OF:

‘

“oe

she
Fx

gross disturbances in physicleyy are wilikeiswithout

Yargerdoses
(2).

"Of the manyt pes ofchanges. which radiation can

ispaererere
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cre
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cause in cells
cr isis.
ne
ie
Conta

Unigue for regiacion,

fany, ii na

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be

- 4

can presumably result from a varie

This summary view aon carcinogenesis is conpativle 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 acknowlecged, and in particular, mention is
made of a pathway mediated by tissue disruption.
Disease proriies are highly species specific.
exception.
also.

.
Cancer 3s

na

Gross characteristics are obviously highly species specific

A rat and a mouse are distinct and yet incredibly similar.

The

gross tissue cifferen ces are articulated out through subtly different
cr

informational resonances amongst cell populations, - the collective pehaviar
being phased ultimately, though perhaps reisotely, 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 tissus, by tissue

disruption seer, as acceptable an origin Tor 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 jungs.

Host of what has been said earlier

in this comnent has been general, and has been aimed at showing that there
was no inherent conservetism in the method of estimating cancer risks set
forth in the first sentence oF 4.6.5, and that riorcever the method could
be far from conservatiy

The conclusion could as weil ba applied to

Vyitphatic tissue ar te bronchial tissue.

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