The carcinogenicity of radon By Rhonda S. Berger Numerous studies of underground miners exposed to radon daughters (elements that result from the disintegration of radon) in the air of mines have shown an increased risk of lung cancer in comparison with nonexposed populations. Laboratory animals exposed to radon daughters also develop lung cancer. The abundant epidemiological and
experimental data have established the carcinogenicity of radon progeny. These observations are of considerable importance because uranium, from which radon and its progeny arise, is ubiquitous in the Earth's crust, and radon in indoor environments can reach relatively high concentrations. Although the carcinogenicity of radon daughters is established, and the hazards of exposure during mining are well recognized, the hazards of exposure in other environments have not yet been adequately quantified. Risk estimates of the health effects of long-term exposures at relatively low levels are required to address the potential health effects of radon and radon daughters in homes and to refine estimates of the risk in work places. Two approaches are currently being used to characterize the lung cancer risks associated with radon daughter exposure: mathematical representations of the respiratory tract that model radiation doses to target cells and epidemiological investigation of exposed populations, mainly underground miners.
Radon daughter exposure Of the several isotopes of radon, radon-222 has the most important impact on human health. An inert gas at temperatures above - 61.8 O C , radon-222 is a naturally occurring decay product of radium-226, the fifth daughter of uranium-238 (see Figure 1). Both ura-
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Rhonda Berger
nium-238 and radium-226 are present in most soils and rocks in widely varied concentrations. As radon forms from the decay of radium-226, it can leave the soil or rock and enter the surrounding air or water. Radon gas thus becomes ubiquitous, and its concentration is increased by the presence of a rich source and by low ventilation in the vicinity of the source. Radon decays with a half-life of 3.82 days into a series of solid, short-lived radioisotopes collectively referred to as radon daughters or progeny. The first four short half-life radioactive decay products of radon are the most important sources of cancer risk. These are poloniwn-2 18, lead-2 14, bismuth-214, and polonium-2 14. Polonium-2 18, the first decay product, has a half-life of just over three minutes. This is long enough for most of the electrically charged polonium atoms to attach themselves to microscopic airborne dust particles. When inhaled, these small particles have a good chance of sticking to the moist epithelial lining of the bronchi. Most inhaled particles are eventually cleared from the bronchi by mucus, but not quickly enough to keep the bronchial epithelium from being exposed to alpha particles from the decay of polonium-2 1 8 and polonium-2 14. This highly ionizing radiation passes through and delivers radiation doses to several types of lung cells. When alpha
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1989 American Chemical Society
INTERESTED IN REPLACING HAZARDOUS CHLORINATED SOLVENTS? particle emissions occur, these cells lining the airways can be damaged. The resulting biological changes can ultimately lead to lung cancer. Underground mining was the first occupation associated with an increased risk of lung cancer. Uranium ores contain particularly high concentrations of radium, and radon daughter exposure has been associated with lung cancer in uranium miners. Miners of other types of ore can also be placed at risk by the combination of a sufficiently strong source of radon and inadequate ventilation. Radon progeny are also present in the air of dwellings. The source is predominantly the underlying soil, Building materials, groundwater used routinely in the building, and utility natural gas can be contaminated with radon gas as well. The concentration of radon progeny in dwellings is highly variable and depends mainly on the air pressure and ventilation in the home. Because of their wide distribution, radon daughters are a major source of exposure to radioactivity for the general public as well as for special occupational groups. The estimated dose to the bronchial epithelium from radon daughters far exceeds that to any other organ from natural background radiation. The recent recognition that some homes have high concentrations of radon has focused concern on the potential lung cancer risk associated with environmental radon.
Indoor radon and risk The radiation dose from inhaled daughters of radon-222 constitutes about half of the total effective dose equivalent that the general population receives from natural radiation. A variety of study results in the United States suggest that radon-222 concentrations in residences average about 1 pCi/L (a picocurie, pCi, is the amount of any radionuclide that undergoes exactly 3.7 x radioactive disintegrations per second). Estimation of the incidence of lung cancer due to the daughters associ-
ated with this quantity of radon-222 yields thousands of cases per year among the U .S. population. Indoor levels are sometimes an order of magnitude or more higher than the average; it is the common experience of communities that survey homes to find concentrations in the range of 10 to 100 pCi/L. Whereas the risk associated with even 1 pCi/L is very large compared with many environmental insults, exposure to these higher concentrations for prolonged periods leads to estimated individual lifetime risks of lung cancer that exceed 1% . For the extreme concentrations that have been reported, the risk appears to approach that from cigarette smoking. Table 1 is an excess risk evaluation chart based upon exposure to radon for individuals who spend 75% of their time in the home for 70 years.
Recommended exposure levels There is currently no federal legislation that might be invoked as the statutory basis for a generalized program regulating the radon level in homes. The thrust of the Clean Air Act is toward prevention of atmospheric pollution and the maintenance of ambient air quality. The Toxic Substances Control Act (TSCA) is aimed at chemical substances or mixtures subsequent to manufacture. Therefore, only recommended guideline exposure levels have been issued by EPA at 4 pCi/L and by the National Council on Radiation Protection at 8 pCi/L. These agencies suggest implementation of remedial actions for exposures above these levels.
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Rhondu S. Berger is an environmental control engineer in the Engine Division of the Ford Motor Company in Dearborn, MI. She received her B.S. degree in environmental sciences from Michigan State University and her M.S. degree in toxicology from Wayne State University in Detroit.
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