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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.
SCAM NUMBER TWENTY-SEVEN: Underestimate the risks posed by low-level radiation by failing to take into account known physical and biological phenomena.
According to the model of risk assessment upheld by the ICRP, the density of ionization events within a target mass is the key determinant of biological effect. To account for the fact that the same quantity of energy will create different patterns of ionization depending on whether it is delivered by alpha, beta, or gamma radiation, the equations of the ICRP allow for the introduction of a weighting factor to make allowance for these differences, called the radiation weighting factor. As an example, if the equivalent dose of radiation is delivered to a tissue by x-rays and alpha particles, the biological effect of alpha particles is weighted as 20 times greater than that produced by the x-rays due to the denser pattern of ionization (more destruction per unit length along a track of alpha particles.) A second weighting factor is added to calculations: the tissue weighting factor. This mathematical expression is inserted into equations to capture the differing sensitivities of the various organs of the body, and to offer an expression for the contribution of each organ to total health detriment resulting from uniform external irradiation to the whole body.
The addition of the two weighting factors into the complex modeling of the ICRP is an attempt to create a realistic model that connects the quantity and quality of radiation to the probable biological effects. Unfortunately, the model is archaic. It fails to take into account known physical and biological phenomena that add to the hazard of the organism. This conveniently leads to an underestimation of risk.
To address these shortcomings, the European Committee on Radiation Risk proposes that, to salvage the ICRP methodology from irrelevance, additional weighting factors need to be included in calculations to address current understanding. (It must be emphasized that the ECRR has absolutely no influence at this point in time over the methodology of the mainstream radiation protection community. Their suggestions can easily go unheeded, and the ICRP and related organizations can continue to ignore biological realities in their questionable risk assessments. Of course, such intransigence will only further weaken their credibility.) To fully capture the hazard to the organism posed by radiation, the ECRR sees the need for the addition of a hazard enhancement weighting factor. This would inject into calculations known physical and chemical effects that at this point in time are completely overlooked by the ICRP. A few examples will be given to illustrate current shortcomings in the accepted methodology that lead to an underestimation of the hazard to health from low-level radiation.
1) Radioisotopes which gain access to the interior of the human body behave in accordance with their chemical composition. Thus, different radioisotopes pose different hazards depending on how they migrate through the human body and where they are retained. It has been proven that isotopes of strontium, barium, and plutonium have a propensity to bind to DNA. Due to their intimate proximity to DNA, the likelihood is increased that these radioisotopes will induce irreparable genetic damage. The ECRR recommends acknowledging this increased hazard in comparison to other radioisotopes that don’t bind to DNA inside the body. This observation is important when discussing the hazards created by the inhalation of depleted uranium. It has been observed that uranyl UO2++ ions bind strongly to DNA [1]. As a consequence, internalized uranium poses enhanced hazards that are totally ignored by all agencies.
2) Cells have a range of sensitivity to radiation depending on where they are in the cell cycle, but this variation in sensitivity is not considered in risk assessment. Cells undergoing replication are more sensitive to radiation effects than cells which are not in the process of cell division. This can enhance radiation effects under certain circumstances. “For external low LET radiation there is a 600-fold variation in the sensitivity for cell killing over the whole cell cycle” [2]. Take the example of two separate doses of external radiation delivered in a 24-hour period. The first dose will induce some portion of the targeted cells to initiate cell repair and replication processes. Once these are underway, a second dose hitting them in this heightened phase of sensitivity will be more hazardous than if the second dose were delivered after the cell population had returned to stasis. Second Event theory postulates a similar phenomenon for certain types of internal emitters. For instance, an atom of strontium-90 may be bound to a chromosome. When it decays to the radioisotope yttrium-90, it will produce a track of ionization through the cell that may produce sublethal damage. This may signal the cell to enter a repair-replication sequence. Yttrium-90 has a half-life of 64 hours. Consequently, a probability exists that it will undergo decay during the phase of enhanced sensitivity of the reproducing cell, when DNA damage can no longer be repaired. Conditions at this point are ripe for irreparable mutations to be created that, if not lethal, will be passed on to all descendants of the daughter cells created from the original cell division. The ECRR recognizes increased hazard in the two scenarios mentioned here and proposes increased weighting factors in calculations of risk under these conditions.
3) Certain types of insoluble hot particles lodged in tissue represent a hazard that is not addressed by current estimates of risk. The biological effect of this type of contamination depends on the size of the embedded particle, the activity, and the dose. Being insoluble, these particles may remain lodged in their place of deposition for long periods of time. As such, they represent an enhanced hazard to surrounding cells when compared to single atoms of the radionuclide dispersed throughout greater volumes. The ECRR believes that this phenomenon warrants inclusion in determinations of risk from internal emitters.
The first publication of the ECRR contains a deep discussion of the ICRP model, its shortcomings and recommendations for bringing it into harmony with current knowledge of radiation effects. The work of the ECRR, however, sets it on a collision course with the nuclear establishment. When applying its risk factors to estimates of health detriment following exposure, radiation is revealed to be much more hazardous than currently assumed. For instance, the risk factors (the probability of injury) per sievert for whole populations for whole-body effects is double that of the ICRP for fatal and nonfatal cancers, severe hereditary defects, and cancer and severe retardation after in utero exposure.
Bibliography
[1] 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.
[2] 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.
