Radon, radioactive

CAS RN: 10043-92-2

Health Effects

    • A) SOURCES: IONIZING RADIATION: Nuclear emissions that have sufficient energy to ionize atoms and remove one or more electrons from the orbit of other atoms. Radiation injuries occur secondary to exposure to ionizing radiation (eg, alpha particles, beta particles, gamma rays, x-rays, and neutrons). The radioactive exposure may be due to external irradiation (source at some distance from the body) or internal contamination (ingestion, inhalation, absorption through skin or wounds). Acute radiation syndrome may occur after total or near total body irradiation with a high dose of ionizing radiation over a short period of time. The most common radionuclides in the atmosphere are: radon-222, tritium, iodine-129, strontium-90, cesium-137, and krypton-85. Radioactive materials of military significance (Military Five) include: Tritium (3H), uranium (235U, 238U), plutonium (239Pu), and americium (241Am).
    • B) TOXICOLOGY: The response to exposure to ionizing radiation varies by cell type and is largely a function of the rate of cell replication or the cell cycle length. Cells are most vulnerable to the effects of radiation during mitosis; therefore, the tissue with the most mitotically active cells will be the most damaged. Spermatogonia, the cells of the gastrointestinal tract, and hematopoietic cells such as lymphocytes and erythroblasts are the most sensitive, while collagen-producing cells, muscle cells, and bone cells are less affected since they are not as mitotically active. Thus, the 3 syndromes that result are hematopoietic, gastrointestinal, and neurovascular, based on these decreasing radiation sensitivities. Increasing doses of ionizing radiation lead to increasing damage to the cells that are more radioresistant.
    • C) EPIDEMIOLOGY: Radiation exposures are rare, but can be life-threatening.
      • 1) The clinical syndromes described for acute radiation syndrome (ARS) follow 4 clinical phases: prodromal, latent, manifest illness, and recovery (or death).
        • a) HEMATOPOIETIC SYNDROME: Dose (gamma equivalent values): Greater than 0.7 Gy (greater than 70 rads); mild symptoms may develop following doses as low as at 0.3 Gy (30 rads).
      • 1) Prodromal stage: Anorexia, nausea, vomiting; onset 1 hour to 2 days postexposure; lasts minutes to days
      • 2) Latent stage: Patients may appear well; stem cells are dying; lasts 1 to 6 weeks
      • 3) Manifest illness stage: Anorexia, fever, malaise. All blood cell counts decrease for weeks. Death from infection or hemorrhage. Increasing dose decreases survival. Most deaths within few months.
      • 4) Recovery: Bone marrow cells begin to repopulate the marrow. Large proportion will recover from few weeks up to 2 years. Death may occur at 1.2 Gy (120 rads). LD50/60 approximately 2.5 to 5 Gy (250 to 500 rads).
        • b) GASTROINTESTINAL SYNDROME: Dose (gamma equivalent values): Greater than 10 Gy (greater than 1000 rads); some symptoms may develop following doses as low as 6 Gy (600 rads).
      • 1) Prodromal stage: Anorexia, severe nausea, vomiting, cramps, diarrhea. Onset within few hours; lasts 2 days.
      • 2) Latent stage: Patients may appear well. Stem cells and gastrointestinal lining cells are dying; lasts less than 1 week.
      • 3) Manifest illness stage: Malaise, anorexia, severe diarrhea, fever, dehydration, electrolyte imbalance. Death from infection, dehydration, and electrolyte imbalance. Death may occur within 2 weeks.
      • 4) Recovery: LD100 is about 10 Gy (1000 rads).
        • c) CNS/CARDIOVASCULAR SYNDROME: Dose (gamma equivalent values): Greater than 50 Gy (greater than 5000 rads). Some symptoms may develop following doses as low as 20 Gy (2000 rads).
      • 1) Prodromal stage: Extreme nervousness, confusion, severe nausea, vomiting, watery diarrhea, loss of consciousness, burning skin sensation. Onset within minutes; lasts minutes to hours.
      • 2) Latent stage: Partial functionality may return. May last for hours but usually less.
      • 3) Manifest illness stage: Return of watery diarrhea, seizures, coma. Onset 5 to 6 hours postexposure. Death within 3 days.
      • 4) Recovery: No recovery expected.
      • 2) CUTANEOUS RADIATION SYNDROME (CRS): Exposure to radiation can damage the basal cell layer of skin, resulting in inflammation, erythema, and dry or moist desquamation. Epilation may occur when hair follicles are damaged. A transient and inconsistent erythema and pruritus may occur within a few hours of exposure. Patients may develop intense reddening, blistering, and ulceration of the irradiated site during a latent phase that lasts from a few days up to several weeks. Although healing can occur, very large doses can cause permanent hair loss, damage sebaceous and sweat glands, atrophy, fibrosis, decreased or increased skin pigmentation, and ulceration or necrosis of the tissue. Patients may develop skin damage without ARS following radiation dose to the skin, especially after acute exposures to beta radiation or X-rays.
      • 3) Hypothyroidism or hyperthyroidism may occur. Both benign and malignant thyroid tumors have been associated with ionizing radiation exposure.
      • 4) COMBINED INJURY: Patients with combined injuries (trauma, thermal, chemical injury, and radiation exposure) may develop immunosuppression, delayed healing, pancytopenia, and other symptoms.
  • A) Four major effects of ionizing radiation on the fetus include: growth retardation; severe congenital malformations (including errors of metabolism); embryonic, fetal, or neonatal death; and carcinogenesis. Fetal risk is noted at exposures above 10 rem. In early pregnancy, fetal death may occur. Later in pregnancy, radiation exposure may be teratogenic or may cause fetal growth retardation.
  • B) Occupational limits: Fetal dose (declared pregnancy): 0.5 rem (5 mSv). Although radiation doses to the embryo or fetus in the uterus is lower than the doses to its mother, health effects of exposure to ionizing radiation in human embryo and fetus can be severe, even at radiation doses too low to immediately affect the mother. Low-level ionizing radiation does not appear to increase the risk of teratogenicity. Consider doses of radioactive materials in specific fetal organs or tissues (eg, iodine-131 or iodine-123 in thyroid; iron-59 in the liver; gallium-67 in the spleen, strontium-90 and yttrium-90 in the skeleton). Approximately 5 Gy (500 rads) dose before 18 weeks' gestation can kill 100% of human embryos or fetuses; 50% of embryos may die with a fetal dose of 1Gy (100 rads).
  • C) Cesium has been shown to penetrate the human placenta and be present in breast milk in mothers following exposures.
  • D) Impaired fertility, including abnormal sperm production and impaired sexual function, has been reported in men. It is possible that radiation exposure in women may affect the viability of the ova and the function of the endocrine system which is responsible for production of some female sex hormones.
    • A) Ionizing radiation has carcinogenic effects in many tissues. The major toxicity of low- and moderate-dose ionizing radiation is cancer induction. Acute ionizing radiation exposure survivors have increased long-term cancer risks. A dose-response relationship exists between exposure to ionizing radiation and the risk for the subsequent development of cancer.
  • A) Ionizing radiation is genotoxic and causes breaks in the structure of DNA, resulting in mutations or chromosomal structural aberrations. Double strand breaks in the mutagenic and carcinogenic effects of radiation have been reported. Incorrectly rejoined break leads to DNA mis-repair which in turn leads to DNA deletions and rearrangements. Large scale changes in DNA structure appear to be typical of most radiation-induced mutations.
    • 1) Hospital workers exposed to low levels of ionizing radiation had 13 and 11 times greater frequencies of chromosomal aberrations in peripheral lymphocytes compared with unexposed controls. Workers were exposed to mean x-ray doses of 1.84 millisieverts/yr and 1.67 millisieverts/yr for 3 to 20 years. These workers had a higher frequency of chromosomal gaps and breaks, endoreduplications, hyperdiploidies, and chromosomal loss (Paz-y-Mino et al, 1995).
    • 2) Nuclear medicine and radiology hospital workers had a mean group frequency of chromosomal aberrations (chromosomal gaps and breaks) in peripheral lymphocytes significantly higher than that of unexposed controls (Hagelstrom et al, 1995).
    • 3) The frequency of chromosomal aberrations in the peripheral lymphocytes of hospital radiodiagnostic, radiotherapy, and nuclear medicine employees was greater than in controls. There were no significant differences between exposed and control groups in the frequency of chromatid gaps and breaks, while significant differences were noted for acentric fragments with or without chromosomal gaps and breaks and total structural aberrations (Barquinero et al, 1993).
    • 4) The was a statistically significant increased total aberration frequency in peripheral lymphocytes in a small group of civilian air crew members compared with controls (Romano et al, 1997). Air crew members are presumed to have increased exposure to cosmic radiation than the general public because of more time spent at high altitudes during flight (Zwingmann et al, 199
    • 8) Okansen, 1998; (Friedberg et al, 1989).
    • 5) Two years after total-body or total-body plus partial-body exposure to gamma radiation from an accident in Estonia, 5 persons had a stable level of translocations present in peripheral blood lymphocytes (Lindholm et al, 1998).
    • 6) In 100 medical workers exposed to x-rays, there was no time-dependent recovery of chromosomal aberrations in peripheral blood lymphocytes (Kasuba et al, 1998).
    • 7) Children exposed to low doses of ionizing radiation from the Chernobyl disaster had more acentric fragments in peripheral blood lymphocytes than did control subjects, but there were no significant differences in chromosome or chromatid breaks (Grollino et al, 1998).
    • 8) Chromosome aberrations in Norwegian reindeer following the Chernobyl accident (radiocesium exposure) appeared to affect mainly calves during the immediate post-accident period in the highest radiation fallout areas (Roed & Jacobsen, 1995).
    • 9) Increased chromosomal aberrations, especially acentric fragments, were found in lymphocytes from hospital workers exposed to low doses of ionizing radiation (1.6 to 42.71 millisieverts). No dose-effect relationship was seen (Barquinero et al, 1993). In a group of 47 children exposed to radiation in the Chernobyl incident, low frequencies of chromosome aberrations were evident several years later (Padovani et al, 1993). 1
    • 0) Chromosomal translocations in persons who lived in houses (up to 16 years) in Taiwan contaminated with cobalt-60 has been reported. Compared with controls (no exposure to cobalt-60), the overall translocation yield in the residents was 5 times higher. Chromosomes 2, 4 and 12 were affected in 500 metaphases per person. The FISH method for reciprocal chromosomal translocations was used (Chen et al, 2000).
    • 1) Japanese atomic bomb survivors have been followed for possible heritable effects from acute ionizing radiation exposure. Even in this population, no clearly demonstrable induced heritable defects have been found (Otake & Schull, 1984). No significant differences in mutation rates in DNA repetitive sequences were found in children of atomic bomb survivors whose parents received a mean gonadal dose of 1.9 sieverts, in comparison with unexposed controls (Satoh et al, 1996).
    • 2) Workers exposed to low levels of ionizing radiation had increased frequencies of hprt-mutated lymphocytes and changed CD4/CD8 lymphocyte subset ratios (Siefert et al, 1993). A 4.6-fold increase in hprt mutations in blood cells was seen in Brazilian children exposed to 15 to 70 centi-gray units (cGy) during a radiological accident (Saddi et al, 1996). A doubling dose of 173 (+/- 4
    • 7) cGy was seen for inducing hprt mutation and micronuclei in victims of a Cs-137 radiological accident in Goiania, Brazil (Dacruz et al, 1997).
    • 3) Persons living near a uranium processing site did not have increased frequencies of mutated somatic cells, as measured by hprt mutations, loss of glycophorin A alleles, or micronuclei (Wones et al, 1995).
    • 4) Increased glycophorin A mutations were seen in former Australian uranium miners 30 years after last exposure (Shanahan et al, 1996).
    • 5) Human cells containing mutant p53 proteins did not have delayed cell replication after irradiation; this is consistent with the occurrence of mutated p53 proteins in some cancers (Zolzer et al, 1995). In related studies, cells from patients with ataxia telangiectasia (AT) had a reduced or delayed increase in p53 protein after gamma-irradiation (Birrell & Ramsay, 1995). Cells from persons heterozygous for AT had an intermediate response. Cells from most breast cancer patients were essentially normal in their response, but 18% of the patients responded in the range of AT heterozygotes. This test of p53 induction may be useful in identifying persons at increased risk of DNA-damaging effects of ionizing radiation (Birrell & Ramsay, 1995). AT is a heritable disease characterized by increased radiation sensitivity and risk for cancer.
    • 6) In limited studies, the serum of persons exposed to ionizing radiation contains clastogenic factors, which have persisted for over 30 years in A-bomb survivors. Such factors have been found in dose-related levels in the serum of 33 of 47 recovery workers from the Chernobyl incident (Emerit et al, 1995).
    • A) Radon is odorless, colorless, tasteless, and not irritating; there is no way to detect its presence other than sampling and laboratory measurement. Radon is a naturally occurring radioactive gas.
      • 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.
    • B) 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.
    • C) 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. After cigarette smoking, indoor radon is the second leading cause of lung cancer. Radon exposure is considered the leading cause of lung cancer in never smokers and the second leading cause of lung cancer in smokers.
      • 1) EPIDEMIOLOGY: It is estimated that radon exposure may represent 30% of lung cancer deaths in never smokers. Several studies have found a linear and statistically significant increase on the risk of lung cancer with residential radon exposure.
      • 2) Smokers are at greater risk for the development of lung cancer. The risk of lung cancer in cigarette smokers is 10 times that of nonsmokers.
      • 3) Lifetime exposure to the EPA recommended guideline of 4 pCi/L is estimated to pose a 1 to 5% risk for developing lung cancer depending if a person is a nonsmoker or smoker.
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.
    • 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.
    • 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.
    • A) Excess mortality from nonmalignant renal disease (chronic and unspecified nephritis) has been noted in radon-exposed miners.
    • A) Radiation dermatitis has developed following gold radon seed implants or wearing gold rings made from spent gold radon seeds.
  • 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. In one study, there was an association between high radon levels and certain birth defects (ie, cleft lip with or without cleft palate) and cystic hygroma.
  • 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.
    • 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.
    • 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 5,000 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. Further research suggests a potential relationship between residential radon exposure and lung cancer in never smokers.
  • 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.
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