develop intrathoracic malignancy, which was shown to be primary cancer of the lung. Early in the twentieth century, high concentrations of radon were measured in the Schneeberg mines and in the nearby mines of Joachimsthal, where underground miners also developed lung cancer. Radon was considered to be a possible cause of the lung cancer, and this was confirmed through epidemiologic studies of miners of uranium and other ores (for a review, see National Research Council, 1988; Samet, 1989).

Many populations of underground miners exposed to radon and its progeny have been shown to be at increased risk of lung cancer. Except at the highest levels of exposure, the lung-cancer risk in these miners is related roughly linearly to exposure. The information available from miners on the combined effect of cigarette smoking and exposure to radon progeny is consistent with synergism between the two carcinogens. Exposure of animals to radon has provided confirming evidence of carcinogenicity, and laboratory systems have been used to understand mechanisms of genetic injury by particles. The newer techniques of molecular and cellular biology are now being applied to -particle carcinogenesis; the initial findings indicate the potential for these techniques to improve understanding.

Research over the last 20 years has shown that radon is a ubiquitous indoor air pollutant, reaching concentrations in some residences as high as were found in mines where excess lung cancers occurred in underground workers. The predominant source of radon in indoor air in homes is the soil beneath the structures, but building materials, water used in the homes, and utility natural gas can also contribute. Radon concentrations are readily measured with passive devices, and early data showed that the distribution of concentrations was approximately lognormal with a mean of about 1.5 picocuries per liter (pCi/L) (Nero et al., 1986). Data gathered from over 4,000 U.S. homes in 1989-1990 showed that the average



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