°
6
Ct.
target afforded by the cell chromosomes.
"
ir
This follows necessarily from
the fact that most alpha interactions with ceil chromosomes lead to the
(17,18)
subsequent mitotic death of the cell, as Barendsen has shown
The
production of a malignant cell calls for a sequence of two or more low
probability events and thus cannot be speeded up by the application of .
massive alpha doses, but rather only 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 is proportional
to Re (e/TDs expiained above, it is apparent that the- alpha activity
concentration or the activity per particle which is eauated to a given
tumor risk decreases with increasing time of exposure and also that 4 given
risk can be attributed to smaller cumulative doses when the time of exposure
t ir appreciably longer than the mean life of the cell, To.
Brues ‘27? and
Burch (28) both pointed out that the two-mutation theories of carcinosepesis
(20,21)
would imply an exceptionally high effectiveness of widely
spaced radiation for tumor production.
It is proposed that just such a
‘dose rate relationship serves to reconcile the observed significant tumor
risk in cigarette smokers with the presence of a persistent lung burden of
insoluble smoke particles: involving a total of only a few picocurirs of
2120p, (14) |
3.
?
2
“Hot” Pud,, Particle Risks:
If the above tentative conclusions are
correct, then the same considerations must 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.
1
Raabe et al. 62%) report an apparent rate of dissolution of ***Pu0,
dn lung fluid which is two orders of magnitude higher than that observed
for ***Pud, particles.
Such a dramatic difference in the chemical behavior