92 YH SHORTER-TERM BIOLOGICAL HAZARDS OF A FALLOUT FIELD of deleterious mutations and at the same time survive with reasonable vigor. The level of the load carried—genetic guality—-varies naturally withthe rate at which deleterious mutations are added to and removed from the gene pool. Tf, then, it can be said that a stock has been weak- ened by an excess of deleterious mutations, the obvious steps for achieving recovery, or reduc- tion of the load, would be decreasing the rate of mutogenésis and increasing the rate of removal. This means lowering exposure to mutogens like radiation on the one hand, and lessening the factors conducive to maintenance of the lesa fit on the other. In summary, the attempt in this brief paper has been to consider someof the effects induced in living systems by radiation from pervasive sources such as fallout and the kinds of repair that accompany them. Three types of erosive effect have been identified: (1) That resulting from necrosis of growing tissues in individuals and leading to various forms of cytopenia, eventual organ failure and death; (2) that resulting from generalized degenerative change in growing tissues and culminating in earlier time of death; and (3) that resulting from mutational changes in the germ plasm of population groups andleading to loss of group vigor and stamina. It was pointed out that recovery in connection with the first consists of tissue” replenishment—a biological factor; that recovery in connection with the second had no meaning with respect to mutational changes but did have in terms of competition between normal and mutated tissue materials; and that recovery in connection with the third consisted of lowering the rate of inducing mutations and also inereasing the rate at which mutations are removed from the gene pool. DISCUSSION Paul S. Henehaw Dr. Bonn (Brookhaven). Y would hike to RATE OF REPAIR OF RADIATION DAMAGE IN MICE make a comment on the steepness of the slope that Dr. Henshaw presented that presumably applies to human beings. I cannotcertainly argue with this slope, because I know of no definitive data on human beings that would allow us to define this. However, I would like to say that the slope for most mammals that have been studied is considerably steeper than the slope indicated by Dr. Henshaw. The factor that would apply in his case in his curve in going from LD-zero to LD-50 would be about two. In most mammals this factor is about1.2. Dr. Beran. Thenk you, Dr. Bond. Is there any other discussion? Dr. Henshaw? Dr. Hensuaw. My main experience has been with laboratory animals also. When I began to consider this question, I, too, had in mind that the time intervals involved, and indeed the slope of the curves presented, would be somewhat different from this picture as presented. But in asking these questions in relation to human beings and taking the frag- ments of information as we are able to get them from those who have had experience in con- nection with the Japanese damage, the few radiation accidents, and some other kinds of considerations, the indications are that the time intervals involved are longer in the case of human beings than in the usual laboratory animals, like rats and mice. So I concur completely with the implications of the question that was raised. By Joun B. Srorer Los Alamos Scientific Laboratory, University of C‘alifornia, Los Alamos, New Merico In the following study tho repair rates of tissues exposed to ionizing radiation were not measured directly, Rather, the rate of repair where R,=percent of initial damage (or dose) remaining at time ¢ D,=initial dose in r LDyo, TDyp dose at. time ¢ LDoe= Dy dose for controls of damage contributing to the death of mice by two different mechanisms was determined, The end-points used were median lethal dose for death in the first 30 days following exposure (LDj-30 days) and the medianlethal close for death in the first 100 hours after exposure (LDg-100 hours). In the ease of X-radiation exposure, deaths occurring in the first 100 hours are generally due to radiation damage to the gastrointestinal tract (in the doserange below 10,000 r). The later deaths associated with the LD,»-30 days are believed due primarily to hematopoietic damage. Thus, it was possible to measure indirectly the rate of repair of two radiosensitive organ systems. The split-dose technique as described by a number of authors was used. Large groups of mice were exposed to an initial sublethal dose of X-rays and at various time intervals there- after they were divided into subgroups and given graded doses of X-rays in order to deter- mine the LDj»-30 days or LDy-100 hours. The extent to which the LD was lower than the value for the control group then gave a measure of the amount of the damage remaining from the first exposure. This residual was necessarily measuredin roentgens but since the dam- age is proportional to dose, this system of measure is probably sound. The residual was then converted to percent. of initial damage by dividing “residual roentgens” by roentgens” and multiplying: by 100. Thus: LDg,—LD. “5 X10 “initial Female CF.--1 mice, 2-3 months of age, were used throughout these studies. X-rays were delivered from a G. E. Maxitron operated at 250 KVP and 30 Ma. added. A Thoraeus I filter was HVLof the filtered beam was 2.6 mm Cu. Mice were exposed 15 at atime in a shallow Lucite cage curved on a radius of 50 cm. The TSD was 50 cm. In the study utilizing 30-daylethality as the biological end-point, groups of mice were exposed to aninitial dose of 100, 200 or 400 r, At intervals of 4, 8, 18, 32, 72, 144, 264,504, 1,920, or 3,000 hours, the LDj-30 days was determined in groups of these mice and(at similar intervals) in control mice from the same initial population. The results are shown in Table I. A plot of these data showed that. the best empirical fit to a regression line was obtained when percent residual was plotted as a function of log time. The least squares calculation gave an equation Y= 106.03 26.79 log X where ¥ is percent residual and X is time in hours. This line and the experimentally determined points are shownin Figure 1. It is apparent from this line that, over the range of doses tested, the percent residual injury was independent of dose. Since this type of exponential is difficult to integrate into a biological model for the repair process, the data 98