"...its existence in the laboratory is beyond question and its mechanism of action appears well understood."lt;/blockquote> They go on to outline the growing body of research that illustrates that the human body is not a passive accumulator of Ionizing radiation damage but it actively repairs the damage caused via a number of different processes, including: * Mechanisms that mitigate reactive oxygen species generated by ionizing radiation and oxidative stress * Apoptosis of radiation damaged cells that may undergo tumorigenesis is initiated at only few mSv. * Cell death during meiosis of radiation damaged cells that were unsuccessfully repaired. * The existence of a cellular signaling system that alerts neighboring cells of cellular damage. * The activation of Enzyme DNA repair mechanisms around 10 mSv. * Modern DNA microarray studies which show that numerous genes are activated at Ionizing radiation doses well below the level that mutagenesis is detected. * Ionizing radiation induced tumorigenesis may have a threshold related to damage density, as revealed by experiments that employ blocking grids to thinly distribute Ionizing radiation * A large increase in tumours in immunosuppressed individuals illustrates that the immune system efficiently destroys aberrant cells and nascent tumors. * Increased sensitivity to radiation induced tumourgenesis in the rare inherited condition taxia-telangiectasia#Differential_diagnosis illustrates the damaging effects of loss of the DNA repair gene HMre11 (with Nibrin & RAD50 (gene) .lt;/ref> Image:New radiation symbol ISO 21482.svg 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 and the 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".BEIR VII, page 245 Most epidemiological studies on populations of people have upheld linear no-threshold model without noting a contradiction, these studies reject radiation hormesis. Epidemiological studies at the lowest levels of radiation are very difficult to interpret because of confounding factors. For example, smoking rates (or even patterns in reporting smoking) cause huge problems in estimating excess cancer rates in observational studies. In addition, measurement error biases estimates towards zero so that a study of a hundred of thousand contaminated with less than perfect smoking information can be less powerful at identifying an effect of radiation hormesis than a clean study of under a thousand.citing 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/m^3 (4 pCi/L).lt;/ref> 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.lt;/ref> 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 studies In addition, Darby et al. argue that radon exposure is negatively correlated with the tenancy to smoke, so environmental studies need to accurately control for this. When doing so they found a significant increase in lung cancer for those with doses as low as 100 to 199 Bq m⁻³.lt;/ref> Furthermore, particle microbeam studies show that passage of even a single alpha particle (specifically such as that from radon and radon progeny) through cell nucleus is highly mutagenic, and that alpha radiation may have higher mutagenic effect at low doses (when only a small fraction of cells are directly hit by alpha particles) than predicted by linear no-threshold model fitted to higher doses (when most cells are hit), which is attributed to bystander effect (radiobiology) saturation at higher doses.lt;/ref> Given the uncertain effects of low-level radiation, there is a pressing need for good quality research in this area."Ultra-Low-Level Radiation Effects Summit." January 2006. ORION International Technologies, Inc. (ORION) and sponsored by the U.S. Department of Energy’s Waste Isolation Pilot Plant (WIPP) 03 Apr. 2008. http://www.orionint.com/projects/ullre.cfm] 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 The laboratory, if built, will investigate the effects of almost no radiationon laboratory animals and cell culture , and it will compare these groups to control group 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. Linear no-threshold model threshold and radiation hormesis.

Statements by leading nuclear bodies

Radiation hormesis has not been accepted by either the United States National Research Council lt;ref>http://books.nap.edu/catalog/11340.html Health Risks from Exposure to Low Levels of Ionizing Radiation: BEIR VII Phase 2, or the National Council on Radiation Protection and Measurements http://www.ncrppublications.org/index.cfm?fmProduct.AddToCart&pid6714063164 NCRP Report No. 136 — Evaluation of the Linear-Nonthreshold Dose-Response Model for Ionizing Radiation] In addition, the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) wrote in its most recent report: UNSCEAR 2000 REPORT Vol. II: Sources and Effects of Ionizing Radiation: http://www.unscear.org/docs/reports/annexg.pdf Annex G: Biological effects at low radiation doses]. page 160, paragraph 541.

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 Councils (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.lt;/ref>lt;/ref>

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.

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.lt;/ref> 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.lt;/ref>

Animals

A study by Otsuka and collaborators find hormesis in whole animals.lt;/ref> 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.lt;/ref> In another rodent study, Sakai and collaborators found that (1 mGy hr-1) gamma irradiation prevents the development of cancer (induced by chemical means, injection of methylcholanthrene . In a 2006 paper,lt;/ref> 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.lt;/ref> 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.lt;/ref> 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).

=== 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 96.4% lower than in the population as a whole.{{cite journal| author= Chen W.L., Luan Y.C., Shieh M.C., et al.| title=Is Chronic Radiation an Effective Prophylaxis Against Cancer? |journal= J Am Phys Surg |volume=9(1)|pages=6–10|year=2004}} [http://www.jpands.org/vol9no1/chen.pdf (pdf file)] 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 t 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.{{Cite journal | doi = 10.1080/09553000601085980 | volume = 82 | issue = 12 | pages = 849–58 | last = Hwang | first = S-L | coauthors = H-R Guo, W-A Hsieh, J-S Hwang, S-D Lee, J-L Tang, C-C Chen, T-C Chang, J-D Wang, W P Chang | title = Cancer risks in a population with prolonged low dose-rate gamma-radiation exposure in radiocontaminated buildings, 1983-2002 | journal = International Journal of Radiation Biology | accessdate = 2008-12-13 | date = 2006-12 | url = http://www.informaworld.com/smpp/content~db=all?content=10.1080/09553000601085980 | pmid = 17178625 }} ==See also== * [[Hormesis]] * [[Dose fractionation]] * [[Linear no-threshold model]] * [[Petkau effect]] * [[Radioresistance]] ==References== {{Reflist|2}} ==External links== *[http://www.dose-response.org/ International Dose-Response Society]. University of Massachusetts center for research on hormesis. Many papers on radiation hormesis. *[http://books.nap.edu/catalog/11340.html?onpi_newsdoc062905 Health Risks from Exposure to Low Levels of Ionizing Radiation: BEIR VII Phase 2] *[http://www.radpro.com/641luckey.pdf Radiation Hormesis Overview] by T. D. Luckey, who wrote a book on the subject (Luckey, T. D. (1991). adiation Hormesis. Boca Raton, FL: CRC Press. ISBN 0-8493-6159-1) * [http://www.pnas.org/content/100/24/13761.full Cancer risks attributable to low doses of ionizing radiation: Assessing what we really know], Proceedings of the National Academy of Sciences of the USA. {{Radiation}} {{DEFAULTSORT:Radiation Hormesis}} [[Category:Radiobiology]] [[Category:Radiation health effects]] [[pl:Hormeza radiacyjna]] [[ru:Гормезис]]

---

System.IndexOutOfRangeException: Index was outside the bounds of the array. at _Default.parseWiki(String inContent)

---

at _Default.parseWiki(String inContent)