5.
Irradiation would advance such an increase of the histohematic barrier
and ensuing consequences, to various degrees in various tissues, depending on
the sensitivity of the constituent parenchymal cells.
Non-specific damage to
the endothelium of the fine vasculature directly or indirectly caused by radiation would be the primary
cause.
The consequent morphological (intersti-
tial edema, increased fibrillar density, spotty at first and then more generalized) and functional changes (loss of reserve capacity of single organs
reflecting gradually and progressively on other parts or on dependent organs )
would tend to perpetuate and to increase themselves by circular reactions where
the natural and radiation-induced aging would not be separable any longer.
46.
The basic notions of Casarett's model [C7] appear on the whole biologi-
eally well founded, since it is known that radiation may cause an interstitial
fibrillar density and capillary fibrosis.
The mechanisms of these phenomena
have recently been discussed by Gerber [G1] who has examined the possible
pathways responsible for fibrosis and by Hopewell
addressed himself to vascular changes.
|H16] who has particularly
But whether the initial endothelial
and connective changes operating in natural and in radiation-induced aging
may indeed be the same remains to be demonstrated and so do the further steps
of Casarett's hypothesis, which should be set on firmer ground /W1].
In addi-
tion, more recent information on the radiosensitivity of the endothelial cells
[R11] seem to cast considerable doubt on the applicability of the hypothesis
to the very low doses and dose-rates and to confine presumably its interest
to the region of the intermediate to high doses.
7.
The hypothesis could also be entertained that late effects of radiation
on the duration of life might be brought about viaalterations of the immune
system and in this respect two possible mechanisms of action could be envisaged.
The first would imply auto-immune diseases as possible causes of a
diffuse deleterious action; alternatively, life-shortening could be viewed
as the result of an earlier appearance and a higher incidence of tumours,
elicited in turn by radiation-induced immune disturbances.
In no case would
the effect of life-shortening have a truly non-specific character, because an
acceleration or an advancement in time of old-age diseases without changes in
their spectrum could hardly be expected as a result of such mechanisms.
48.
In 1972 the Committee reviewed extensively the effects of radiation on
the immune response and considered the general question of radiation as it