32 BIOLOGICAL EFFECTS OF ATOMIC RADIATION 



of variation in overall life shortening between strains is less than a factor of two. There is as 

 yet no way to determine what the genetic heterogeneity of a human population signifies in 

 terms of differences in radiosensitivity between members of the population. The evidence of 

 ethnic differences in the incidence of spontaneous leukemia suggests that in man, as in the 

 mouse, genetic constitution will play a role in the susceptibility to radiogenic leukemia. The 

 consistency of the experimental data and estimates suggests that the nonspecific life shortening 

 action has a common basis in all mammalian forms that may be conceived to be in cellular 

 and subcellular mechanisms that exhibit little genetic variability. 



There may be a correlation between "vigor" or "fitness" and acute radiosensitivity in 

 man, as there is in experimental animals. Judgments about the effect of physical or clinical 

 status or pre-existing disease, etc., on short- or long-term effects of radiation must be based 

 at present almost entirely on incidental clinical and experimental observations, because only 

 the barest beginnings have been made on the study under controlled conditions of the influence 

 of nutrition, exercise, disease, and other environmental and physiological variables on radia- 

 tion effects. It is common knowledge that any of a variety of stresses can have an activating 

 effect on chronic or latent disease. Radiation can have such an effect on certain diseases. 



Cancer: Local radiation in sufficient amount to almost any part of the body may produce 

 cancer, the chance of tumor development being somewhat related to dose. 



All types of induced and spontaneous tumors appear not to arise at once, but to pass 

 through a series of preliminary stages; radiation-induced tumors often take a particularly long 

 time to develop. They do not begin to develop immediately after the radiation has altered the 

 cells. There is much evidence indicating that malignant change ordinarily develops only after 

 a series of "precancerous" changes or a state of tissue disorder has taken place. This tissue 

 disorder need not exist at the site of origin of the cancer, as there are examples of the radia- 

 tion-induction of malignant disease through physiological or hormonal mechanisms which are 

 clearly indirect, i.e., where irradiation of the cells of origin is clearly not the critical factor. 

 Mouse experiments show that shielding of a part of the body will prevent radiation leukemia 

 and that shielding of one ovary will prevent a tumor from developing in the other. 



Some recent reviews have expressed the opinion that the incidence of tumors induced in 

 a population may bear a direct proportion to radiation dose, based on the somatic mutation 

 theory. So far it has been impossible to test this on human populations and in general animal 

 experiments have shown that the picture may be much more complicated. It has been sug- 

 gested by others that amounts of radiation below a certain threshold quantity may have no 

 effect at all. It is conceivable that very small doses of radiation might induce tumors, but in 

 a much lower incidence than would be predicted by the theory of proportionality. This would 

 be true if somatic mutation was a part of the cancer induction process, but played a minor 

 role. In view of the many uncertainties, the Committee does not consider it justifiable to pre- 

 dict human tumor incidences from small radiation doses based on extrapolation from the 

 observed incidences following high dosage. 



Radioactive Fallout: Data on Rongelap inhabitants and Japanese fishermen indicate that 

 during exposure to radioactive fallout the amount of radioactive material deposited within the 

 body may barely exceed permissible levels at a time when exposure to external radiation has 

 reached a considerable proportion of the lethal dose. 



There are two notable instances of isotopes occurring in fallout that are much less con- 

 centrated in the gonads than they are in some other tissues, so that somatic damage might 

 occur relatively in excess of genetic damage. Widespread contamination with strontium-90 



