Exposure to radon can occur from inhalation or dermal contact. It can also enter the body via ingestion if dissolved in water. Radon distributes mainly to the fat. It is not metabolized and may be eliminated in the urine, faeces, or expired air. (L1836)
IDENTIFICATION AND USE: Radon, a naturally occurring gas formed from the decay of uranium in the earth. Radon was produced commercially for use in radiation therapy, but for the most part has been replaced by other radionuclides. Some radon is produced in research laboratories and universities for use in experimental studies. HUMAN STUDIES: Radon and its isotopic forms radon-222 and radon-220 are known to be human carcinogens based on sufficient evidence of carcinogenicity from studies in humans. Increased incidences of lung cancer have been reported in numerous epidemiological studies of groups occupationally exposed to radon at high doses. In one of the largest prospective studies, two cohorts totaling 3,400 white and 780 Native American uranium miners and millers in Colorado were followed from 1950 to 1977. Among white males, the risk of lung cancer was significantly increased 4- to 6-fold. In some other cohorts, radon exposure was also associated with increased risks of tracheal and bronchial cancer. Smaller case-control studies also suggested an association between lung-cancer risk and indoor residential exposure to radon, mainly from ground sources. There is evidence of association between chronic exposure to indoor radon and the occurrence of chromosome damage in human oral epithelial cells. In an effort to mimic human in vivo exposures to ionizing irradiation, G(0) phase T lymphocytes from human peripheral blood samples were utilized for in vitro studies of the genotoxic effects of radon-222 irradiation. The spectrum of radon-222 irradiation-induced mutation was characterized by an increase in small alterations, especially multiple single base deletions/substitutions and micro-deletions. However, radon therapy is clinically useful for the treatment of pain-related diseases. Radon bath is a well-established modality of balneotherapy for the management of degenerative musculoskeletal disorders. ANIMAL STUDIES: In male rats, inhalation exposure to radon caused lung cancer (adenoma, adenocarcinoma, alveolar/bronchiolar carcinoma, and squamous-cell carcinoma). In dogs of both sexes, inhalation exposure to a combination of radon, radon decay products, and uranium ore dust caused lung cancer and nasal cancer. A review of studies in rats exposed to radon by inhalation also reported increased incidences of tumors of the upper lip and urinary tract. In a study in hamsters, only three animals developed features of squamous-cell carcinoma after 16 to 17 months of exposure to radon decay products or radon decay products and uranium ore dust. The cytotoxic and mutagenic effects of radon and its progeny in murine lymphoblast L5178Y-R16 cells were compared after exposure in vitro to a steady-state ratio of radon and its progeny (radon-222:polonium-218:polonium-214=1:3.5:4.5) under various experimental conditions. In all cases, a dose-dependent increase in the induced frequency of mutation at the thymidine kinase locus was found. However, radon inhalation activates antioxidative functions in the liver and inhibits carbon tetrachloride-induced hepatopathy in mice. Radon inhalation activates superoxide dismutase (SOD) inhibiting transient global cerebral ischemic injury in gerbils. ECOTOXICITY STUDIES: Radon retention by the bluegill increased much more rapidly with time after injection than did radon retention by the mouse.
The ionizing radiation produced by radon causes cellular damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and genetic instability. This leads to loss of normal cell and tissue homeostasis, and development of malignancy. Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that directly affect the stability of p53, an important enzyme in cell-cycle regulation, and produce oxidative damage to individual bases in DNA and point mutations by mispairing during DNA replication. (L1836)
Evaluation: There is sufficient evidence for the carcinogenicity of radon and its decay products in experimental animals. There is sufficient evidence for the carcinogenicity of radon and its decay products in humans. Overall evaluation: Radon and its decay products are carcinogenic to humans (Group 1).
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌性证据
辐射性辐射，氡：已知是人类致癌物。/辐射性辐射：氡/
Ionizing Radiation, Radon: known to be a human carcinogen. /Ionizing Radiation: Radon/
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌物分类
国际癌症研究机构致癌物：氡-222及其衰变产物
IARC Carcinogenic Agent:Radon-222 and its decay products
来源:International Agency for Research on Cancer (IARC)
吸收、分配和排泄
气体和蒸汽已知被皮肤吸收（或排出）包括...氡...。
Gases and vapors known to be absorbed (or excreted) by the skin include ... radon ... .
来源:Hazardous Substances Data Bank (HSDB)
吸收、分配和排泄
氡气的存在与肺癌发生率的增加有关，这是由于放射性物质在支气管区域的沉积。
The presence of radon is associated with an increase in the occurrence of lung cancer due to the deposition of radioactive substances in the bronchial region.
Following ingestion of radon dissolved in water, greater than 90% of the absorbed radon was eliminated by exhalation within 100 minutes. By 600 minutes, only 1% of the absorbed amount remained in the body.
Experiments in animals have reported the retention of radon after exposure by the intraperitoneal and intravenous routes. After intravenous administration , 1.6% to 5.0% of the administered activity was retained in the animals after 120 minutes. Retention was greatest after intraperitoneal administration at 120 minutes, but by 240 minutes it was nearly the same for both routes of administration.
