Research Papers in Physics and Astronomy

 

Date of this Version

June 1982

Comments

Published in Nuclear Instruments and Methods 203 (1982), pp. 433-442. Copyright © 1982 North-Holland Publishing Company/Elsevier. Used by permission. http://www.sciencedirect.com/science/journal/01689002

Abstract

A radiation field is made up of a tangle of particle tracks, from the primary particle and secondary and higher generation electron interactions, well isolated at low doses and with multiple intersections in cell nuclei at high doses. Low dose effects in multicellular systems are therefore the sum of individual track structures. Until we can state with confidence the structure of a particle track in biological matter for all end-points of interest, at least as well as we can for nuclear emulsions, our knowledge of low dose effects should be regarded as uncertain and inadequate. In this context “track structure” means the response of physical and biological systems along the path of the particle, and depends on the observed end-point as well as on the identity of the particle. For mammalian cell killing and a few other biological end-points, track theory and experimental radiosensitivity parameters allow us to construct schematic models. If we take a particle track to consist of a sequence of inactivated cells strung along the path of a particle, neither electrons nor protons leave a track in a compact mammalian cell structure. At most there is an occasional killed cell at the end of the range of a proton or an electron where the particle stops in the nucleus of a cell, with probability less than 0.3 for a proton, and less than 0.01 for an electron. The variety of potential targets whose size may be compared to the measured inactivation cross-section and the lack of a fully consistent theory of RBE make it impossible to decide, from this information alone, whether cell killing is an individual (1-hit) or cooperative (many-hit) phenomenon, especially for electrons. A similar analysis of epidemiological data for cancer induction leads to probabilities and action cross-sections so low as to make a linear extrapolation implausible. In assigning quality factors at highest LET values we should consider that heavy ions inactivate cells, so that neither mutation nor transformation can represent a hazard. At low doses, when only isolated inactivated cells are produced whose function may be restored by repopulation, it is difficult to see why high LET radiations are assigned the highest quality factors.

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