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Exhibit D
The astute reader may have asked at some point why the history of radiation safety provided earlier in this chapter stopped where it did in the 1950s following publication by the ICRP and NCRP of the first standards of safety for internal contamination. What happened to the second half of the Twentieth Century? This is the million-dollar question. The model used today by international agencies formulating safety for internal contamination by radionuclides is essentially the same model, with updated modifications, developed during the Manhattan Project, the Tri-Partite Conferences, and the meetings of the committees on internal emitters of the NCRP and the ICRP. This model was developed prior to the discovery of DNA! Since the 1950s, a revolution has taken place in biology. Entire vistas of cellular and molecular biology, totally unsuspected by World War II physicists, have opened up for scientific exploration. The rapid advancement in technology has created powerful tools for imaging cellular structures and probing the mysteries of the molecular chemistry that orchestrates cellular processes. Advances have been so profound that, today, microbeams can deliver individual alpha particles to cells in vitro and the altered morphology of cellular structures can be determined by DNA sequencing and correlated with functional aberrations. Over this amazing new world of microscopic wonders and the deepening understanding of the cellular and molecular basis of life, the ICRP, NCRP, NRPB, UNSCEAR, and BEIR, like Fascist dictators, inflexibly demand that their archaic model of radiation effects be the basis for radiation protection. They tyrannize all discussions on the biological effects of ionizing radiation, and are rigidly intolerant of allowing other points of view from gaining a footing. Despite the fact that cellular response to radiation can now be studied as never before, these “august” bodies of self-declared experts insist that radiation effects can only be properly modeled as they were modeled in the early 1950s. This state of affairs is despotic. The ruling paradigm on radiation effects maintains its supremacy by ignoring a half-century of research in the biological sciences.
A review of a half-century of radiation biology is beyond the purview of this book. The purpose of Exhibit D is to introduce to the reader a small number of fascinating, well-established, scientific facts pertaining to how cells respond to ionizing radiation. What is significant is that these phenomena cannot be adequately taken into account by the current methods used by the radiation protection agencies for determining the health risks from internal, low-level radiation exposure. Their models cannot accommodate these facts. Exhibit E will then offer an explanation for why an antiquated system of radiation safety is being propped up in defiance of advancing knowledge.
According to conventional wisdom, when the DNA of a cell’s nucleus is “hit” by radiation, one of three outcomes is possible: (1) The DNA lesion is readily repaired and the cell emerges from the event unharmed. (2) The damage is of such a nature that it brings about death to the cell. (3) The cell survives in an altered form with radiation-induced mutation(s) to its DNA which are subsequently passed on to daughter cells during cell replication. These inheritable mutations may produce alteration in function within the cell. These in turn may instigate a cancer. It was not until the 1990s that a number of studies confirmed that a fourth avenue was possible for cells hit by radiation. At the moment of exposure, instability to the genome of a cell can be introduced which is not immediately apparent. The cell emerges from the event seemingly unscathed. No detectable aberrations are observable. Only with the passage of time, after a number of generations of cell division, does an instability begin to manifest itself as “abnormally high rates (possibly accelerating rates) of genetic change occurring serially and spontaneously in cell-populations, as they descend from the same ancestral cell [originally hit by the radiation]” (Gofman 1998). What is of interest is that the descendant cells that begin to manifest genetic abnormalities are not the original cells that received the radiation exposure. Moreover, after the first manifestation of chromosomal aberrations, continued cell division introduces yet further aberrations and DNA lesions which have no apparent relationship to the aberrations appearing first. The tentative conclusion at this point is that the initial radiation exposure damages the whole genome of the cell in such a way as to render it incapable of maintaining its stability over time.
Within the nucleus of each of the approximately ten trillion cells in the body of a human being, an exact copy of that individual’s genetic code can be found. The integrity of this operating system is maintained by the ordered sequence of nucleotides along the length of the DNA molecules. DNA is not inherently stable. Agents from both within and outside the cell can induce changes to its structure. To counter these influences and ensure stability to the genome, an elaborate molecular system continually monitors the accuracy of the sequencing along the DNA and repairs any deviations. As a consequence, when a cell undergoes division, each progeny cell contains a faithful reproduction of the genetic sequences present in the parent cell.
Exposure to radiation can adversely affect this system of stabilization of the genome. This can be induced by even the removal of a single nucleotide in the DNA sequence.
"The nature of the genetic code is such that mutations need not be gross in order to have gross biological consequences. For instance, permanent removal of a single nucleotide (a micro-deletion) can totally garble much of a gene's code, by causing what is called a “frame-shift.” Then this nonfunctional gene can be the phenomenon which wrecks part of the system which would otherwise maintain genetic stability.
In the mass media, some writers have expressed astonishment that radiation-induced genomic instability is not detected until several cell-divisions have occurred after the radiation exposure. They seem to imagine that the delay reflects a mysterious discontinuity between cause and effect. There is no discontinuity, of course. With current techniques, and with uncertainties about where to search closely among a billion nucleotides, it is just not possible to detect every intermediate step.
The induction of genomic instability in a cell does not guarantee that it will become malignant. Genomic instability increases the rate of mutation in that cell and its descendants, and with this higher rate, the cells each have a higher probability that at least one of them will accumulate all the genetic powers of a killer-cancer. These powers include the ability to thrive better than normal cells, to invade inappropriate tissue, to adapt to the new conditions there, to recruit a blood supply, to fool the immune system, and many other properties" [1].
The exact mechanism responsible for the initiation of genomic instability has yet to be identified. Perhaps more than one mechanism exists. Or, perhaps a chorus of combined mechanisms needs to be activated to induce the phenomenon. To date, no identifiable single lesion in a gene or chromosome has been identified as the trigger for genomic instability. A more pervasive intrusion on the cell’s regulatory functions is hypothesized. A possible explanation is that a radiation-induced interference disrupts the system governing DNA repair, the system responsible for the accurate duplication and distribution of DNA to progeny cells, or the system that regulates gene expression. Further, it may be the case that some individuals carry a genetic predisposition to these destabilizing influences. If such variation exists in human beings, standards of radiation safety presumed to be applicable to all human beings may be very shortsighted. It is important to note in passing that observations of mammals has confirmed that genomic instability can be induced in germ cells and be passed on to the genome of developing offspring. Thus, it is plausible that inherited genomic instability plays a part in the initiation of developmental abnormalities, stillbirths, birth defects, and infant mortality. In light of this, the finding that depleted uranium has been found in the semen of Gulf War veterans, when added to the accumulating anecdotal evidence of an increased frequency of birth defects in the population of Iraq, makes the indiscriminate scattering of depleted uranium in the environment truly alarming.
Bibliography
Gofman J.W. What Is Genomic Instability, and Why Is It So Important. San Francisco: Committee for Nuclear Responsibility; 1998. http://www.ratical.org/radiation/CNR/GenomicInst.html
