Posts
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
There are numerous other examples of biological effects not adequately considered by ICRP risk assessments. For instance, some people are genetically predisposed to a heightened sensitivity to radiation damage. Are these people adequately protected by current radiation standards developed in the one-size-fits-all model of the ICRP?
"Animal and human studies have identified genetic subgroups with enhanced sensitivity to radiation e.g. Japanese LSS study and women developing early breast cancer. In the extreme cases of those carrying the ATM gene for ataxia telangiectasia, there is extreme radiosensitivity and tendency to leukemia, lymphoma, and some solid tumors" [1].
Footnote: ataxia telangiectasia is a rare, inherited, progressive, degenerative disease of childhood that causes loss of muscle control, a weakened immune system, and an increased risk of cancer. http://www.cancer.gov/dictionary/db_alpha.aspx?expand=A#ataxia-telangiectasia
Take another example of biological variations among people outside the purview of ICRP models. Not everyone’s immune system functions identically. Immune response to radiation insult may differ significantly from person to person. Models ignoring the variations may put segments of the population at greater risk to radiation injury. Further, the immune system performs defensive surveillance on behalf of the body and can mitigate the effects of mutation or tumor progression induced by radiation. However, the effectiveness of this system can be suppressed by exposure to certain stressors such as ultraviolet light. This suppression of immune system response may, under some circumstances, be another factor involved in the enhancement of hazard from low doses of radiation.
Take a third example. It is a well-established fact that different radioisotopes, due to their chemistry, have an affinity for different organs of the body. This fact is acknowledged in ICRP models, and the hazard posed by different radioisotopes to different organs is adequately taken into account. But the same consideration is not given to radioisotope affinity on the molecular level. For example, it has been proven that Uranyl UO2++ ions bind strongly to DNA [2]. This suggests that internalized depleted uranium may have an affinity for DNA molecules. Thus, depleted uranium may pose an enhanced hazard to genetic damage out of all proportion to its “dose.” The same is true for strontium isotopes which have affinity for the phosphate backbone of DNA. It is essential that such molecular affinities be incorporated into assessments of risk from radiation because molecular effects at extremely low doses may nonetheless induce serious consequences to health in the form of mutations.
Another phenomenon ignored by ICRP models is the chemical transmutation radioisotopes undergo upon radioactive decay. When an atom undergoes transformation from one element to another, the chemical bonds which it has formed can be broken leading to significant alteration of the molecular structure of which it was a part. The impact of this chemical change is mentioned in the publication of the European Committee on Radiation Risk.
"The macromolecules which are the operators of living systems — proteins, enzymes, DNA and RNA — depend upon their tertiary structure, or shape, for their activity and biological integrity. Alteration of this shape results in inactivity of the macromolecule. This inactivation could in principle be effected by the sudden transmutation or alteration of one atom in the macromolecule. Since the molecular weight of these macromolecules is usually greater than 100,000, it is clear that incorporation of one atom (of e.g. C-14 which decays to Nitrogen) may result in an enhancement of effect of many thousand-fold" [1] .
When radioisotopes enter the internal environment of the body, they are available to become incorporated into the structure of significant macromolecules. Upon radioactive decay of just one atom in such a molecule, the function of the entire molecule may be altered or destroyed. A question yet to be addressed in risk assessment is the impact to health on individual cells, organs, and the whole organism of such altered molecular junk flooding the human body.
The ECRR mentions another interesting biological phenomenon that may in time prove important in risk assessment. In a recent theory of cancer expression hypothesized by Sonnenschein and Soto, a communication field exists between cells, and a threshold number of genetically damaged cells must come into existence before cancer can develop [3]. This idea is based on the theory that cell proliferation is the default state in multicellular organisms and that some permanent inhibitory signal must exist to deter proliferation. It is postulated that this inhibitory signal is carried by cell-to-cell communication and is perpetuated in the field of this communication network. “If this is found to be generally so then the effects of high local doses, as occur in the region near hot particles, may be particularly effective in causing cancer, since the damaged cells are all close to one another” [1]. By this theory, hot particles can create sufficient local damage to disrupt the inhibitory signal generated between cells and lead to cancerous proliferation.
One last biological phenomenon mentioned by ECRR that has yet to enter into consideration by ICRP models is the transfer of radioisotopes to the developing fetus in a woman who is internally contaminated. Once again, alpha emitters released at extremely minute concentrations may have consequences out of all proportion to the “dose” as currently calculated by ICRP models.
"For early developing fetuses, the local dose from particles of plutonium oxide or other actinide alpha emitters will be massively high and may result in a range of effects from fetal death and early miscarriage to effects in childhood. This is a case where the biological end-point may result from a very low probability, high risk event" [1].
Bibliography
[1] European Committee on Radiation Risk (ECRR). Recommendations of the European Committee on Radiation Risk: the Health Effects of Ionising Radiation Exposure at Low Doses for Radiation Protection Purposes. Regulators' Edition. Brussels; 2003. www.euradcom.org.
[2] Wu O., Cheng X., et al. Specific Metal Oligonucleotide Binding Studied By High Resolution Tandem Mass Spectrometry. Journal of Mass Spectrometry. 1996; 321(6) 669-675.
[3] Sonnenschein C., Soto A,M. The Society of Cells: Cancer Control and Proliferation. Oxford: Bios Scientific Publishers; 1999.
