The first fruits of the US DOE Low Dose research contract by Flinders University
I have purchased the full paper. However, for copyright reasons (though its funded by the United States Government, and normally taxpayer funded material of this nature is freely available, particularly at DOE Opennet), I will confine myself to the material released actually for the public to see (Despite the Executive Order which mandates openness of the US Department of Energy). This is of course a matter for the United States of America, not its Australian contractors.
“The Linear No-Threshold Model does not Hold for Low-Dose Ionizing Radiation
Antony M. Hooker, a Madhava Bhat,b Tanya K. Day, a Joanne M. Lane, a Sarah J. Swinburne, a Alexander A. Morley a and Pamela J. Sykes a,
(a Department of Haematology and Genetic Pathology, Flinders University and Flinders Medical Centre, Australia; and b Department of Medical Physics, Royal Adelaide Hospital, Adelaide, Australia)
The following abstract is available as free content at the above web address and is cited and quoted as minimally here here as possible in order to allow non-peer review.
“……… Regulatory limits for radiation exposure are based on the linear no-threshold model, which predicts that the relationship between biological effects and radiation dose is linear, and that
any dose has some effect. Chromosomal changes are an important effect of ionizing radiation because of their role in carcinogenesis. Here we exposed pKZ1 mice to single wholebody
X-radiation doses as low as 1 mGy. We observed three different phases of response………These results do not fit a linear nothreshold model, and they may have implications for the way in which regulatory standards are presently set and for understanding radiation effects.” copyright 2004 by Radiation Research Society”
This portion of the paper is freely available at the above link.
However, I refer the reader to the paper quoted in the first post of this blog here: https://hormesishistory.wordpress.com/2012/02/15/radiation-hormesis-and-adaptive-response-definitions/
That is, “Low-dose ionizing radiation exposure: Understanding the risk for cellular transformation” By L. DE SAINT-GEORGES,*
SCK•CEN, Department of Radiobiology, Mol, Belgium. Published in: Journal of Biological Regulators and Homeostatic Agents
Received:May 15, 2004\, Accepted:June 26, 2004. This paper states in part ” According to the hormesis model, people should be exposed to low radiation dose unless it is demonstrated with certitude that there is no benefit from such exposure. The possibility of adverse effects is not even considered.
We may wonder why the proponents of the hormesis model acknowledge a radiation threshold value for harmful effects, but reject it for beneficial effects.
Considering the essentially random interaction between radiation and target molecules leading to unpredictable molecular damage, it appears surprising that at low doses only beneficial effects would occur while noxious effect would require a dose above a certain threshold. To consider hormesis as an argument against actual dose limits would only be valid if the efficacy of hormesis could be demonstrated for the effects against which one wants to protect at low radiation doses, i.e. cancer and genetic damages.
Unfortunately this is not yet demonstrated in an unequivocal way. Therefore, the hormesis model is currently not considered in radioprotection.
The theory of “adaptive response”, (not to be confused with hormesis) shows that a low dose can reduce the effect of a higher dose when administered after a short time delay. This theory is based on substantial evidence.
To reduce a risk appears beneficial, but it does not mean that the risk is eliminated. According to the “adaptive response” model, a first low dose (conditioning dose) is considered to stimulate the DNA repair mechanisms that contribute to reduce the effect of a subsequent higher dose. But the initial low dose can only stimulate the limited number of cells actually hit, the total of which in function with the dose. This situation never excludes the possibility of a transformation of one of the cells.
The next higher dose concerns all cells. Some of them having the repair mechanisms stimulated by the first conditioning dose, and may repair the damage more easily. The other cells, that were not previously hit, are not protected. The total damage can be reduced by a factor depending on the number of the cells conditioned but will always be dependent on the total number of the cells exposed to both doses.
Would the conditioning of all cells solve the question? No, because to reach such a goal we have to increase the conditioning dose and the risk remains proportional to the dose and to the number of cells irradiated.
Therefore the adaptive response does not appear to be a relevant mechanism for radiation protection because the (low) conditioning dose that defines it, also generates a risk of transformation. On the other hand the challenging dose is not a low dose.”
end quote. I suppose it’s all in the eye of the beholder. There was at the time of the publication of this first DOE contracted paper by Flinders University sufficient qualified pondering and explanation of alternate views to cause an open minded person aware of the pros and cons that Bhat et al did not have a monopoly on the truth and that in 2004 it was pointed out by a qualified person with decades of experience in the field that the effect observed and reported was merely one of many. It is self evident in the Bhat et al paper that the effect reported on was merely one of many.
Bhat et al state: “The Linear No-Threshold Model does not Hold for Low-Dose Ionizing Radiation”
At around the same time – 2004 – L. DE SAINT-GEORGES writes : The Linear No Threshold hypothesis should remain so far the basic guide line for the radioprotection authorities. It appears clearly that the ALARA (As Low As Reasonably Achievable) principle, which is currently the basis of radiation protection policies, should be followed as long as no relevant scientific facts provide other insights. The very weak probability of oncogenic events at low dose should reassure everybody.
If any beneficial effects from low-dose radiation should exist, we can not exclude them, there is no reason to expect a higher occurrence probability for them than for cell transformation and the one would never exclude the other possibility in other cells. Therefore, such concepts aimed to attenuate the risk perception, will only lead toward more confusion, which in turn will generate more unwarranted anxiety and will finally be totally counterproductive.”
And while Bhat et al claim that they are especially qualified to comment and to prescribe doses of radiation to entire populations who are not their patients, I point out that Dr. Louis de Saint-Georges
has many decades of experience in the field. He has long since finished his training.
On the other hand Pamela Sykes has stated in her letter to me dated 2002 that “the area of low dose X rays is relatively new to me…” Pam was the Chief scientist in the course of that DOE research.
I would trust the decades of expertise in low dose radiation research owned by Dr. Louis de Saint-Georges
than the entire combined person years of understanding of Pam Sykes B.Sc and the rest of her team and their relative inexperience.
Not that I agree with everything anyone has ever said. I’m just an average voter wanting access to the whole truth before I cast my ballot.