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gross disturbances in physiology are unlikely without
Vargqer cases (2).
"Of the manytypes of changes which radiation can
cause in cells cr tissues, none 1s. considered to bs
unique for rediaticn. Many, if not all, such changes
can presumably resuit from a variety of other agents.
This summary view on carcinogenesis is compatible with the ideas leading
to the conclusion reached earlier, that fictitious dose averaging to
larger tissue masses need not be conservative.
The possibility of various
. modes of carcinogenesis is acknowledged, and in particular, mention is
exception.
also.
Cancer is no
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Disease profil s are highly
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made of a pathway mediated by tissue disruption.
Gross characteristics are obviously highlyspecies specific
A rat and a mouse are distinct and yet incredibly similar.
The
gross tissue differences are articulated out through subtly different
“informational resonances amongst cell populations, - the collective behavior
being phased ultimately, though perhaps remotely, by the genetic controls
of the cells.
Not to belabor this point unnecessarily, - cancer profiles
°
are species specific; gross characteristics and, of course, genetic material
_ are also species specific.
Collective detuning of tissue, by tissue
disruption seen as acceptable an origin for the tissue instabilities of
cancer as does an isolated single cell event.
.
.
Return now to the problem of risk estimates associated with
radioactive particulates in human lungs.
Most of what has been said earlier
in this comment has been general, and has been aimed at showing that there
was no inherent conservatism in the riathod of estimating cancer risks set
forth in the first sentence of 4.4.5, and that moreover the method could
--
be far from conservative.
The conclusion could as wel] ba applied to
lymphatic tissue or to bronchial tissue.
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