associated with indoor radon. For example, the precursor to this committee, the BEIR IV committee, developed one such model on the basis of statistical analysis of data from 4 epidemiologic studies of underground miners. The BEIR IV model has been widely used to estimate the risk posed by indoor radon. Since the 1988 publication of the BEIR IV report, substantial new evidence on radon has become available: new epidemiologic studies of miners have been completed, existing studies have been extended, and analysis of the pooled data from 11 principal epidemiologic studies of underground miners has been conducted involving a total of 68,000 miners and to date, 2,700 deaths from lung-cancer. Other lines of scientific evidence relevant to assessing radon risks have also advanced, including findings on the molecular and cellular basis of carcinogenesis by alpha particles. Radon itself does not directly cause lung-cancer but alpha particles from radon progeny directly damage target lung cells to cause cancer. There is additional information for calculating the dose of alpha particles received by the lung from inhaled radon progeny, the topic of a 1991 follow-up report to the BEIR IV report, the report of the National Research Council's Panel on Dosimetric Assumptions. Finally, during the last decade, a number of epidemiologic case-control studies that estimated the risk associated with indoor radon directly have also been implemented.
The BEIR VI committee faced the task of estimating the risks associated with indoor radon across the full range of exposures and providing an indication of the uncertainty to be attached to risk estimates across this range. In preparing this report, the BEIR VI committee, in response to its charge, reviewed the entire body of data on radon and lung-cancer, integrating findings from epidemiologic studies with evidence from animal experiments and other lines of laboratory investigation. The committee also considered the substantial evidence on smoking and cancer and the more limited evidence on the combined effect of smoking and radon. The report's elements include comprehensive reviews of the cellular and molecular basis of radon carcinogenesis and of the dosimetry of radon in the respiratory tract, of the epidemiologic studies of miners and the general population, and of the combined effects of radon and other occupational carcinogens with tobacco-smoking. The committee describes its preferred risk models, applies the models to estimate the risk posed by indoor radon, and characterizes uncertainties associated with the risk estimates.
Information on radon carcinogenesis comes from molecular, cellular, animal, and human (or epidemiologic) studies. Radiation carcinogenesis, in common with any other form of cancer induction, is likely to be a complex multistep process that can be influenced by other agents and genetic factors at each step. Since our current state of knowledge precludes a systematic quantitative description of all steps from early subcellular lesions to observed malignancy, the com-