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Cell damage by high linear energy transfer (LET) radiations has been described by a phenomenological model (track theory) for more than 20 years. With track theory, molecules of biological significance (dry enzymes and viruses) act as one-hit detectors. Recent additions to tire class of one-hit detectors arc Escherichia coil B, and single- and double-strand breaks in SV-40 virus in EO buffer, where indirect effects predominate. The response of cells (survival, transformation, and chromosome aberration) to these radiations is typically described by a four-parameter model whose numerical values are determined from the equations of the theory being fit to experimental data at high dose (typically above 1 Gy), with tile cells bombarded by gamma rays and high-charge-and-energy (HZE) particle beams, of tile widest possible dynamic range. Once these parameters are determined, the model predicts cellular response in any radiation environment for which the particle-energy spectrum is known. The important feature of this track structure model is its ability to estimate from a limited set. of laboratory data the response of a complex radiation environment with many components. For example, we have calculated cell survival after neutron irradiation with mixtures of neutrons and gamma rays and cell survival and transformation after irradiation with HZE of different energies. Tile model does not yet include cellular repair, although some hopeful approaches to repair dependence are now being (developed. It also does not include cancer induction because tile available data give neither tile number of cells at risk nor tile number of cancers induced and are thus not suited to our formulation.