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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