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What follows is the continuation, in serial form, of a central chapter from my book A Primer in the Art of Deception: The Cult of Nuclearists, Uranium Weapons and Fraudulent Science.
Exhibit D continued
When one takes into account the differences in cell sensitivity to radiation at different times in the cell life cycle, the hazards of low doses of radiation may be much greater than that supposed by ICRP models. According to the ICRP, radiation effects are proportional to dose. This linear relationship is well-documented at high doses, and via mathematical extrapolation, it is assumed to be equally true at low doses. However, when taking cell sensitivity into account, the dose-response relationship at low doses takes on a different picture. It is not unreasonable to assume that throughout an organ or throughout the whole body, some portion of cells at any one time are undergoing replication. Normal replacement of dead or aging cells can account for this turnover. When this subgroup of sensitive cells is factored into consideration, the concept of averaging a dose over an undifferentiated mass to derive an organ dose once again seems out of touch with reality and the linear dose-response model breaks down at low doses. A biphasic dose-response relationship would offer a more accurate model of low-dose effects to cell populations that include among them cells in a state of hypersensitivity to radiation damage. Such a response has been observed by Burlakova [1,2]. To explain, let’s assume that one percent of a cell population is actively dividing and in repair replication sequences, and for argument’s sake, that these cells are 200 to 600 times more sensitive to a hit from a radiation track. What would the dose-response look like?
"Well, as the dose was increased from zero, the sensitive cells would begin to be damaged and a proportion of these hits would result in fixing a mutation and increasing the possibility of cancer. As the dose increased further, eventually this rise in response would peak as these sensitive cells were killed. The mutation yield would then begin to fall. However, at some point, the insensitive G0 cells would begin to be damaged and the whole process would begin again, with a rise in cancer" [3].
It can be seen from this model that the lowest doses of radiation can induce mutations in the most sensitive cells. Thus, the likelihood of developing cancer may be enhanced at low doses. As the dose rises, these most sensitive of cells are killed preventing cancer expression. This has the effect of masking the low-dose mutagenic effect. As the dose increases further, the cells in G0 begin to be damaged and the dose response begins to take on the linear appearance that is currently assumed to be true for all doses. Within this theoretical framework, the possibility emerges yet again that internal emitters releasing low doses of radiation may pose a greater hazard than currently assumed by a simple linear extrapolation from high doses of radiation delivered external to the body.
It is reasonable to hypothesize that in the case of fetal injury, dose-response cannot be linear, but must be biphasic. This point is clearly addressed within the Minority Report of CERRIE, the Committee Examining Radiation Risk in the Environment:
"The Committee [CERRIE] considered the effect that the assumption of a continuous linear dose response relationship would have on the interpretation of findings in epidemiological studies. We [those who authored the Minority Report] argued that this (assumption that increasing dose would consistently produce increasing effect) was biologically implausible — for example, increasing dose to the fetus would ultimately result in its death. As a consequence, if an analysis of any endpoint in infants were expressed in terms of increasing dose it would show a maximum followed by a reduction. If there were sub populations of cells or people of different sensitivity, there could then be a subsequent increase (a biphasic dose response)" [4].
The biphasic dose response to low-dose/slow-dose rate exposure was proven by Burlakova and her colleagues after extensive research on animals and humans. This work was summarized in an article by Rosalie Bertell entitled Gulf War Syndrome, Depleted Uranium and the Dangers of Low-Level Radiation:
"They [Burlakova and fourteen other scientists] examined carefully the following biological phenomena under ionizing radiation exposure situations:
* alkaline elution of DNA of lymphocytes and liver
* neutral elution and adsorption of spleen DNA on
nitrocellulose filters
* restriction of spleen DNA by EcoRI endonuclease
* structural characteristics (using the ESR spin probe
technique) of nuclear, mitochondrial, synaptical, erythrocyte and leukocyte membranes
* activity and isoforms of aldolase and lactate hydrogenase enzymes
* activity of acetycholine esterase, superoxide dismutase, and glutathione peroxidase
* the rate of formation of superoxide anion radicals
* the composition and antioxidizing activity of lipids of the above mentioned membranes
* the sensitivity of cells, membranes, DNA, and organisms to the action of additional damaging factors.
For all of the parameters a bimodal dose-effect dependence was discovered, i.e. the effect increased at low doses, reached its [low-dose] maximum, and then decreased (in some cases, the sign of the effect changed to the opposite, or “benefit” effect) and increased again as the dose was increased. Dr. Burlakova has speculated that at the lowest experimental doses used in this research, the repair mechanism of the cells was not triggered. It became activated at the point of the low-dose maximum, providing a “benefit” until it was overwhelmed and the damage began again to increase with dose. This may well be the case" [5].
Footnote: It is important to note that it is only within this narrow dose range, where cell repair mechanisms begin to kick in, that the concept of hormesis makes sense. The concept, however, is abused when cited to prove that low-dose exposure is “beneficial” to the organism. Burlakova has demonstrated that numerous detrimental effects occur at lower doses before this seeming “benefit” appears.
Bibliography
[1] Burlakova E. B. Radiation Protection Dosimetry. In E.B. Burlakova, V. Naidich, J.B. Reitan (eds.): Radiobiological Consequences of Nuclear Accidents-Contamination, Radioecology, Radiobiology and Health. Nuclear Technology Publications. 1995.
[2] Burlakova E.B., Goloshchapov A.N., Gorbunova N.V., Zhizhina G.P., Kozachenko A.I., Korman D.B., Konradov A.A., Molochkina E.M., Nagler L.G., Ozewra I.B., Rozhdestvensko L.M., Shevchenko V.A., Skalatskaya S.I., Smotryaeva M.A., Tarasenko O.M., Treshchenkova Y.A. Mechanisms of Biological Action of Low Dose Irradiation. In E.B. Burlakova (ed.): Consequences of the Chernobyl Catastrophe for Human Health. Moscow: Co-published by the Centre for Russian Environmental Policy and the Scientific Council on Radiobiology. Russian Academy of Science. 1996.
[3] Busby C. Science on Trial: On the Biological Effects and Health Risks following Exposure to Aerosols Produced by the Use of Depleted Uranium Weapons. Invited Presentation to the Royal Society. London. July 19, 2000
Also given in part to the International Conference against Depleted Uranium. Manchester. November 4-5, 2000. Occasional Paper 2000/11. Aberystwyth: Green Audit. October 2000. http://www.llrc.org/du/subtopic/durs.htm
[4] CERRIE Minority Report. Minority Report of the UK Department of Health / Department of Environment (DEFRA) Committee Examining Radiation Risk from Internal Emitters (CERRIE). Aberystwyth: Sosiumi Press; 2005.
[5] Bertell R. Gulf War Syndrome, Depleted Uranium, and the Dangers of Low-Level Radiation. 1999b. http://www.ccnr.org/bertell_book.html
