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Re: Do Low Dose-rate Bystander Effects Influence Domestic Radon Risks?
David,
Bystander effect for high LET radiation causes genomic
instability including cell death (which is probably
better than mutation), specific gene mutations and
sister chromatid exchanges in non irradiated bystander
cells.
There is a sizable body of literature on this now.
I will be away from the computer for the next 10 days
and will not be able to respond to emails.
Regards, Bill Field
> RADSAFERS:
>
> I readily acknowledge that I am not a so-called "radon expert." That said,
> however, I am well aware of the controversy that continues to rage in the
> field of radiation biology regarding the significance of the so-called
> "bystander" cell effect. In the summary of the Brenner & Sachs paper
> below, the authors appear to be of the radiobiological school of thought
> that construes any detected bystander cell response to be "bad" rather than
> benign, let alone "good." I submit, however, that merely detecting some
> sort of bystander cell response does not necessarily permit the conclusion
> that the bystander cell response was "bad"--it depends on the nature and
> magnitude of the bystander cell response. I am unable to discern in the
> summary of the Brenner & Sachs paper below precisely what response the
> bystander cells manifested; consequently, I cannot draw any conclusions as
> to whether or not the manifested bystander cell responses were "bad,"
> "benign," or "good" for the bystander cells, much less conclude that the
> bystander cell effects ought to be superpositioned with the effects
> manifested by the cells directly hit.
>
> To offer a crude analogy, let's say I am following a car on the highway
> home from work this afternoon. For some reason the car in front of me is
> hit by a lightening bolt and catches fire. As a "bystander" car, I respond
> to the signal sent out by lightening-struck car in front of me by slamming
> on my brakes and hoping my anti-lock braking system works properly. But
> whether the effect manifested by me (the "bystander" car) is "bad" or
> "good" depends on whether or not my bystander car sustains any ill
> effects. If my brakes work properly and I was not following too closely, I
> would manifest no ill bystander car effects. If, however, I was following
> too closely and crashed into the car that was directly hit by lightening,
> presumably I would manifest bystander effects that would be injurious. One
> simply cannot conclude a priori that my bystander car response that I
> manifested of "slamming on the brakes" is categorically "bad" or "good"
> merely because one detected that I slammed on the brakes.
>
> Best regards David
>
>
>
>
> At 04:04 PM 6/26/2002 +0000, you wrote:
> >Int J Radiat Biol 2002 Jul;78(7):593-604
> >
> >Do low dose-rate bystander effects influence domestic
> >radon risks?
> >
> >Brenner DJ, Sachs RK.
> >
> >Center for Radiological Research, Columbia University,
> >630 West 168th Street, New York, NY 10032, USA.
> >
> >PURPOSE: Radon risks derive from exposure of bronchio-
> >epithelial cells to high-linear energy transfer (LET)
> >alpha-particles. alpha-particle exposure can result in
> >bystander effects, where irradiated cells emit signals
> >resulting in damage to nearby unirradiated bystander
> >cells. This can result in non-linear dose-response
> >relations, and inverse dose-rate effects. Domestic radon
> >risk estimates are currently extrapolated from miner
> >data, which are at both higher doses and higher dose-
> >rates, so bystander effects on unhit cells could play a
> >large role in the extrapolation of risks from mines to
> >homes. Therefore, we extend an earlier quantitative
> >mechanistic model of bystander effects to include
> >protracted exposure, with the aim of quantifying the
> >significance of the bystander effect for very prolonged
> >exposures. MATERIALS AND METHODS: A model of high-LET
> >bystander effects, originally developed to analyse
> >oncogenic transformation in vitro, is extended to low
> >dose-rates. The model considers radiation response as a
> >superposition of bystander and linear direct e It
> >attributes bystander effects to a small subpopulation of
> >hypersensitive cells, with the bystander contribution
> >dominating the direct contribution at very low acute
> >doses but saturating as the dose increases. Inverse dose-
> >rate effects are attributed to the replenishment of the
> >hypersensitive subpopulation during prolonged
> >irradiation. RESULTS: The model was fitted to dose- and
> >dose-rate-dependent radon-exposed miner data, suggesting
> >that one directly hit target bronchio-epithelial cell
> >can send bystander signals to about 50 neighbouring
> >target cells. The model suggests that a naive linear
> >extrapolation of radon miner data to low doses, without
> >accounting for dose-rate, would result in an
> >underestimation of domestic radon risks by about a
> >factor of 4, a value comparable with the empirical
> >estimate applied in the recent BEIR-VI report on radon
> >risk estimation. CONCLUSIONS: Bystander effects
> >represent a plausible quantitative and mechanistic
> >explanation of inverse dose-rate effects by high-LET
> >radiation, resulting in non-linear dose-response
> >relations and a complex interplay between the effects of
> >dose and exposure time. The model presented provides a
> >potential mechanistic underpinning for the empirical
> >exposure-time correction factors applied in the recent
> >BEIR-VI for domestic radon risk estimation.
> >
> >
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>
> DAVID W. LEE, CHP
> Los Alamos National Laboratory
> Radiation Protection Services
> HSR-12, MS K483
> Los Alamos, NM 87545
> PH: (505) 667-8085
> FAX: (505) 667-9726
> lee_david_w@lanl.gov
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