Low doses of ␣ radiation in basements have been causally implicated in lung cancer. Previous studies have concentrated on high dose effects, for which no significant repair was found. In the present study, the methodology for measuring mutation by quantitating mitotic breaks and gaps was found to be applicable to G2-phase Chinese hamster ovary cells irradiated with 10 -50 cGy of ␣ radiation. The mutation yield in such cells closely resembles that of ␥ irradiation. Caffeine, which inhibits repair, produces the same straight line increase of ␣ and ␥ mutation yields plotted against the dose. In the absence of caffeine, the repair of ␣ radiation lesions is almost twice as great as for ␥ radiation. Mitotic index changes substantiate these interpretations. It is proposed that the higher ion density associated with ␣ radiation may result in fewer lesions being missed by the repair processes. The quantitation of chromosomal lesions for G2 cells exposed to low doses of ␣ radiation, ␥ radiation, or chemical mutagens in the presence and absence of caffeine is a rapid and reproducible methodology. Protection from mutational disease in a fashion similar to the use of sanitation for infectious disease appears practical. R eports on the effects of ␣ radiation of mammalian cells usually concentrate on high doses, where cell killing is extensive, and complex multihit chromosomal lesions are obtained (1-3). In this paper, we report results on the effects of doses less than 50 cGy, a dose region that should be easier to understand theoretically and that presumably is responsible for a significant amount of human lung cancer. We have earlier shown for ␥ radiation that high doses produce complex chromosomal rearrangements as opposed to the simple breaks and gaps from low doses (4).In previous papers, a methodology for measuring chromosomal aberrations produced by physical and chemical agents in mammalian cells has been described (5, 6). The procedure is rapid, sensitive, and reproducible, and yields quantitative measurement of breaks and gaps in mitotic chromosomes resulting from mutagenesis in G 2 cells. The principle used consists of scoring microscopically identifiable breaks and gaps in mitotic chromosomes. In these chromosomes, condensation has reduced the overall length by approximately 20,000-fold, so that the corresponding increase in thickness renders each chromosome visible under the microscope. The condensation is accomplished by means of successive coiling, supercoiling, folding, and other highly specific molecular interactions that are attended by attachment of specific macromolecules, e.g., proteins, to designated points in the chromosome. Thus, even a small mutational lesion at an appropriate position, by preventing normal attachment of the supercoiling protein to the mutated DNA, can presumably prevent condensation at a given point resulting in an apparent discontinuity (break or gap) in the resulting mitotic figure. An example of a gap without a discontinuity is illustrated by the work of Kremer et al. (7), who demo...