miners is based on cumulative exposures at least 10 times the estimates of typical lifetime residential exposure, that is, about 0.049 Jhm-3 (14 WLM) (NCRP 1984). Consequently, extension of risk models based on data from miners to the general population rests on extrapolation below the exposure range of most of the miner data. A linear-nonthreshold model has been assumed for this purpose by other groups developing radon risk models, including the BEIR IV committee (NRC 1988). Risk projections are sensitive to the extrapolation model chosen. For example, a model that incorporated a threshold at lower levels of exposure, such as, below the mean of about 0.0035 Jhm-3 (1 WLM), would project far fewer radon-caused lung-cancers than a nonthreshold model, because of the distribution of population exposures (Figure 1-4).

Extrapolation from Higher to Lower Exposure Rates

The underground miners included in the epidemiologic studies typically received their occupational exposures to radon over several years (Lubin and others 1994). However, exposure to indoor radon takes place across the full lifetime, so exposure rates are generally far lower for the radon exposures received by the general population than for the exposures received by the miners in the epidemiologic studies. The analysis of pooled data on 11 cohorts of underground miners indicated an inverse exposure-rate effect; that is, the effect of exposure increased as the rate at which the exposure was received diminished (Lubin and others 1994). Laboratory systems have shown a parallel inverse dose-rate effect for some end points (NRC 1994). The BEIR VI phase 1 committee recognized that the full BEIR VI committee would need to address the extrapolation of exposure-rate effects for exposures received by the miners to those typically received by the general population.

Interactions of Radon Progeny with Other Agents

Lung-cancer can be caused by a number of inhaled environmental agents, including tobacco smoke (Table 1-1) (Lubin and others 1995). Agents in the mining environment other than radon progeny have been associated with lung-cancer, including diesel exhaust, arsenic, and silica. Those agents might potentially confound the relationship between radon progeny and lung-cancer or modify the risk associated with radon progeny. The majority of the miners included in the epidemiologic studies also were probably cigarette smokers, although the information on smoking in the various cohorts is incomplete (Lubin and others 1994). Exposure to radon progeny is an established cause of lung-cancer in those who have never smoked (NRC 1988), but the risks to ever-smokers and never-smokers have not been separately characterized with great precision. Lack of information on the combined effect of smoking and radon introduces uncertainty in extending a risk model based on data from miners to the general population.

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