Evidence For Radiation Hormesis Research Articles

Evidence of a Dose Threshold for Radiation-Induced Leukemia.

In 1958, Neil Wald presented data on the incidence of leukemia among the Hiroshima atomic bomb survivors. These data, which suggested a dose–response threshold for radiation-induced leukemia, were included in the first UNSCEAR report (1958). However, this evidence of a threshold was not recognized. It was obfuscated and concealed. In 2010, Zbigniew Jaworowski identified these data as evidence of radiation hormesis. A letter to the editor in 2014 and 2 articles in 2014 and 2015 presented a graph of these UNSCEAR 1958 data, which revealed a threshold at about 500 mSv. Since the blood-forming stem cells of bone marrow are more radiosensitive than most other cell types, it is reasonable to expect thresholds for inducing other types of cancer by ionizing radiation—their thresholds are likely higher than 500 mSv. A careful examination of the Wald data reveals the suprisingly low incidence of radiogenic leukemia, only 0.5% of the survivors who were in the high radiation zone. Many articles on radiation risk have been published since 2015 by other authors, but none makes reference to this evidence of a threshold, either to challenge or endorse it. In this commentary, the author addresses the comments from a colleague.

Are We Approaching the End of the Linear No-Threshold Era?

The linear no-threshold (LNT) model for radiation-induced cancer was adopted by national and international advisory bodies in the 1950s and has guided radiation protection policies worldwide since then. The resulting strict regulations have increased the compliance costs for the various uses of radiation, including nuclear medicine. The concerns about low levels of radiation due to the absence of a threshold have also resulted in adverse consequences. Justification of the LNT model was based on the concept that low levels of radiation increase mutations and that increased mutations imply increased cancers. This concept may not be valid. Low-dose radiation boosts defenses such as antioxidants and DNA repair enzymes. The boosted defenses would reduce the endogenous DNA damage that would have occurred in the subsequent period, and so the result would be reduced DNA damage and mutations. Whereas mutations are necessary for causing cancer, they are not sufficient since the immune system eliminates cancer cells or keeps them under control. The immune system plays an extremely important role in preventing cancer, as indicated by the substantially increased cancer risk in immune-suppressed patients. Hence, since low-dose radiation enhances the immune system, it would reduce cancers, resulting in a phenomenon known as radiation hormesis. There is considerable evidence for radiation hormesis and against the LNT model, including studies of atomic bomb survivors, background radiation, environmental radiation, cancer patients, medical radiation, and occupational exposures. Though Commentary 27 published by the National Council on Radiation Protection and Measurements concluded that recent epidemiologic studies broadly support the LNT model, a critical examination of the studies has shown that they do not. Another deficiency of Commentary 27 is that it did not consider the vast available evidence for radiation hormesis. Other advisory body reports that have supported the LNT model have similar deficiencies. Advisory bodies are urged to critically evaluate the evidence supporting both sides and arrive at an objective conclusion on the validity of the LNT model. Considering the strength of the evidence against the LNT model and the weakness of the evidence for it, the present analysis indicates that advisory bodies would be compelled to reject the LNT model. Hence, we may be approaching the end of the LNT model era.

Molecular evidence of radiation hormesis at occupational exposure

The idea of favourable effects of low dose ionising radiation in biological systems has existed for many years and is the basis of radiation hormesis hypothesis. New evidence at subcellular levels might contribute to further clarify this problem. We used molecular epidemiological biomarkers (DNA/protein changes in peripheral blood; immunological changes in lymphocytes) in occupationally-exposed individuals (400 Nuclear Power Plant (NPP) workers). Two levels of investigations were studied: molecular (spontaneous and induced DNA repair by unscheduled DNA synthesis, induced protein synthesis, DNA damage) and cellular (lymphocyte subsets, immunofluorescent-stained mouse monoclonal antibodies). Potentially lethal damage is decreased in persons with mean annual dose ≤5 mSv. The highest repair capacity (after 2 Gy γ-rays) was also evaluated. Significant decreases of CD3+4+, CD4+25+, CD4+62L+ lymphocytes and CD4/CD8 ratio were observed at <200 mSv. Simultaneously, increased natural killer cells, CD57+8+, CD8+28+ and CD8+38 were recorded. Our study showed DNA repair capacity elevation following high dose irradiation and increased cellular resistance at annual doses twice lower than natural radiation background. We postulated that the positive dose correlation with CD4+25+ and CD57+8+ as well as the negative one with CD4+62L+, CD8+28+ and CD8+38+ could reflect adaptive processes and compensatory activated immune system due to the low dose irradiation.

Evidence for radiation hormesis after in vitro exposure of human lymphocytes to low doses of ionizing radiation.

Previous research has demonstrated that adding a very small gamma-ray dose to a small alpha radiation dose can completely suppress lung cancer induction by alpha radiation (a gamma-ray hormetic effect). Here we investigated the possibility of gamma-ray hormesis during low-dose neutron irradiation, since a small contribution to the total radiation dose from neutrons involves gamma rays. Using binucleated cells with micronuclei (micronucleated cells) among in vitro monoenergetic-neutron-irradiated human lymphocytes as a measure of residual damage, we investigated the influence of the small gamma-ray contribution to the dose on suppressing residual damage. We used residual damage data from previous experiments that involved neutrons with five different energies (0.22-, 0.44-, 1.5-, 5.9-, and 13.7-million electron volts [MeV]). Corresponding gamma-ray contributions to the dose were approximately 1%, 1%, 2%, 6%, and 6%, respectively. Total absorbed radiation doses were 0, 10, 50, and 100 mGy for each neutron source. We demonstrate for the first time a protective effect (reduced residual damage) of the small gamma-ray contribution to the neutron dose. Using similar data for exposure to gamma rays only, we also demonstrate a protective effect of 10 mGy (but not 50 or 100 mGy) related to reducing the frequency of micronucleated cells to below the spontaneous level.

Low-dose irradiation therapy to cure gas gangrene infections

Infection with clostridium bacteria, which live in the soil, is most often associated with war wounds, car accidents, complicated abortions, etc. The incidence is highest in areas with poor access to proper wound care. Such infections lead to gas gangrene, a deadly disease that spreads very quickly in the body and causes rapid death. Present-day treatment consists of administering antibiotics and surgical removal of dead, damaged and infected tissue. Amputation is usually necessary to control the spread of the infection, which, once established, generally advances at the rate of six inches per hour. From the late 1920s until the early 1940s, this disease was treated successfully with low doses, approximately 50 rad, of radiation (X-rays) in the area of infection. A review of 364 cases treated in this manner, from 1928 until 1940, indicated that patient mortality would be reduced from 50% (or higher) to ∼5% if patients were treated before severe progression of the disease and with the correct technique. X-ray therapy stopped the infection without the need for amputation to control its spread. Low-dose irradiation (LDI) therapy, given immediately, acted as a prophylaxis to prevent the onset of gas gangrene. This is but one example of the extensive use of radiation treatment of many types of infections, before the advent of antibiotics. Low doses are not adequate to kill invading bacteria directly; but, they will increase the activity of a patient's damage-control biosystem to destroy the infection. The observed beneficial effects are consistent with the large amount of scientific evidence of radiation hormesis – the stimulation by low doses of radiation of an organism's own defences (to destroy invaders and heal wounds). In view of the ineffectiveness of antibiotics in many cases and the evolution of antibiotic-resistant strains of bacteria, current use of LDI therapy is needed. Many patients would benefit greatly.

The risk of leukemia from low doses of low-LET radiation

In this communication, we examine the evidence (if any) for a nonlinear dose response in relation to leukemia mortality in the Japanese A-bomb population. Specifically, we seek an estimate of the probability that, at low doses of radiation, the relative risk (RR) is smaller than one. Using Bayesian bootstrap techniques, we find that there is a 90% probability that—for at least one dose group at or below 200 mSv—there is a reduction of effect relative to the control group. We take this as evidence for radiation hormesis (end point: leukemia mortality) at low doses of radiation.