WAS-1535,
There, u? introducing a fictittcusly léree mist of oxposed
tissuc, the calculated dose becomes covmensurately smal}.
In passing from
the real situation in which a hot particle irradiates 10 to 100 alveoli,
‘o the fictional situation in which the jonizing radiation from the hot
nsrticle is averaged over 108 alveoli, the dose scale has decreased dy
»eughly a factor of &@ million.
.
Living tissue shows extensive intre-cellular and inter-cellular
organization. Several regimes of biological response would be exnected
as physical characte.istics of exposure are varied.
Carcinogenic response
to whole organ exposure by non acute doses of radiation will fall in one
of these regimes, and this will be a regime in which there is human
experience.
Fron the physical characteristics of plutonium aerosols, from
the lung deposition experience with aerosols, and from tne lung clearance
evperjence with plutcniua particulates, it can be inferred that at Teast
one class of parcicles exist which suogect lung tissue to an exposure
associated with a different carcinogenic response regime.
This is because
other biological phenomenon has intervened.
For hot particle exposure that phenomencn is mitotic death of
cells, 7.e., Toss of the cell's ability to divide.
literature on the subject.
There is anextensive
Radiclogically induced mitotic death is, in
fact, the basis for treating malignant tissue with tenizing radiation, and
is the cause of most acute syep toms consequent to raagiation exposure.
Even though the intercession of extensive mitotic death of cells must
eee
inovitably piace certain particulate exposures in a different response
regime from whole Tung, non acute exposures, a compelling araument might
be made that the carcinovenic response in tho forviser case is necessarily