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

Thursday, September 2, 2010

The Trial of the Cult of Nuclearists: SCAM NUMBER THIRTY

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 THIRTY: Use current theories of cancer etiology as a multistage process to deny that exposure to low doses of radiation is hazardous.

In 1927, Hermann Muller published his research on x-ray induced mutations in populations of male fruit flies. In the course of his investigations, Muller observed that the frequency of mutations was directly proportional to the dose, and that no-threshold dose existed for the onset of genetic damage. With decreasing dosages, the frequency of mutations decreased, but they did not entirely cease to occur. No dose, however small, was found to be 100% risk-free for genetic damage. This discovery was the historical foundation for what later developed into the Linear No-Threshold Hypothesis for cancer induction. The rudiments of this hypothesis and its implications for the standards of radiation safety first appeared in Publication 1 of the ICRP in 1958. Further articulation of the hypothesis appeared in ICRP publications in 1962 and 1965. In 1991, for the purpose of radiation protection, the ICRP officially endorsed the LNT Hypothesis.

A vocal opposition has always questioned the validity of the LNT Hypothesis. Gunnar Walinder made the following observation in an article that ended with the remark, “the LNT hypothesis is one of the greatest scientific scandals of our time.” As he went on to say:

However, there were many people who were reluctant to accept the new idea of the LNT. Rolf Sievert found it difficult to reduce complex biological phenomena such as heredity and cancer to a straight line. He simply did not believe in stochastic, biological effects and his arguments were very similar to those later expressed by Lauriston Taylor. The same opposition could also be found among the oncologists at Radiumhemmet in Stockholm, of whom the perhaps most eloquent spokesman was Dr. Lars-Gunnar Larsson. They claimed that the drawing of straight lines has nothing to do with biology and such methods could never constitute a model of a biological process and, least of all, the complex kind of dysdifferentiation that we call cancer” [1].

Walinder continues with an interesting observation about the shortcomings of a linear mathematical model for cancer rates within populations.

The basic doctrine in the radiation protection is expressed (after low doses and dose-rates) by the simple formula: N = 0.05 x D where N is the number of radiogenic cancer cases and D is the collective dose (expressed in manSv). This formula is considered valid for all populations and independent of living habits and other factors that normally are considered of significance for tumor formation. Advocates of this equation cannot possibly have any knowledge of the generic category of disparate diseases which we have given the common name cancer. Nor can they have any idea about the epistemological prerequisites for using mathematical models. As a physicist, I have, of course, always applied mathematics to my problems. However this mathematics has to be adjusted to the specific task. To me, it is impossible to understand how one and the same formula can be used as a collective model for all disparate forms of cancer. How should we explain the fact that various forms of cancer have different dose-response relationships and that some tumors cannot, on the whole, be induced by ionizing radiation (for example, such common forms as the uterine cancer and those in the prostate). How can anyone believe that such extremely complex processes as the general carcinogenesis can be adequately described by an equation of the first degree? This model obviously does not fulfill any demands for consistence or generality. The formula is not only generally considered valid, it is also said to be applicable at “homeopathic” radiation doses. What an unbelievable pretension to knowledge: “We know everything and we are able to give quantitative figures of infinitesimally small radiation risks.” It reminds me of Moliere's comedies. Could we not hope that, in a reasonably short future, such pretensions of knowledge will give rise to the same roar of laughter as is the case with the precious figures in Moliere's comedies? In no other scientific field have such deeply unscientific claims been made.”

Today, the steps leading from radiation-induced genetic alteration to the expression of cancer in the organism are mired in controversy. Many researchers believe that the popular idea of a single cell being transformed into a malignant state in one step is overly simplistic. Evidence has accumulated that the initiation of cancer is most likely a multistage process. As the ECRR notes: “As a result of examining the variation of cancer rates with age, cancer is now believed to be the result of up to six separate genetic changes. These include acquisition of specific oncogenes and loss of tumor suppressor genes.” The onset of uncontrolled cell proliferation is further impeded by a number of biological defense mechanisms that intercede at an early stage to repair radiation damage or prevent an altered cell from reproducing. These defense mechanisms include such things as immune system removal of cells with persistent DNA alterations, enzymatic reactions, apoptosis (suicidal elimination of altered cells), activation of tumor suppressor genes, cell cycle regulation, and various intercellular interactions. On the basis of this repair capacity and the complex, multistage process of cancer etiology, many researchers advocate that radiation protection standards need not be as stringent as they are today. They hypothesize that the human organism can tolerate greater levels of exposure than permitted today without undergoing ill effects. The body has a generous capacity for eliminating the effects of low-dose radiation before such effects induce cancer.

The conclusion of this line of reasoning is succinctly stated by Walinder:

“Modern oncology has also clearly shown that the transformation of a cell into a malignant phenotype is a multistep process that demands several changes in different parts of the genome. All these changes cannot be caused by a low radiation dose. Thus, here too, the malignant contribution of the radiation is dependent on the presence or future emergence of other, necessary genetic effects.”

The complexity of cancer etiology is becoming an increasingly popular theme of nuclear apologists intent on loosening standards for radiation protection. However, those who advocate that low levels of radiation cannot possibly induce cancer and that regulation of low levels of exposure is unnecessary fail to see that their argument is deeply flawed and reckless. With cancer being a multistage process, it is reasonable to assume that some unknown percentage of a population carries within its cells precancerous genetic alterations from any number of environmental or hereditary sources. In these people, exposure to even low levels of radiation may be sufficient to induce that final genetic mutation necessary to ignite a malignant proliferation of cells. Even with cancer understood as a complex, multistage process, low-level radiation, being a mutagen, must be considered hazardous. The ECRR makes this point perfectly clear:

“The outcome of radiation exposure in the exposed individual follows the effects of somatic damage to cells. In the case of cancer as an outcome, there is seen both an immediate effect and a delayed effect. This pattern of risk with time is a consequence of the multistage etiology of cancer. Cancer is now believed to result from the accumulation of genetic damage in cells or their descendants. The particular pattern of incidence of cancer with age is most easily explained by assuming that a geometric increase in the number of a damaged cell clone ultimately results in a high enough probability that one of the cell descendants will acquire a second or subsequent necessary genetic mutation for cancer to develop in that cell (or group of cells). It follows that an exposure episode may either cause initial genetic damage in cells which have none or add to genetic damage which is already present. For those cells which have already acquired the initial set of genetic damage, the exposure may produce the final requirement for cancer. For undamaged cells the episode will supply the initial damage and start the process [emphasis added]".

In summarizing the current theory of the etiology of cancer, Lars Persson of the Swedish Radiation Protection Institute makes the same point:

“Neoplastic initiation encompasses the irreversible cellular damage, which provides the potential in cells for neoplastic development. There is good evidence that this initiation process results from damage to DNA leading to gene or chromosomal mutations in single cells in tissues. The critical event in relation to ionizing radiation is likely to be DNA double-strand breaks for which error-free repair is not likely at any dose.


Once the necessary gene mutation is present in a cell, further neoplastic development is believed to be highly dependent upon the cellular environment. Promotional events, influenced by growth factors in cells, dietary constituents, hormones, or other environment agents, may increase cell proliferation and may, in some instances, interfere with communication processes between cells that act to maintain cellular stability in tissues.

Conversion of these pre-neoplastic cells to a form in which they are committed to be malignant is believed to be driven by further gene mutations.

Progression of the disease, once the potential for a malignancy has been established, may depend upon further cellular changes that allow for the invasion of adjacent normal tissues, the circulation of neoplastic cells in the blood and lymphatic systems and the establishment of metastases at other sites in the body.

Radiation-induced mutations may influence all stages of the neoplastic process. Consequently, at the level of DNA damage, there is no basis for assuming that there is a dose threshold below which the risk of tumor induction is zero” [2].

The bottom line is that radiation, at any level of exposure, poses a hazard to the health of some portion of the population. Arguments that try to deny this fact are ill-conceived and politically motivated. Low-level radiation can be responsible for initiating the first step of a multistage process or for tripping precancerous cells into the final stage where malignancy commences. This is a plausible mechanism for explaining elevated incidences of cancer among populations exposed to low levels of radiation released from nuclear installations. Our theories of cancer may change, but they cannot repudiate the capacity of ionizing radiation to structurally alter DNA, and thus, be a mechanism in the process of carcinogenesis.


[1] Walinder G., Ahlquist J. About the Validity of the LNT Hypothesis. Health Physics Society Newsletter. January 2002.

[2] Persson L. Effects of Low-Dose Ionising Radiation. Swedish Radiation Protection Institute. SE-17111 Stockholm, Sweden.