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National Research Council (US) Committee on the Biological Effects of Ionizing Radiations. Health Risks of Radon and Other Internally Deposited Alpha-Emitters: Beir IV. Washington (DC): National Academies Press (US); 1988.

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Health Risks of Radon and Other Internally Deposited Alpha-Emitters: Beir IV.

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Appendix IIIThe Effects of Radon Progeny on Laboratory Animals

Animal studies have been conducted for over 50 yr to examine the respiratory effects of pollutants in the air of mines. This work, emphasizing respiratory cancer, has provided important data on exposure-response relationships and the interactions among the harmful agents to which miners are exposed. Many of the initial studies were concerned with early effects or short-term pathological changes.21,22,29 In many of the studies, exposures were based primarily on radon-gas concentrations, with little or no consideration of radon-daughter concentrations, which have been shown to contribute the greatest radiation dose to the lung. Two American research centers—the University of Rochester and the Pacific Northwest Laboratory (PNL)—and the Compagnie Generale des Matieres Nucleaires (COGEMA) laboratory in France have contributed most of the experimental data on radon-daughter inhalation by laboratory animals.

Inhalation Studies at the University of Rochester

Beginning in the 1950s, investigators examined the biological and physical behaviors of radon daughters and the dosimetry of radon daughters in the respiratory tract.1,20,25 Shapiro31 exposed rats and dogs to radon alone at several concentrations and to radon with radon daughters attached to room-dust aerosols. The degree of attachment of radon daughters to carrier dust particles was shown to be an important determinant of the alpha-radiation dose to the airway epithelium and that more than 95% of the dose to the airway epithelium was due to the short-lived radon daughters radium A (218Po) and radium C' (214Po), rather than to the parent radon. In 1953, Cohn et al.9 reported the relative levels of radioactivity found in the nasal passages, the trachea and major bronchi, and the other portions of rat lungs after exposure to radon or radon daughters. The respiratory tracts of animals that inhaled radon with its daughters contained 125 times more activity than those of animals that inhaled radon alone. Beginning in the mid-1950s, Morken,2527 and Morken and Scott28 initiated a series of experiments to evaluate the biological effects of inhaled radon and radon daughters in mice; later experiments also used rats and beagles. The negative results of these studies suggested that alpha irradiation was inefficient in producing tumors in the respiratory system.

These experiments were noteworthy in describing exposure-dose relationships in the whole lung, in regions of the lung, and in other organs. The paucity of pathological effects did not permit examination of exposure-response relationships for carcinogenesis, as demonstrated later by experiments at COGEMA and PNL. In the early experiments, the only apparent late, permanent changes occurred in the alveolar and possibly the bronchiolar regions of the lung. They were observed for a wide range of doses and developed after 3 yr in the dog and 1 and 2 yr in the rat and mouse, respectively. Some of these changes might have been preneoplastic, but the high-level exposures (associated with life-span shortening) and the early termination of experiments precluded further development to neoplasia. The influence of the radon-daughter carrier aerosol (laboratory air) on the results of these experiments is uncertain, but it might have led to more rapid solubilization of the daughters into blood and a resulting decrease in irritation or fibrosis, in comparison with ore-dust and silica aerosols.

Inhalation Studies at Cogema

The studies by Chameaud and colleagues28 were begun in the late 1960s and early 1970s to determine whether radon and its daughters induced tumors in rats and to provide experimental data to support the epidemiological data on radon-daughter carcinogenesis. Before 1972, rats were exposed to ambient air that was enriched with radon after passage through trays of finely ground ore containing 25% uranium. Resulting radon concentrations were 0.75 µCi/liter; radon-daughter equilibrium factors were about 30%. With filters and electrostatic purifiers, the equilibrium factor was reduced to about 1%. Radon-daughter concentrations were calculated to be around 2,300 and 75 working levels (WL), respectively, for the two radon-daughter equilibrium conditions.

After 1972, animals were exposed to radon derived from underground barrels of radium-rich lead sulfate. Radon was pumped by a closed circuit into a 1-m3 equilibration container and then to two 10-m3 metal inhalation chambers. Up to 600 rats could be exposed for as long as 16 h when oxygen was added to the inhalation chambers. The maximum radon concentration was 1.25 µCi/liter, generally at 100% equilibrium with radon daughters. By calculation, the maximum radon-daughter concentration was 12,500 WL. Because of radon-daughter deposition on the cages and the hairs of rats, the disequilibrium of the radon daughters increased as the number of animals in the inhalation chambers increased. Exposure periods ranged from about 1 to 10 months; exposure rates ranged from less than 10 to hundreds of working-level months (WLM)/wk, the majority averaging approximately 200–400 WLM/wk.*

In two major experiments,2 rats were exposed by inhalation to stable cerium hydroxide or to uranium-ore dust concentrations with and without radon daughters, at 130 mg/m3, to determine whether the presence of dust altered the carcinogenic effect of radon daughters. Exposure to stable cerium hydroxide before exposure to radon daughters shortened the induction latent period by 2–3 months. Uranium-ore dust (given on days alternating with days of radon-daughter exposure) appeared to have little influence on the tumorigenic process, although too few animals were used to permit a firm conclusion.5 Radon-daughter exposures varied from 500 to 8,500 WLM. The effect of the radon daughters did not change with the various equilibrium ratios. These experiments confirmed that radon daughters alone induced tumors in rats.

Other changes were observed in these experiments. These are given below.

  • After large radon-daughter exposures, large areas of diffuse interstitial pneumonia with hyaline membrane formation and with severe fibrosis of interalveolar septa surrounding capillaries were noted. Death generally occurred within a few weeks to a few months if exposure exceeded 6,000 WLM. No lung cancers were produced.
  • Animals lived longer after smaller radon-daughter exposures, with lung carcinomas appearing 12–24 months after the beginning of exposure. The time to appearance of tumors increased with decreasing cumulative radon-daughter exposure. Exposures of 2,000–5,000 WLM, delivered over 300–500 h (during 3–4 months) produced the highest incidence of tumors.
  • Bronchiolar metaplasia occurred at the bronchioloalveolar junction and in neighboring alveoli. It consisted of large columnar cells with basal nuclei and light-colored protoplasm that were often ciliated. Alveolar metaplasia of cuboidal cells, with darker protoplasm, appeared in peripheral regions of the lungs.
  • Adenomatous lesions of varied size and cell layers covered areas of the alveolar septa. Adenomas consisting of round tumors with cells often clustered together occurred. Some adenomas showed malignant characteristics.
  • Malignant tumors of several different types occurred, often in the same animal. These included epidermoid carcinomas, not always clearly differentiated, often keratinized or necrosed, and occasionally extending into the mediastinum; bronchiolar adenocarcinomas, sometimes mucus-producing, containing numerous cellular anomalies, and characterized by a high number of mitoses and invasion of other lung lobes, but seldom metastatic; and bronchioloalveolar adenocarcinomas with few mitoses, but later invading the mediastinum, diaphragm, and thoracic wall.
  • The relationship of exposure to tumor incidence, uncorrected for life-span shortening, was not linear over a wide range of exposures; the incidence per unit exposure increased with decreasing high cumulative exposure.

Later experiments, which confirmed these pathological findings, extended the radon-daughter exposures to approximately 20–50 WLM.5,7,8 Tumor-incidence and survival-time data and lifetime lung-tumor risk coefficients are shown in Table III-1. Although the risk data are uncorrected for life-span shortening, hazard-function analysis demonstrated that when the data are adjusted for competing causes of death, the excess risk of developing pulmonary tumors is approximately linearly related to exposure throughout the range of exposures studied.19 Further findings are given below.

TABLE III-1. Summary of Tumors Primary to Lungs of Rats, Median Survival Times, and Lung-Tumor Risk Coefficients for COGEMA Radon-Daughter Exposures.


Summary of Tumors Primary to Lungs of Rats, Median Survival Times, and Lung-Tumor Risk Coefficients for COGEMA Radon-Daughter Exposures.

  • The tumor latent period, defined as the interval between the start of radon-daughter exposure and death or killing, of the animal increased with decreasing cumulative WLM. Mean latent periods of tumor-bearing animals were around 750 days for exposures of less than 300 WLM and 650 days for exposures of over 1,000 WLM.
  • Lung cancers in rats invaded pulmonary lymph nodes, but metastases to other tissues were rare. Tumor size increased with increasing cumulative WLM.
  • No radiation-induced small-cell carcinomas were observed in rats; however, other histological types of lung carcinomas were similar to those observed in humans.
  • Cutaneous epitheliomas of the upper lip and cancers of the urinary system were the only two sites other than the lungs where cancers were noted in exposed rats.
  • The incidence of lung cancer increased with decreasing high radon-daughter exposure rate. The greatest effect was noted in exposure-fractionation experiments. Rats exposed to radon daughters for approximately 3,000 WLM, at 1,500 WL for 7 h/day or 5 days/wk (average exposure rates are calculated to be above 50 and 300 WLM/wk) had a nearly fourfold increase in cancer incidence with exposure protraction.
  • While the latency period decreased, the lung-cancer incidence did not change with increasing age at first exposure. For 3,000-WLM exposures, the latent periods for ages at first exposure of 150, 280, 400, and 520 days were 640, 510, 450, and 305 days, respectively.
  • Synergism was observed between exposure to radon progeny and whole-body cigarette-smoke exposures if the exposure to smoke followed the exposure to radon daughters. However, if the cumulative cigarette-smoke exposure preceded the radon-daughter exposure, no increase in cancer incidence was noted over that produced by radon daughters alone. Thus, the effect of cigarette smoke depended on the sequence of exposures and was attributed to its promoting action.5 The histological types of cancers observed were not altered by cigarette-smoke exposures. The investigators have not reported whether the latent period for cancer was influenced by smoke exposure; the observation that tumors in the radon-daughter-and smoke-exposed animals were larger and more invasive than those in animals exposed only to radon daughters might be indicative of a shorter latent period for smoking-related tumors.

The COGEMA studies have produced more than 800 lung cancers in about 10,000 rats exposed to radon daughters with ambient aerosols and in mixtures with other pollutants. The exposure-response relationship data shown in Table III-1 therefore constitute only a portion of the data from these experiments. The derived range in mean lifetime risk coefficients, uncorrected for life-span differences from control animals, is about 1.5 × 10-4-7.5 × 10-4/WLM for exposures between about 20 and 5,000 WLM. The risk decreases at larger exposures because of life-span shortening. No evidence of a threshold below 20 WLM was apparent.8

Inhalation Studies at the Pacific Northwest Laboratory

Exposures of dogs and rodents to uranium-mine air contaminants were begun in the late 1960s and early 1970s to identify agents and the magnitude of exposures to them that were responsible for producing lesions of the respiratory tract similar to those observed in uranium miners. The early experiments concentrated on lifetime inhalation exposures of hamsters and beagles to mixed aerosols of radon, radon daughters, carnotite uranium-ore dust, diesel-engine exhaust, and cigarette smoke. Most of the final data from these early experiments have been published.1113 To provide data that were missing from the earlier dog study, follow-up studies have included exposures of beagles to uranium-ore dust alone (but not to radon daughters alone) and exposures of rats to mixtures of radon, radon daughters, and uranium-ore dust.10,1418,33 Because the studies in rats were designed to develop exposure-response relationships, the exposures were truncated rather than extended through the animals' lifetimes. They were also designed to study the roles of carnotite uranium-ore dust concentration and radon-daughter exposure rate, unattachment fraction, and disequilibrium in the production of lung lesions. Histopathological examination, clinical pathological examination, and pulmonary physiology tests were the primary means of measuring response. Urinalyses have recently supplemented serum tests as more sensitive evaluations for kidney damage. Radiometric analyses of tissues have been used to determine mean radon-daughter tissue doses and the body distribution of long-lived radioactivity from the ore dust.

Lifetime exposures of hamsters to radon daughters alone or in combination with uranium-ore dust and diesel-engine exhaust caused no significant (P > 0.05) changes in mortality patterns compared with those of controls. The mean radon-daughter exposure in the hamster experiments was about 10,000 WLM. Lifetime exposures of beagles to mixtures of radon daughters, uranium-ore dust, and cigarette smoke caused significant life-span shortening compared with that of controls. Mean survival times of the dogs exposed to mixtures of radon daughters and ore dust, with or without cigarette smoke, were 4–5 yr. Mean survival times of controls and dogs exposed to smoke only were equivalent during the same period. The mean radon-daughter exposure of the dogs was about 13,000 WLM.

Studies in progress show that chronic exposure of rats to mixtures of radon daughters and uranium-ore dust shortens the life span. The data thus far generally show no significant differences in mortality patterns compared with those of controls for exposures up to about 2,500 WLM. Exposures exceeding 5,000 WLM have caused significant life-span shortening, with the effect increasing with exposure. In general, rats that showed life-span shortening also showed weight loss.

Thus far, two life-span-shortening anomalies have been noted in the rat experiments. First, in an interim study to determine any influence of radon-daughter exposure rate, rats exposed to about 640 WLM at the lowest rate (about 44 WLM/wk) died earlier than other animals given comparable cumulative exposures. Second, in a study to determine the influence of unattached radon daughters versus that of attached radon daughters, rats exposed to about 5,100 WLM with the highest unattachment fraction (f a = 24%) died earlier than other animals given comparable cumulative exposures. Life-table analyses of the survival-time data in the unattachment fraction study18 showed that the estimated probabilities that a rat would die with a lung tumor before 600 days were 0.42, 0.65, and 0.75 for 6, 10, and 24% 218Po (radium A) unattachment, respectively. Expressed as percentages of radon concentration, rather than radium A concentration, the unattachment was 1.3, 5.2, and 9.5%. Later experiments at 640 and 53 WLM/wk showed no appreciable life-span shortening.

The mean survival time of tumor-bearing rats (as in the COGEMA data) was always significantly longer than that of non-tumor-bearing rats. The latent period of lung tumors is a large fraction of the rat life span, and tumors must grow to a else sufficient for detection; the shorter-lived animals might have died too soon for tumors, if any, to be detected.

In the life-span studies with dogs, animals with tumors of the respiratory tract generally had cumulative radon-daughter exposures exceeding 13,000 WLM; the exposure rate was 71 WLM/wk. Concomitant exposure to cigarette smoke had a mitigating effect on radon-daughter-induced tumors, possibly because smoking caused thickening of the mucus layer and stimulated mucociliary clearance. The overall incidence of lung primary tumors was 21% for a mean exposure of 13,100 WLM to radon daughters, 37% in the group exposed to radon daughters and uranium-ore dust, but only 5% in the comparable group that was also exposed to cigarette smoke. The overall incidence of nasal carcinoma was 8%. The lung cancers were about 70% bronchogenic carcinomas and 30% bronchioloalveolar carcinomas.15 The simplified convention used was that squamous cell carcinomas and mucus-staining adenocarcinomas were bronchogenic carcinomas and that tumors of Clara cell or type II alveolar cell origin and non-mucus-staining adenocarcinomas were bronchioloalveolar carcinomas.

Lifetime inhalation exposures of hamsters produced severe radiation pneumonitis but only four squamous cell carcinomas (three in the radon daughters-only group and one in the group exposed to radon daughters and uranium-ore dust) in 306 radon-daughter-exposed animals (1.3% incidence). Squamous cell carcinoma occurred only in association with squamous metaplasia of the alveolar epithelium, which was found only in hamsters exposed to radon daughters. Thus, it appears that after exposure to radon daughters, the development of squamous metaplasia and the development of carcinoma were related. Because so few lung cancers were produced in these high-exposure experiments, it was concluded that the hamster was an inappropriate surrogate for further study of the carcinogenic potential of inhaled (as opposed to instilled) mine-air pollutants.

Over 4,000 male rats have received chronic exposures to ambient air or to mixtures of radon daughters and uranium-ore dust since 1978. Data are still accumulating, But some general trends can be observed. Lung-cancer risk tended to increase (sometimes significantly) with decreasing radon-daughter exposure rate, increasing unattached fraction of radon daughters, and increasing radon-daughter disequilibrium. The lung cancers induced after exposures of approximately 300–5,000 WLM were about 70% bronchogenic carcinomas and 30% bronchioloalveolar carcinomas. The tumors were most often estimated (by sizing associated bronchi and bronchioles) to be about 50% proximal (bronchus-associated) and 50% distal (bronchiole-and alveolus-associated), in contrast with the greater proportion of proximal lung cancers in humans.30 The prevalence of squamous metaplasia, and generally carcinoma, of the respiratory tract increased with an increasing unattached fraction of radon daughters.

The PNL data are inadequate for firm conclusions regarding the effect of radon-daughter exposure rate and the magnitude of the lifetime risk coefficient below 100 WLM. However, the data to date indicate an increasing lifetime lung-tumor risk coefficient with decreasing cumulative radon-daughter exposure. Like the COGEMA data, the PNL risk-coefficient data have not Been corrected for life-span shortening due to competing causes of death, such as radiation pneumonitis (see Table III-1). It cannot be concluded that the increase in the risk coefficient continues with further decreases in cumulative exposure and exposure rate. The PNL experiments include exposures as low as 20 WLM. The tumor-incidence data, particularly those derived from high-exposure-rate experiments, are similar not only to those from COGEMA But also to present estimated lung-tumor incidence data in humans.

Animal exposure studies show that the tumorigenic efficiency of radon daughters varies with cumulative exposure, exposure rate, unattached fraction, disequilibrium, and concomitant exposures to other pollutants (i.e., cigarette smoke). The COGEMA and PNL data indicate that tumor incidence increases with an increase in radon-daughter cumulative exposure and a decrease in radon-daughter exposure rate. Chameaud et al.5 concluded that lung-cancer incidence at comparable cumulative exposures increased as the radon-daughter concentration decreased from 12,000 to less than 3,000 WL. In a related dose-fractionation study with a cumulative exposure of 3,000 WLM and a radon-daughter concentration of 1,500 WL, an approximately fourfold increase in lung cancers was observed when the exposure rate decreased from about 300 to 50 WLM/wk; it is not known whether this exposure-rate dependence persists at the far lower rates. A trend toward increasing a lung tumor risk with decreasing exposure rate was noted in the earlier PNL rat experiments14,18 when the rates changed from 180 to 88 and to 44 WLM/wk. Inasmuch as the increase was not significant and results were uncertain at 44 WLM/wk as a result of life-span shortening in that group, the exposure-rate dependence in rats might be lessened at the lower weekly rates of exposure. However, more recent data confirm the increase in lung-tumor risk with decreased exposure rate down to 53 WLM/wk.

Data from the PNL rat experiments also indicate an increase in the risk of lung tumors with increases in radon-daughter unattached fraction and disequilibrium.18 The risk increase from 1.6 to 10% unattached radium A is significant (P < 0.05), but the positive trend reverses at 24% unattachment as a result of life-span shortening in that exposure group. In contrast with the results of the COGEMA experiments, the increase is also significant with radon-daughter disequilibrium (an equilibrium of 10 versus 40%) when the total numbers of lung cancers are compared. However, the trend is of borderline significance (P = 0.10) when the total numbers of rats with lung tumors are compared. The data on nasal carcinoma show an increasing trend with increasing unattachment and, as with the neoplastic lesions of a the lung, a reverse trend at 24% unattachment. There is no indication that high-disequilibrium radon-daughter exposures, without concomitant high unattachments, produce more nasal carcinomas than do low-disequilibrium exposures.

The role of concomitant exposures to other pollutants depends not only on the nature of those pollutants but also on the sequence of exposures. Simultaneous or same-day exposure to radon daughters and uranium-ore dust, diesel-engine exhaust, or cigarette smoke increased the incidence of preneoplastic lesions but, except for cigarette smoke, did not change the incidence of lung tumors in the PNL experiments. In the COGEMA rat experiments, cigarette smoke was cocarcinogenic with radon daughters if exposure to smoke followed completion of exposure to the radon daughters,4 but not if smoking preceded the radon-daughter exposures. In the PNL dog experiments, lung-tumor incidence decreased when animals were exposed to radon daughters and cigarette smoke alternately on the same day.

Lung Cancer

In Figure III-1 the mean lifetime lung-tumor risk per WLM (uncorrected for life-span differences from control animals) is plotted against the radon-daughter exposure (WLM) for PNL rats and dogs and COGEMA rats. The higher tumor efficiencies in the PNL studies (in contrast with the COGEMA studies) are probably due to the lower average exposure rates of the PNL experiments.

Figure III-1. Lifetime risk coefficients for radon-daughter exposure for PNL rat and dog data and COGEMA rat data; error bars are omitted.

Figure III-1

Lifetime risk coefficients for radon-daughter exposure for PNL rat and dog data and COGEMA rat data; error bars are omitted. Source: Personal communication, Dr. F. Cross, Pacific Northwest Laboratories.

The uncertainties in the PNL lung-cancer incidence and risk-coefficient data' are considered to be due mainly to uncertainties in the exposure data (standard deviations were generally well within ±20% of the means). Whenever PNL exposures were repeated, reproducibility of tumor-incidence data was generally within ±20% of the mean tumor incidence, which included the statistical uncertainties in the exposure data. Because the normal lung-tumor incidence in the absence of appreciable background radon exposures is very low (<0.2%) in the COGEMA and PNL rats, the risk-coefficient data, except for the 20- to 50-WLM COGEMA group of rats, have not been corrected for the incidence in control animals.

Current experiments at PNL, which involve mixtures of radon daughters and uranium-ore dust, will further define the shape of the risk-coefficient curve for very low exposures and exposure rates. For the present, COGEMA data on low exposures and low exposure rates indicate a leveling-off of the risk to a value of 6 × 10-4-8 × 10-4/WLM.

Kushneva23 reported that rats given 50 mg of silica by instillation with inhalation exposures to radon at 8 µCi/liter developed many more pulmonary effects, including both adenomas and carcinomas, than did animals exposed to silica alone; the number of tumors and control animals was small. When silica dusts were included in the exposures, the radon-daughter inhalation studies at COGEMA and PNL showed no increased tumorigenic efficiency over exposures to radon daughters alone if these exposures exceeded a few hundred WLM. However, in contrast with the rat data of Kushneva23 and the dog data from PNL, Chameaud et al.5 have not found the silicotic process to be accelerated by the presence of radon daughters.

Little et al.24,32 have shown in hamsters that when benzo(a)pyrene or saline instillations followed low-dose 210Po instillations, the carcinogenic action of polonium was increased. Because radioactivity appears to Be the initiator of the lung cancer, as in all the animal experiments with radon described here, any later exposure to an irritant that stimulates cell proliferation appears to increase the incidence of cancer.

Summary and Conclusions

Laboratory animal research programs on the effects of radon-daughter inhalation are being carried out in laboratories in both the United States and France. While much of the early work explored acute effects, more recent experiments involving chronic exposure have resulted in the induction of lung cancer in both rats and dogs. It should be noted, however, that the location and histopathology of such cancers are not analogous to humans, and caution is warranted in extrapolating from experiments with laboratory animals to humans. Nevertheless, substantial information has accumulated that provides insights into radon-daughter carcinogenesis. Table III-2 summarizes recent findings in animal studies of lung-cancer induction by radon decay products.

TABLE III-2. Summary of Factors Influencing the Tumorigenic Efficiency of Radon-Daughter Exposure.


Summary of Factors Influencing the Tumorigenic Efficiency of Radon-Daughter Exposure.

In rats, lung tumors have been induced at relatively low exposures (20 WLM).7 As yet, experiments with dogs do not extend to this low-dose range, but tumors have been observed for exposures at the 600-WLM level.13 It is of interest that lung-cancer incidence in animals increases with a decreasing rate of exposure for fixed cumulative exposure—a finding that has yet to be confirmed in studies of exposed underground miners (Annex 2A). The difficulty of documenting exposure rate for the miners may explain the failure to find a dose-rate effect in the epidemiological studies.

Large-scale animal studies may become useful for elucidating the interactions between radon daughters and other inhaled pollutants. Information on the extent and duration of smoking is incomplete for human studies, but smoking can be controlled in experiments with animals. It is clear from such experiments that the interactions between smoking and lung cancer induced by radon decay products reflect a complex interplay of these agents in the host. Well thought out experiments with dogs and rats can provide models that aid our understanding of how smoking modulates radiogenic lung cancer. Nevertheless, application to humans is indirect, and confirming experiments with primates may be necessary. However, findings in humans and animals to date are generally parallel for short-half-life radon progeny.


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Some of the exposure values in these French studies have been supplied by COGEMA investigators and might be different from previously published values. (J. Chameaud, personal communication to F. T. Cross, 1986.)

Copyright © 1988 by the National Academy of Sciences.
Bookshelf ID: NBK218115


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