os would be lost, and at birth, the frequency of males would be greater than would be true if the father were not exposed. If, on the other hand, the mother were exposed, more male embryos would be lost, and at birth, the frequency of males would decrease. If both parents were exposed, the resulting proportion of male births, would be related to the individual parental doses and the frequency of dominant versus recessive lethal mutations. As can be seen, this theory of sex determination made fairly specific predictions that could be compared with the actual observations that were accumulating. When the data from the initial study were examined, it appeared that the frequency of male births was, in fact, declining with dose when the mother was exposed, and increasing, albeit modestly, with increasing paternal dose. The rate of change with dose was not, however, statistically significant, although in the direction predicted by theory. It was for this reason that when the clinical phase of the studies ended, data on the sex ratio continued to be collected on the supposition that the rate of change might become statistically significant with further information. To this end, observations on the frequency of male births were continued through 1966, when information was available on 140,542 births of which 73,994 were to parents one or both of whom were exposed. However, when these additional observations were analyzed, the results did not support the earlier findings; indeed, the modest changes seen were opposite to those predicted by theory. Today, the earlier arguments regarding sex determination are known to have been overly simplistic. First, they did not take into account the occurrence of X chromosome aneuploids (errors in X-chromosome number), such as the Klinefelter and Turner syndromes, which might confuse the determination of the gender of an individual as revealed by a clinical examination shortly after birth. The first of these a...
