Cancer is the result of mutations and alterations in the genes in somatic cells (all cells but the gonadal cells) that affect the individual who has them. Hereditary effects, also frequently known somewhat confusingly as genetic effects, result from mutations in the gonadal germ cells and affect following generations. The ability of radiation to cause hereditary mutations in genes was first discovered and stud­ied in detail in the fruit fly, Drosophila melanogaster, by Hermann Muller in 1927. He showed that the number of mutations increased linearly with dose. Clearly, humans are more complex and very different from fruit flies, so a huge study known as the Megamouse Project was done at Oak Ridge National Laboratory in the 1950s by the husband and wife team of William and Liane Russell. They demonstrated that mutations in mice also increased linearly with dose, but that it depended greatly on the dose rate, so that the effects were much less at a low dose rate (7). The BEIR committees have used these results to calculate what is known as the “doubling dose”—the dose that would cause an additional number of muta­tions in a human population equal to the number normally present, so the total number would be doubled. They conclude that the doubling dose is 1 Gy (29, 36).

You might ask, why use mouse results when we really care more about humans? Once again, the Japanese atomic bomb survivors constitute the largest human pop­ulation carefully studied for hereditary effects, and there simply are no hereditary effects that can be attributed to the radiation. These negative results lead to the likelihood that the doubling dose for humans is actually between 1.5 and 2 Gy. The overall conclusion is that there have been no measurable hereditary effects from exposure of human populations to radiation. The main concern when a human population is exposed to radiation is the risk of cancer, not the hereditary risk.