Voy ty
extrapolction to low dese rates {is not only not conservative for alpha
radiation induced tumors, but rather that there is a marked inverse doserate vs risk relationsnin.
There is an increising body of published
experimental evidence that reilects this trend.
Speiss and says?” observed that for ““*sa alpha radiation induced bone |
sarcema in man, the tumor incidence per rad approximately doubled for a four-
fold increase in the spacing of 7*"Ra injections and that the observed incidence
of bone tumors per rad in children was nearly twice that for adults.
Upton
et ar, 23) show a significantly higher incidence of tumors in mice for a
given neutron dose at more protracted periods. of exposure.
Moskalev and
Buldakov (24) showed that fractionation of the administered *3°Pu dose over
larger periods of tine increased bone tumor induction.
The higher tumor
incidence per rad for the smaller lung burdens of crushed "Pad, nicrospheres observed by sanders 1) seems best
explained by the limsited aloha
irradiation of large numbers of cells by numerous very small, mobile
particles of low activity per particle (see below).
Hamsters subjected to
low alpha doses from ?!°Po distributed quite homogeneously in the bronchiolaralveolar region show a marked increase in the lung tumor incidence per rad
at very low doses and dose rates (25) .
t
And the incidence of bronchial cancer
2
in uranium miners refiects a higher tumor risk per rad at the lower doses ‘79?
for this low dose rate exposure group.
The tobacco radioactivity results
(14)
indicate a significant tumor risk for the cumulative alpha radiation dose
‘from 7)?°po in insoluble particles in the bronchi of smokers, invelving much
lower dose rates.
Based on the above considerations it is evident that the tumor risk is
optimized when a very large number of cells and their descendants are
subjected to only a few widely spaced alpha interactions with the smal]
: