Both the great Truths and the great Falsehoods of the twentieth century lie hidden in the arcane, widely inaccessible, and seemingly mundane domain of the radiation sciences

Monday, March 29, 2010

The Trial of the Cult of Nuclearists: Exhibit D continued

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

In addition to genomic instability and the bystander effect, there are other biological phenomena not adequately represented in the ICRP model of the health effects of radiation. For instance, cells vary in their sensitivity to radiation at different times throughout their lifespan. In an experiment conducted in 1966 on Chinese hamster cells, a 600-fold variation was observed in cell radiation sensitivity throughout the entire cell cycle [1]. At any one time during the life of an organism, most cells inhabit a phase commonly referred to as Gap 0 (G0). In this phase, the cell is in a non-replication mode of stasis. It is living out its life while contributing to the normal living processes of the system of which it is a part. While in this phase, the cell is relatively insensitive to radiation damage. At some point, as a result of such factors as tissue growth, damage, or senescence, a signal is generated to initiate cell replication and the cell moves into Gap 1 (G1) phase. At this point in the cell cycle, preparations are initiated for the replication of the chromosomes. The cell increases in size, produces RNA, and synthesizes proteins. Also, an important cell-cycle control mechanism is activated. A process of proofreading of the integrity of the DNA gets underway where complementary strands are compared and damage is repaired. During G1, the cell is in an intermediate state of sensitivity. If the cell is damaged at this point by radiation, a period of delay is introduced into the process of cell replication while any newly incurred damage is repaired. In this controlled sequence of preprogrammed operations, the cell then moves on to Synthesis (S) phase where the chromosomes replicate. From there, Gap 2 (G2) phase follows. During this gap between DNA synthesis and cell division, the cell continues to grow and produce new proteins. Late in G2, a last checkpoint is reached in the cell cycle to verify that the cell is ready to enter mitosis and divide. Once this transition point (TP) is passed, the cell has reached a point of no return in the sequence of events and it will undergo mitosis. At this transition point, the cell is at its most sensitive point for radiation damage. If a sublethal hit is incurred at this time and damage is introduced into a chromosome, repair is not possible. The damage will be copied and replicated in the two daughter cells regardless of the amount of damage.

The ICRP model makes no allowance for the varied sensitivity of cells throughout their lifetime. Yet again ignoring radiation effects on the cellular level, the model is out of touch with basic biological realities. This gross inconsistency, however, does serve one important purpose. It bolsters the archaic and inappropriate concept of dose which averages energy over large volumes of undifferentiated, noncellular, masses. By this means, low-level radiation effects to individual cells is afforded no room for consideration within the current paradigm of radiation safety. The hazard posed by internal emitters is thus conveniently sidestepped. The enhanced sensitivity of cells to radiation damage at the time of replication suggests that the energy/particle flux from internal emitters, even at low doses, may represent an enhanced hazard to radiation injury when compared to photons impinging on the body from the outside from naturally occurring background radiation due to ionization density. It has been determined that, as a result of the natural radiation from the environment impinging on the body externally, each cell receives on average one hit per year. In contrast to this low-level external radiation, low-level radiation emitted by radioactive particles embedded within the body have a greater likelihood (dependent, of course, on quantity and activity) of hitting cells in their immediate proximity during the period of heightened sensitivity of cell replication.


[1] Sinclair W.K., Morton R.A. X-ray Sensitivity during the Cell Generation Cycle of Culture Chinese Hamster Cells. Radiation Research. 1966; 29:450-474.

Thursday, March 25, 2010

The Trial of the Cult of Nuclearists: Exhibit D continued

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

The bystander effect introduces an entirely new type of effect produced by ionizing radiation, namely a disruption of intracellular and intercellular communication pathways. The study of this phenomenon is in it infancy and may lead to a revolution in understanding radiation effects. Rosalie Bertell has provided a few insights into this fascinating avenue of research:

"In addition to these general affects on the whole organism, there are micro-biological effects and biomarkers of exposure which have been neglected by the ICRP because of their focus on cancer death and only one mechanism, namely, direct damage to the DNA molecule initiating a malignant growth. Professor Michael Vicker, University of Bremen, has documented the acute radiosensitivity of blood to micro-Gray doses of radiation, causing the arachidonic acid cascade (Vicker). Rather than trying to extrapolate the DNA damage hypothesis from the high dose exposures to radiation into theoretical happenings in the low dose range, researchers would do better to expand the mechanisms studied to include those which actually occur at the low dose and their sequelae.

With all of the sweeping changes which have occurred in biology and microbiology since the 1952 discovery of DNA by Watson and Crick, radiobiology has stayed focused on cancer and direct damage to DNA. Other branches of biology have expanded to consider the entire cell, systems influencing cellular behavior including functional levels and coupled feedback reactions of networks of inter- and intracellular responses regulating cell communication. Without a holistic view of biology and physiology, radiobiology has been consumed with detail and elaborate mathematical picture of the small world which was delimited by the very first administrative decisions of the nuclear bomb era.

In an organism, cells communicate with one another through the exchange of specific information, for example through a hormone, and the translation of this signal into intracellular messages. Paracrine (hormones secreted from tissues other than endocrine glands) and endocrine hormones are unable to pass through cell membranes. Therefore their information (the hormone) requires a cellular receptor on the outside surface of the cell, a transmembrane signaling that is connected to the receptor, called a “second messenger-generating enzyme”, and a correct interpretation of the second messenger system. Various second messengers are released into the cell after stimulation of a particular receptor enzyme system, and which systems may be activated depends on the genetically determined receptors possessed by the cell. This communication system between cells in complex systems, can be modified, for example by phosphorylating particular proteins, and two second messengers can interact through feedback and cross talk. Ionizing radiation causes many interferences and disruption in this delicately balanced intercellular communication system. In radiobiology, these problems are dismissed and assume to be either trivial or perfectly repaired. Ionizing radiation induces oxidative stress, something admitted by radiobiology but discussed only in terms of its thermal effects. This same oxidative stress induces measurable inflammation, including a massive cascade of fatty acids in various states of oxidation. These mediate inflammatory reactions in the blood and other tissues, such as blood vessel endothelium, and function as second messengers, even controlling such things as pain and chemiluminescence.

The perturbation of cellular communication, regulation and homeostasis by low doses has major consequences for human health and development. It is irrational, as the physicists are now doing, to count on the failure to observe high dose effects at low doses as “proof” that such doses are “safe”. DNA damage is a statistical phenomena, called stochastic by the physicists, while the inflammatory response is nonstochastic, or deterministic as it is now called. Unlike skin burns, these internal inflammatory responses occur at microGray doses. The ICRP assumes that deterministic effects do not occur below 500 mGy doses.

The ionizing radiation stimulations are “illicit” in the sense that there is no equivalent stimulation of the arachidonic pathway after non-radiological physiological stimulation, making it pathogenic in character, difficult for the body to regulate and return to homeostasis. This response activates the monocytes, which kill themselves by the oxidants they produce, often ending up as pus along with their digested cellular victims. They can endanger the host by killing other tissue, for example, transplants or infarcted heart tissue.

Activated monocytes are carcinogenic, provoking hitherto latent oncogenic systems and genomic errors to replicate. This may well be one of the mechanisms by which cancers were increased within the first ten years after the Chernobyl disaster. These cancers were dismissed by the IAEA as not radiation related because the ICRP required latency period of ten years had not been completed. These were radiation promoted or accelerated cancers, not radiation induced cancers. Again, we see ICRP recognizing only radiation induced cancers, whereas the victim will experience both mechanisms as due to the disaster" [1].


[1] Bertell R. Limitations of the ICRP Recommendations for Worker and Public Protection from Ionizing Radiation. For Presentation at the STOA Workshop: Survey and Evaluation of Criticism of Basic Safety Standards for the Protection of Workers and the Public against Ionizing Radiation. Brussels: European Parliament, February 5, 1998a.

Monday, March 22, 2010

The Trial of the Cult of Nuclearists: Exhibit D continued

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

In the cold, mechanistic, clockwork universe of the physical scientist, the phenomena of love, compassion and empathy are driven into exile. There is no mechanism that can account for these experiences. When I am hit, I suffer alone. You standing beside me remain untouched by my misery. This state of affairs, however, is not true to the human experience. In the world of relatedness and relationship, when I am hit, you beside me bleed. Reclaiming mechanistic science from out-of-touch abstraction is biology, the study of life. This is the metaphorical significance of the recently discovered “bystander effect,” a second intriguing biological phenomenon that calls into question current assessments of risk from exposure to low doses of radiation.

Up until the closing years of the twentieth century, research in radiation biology was guided by the foundational assumption that radiation-induced damage to cells was a direct consequence of the transfer of energy to cellular molecular structures, DNA being the primary target. Those cells “hit” by radiation were damaged at the instant of exposure or shortly thereafter, and the consequences were expressed within one or two cell generations. Those cells not hit by radiation escaped damage altogether. Within the physicist’s paradigm, there was no mechanism by which non-targeted cells could receive injury from radiation. Discovery of the bystander effect dashed this shortsighted, unfounded assumption. In the realm of the living, cells hit by radiation communicate the assault to cells in their immediate vicinity, and the non-targeted cells respond by undergoing similar destructive transformations as if they had actually received the blow themselves.

The ‘bystander effect’ is the name given to a cell-to-cell communication process by which the damage created in cells hit by radiation is communicated to non-hit cells. These cells in turn manifest damage — often very extensive damage — similar in kind to that received by the targeted cells. “The radiation-induced bystander effect is a phenomenon whereby cellular damage (sister chromatid exchanges, chromosome aberrations, micronucleation, transformation, gene expression) is expressed in unirradiated neighboring cells near to an irradiated cell or cells” [1]. Besides immediately observable genetic damage and mutations, bystander damage may also include genomic instability which manifests only after many generations of cell divisions among populations of non-targeted cells. The mechanisms responsible for the bystander effect are not currently known. Two separate pathways seem to be involved. In cells which are in direct contact with each other, chemical communication from the irradiated cell to unirradiated neighbors occurs through channels called gap junctions. For communication with more distant cells, the prevailing hypothesis is that the hit cell releases damage-response chemical signals into the intercellular medium which are then absorbed by cells not directly targeted by the radiation.

The bystander effect shakes the foundation of orthodox dogma as to how radiation interacts with living systems and calls into question the adequacy of current models of radiation risk. Although as yet unproven, it suggests that internal exposure to low doses of radiation may be more hazardous than currently assumed. Further, it poses a serious challenge to the reigning assumption that the effects of low doses of radiation can be determined by a simple linear extrapolation from high doses.

"[The bystander effect] would have significant consequences in terms of radiation risk extrapolation to low doses, implying that the relevant target for radiation oncogenesis is larger than an individual cell, and that the risk of carcinogenesis would increase more slowly, if at all, at higher doses. Thus a simple linear extrapolation of radiation risk from high doses (where they can be measured) to lower doses (where they must be inferred) would be of questionable validity" [2].

"The bystander effect does not demonstrate a linear relationship to dose. It is maximally induced by very low doses, suggesting a switch on/off mechanism for its activation" [1].

"On the basis of this [bystander] effect and its possible contribution to cancer induction in body tissues via the induction of DNA damage, the authors question the assumed linearity of low dose carcinogenic response for alpha particles; this assumption is an important element in radiological protection" [3].

"The main report [CERRIE Majority Report] notes that the existence of genomic instability together with the bystander effect draws attention to the existence of organization levels for cell communication midway between the cell and the organ. Sonnenschein and Soto have recently suggested that such cell communities are pivotal in the development of cancer as it is cell communication from local cells that tends to prevent any cells in a community from running away from growth control. They see replication as a default state and quiescence as a response to control by local cells. This suggests that damage to such a cell community results in transformation and may be critical in the ultimate expression of cancer. For this reason sublethal damage from multiple decays from hot or warm particles would confer risks not accommodated within presently accepted paradigms" [4]

It is interesting to note that the existence of the bystander effect lends support to the idea put forth in Exhibit A that radiation effects cannot be adequately modeled by the simple concept of a transfer of energy. “Because of bystander effects, the distribution of energy in cells is not related to the distribution of cellular damage" [5].


[1] Belyakov O.V., Folkard M., Mothersill C., Prise K.M., Michael B.D. Bystander Effect and Genomic Instability-Challenging the Classic Paradigm of Radiobiology. Timofeeff- Ressovsky Centennial Conference, "Modern Problems of Radiobiology, Radioecology and Evolution." Joint Institute for Nuclear Research. Dubna, Russia. 2000.

[2] Hall E.J. Genomic Instability, Bystander Effect, Cytoplasmic Irradiation and other Phenomena that may Achieve Fame without Fortune. Physica Medica. Vol. XVII, Supplement 1, 2001.

[3] Zhou H., Randers-Pehrson G., Waldren C.A., Vannais D., Hall E.J., Hei T.K. Induction of a Bystander Mutagenic Effect of Alpha Particles in Mammalian Cells. Proceedings of the National Academy of Sciences. 2000; 97:2099-2104.

[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] Brooks A.L. Bystander Effects from High-LET Radiation. Powerpoint Presentation. US Department of Energy Low Dose Radiation Research Program.

Thursday, March 18, 2010

The Trial of the Cult of Nuclearists: Exhibit D continued

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

One of the landmark studies on genomic instability was published in 1992 by Eric Wright, Munira Kadhim, and colleagues [1]. In the course of their research, they exposed stem cells from the bone marrow of mice to plutonium-238, giving them a dose of from 0 to 5 grays of alpha radiation.

"The cells were kept in Petri dishes for 11 days until they had divided between 10 and 13 times, each producing between 10 000 and 100 000 daughter cells. Wright found that the progeny of the irradiated cells contained three and a half times as many chromosome aberrations as the descendants of cells that were not irradiated. In a letter to Nature, he concluded that the “relative biological effectiveness” — a measure of how damaging low-level radiation can be in the body — for isotopes that emit alpha particles is “effectively infinite [emphasis added]" [2].

In the fall of 1995, more than thirty radiation biologists and health specialists attended a workshop in Helsinki to discuss the health consequences to the public of radiation-induced genomic instability. When compiling the available published information on genomic instability, attendees cited twenty-six studies that suggested that the “accepted rules for calculating the biological impact of radiation should be rewritten” (Edwards). According to Jack Little, professor of radiobiology at the Harvard School of Public Health and an attendee of the workshop: “Genomic instability changes our way of thinking about how radiation damages cells and produces mutations.” After the workshop, participants prepared a report for the World Health Organization. This report was never published. However, the magazine New Scientist acquired a copy and published excerpts. Included in the report was the observation that genomic instability is a key event not only in the process leading to cancer but to the development of other diseases as well. This insight is revolutionary. If confirmed, it will effectively destroy current concepts of radiation safety.

"Instability is also a “plausible mechanism” for explaining illnesses other than cancer, the report says. “It would seem likely that if genomic instability led to health effects these would not be specific but may include developmental deficiencies in the fetus, cancer, hereditary disease, accelerated aging and such nonspecific effects as loss of immune competence.” Epidemiology would be “powerless” to detect any relationship between the incidence of such diseases and exposure to radiation, the report says, because the number of people who would suffer any single disease would be too low. [Keith] Baverstock, who was the main organizer of the Helsinki workshop, and Wright believe that the world should be more wary of low-level radiation. If genomic instability is causing unpredicted disease, and if some people are genetically predisposed to it, the regulatory system starts to look inadequate. Existing measures meant to protect people, argue Wright and Baverstock, are less than reassuring" [3].

In response to these observations, people who support the reigning ICRP paradigm will argue that any illness induced by genomic instability will already be accounted for within existing safety limits. This position is untenable. It is based on the unfounded assumption that the frequency of all possible endpoints of radiation damage (not just cancer) are linearly related to dose and valid extrapolations about low internal doses of radiation can be made from high doses of radiation delivered exterior to the body. According to the model of radiation effects upheld by the nuclear establishment, cancer is the fundamental endpoint of concern following radiation exposure. Further, the frequency of cancer expressed in a population after exposure is directly related to the dose of radiation received by that population. In sharp contrast, as illustrated in the quotation above, radiation-induced genomic instability may produce “developmental deficiencies in the fetus, cancer, hereditary disease, accelerated aging and such nonspecific effects as loss of immune competence.” This hypothesis is revolutionary and in direct conflict with mainstream adherence to the belief that radiation damage to the human organism is confined to cancer. If this proves to be the case, it is totally without justification at this point in time to assume that these results are similarly in a linear relationship to dose and that current standards of safety protect the population from these endpoints. As has already been discussed, dosage is too imprecise a concept to account for radiation-induced changes on the cellular level from low levels of radiation. The number and rate of charged particles passing through the cell is a more fundamental phenomenon. This shift of perspective is essential for explaining newly discovered cellular effects of radiation.

The subject of depleted uranium will be explored in depth in subsequent chapters. But one observation is relevant at this point. Within the currently accepted framework for understanding radiation effects, battlefield dispersal of depleted uranium cannot possibly pose a radiological hazard. The “dose” of radiation is just too small. But in the light of current research, this point of view is no longer defensible. Two in vitro studies were recently conducted involving exposure of human osteoblast cells to depleted uranium. Both studies demonstrated that depleted uranium induces genomic instability in the progeny of cells receiving exposure. One study exposed cells to uranyl nitrate created from various isotopes of uranium and compared their toxic effects to cells exposed to the heavy metals nickel and tungsten [4]. Those cells exposed to DU evidenced an increased frequency of dicentric chromosomes — chromosomes with two centromeres — when compared to the nonradioactive metals. Further, the frequency of dicentric abnormalities was dependent on the specific radioactivity of the different isotopes. The conclusion was that it was alpha radiation emitted by uranium that induced the chromosomal aberrations. According to Miller and her colleagues, Published data from our laboratory have demonstrated that DU exposure in vitro to immortalized human osteoblast cells (HOS) is both neoplastically transforming and genotoxic.” A second study conducted by the same research team exposed osteoblast cells to gamma radiation and alpha radiation from depleted uranium and compared the effects to nickel exposure [5]. Cell lethality and micronuclei formation were measured at various times after exposure. (Micronuclei arise from DNA double-strand breaks that are not rejoined. These have been implicated in carcinogenesis.) It was found that DU stimulates delayed reproductive death and the production of micronuclei up to thirty-six days (thirty population doublings) after exposure. This is evidence of induced destabilization in the genome. In contrast, the cell populations exposed to gamma radiation returned to normal after a period of twelve days. Further, micronuclei formation from DU exposure occurred at a greater frequency than for equal doses delivered by gamma irradiation. The authors summarized their results as follows: “These studies demonstrate that DU exposure in vitro results in genomic instability manifested as delayed reproductive death and micronuclei formation.” Together these two studies demonstrate that the alpha radiation emitted from depleted uranium can damage DNA and that DU can induce instability to the genome that initiates abnormal growth in progeny cells. Only in political defiance of these observed phenomenon can propagandists continue to affirm that depleted uranium poses no radiological hazard.


[1] Kadhim M.A., Macdonald D.A., Goodhead D.T., Lorimore S.A., Marsden S.J., Wright E.G. Transmission of Chromosomal Instability after Plutonium Alpha-Particle Irradiation. Nature. 1992; 355:738-740.

[2] Edwards R. Radiation Roulette.

[3] Edwards R. WHO ‘Suppressed’ Scientific Study Into Depleted Uranium Cancer Fears in Iraq. Sunday Herald Online. February 22, 2004.

[4] New Scientist. No. 2103. October 11, 1997. pp. 36-40.

[5] Miller A.C., Xu J., Stewart M., Prasanna P.G.S., Page N. Potential Late Health Effects of Depleted Uranium and Tungsten Used in Armor-piercing Munitions: Comparison of Neoplastic Transformation and Genotoxicity with the Known Carcinogen Nickel. Military Medicine. 2002a; 167(Supplement 1):120-122.

[6] Miller A.C., Brooks K., Stewart M., Anderson B., Shi L., McClain D., Page N. Genomic Instability in Human Osteoblast Cells after Exposure to Depleted Uranium: Delayed Lethality and Micronuclei Formation. Journal of Environmental Radioactivity. 2003; 64:247-259.

Monday, March 15, 2010

The Trial of the Cult of Nuclearists: Exhibit D

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

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.


Gofman J.W. What Is Genomic Instability, and Why Is It So Important. San Francisco: Committee for Nuclear Responsibility; 1998.