Re: Another question re: dose

[Muckerheide <muckerheide@attbi.com>]

on 9/6/02 10:19 PM, BLHamrick@AOL.COM at BLHamrick@AOL.COM wrote:



> In a message dated 09/06/2002 5:20:46 PM Pacific Daylight Time,

> idias@interchange.ubc.ca writes:

> 

>> A whole body Esub(eff) of 10 mSv/year has a much higher risk than the same

>> Esub(eff) to a smaller tissue.

>

> 

> I think the original question was why this is so.

> 

> And, I think the simplistic explanation is that you're simply irradiating

> more cells.  I.e., the risk of inducing cancer is proportional both to the

> dose to an individual cell and the number of cells receiving that dose.



Unfortunately (fortunately) this is too simplistic :-)



The question relates to confirmed, consistent, experiments, in which, e.g.,

mice irradiated whole-body induce high cancer rates, but animals irradiated

half-body, either front half or back half, have no increase vs. controls.

This isn't "a factor of two" :-)



> Since cancer induction is a statistical phenomena, the more tissue

> irradiated, the more opportunities for cancer induction.  Thus, if I

> irradiate one cell in my body (I realize that's a spherical cow type of

> problem), and the theoretical risk for that cell cancerously mutating at that

> dose is 5E-24, then my total risk of cancer incidence increases by 5E-24.

> But, if I irradiate the 5E+13 cells in my body at the same dose, I now

> increase the total risk of cancer induction to 5E-24 x 5E+13 = 2.5E-10.



Not consistent with biology :-)  The mechanism relates to the known

cancer-causing factors.  Damaged cells do not cause cancer. The body removes

millions of damaged cells all the time. The amount of "damage" to cells, and

removal of cells, is thousands to hundreds of thousands, even millions of

times, greater from normal metabolism than from background radiation levels.

Many multiples of background radiation are hardly a noise level to the

organism. 



Cancer is caused by a failure of the damage repair functions. In a large,

but not too large, half-body exposure, the organism's undamaged repair

functions are sufficient to maintain repair performance to 'clean up the

mess.' In a whole-body exposure, they aren't. So the organism "fell-behind"

in the ability to repair the damage. The organism did "emergency repairs"

(error-prone repairs" that left a lot of damage. If this isn't too bad,

later stimulation of the repair functions may remove enough of the legacy of

damaged cells to have minimal long-term effect. If the legacy of damage is

relatively large, many of the animals will get cancer before the damage can

be removed.



This is straightforward, known, biology. It's ignored in radiation biology

only because the funding agencies do not want to abandon "the golden goose"

of the LNT. (From the outraged statement - 'personal communication' :-)  by

Helen Garnett, Head of RP in Australia, in response to some equivalent data

sources I presented in comments at the Dec 1999 by-invitation Int'l BRPS

Conference at Airlie House in Warrenton, Virginia: "We know what you want!

You want to kill the golden goose!"  It's good when such a great commitment

to 'open dialog' can reach such clear consensus among parties on both sides

of the issue of the justification of the $ trillion rad protection mission!

Unfortunately the organizers and authors of the final report didn't consider

'open dialog' to be on the agenda! :-)  See, e.g.:



http://cnts.wpi.edu/RSH/Docs/BRPS_Docs/index.html



Regards, Jim Muckerheide





 

> All this is also tempered by the fact that some cells are more radiosensitive

> than others.  So, for example, irradiating a finger skin cell does not result

> in the same effect as irradiating a bone marrow cell.  There will be,

> effectively, a weighted average that determines the end risk value.

> 

> Ultimately, however, these numbers are not known.  The risk factors used by

> the standard-setting community are extrapolated from high dose/high dose-rate

> exposures that have caused cancers at some reasonably statistically

> significant rate.  One can extapolate downward in a simplistic manner to

> (theoretically) save time and argument over the matter, but, as the Health

> Physics Society acknowledges, below 5 rem acute dose, and 10 rem lifetime,

> any assignment of risk is not scientifically sound.  Even well above those

> doses the matter is still very much up for grabs, but may well fall into the

> area where it is appropriate to begin a discussion.

> 

> Barbara

> 



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