The reigning paradigm is out of step with the current knowledge base. It is completely inadequate for modeling the effects of low-level radiation on the cellular level. The problem is that it is grounded on an “unsound premise.” As mentioned in Radiation Protection Dosimetry: A Radical Reappraisal: “In the present context, the unsound premise is that absorbed dose is a fundamental concept that can be used as an effective predicator of radiation effects.” Simmons and Watt then continue:
"Criticisms of the use of absorbed dose as a basis for assessing the effects of low levels of radiation are not new. At the 17th meeting of the NCRP in 1981, V. Bond, the Head of the Medical Department of the Brookhaven National Laboratory, observed that for stochastic processes such as the induction of cancer at low levels of radiation, it is the effect within a cell (or a small number of cells) that is important. [The outcome of stochastic processes involve chance or probability. Their end result is not fixed or causally determined.] However, because at low levels of radiation (i.e., those of significance in radiation protection) a large proportion of the cells will have received no radiation, the mean dose per cell represented by the average tissue dose is not the same as the mean dose per dosed cell. A better quantity to use in this context is the fluence of charged particles through the critical volumes. Only when all the cells have received at least one hit (i.e., at “doses” of ~ 10 cGy [10 rad] for low-LET radiation and ~ 1 Gy [100 rad] for high-LET radiation) does dose become a suitable surrogate for charged-particle fluence" .
To translate, the current model is adequate to explain radiation effects as long as the radiation dose received is great enough that the critical volume of each cell of the target [i.e., the cell nucleus] receives at least one hit by tracks of ionization laid down by alpha, beta, or gamma radiation. In doses smaller than this, a better predictor of biological effects is the fluence of charged particles passing through the nuclei of the cells actually hit. [The term “fluence” refers to the number of charged particles traversing a given target volume.] Why is this? When low levels of radiation traverse tissue, not all cells are hit. Thus, the averaging of energy over large volumes is an erroneous concept. Biological effect is only induced in cells that are actually hit. Of those cells that are hit, the greater the number of tracks of ionization passing through the nucleus, the greater the likelihood for irreparable damage to critical cellular structures such as the DNA molecules. Thus, the fluence of charged particles is the fundamental phenomenon in gauging radiation effects. As Simmons and Watt explain, “Energy deposited is not the cause of an interaction; it is a secondary effect. The interaction is best described by fluence and cross section.” From this point of view, dose “can be expressed as ‘hits per unit volume or mass’ or ‘passage of particles per unit area’” .Here physics and biology merge in a successful model that accurately depicts what takes place when radiation interacts with living systems composed of individual cells.
In the opinion of many radiobiologists, the most critical lesion created in a cell traversed by radiation is a double-strand break (dsb) in the DNA molecule. Single-strand breaks along one half of the double-helix molecule are effectively repaired by cellular mechanisms. Two breaks, each occurring along each half of the double helix, are much less likely to be accurately repaired. Such a lesion either goes unrepaired or is misrepaired. This can lead to cell death or various types of mutation that may or may not be lethal to the cell. Mutations within cells that do survive may be the precursor to a cancer. The distance between the two strands of a DNA molecule is approximately 2 nanometers (2 billionths of a meter). There are a number of patterns of radiation fluence that can be responsible for creating successive ionizations within this critical 2 nm distance. At high doses of gamma irradiation, a number of tracks may intersect the same cell nucleus and successfully cause breakage in the two arms of the same DNA molecule. As dosage decreases, the likelihood of double-strand breaks diminishes. It is at this point that the current model of energy effects begins to break down. (Although the dose delivered by photons makes dsbs unlikely, an equivalent dose delivered by marauding alpha particles still retains the capacity for creating dsbs.) A second possible initiator of a double-strand break is a decelerating electron coming to the end of its track and ionizing both strands of a DNA molecule. The geometry of this type of event makes the probability of its occurring relatively low. A third and very effective cause of double-strand breaks is a heavy particle such as an alpha particle. Its dense pattern of ionization permits it to breach, at a single blow, both strands of the double helix. This is what makes alpha-emitting radionuclides so potentially hazardous. Just one alpha particle has the capacity of creating a dsb.
So far, what has been mentioned are double-strand breaks created by direct hits to the DNA molecule. Indirect hits can also contribute to double-strand breaks. The most frequent type of molecule to be ionized in a cell from radiation is water. This can lead to the formation of free radicals which can diffuse up to a distance of about 15 nm from the particle path that created it. Created in close enough proximity to the DNA molecule, the free radical can induce rupture along one of the strands, creating a point mutation. Similarly, the hydroxyl radical (OH) produced from the ionization of water can diffuse 2 to 3 nm and promote chemical rupture in a DNA strand. Thus, it is the combination of both direct and indirect hits to the nucleus that combine to create double-strand breaks.
"The radiation track must, so to speak, match the ‘template’ of the strands of the DNA for an effective interaction to occur. Those interactions which occur at positions not so matched will have no effects, a situation that accounts for the irrelevance of energy transfer. There are on average ~15 pairs of strands at risk across the cell nucleus. The observed saturation cross section depends on the number of target DNA segments penetrated (determined by the particle’s projected range) and the interaction spacing along the relevant track" .
Under this scheme, the probability of hits created by the respective fluences of variously charged particles delivered at different rates becomes a basis for establishing relative hazard.
"The conclusion to be drawn is that the basic mechanism of radiation damage to normal mammalian cells is the correlation of two ionizations, which are spaced at about 1.5 to 2 nm along single-particle tracks in the relevant charged-particle spectrum, with the similarly spaced strands of the intranuclear DNA. The biological effects discussed are found to depend on the number of such paired interaction events, which are independent of the energy transfer" .
Within this new paradigm, it is the breakage of the chemical bonds of the two strands of a DNA molecule that is critical, AND, for this to occur, no more energy is required than the binding energy of these two bonds. Thus, the old paradigm, in which radiation effects were pegged to total energy absorbed, mistakes the fundamental phenomenon in the interaction of radiation with living systems.
"If one accepts the argument, based on experimental evidence, that the amount of energy transfer in excess of bond energies is irrelevant to the induction of radiation effects, then it is fundamentally wrong to use energy deposition as a quantifying parameter."
"Two ionizations, if appropriately placed, are sufficient to break two single strands of the DNA whether the energy transfer is 10 eV or 1 MeV. All the evidence obtained here points to the conclusion that it is the number of events (double-strand breaks in the DNA) caused by correlated pairs of ionizations that matter, not the energy transfer. Thus, two ionizations produced in the critical volume of a DNA segment need not induce a dsb. To do this the ionizations produced by the track must be correlated with the strands of DNA, like a template. If this is correct, then it would invalidate, on conceptual grounds, the use of volume quantities such as absorbed dose; the quality parameters ionization density and restricted LET; and the microdose quantities, linear energy and specific energy density, because these quantities include the interactions of low-energy delta electrons" .
Simmons and Watt title their book Radiation Protection Dosimetry: A Radical Reappraisal. Their proposal for a new paradigm in understanding radiation effects is both unorthodox and revolutionary. It challenges the very foundation of current thinking on how to best conceptualize what transpires when radiation interacts with life. It has been presented here in order to highlight the inadequacies of the reigning paradigm. It is evidence that the knowledge base has expanded tremendously since the Tri-Partite Conferences. Further, it is evidence of how antiquated the currently accepted model of radiation effects has become. The puzzle that must be unraveled is why such an outdated, inaccurate model continues to be used to protect mankind from exposure to low levels to ionizing radiation. The answer to this question will be addressed in Exhibit E.
 Simmons J.A., Watt D.E. Radiation Protection Dosimetry: A Radical Reappraisal. Madison, Wisconsin: Medical Physics Publishing; 1999.