ability to model without assuming any underlying biologic mechanism of disease, leads to the characterization of the modeling approach as empirical or descriptive. The empirical modeling approach also allows for evaluation of diverse factors that modify risk, such as attained age and exposure rate, through formal statistical testing. Given the limitations of the available data and the resulting difficulty in discriminating among plausible alternative models, the empirical approach undoubtedly results in models that are relatively crude and at best yield rough approximations of actual patterns of risk. While the committee relied on data on lung-cancer mortality in underground miners to construct its proposed risk models, a series of assumptions is needed to extend the miner-based model to the general population. For example, the committee used models in which the exposure-risk relation is linear at low exposures, based on the mechanistic considerations discussed in chapter 2. Other assumptions made in projecting population risks are described later in this chapter.


The committee critically assessed the principal approaches (see Figure 1-3) that could be used to estimate the risk associated with exposure to indoor radon, with respect both to sources of data for developing risk models and to techniques for modeling. The combinations of data resources and risk estimation approaches of present interest are as follows:

  1. Biologically motivated analysis of miner data.

  2. Dosimetric approach using low-LET data (for example, atomic-bomb survivor data).

  3. Empirical analysis of miner data.

  4. Empirical analysis of data from residential case-control studies.

The strengths and limitations of the three different data sources are summarized in Table 3-1.

With regard to the first approach, the committee recognized that use of biologically motivated risk models is a highly desirable goal, but it felt that such models have not reached a stage at which they can be used for radon risk assessment. Specifically, the complexity and multiplicity of the processes involved in radiation carcinogenesis were noted, as were the gaps in knowledge of the most-basic relevant processes. The paradigms describing carcinogenesis in general and radiation carcinogenesis in particular are changing rapidly. For example, the potential importance of delayed genomic instability (Chang and Little 1992; Kadhim and others 1992; Morgan and others 1996), not incorporated in currently formalized biologically motivated models, was not apparent until within the last few years.

The second approach, the dosimetric approach based on the atomic-bomb

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