220.
In the experiments of Lamson, Billings and Meek [L3] and Lamson, Billings,
Ewell and Bennett
[L5]| acceleration of tumour appearance and nephrosclerosis
were associated with life-shortening in the rat; and the same was true for the
dog in the series of Andersen and Rosenblatt
[A2], according to the author's
opinion and to the reanalysis of Walburg [W1].
221.
Concerning duration-of-life exposure, the paper by Grahn, Fry and Lea
[G5] contains a comprehensive discussion of the problem of specificity, based
on data from different mouse strains.
According to this analysis, the incre-
ment in long-term mortality at exposure rates up to a few R/day is associated
with an increment of the neoplastic deaths which can entirely account (both as
increased incidence and as accelerated appearance) for the relevant reduction
of life.
At exposure rates above 6 R/day an excess mortality from non-tumorous
conditions becomes apparent.
It should also be added that whatever conclusion
may be drawn up to the present from the Argonne series on the life-time irra-
diation of dogs seems to be in agreement with the above conclusion.
222.
Thus, the vast majority of data on rodent and non-rodent mammals, irra-
diated with sparsely- and densely-ionizing radiation and with acute or chronic
doses, when properly analysed, appears to be consistent with the following con-
clusions.
The life-shortening action observed on animals surviving the acute
effects of irradiation, that is, after low-to-medium doses up to about the
1S 9/30? may be essentially accounted for by an acceleration or an increased
incidence of neoplastic conditions taking some animals to premature death. From
doses around the P59 /30 - but progressively more so at higher doses - other
pathological conditions may also advance or accelerate death and among them the
vascular changes leading to organ fibrosis, particularly of the kidney, have
been described on irradiated animals.
The hypothesis of a general deleterious
action of radiation formally analogous to aging could, in principle, be entertained and, if so, it could not be disproved.
However, if non-specific life-
shortening is viewed as an advancement in time of diseases normally associated
with senescence without apparent changes in the spectrum of these diseases, no
data are found to support such a concept.
The notion of non-specific aging,
based only on actuarial analogies and on superficial resemblances between irra-
diated and aging animals, cannot be substantiated by accurate pathology.
Par-
ticularly at the low doses and dose rates of interest in radiation protection
there appears to be no need to invoke any general non-specific noxious effect,
because all the experience on animals does not require to postulate any other
effect than tumour induction or acceleration to explain the reduced life expectancy observed after irradiation.