to 33,0001. Nonetheless, this indicates a public-health problem and makes indoor radon the second leading cause of lung-cancer after cigarette-smoking.
The full number of attributed deaths can be prevented through radon mitigation only by eliminating radon in homes, a theoretical scenario that cannot be reasonably achieved. Nonetheless, the burden of lung-cancer deaths attributed to the upper end of the exposure distribution is expected to be reduced by lowering radon concentrations. Perhaps one-third of the radon-attributed cases (about 4% of the total lung-cancer deaths) would be avoided if all homes had concentrations below the Environmental Protection Agency's action guideline of 148 Bqm-3 (4pCiL-1); of these, about 87% would be in ever-smokers. It can be noted that the deaths from radon-attributable lung-cancer in smokers could most efficiently be reduced through tobacco-control measures, in that most of the radon-related deaths among smokers would not have occurred if the victims had not smoked.
The committee's model and general approach to assessing lung-cancer risks posed by indoor radon and cigarette-smoking are subject to considerable uncertainty because of gaps in our scientific knowledge of effects at low levels of exposure. This uncertainty should be reduced as an improved understanding develops of molecular and cellular events in the induction of lung-cancer at low levels of exposure to radon and other toxicants and of the role of various factors influencing susceptibility to lung-cancer. The long-term follow-up of miner populations is strongly encouraged, as is completion of the case-control studies of residential exposures now in progress. The committee encourages further meta-analysis and pooling of case-control data. However, the committee recommends that new case-control studies not be initiated until those in progress are completed, data are analyzed and synthesized, and judgments rendered as to the likely value of further residential studies.
Despite the limitations of existing data, the committee found key observational and experimental data that, along with theoretical considerations in radiobiology and carcinogenesis, provided a basis for the models developed and used to estimate radon-attributable lung-cancer risks. The major shortcomings in the existing data relate to estimating lung-cancer risks near 148 Bqm-3 (4 pCiL -1) and down to the average indoor level of 46 Bqm-3 (1.24 pCiL-1), especially the risks to never-smokers. The qualitative and quantitative uncertainty analyses indicated the actual number of radon-attributable lung-cancer deaths could be either greater or lower than the committee's central estimates. This uncertainty did not change the committee's view that indoor radon should be considered as a cause of lung-cancer in the general population that is amenable to reduction. However, the attributable risk for smoking, the leading cause of lung-cancer, is far greater than for radon, the second leading cause. Lung-cancer in the general population and in miners is related to both risk factors and is amenable to prevention.