(chromosome inversions, durlications, translocations, deletions, etc.)
and remain viable.
However, although only a very small fraction of alpha
interactions give rise to-viable mutated cells, these survive to
preliferate, whereas cells which suffer lethal changes are elininated
from the cell population.
Thus in the case of long-tern exposure of
tissue to internal alpha emitters at low dose rates there is a cumulative
‘increase in the population of cells which have survived one or more
chromosome structural changes.
However it is equally obvious that a
cell whose nucleus is subjected to repeated alpha interactions within
the mean life of the cell hes only a negligible chance of survival.
It is likely that the production of a radiation-induced tumor begins
with the formation of a single malignant cell characterized by a combina
tion of two or more chromosome changes and/or gene mutations.
The alpha
radiation-induced bone tumor incidence in dogs is observed to be proportional to the square of the alpha dose (13) implying that a sequence of
two or more low probability events must be involved. This is consistent
with the two-mutation and nultiple-nutation theories of cancer
on the age distribution of cancer in man.
(20,21)
based
On the basis of these consider-
ations the production of a pilignant cell involves a sequence of events,
as follows:
(3) production of a viable mutated cell;
(2) clone growth
from the mutated cell; (3) production of a second viable mutation in
one or more of the clone; »(4) growth of a clone of doubly-mutated cells;
etc.
Thus, for a two-mutation sequence, the tumor risk would be proportional
to the Re? (t/t), where R is the alpha dose rate, t is the time of
exposure, and T is the mean life of the normal cell and singly mutated
cell,
The term (t/t.) represents the influence of the growth of the clone
of the singly-mutated cell on the long-term risk.
This tumor risk relationship makes it abundantly clear that a linear
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