiu, and Alba counties. Measurements were performed using CR-39 track detectors, exposed for a minimum of 3 mo. Average annual radon concentrations were 232, 114, 71, 62, and 161 Bq m -3 for Stei area, Cluj, Bistrita-Nasaud, Sibiu, and Alba, respectively. The linear risk model of Darby was used to simulate the dose-effect relationship and relative lung cancer risk at low doses of alpha particles specific to residential radon exposures. Predicted relative risks at the measured exposure levels, together with information on the total number of reported lung cancer deaths and the number of people living in these regions, enabled us to estimate the fraction of lung cancer cases in each area that is attributable to radon. These percentages are 16.67% for Stei area, 9.09% for Cluj, 5.66% for Bistrita-Nasaud, 4.76% for Sibiu, and 12.28% for Alba county among lifetime non-smokers. Assuming that the smoking rates are similar for the investigated regions (10.72% smokers among men and 5.95% among women), around 64 to 69% of the total number of annual lung cancer deaths, stratified by sex, would be attributed to radon and occur among smoking male population, and around 35 to 44% would be attributed to radon and occur among smoking female population.

Deposits of intravascularly injected Thorotrast in the reticulo-endothelial system of Thorotrast patients are a continuous source of {sup 220}Rn. In this study, we modeled the transport of {sup 220}Rn from these deposits through the body into the lungs, exhalation of {sup 220}Rn from the lungs, production of {sup 220}Rn progeny in the lungs and their exhalation, and mucociliary clearance of {sup 220}Rn progeny deposited on airway surfaces. The injection of 1 mL Thorotrast produces annual doses of 0.48 mGy y-1 to the bronchial epithelium and 0.95 mGy y-1 to pulmonary tissue. Based on a mean injected volume of about 25 mL and an average exposure time of 30 y, German Thorotrast patients received a mean bronchial lifetime dose of 357 mGy. Despite these relatively high doses, comparable to exposure in uranium miners, no excess lung cancers could be observed in the epidemiologic follow-up study. This apparent discrepancy between predicted and observed bronchial tumors may have important implications for lung dosimetry and risk assessment of inhaled {sup 222}Rn progeny.

Energy deposition and cellular radiation effects arising from the interaction of single {sup 218}Po and {sup 214}Po alpha particles with basal and secretory cell nuclei were simulated for different target cell depths in the bronchial epithelium of human airway generations 2, 4, 6, and 10. To relate the random chord lengths of alpha particle tracks through spherical cell nuclei to the resulting biological endpoints, probabilities per unit track length for different cellular radiation effects as functions of LET were derived from in vitro experiments. The radiobiological data employed in the present study were inactivation and mutation (mutant frequency at the HPRT gen) in V70 Chinese hamster cells and inactivation and transformation in C3H 10T1/2 cells. Based on computed LET spectra and relative frequencies of target cells, probabilities for transformation, mutation, and cell killing in basal and secretory cells were computed for a lifetime exposure of 20 WLM. While predicted transformation probabilities were about two orders of magnitude higher than mutation probabilities, they were still about two orders of magnitude lower than inactivation probabilities. Furthermore, transformation probabilities for basal cells are generally higher than those for secretory cells, and {sup 214}Po alpha particles are primarily responsible for transformation in bronchial targetmore » cells.« less

Aerosol deposition studies with tracheobronchial casts and models have demonstrated that inhaled particles are preferentially deposited within transitional bifurcation zones, exhibiting hot spots in the vicinity of carinal ridges. The goal of the present study is to quantify the inhomogeneity of theoretically predicted deposition patterns by local deposition enhancement factors. First, inspiratory particle deposition patterns of unattached (1 nm), ultrafine (10 nm and 20 nm), and attached (100 nm and 200 nm) radon progeny within three-dimensional models of segmental bronchial airway bifurcations were simulated by a numerical fluid dynamics and particle trajectory model. Second, local deposition enhancement factors were computed by scanning along the surface of the bifurcation models with prespecified surface area elements. Maximum values and frequency distributions of local deposition enhancement factors of inhaled radon progeny were derived for different sizes of the scanning element in a "narrow" and a "physiologically realistic" bifurcation model and for two different flow rates (10 L min(-1) and 60 L min(-1) in the trachea). Computed enhancement factors indicate that cells located at carinal ridges may receive localized doses which are 20-40 times (1 nm) and 50-115 times higher (10 nm-200 nm), respectively, than the corresponding average doses. This may have important implications for the microdosimetry of inhaled radon progeny and the resulting lung cancer risk.

The cumulative deposition of the 137Cs fallout in Austria resulting from the passage of the Chernobyl cloud has been investigated by applying correlation dimension and hyperbolic frequency distribution methods. For the analysis, a total of 1,881 deposition values were used, which were collected by the Federal Environmental Agency of Austria and the Federal Ministry of Health, representing all available measurements of 137Cs in soil made in Austria after the Chernobyl accident. From these data a hyperbolic exponent for the frequency distribution of 4.0 and a set of fractal correlation dimensions, which decrease from 1.426 +/- 0.022 (for the whole network) to 0.706 +/- 0.047 (for 137Cs values > or = 100 kBq m(-2)), were derived, thus confirming that the fallout pattern can be described as a multifractal.

137 Cs activities were measured in a variety of epigeic and epiphytic lichens in Austria before and after contamination by the Chernobyl fallout. For comparison, the activity of the naturally occurring 40 K was also determined in each lichen sample. The high 137 Cs activities found after Chernobyl suggest that lichens are suitable and inexpensive biological detectors of the fallout pattern

A survey of inhabitant exposures arising from the inhalation of /sup 222/Rn and /sup 220/Rn progeny, and lung cancer mortality has been carried out in two adjacent areas in Guangdong Province, People's Republic of China, designated as the high background and the control area. Annual exposure rates are 0.38 working level months (WLM) per year in the high background, and 0.16 WLM/yr in the control area. In 14 yr of continuous study, from 1970 to 1983, age-adjusted mortality rates were found to be 2.7 per 10(5) living persons of all ages in the high background area, and 2.9 per 10(5) living persons in the control area. From this data, we conclude that we are unable to determine excess lung cancers over the normal fluctuations below a cumulative exposure of 15 WLM. This conclusion is supported by lung cancer mortality data from Austrian and Finnish high-background areas. A theoretical analysis of epidemiological data on human lung cancer incidence from inhaled /sup 2/)2''/sup 2/Rn and /sup 220/Rn progeny, which takes into account cell killing as competitive with malignant transformation, leads to the evaluation of a risk factor which is either a linear-exponential or a quadratic-exponential function of the alpha-particle dose. Animal lungmore » cancer data and theoretical considerations can be supplied to support either hypothesis. Thus we conclude that at our current stage of knowledge both the linear-exponential and the quadratic-exponential extrapolation to low doses seem to be equally acceptable for Rn-induced lung cancer risk, possibly suggesting a linear-quadratic transformation function with an exponential cell-killing term, or the influence of risk-modifying factors such as repair or proliferation stimuli.« less

A deterministic aerosol deposition model, previously validated by data from adult inhalation exposure experiments, is used to study particle deposition within the developing human lung. Here, two age-dependent lung morphologies are presented, in which the number of tracheobronchial (TB) generations is complete at birth but airway dimensions vary with age; the number of pulmonary (P) generations, however, changes with age, as do the alveolated airway dimensions. Deposition patterns within the two morphologies are compared. For the light and heavy respiratory-activity levels considered, regional TB and P, and total (TB + P) lung deposition fractions are calculated. For alI particle sizes (0.2–9.0 μm diameters) tested, total deposition in both morphologies was minimal for the 30-y-old adult and maximal for either of the youngest subjects (7 and 22 mo old). A breakdown of total deposition into lung compartments was specifically addressed for one morphological model. Age-dependent deposition models are intended to aid in future extrapolation efforts to assess the threat to human health from airborne contaminants.

The geometrical structure of the lung is one of the main factors governing inhaled particle deposition; structural differences among different species are, therefore, of great importance for extrapolation modeling. A statistical analysis of morphometric data for the human and rat tracheobronchial tree reveals significant interspecies differences in airway branching patterns: compared to the relatively dichotomous and symmetric structure of the human lung, the rat lung displays a more monopodial airway branching pattern. Thus, for the rat lung, we recommend characterizing the properties of a given airway, i.e., its size, physiologic function, and distance from the trachea, by its diameter rather than by a theoretically assigned generation number. A Monte Carlo method is used to construct an airway geometry along each inhaled particle's path by randomly selecting airway parameters from their frequency distributions and the correlations among them. While the airway geometry is selected randomly, particle deposition in individual airways is calculated analytically. These stochastic deposition calculations allow for structural differences between the human and rat lung, and the variability of the airway system within each species.

Although dose is the simplest and most widely used measurement of a radiation field, it does not always lead to an unambiguous estimate of response. This is reflected in the very wide range of relative biologic effectiveness (RBE) values for biological systems. The ambiguity arises from the focus on energy deposition as the source of biological effect, whether in macroscopic or microscopic volumes. The properties of the biological detector play a role equally important to the properties of the radiation field in their interaction. To predict even the most experimentally accessible biological response, cell killing, we must know the probability per unit path length for generating the observed end point. Especially for high LET radiations we need the action across sections and the particle-energy spectrum. No one parameter reduction of a radiation field can predict biological effect. For cell killing such a prediction can be made, however, from a two-parameter reduction of the interaction between the radiation field and a specific cell line and a specific ambience of the survival curve for the specific radiation field. The determination of these two parameters leads to a suggested new procedure for evaluating the dose equivalent.

The atmospheric content of radon and its decay products contributes significantly to the radiation exposure of man even in the normal environment. In this study, the risk for lung cancer induction associated with normal exposure to natural radionuclides is assessed in Salzburg, Austria. Altogether more than a thousand rooms have been investigated by using combined radon grab-sampling methods together with continuous measurements of radon and daughters at different control stations. Dose calculations were carried out for 729 demoscopically selected test persons, considering individual differences in age, sex and life-style and atmospheric nuclide concentrations at different sites. Using a specially developed age-dependent lung model, the dose frequency distribution of the absorbed dose to the basal cells of the bronchial epithelium could be evaluated for the population of Salzburg. Dose modifications caused by anatomical and physiological variabilities as well as microdosimetric considerations of the stochastic events during energy deposition result in a significantly increased dispersion of the dose histogram. Induction of lung cancer due to inhalation of radon and decay products can be correlated with cumulative exposure based on experience with lung cancer incidence amongst uranium miners. Using the recommended range of lifetime risk values of 20-45 X 10(-5)/WLM (UN77), it is shown for Salzburg that about 15% of the observed number of lung cancer cases may be induced by natural radionuclides.

The deposition and retention models and the anatomical and physiological data as proposed by the ICRP Task Groups on Lung Dynamics and Reference Man are valid only for adult dosimetry. However, the change of the growing organism causes an age-dependent variation of the radiation burden to the respiratory tract. Therefore, age-dependent functions of anatomical and physiological parameters were defined. For this purpose data were either interpolated from literature or calculated from theoretical modeling. With these functions and defined aerosol composition, age-dependent deposition probabilities in the single regions of the respiratory tract were determined. For the demonstration of lung dosimetry as a function of age the naturally occurring radon daughters were used as an example. By applying typical mean nuclide concentrations found in the atmosphere of an urban environment and defined age-dependent daily life patterns, the annual inhaled amount of radioactivity was computed. With the above data, dose calculations for the single ICRP lung model compartments were performed. This revealed that the inhaled dose in both the tracheobronchial and pulmonary regions showed a strong dependence on age; a pronounced maximum value was reached at the age of about 6 yr for radon and thoron decay products.