d . o hea Sea ee oc cmeeeramiomenWBtite at Se at Leeet” 1aeedBE ESE DISCUSSION The above-presented cell dose approach to radiation risk evaluation differs drastically from that presently used. Cell populations and the energy deposited in each cell replace the organ and organ dose concepts. - A Ph and statistical mechanics approach to evaluating cell-charged particle ° obtata {ateractions, replaces the Md approach currently used. s as. see ch the REE in tissues is abandoned in favor of use of the HSEF to evaluate risk to the single cell. Mean values of LET Object-oriented physical quantities that are closely related to cell damage replace the more remote field quantities, distributions of cells, Thus the HSEF, and the associated distribution of ‘quantally responding cells replace “linear, non-threshold" relationships. The approach, in principle, appears to be far more coherent, internally consistent and logical than is the present system that must employ various factors and various versions of "dose equivalent" to permit it to be operable at all. The present system could in principle obviate the need, while LLE, for radiation quality and LET; field quantities; a “standard radiation”, linear "dose effect" and “dose response” relationship; risk coefficlents; RBE; Q, dose equivalent and rem. i The proposed approach embracing the HSEF permits the estimation, with ; any exposure, of the (fractional) number of cells in the individual that 7 are transformed. | Assuming all exposed normal individuals have approximately the same number of relevant cells, we then can have, ina principle, @ population of individuals with known and equal numbers of transformed cells. With a graded series of exposures, these numbers could then be correlated with cancer incidence, in anittals or in human beings. The result would be a relationship for cancer risk as a function of number of transformed cells ia the individual. HSEF's for macro accidents, although they the , on be and are obtained in experiments in which stochastic energy weanater le simulated, are not used or even teferred to operationally. response which may result can be stlone . = -3s¢* readily observed, so that neither a dose concept nor dose-response relationships are required for practical risk evaluation. atively one The obvious reason is that a quantal Similarly, quantal responses of cells can, in aost laboratory experiments using “single cell systems”, be observed promptly. Thus it {s only for appreciably delayed responses, such as cancer or herttable ~225- 4