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| year = 2009
| year = 2009
| url = http://www.mendeley.com/research/assessing-cancer-risks-of-lowdose-radiation/#page-1
| url = http://www.mendeley.com/research/assessing-cancer-risks-of-lowdose-radiation/#page-1
| pmid = 19629073}}</ref><ref name=Tubiana
| pmid = 19629073}}</ref><ref name=Tubiana>{{Cite journal| doi = 10.1148/radiol.2511080671
>{{Cite journal| doi = 10.1148/radiol.2511080671
| volume = 251
| volume = 251
| issue = 1
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| date = 2009-04
| date = 2009-04
| url = http://radiology.rsna.org/content/251/1/13.short| pmid = 19332842| pmc = 2663584
| url = http://radiology.rsna.org/content/251/1/13.short| pmid = 19332842| pmc = 2663584
}}</ref> While [[epidemiological]] studies on populations of people exposed to an acute dose of high level radiation such as [[Hibakusha|Japanese Atomic Bomb Survivors]] ({{nihongo|hibakusha|被爆者}}) have robustly upheld the [[linear no-threshold model|LNT]],<ref name=Samartzis>{{Cite journal| doi = 10.2106/JBJS.J.00256| pages = JBJS.J.00256| last = Samartzis| first = Dino| coauthors = Nobuo Nishi, Mikiko Hayashi, John Cologne, Harry M. Cullings, Kazunori Kodama, Edward F. Miles, Sachiyo Funamoto, Akihiko Suyama, Midori Soda, Fumiyoshi Kasagi| title = Exposure to Ionizing Radiation and Development of Bone Sarcoma: New Insights Based on Atomic-Bomb Survivors of Hiroshima and Nagasaki| journal = J Bone Joint Surg Am| accessdate = 2011-04-30| date = 2011-03-31| url = http://www.ejbjs.org/cgi/content/abstract/JBJS.J.00256v1}}</ref> studies involving low doses and low dose rates have failed to detect any increased cancer rate.<ref name="Tubiana"/> This is because the baseline cancer rate is already very high (causing 13% of all deaths in 2008) and it fluctuates wildly because of life style choices and viral disease,<ref>{{Cite web
}}</ref> While [[epidemiological]] studies on populations of people exposed to an acute dose of high level radiation such as [[Hibakusha|Japanese Atomic Bomb Survivors]] ({{nihongo|hibakusha|被爆者}}) have robustly upheld the [[linear no-threshold model|LNT]],<ref name=Samartzis>{{Cite journal| doi = 10.2106/JBJS.J.00256| pages = JBJS.J.00256| last = Samartzis| first = Dino| coauthors = Nobuo Nishi, Mikiko Hayashi, John Cologne, Harry M. Cullings, Kazunori Kodama, Edward F. Miles, Sachiyo Funamoto, Akihiko Suyama, Midori Soda, Fumiyoshi Kasagi| title = Exposure to Ionizing Radiation and Development of Bone Sarcoma: New Insights Based on Atomic-Bomb Survivors of Hiroshima and Nagasaki| journal = J Bone Joint Surg Am| accessdate = 2011-04-30| date = 2011-03-31| url = http://www.ejbjs.org/cgi/content/abstract/JBJS.J.00256v1}}</ref> studies involving low doses and low dose rates have failed to detect any increased cancer rate.<ref name="Tubiana"/> This is because the baseline cancer rate is already very high (causing 13% of all deaths in 2008) and it fluctuates 40% because of suboptimal life style choices and and environmental risk factors,<ref>{{Cite web
| title = WHO Cancer Fact sheet N°297
| title = WHO Cancer Fact sheet N°297
| accessdate = 2011-04-29
| accessdate = 2011-04-29
| url = http://www.who.int/mediacentre/factsheets/fs297/en/}}</ref><ref name=parkin2011>{{Cite journal
⚫
| url = http://www.who.int/mediacentre/factsheets/fs297/en/}}</ref> obscuring the subtle effects of low level radiation (an acute dose of 100 [[Sievert|mSv]] may cause a ~0.8% increase in cancer risk). In particular, variations in smoking prevalence or even patterns in reporting smoking cause wide variation in excess cancer and measurement error bias. Thus, even a large study of many thousands of subjects with imperfect smoking prevalence information will fail to detect the effects of low level radiation than a smaller study that properly compensates for smoking prevalence.<ref>{{cite journal
| issn = 0007-0920
| volume = 105
| issue = S2
| pages = S77-S81
| last = Parkin
| first = D M
| coauthors = L Boyd, L C Walker
| title = 16. The fraction of cancer attributable to lifestyle and environmental factors in the UK in 2010
| journal = Br J Cancer
| accessdate = 2011-12-08
| date = 2011-12-06
| url = http://dx.doi.org/10.1038/bjc.2011.489
}}</ref> obscuring the subtle effects of low level radiation (an acute dose of 100 [[Sievert|mSv]] may cause a ~0.8% increase in cancer risk).

⚫
In particular, variations in smoking prevalence or even patterns in reporting smoking cause wide variation in excess cancer and measurement error bias. Thus, even a large study of many thousands of subjects with imperfect smoking prevalence information will fail to detect the effects of low level radiation than a smaller study that properly compensates for smoking prevalence.<ref>{{cite journal
| last = Samet
| last = Samet
| first = Jonathan
| first = Jonathan

Revision as of 08:55, 8 December 2011

Alternative assumptions for the extrapolation of the cancer risk vs. radiation dose to low-dose levels, given a known risk at a high dose: supra-linearity (A), linear (B), linear-quadratic (C) and hormesis (D).

Radiation hormesis (also called radiation homeostasis) is the hypothesis that low doses of ionizing radiation (within the region and just above natural background levels) are beneficial, stimulating the activation of repair mechanisms that protect against disease, that are not activated in absence of ionizing radiation. The reserve repair mechanisms are hypothesized to be sufficiently effective when stimulated as to not only cancel the detrimental effects of ionizing radiation but also inhibit disease not related to radiation exposure (see hormesis).[1][2][3][4] This counter-intuitive hypothesis has captured the attention of scientists and public alike in recent years.[5]

Quoting results from a litterature database research, the Académie des Sciences — Académie nationale de Médecine (French Academy of Sciences — National Academy of Medicine) stated in their 2005 report concerning the effects of low-level radiation that many laboratory studies have observed radiation hormesis.[6][7] However, they cautioned that it is not yet known if radiation hormesis occurs outside the laboratory, or in humans.[8]

Consensus reports by the United States National Research Council and the National Council on Radiation Protection and Measurements and the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) argue that there is no evidence for hormesis in humans and in the case of the National Research Council, that hormesis is outright rejected as a possibility. Therefore, the Linear no-threshold model (LNT) continues to be the model generally used by regulatory agencies for human radiation exposure.

Proposed mechanism and ongoing debate

A very low dose of a chemical agent may trigger from an organism the opposite response to a very high dose.

Radiation hormesis proposes that radiation exposure comparable to and just above the natural background level of radiation is not harmful but beneficial, while accepting that much higher levels of radiation are hazardous. Proponents of radiation hormesis typically claim that radio-protective responses in cells and the immune system not only counter the harmful effects of radiation but additionally act to inhibit spontaneous cancer not related to radiation exposure. Radiation hormesis stands in stark contrast to the more generally accepted linear no-threshold model (LNT), which states that the radiation dose-risk relationship is linear across all doses, so that small doses are still damaging, albeit less so than higher ones. Opinion pieces on chemical and radiobiological hormesis appeared in the journals Nature[1] and Science[3] in 2003.

Assessing the risk of radiation at low doses (<100 mSv) and low dose rates (<0.1 mSv.min−1) is highly problematic and controversial.[9][10] While epidemiological studies on populations of people exposed to an acute dose of high level radiation such as Japanese Atomic Bomb Survivors (hibakusha (被爆者)) have robustly upheld the LNT,[11] studies involving low doses and low dose rates have failed to detect any increased cancer rate.[10] This is because the baseline cancer rate is already very high (causing 13% of all deaths in 2008) and it fluctuates 40% because of suboptimal life style choices and and environmental risk factors,[12][13] obscuring the subtle effects of low level radiation (an acute dose of 100 mSv may cause a ~0.8% increase in cancer risk).

In particular, variations in smoking prevalence or even patterns in reporting smoking cause wide variation in excess cancer and measurement error bias. Thus, even a large study of many thousands of subjects with imperfect smoking prevalence information will fail to detect the effects of low level radiation than a smaller study that properly compensates for smoking prevalence.[14] Given the absence of direct epidemiological evidence, there is considerable debate as to whether the dose-response relationship in the low dose regime is supralinear, linear (LNT), has a threshold or sub-linear i.e. a hormetic response.

While most major consensus reports and government bodies currently adhere to LNT,[15] the 2005 French Academy of Sciences-National Academy of Medicine's report concerning the effects of low-level radiation rejected LNT as a scientific model of carcinogenic risk for doses below 100 mSv.[8] They consider there to be several dose-effect relationships rather than only one, and that these relationships have many variables such as target tissue, radiation dose, dose rate and individual sensitivity factors. They request that further study is required on low doses (less than 100 mSv) and very low doses (less than 10 mSv) as well as the impact of tissue type and age. The Academy considers the LNT model is only useful for regulatory purposes as it simplifies the administrative task. Quoting results from literature research,[7][6] they furthermore claim that approximately 40% of laboratory studies on cell cultures and animals indicate some degree of chemical or radiobiological hormesis, and state:

"...its existence in the laboratory is beyond question and its mechanism of action appears well understood."

They go on to outline a growing body of research that illustrates that the human body is not a passive accumulator of radiation damage but it actively repairs the damage caused via a number of different processes, including:[8][10]

Furthermore, increased sensitivity to radiation induced cancer in the inherited condition Ataxia-telangiectasia like disorder, illustrates the damaging effects of loss of the repair gene Mre11h resulting in the inability to fix DNA double-strand breaks.[16]

However, as the BEIR-VII report points out, "the presence of a true dose threshold demands totally error-free DNA damage response and repair." The specific damage they worry about is double strand breaks (DSBs) and they continue, "error-prone nonhomologous end joining (NHEJ) repair in postirradiation cellular response, argues strongly against a DNA repair-mediated low-dose threshold for cancer initiation".[17]

Radon gas in homes is the largest source of radiation dose for most individuals and it is generally advised that the concentration be kept below 150 Bq/m³ (4 pCi/L).[18] A recent retrospective case-control study of lung cancer risk showed substantial cancer rate reduction between 50 and 123 Bq per cubic meter relative to a group at zero to 25 Bq per cubic meter.[19] This study is cited as evidence for hormesis, but a single study all by itself cannot be regarded as definitive. Other studies into the effects of domestic radon exposure have not reported a hormetic effect; including for example the respected "Iowa Radon Lung Cancer Study" of Field et al. (2000), which also used sophisticated radon exposure dosimetry.[20] In addition, Darby et al. (2005) argue that radon exposure is negatively correlated with the tendency to smoke and environmental studies need to accurately control for this; people living in urban areas where smoking rates are higher usually have lower levels of radon exposure due the increased prevalence of multi-story dwellings.[21] When doing so, they found a significant increase in lung cancer amongst smokers exposed to radon at doses as low as 100 to 199 Bq m−3 and warned that smoking greatly increases the risk posed by radon exposure i.e. reducing the prevalence of smoking would decrease deaths caused by radon.[21][22]

Furthermore, particle microbeam studies show that passage of even a single alpha particle (e.g. from radon and its progeny) through cell nuclei is highly mutagenic,[23] and that alpha radiation may have a higher mutagenic effect at low doses (even if a small fraction of cells are hit by alpha particles) than predicted by linear no-threshold model, a phenomena attributed to bystander effect.[24] However, there is currently insufficient evidence at hand to suggest that the bystander effect promotes carcinogenesis at low doses.[25]

Given the uncertain effects of low-level radiation, there is a pressing need for good quality research in this area. An expert panel convened at the 2006 Ultra-Low-Level Radiation Effects Summit at Carlsbad, New Mexico, proposed the construction of an Ultra-Low-Level Radiation laboratory.[26] The laboratory, if built, will investigate the effects of almost no radiation on laboratory animals and cell cultures, and it will compare these groups to control groups exposed to natural radiation levels. The expert panel believes that the Ultra-Low-Level Radiation laboratory is the only experiment that can explore with authority and confidence the effects of low-level radiation; that it can confirm or discard the various radiobiological effects proposed at low radiation levels e.g. LNT, threshold and radiation hormesis.

Statements by leading nuclear bodies

Radiation hormesis has not been accepted by either the United States National Research Council,[27] or the National Council on Radiation Protection and Measurements.[28] In addition, the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) wrote in its most recent report:[29]

Until the [...] uncertainties on low-dose response are resolved, the Committee believes that an increase in the risk of tumour induction proportionate to the radiation dose is consistent with developing knowledge and that it remains, accordingly, the most scientifically defensible approximation of low-dose response. However, a strictly linear dose response should not be expected in all circumstances.

This is a reference to the fact that very low doses of radiation have only marginal impacts on individual health outcomes. It is therefore difficult to detect the 'signal' of decreased or increased morbidity and mortality due to low-level radiation exposure in the 'noise' of other effects. The notion of radiation hormesis has been rejected by the National Research Council's (part of the National Academy of Sciences) 16 year long study on the Biological Effects of Ionizing Radiation. "The scientific research base shows that there is no threshold of exposure below which low levels of ionizing radiation can be demonstrated to be harmless or beneficial. The health risks – particularly the development of solid cancers in organs – rise proportionally with exposure" says Richard R. Monson, associate dean for professional education and professor of epidemiology, Harvard School of Public Health, Boston.[30][31]

The possibility that low doses of radiation may have beneficial effects (a phenomenon often referred to as “hormesis”) has been the subject of considerable debate. Evidence for hormetic effects was reviewed, with emphasis on material published since the 1990 BEIR V study on the health effects of exposure to low levels of ionizing radiation. Although examples of apparent stimulatory or protective effects can be found in cellular and animal biology, the preponderance of available experimental information does not support the contention that low levels of ionizing radiation have a beneficial effect. The mechanism of any such possible effect remains obscure. At this time, the assumption that any stimulatory hormetic effects from low doses of ionizing radiation will have a significant health benefit to humans that exceeds potential detrimental effects from radiation exposure at the same dose is unwarranted.[31]

Studies of low level radiation

Cultures

Studies in cell cultures can be useful for finding mechanisms for biological processes, but they can be criticized for not effectively capturing the whole of the living organism.

A study by E.I. Azzam suggested that pre-exposure to radiation causes cells to turn on protection mechanisms.[32] A different study by de Toledo and collaborators, has shown that irradiation with gamma rays increases the concentration of glutathione, an antioxidant found in cells.[33]

Animals

A study by Otsuka and collaborators find hormesis in whole animals.[34] Miyachi conducted a study on mice and found that a 200 mGy X-ray dose protects mice against both further X-ray exposure and ozone gas.[35] In another rodent study, Sakai and collaborators found that (1 mGy/hr) gamma irradiation prevents the development of cancer (induced by chemical means, injection of methylcholanthrene).[36]

In a 2006 paper,[37] a dose of 1 Gy was delivered to the cells (at constant rate from a radioactive source) over a series of lengths of time. These were between 8.77 and 87.7 hours, the abstract states for a dose delivered over 35 hours or more (low dose rate) no transformation of the cells occurred. Also for the 1 Gy dose delivered over 8.77 to 18.3 hours that the biological effect (neoplastic transformation) was about 1.5 times smaller than that which that had been observed using a single high dose rate of X-ray photons of similar energy. Likewise it has been reported that fractionation of gamma irradiation reduces the likelihood of a neoplastic transformation.[38] Pre-exposure to fast neutrons and gamma rays from Cs-137 is reported to increase the ability of a second dose to induce a neoplastic transformation.[39]

However, caution must be used in interpreting these results, as it noted in the BEIR VII report, these pre-doses can also increase cancer risk:

In chronic low-dose experiments with dogs (75 mGy/d for the duration of life), vital hematopoietic progenitors showed increased radioresistance along with renewed proliferative capacity (Seed and Kaspar 1992). Under the same conditions, a subset of animals showed an increased repair capacity as judged by the unscheduled DNA synthesis assay (Seed and Meyers 1993). Although one might interpret these observations as an adaptive effect at the cellular level, the exposed animal population experienced a high incidence of myeloid leukemia and related myeloproliferative disorders. The authors concluded that “the acquisition of radioresistance and associated repair functions under the strong selective and mutagenic pressure of chronic radiation is tied temporally and causally to leukemogenic transformation by the radiation exposure” (Seed and Kaspar 1992).[31]

Humans

2004 Taiwan cobalt-contaminated steel

In popular treatments of radiation hormesis, a study of the inhabitants of apartment buildings in Taiwan has received prominent attention. The building materials had been accidentally contaminated with Cobalt-60 but the study found cancer mortality rates more than 20 times lower than in the population as a whole.[40] However, this study compared the relatively young irradiated population with the much older general population of Taiwan, which is a major flaw. A subsequent study by Hwang et al. (2006) found a significant exposure-dependent increase in cancer in the irradiated population, particularly leukemia in men and thyroid cancer in women, though this trend is only detected amongst those who were first exposed before the age of 30. This study also found that rate of total cancer cases was lower than expected:[41].

Besides the excess risks of breast cancer and leukemia, a later publication recalls the observations of various cytogenetic anomalies and health effects among this population:[42]

There have been several reports concerning the radiation effects on the exposed population, including cytogenetic analysis that showed increased micronucleus frequencies in peripheral lymphocytes in the exposed population, increases in acentromeric and single or multiple centromeric cytogenetic damages, and higher frequencies of chromosomal translocations, rings and dicentrics. Other analyses have shown persistent depression of peripheral leucocytes and neutrophils, increased eosinophils, altered distributions of lymphocyte subpopulations, increased frequencies of lens opacities, delays in physical development among exposed children, increased risk of thyroid abnormalities, and late consequences in hematopoietic adaptation in children.

See also

References

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  34. ^ Kensuke Otsuka, Takao Koana, Hiroshi Tauchi and Kazuo Sakai (2006). "Activation of Antioxidative Enzymes Induced by Low-Dose-Rate Whole-Body γ Irradiation: Adaptive Response in Terms of Initial DNA Damage". Radiation Research. 166 (3): 474–478. doi:10.1667/RR0561.1. PMID 16953665.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  35. ^ Y Miyachi (2000). "Acute mild hypothermia caused by a low dose of X-irradiation induces a protective effect against mid-lethal doses of X-rays, and a low level concentration of ozone may act as a radiomimetic". The British Journal of Radiology. 73 (867): 298–304. PMID 10817047.
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External links

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