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Home and Away
Published in Alan Perkins, Life and Death Rays, 2021
The highest levels of radon have been found in Scandinavia, the US, Iran and the Czech Republic. Being a gas, radon seeps out of the earth and into the atmosphere. Radon-222 with a half-life of 3.8 days is the most stable radionuclide of radon and is responsible for the majority of public exposure to background radiation. It becomes a particular hazard to health when it enters buildings and closed spaces with poor air flow. The increasing use of building insulation and double glazing has resulted in the build-up of dangerously high concentrations of radon in some domestic properties, schools and workplace buildings. The main health hazard from radon is from lung intake through normal breathing. The biological damage occurs from the radon decay products, mainly polonium-218 and polonium-214 which become deposited in the bronchial tissues of the airways delivering the majority of the radiation dose to the lungs in the form of alpha particles. Epidemiological studies have shown conclusively that this is carcinogenic to humans and can cause lung cancer. In fact, radon is considered to be the second largest cause of lung cancer after cigarette smoking. Low levels of radon can also be found in drinking water but the release of the gas from water is negligible compared to other sources. Scientific studies have shown that the risk of stomach cancer and other gastrointestinal malignancies from radon in drinking water is small.
Environmental Inhaled Agents and Their Relation to Lung Cancer
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Uranium in the earth's crust gives rise to decay chain products through radium 226 to the gas radon 222, which in turn gives rise to other isotopes collectively termed radon daughters (Parkes, 1982a). Radon 222 and the three radon daughters, polonium 218, polonium 214, and polonium 210, are important a-particles emitters. Thorium likewise decays into decay chain products of which thorium B (lead 212) and thorium C (bismuth 212) are a-particles emitters. All these products are emitted by soil, rocks, and building materials and are dispersed in the atmosphere to attach to water vapor, dust, or cigarette smoke particles, attaining aerosol sizes of 0.25-0.4 /rm (Davies, 1967). In this state, they can, on inhalation, penetrate well to the trachea, bronchi, and beyond (Parkes, 1982b) and exert their ionizing effect.
Radiation Hormesis in Cancer
Published in T. D. Luckey, Radiation Hormesis, 2020
Radon, 222Rn, is produced from radium decay; it has a half life of 3.82 d and decays with ejection of an alpha particle. 219Rn and 220Rn have half lives so short they have little time for identity separate from their source atoms. 222Rn decay triggers a cascade of several short lived progeny which produce four alpha, four beta, and four gamma emmissions within 4 h (Table 1.5). All three types of radiation produce free radicals. The cascade stops with 210Pb, half life of 22 years. When 210Pb decays to stable 206Pb, one alpha and two beta rays are produced.
Radioactivity in building materials and assessment of risk of human exposure in the East Khasi Hills District, Meghalaya, India
Published in Egyptian Journal of Basic and Applied Sciences, 2020
The external hazard index (Hex) is an evaluation of the hazard of the natural gamma radiation emitted by the concerned radionuclides. This index value must be less than 1 (unity) to keep the contribution to the radiation hazard insignificant (European Commission, 1999). When the value of this index is less than 1 (unity), then the radiation received by occupants will be less than 1.5 mGy y−1. The inhalation of radon (222Rn) gas and its progeny products or ingestion of other radionuclides give rise to internal exposure. This exposure was measured by the parameter Hin. The expression for calculating Hex and Hin is given below [21,29]:
Primary and secondary bystander effect and genomic instability in cells exposed to high and low linear energy transfer radiations
Published in International Journal of Radiation Biology, 2019
K. Kanagaraj, V. Rajan, Badri N. Pandey, K. Thayalan, P. Venkatachalam
Human exposures to radiation are either from natural or man-made sources. The sources of high-LET exposures are radon gas and its decay products from the environment; the roots of accumulation are ingestion through food and or inhalation from the air. Of late, use of high LET radiation in cancer treatment (α-particle emitting radionuclides administered for therapeutic purposes) is the preferred choice, because of its enhanced therapeutic benefit; but this also results in a source of human exposure to high LET radiation. While for the exposure to the latter the benefit outweighs the risk, the exposure to the former remains a concern. For example, occupational exposure to high LET radionuclide from radon (222Rn), and its decay products has been associated with the development of lung cancer and leukemia’s in Uranium miners (Zölzer et al. 2012; Widel 2017). High LET has become a prominent public health concern because of the growing evidence on its presence in the residential environment, occupational environment and for astronauts in space flights (Kawata et al. 2004). The RIBE have been reported in multiple experimental models, challenging the traditional central dogma in radiation biology. The situation further raises the concern that these effects like bystander response and GI has been demonstrated even in the bystander cells. Keeping the importance of the emerging literature, the property of RIBE was investigated in the HADF cells and human blood lymphocytes.
Correlation between cytogenetic biomarkers obtained from DC and CBMN assays caused by low dose radon exposure in smokers
Published in International Journal of Radiation Biology, 2019
Radon and its decay products emit high LET alpha radiation. Half of the human annual background radiation exposure occurs because of the Radon-222 (Robertson et al. 2013). High doses of ionizing radiation causes detrimental effects in humans such as chromosomal damage (Ulsh et al. 2015), mutations (Vilenchik and Knudson 2006), carcinogenesis (Evrard et al. 2005; Krewski et al. 2006) etc. Data related to low dose ionizing radiation effects is limited and there is an increasing concern towards the risk of low dose exposure because of frequent flyer risks, screening tests for cancer, occupational exposure, manned space exploration etc. (ICRP 1999; Gilbert 2001). At present, risks of low dose exposure are derived by linear extrapolation from higher doses which might not truly reflect the low dose risk (Mitchel 2007; Matsumoto et al. 2009; Wheeler and John Bailer 2013; Desouky et al. 2015). Because of lack of understanding of the molecular consequences of low dose exposure, ambiguity exists on the risks of low dose in human beings (Kim et al. 2015).