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We have developed a model to calculate the dose to the cell nucleus in cells exposed in suspension to radon and/or radon progeny. The model addresses the influence of (1) different radiation qualities and energies in the irradiation milieu; (2) the contribution to dose from radioactivity in the medium surrounding the cell after exposure to the radon gas as well as that from excess radon progeny associated with the cell; (3) the geometry of the cell and of the radiosensitive target, the cell nucleus; (4) the intracellular localization of the radionuclides; (5) attenuation of the alpha particles by the cytoplasm; (6) the radionuclide concentrations in the medium; and (7) the length of exposure. Investigation of the influence of these various parameters was made using an irradiation system in which cells were exposed to 212Bi, which decays to stability with the emission of an alpha particle (either 6.05 or 8.78 MeV). The information from these studies was then used to develop the system further for more complex systems in which 222Rn and its progeny are present. The model takes into account the contribution of dose from different radiation sources using scintillation counts of the medium and the cells, and it is useful for calculations of dose in situations where cells are exposed in suspension culture.

A linear dose response was observed for radon-induced mutations at the CHO-hprt locus with an induction frequency of 1.4 x 10(-4) mutants per viable cell per gray. Mutants isolated after two levels of radon exposure were evaluated using Southern blot techniques and polymerase chain reaction (PCR) exon amplification. No significant differences in mutational spectra were detected at these two exposure levels. Of 52 radon-induced mutations, 48% sustained a gene deletion, 23% underwent a rearrangement of the banding patterns or loss of one or more exons, and 29% showed no change from the parental line. These mutants were compared with mutants produced after X irradiation (3 Gy) and with spontaneous mutants from untreated cells. The spectra of mutation types in cells treated with radon and X rays were not significantly different. In contrast, 31 spontaneous mutations exhibited a low percentage of gene deletion events (16%); most spontaneous mutants showed no change (74%); the remaining 10% were classified as alterations. In conclusion, the principal lesion seen at the CHO-hprt locus after radiation exposure is gene deletion, while the predominant class of spontaneous mutations is composed of smaller events not detectable by Southern blot or PCR exon analysis.

DNA damage was induced in isolated human peripheral lymphocytes by exposure at 5 Gy to 60Co radiation. Cells were permitted to repair the DNA damage while exposed to 60-Hz fields or while sham-exposed. Exposed cells were subjected to magnetic (B) or electric (E) fields, alone or in combination, throughout their allotted repair time. Repair was stopped at specific times, and the cells were immediately lysed and then analyzed for the presence of DNA single-strand breaks (SSB) by the alkaline-elution technique. Fifty to 75 percent of the induced SSB were repaired 20 min after exposure, and most of the remaining damage was repaired after 180 min. Cells were exposed to a 60-Hz ac B field of 1 mT; an E field of 1 or 20 V/m; or combined E and B fields of 0.2 V/m and 0.05 mT, 6 V/m and 0.6 mT, or 20 V/m and 1 mT. None of the exposures was observed to affect significantly the repair of DNA SSB.