Radiation hormesis
From Wikipedia, the free encyclopedia
| It has been suggested that this article or section be merged with Radiation homeostasis. (Discuss) |
Radiation hormesis is the controversial hypothesis that chronic low doses of ionizing radiation (at the level of natural background radiation) stimulates repair mechanisms that protect against disease.[1][2][3][4]
The Académie des Sciences - Académie nationale de Médecine (French Academy of Sciences - National Academy of Medicine) in their 2005 report concerning the effects of low level radiation, acknowledged that 40% of laboratory studies have observed radiation hormesis.[5][6] However, they cautioned that it is not yet known if radiation hormesis occurs outside the laboratory, in humans.[7]
Additionally, the other major 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) have all upheld the Linear no-threshold model (LNT) (that radiation is dangerous no mater how low the exposure) and discounted the existence of radiation hormesis in humans.
Contents |
[edit] Non Acceptance of Radiation Hormesis
Radiation hormesis has been rejected by both the United States National Research Council (part of the National Academy of Sciences)[8] and the National Council on Radiation Protection and Measurements (a body commissioned by the United States Congress).[9] In addition, the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) wrote in its most recent report:[10]
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 [7]. See the National Academies Press book Health Risks from Exposure to Low Levels of Ionizing Radiation: BEIR VII Phase 2.
- 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 [8].
- 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) [9]. See also Hormesis under "Non-acceptance".
[edit] Ongoing Debate
| The neutrality of this article is disputed. Please see the discussion on the talk page.(March 2008) Please do not remove this message until the dispute is resolved. |
Radiation Hormesis is the controversial hypothesis that low level radiation has negative risk; that ionizing radiation at levels that occur in the natural environment may increase health by stimulating natural defense mechanisms. Radiation hormesis accepts that radiation above natural background levels has positive risk; that intense artificial radiation, for example, is toxic. The subject of radiation hormesis has captured the attention of scientists and public alike in recent years, perhaps because of its counter-intuitive properties. Opinion pieces on chemical and radiobiological hormesis appeared in the journals Nature[1] and Science[3] in 2003.
While most major studies have upheld the Linear no-threshold model (LNT) and rejected the existence of radiation hormesis in humans, according to the 2005 French Academy of Science-National Academy of Medicine's report concerning the effects of low level radiation (only they rejected LNT), 40% of laboratory studies on cell cultures and animals have observed radiobiological hormesis - "its existence in the laboratory is beyond question and its mechanism of action appears well understood."[7] However, they cautioned that it is not yet known based on laboratory studies if radiation hormesis occurs in humans.[7]
In their 2005 report, the French Academy of Sciences-National Academy of Medicine acknowledged the 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 number of different processes, including:[7]
- Mechanisms that mitigate reactive oxygen species generated by ionising 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 activation of enzymatic DNA repair mechanisms c. 10 mSv.
- The existence of a cellular signaling system that alerts neighboring cells of cellular damage.
- Modern DNA microarray studies which show that numerous genes are activated at radiation doses well below the level that mutagenesis is detected.
- Radiation induced tumorigenesis may have a threshold related to damage density, as revealed by experiments that employ blocking grids to thinly distribute radiation.
- A large increase in tumours in immunosuppressed individuals illustrates that the immune system efficiently destroys aberrant cells and nascent tumours.
Examples of studies that observed radioadaptive and hormetic effects include experiments on cells[11][12][13][14][15][16], in animals[5][6][17][18] and tests on individual humans.[19][20]
Another question is the effect of prolonged exposure to low level radiation on populations of people. Most epidemiological studies have upheld LNT and by default reject radiation hormesis, but epidemiological studies are very difficult do carry out due to compounding factors. For example, a town may have a lower cancer rate, not because of slightly elevated background radiation but because it has more new houses with young families who have a lower cancer rate. The few epidemiological studies that appear to refute LNT and suggest radiation hormesis include, most notably:
- Bernard Cohen's 1995 study of lung cancer rates vs. average radon concentration in homes for 1,601 U.S. counties, that questioned the validity LNT.[21]
- Thompson et al. (2008) 7 year long case-controlled study of residential radon exposure in Worcester County, Massachusetts, that found an apparent 60% reduction in lung cancer risk amongst people exposed to low levels (0-150 Bq/m3) of radon gas; levels typically encountered in 90% of American homes.[22]
Significantly, both studies reportedly found a very similar exposure/risk relationship curve that appears to match the predictions of radiation hormesis.[23] Donald Nelson, co-author of Thompson et al. (2008), indicated that the hormetic effect was detected because of the studies application of improved radon exposure dosimetry.[24] However, a single study cannot be regarded as definitive unless later studies using the same methods of Thompson et al. (2008) reproduce the same results.[24] Additionally, all other studies into the effects of domestic radon exposure have failed to detect 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.[25]
Given the uncertain effects of low level radiation, there is a pressing need for quality research in this area.[26] 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.[27] 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.[28] 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.
Cadmium poisoning is cited as a similar model. It is known that many toxic metals can induce oxidative stress in tissue which may result in free radical-induced damage. Also it is known that prior exposure to a small dose of cadmium can mitigate the effects of a second larger dose, this suggests that the first lower dose of the poison stimulates the DNA repair processes in the exposed tissue. [29][30][31][32]
[edit] See also
[edit] External links
- " Radiation and Risk: A Hard Look at the Data" by M.E. Schillaci of Los Alamos National Laboratory - A non-academic magazine article that discusses the hazards of radiation and radiological protection schemes.
- Health Risks from Exposure to Low Levels of Ionizing Radiation: BEIR VII Phase 2
- Abstract of a study showing that radiation increases the rate of natural antioxidant (glutathione) production. The study found that this does not act as a radiation protection, but seems to protect against other cellular insults such as oxidation.
- History of the idea by a supporter of the concept.
- Radiation Hormesis Overview by T. D. Luckey, who wrote a book on the subject (Luckey, T. D. (1991). Radiation Hormesis. Boca Raton, FL: CRC Press. ISBN 0-8493-6159-1)
- Radiation Hormesis: Demonstrated, Deconstructed, Denied, Dismissed, and Some Implications for Public Policy by Joel M. Kauffman: "evidence is presented that chronic doses up to 100 times those of normal ambient (including medical) exposures are beneficial..."
- Exposure To Low Levels Of Radon Appears To Reduce The Risk Of Lung Cancer From Sciencedaily.com
- News release from the Worcester Polytechnic Institute describing the study of Thompson et al. (2008) that found low levels of radon gas appears to reduce the risk of Lung Cancer.
[edit] References
- ^ a b Calabrese, Edward J; Linda A Baldwin (2003-02-13). "Toxicology rethinks its central belief". Nature 421 (6924): 691-692. doi:. ISSN 0028-0836.
- ^ Feinendegen, L.E. (2005). "Evidence for beneficial low level radiation effects and radiation hormesis". British Journal of Radiology 78: 3-7. doi:.
- ^ a b Kaiser, Jocelyn (2003-10-17). "HORMESIS: Sipping From a Poisoned Chalice". Science 302 (5644): 376-379. doi:.
- ^ Wolff, S. (1998-02). "The adaptive response in radiobiology: evolving insights and implications". Environmental Health Perspectives 106 (1): 277–283.
- ^ a b Calabrese, Edward J. (2004-06-01). "Hormesis: from marginalization to mainstream: A case for hormesis as the default dose-response model in risk assessment". Toxicology and Applied Pharmacology 197 (2): 125-136. doi:.
- ^ a b Duport, P. (2003-09-11). "A database of cancer induction by low-dose radiation in mammals: overview and initial observations" 1 (11): 120-131. doi:.
- ^ a b c d Aurengo et al. (2005-30-03). "Dose-effect relationships and estimation of the carcinogenic effects of low doses of ionizing radiation.". . Académie des Sciences & Académie nationale de Médecine Retrieved on 2008-03-27.
- ^ http://books.nap.edu/catalog/11340.html Health Risks from Exposure to Low Levels of Ionizing Radiation: BEIR VII Phase 2
- ^ NCRP Store - Add Product to Cart
- ^ UNSCEAR 2000 REPORT Vol. II: Sources and Effects of Ionizing Radiation: Annex G: Biological effects at low radiation doses. page 160, paragraph 541. Available online at [1].
- ^ Azzam, E.I.; G.P. Raaphorst, R.E.J. Mitchel (1994). "Radiation-Induced Adaptive Response for Protection against Micronucleus Formation and Neoplastic Transformation in C3H 10T1/2 Mouse Embryo Cells.". Radiation Research 138 (1): S28-S31.
- ^ Azzam, E.I.; S.M. de Toledo, G.P. Raaphorst, R.E.J. Mitchel (1996.). "Low-Dose Ionizing Radiation Decreases the Frequency of Neoplastic Transformation to a Level below the Spontaneous Rate in C3H 10T1/2 Cells.". Radiation Research 146 (4): 369-373. doi:.
- ^ Ko, S J; X-Y Liao, S Molloi, E Elmore, J L Redpath (2004-12). "Neoplastic transformation in vitro after exposure to low doses of mammographic-energy X rays: quantitative and mechanistic aspects". Radiation research 162 (6): 646-54. ISSN 00337587.
- ^ Stoilov, LM; LHF Mullenders, F Darroudi, AT Natarajan (2007-03-01). "Adaptive response to DNA and chromosomal damage induced by X-rays in human blood lymphocytes". Mutagenesis 22 (2): 117-122. doi:.
- ^ Wolff, S; R Jostes, F T Cross, T E Hui, V Afzal, J K Wiencke (1991). "Adaptive response of human lymphocytes for the repair of radon-induced chromosomal damage". Mutation research 250 (1-2): 299-306. ISSN 00275107.
- ^ Wolff, S.; V. Afzal, R F Jostes, J K Wiencke (1993-10). "Indications of repair of radon-induced chromosome damage in human lymphocytes: an adaptive response induced by low doses of X-rays.". Environmental Health Perspectives 101 (3): 73-77.
- ^ Miyachi, Y (2000-03-01). "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". British Journal of Radiology 73 (867): 298-304.
- ^ Pathak, Chander Mohan; Pramod Kumar Avti, Surender Kumar, Krishan Lal Khanduja, Suresh Chander Sharma (2007-03). "Whole body exposure to low-dose gamma radiation promotes kidney antioxidant status in Balb/c mice". Journal of radiation research 48 (2): 113-20. ISSN 04493060.
- ^ Ghiassi-Nejad, M.; M.M. Beitollahi, N. Fallahian, M. Saghirzadeh (2005-02). "New findings in the very high natural radiation area of Ramsar, Iran". International Congress Series 1276: 13-16. doi:.
- ^ Durante, M.; G. Snigiryova, E. Akaeva, A. Bogomazova, S. Druzhinin, B. Fedorenko, O. Greco, N. Novitskaya, A. Rubanovich, V. Shevchenko, U. Von Recklinghausen, G. Obe (2003). "Chromosome aberration dosimetry in cosmonauts after single or multiple space flights". Cytogenetic and Genome Research 103 (1-2): 40-6. ISSN 1424859.
- ^ Cohen, B L (1995-02). "Test of the linear-no threshold theory of radiation carcinogenesis for inhaled radon decay products". Health physics 68 (2): 157-74. ISSN 00179078.
- ^ Thompson, Richard E; Donald F Nelson, Joel H Popkin, Zenaida Popkin (2008-03). "Case-control study of lung cancer risk from residential radon exposure in Worcester county, Massachusetts". Health physics 94 (3): 228-41. ISSN 00179078.
- ^ Raabe, Otto G. Radon hormesis suggested by a careful case-controlled study [2] Retrieved on 2008-03-30
- ^ a b Physorg. Exposure to low levels of radon appears to reduce the risk of lung cancer, new study finds. [3] Retrieved on 2008-03-30
- ^ Field, R. William; Daniel J. Steck, Brian J. Smith, Christine P. Brus, Eileen L. Fisher, John S. Neuberger, Charles E. Platz, Robert A. Robinson, Robert F. Woolson, Charles F. Lynch (2000-06-01). "Residential Radon Gas Exposure and Lung Cancer: The Iowa Radon Lung Cancer Study". Am. J. Epidemiol. 151 (11): 1091-1102. studies
- ^ "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. [4]
- ^ "Ultra-Low-Level Radiation Effects Summit Report." 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. [5]
- ^ "Ultra-Low-Level Radiation Effects Summit - Report Summary." 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. [6]
- ^ Wahba, Z. Z.; Hernandez, L.; Issaq, H. J.; Waalkes, M. P. (1990): Involvement of sulfhydryl metabolism in tolerance to cadmium in testicular cells. Toxicology and Applied Pharmacology, 104:157-166.
- ^ Waalkes, M. P.; Perantoni, A. (1986): Isolation of a novel metal-binding protein from rat testes: characterization and distinction from metallothionein. Journal of Biological Chemistry, 261:13079-13103.
- ^ Waalkes, M. P.; Rehm, S.; Riggs, C.W.; et al. (1988): Cadmium carcinogenesis in male Wistar (Crl:(WI)BR) rats: dose-response analysis of tumor induction in the prostate and testes, and at the injection site. Cancer Research, 48:4656-4663.
- ^ Rugstad, H. E.; Norseth, T. (1975): Cadmium resistance and content of cadmium-binding protein in cultured human cells. Nature, 257:136-137.

