Table of Contents
Introduction
Lung cancer is the leading form of cancer-related deaths. Carcinogens breathed into the lung from the burning of cigarette, wood, or anything chemical combustion in general, can damage the lungs and cause lung cancer. Studying why there is such a high probability of lung cancer is important to lower the rate of lung cancer in the future. Smokers are expected to have a high risk of lung cancer due to exposure to high concentration of carcinogens for a long period of time but why are non-smokers also experiencing a high risk for lung cancer. One of the possible causes of lung cancer is exposure to radon a radioactive gas that can give off radiation in the lungs, damage DNA and cause cancer.
According to EPA radon is the second most frequent cause of lung cancer after cigarette smoking in the United States and the first frequent cause of lung cancer for non-smokers. The correlation between radon and lung cancer was first discovered in miners. A lot of miners in uranium mine have a very high rate of lung cancer death and discovery of high concentration of radon in mines correlate radon as a carcinogen. After further study of how radon can cause cancer in lab animals, there is no doubt radon is a carcinogen.
Radon concentration in the different area varies and it is important to make sure there isn’t a high concentration of radon in your house. High level of radon exposure in homes, workplace, schools can be avoided with proper education and testing so educating the public about radon gas is very important. The questions remain to be answered with more research is whether the average household concentration of radon can cause cancer in the general population and if a low level of radon radiation can be beneficial for medical purpose.
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Physical and Chemical Properties
Radon is a colorless, tasteless and odorless noble gas that cannot be detected without testing. Radon is naturally occurring gas that is formed when uranium, thorium or radium in soil or rocks or groundwater is broken down. It has 36 known isotopes and isomers but no known stable isotope Radon-222 has a half-life of 3.825 days. It is a gas that can enter buildings through cracks and be trapped in the basement or lower floor of buildings due to its high density of 9.73 g/L. Due to the fact that it is a gas, it is more mobile and able to diffuse through the environment, unlike its radioactive progeny which are solid. When radon decays it releases radioactive progeny that can bind to dust and when inhaled the radioactive particles will be trapped in the lung.
ADME
When radon gas is breathed most of it is immediately exhaled. Radon progeny is breath in along with dust particles and accumulates in the mucus along bronchial epithelial lining. From there the progeny continues to release alpha-radiation. If radon and its progeny travel into the lungs it will be transferred into the blood and carried throughout the body. If radon in water is ingested it will give off radiation in the stomach, GI tract, be transferred into the blood and carried throughout the body. Most of it will be deposited in adipose tissue and retention once it enters the blood. Radon and its progeny will decay in the body and stable decay product can be eliminated by the body urinary and fecal excretion but due to the short half-life of the progeny radiative energy will be released before entering metabolic pathways.
Mechanism of Action
When uranium-238 decays radon-222 is formed. When radon-222 decays it emits a-particles and different radioactive progeny. The progeny polonium-218 and polonium-214 are solid and they also emit a-particles when they decay. Progeny can also emit beta and gamma radiation, but their effects are minimal compared to alpha particle radiation. These solids will bind to dust particles, be breath in and remain in bronchial epithelium. When they break down cells will be exposed to ionizing radiation. A-particle deposit energy in increasing linear amount as they travel through the body, but they cannot travel very far so bronchial tumors are typical lung cancer caused by radon.
A-particle creates ion pair clusters that damage cells. It can react with DNA causing DNA damage like double-strand breaks and generate reactive oxygen species which will damage the cell. The cell will utilize its repair mechanism to fix those DNA damages but during the process base insertion, deletion, mismatch, rearrangement is increased and the likelihood for mutation is also increased. Along with chromosomal aberrations which are a result of repair mechanisms, micronuclei formation which are short pieces of DNA fragments that are not rejoined are common sign of radiation damage. Alteration in gene expression, cell cycle regulation cytokine up and down regulation are also permanent effects of radiation.
Research in vitro with lab animals and in vivo with uranium miners demonstrate the ability of radon progeny to cause biological damage. TP53 gene which is a tumor suppressor is often mutated or deleted in radon-induced cancer, but research showed there is no hotspot mutation identified. The effect of radon radiation might be extended beyond directly irradiated cells due to the bystander effect. This means that damage cells will be sent out a signal that will further damage surrounding cells. The mechanism radon causes cancer varies and damages on DNA are nonspecific. Even though cells will survive the damage caused by ion clusters and reactive oxygen intermediates due to different DNA repair mechanisms there will still be permanent damage to the cell’s DNA and the stability of the p53 gene on cell regulation.
Controversy
There remain much debated about how low levels of radon radiation affects the body. Research shows that radon exposure at a lower concentration in homes does not increase the risk of cancer but instead sometimes decrease the risk of cancer. Some clinical studies use radon-rich air or water to treat rheumatoid arthritis. A possible explanation for why radiation is beneficial is the theory of radiation hormesis when radiation actives free radicals, protective mechanism of the body also actives and mend damage caused by radiation and pre-existing damage.
Superoxide dismutase which one of the protective mechanisms against free radicals has increased activity in the female in Misasa Japan that are living in an area with elevated radon level. So contrary to previous belief that the dose-response curve of radon is linear no-threshold new research indicates that there is one set of gene response at a low dose and another set of gene response at a high dose. The concentration of radon in homes also varies a lot from concentration and condition in mines where radon radiation case is first looked at. There is an increasing amount of ventilation in homes and decreasing amount of other toxic gas. Even with a large group of data, it’s hard to produce a conclusive risk model for radon risk at low concentration.
Conclusion
With new research proving a low level of radon can be beneficial our future understanding of radon might change. Radiation concentration is the key to the debate within groups of the scientist. Cells have its own repair mechanism to fix small amount of radiation damage but when the damage occurs too often, and the damage cannot be correctly repaired the cell survive with mistakes accumulating until it becomes a tumor. With not enough cases directly linking radon exposure in homes to lung cancer, it’s hard to determine what level is considered safe and what level is dangerous.
Radiation damage is something that cannot be measured until it becomes cancer. Many federal organizations like EPA still recommend living in a house with radon concentration below 4pCi/L. It is still important to learn about radon exposure when living in an area of high radon concentration because even though studies cannot identify specific health effects there is enough circumstantial evidence they occur.
