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RADON

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Radon is a radionuclide derived from the radioactive decay of radium, and can be obtained by bubbling air through a radon salt solution (HSDB , 2002; Lewis, 2001). Radon daughters or progeny are radioactive decay products of radon (Berger, 1990).
    1) Radon-222 (radon) is the natural decay product of radium-226, and the sixth decay product of uranium-238 (Berger, 1990).
    2) Besides its natural occurrence in the environment, radon has been used as a tracer gas for leak detection, in chemical research, and in radiography (HSDB , 2002; Lewis, 2001). Radon has been used in radiation therapy (HSDB , 2002).

Specific Substances

    A) Radon
    1) Alphatron
    2) Niton
    3) Radium Emanation
    4) Radon 222
    5) Radon-222
    6) Molecular Formula: Rn
    7) CAS 10043-92-2
    8) References: HSDB, 1990
    RADON DAUGHTERS
    1) Radon Progeny
    2) Radon Degradation Products
    3) Polonium-218
    4) Lead-214
    5) Bismuth-214
    6) Polonium-214
    7) Polonium-210
    8) References: Berger, 1990; ATSDR, 1992

    1.2.1) MOLECULAR FORMULA
    1) Rn

Available Forms Sources

    A) FORMS
    1) Radon is a colorless, odorless, inert gas. All 21 isotopes of radon are radioactive, with mass numbers ranging from 202 to 224. The common isotopes are Rn-222, Rn-220, and Rn-219, with half-lives of 3.82 days, 55.3 seconds, and 4.0 seconds, respectively ((ATSDR, 2000)) Patnaik, 1992).
    2) Radon is an alpha-emitter and a member of the decay chain of uranium 238. Known artificial radioactive isotopes include radon 200-221 and 223-226 (Budavari, 2000).
    3) With a half-life of 3.823 days, radon-222 is the longest-lived known radon isotope (Budavari, 2000).
    B) SOURCES
    1) Radon is derived from the radioactive decay of uranium to radium then radon. Uranium exists in soil and rocks in small amounts. Approximately 1 gram of radium exists for each 6-inch-deep square mile of soil. Radon is released from this radium into the atmosphere (ATSDR, 1990; (ATSDR, 2000)). At normal temperature and pressure, 1 gram of radium produces approximately 0.0001 mL of radon per day (HSDB , 2002).
    2) Radon is produced by alpha-disintegration of radium and its isotopes (Patnaik, 1992). "Radon is [also] obtained by bubbling air through a radon salt solution and collecting the gas plus air" (Lewis, 2001).
    3) Both uranium-238 and radium-226 occur naturally in most soils and rock (Berger, 1990).
    4) The radon decay product leaves the soil or rock as it is formed and becomes ubiquitous in the environment (Berger, 1990). Higher radon concentrations are produced in areas with richer sources of the precursor radionuclides, especially when ventilation is poor (Berger, 1990).
    5) Radon levels are higher in areas with uranium and thorium ore deposits and granite formations. Natural uranium exists in these locations in high concentrations. In the United States, eastern Pennsylvania and parts of New York and New Jersey have high radon concentrations because of the presence of granite formations (ATSDR, 1990).
    6) Other natural sources of radon are plants, groundwater, and oceans (WHO, 1983).
    7) Other radon sources include natural construction materials such as alum slate and by-products from the treatment and production of such materials (ILO , 1998).
    8) Radon and its daughters can be present in indoor air in homes from such sources as underlying soil, various building materials, ground and well water, and contaminated natural gas (Berger, 1990) NTP, 2001; (WHO, 1983).
    9) Certain building materials, such as aerated concrete with alum shale and phospho-gypsum from sedimentary ores, have a higher radon content. Excluding these, the average radium radiation concentration in building materials is about 100 becquerels/kilogram (WHO, 1983).
    10) Radon levels in homes can vary widely, and are largely dependent on such factors as ventilation and air pressure in the building. The average home air level is about 1 picocurie/liter (pCi/L), with some homes having concentrations as high as 10 to 100 pCi/L (Berger, 1990). An estimated six million homes in the United States have radon levels greater than 4 pCi/L ((ATSDR, 2000)).
    a) Homes in areas with significant deposits of granite, uranium, shale, and phosphate are more likely to have elevated levels of radon ((ATSDR, 2000)).
    C) USES
    1) Radon is used to start and affect chemical reactions, in surface reaction studies as a surface label, in the determination of thorium and radium, in filtration studies, and as a source of neutrons in combination with beryllium or other light filters. Radon is also used as a therapeutic catalyst for antineoplastic radiation (Budavari, 2000). This noble gas is also used as a tracer to detect leaks, in measurement of flow-rates, radiography, chemical research, and as a cancer treatment (Lewis, 2001).
    2) In some countries, "radon mines," caves with high radon concentrations, and radon "spas" are being used as health treatments for ailments such as arthritis, asthma, allergies, diabetes, hypertension, ulcers, and cancer (ATSDR, 1990).
    3) Radon is also being used as part of new earthquake prediction technology. This technology uses radon emanation from soil and groundwater concentrations as crustal activity indicators (ATSDR, 1990).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Radon is a naturally occurring radioactive gas. The main concern after exposure to radon and its daughters (decay products) exposure concern is the development of lung cancer. An increased risk of lung cancer has been clearly documented in uranium and certain other miners exposed to radon and its daughters, as well as in experimental animals.
    1) Radon and its daughters are absorbed into the lungs by inhalation after becoming attached to microscopic particles of environmental airborne dust. Inhaled dust particles with attached radon daughters are distributed in the lungs, where they may stick to the moist bronchial epithelial lining.
    2) Mucociliary clearance may not be rapid enough to prevent ionizing radiation (alpha particles) released from the decay of the radon daughters, polonium-218 and polonium-214, from affecting several types of pulmonary cells and eventually leading to cancerous transformation.
    3) Uranium ore has particularly high concentrations of radium. Other types of ore (zinc, lead, fluorospar, tin, niobium, and iron) containing uranium and radium can also release radon and its daughters. When ventilation is not adequate, miners can be at risk for an increased incidence of lung tumors. Cutting uranium metal may release dust containing radon and its daughters.
    B) Radon exposure is thought to be an important environmental cause of death. The US EPA and the National Cancer Institute estimate that there are 15,000 deaths annually in the US from radon induced lung cancer. Of the 164,100 cases of lung cancer diagnosed each year, approximately 14% are attributable to radon exposure. After cigarette smoking, indoor radon is the second leading cause of lung cancer.
    1) Smokers are at greater risk for the development of lung cancer. The risk of lung cancer in cigarette smokers is 10 times that of non-smokers.
    2) Lifetime exposure to the EPA recommended guideline of 4 pCi/L is estimated to pose a 1-5% risk for developing lung cancer depending if a person is a nonsmoker or smoker.
    C) Radon is odorless, colorless, tasteless, and not irritating; there is no way to detect its presence other than sampling and laboratory measurement.
    1) The dose of ionizing radiation received by the bronchial epithelium in the general population from radon is far in excess of the dose received by any other organs from natural background radiation.
    0.2.4) HEENT
    A) Radiation cataracts have developed in patients who previously had gold radon seed implants for the treatment of skin cancer on or near the eyelids.
    0.2.5) CARDIOVASCULAR
    A) A false aneurysm of the vertebral artery at the level of the axis vertebra developed in a patient previously treated with gold radon seed implants for sarcoma of the pharynx.
    0.2.6) RESPIRATORY
    A) The main concern with exposure to radon and its daughters is the development of lung cancer. Most radon-induced lung cancers are bronchogenic.
    1) Histologic lung cancer types that have been associated with radon exposure are squamous cell carcinoma and adenocarcinoma. Histologic lung cancer types noted in uranium miners were predominantly small cell carcinomas, although all cell types were represented.
    B) There is at least an additive relationship between radon exposure and smoking for lung cancer risk.
    0.2.10) GENITOURINARY
    A) Excess mortality from non-malignant renal disease (chronic and unspecified nephritis) has been noted in radon-exposed miners.
    0.2.14) DERMATOLOGIC
    A) Radiation dermatitis has developed following gold radon seed implants or wearing gold rings made from spent gold radon seeds.
    0.2.20) REPRODUCTIVE
    A) High rates of congenital malformations and spontaneous abortions have been noted at an Indian Health Service hospital serving an area where extensive uranium mining occurred.
    B) Changes in the secondary sex ratio have been noted in the offspring of male underground miners exposed to radon.
    C) An increase in rat prenatal mortality and macroscopic hemorrhages in the surviving offspring were noted when female rats were injected with radon solutions.
    0.2.21) CARCINOGENICITY
    A) The main concern with exposure to radon and its daughters is the development of lung cancer. An increased risk of lung cancer has been clearly documented in uranium and certain other miners exposed to radon and its daughters, as well as in experimental animals.
    B) The EPA estimates that from 5000 to 20,000 cases of lung cancer occur annually in the US from indoor environmental radon exposure, and that as many as 11% of current lung cancer cases may be due to radon exposure.
    C) RISK ASSESSMENTS -
    1) With Lifetime Exposure to 4 pCi/L
    a) EPA - Lung Cancer Risk is 1 to 5%
    b) National Research Council (NRC): Lung Cancer Risk is 0.8 to 1.4%

Laboratory Monitoring

    A) There are no clinical tests specific for radon exposure.
    B) In patients suspected of having radon-induced lung cancer, bronchial washings for cytology or biopsy of suspected lesions for histology may be indicated.
    C) In patients suspected of having radon-induced lung cancer, chest x-rays and CT or MRI scans may be clinically indicated.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Radon is not irritating, and there is no current evidence that it can cause toxicity or cancer following ingestion of the daughters either attached to airborne dust particles or in contaminated groundwater.
    0.4.3) INHALATION EXPOSURE
    A) Treatment of patients with lung cancer is best done in consultation with an oncologist who specializes in lung cancer.
    0.4.4) EYE EXPOSURE
    A) Radon is not irritating, and there are no data indicating that eye injury can occur from acute radon exposure.
    B) Radiation cataracts have developed following implantation of gold radon seeds near the eyes. Treatment would be the same as for similar cataracts from any etiology.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Treatment of patients with possible radon-induced skin cancer is best done in consultation with a dermatologist.

Range Of Toxicity

    A) An increased risk of lung cancer has been associated with radon exposure from somewhat less than to greater than 100 Working Level Months (WLMs) in uranium miners. The lung cancer risk in uranium miners has also been found to be a function of age at first exposure.

Clinical Effects

Summary Of Exposure

    A) Radon is a naturally occurring radioactive gas. The main concern after exposure to radon and its daughters (decay products) exposure concern is the development of lung cancer. An increased risk of lung cancer has been clearly documented in uranium and certain other miners exposed to radon and its daughters, as well as in experimental animals.
    1) Radon and its daughters are absorbed into the lungs by inhalation after becoming attached to microscopic particles of environmental airborne dust. Inhaled dust particles with attached radon daughters are distributed in the lungs, where they may stick to the moist bronchial epithelial lining.
    2) Mucociliary clearance may not be rapid enough to prevent ionizing radiation (alpha particles) released from the decay of the radon daughters, polonium-218 and polonium-214, from affecting several types of pulmonary cells and eventually leading to cancerous transformation.
    3) Uranium ore has particularly high concentrations of radium. Other types of ore (zinc, lead, fluorospar, tin, niobium, and iron) containing uranium and radium can also release radon and its daughters. When ventilation is not adequate, miners can be at risk for an increased incidence of lung tumors. Cutting uranium metal may release dust containing radon and its daughters.
    B) Radon exposure is thought to be an important environmental cause of death. The US EPA and the National Cancer Institute estimate that there are 15,000 deaths annually in the US from radon induced lung cancer. Of the 164,100 cases of lung cancer diagnosed each year, approximately 14% are attributable to radon exposure. After cigarette smoking, indoor radon is the second leading cause of lung cancer.
    1) Smokers are at greater risk for the development of lung cancer. The risk of lung cancer in cigarette smokers is 10 times that of non-smokers.
    2) Lifetime exposure to the EPA recommended guideline of 4 pCi/L is estimated to pose a 1-5% risk for developing lung cancer depending if a person is a nonsmoker or smoker.
    C) Radon is odorless, colorless, tasteless, and not irritating; there is no way to detect its presence other than sampling and laboratory measurement.
    1) The dose of ionizing radiation received by the bronchial epithelium in the general population from radon is far in excess of the dose received by any other organs from natural background radiation.

Heent

    3.4.1) SUMMARY
    A) Radiation cataracts have developed in patients who previously had gold radon seed implants for the treatment of skin cancer on or near the eyelids.
    3.4.3) EYES
    A) RADIATION CATARACTS - Segmental or sector-shaped radiation cataracts have been reported in patients previously treated with radon gold seed implants for squamous or basal cell carcinomas on or near the eyelids (Britten et al, 1966).
    1) The incidence of such cataracts was progressive from 6 to 11 years after treatment (Britten et al, 1966).

Cardiovascular

    3.5.1) SUMMARY
    A) A false aneurysm of the vertebral artery at the level of the axis vertebra developed in a patient previously treated with gold radon seed implants for sarcoma of the pharynx.
    3.5.2) CLINICAL EFFECTS
    A) VERTEBRAL ARTERY ANEURYSM
    1) CASE REPORT - A false aneurysm of the vertebral artery at the level of the axis vertebra developed in one patient nearly 30 years following implantation of radon seeds for the treatment of sarcoma of the pharynx; the presenting sign was hemorrhage from the posterior pharynx (Early et al, 1966).

Respiratory

    3.6.1) SUMMARY
    A) The main concern with exposure to radon and its daughters is the development of lung cancer. Most radon-induced lung cancers are bronchogenic.
    1) Histologic lung cancer types that have been associated with radon exposure are squamous cell carcinoma and adenocarcinoma. Histologic lung cancer types noted in uranium miners were predominantly small cell carcinomas, although all cell types were represented.
    B) There is at least an additive relationship between radon exposure and smoking for lung cancer risk.
    3.6.2) CLINICAL EFFECTS
    A) PRIMARY MALIGNANT NEOPLASM OF RESPIRATORY TRACT
    1) The main concern with exposure to radon and its daughters is the development of lung cancer (Berger, 1990; HSDB , 2002; ATSDR, 1992). An increased risk of lung cancer has been clearly documented in uranium and certain other miners exposed to radon and its daughters, as well as in experimental animals (Berger, 1990; HSDB , 2002; IARC, 1988; NIOSH, 1987). Most radon-induced lung cancers are bronchogenic (ATSDR, 1992).
    2) Histologic lung cancer types that have been associated with radon exposure are squamous cell carcinoma and adenocarcinoma (Lees et al, 1987).
    3) Histologic lung cancer types noted in smoking uranium miners were predominantly small cell carcinomas (IARC, 1988; BEIR IV, 1988), although all cell types were represented (ATSDR, 1992).
    4) CIGARETTE SMOKING - There is at least an additive relationship between radon exposure and smoking for lung cancer risk (Edling & Axelson, 1983; Saracci, 1987) Harely et al, 1986; (BEIR IV, 1988; BEIR VI, 1999).
    a) In a study comparing periodic sputum cytology evaluation of underground uranium miners versus controls, uranium miners who smoked had a significantly higher incidence of abnormal sputum cytology (moderate atypia, marked atypia, or cancer cells) than did control smokers (Band et al, 1980).
    1) In control smokers, the frequency of abnormal sputum cytology was dependent on the duration of smoking, while in the smoking uranium miners, it was dependent on the duration of both smoking and mining (Band et al, 1980).
    B) FIBROSIS OF LUNG
    1) Nonmalignant respiratory disease in the form of pulmonary fibrosis has been reported in uranium miners. It is suspected that exposure to radon and its daughters may cause fibrosis of the pulmonary interstitium, although there is insufficient evidence to specifically establish a causal link with radon progeny (Archer et al, 1998; BEIR VI, 1999).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) PULMONARY CARCINOMA
    a) RATS - In a rat study, lung tumors noted were bronchiolar or bronchiolar-alveolar in origin; extrapulmonary metastases were only noted in one animal (IARC, 1988). In another rat study, squamous cell carcinomas, adenocarcinomas, and bronchiolar-alveolar carcinomas were seen (IARC, 1988).
    b) HAMSTERS - Squamous cell carcinomas were seen in some exposed hamsters (IARC, 1988).

Genitourinary

    3.10.1) SUMMARY
    A) Excess mortality from non-malignant renal disease (chronic and unspecified nephritis) has been noted in radon-exposed miners.
    3.10.2) CLINICAL EFFECTS
    A) NEPHRITIS
    1) An excess risk of mortality from non-malignant renal disease, with a particularly elevated risk of chronic and unspecified nephritis following a 10-year latent period, has been noted in underground uranium miners from the Colorado plateau area (BEIR IV, 1988).
    a) It is unclear whether this excess of renal toxicity is a chance finding, or whether it represents an occupational risk (BEIR IV, 1988).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) NEPHROPATHY TOXIC
    a) Soluble uranium is nephrotoxic in experimental animals, but most of the uranium found in mines is in the form of less soluble uranium oxides (BEIR IV, 1988).

Dermatologic

    3.14.1) SUMMARY
    A) Radiation dermatitis has developed following gold radon seed implants or wearing gold rings made from spent gold radon seeds.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) A patient who had radon seeds implanted in both cheeks 25 years previously for the treatment of acne developed ulcerative radiation dermatitis (Auerbach & Pearlstein, 1973).
    2) Wearing unrefined gold rings made from decayed gold radon seeds or gold tubing from a radon plant has caused radiation dermatitis (Simon & Harley, 1967).
    B) NEOPLASM OF SKIN
    1) CASE REPORT - One case of a squamous cell carcinoma of the skin on a finger caused by wearing a gold ring contaminated with radon and its daughters has been reported (Helm, 1974).

Reproductive

    3.20.1) SUMMARY
    A) High rates of congenital malformations and spontaneous abortions have been noted at an Indian Health Service hospital serving an area where extensive uranium mining occurred.
    B) Changes in the secondary sex ratio have been noted in the offspring of male underground miners exposed to radon.
    C) An increase in rat prenatal mortality and macroscopic hemorrhages in the surviving offspring were noted when female rats were injected with radon solutions.
    3.20.2) TERATOGENICITY
    A) HUMANS
    1) CONGENITAL ANOMALY
    a) High rates of congenital malformations and spontaneous abortions have been noted at an Indian Health Service hospital serving an area where extensive uranium mining occurred. The only statistically significant finding between poor birth outcomes and uranium mining was identified with the mothers living near mine tailings or dumps (Shields,1992; (BEIR IV, 1988).
    3.20.3) EFFECTS IN PREGNANCY
    A) HUMANS
    1) High rates of congenital malformations and spontaneous abortions have been noted at an Indian Health Service hospital serving an area where extensive uranium mining occurred. The only statistically significant finding between poor birth outcomes and uranium mining was identified with the mothers living near mine tailings or dumps (Shields,1992; (BEIR IV, 1988).
    2) A temporal decline in the secondary sex ratio (male to female births) was also noted in New Mexico, associated with extensive uranium mining, and was greatest in the counties with the greatest mining activity (BEIR IV, 1988).
    3) However, in a comparison study of New Mexico uranium miners with other miners, there were no significant differences in the frequency of low-birth-weight infants, sex ratio, miscarriages, or infertility (BEIR IV, 1988).
    4) It is currently unclear whether or not uranium mining might represent a reproductive risk for the general population (BEIR IV, 1988).
    B) ANIMAL STUDIES
    1) When radon and its progeny were injected subcutaneously into female rats before mating or during conception at a dose of 5 mCi, there was an increase in prenatal mortality and macroscopic hemorrhages in the surviving offspring (BEIR IV, 1988).
    2) These effects were noted even when the radionuclides were injected as early as 22 days before mating (BEIR IV, 1988).
    3) By analogy with (85)Kr, radon and its progeny are inferred to cross the placenta freely (BEIR IV, 1988).
    4) The fetal effects may be due to placental or yolk sac effects of the radionuclides, rather than direct effects on the conceptus (BEIR IV, 1988).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) LACK OF INFORMATION
    1) At the time of this review no data were available to assess the potential effects of exposure to this agent during lactation.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS10043-92-2 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) IARC Classification
    a) Listed as: Radon-222 and its decay products
    b) Carcinogen Rating: 1
    1) The agent (mixture) is carcinogenic to humans. The exposure circumstance entails exposures that are carcinogenic to humans. This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent (mixture) may be placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent (mixture) acts through a relevant mechanism of carcinogenicity.
    3.21.2) SUMMARY/HUMAN
    A) The main concern with exposure to radon and its daughters is the development of lung cancer. An increased risk of lung cancer has been clearly documented in uranium and certain other miners exposed to radon and its daughters, as well as in experimental animals.
    B) The EPA estimates that from 5000 to 20,000 cases of lung cancer occur annually in the US from indoor environmental radon exposure, and that as many as 11% of current lung cancer cases may be due to radon exposure.
    C) RISK ASSESSMENTS -
    1) With Lifetime Exposure to 4 pCi/L
    a) EPA - Lung Cancer Risk is 1 to 5%
    b) National Research Council (NRC): Lung Cancer Risk is 0.8 to 1.4%
    3.21.3) HUMAN STUDIES
    A) PULMONARY CARCINOMA
    1) The main concern of exposure to radon and its daughters is the development of lung cancer (Samet & Nero, 1989; Berger, 1990; HSDB , 2002; ATSDR, 1992). An increased risk of lung cancer has been clearly documented in uranium and certain other miners exposed to radon and its daughters, as well as in experimental animals (Gottlieb & Husen, 1982; Mays, 1973; Sevc et al, 1988) Whittemore & McMillan, 1987; Roscoe et al, 1989; (Berger, 1990; HSDB , 1990; IARC, 1988; NIOSH, 1987). Most radon-induced lung cancers are bronchogenic (ATSDR, 1992).
    2) Uranium ore has particularly high concentrations of radium (Berger, 1990; BEIR IV, 1988; Morgan & Samet, 1986). Other types of ore, such as zinc, lead, fluorospar, tin, niobium, and iron, can also release radon and its daughters, and when ventilation is not adequate, miners can be at risk for an increased incidence of lung tumors (Berger, 1990; Axelson & Sundell, 1978; Battista et al, 1988; BEIR IV, 1988; Bramwell, 1986; Edling & Axelson, 1983; Lubin et al, 1990) Radford & Renard, 1984; Solli et al, 1987; Wright & Coures, 1977). Cutting uranium metal may release dust containing radon and its daughters (Eisenbud & Quigley, 1956).
    a) However, studies of uranium miners have generally NOT separated the effects of exposure to other atmospheric contaminants found in mines (ie, silica, diesel-engine exhaust, blasting fumes) from the effects of radon and its progeny (BEIR IV, 1988).
    3) Miners having a cumulative radon and daughters exposure somewhat below 100 to greater than Working Level Months (WLMs) have an excessive lung cancer mortality (Harley et al, 1986; HSDB , 1990).
    4) Histologic lung cancer types that have been associated with radon exposure are squamous cell carcinoma and adenocarcinoma (Lees et al, 1987). Histologic lung cancer types noted in uranium miners were predominantly small cell carcinomas (IARC, 1988; BEIR IV, 1988), although all cell types were represented (ATSDR, 1992).
    a) In a case-control study of residential radon exposure, histologic lung cancer types included epidermoid, small cell, and adenocarcinoma. In a combined analysis of 7 North American case-control studies, cancer types included adenocarcinoma in 38% of cases, squamous cell carcinoma in 22%, and small/oat cell carcinoma in 16% of cases (Bochicchio et al, 2005; Krewski et al, 2005).
    5) The EPA estimates that from 5000 to 20,000 cases of lung cancer occur annually in the US from indoor environmental radon exposure, and that as many as 11% of current lung cancer cases may be due to radon exposure (ATSDR, 1992). Indoor radon is the second leading cause of lung cancer after cigarette smoking (BEIR VI, 1999).
    6) RISK ASSESSMENTS (ATSDR, 1992) -
    a) With Lifetime Exposure to 4 pCi/L
    1) EPA - Lung Cancer Risk is 1 to 5%
    2) National Research Council (NRC): Lung Cancer Risk is 0.8 to 1.4%
    3) BEIR IV - Lifetime risk of lung cancer mortality due to lifetime exposure to radon progeny of 350 cancer deaths per 10(6) person working level months (WLM) (BEIR IV, 1988)
    4) Evans et al (1981): General population; 10(-4) lifetime risk lung cancer cases per WLM
    7) CIGARETTE SMOKING - There is at least an additive relationship between radon exposure and smoking for lung cancer risk (Edling & Axelson, 1983; Saracci, 1987; Harley et al, 1986; Axelson et al, 1988; Axelson, 1984; BEIR IV, 1988; Cothern, 1989; Hoffmann & Wynder, 1976; Lubin, 1988; Martell, 1983) Solli et al, 1987; (Steenland & Thun, 1986; Whittemore & McMillan, 1983).
    a) In a study comparing periodic sputum cytology evaluations of underground uranium miners versus controls, uranium miners who smoked had significantly higher incidence of abnormal sputum cytology (moderate atypia, marked atypia, or cancer cells) than did control smokers (Band et al, 1980).
    b) In control smokers, the frequency of abnormal sputum cytology was dependent on the duration of smoking, while in the smoking uranium miners, it was dependent on the duration of both smoking and mining (Band et al, 1980).
    c) In an epidemiologic study from Ontario, Canada, smoking was a confounding variable, although a marginally significant association was shown between environmental radon exposure in the home and lung cancer (Lees et al, 1987). In this study, more than 90% of lung cancers were associated with cigarette smoking (Lees et al, 1987).
    d) Stopping cigarette smoking has been cited as the most effective way to decrease lung cancer risk from indoor radon exposure (Lubin & Boice, 1989) Roach & Weaver, 1992; (Samet & Nero, 1989).
    e) In a collaborative analysis of individual data from 13 European case-control studies of residential radon and lung cancer, there was evidence of an association between the radon concentration at home and lung cancer. The absolute risk to smokers and recent ex-smokers was much greater than to lifelong non-smokers. Based on the data from this study, the risk of developing lung cancer by age 75 years with radon exposure of 0, 100 and 400 Bq/m(3) was 0.4%, 0.5% and 0.7% respectively for lifetime non-smokers. This risk increased to 10%, 12% and 16% respectively for smokers (Darby et al, 2005).
    f) Ontario uranium miners had a 3-fold elevated risk for incidence of lung cancer. The risk to miners who had stopped smoking was half that of smokers, but there was no interaction between smoking and radon. Risk for lung cancer was higher in subjects who had reduced pulmonary function consistent with obstructive lung disease. Presence of silicosis did not affect risk for lung cancer. Exposure accumulated between 4 and 14 years prior to diagnosis was the critical period for subsequent development of lung cancer (Finkelstein, 1996).
    8) ENVIRONMENTAL EXPOSURE - While environmental exposures have been thought to also result in an increased lung cancer risk, the level of risk has not been well quantitated (Berger, 1990). At least one review has suggested that the lung cancer risk from environmental radon and its daughters is possibly negligible in relationship to other environmental carcinogens (Steinhausler, 1987).
    a) In Swedish epidemiologic studies of lung cancer cases in both urban and rural areas, there was a relationship between higher radon concentration in ground-level dwellings where lung cancer cases had lived (Svensson et al, 1986; (Edling et al, 1984).
    b) Estimates of lung cancer risk from exposure to environmental levels of radon in indoor air are based on mathematical models, and are extrapolated from high-level occupational radon exposure in underground miners (BEIR IV, 1988; Lubin & Boice, 1989; Lubin, 1988; Samet, 1992) ACOEM, 1992.
    c) An Iowa study of 1027 women between the ages of 40 and 84 who resided in their current home for at least 20 years suggested that residential radon exposure is a significant risk for lung cancer. The study found excess risks of 0.50 for exposures that were approximately the same as 15-years spent at an average radon exposure of 4pCi/L.
    1) Close to 60 percent of the control group without lung cancer and participants with lung cancer exceeded the Environmental Protection Agency's action level of 4pCi/L (Field et al, 2000).
    d) These last few studies suggest that the risk of lung cancer from indoor radon exposure may be difficult to measure using traditional epidemiological studies. In a meta-analysis of 4263 lung cancer cases in 8 studies on at least 200 subjects where long-term radon measurements were available, a slightly elevated risk of 1.14 at 150 Bq/m(3) was found and was not markedly greater than what would have been predicted from studies on miners (Lubin & Boice, 1997).
    e) The estimated incidence of lung cancer due to environmental radon exposure is in the thousands of cases yearly. In homes with high (10 to 100 pCi/L) radon concentrations, the estimated lifetime lung cancer risk is greater than 1% (Berger, 1990).
    f) A meta-analysis was conducted to delineate the association between residential exposure to radon gas and lung cancer. An analysis of 17 case-control studies suggested that there is a significantly increased risk of lung cancer in people who are exposed to radon in their homes. The analysis also indicated a possible dose-related association. At an exposure of 150 Becquerels/cubic meter (Bq/m(3)), the odds ratio of developing lung cancer was 1.24 (95% CI, 1.11 to 1.38). At an exposure of 250 Bq/m(3) the odds ratio was 1.43 (95% CI, 1.19 to 1.72) (Pavia et al, 2003).
    g) A case control study was conducted to determine the risk of lung cancer following residential exposure to radon in Eastern Germany. Study subjects included histologically confirmed lung cancer patients from hospitals with a random sample of well-match population controls. One-year radon measurements were conducted in houses occupied during 5 to 35 years prior to the subject's interview. The average radon concentration measured was 76 Bq/m(3) among the cases and 74 Bq/m(3) among the controls. The odds ratio of lung cancer risk, adjusted for cigarette smoking and exposure to asbestos, were 0.95 (0.77 to 1.18), 1.13 (0.86 to 1.50), and 1.30 (0.88 to 1.93) for the radon exposure categories of 50 to 80 Bq/m(3), 80 to 140 Bq/m(3), and greater than 140 Bq/m(3), respectively, as compared with the adjusted odds ratio of 1.00 for the radon exposure category of 0 to 50 Bq/m(3) (Kreuzer et al, 2003). There are several potential limitations to this study that need to be taken into account, including a low response rate among controls, exclusion of 33% of the interviewed cases and 14% of the controls due to missing radon measurements, possible inaccuracy of exposure assessment, and radon exposures outside of the home were not measured.
    9) EPIDEMIOLOGICAL STUDIES -
    a) READING PRONG AREA - Both total cancers and lung cancer were significantly higher amongst persons living in close proximity to the Reading Prong formation in counties of New York, Pennsylvania, and New Jersey when compared to controls (Archer, 1987). However, there were no controls for cigarette smoking in this study.
    b) MAINE - Radon levels in domestic water supplies were significantly correlated with cancer rates in one study (Hess et al, 1983).
    B) CARCINOMA
    1) Some, but not all, epidemiologic studies in miners have also shown excess skin and stomach cancers (Cothern, 1989; Wilkinson, 1985).
    a) In an analysis of miner studies, increases in mortality from leukemia, stomach, liver and pancreatic cancers were felt to be unlikely to have been caused by radon since they were unrelated to cumulative exposures. This study felt that there was considerable evidence that high radon concentrations do not cause an increased mortality from cancers other than lung cancer (Darby et al, 1995).
    2) One case of a squamous cell carcinoma of the skin on a finger caused by wearing a gold ring contaminated with radon and its daughters has been reported (Helm, 1974).
    3) Death from bone cancer among persons under 26 years of age in Ontario, Canada was associated with exposure to radium in drinking water. Increased risk was similar for all forms of bone cancer and was much higher than expected (Finkelstein, 1994).
    4) Exposure to indoor radon did not increase the risk for lung cancer in a case-control study on 1055 patients in Finland (Auvinen et al, 1996). Similar results were found in Cornwall, where exposure to radon is the highest in England (Etherington et al, 1996; Thorne et al, 1996). Cornwall adults did have increased non-melanoma skin cancers in the highest exposure group (greater than or equal to 100 Bq/m(3)), and Cornwall children had increased risk for neuroblastoma (Etherington et al, 1996; Thorne et al, 1996).
    3.21.4) ANIMAL STUDIES
    A) PULMONARY CARCINOMA
    1) In a rat study, the lung tumors noted were bronchiolar or bronchiolo-alveolar in origin; extrapulmonary metastases were only noted in one animal (IARC, 1988). In another rat study, squamous cell carcinomas, adenocarcinomas, and bronchiolar-alveolar carcinomas were seen (IARC, 1988).
    2) Mice exposed to radon levels 1000 to 2500 times acceptable workplace concentrations had changes in lymphocytes and macrophages. These signs of depressed immunity may contribute to the development of lung cancer (Nagarkatti et al, 1996).
    3) Inhalation studies in male rats and hamsters and in dogs of both sexes showed a significant increase in the occurrence of respiratory tract tumors in the rats and dogs when compared with unexposed animals ((IARC, 1998)).
    4) Another rat study also found that exposure to radon and its daughters increases the incidence of benign and malignant lung tumors (Collier et al, 1999).
    B) CARCINOMA
    1) Squamous cell carcinomas were seen in some exposed hamsters (IARC, 1988).
    2) Radon causes thoracic malignancies in experimental animals and has been shown to be co-carcinogenic with asbestos and other mineral dusts (Bignon et al, 1983).
    3) In rats, equivalent pulmonary carcinogenic dose is 3 working level months (WLM) of radon to 1 mGy of fission neutrons (Chmelevsky & Kellerer, 1984).

Genotoxicity

    A) Aberrations were noted in the chromosomes of circulating lymphocytes from underground uranium miners.
    B) An increase in sister chromatid exchanges was noted in the bone marrow of rats exposed to 100 to 6000 Working Level Months (WLMs) radiation from radon and its daughters.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) There are no clinical tests specific for radon exposure.
    B) In patients suspected of having radon-induced lung cancer, bronchial washings for cytology or biopsy of suspected lesions for histology may be indicated.
    C) In patients suspected of having radon-induced lung cancer, chest x-rays and CT or MRI scans may be clinically indicated.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) In patients suspected of having radon-induced lung cancer, chest x-rays and CT or MRI scans may be clinically indicated.

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) An electronic dosimetry system can be used to continuously monitor ambient air in mines where radon may be present (Durkin, 1979). Ambient air is drawn through paper filter heads, and the alpha emissions from decay of the radon and its daughters are monitored with a solid state barrier detector (Durkin, 1979).
    2) Charcoal canisters and alpha track detectors are the most common and practical devices used to determine radon levels in a home and can be used at a reasonable cost (Doege & Hendee, 1988).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.3) CONSULT CRITERIA/INHALATION
    A) Treatment of patients with lung cancer is best done in consultation with an oncologist who specializes in lung cancer.
    6.3.5) DISPOSITION/DERMAL EXPOSURE
    6.3.5.3) CONSULT CRITERIA/DERMAL
    A) Treatment of patients with possible radon-induced skin cancer is best done in consultation with a dermatologist.

Monitoring

    A) There are no clinical tests specific for radon exposure.
    B) In patients suspected of having radon-induced lung cancer, bronchial washings for cytology or biopsy of suspected lesions for histology may be indicated.
    C) In patients suspected of having radon-induced lung cancer, chest x-rays and CT or MRI scans may be clinically indicated.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) GENERAL -
    1) Radon is not irritating, and there is no current evidence that it can cause toxicity or cancer following ingestion of the daughters either attached to airborne dust particles or in contaminated groundwater. Most exposure to radon involves chronic low level exposure and acute ingestion is unlikely. Routine use of gastrointestinal decontamination is not recommended.
    6.5.3) TREATMENT
    A) GENERAL TREATMENT
    1) Radon is not irritating, and there is no current evidence that it can cause toxicity or cancer following ingestion of the daughters either attached to airborne dust particles or in contaminated groundwater.

Inhalation Exposure

    6.7.2) TREATMENT
    A) NEOPLASM OF LUNG
    1) Treatment of patients with lung cancer is best done in consultation with an oncologist who specializes in lung cancer.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.2) TREATMENT
    A) GENERAL TREATMENT
    1) Radon is not irritating, and there is no current data that eye injury can occur from acute radon exposure.
    B) CATARACT ASSOCIATED WITH RADIATION
    1) Radiation cataracts have developed following implantation of gold radon seeds near the eyes.
    2) Treatment would be the same as for similar cataracts from any etiology.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.2) TREATMENT
    A) SQUAMOUS CELL CARCINOMA OF SKIN
    1) One case of a squamous cell carcinoma of the skin on a finger caused by wearing a gold ring contaminated with radon and its daughters has been reported (Helm, 1974).
    2) When feasible, surgical excision would be the treatment of choice.
    B) RADIATION DERMATITIS
    1) A patient who had radon seeds implanted in both cheeks 25 years previously for the treatment of acne developed ulcerative radiation dermatitis (Auerbach & Pearlstein, 1973).
    2) Treatment includes close medical surveillance for the rest of the patient's life, with surgical excision and histopathologic examination whenever tissue breakdown is clinically evident (Auerbach & Pearlstein, 1973).
    3) Frankly malignant growths should be surgically removed (Auerbach & Pearlstein, 1973).
    4) Patients with radiation dermatitis should be counseled to avoid further exposure to ionizing radiation, as well as ultraviolet exposure (Auerbach & Pearlstein, 1973).
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) An increased risk of lung cancer has been associated with radon exposure from somewhat less than to greater than 100 Working Level Months (WLMs) in uranium miners. The lung cancer risk in uranium miners has also been found to be a function of age at first exposure.

Minimum Lethal Exposure

    A) Uranium miners exposed to 100 to 10,000 pCi radon-222/L in air died as a result of nonneoplastic respiratory diseases. Cumulative exposure to radon and radon daughters ranged from 50 WLM (Working Level Months) to greater than 3720 WLM. It should be noted, however, that in these studies, when considering the cause of these diseases, confounding factors such as exposure to other substances, history of smoking, etc., were not taken into account (ATSDR, 1990).
    B) Several studies of uranium miners "indicate that lung cancer mortality was influenced by the total cumulative radiation exposure, by the age at first exposure, and by the timecourse of the exposure accumulation. Most deaths from respiratory cancers occurred 10 or more years after the individual began uranium mining" (ATSDR, 1990).
    C) Researchers pooled information from 11 studies of radon-exposed miners and used various relative risk regression models that resulted in the following conclusions: "40% of all lung cancer deaths may be due to radon progeny exposure, 70% of lung cancer deaths in never-smokers, and 39% of lung cancer deaths in smokers. In the United States, 10% of all lung cancer deaths might be due to indoor radon exposure, 11% of lung cancer deaths in smokers, and 30% of lung cancer deaths in never-smokers" (Lubin, et al, 1995).
    D) In an analysis of 11 studies of underground miners, researchers conclude that, in terms of cancers, the material risk of mortality from exposure to radon is linked to lung cancer only. The incidences of death due to leukemia and cancers of the liver and stomach are not related to cumulative exposure to radon and therefore are unlikely to have been caused by radon (Darby et al, 1995).
    E) In one study, many more lung cancer deaths occurred at mine air concentrations of 30 pCi radon-222/L of air and greater. Miners were exposed to the radon for a minimum of 10 years with approximate cumulative exposure at 36 WLMs or more (ATSDR, 1990).
    F) "Lung cancer is the only malignancy clearly associated with exposure to radon" (HSDB , 2002). Residential exposure to radon has been associated with as many as 20,000 lung cancer fatalities per year (NTP, 2001).
    G) "There is sufficient evidence for the carcinogenicity of radon and its decay products in experimental animals [and] in humans. Radon and its decay products are carcinogenic to humans" (IARC, 1988) NTP, 2001).

Maximum Tolerated Exposure

    A) LEVEL OF EXPOSURE -
    1) Calculated absorbed alpha radiation dose to basal cells in bronchial epithelium at a 0.2 Working Level Month (WLM) exposure to radon: 0.1 rad/year (adult men and women); 0.24 rad/year (children); 0.15 rad/year (infants) (Harley & Pasternack, 1982).
    2) In one study of "high background" and "control" areas in China, it was concluded that excess lung cancers could not be separated from background normal fluctuations at radon exposures below cumulative 15 WLM (Hofmann et al, 1986).
    3) The main floor household radon concentration is the primary determinant of body radon contamination in the general public; females may have higher body contamination than males, and nonsmokers may have more body contamination than smokers (Stebbings & Dignam, 1988).
    4) Of 2552 uranium miners exposed to radon over an 8-year period in the 1950s, 419 had developed lung cancer by the end of 1995. Those miners exposed at younger ages were at higher risk to develop lung cancer. (Under age 30, risk increased by a factor of 2). Epidermoid tumors occurred more frequently in miners under the age of 30, while the risk of contracting the small cell type cancers was double that of the epidermoid tumors, but mostly occurred 5 to 14 years after radon exposure (Tomasek and Placek, 1999).
    5) In one study, more than 8000 uranium miners were studied and after approximately 14 years, researchers found that 17 had lung cancer (the expected number was 2.21 (p > 0.05). The lung cancer risk to the miners appeared to be dependent upon the age at which they were first exposed to radon (HSDB, 2002).
    6) Individuals who worked as uranium miners for 10 years or more and who were exposed to approximately 3.08 pCi/L air and thus 6.22 pCi radon-222/cm(2) skin surface area, had a statistically significant increase in the chance of developing a basal cell skin cancer. The researchers acknowledge that factors other than radon exposure may influence health outcomes (ATSDR, 1990).
    B) ANIMAL DATA
    1) In rats, the natural occurrence of lung cancer doubles following exposure to 20 WLM of radon and radon-daughter (HSDB , 2002).
    2) In rats, exposure to radiation from radon and its daughters at 20 and 40 WLM caused an increased incidence of lung tumors (HSDB , 2002).
    C) CARCINOGENICITY
    1) Radon and its decay products are categorized in Group 1 (carcinogenic to humans) (IARC, 1988).
    2) Radon and its isotopes (radon-222 and radon-220) are listed as Known to be Human Carcinogens (NTP, 2001).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) THRESHOLD DOSE -
    a) There is no defensible evidence for or against the possible existence of a threshold dose for radon-induced lung cancer, although some investigators believe that a threshold dose exists and that it may be greater than 4 pCi/L (Cothern, 1989).
    b) It is advised that indoor radon levels be kept at or below the ambient outdoor levels of 0.2 - 0.7 pCi/L (NTP, 2001).
    c) An increased risk of lung cancer has been associated with radon exposure from somewhat less than to greater than 100 WLM in uranium miners (HSDB , 2002; Howe et al, 1986).
    d) NIOSH recommends that radon exposure not exceed 1 WLM per year and 0.083 WLM per shift (NTP, 2001).
    e) The lung cancer risk in uranium miners has also been found to be a function of age at first exposure (Howe et al, 1986).

Workplace Standards

    A) ACGIH TLV Values for CAS10043-92-2 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS10043-92-2 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS10043-92-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 1 ; Listed as: Radon-222 and its decay products
    a) 1 : The agent (mixture) is carcinogenic to humans. The exposure circumstance entails exposures that are carcinogenic to humans. This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent (mixture) may be placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent (mixture) acts through a relevant mechanism of carcinogenicity.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): K ; Listed as: Radon
    a) K : KNOWN = Known to be a human carcinogen

    D) OSHA PEL Values for CAS10043-92-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) Reference: HSDB, 2002
    1) LD50- (INHALATION)MOUSE:
    a) 2.2 X 10(8)pCi/L (8.1 X 10(9) Bq/m(3)) for 5-40H

Pharmacology Toxicology

Toxicologic Mechanism

    A) Radon and its daughters are absorbed into the lungs by inhalation after becoming attached to microscopic particles of environmental airborne dust (Berger, 1990).
    1) Inhaled dust particles with attached radon daughters are distributed to the lungs, where they may stick to the moist bronchial epithelial lining (Berger, 1990).
    a) Mucociliary clearance may not be rapid enough to prevent ionizing radiation (alpha particles) released from the decay of the radon daughters, polonium-218 and polonium-214, from affecting several types of pulmonary cells and eventually leading to cancerous transformation (Berger, 1990).

Physicochemical

Physical Characteristics

    A) Radon exists as a colorless, tasteless, odorless, inert, very dense, monotomic radioactive gas (Budavari, 2000; (Lewis, 1998; Lewis, 2000; Lewis, 2001). Radon "can be condensed to a colorless, transparent liquid and to an opaque, glowing solid" (Lewis, 2001). Radon is an inert gas at temperatures greater than -61.8 degrees C (Berger, 1990) and is the heaviest known gas (Lewis, 2001).
    B) The solid form exists as cube-shaped, face-centered crystals (Budavari, 2000).
    C) "When cooled below the freezing point, radon exhibits a brilliant phosphorescence which becomes yellow as the temperature is lowered and orange-red at the temperature of liquid air" (HSDB , 2002).

Molecular Weight

    A) 222.0176 (atomic mass 222Rn)

References

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