. "2: Issues of Concern to NASA: Discussion and Conclusions." Radiation Hazards to Crews of Interplanetary Missions: Biological Issues and Research Strategies. Washington, DC: The National Academies Press, 1996.
NOTE: All values relate to the radiation incident on the body or, for internal sources, emitted from the source.
a Excluding auger electrons emitted from nuclei bound to DNA.
b ICRP recommends a WR of 5 for protons, other than recoil protons, with energy >2 MeV (see International Commission on Radiological Protection. 1991. 1990 Recommendations of the International Commission on Radiological Protection. ICRP Publication 60. Annals of the ICRP 21. Pergamon Press, Elmsford, N.Y.).
SOURCE: National Council on Radiation Protection and Measurements (NCRP). 1993. Limitation of Exposure to Ionizing Radiation. NCRP Report No. 116. National Council on Radiation Protection and Measurements, Bethesda, Md.
dose rates expected from heavy ions, dose rate considerations should not be as important because the probability that two different heavy ions will traverse the same human cell is small.
Because essentially no data from human populations are available to allow investigators to make direct estimates of risk from exposure to these types of radiation, or which address the factors influencing sources of uncertainty in risk estimation, such estimates are heavily dependent on data from other studies. Hence, both an adequate understanding of the relationships between RBE and particle type and energy, as well as information on dose response and dose rate effects derived from experimental studies are essential to understanding the cancer risks associated with deep-space travel. Existing experimental data are inadequate.
Even in animal systems, data on tumor induction following exposure to protons and heavy ions are sparse. Critical data on cellular responses to irradiation, required to support the use of laboratory animal tumor data for estimating risks to humans, are also lacking in many instances. Cell survival studies, while not directly applicable to estimation of cancer risks, do permit comparisons of the effectiveness of different types and levels of radiation and determination of the repairability of induced DNA damage. Cellular studies of the induction of somatic mutations and chromosomal aberrations provide data that can be linked fairly directly to carcinogenic effects. Such studies, particularly in human cell systems, are important for understanding possible mechanisms of carcinogenicity and in the appropriate application of animal data to the estimation of risks to humans.
As described in Chapter 1, data for tumor induction following proton irradiation are available for only a few tumor types following acute exposure. The limited dose-response data that can be obtained from these studies suggest similarities to responses that would be seen after gamma ray irradiation.37–39 Only one study found evidence to support an RBE of greater than 1.40 Additional support for similarities in effects from exposure to proton and to low-LET radiation comes from the work of Burns et al., who have reported a curvilinear dose response for rat skin tumor induction similar to that occurring after exposure to electrons and a reduction in the carcinogenic effects of exposure to protons.41
Cellular studies have been conducted using protons of different energies to examine cell survival and induction of chromosomal aberrations. 42–45 Although the range of energies used is lower than that encountered in the space environment, these data also suggest similarities in effects between protons, gamma rays, and x rays. The dose responses tend to be linear/quadratic, and there is clear evidence for repair of proton-induced DNA damage.
While most data tend to support the view that the risks for carcinogenic effects, as a result of irradiation by high-energy protons, will be similar to those for low-LET radiation, additional studies of protons in the