high-and low-LET radiation-induced mutagenesis in the fraction of mutations that lost the entire active gene (Thacker 1986; Kronenberg and Little 1989; Evans 1991, 1993; Jostes and others 1994), whereas in an episomal shuttle-vector model, deletions were observed to be more frequent after alpha-particle exposure than x-ray exposure but were of comparable size (Lutze and others 1992, 1994).
Those observed differences in the patterns of mutation induced by high-LET radiation in different cell lines seem to be partially resolved by the observation that in cell systems in which genes that were critical to cell survival were close to the marker gene, a rather low frequency of mutations was induced by deletions. In cell systems in which the marker gene was not near a critical gene and the marker gene was not involved in cell survival, a larger fraction of the total mutations were produced by large deletions after alpha-particle exposure than after low-LET radiation exposure (Evans 1991; Bao and others 1995).
A variety of additional differences have been reported between the spectra of deletions caused by high-and low-LET radiation. These include a higher proportion of smaller but more complex deletions and rearrangements caused by alpha particles (Bao and others 1995; Jin and others 1995; Thacker 1995; Chaudhry and others 1996) and differences in growth characteristics (Metting and others 1992; Chaudhry and others 1996; Amundson and others 1996). Hence, radiation produces a spectrum of mutations different from those which arise spontaneously or are caused by other agents, and the spectrum can depend on radiation quality.
Research at the sequence level is continuing in a number of laboratories to evaluate the molecular nature of mutations induced by alpha particles from radon (Jostes 1996). It should add to the understanding of the nature of the mutagenic lesions induced by high-LET radiation. One of the objectives of such research is to determine whether unique changes associated with high-LET damage can be used as a ''signature" of alpha-particle-induced damage. Such a signature could help to identify environmental agents that are responsible for observed mutagenic damage (Schwartz and others 1994). Other studies also have proposed signatures for alpha-particle-induced biologic damage in the form of the induction of specific point mutations in the tumors of uranium miners (Taylor and others 1994; Vahakangas and others 1992); however, the results are not consistent, nor have they been confirmed by larger-scale animal studies (McDonald and others 1995; Kelly and others 1995).
The primary approach to radon risk estimation involves epidemiologic studies of underground miners whose mean exposure was typically much larger than average residential exposures. For example, the average radon-progeny exposure of the Colorado miner cohort was about 2.8 Jhm-3 (800 WLM) over an average duration of 5 y. That implies that an average of about 7–26 alpha particles would