ever, that the dose-rate reduction factor traditionally used by UNSCEAR and the BEIR committees is 3, based on specific locus mutation experiments with male mice.

For reasons discussed in the main text, the DDs estimated from these data cannot readily be compared with those used by UNSCEAR and the BEIR committees. However, the results with one indicator of damage used in the Japanese studies, namely, untoward pregnancy outcome, which includes stillbirths, congenital abnormalities, and early neonatal deaths, permit a crude comparison with the risk of congenital abnormalities estimated in this report. The rate of induction defined by the regression coefficient for UPO is (26.4 ± 27.7) × 10−4 per parental sievert, compared to the background risk of 500 × 10−4 assumed in the calculations. The risk of congenital abnormalities (estimated from mouse data in this document) is 60 × 10−4 per Gy−1 for acute X-irradiation, compared to the background risk (human data) of 600 × 10−4. Considering the uncertainties involved in both of these estimates, one can conclude that they are of the same order.

The other end points—namely, F1 mortality, F1 cancers, sex chromosomal aneuploidy, and electrophoretic mobility or activity mutations—that have been used in the Japanese studies have not been used in this report and so do not lend themselves to comparisons. It should be noted that the first two of the above (i.e., F1 mortality, F1 cancers) are multifactorial traits (similar to UPO), and their responsiveness to an increase in mutation rate will depend on the magnitude of the mutation-responsive component, which is quite small, as Neel and colleagues point out. Consequently, the rates of induced genetic damage underlying these traits are expected to be small, and increases will be undetectable with the available sample sizes at the relatively low radiation doses (about 0.4 Sv) sustained by most of the survivors.

The reasons for the lack of significant effects on sex chromosomal aneuploidy and electrophoretic mutations are different. There is no evidence from mouse studies that radiation is capable of inducing chromosomal nondisjunction (the principal basis for the origin of sex chromosomal aneuploidy). Since radiation is a poor inducer of point mutations, a priori one would not expect electrophoretic mutations to be induced by radiation to any great extent as they are known to be due to base-pair changes. Null enzyme mutations would be expected to be induced, but they are unlikely to be found at the low dose levels experienced by most survivors. Consequently, it is not surprising that the DD estimates of Neel and colleagues for these end points (1.60 Sv for sex-chromosomal aneuploids and 2.27 Sv for electrophoretic mutations) are higher than those for the other end points.



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