ary photons; the straight lines represent the paths of ejected electrons. For clarity of presentation, the size of the tracks is increased relative to the cell and is not drawn to scale. As the energetic electron interacts with atoms of the material, secondary electrons are produced and kinetic energy is lost. Such collisions can result in deflection of the primary electron from its original path (Figure 1-8, panel A). Important components of the track structure are the clusters of secondary ionizations that occur in a very small volume (see Figure 1-8, panel B). These clusters, acting directly or indirectly on the DNA molecule, may produce clustered damage, LMDS, that may in turn be refractory to repair. The likely site of health effects of low-dose radiation is the genetic material, which directs the structure and function of the organism. This genetic material is made up of DNA organized into genes and chromosomes (for a brief description, see Appendix A). Radiation can damage DNA as described in this chapter, and the damage can result in cell lethality, impaired cell function, or may produce damage involved in the carcinogenic process. Radiation has also been shown to produce heritable gene mutations in animals. For a basic description of gene mutations, see Appendix A.
This report assesses the biological effects of low-LET radiation, that is, photons and electrons. It does not deal with densely ionizing radiation, such as heavy ions (including α-particles) and fast neutrons. Although neutrons need not be considered here on their own account, they must be accounted for in the analysis of the most important source of information on radiation risks, observations on the atomic bomb survivors of Hiroshima and Nagasaki. Such analysis requires consideration of the relative biological effectiveness of neutrons. The following remarks deal with the RBE of neutrons in general terms.
According to the 1986 dosimetry system, DS86, only a small fraction of the absorbed dose to atomic bomb survivors was due to neutrons—about 2% in Hiroshima in the most relevant dose range and 0.7% in Nagasaki (Roesch 1987). The current reevaluation of the Hiroshima and Nagasaki dosimetry, DS02, is in general agreement with these observations. However, although the absorbed dose fraction of neutrons was small in both cities, it is known from a multitude of radiobiological investigations that the RBE of small neutron doses can be large enough for even the small absorbed dose fraction to add appreciably to the late health effects among atomic bomb survivors.
Fast neutrons interact with exposed tissue predominantly by releasing recoil nuclei. At neutron energies up to a few million electronvolts, the energy transfer is predominantly to protons. On the average, a neutron transfers half its energy to a recoil proton in a collision. Neutrons of 1 MeV therefore produce recoil protons with an average initial energy of 500 keV. At a neutron energy of 0.4 MeV, the typical recoil proton energy is 200 keV, enough to allow the proton to go through its maximal LET of about 100 keV/μm, which is reached at its Bragg peak energy of 0.1 MeV. The ionization density in such proton tracks is far greater than that in an electron track, as depicted in Figure 1-1. It is evident that the resulting high local energy concentration will produce far more clusters of closely spaced ionizations than do low-LET photons and thus more LMDS (clustered damage) that may remain unrepaired or misrepaired. In addition, recoil protons have track lengths of a few micrometers, so critical damage can, with fairly high probability, be caused in neighboring chromosomal structures. The interaction of closely spaced chromosomal damage has long been noted to