target afforded by the cell chromosozes.
This follaws necessarily from
the fact that most alpha interactions with cell chromosomes lead to the
subsequent mitctic death of the cell, as Bazendsen hes she
(17518)
on,
Ane
production of a malignant cell calls for a sequence of two or more low
probability events aad thus cannct be specded up by the applscation of
massive alpha doses, but rather onsly by subjecting a much larger number
of cells to a limited number of interactions.
Additionally, assuming that
the tumor risk to the tissue subjected to alpha irradiation {s proportional
to Re? (t/t), explained above, it is apparent that the: alpha activity
concentration or the activity per particle which is equated to a given
tumor risk decreases with increasing time of exposure and also that a given
risk can be attributed to smaller cumulative doses when the time of exposure
t is appreciably longer than the mean life of the cell, TOs
Purch
(28)
genesis
Brues 2”)
both peinted out that the two-mutation theories of carcino-
(20,22)
would imply an exceptionally high effectiveness of widely
spaced radiation for tumor production.
It is proposed that just such a
dose rate reiationship serves to reconcile the observed significant tunor
can
risk in cigarette smokers with the presence of a persistent lung burden of
insoluble smoke particles involving a total of only a few picocuries of
a ogy Ne DEage Sehg Se OY ohEe, a:
.
se,
hee et
. gb > eG
seg
210p. (14) |
3.
e
>
"Hot" Pu0, Particle Risks:
If the above tentative conclusions are
correct, then the same considerations mus‘ apply in the assessment of
tumor risks for hot particles.
In this connection a preliminary considera-
tion of the influence of specific alpha activity and particle size of the
hot
-
alpha emitting particles is in order.
Raabe et ar, (29) report an apparent rate of dissolution of *7°PUC,
in ling fluid which is two orders of magnitude higher than that observed
for **°Pu0, particles.
Such a dramatic difference in the chemical behavior