the important modification being a term for reduction in risk with time since exposure. Publication 50 of the International Commission for Radiological Protection (1987) describes a multiplicative model, as does Publication 65, published in 1993. The Commission assumed a multiplicative projection model because such models were assumed "... to be more representative of the time distribution of the excess risk," while acknowledging the inconsistency of the evidence from the miners. The U.S. Environmental Protection Agency (1992b) also assumes a multiplicative interaction in making its risk projections.

Passive Smoking and Lung-Cancer

Because passive smoking is also a cause of lung-cancer, there has also been interest in the combined effect of passive smoking and radon exposure on lung-cancer risk (Samet 1989). Interaction between passive smoking and lung-cancer could occur at several levels. Smoking adds particulate matter to the air of a room, thereby increasing the attached fraction and concentration of radon progeny because plateout of unattached progeny onto surfaces is reduced. Tobacco smoke has been shown to increase radon progeny level but the reduction of the unattached fraction by tobacco smoke would be anticipated to reduce the dose to target cells.

The 1991 report of the National Research Council (NRC 1991) addressed the effect of passive smoking on dose of delivered alpha energy. The modeling compared delivered doses under average circumstances of smoking (unattached fraction of 0.03) and during the circumstance of exposure to average smoking passively (unattached fraction of 0.01). The aerosol generated by smoking was considered to have a larger aerodynamic diameter compared with that normally present (0.25 versus 0. 15 µm). Smoking was projected to reduce the dose. In the extreme circumstance of the aerosol generated at the time of active smoking, the projected exposure-dose coefficient was only half that under normal conditions. There has not yet been formal epidemiologic investigation of the combined effect of passive smoking and radon and statistical power for assessing the joint effect would be anticipated to be extremely limited.


Tobacco-smoking, primarily in the form of smoking manufactured and hand-rolled tobacco, is the cause of most lung-cancer cases in the United States and many other developed countries. The trends of lung-cancer occurrence across the century are largely reflective of smoking patterns. Consequently, any risk assessment for indoor radon needs to address the effect of radon on never-smokers and ever-smokers of tobacco. The evidence from the epidemiologic studies of underground miners shows differing patterns of effect of radon-progeny exposure on never-smokers and ever-smokers. Although the data are not sufficiently abun-

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