dant to describe this effect modification in great detail, the data indicate synergism between the two agents that is most consistent statistically with less than multiplicative interaction for describing the joint effect. The committee's risk projection models separately characterize the risks in ever-smokers and never-smokers. The miner data remain the principal basis for this separate characterization. The case-control studies in the general population have not proved informative on this issue and valid signatures at the histologic and molecular levels have not yet been identified.
Some have argued that indoor radon could not contribute substantially to lung-cancer in the population because mortality rates from lung-cancer in never-smokers are substantially lower than overall rates in the general population. By implication, all lung-cancer is assumed to be caused by smoking, or preventable by smoking prevention and control. However, the synergism between radon exposure and smoking implies that the number of radon-attributable cases will vary with the background rate. From the public health perspective, it would be inappropriate to dismiss the large numbers of cases that occur in ever-smokers because of their high background rate. The historical record of lung-cancer rates across the century provides little insight into the significance of radon as a public health problem. The validity of the diagnosis has probably varied over time. Mortality rates from lung-cancer earlier in this century and rates in never-smokers offer at most a biologically inappropriate upper bound for the numbers of lung-cancers attributable to radon progeny absent cigarette-smoking.