9
The Committee's Dosimetric Model for Radon and Thoron Progeny

INTRODUCTION

The purpose of this chapter is to describe the underlying assumptions, the specific experimental data, and the formulation of the theoretical dosimetry model that the committee has used to carry out its task of comparing the dose per unit exposure received by underground miners with those received by subjects exposed to radon progeny at home. The modeling procedures that are reviewed and adapted here by the committee were developed as part of an overall review of models and experimental data for radon progeny dosimetry that was sponsored by the U.S. Department of Energy (James, 1990).

DOSIMETRIC ASSUMPTIONS AND MODEL

Both secretory and basal cells in the bronchial epithelium and, to a lesser extent, secretory cells in the bronchioles were identified in Chapter 8 as the principal targets for induction of bronchogenic cancer. The location of these cells within the ciliated epithelium is illustrated schematically in Figure 9-1, which shows a diagrammatic section through the wall of a bronchus. When radon progeny decay, the alpha particles that they emit lose all of their energy within very short distances in the fluid lining the bronchial or bronchiolar airway surfaces and in the epithelial tissue that contains the target cells. The range of the 6-MeV alpha particle from polonium-218 (218Po) in fluid or tissue is 48 µm, and that for the 7.7-MeV alpha particle of 214Po is 71 µm. The location of the target cells in relation to the points at which radon progeny decay (the source



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Comparative Dosimetry of Radon in Mines and Homes 9 The Committee's Dosimetric Model for Radon and Thoron Progeny INTRODUCTION The purpose of this chapter is to describe the underlying assumptions, the specific experimental data, and the formulation of the theoretical dosimetry model that the committee has used to carry out its task of comparing the dose per unit exposure received by underground miners with those received by subjects exposed to radon progeny at home. The modeling procedures that are reviewed and adapted here by the committee were developed as part of an overall review of models and experimental data for radon progeny dosimetry that was sponsored by the U.S. Department of Energy (James, 1990). DOSIMETRIC ASSUMPTIONS AND MODEL Both secretory and basal cells in the bronchial epithelium and, to a lesser extent, secretory cells in the bronchioles were identified in Chapter 8 as the principal targets for induction of bronchogenic cancer. The location of these cells within the ciliated epithelium is illustrated schematically in Figure 9-1, which shows a diagrammatic section through the wall of a bronchus. When radon progeny decay, the alpha particles that they emit lose all of their energy within very short distances in the fluid lining the bronchial or bronchiolar airway surfaces and in the epithelial tissue that contains the target cells. The range of the 6-MeV alpha particle from polonium-218 (218Po) in fluid or tissue is 48 µm, and that for the 7.7-MeV alpha particle of 214Po is 71 µm. The location of the target cells in relation to the points at which radon progeny decay (the source

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Comparative Dosimetry of Radon in Mines and Homes Figure 9-1 Diagrammatic section through the wall of a bronchus showing the types of cells found in the epithelium. of alpha particles) is therefore a critical factor in determining dose. To evaluate the dose received by the respective populations of secretory or basal target cells from each decay of 218Po or 214Po, it is necessary to represent the positions of the source and targets by a geometrical model. The geometry of each bronchial or bronchiolar airway is approximated by a cylindrical tube (Figure 9-2). In the model, the inner surface of the tube is considered to be lined by a thin layer, or sheath, of fluid representing mucus. This inner sheath of mucus is separated from the underlying epithelium by a band of hair-like cilia, which are responsible for clearing the mucus in the direction of the trachea. The cilia are bathed in an aqueous fluid that forms a second, thin layer of shielding material. Both fluid layers have the protective effect of absorbing some of the energy from radon progeny alpha particles. The geometrical model of the airway wall is used to calculate the radiation dose at all points in the underlying epithelium where sensitive targets are found, and particularly the doses received by the nuclear DNA of sensitive cells from alpha-particle decays of the radon progeny source wherever this may be located. Figure 9-2 illustrates two possible locations of the source, within the sheath of mucous ''gel'' overlying the cilia and within the epithelium itself, if the progeny move into the epithelium. In a dosimetric model, the distribution of target cell nuclei in the bronchial epithelium can be approximated by the idealized structure shown in Figure 9-3. A recent, detailed study has shown that the thickness of histologically normal human bronchial epithelium is typically about 58 µm in the larger bronchial airways and 50 µm in the most distal bronchi (Mercer et al., in

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Comparative Dosimetry of Radon in Mines and Homes press). Mercer and colleagues found that secretory cell nuclei are distributed approximately uniformly between about 10 and 40 µm below the epithelial surface and that basal cell nuclei are located between about 35 and 50 µm below the surface, as illustrated schematically in Figure 9-3. The thickness of the mucous gel overlying the cilia is difficult to determine in histological preparations. Using the technique of fixation by vascular perfusion, Mercer et al. (1989)estimated that the gel is typically only 2-µm thick in the bronchi. It has been assumed previously that bronchial mucus is substantially thicker, for example, Harley and Pasternack (1982) and National Council on Radiation Protection and Measurements (NCRP, 1984) assume a value of 15 µm for the overall thickness of protective mucus (which, in their case, includes the 6-µm-thick fluid layer bathing the cilia). In view of the uncertainty in the actual value, the committee assumed for the purpose of modeling bronchial doses that the normal thickness of the mucous gel has an intermediate value of 5 µm (Figure 9-3). The thickness of mucus in smokers, and particularly in subjects with chronic bronchitis, may be substantially greater (Chapter 7). The calculated variation of dose with depth below the surface of the normal bronchial epithelium for the decay of one alpha particle of 218Po or 214Po per cm2 of airway surface is shown in Figure 9-4. The calculation is based on the mathematical technique described by Harley (1971), except that it uses Armstrong and Chandler's (1973) theoretical stopping power of tissue as a function of alpha-particle energy (Nuclear Energy Agency Group of Experts [NEA], 1983). Both calculations take into account. the additional dose contributed by any alpha particles that cross the airway lumen from the opposite wall. An airway caliber of 5 mm in diameter is assumed to typify a bronchus. In adults, the actual airway caliber varies from about 1 cm in Figure 9-2 Cylindrical model of a bronchial or bronchiolar airway used to calculate doses received by target cell nuclei from alpha-particle decays of radon progeny located in mucus or in the epithelium.

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Comparative Dosimetry of Radon in Mines and Homes Figure 9-3 Model of the location of secretory and basal cell nuclei in bronchial epithelium and of the structure of the mucous layers at the epithelial surface. the main bronchi (referred to as the first bronchial generation) to about 2 mm in the eighth generation, which the committee took to represent the last and smallest bronchi. Since the range of radon progeny alpha particles in air is on the order of 5 cm, however, it is found that the actual airway caliber has little effect on the dose received by epithelial target cells from a given number of alpha-particle decays per unit surface area. Figure 9-4 shows two curves, labeled activity in mucus, for each of 218Po and 214Po. In each case, the lower curve represents activity retained in the 5-µm-thick mucous gel overlying the cilia (see Figure 9-3). The corresponding upper curves represent the higher doses calculated for activity mixed in the 6-µm-thick aqueous layer that bathes the cilia. This amount of variation in the location of the mucous source has a relatively minor impact on calculated doses. In contrast, however, the same number of alpha-particle decays from radon progeny located in the epithelium gives rise to a relatively constant dose throughout the tissue. Figure 9-4 also indicates the range of depths at which secretory or basal cell nuclei are assumed to occur. When the depth-dose curves are averaged over these ranges of target depths, it is found that the average dose received by secretory cell nuclei is relatively independent of the location of radon progeny alpha-particle decays, but the dose received by basal cell nuclei is significantly higher if radon progeny decay in the epithelium rather than in mucus. The degree to which radon progeny are taken up by the epithelium is an uncertain factor in the dosimetry model. Its overall impact on the calculated

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Comparative Dosimetry of Radon in Mines and Homes Figure 9-4 Variation of dose with depth below the surface of bronchial epithelium for alpha-particle decays of radon progeny in mucus or in the epithelium itself. The ranges of depth at which secretory or basal cell nuclei occur are shown for comparison. conversion coefficient between exposure and critical dose is examined later in this chapter. Figure 9-5 illustrates the model of target cell nuclei and mucus assumed by the committee to represent the epithelial lining of the bronchioles. These airways are devoid of basal cells. The sensitive targets are assumed to be the nuclei of secretory cells, which are located between 4 and 12 µm below the epithelial surface (Mercer et al., in press). Both the cilia (the mucous sol layer) and the overlying mucous gel are assumed to be thinner than those in the bronchi (4-µm high and 2-µm thick, respectively). The depth-dose curves calculated for secretory cell nuclei in the bronchiolar epithelium are shown in

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Comparative Dosimetry of Radon in Mines and Homes Figure 9-5 Model of the location of secretory cell nuclei in bronchiolar epithelium and of the structure of bronchiolar mucus. Figure 9-6. In this case, it is found that the average dose received by target cell nuclei does not vary significantly with the location of the radon progeny alpha-particle decays, whether or not these occur in mucus (of the assumed normal thickness) or in the epithelium itself. The values of target cell dose calculated respectively for bronchial and bronchiolar epithelia from the alpha decay of 218Po or 214Po per cm2 of airway wall are given in Table 9-1. It has been found that the epithelial thickness is the same in infants and children as that in the adult (Gehr, 1987). The tabulated dose conversion coefficients are therefore assumed to apply to all subjects. The doses received by these various target cell populations for a given subject, under given conditions of exposure, are evaluated by first modeling the number of 218Po and 214Po alpha decays that occur in each airway generation, using the procedures described below. In order to apply the dose conversion coefficients given in Table 9-1, it is necessary to specify the surface areas of the respective airways in each subject. To do this, a model of the variation of airway caliber and length throughout the bronchial tree must be assumed. Several, more or less complete, models of bronchial and bronchiolar airway dimensions in the adult male have been used previously for radon progeny dosimetry (Weibel, 1963; Yeh and Schum, 1980; Phalen et al., 1985). The airway models of these investigators were derived by measuring casts of human lungs that were made

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Comparative Dosimetry of Radon in Mines and Homes Figure 9-6 Variation of dose with depth below the epithelial surface in the bronchioles. This is shown over the range of depths at which secretory cell nuclei are assumed to occur. at different degrees of inflation in each case. However, even when the reported airway dimensions are scaled to a common lung volume, the different models still exhibit significantly different dimensions (Yu and Diu, 1982). For the purpose of dosimetry, the committee assumes that a "representative" model for the adult male is obtained by averaging the airway dimensions reported in the three studies cited above, after these have been scaled to the normal functional residual capacity (FRC) of 3,000 ml (James, 1988). The model of airway dimensions is needed for two purposes: first, to calculate the fractions of inhaled radon progeny activity that are deposited in each airway generation throughout the bronchial tree (and also in the alveolated respiratory airways) and then to calculate the surface densities of alpha-particle decays throughout the bronchi and bronchioles, in order to evaluate target cell doses. Previous models of radon progeny dosimetry for adult females (who

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Comparative Dosimetry of Radon in Mines and Homes TABLE 9-1 Calculated Mean Doses to Bronchial and Bronchiolar Target Cell Nuclei (in nGy) from 1 α-Decay of 218Po or 214Po per cm2 of Airway Surface   Mucous Gel Epithelium Location of Radon Progeny 218Po 214Po 218Po 214Po Target Cell Nuclei in Bronchi: Secretory cells 78 142 131 264 Basal cells 3 68 126 132 Target Cell Nuclei in Bronchioles: Secretory cells 251 250 264 271 typically have lungs smaller than those of adult males) and children have assumed uniform scaling of airway dimensions with lung volume (Harley and Pasternack, 1982; Hofmann, 1982; NEA, 1983; NCRP, 1984) or, alternatively (James, 1988), have adopted the scaling of bronchial and bronchiolar dimensions with body height reported by Phalen et al. (1985) from measurements of airway casts that were taken from children and infants. However, the data of Phalen et al. surprisingly indicate that the small bronchioles in young children and infants are not substantially different in size from those in adults. These data yield unrealistically high values of the physiological dead space in young subjects. To give values of dead space that are comparable with physiological data (Table 9-2), the committee has adopted the scaling procedure introduced by Yu and Xu (1987) and also used by Egan et al. (1989). The committee assumes that all airway dimensions in the fully grown lungs of adults (male and female) are scaled according to the one-third power of the subject's FRC. The factors reported by Phalen et al. (1985) to scale bronchial airway dimensions for young subjects in terms of their height are based on reasonably complete samplings of all airways. These data can therefore be used to evaluate the size of the trachea and bronchi in growing subjects relative to the standard values adopted for the adult male. However, in the absence of comparable data for the bronchioles, their dimensions must be inferred. It is reasonable to adopt Weibel's (1963) inference that, on average, the diameter and length of bronchioles decrease exponentially in successive generations, until they match the dimensions of the first respiratory bronchioles. The size of the latter is determined by considering how the lung grows from birth to maturity. Once the lung is fully developed, the respiratory airways are scaled replicas of those in the adult. Recent data indicate that this development process is complete by age 2, when the growing lung has a full complement of airways and most of

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Comparative Dosimetry of Radon in Mines and Homes TABLE 9-2 Comparison of Tracheobronchiolar Dead Space Predicted Using the Committee's Model of Airway Dimensions Vis-à-Vis Physiological Data   Anatomical Dead Space (cm3)   Physiological Data Model Subject Age (yr) Cook et al (1955) Hart et al. (1963) Wood et al. (1971) Mean VTOT VTOT VTB VET Newborn 8.5 — — 8.5 — — 1.5 1/12 11 — — 11 13 10.7 1.9 1 — — — — 25 15.9 4.6 5 — 51 — 51 47 33 14 10 — 88 81 85 85 59 26 Woman — 126 127 127 118 78 40 Man — 151 160 155 147 97 50 the final number of alveoli (Gehr, 1987; Zeltner et al., 1987). The respiratory airways are therefore scaled according to the growth in lung volume (FRC). In order to estimate typical dimensions of respiratory airways in the developmental stage from birth to age 2 yr, it is reasonable to assume that the number of airways is virtually complete at birth, but that alveolization of these immature airways is not. The data of Zeltner et al. (1987) indicate that the number of alveoli at age 1 mo is about 20% of the typical adult value, and that at age 1 yr it is about 80%. Hansen et al. (1975) provided a complete description of the branching structure and dimensions of the respiratory acinus in an adult male. This model has been adopted by the committee to derive respiratory airway dimensions for the lungs of children and infants by scaling for lung volume and number of alveoli, respectively (Egan et al., private communication). The derived dimensions of respiratory bronchioles are then used to infer the size of the most distal generation of bronchioles in young subjects. Figures 9-7 and 9-8 show, respectively, the values of airway diameter and length that are given by the above scaling procedures for adult females, children aged 10 or 5 yrs, and infants aged 1 yr or 1 mo. The reference values for the adult male are also shown, for comparison. Table 9-3 gives the corresponding estimates of the total surface area of the airways in each generation of the bronchial and bronchiolar model for each subject. These values are used with the coefficients given in Table 9-1, to convert the calculated number of radon progeny alpha-particle decays in each airway generation into radiation doses absorbed by target cell nuclei. CLEARANCE MODEL The process of breathing continuously deposits radon progeny at all levels in the bronchial tree. The process of mucociliary clearance, which acts in all

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Comparative Dosimetry of Radon in Mines and Homes Figure 9-7 Scaling of airway diameter throughout the lung respiratory pathway assumed for the calculation of radon progeny deposition and dose in each generation for adults, children, and infants. The trachea is labeled generation 0. Airway generations 1-8 represent the bronchi. These are scaled with body height according to data from Phalen et al. (1985). Generations 9-15 represent the bronchioles. Generations 16-26 represent the respiratory airways whose dimensions are based on the model of Hansen et al. (1975). ciliated airways, continually redistributes these progeny in a proximal direction (toward the trachea and larynx). This tends to concentrate the alpha particle decays on smaller areas of airway surface (as shown in Table 9-3), since the number of airways is halved each time subsidiary branches converge into a common parent. The combination of these processes with that of radioactive decay determines the number of alpha decays that occur in each airway generation, the surface density of the decays, and thus the dose received by target cells. This complex movement and decay of radon progeny within the bronchial tree is represented mathematically by a so-called clearance model. Figure 9-9 shows the model used by the committee to calculate the number of radon progeny decays that occur in each airway generation. The model represents the average time taken by a theoretical, discrete packet of mucous gel to traverse a given airway generation by the parameter 1/λ2, where λi is a constant that represents the rate of mucous transport in the ith generation. If k represents each of the short-lived radon progeny in turn (218Po through 214Pb

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Comparative Dosimetry of Radon in Mines and Homes Figure 9-8 Scaling of airway length as described for Figure 9-7. TABLE 9-3 Total Surface Area of the Airways in Each Generation of the Committee's Model of the Bronchial Tree for Adults, Children, and Infants   Surface Area (cm2)   Adult Child Infant Airway Gen. No. Male Female 10 yr 5 yr 1 yr 1 mo Trachea 0 47 41 30 20 9.3 5.1 Bronchi 1 29 25 19 13 7.1 4.4   2 16 14 11 7 4.1 2.6   3 13 11 9 6 3.2 2.0   4 20 17 14 10 6.5 4.6   5 29 25 20 14 8.5 5.7   6 39 33 27 19 11.7 8.0   7 58 50 43 33 22 17   8 85 74 68 55 41 34 Bronchioles 9 113 98 90 70 51 42   10 154 134 120 89 63 52   11 227 196 161 113 77 64   12 298 258 212 142 95 80   13 402 348 284 181 116 99   14 545 476 378 231 145 122   15 824 721 508 297 179 152

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Comparative Dosimetry of Radon in Mines and Homes TABLE 9-6 Summary of Coefficients to Convert Exposure to Radon Progeny Potential Alpha-Energy into the Averagea Dose to Basal Cell Nuclei in the Bronchi of Different Subjects (Normal Nasal Breathers) as a Function of the Radon Progeny Aerosol Size and the Subject's Level of Physical Exertion Subject Radon Progeny AMTD (µm) With Assumed Nasal Deposition Exposure-Dose Conversion Coefficient (mGy per WLM) for the Following Level of Physical Exertion     Sleep Rest Light Exercise Heavy Exercise Adult Male 0.0011b 48.9 59.6 153.0 321.2   0.0011c 23.4 28.9 80.9 210.7   0.02 18.3 20.0 31.5 41.6   0.15 4.66 5.04 7.86 11.8   0.25 3.35 3.64 6.31 14.9   0.3 3.03 3.31 6.22 18.4   0.5 2.63 2.93 7.51 38.6 Adult Female 0.0011b 39.9 48.8 152.5 340.9   0.0011c 18.6 23.1 80.0 223.2   0.02 19.1 21.4 36.2 49.2   0.15 4.66 5.17 8.62 13.4   0.25 3.29 3.64 6.75 17.1   0.3 2.95 3.27 6.59 21.1   0.5 2.48 2.77 7.77 44.4 Child age 10 yr 0.0011b 48.8 60.2 166.5 —   0.0011c 23.0 28.8 87.5 —   0.02 22.3 24.9 40.1 —   0.15 5.38 5.98 9.58 —   0.25 3.81 4.25 7.61 —   0.3 3.43 3.84 7.47 —   0.5 2.89 3.30 8.80 — Child age 5 yr 0.0011b 55.7 74.9 129.4 —   0.0011c 26.1 36.0 65.6 —   0.02 25.8 29.7 38.2 —   0.15 6.04 6.98 8.94 —   0.25 4.34 5.05 6.66 —   0.3 3.93 4.61 6.26 —   0.5 3.33 4.08 6.42 — Infant age 1 yr 0.0011b 63.8 94.3 148.6 —   0.0011c 29.6 45.2 74.3 —   0.02 33.2 39.6 48.2 —   0.15 7.77 9.06 10.9 —   0.25 5.56 6.65 8.19 —   0.3 5.02 6.11 7.69 —   0.5 4.17 5.47 7.67 — Infant age 1 mo 0.0011b 50.1 — 78.8 —   0.0011c 22.4 — 36.7 —   0.02 36.8 — 45.9 —   0.15 9.02 — 10.9 —   0.25 6.25 — 7.35 —   0.3 5.54 — 6.47 —   0.5 4.25 — 5.01 — a Average value of the exposure-dose conversion coefficient calculated on the alternative assumptions that radon progeny are i) insoluble or ii) partially soluble in mucus. b Nasal deposition of unattached progeny according to George and Breslin (1969). c Nasal deposition of unattached progeny according to Cheng et al. (1989).

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Comparative Dosimetry of Radon in Mines and Homes Figure 9-22 Effects of radon progeny aerosol size on calculated dose to secretory cell nuclei—adult male (insoluble/light exercise/nose breather). Figure 9-23 Effects of radon progeny aerosol size on calculated dose to secretory cell nuclei—adult male (soluble/light exercise/nose breather).

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Comparative Dosimetry of Radon in Mines and Homes secretory cells that occurs throughout the bronchi (generations 1 through 8 in the lung model). The reference doses are approximately twofold lower if they are averaged for secretory cells in the bronchioles (generations 9 through 15 in the lung model). It is noted that, for targets in both "lobar/segmental bronchi" and "all bronchi," the dose per unit exposure is approximately 25-fold higher for unattached progeny (with AMTD ≈ 0.001 µm) than it is for attached progeny with equilibrium AMTD in the range 0.3 to 0.5 µm. This ratio is somewhat lower (at approximately 20-fold) for targets in the bronchioles. For ultrafine radon progeny aerosols (AMTD < 0.01 µm), the dose per unit exposure is strongly influenced by the assumed nasal filtration efficiency. Figure 9-23 shows the equivalent exposure-dose conversion coefficients that are calculated if the radon progeny are assumed to be partially (30%) taken up by epithelial tissue at the site of deposition. Comparison with Figure 9-22 shows that this degree of uncertainty in the clearance behavior of radon progeny has a small effect on doses calculated for secretory cell targets. However, if basal cells are instead assumed to be the principal targets, significantly different values of the exposure-dose conversion coefficient are calculated (Figure 9-24). In this case, dose conversion coefficients are approximately twofold lower for ultrafine radon progeny aerosols than they are for secretory cells, and uncertainty in the clearance behavior of radon progeny has a greater impact. Influence of Exercise Figure 9-25 shows exposure-dose conversion coefficients calculated for secretory cell nuclei throughout the bronchi for a man at various levels of physical exertion. It is seen that the calculated doses increase markedly with exercise for both unattached progeny and for large attached aerosols (with AMTD ≈ 0.5 µm) . These findings are significant for the evaluation of doses for exposure of underground miners. Influence of Age and Gender Figure 9-26 shows exposure-dose conversion coefficients calculated for a man, a woman, and children and infants (of either sex) of different age. In this case, the subjects are taken to be resting, and the target cells are taken to be secretory cells throughout the bronchi. It is seen that dose conversion coefficients are calculated to be somewhat lower for a woman than for a man, whereas they are generally higher in children and in the 1-year-old infant.

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Comparative Dosimetry of Radon in Mines and Homes Figure 9-24 Effects of radon progeny aerosol size on calculated dose to basal cell nuclei—adult male (light exercise/nose breather). Figure 9-25 Effects of radon progeny aerosol size and exercise on calculated dose to secretory cell nuclei in the bronchi—adult male (nose breather).

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Comparative Dosimetry of Radon in Mines and Homes Figure 9-26 Effects of radon progeny aerosol size on calculated dose to secretory cell nuclei in bronchi for different subjects (resting/nose breather). Figure 9-27 Modeled effect of bronchitis on calculated dose to secretory cell nuclei in bronchi—adult male (light exercise/nose breather).

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Comparative Dosimetry of Radon in Mines and Homes Figure 9-28 Effect of epithelial hyperplasia on calculated dose to bronchial target cells—adult male (light exercise/nose breather). Figure 9-29 Effect of epithelial regeneration on calculated dose to bronchial secretory cell nuclei—adult male (light exercise/nose breather).

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Comparative Dosimetry of Radon in Mines and Homes Influence of Airway Disease Figures 9-27 through 9-29 illustrate the effects of modeling various disease conditions on the calculated exposure-dose conversion coefficient. In the case of a man with bronchitis (Figure 9-27), the effect of thickened mucus is to reduce the calculated doses by about a factor two. Markedly lower doses are also calculated for target cells in areas of hyperplastic epithelium. Figure 9-28 compares doses calculated for basal cells in hyperplastic epithelium (where no secretory cells are present) with those calculated for both secretory and basal cell targets in normal epithelium. Finally, Figure 9-29 compares doses calculated for secretory cells in thinned epithelium that is undergoing regeneration with those in epithelium of normal thickness. In this case, target cells in the damaged epithelium are calculated to receive about twofold higher doses than those in normal epithelium. REFERENCES Armstrong, T. W., and K. C. Chandler. 1973. SPAR, a FORTRAN Program for Computing Stopping Powers and Ranges for Muons, Charged Pions, Protons and Heavy Ions. ORNL-4869. Oak Ridge, Tenn.: Oak Ridge National Laboratory . Bianco, A., F. R. Gibb, and P. E. Morrow. 1974. Inhalation study of a submicron size lead-212 aerosol. Pp. 1214-1219 in Proceedings of the 3rd International Congress of the International Radiological Protection Association. CONF-730907. Washington, D.C.: U.S. Atomic Energy Commission. Booker, D. V., A. C. Chamberlain, D. Newton, and A. N. B. Stott. 1969. Uptake of radioactive lead following inhalation and injection. Br. J. Radiol. 42:457-466. Cheng, Y. S., Y. Yamada, H. C. Yeh, and D. L. Swift. 1988. Diffusional deposition of ultrafine aerosols in a human nasal cast. J. Aerosol Sci. 19:741-752. Cheng, Y. S., D. L. Swift, Y. F. Su, and H. C. Yeh. 1989. Deposition of radon progeny in human head airways. Proceedings of the DOE Technical Exchange Meeting on Assessing Indoor Radon Health Risks, September 18-19, 1989, Grand Junction, Colo. Department of Energy CONF 8909190. Springfield, Va.: National Technical Information Service. Cheng, Y. S., Y. Yamada, H. C. Yeh, and D. L. Swift. 1990. Deposition of ultrafine aerosols in a human oral cast. Aerosol Sci. Technol. 12:1075-1081. Cohen, B. S. 1987. Deposition of ultrafine particles in the human tracheobronchial tree: A determinant of dose from radon daughters. Pp. 475-486 in Radon and Its Decay Products: Occurrence, Properties, and Health Effects, P. K. Hopke, ed. Washington, D.C.: American Chemical Society. Cohen, B. S., R. G. Sussman, and M. Lippmann. 1990. Ultrafine particle deposition in a human tracheobronchial cast. Aerosol Sci. Technol. 12:1082-1091. Cook, C. D., R. B. Cherry, D. O'Brien, P. Karlberg, and C. A. Smith. 1955. Studies of respiratory physiology in the newborn infant. I. Observations on normal premature and full-term infants. J. Clin. Invest. 34:975-982. Cooper, D. M., and D. Weiler-Ravell. 1984. Gas exchange response to exercise in children. Am. Rev. Respir. Dis. 129(Suppl.):S47-S48. Cotes, J. E. 1979. Lung function assessment and application in medicine. Oxford: Blackwell Scientific Publications.

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