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nonuniform alpha radiation cose distribution in the lung.
The authors
of this study take exception to the conclusions and recormendations of
Seesaman, Tamplin ai:d Cochran
¢
As
28)
and concluce
that
“the nonuniform dose distribution of plutonium particles in
the lung is mot more hozardous end “ay be less hazarctus than
4f the plutonium were unifernly distributed and that the mean
dose iung model is a radi obiologicaliy sound basis for
establishment of plutonium standards."
Bair et ai, (15) fail to take into account the full implications of
gome of the recent published results:
in particular, the observed higher
tumor risks for ?3°Pu0, than for 22%yo, 11) the apparently limited
|
biological response of mammal lung cells from *?°Pu and 7?°Pu incorporated
into ceramic microspheres (17+3) and the tobacco smoke radioactivity
results ‘14,
The latter results imply that as little as a few picocuries
of insolubie alpha emitting particles in the iung may give rise to a
“
significant risk cf lung cancer and other serious heaith eifects in
the chronic exposure case.
"
On the basis of a brief review of the known effects of alpha inter-
.
actions with cells (below) it will become evident that alpha radiation
induced cancer in mammals and man must be brought about by subjecting
a large number of living cells to a limited number of alpha interactions.
Thus, in principie, the hignest risk would be associated with a uniferm
distribution of the alpha dose, in accordance with the conclusion of
Bair et al.
However, in fact, we are almost always concerned with a highly
irregular tissue distribution of alpha emitting particles.
For hot
particles, the tumor incidence must be due to the low dose irradiation
of a large number of cells by a very small fraction of the hot particle
burden.
And for lone tern exposures, unacceptably high tumor risks
appear to be associated with picocurie burdens of internal alpha emitters.
This serious possibility calls for a drastic downward revision of permissible
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