Summary and Recommendations

Epidemiological investigations of uranium and other underground miners have provided extensive and consistent data on the quantitative risk of lung cancer associated with exposure to radon progeny in underground mines (Lubin, 1988; National Research Council [NRC], 1988). To extend these data to radon exposure of the general population in the home environment, a series of assumptions with attendant uncertainties must be made (see Figure 1-2). This report compares relations in the home and mining environments between exposure to radon progeny and the dose of alpha radiation to target cells in the respiratory epithelium. A dosimetric model is used to estimate the quantitative uncertainty introduced by differences in exposure-dose relations for miners and the general population who are exposed in their homes (Chapter 3). Additional sources of uncertainty that relate to the likelihood of lung cancer, including age at exposure, sex, cigarette smoking, and effects of environmental contaminants other than radon, are addressed qualitatively in Chapter 4.

The committee's dosimetric model incorporates a wide range of physical and biological parameters (see Chapter 9), some of which plausibly differ for the circumstances of exposure in the mining and home environments. Among the parameters selected by the committee as being different in the two environments are: aerosol size distribution, unattached fraction, and breathing rate and route. For those parameters, the committee reviewed the available evidence to estimate the values most typical in the two environments and to characterize their ranges. The committee also explored the consequences of various underlying model assumptions for the efficiency of nasal deposition, the efficiency of bronchial deposition, the solubility of progeny in mucus, and



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Comparative Dosimetry of Radon in Mines and Homes Summary and Recommendations Epidemiological investigations of uranium and other underground miners have provided extensive and consistent data on the quantitative risk of lung cancer associated with exposure to radon progeny in underground mines (Lubin, 1988; National Research Council [NRC], 1988). To extend these data to radon exposure of the general population in the home environment, a series of assumptions with attendant uncertainties must be made (see Figure 1-2). This report compares relations in the home and mining environments between exposure to radon progeny and the dose of alpha radiation to target cells in the respiratory epithelium. A dosimetric model is used to estimate the quantitative uncertainty introduced by differences in exposure-dose relations for miners and the general population who are exposed in their homes (Chapter 3). Additional sources of uncertainty that relate to the likelihood of lung cancer, including age at exposure, sex, cigarette smoking, and effects of environmental contaminants other than radon, are addressed qualitatively in Chapter 4. The committee's dosimetric model incorporates a wide range of physical and biological parameters (see Chapter 9), some of which plausibly differ for the circumstances of exposure in the mining and home environments. Among the parameters selected by the committee as being different in the two environments are: aerosol size distribution, unattached fraction, and breathing rate and route. For those parameters, the committee reviewed the available evidence to estimate the values most typical in the two environments and to characterize their ranges. The committee also explored the consequences of various underlying model assumptions for the efficiency of nasal deposition, the efficiency of bronchial deposition, the solubility of progeny in mucus, and

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Comparative Dosimetry of Radon in Mines and Homes TABLE S-1 Summary of K Factors for Bronchial Dose Calculated for Normal People in the General Environment Relative to Healthy Underground Miners   K Factor for the Following Target Cells: Subject Category Secretory Basal Infant, age 1 mo 0.74 0.64 Child, age 1 yr 1.00 0.87 Child, age 5-10 yr 0.83 0.72 Female 0.72 0.62 Male 0.76 0.69 the growth of aerosols in the respiratory tract. Because uncertainty remained after the committee's review concerning the cells of origin of lung cancer, the committee performed the calculations separately for basal and secretory cells in the respiratory epithelium. In addition to adult males, calculations were performed for adult females and for children and infants. Finally, the committee considered the consequences of abnormalities of the airways, such as those that might occur with chronic bronchitis caused by cigarette smoking or exposure to dusts and gases in mines. The committee's findings on the differences in exposure-dose relations in mines and in homes are expressed as a ratio, termed K in the BEIR IV report (NRC, 1988). This ratio represents the quotient of the dose of alpha energy delivered per unit exposure to an individual in the home to the dose per unit exposure to a male miner in a mine. Thus, if the K factor exceeds unity, the delivered dose per unit exposure is greater in the home; if it is less than unity, the delivered dose per unit exposure is less in the home. Across the wide range of exposure scenarios considered by the committee, most values of K were less than unity (see Tables 3-4, 3-5, and 3-6). The K factor was also below unity for adult females and children. The K factors for normal people without respiratory illnesses are summarized in Table S-1. The committee's literature review (see Chapter 2) indicated that homes tended to have higher unattached fractions of radon progeny and room aerosols with smaller aerodynamic diameter than those in mines, although smoking or other activities can lower the unattached fraction and increase the aerosol size. Higher breathing rates were assumed for miners because of the work load imposed by the physical activity of mining. For an adult male exposed in the mining or home environment under typical conditions, the K factors ranged from about 0.8 to 0.6, depending on the assumptions concerning the solubility of radon progeny in mucus. Similar calculations were performed for adult females and children. For adult females, the K factors tended to be somewhat lower than those for adult

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Comparative Dosimetry of Radon in Mines and Homes males. In several risk assessments, children and infants have been considered to be at increased risk for radon-induced lung cancer in comparison with the risk for adults because of heightened susceptibility (International Commission on Radiological Protection [ICRP], 1987; Puskin and Nelson, 1989). Although the K factors for children and infants were somewhat greater than those for adults, none of the values was above unity. The committee examined the sensitivities of these findings to changes in the underlying biological assumptions in its model. The K factors remained below unity regardless of whether radon progeny were assumed to be insoluble or partially soluble in the epithelial tissue. The K factor changed little with the assumption that lobar and segmental bronchi (K = 0.69) rather than all bronchi (K = 0.73) are the target tissues. Similarly, the K values changed little as the assumptions concerning the efficiencies of nasal and airway deposition were changed. The findings were comparable across the range of conditions examined for both secretory and basal cells as well. At the extremes of selection of breathing route, exclusively nasal and exclusively oral, the general pattern of the K values was also unchanged. Using a dosimetric model, the committee comprehensively compared exposure-dose relations for mining and home environments. The committee's calculations indicate that the dose of alpha energy per unit exposure delivered to target cells in the respiratory tract tends to be lower for the home environment—by about 30% for adults of both sexes and by 20% or less for infants and children. Thus, direct extrapolation of risk estimates from the mining to the home environment may overestimate the numbers of radon-caused lung cancer cases by these percentages. The limitations of this analysis are addressed in detail in the report. Any dosimetric model, regardless of its sophistication, inevitably simplifies extremely complex physical and biological phenomena. In this report, however, the same model was applied to people in both the mining and home environments. Substantial uncertainty remains concerning the appropriate values for most of the model's parameters. For example, the data on breathing rate and route (oral versus nasal) of the miners and the general population are extremely limited, as are measurements of the unattached radon fractions in the two environments. The distributions of values for most of the model's parameters have not been described in appropriate samples. The committee's recommendations for research to address these uncertainties are provided at the end of this chapter. Other committees and researchers have also compared exposure-dose relations in mines and homes (see James [1988]). Recent reports of the National Council on Radiation Protection and Measurements (NCRP), the ICRP, and the NRC have addressed this issue. NCRP Report No. 78 (NCRP, 1984) used a dosimetric model to calculate the dose of alpha energy delivered to basal cells. K values calculated from the dose conversion factors provided in that report were 1.40 for adult males, 1.20 for adult females, 2.40 for children, and 1.20

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Comparative Dosimetry of Radon in Mines and Homes for infants. ICRP Publication No. 50 concluded that K is 0.8 for adult males and females in indoor environments. For children ages 0 to 10 yr, the report's authors suggested that the dosimetric correction might be about 1.5 times larger than that for adults. On the basis of a qualitative analysis, the BEIR IV committee (NRC, 1988) concluded that a K value of 1 could justifiably be assumed. The fact that the findings of the present report diverge from those of earlier reports reflects the further evolution of dosimetric models and the availability to the present committee of additional data on input parameters for the dosimetric model. This committee also examined other sources of uncertainty in extrapolating risk coefficients from studies of miners to the general population (see Figure 4-2). These sources of uncertainty related not only to aspects of lung dosimetry but to the biology of lung cancer. The committee could not consider these factors directly in the dosimetric model, and their impact on the extrapolation could not be gauged quantitatively. Nevertheless, because the uncertainties associated with these factors are potentially large, the committee synthesized the available evidence on sex, age at exposure and age at risk, exposure rate, cigarette smoking, and agents that cause epithelial injury and promote cell turnover. The BEIR IV report (NRC, 1988) also considered the evidence on sex, age, and cigarette smoking. The assumption of a greater or lesser risk of lung cancer in children who are exposed to radon has substantial public health implications. ICRP (1987) assumed a threefold greater risk of cancer for exposure during childhood on the basis of dosimetric considerations and the increased lung cancer risk for atomic bomb survivors who were age 20 yr or younger at the time of the blast. The latter evidence is extremely limited, however; on follow-up through 1980, only 10 cases of lung cancer had occurred in persons aged 0 to 10 yr at the time of the bomb (15,564 were at risk) (Yamamoto et al., 1986), and their relative risk of lung cancer through 1985 is less than 1 (Shimizu et al., 1988). Moreover, the relevance of these data, based on low-LET radiation, to the high-LET radiation from radon progeny is uncertain. The present risk assessment approach of the U.S. Environmental Protection Agency incorporates in part ICRP's threefold greater risk for those aged 0 to 20 yr (Puskin and Nelson, 1989). By contrast, the model in the BEIR IV report (NRC, 1988) reduces the risks as the interval since exposure lengthens, implying a lower risk of lung cancer for exposures during childhood. In its analyses, the BEIR IV committee did not find an effect of age at exposure, but little information was available for miners at young ages. A recent case-control study of lung cancer in radon-exposed Chinese tin miners, 37% of whom were exposed by age 13 yr, offers some relevant information (Lubin et al., 1990). The increase in risk of lung cancer did not vary significantly with age at first exposure. Thus, assumption of either an enhanced or a reduced effect for exposure during childhood is subject to substantial uncertainty.

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Comparative Dosimetry of Radon in Mines and Homes The committee considered cigarette smoking, which was also reviewed in depth by the BEIR IV committee (NRC, 1988). On the basis of literature review as well as its own analyses, the BEIR IV committee concluded that cigarette smoking and radon progeny interact multiplicatively. That committee noted the uncertainty inherent in extrapolating from a population of males, predominantly smokers, to smokers and nonsmokers of both sexes. Since publication of the BEIR IV report, evidence has not been published that would justify a revised conclusion on the combined effects of smoking and radon exposure. The present committee did address the consequences of bronchitis and hyperplasia of the epithelium with attendant cessation of mucus flow, both of which are effects of cigarette smoking, in the dosimetric model (see Table 3-6). Underground miners inhale not only radon and progeny but silica and other dusts, blasting fumes, and sometimes engine exhaust as well. Inflammation of the airways with increased cell proliferation may result. This environmental difference should also be considered in extrapolating from miners to the general population in their homes. The increased cell turnover associated with exposures to these other agents in the mining environment may have increased the risk per unit exposure for the miners in comparison with exposure in the absence of these other agents (see Chapter 4). For the general population, radon exposure occurs throughout the life span at a rate principally dependent on the concentrations in homes. Most of the miners included in the epidemiological studies were exposed underground for only a small proportion of their life spans. The extant risk models do not incorporate terms representing possible changes in risk associated with different exposure rates in the mining and general populations. The committee concluded that it is reasonable to assume that risk is proportional to total exposure (i.e., there is no dose rate effect). Although the K factors imply a somewhat lower lung cancer risk for exposure in the home environment, the committee's findings do not imply that radon is not carcinogenic. The dosimetric modeling in this report suggests that the BEIR IV committee's risk assessments based on the data from miners may have overestimated to some extent the numbers of radon-associated cases of lung cancer in the general population. However, the degree of overestimation is not large. In applying the data from miners to the general population, it is now likely that assumptions related to other factors (e.g., age at exposure and cigarette smoking) introduce larger uncertainties than the uncertainties related to dosimetric differences between exposures in mines and in homes. RECOMMENDATIONS FOR FURTHER RESEARCH AND ANALYSIS To have more certain estimates of the dose per unit exposure and the K factors described here, further data are needed for the input parameters of dosimetric models, as is improved biologic understanding of carcinogenesis due

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Comparative Dosimetry of Radon in Mines and Homes to radon progeny. The committee has reviewed these needs and makes the following recommendations for further studies. Assessment of the activity-weighted size distributions of radon progeny in homes, schools, high-rise apartment buildings, and offices is needed. These studies should examine the effects of various indoor aerosol sources on these distributions. Additional data on activity-weighted size distributions of particles in underground mines, comparable to those worked in by the miners in the epidemiological cohorts, are also needed. Further research is needed on radon carcinogenesis to support the development of biologically based mathematical models of the temporal pattern of tumor formation. The roles of age, tissue injury, and interactions with other environmental toxicants in the carcinogenic response to radon need further investigation. Animal experiments are needed to assess modification of the dose-response relation between lung cancer and radon exposure by smoking and other factors. Because of the difficulty of determining the dose of alpha energy delivered by radon progeny to the bronchial epithelium, the development of biological markers should be undertaken. Data on breathing by humans should be gathered in a variety of settings. Methods have been developed that allow measurements of tidal volume from body surface displacements. Alternatively, once calibrated, heart rate can be used as a surrogate for oxygen consumption. This technology should be adapted to field use, and measurements should be made in many places, including mines and homes. More data are also needed on the range of human activities indoors with associated ventilation rates. Additional studies are needed on the anatomic locations in which radon progeny deposit. Little information is available, especially in humans, regarding where these radon progeny are retained. Additional information is needed on respiratory deposition of particles less than 0.1 mm in aerodynamic diameter. Sites of interest are the upper airway, trachea, and bronchi. More data are needed on the location and morphologic types of lung cancers and on temporal trends in these parameters. Information on the effect of smoking on the anatomic distribution of lung cancers should be obtained, both for underground miners and the general population. Additional research should be undertaken to determine whether different histologic types of bronchogenic lung cancer result from different genetic changes in a common bronchial stem cell precursor or from transformation of different types of bronchial cells. For example, further research is needed to determine whether undifferentiated small-cell carcinomas of the lung arise from

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Comparative Dosimetry of Radon in Mines and Homes bronchial Kulchitsky cells of neural crest origin (neurosecretory cells) or from an endodermal precursor or stem cell in the bronchus. More information is needed on the hygroscopicity of radon progeny aerosols, on the degree to which they increase in size within the respiratory tract, on the time taken for any growth to occur, and on the effects of hygroscopic growth on deposition within the bronchial airways. Estimates of the filtration efficiency of the nasal and oral passageways for unattached radon progeny that have been developed from studies with hollow casts need to be confirmed by in vivo measurements of extrathoracic filtration in sufficient numbers of human subjects. It is also necessary to study the nasal and oral filtration efficiencies in vivo in children. It is necessary to extend studies of the deposition efficiency of submicron particles in hollow casts of the human bronchi to much smaller particles in the size range of unattached radon progeny. When coupled with more accurate information on extrathoracic filtration efficiencies, such studies of localized bronchial deposition will resolve some of the uncertainty in evaluating doses from exposure to unattached progeny. A better understanding is needed of the respective roles of secretory and basal cells in the etiology of lung cancer, and of the relative sensitivities of the epithelial lobar, segmental, and subsegmental bronchi. Estimates of doses received by bronchial basal cells are especially sensitive to uncertainties in the thickness and structure of the epithelium, in the thickness of mucus and its variability, and in the degree to which radon progeny migrate from mucus to be retained in epithelial tissue. Further investigation of these parameters is needed. REFERENCES International Commission on Radiological Protection (ICRP). 1987. Lung Cancer Risk from Indoor Exposures to Radon Daughters. ICRP Publ. No. 50. Oxford: Pergamon Press. James, A. C. 1988. Lung dosimetry. Pp. 259-309 in Radon and Its Decay Products in Indoor Air, W. W. Nazarof and A. V. Nero, Jr., eds. New York: John Wiley & Sons. Lubin, J. H. 1988. Models for the analysis of radon-exposed populations. Yale J. Biol. Med. 61:195-214. Lubin J. H., Y. Qiao, P. R. Taylor, S. X. Yao, A. Schatzkin, B. L. Mao, J. Y. Rao, X. Z. Xuan, and J. Y. Li. 1990. Quantitative evaluation of the radon and lung cancer association in a case control study of Chinese tin miners. Cancer Res. 50:174-180. National Council on Radiation Protection and Measurements (NCRP). 1984. Evaluation of Occupational and Environmental Exposure to Radon and Radon Daughters in the United States. NCRP Report No. 78. Bethesda, Md.: National Council on Radiation Protection and Measurements.

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Comparative Dosimetry of Radon in Mines and Homes National Research Council (NRC). 1988. Health Risks of Radon and Other Internally Deposited Alpha-Emitters. BEIR IV. Committee on the Biological Effects of Ionizing Radiation. Washington, D.C.: National Academy Press. Puskin J. S., and C. B. Nelson. 1989. Environmental Protection Agency's perspective on risks from residential radon exposure. J. Air Pollut. Control Assoc. 39:915-920. Shimizu, Y., H. Kato, and W. J. Schull. 1988. Life Span Study Report II. Part 2. Cancer Mortality in the Years 1980-85 Based on the Recently Revised Doses. DS86 RERF TR 5-88. Hiroshima: Radiation Effects Research Foundation. Yamamoto, T., K. J. Kopecky, T. Fujikura, S. Tokuoka, T. Monzen, I. Nishimori, E. Nakashima, and H. Kato. 1986. Lung Cancer Incidence Among A-Bomb Survivors in Hiroshima and Nagasaki. RERF TR 12-86. Hiroshima: Radiation Effects Research Foundation.