[en] The ultimate objective is to predict potential health costs tp man accruing from the effluents or by-products of any energy system or mix of systems, but the establishment of reliable prediction equations first requires a baseline analysis of those preexisting and essentially uncontrolled factors known to have significant influence on patterns of mortality. These factors are the cultural, social, economic, and demographic traits of a defined local or regional population. Thus, the immediate objective is the rigorous statistical definition of consistent relationships that may exist among the above traits and between them and selected causes of death, especially those causes that may have interpretive value for the detection of environmental pollutants

[en] This Projection Paper is in two parts. The first is a general discussion of current knowledge and the present basis of radiation protection policy, the rather dismal prospects in the foreseeable future of getting realistic estimates of the human impact of radiation-induced mutation, and some general remarks about radiation standards and research strategy. The second part deals with specific research projects that might increase basic knowledge and narrow the gap between what is needed and what is known. We should emphasize at the outset that, of all environmental hazards, radiation is one whose genetic effects are best understood. There is good information on the dose-response curve, on the effects of dose rate and fractionation, and on the differential sensitivity of different ages, sexes and cell stages. This includes a great deal of knowledge of one organism closely related to man, the mouse. This information has been the basis for risk assessment and for safety standards that are widely accepted as solidly based

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[en] The relative biological effectiveness (RBE) values for low doses of fission neutrons compared to ⁶⁰Co gamma rays were determined with four separate assessments of genetic damage induced in young hybrid male mice. Both radiations were delivered at low dose levels over about one-half the adult lifetime as 60 once-weekly exposures. Genetic damage assessed included both transient and residual injury. The latter is more critical, as residual genetic injury can be transmitted to subsequent generations long after the radiation exposures have ceased. Assays were performed periodically during the 60-week exposure period and at 10 or more weeks after the irradiations had terminated. RBE values, with few exceptions, ranged between 5 and 15 for transient injury and between 25 and 50 for different types of residual genetic injury. The most important form of residual genetic damage in this study was the balanced reciprocal chromosome translocation. These translocations continue to be transmitted throughout reproductive life and can lead to reduced fertility and increased prenatal mortality. The best estimate of the RBE value for translocations was 45 +- 10. Implications and recommendations with regard to the neutron quality factor will be presented conjointly with the findings from the data obtained in this same project on life shortening and on the risks of incidence or death from neoplastic disease. 64 refs., 23 tabs

[en] Over the last 25 years, the JANUS program in the Biological and Medical Research Division at Argonne National Laboratory (ANL) has compiled a database on the response of both sexes of an F₁ hybrid mouse, the B6CF₁ (C57BL/6 x BALB/c), to external whole- body irradiation by ⁶⁰Co γ-rays and fission neutrons. Three basic patterns of exposure for both neutrons and γ-rays have been investigated: single exposures, 24 equal once-weekly exposures, and 60 equal once-weekly exposures. All irradiations were terminated at predetermined total doses, with dose calculated in centigrays at the midline of the mouse. Three endpoints will be discussed in this paper: (1) life shortening, (2) a point estimate for cumulative mortality, and (3) the hazard function. Life shortening is used as an analysis endpoint because it summarizes, in a single index, the integrated effect of all injuries accumulated by an organism. Histopathological analyses of the mice used in the ANL studies have indicated that 85% of the deaths were caused by neoplasms. Connective tissue tumors were the dominant tumor in the B6CF₁ mouse, with tumors of lymphoreticular origin accounting for approximately 80% of this class. The latter two endpoints will therefore be used to describe the life table experience of mice dying from the lymphoreticular class of tumors. Dose-response models will be applied to the three endpoints in order to describe the response function for neutron exposures, evaluate the effect of dose range and pattern of exposure on the response function for neutrons, and provide a set of neutron relative biological effectiveness (RBE) values of the ANL database. 25 refs

[en] A total of 6316 mice were exposed to 60 once-weekly doses of 0.85 MeV fission neutrons or ⁶⁰Co gamma rays and observed until they died. An additional 1404 mice were entered into the experiment and followed for part of their lifetimes; a few of these mice were lost accidentally, but most were removed for genetic testing. The mean aftersurvival (MAS) times showed dose-response curves for both neutron and gamma-ray exposures to be linear over all doses except the highest neutron dose. The relative biological effectiveness (RBE) value for neutrons, calculated as the ratio of the linear slopes of the dose-response curves for MAS times, was about 20 for both males and females. Essentially the same value was obtained by other analyses of the data. This RBE value of 20 is specific for deaths from all causes after 60 once-weekly exposures to 0.85 MeV fission neutrons, with once-weekly ⁶⁰Co gamma-ray exposures as the reference radiation. The value for the RBE will probably be different for some, but not all, of the other end points (i.e., specific causes of death, especially tumors). 21 refs., 6 figs., 6 tabs

[en] Although the genetic risks of space radiation do not pose a significant hazard to the general population, the risks may be very important to the individual astronaut. The present paper summarizes some experimental results on the induction of dominant lethal mutations and chromosomal damage in the first generation which may be used in the prediction of the genetic risks of radiation exposures of space crews. Young adult male mice were exposed to single, weekly and continuous doses of gamma rays, neutrons in single doses and weekly exposures and continuous doses of Pu-239 alpha particles. Evaluation of fetal survival rates in females mated to the exposed males shows the mutation rate in individuals exposed to gamma rays to decline as the exposure period is prolonged and the dose rate is reduced, while the response to neutrons is in the opposite direction. Cytological determinations show the rate of balanced chromosomal translocations to drop as gamma ray exposures change from one-time to continuous, however little or no dose rate effect is seen with neutron radiation and alpha particle exposure shows no regular dose-response. Based on the above results, it is predicted that the rate of dominant mutations and transmissible chromosome aberrations in astronauts on a 100-day mission will increase by 4.5 to 41.25 percent over the spontaneous rate. 35 references