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Radiation Protection Dosimetry Advance Access originally published online on January 29, 2007
Radiation Protection Dosimetry 2006 122(1-4):354-361; doi:10.1093/rpd/ncl465
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Nuclear fragmentation and the number of particle tracks in tissue

A. L. Ponomarev1,2,* and F. A. Cucinotta1

1 NASA Lyndon B. Johnson Space Center, Houston TX 77058, USA
2 U.S.R.A., Division and Life Space Sciences, Houston TX 77058, USA

* Corresponding author: aponomar{at}ems.jsc.nasa.gov


   Abstract

For high energy nuclei, the number of particle tracks per cell is modified by local nuclear reactions that occur, with large fluctuations expected for heavy ion tracks. Cells near the interaction site of a reaction will experience a much higher number of tracks than estimated by the average fluence. Two types of reaction products are possible and occur in coincidence; projectile fragments, which generally have smaller charge and similar velocity to that of the projectile, and target fragments, which are produced from the fragmentation of the nuclei of water atoms or other cellular constituents with low velocity. In order to understand the role of fragmentation in biological damage a new model of human tissue irradiated by heavy ions was developed. A box of the tissue is modelled with periodic boundary conditions imposed, which extrapolates the technique to macroscopic volumes of tissue. The cross sections for projectile and target fragmentation products are taken from the quantum multiple scattering fragmentation code previously developed at NASA Johnson Space Center. Statistics of fragmentation pathways occurring in a cell monolayer, as well as in a small volume of 10 x 10 x 10 cells are given. A discussion on approaches to extend the model to describe spatial distributions of inactivated or other cell damage types, as well as highly organised tissues of multiple cell types, is presented.


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