By Dr. Theresa R. Pantanella, PhD, MPA, OT/L
Radiation hormesis (also called radiation homeostasis) is a theory surmising chronic low doses of ionizing radiation, combined with natural background radiation, is beneficial to one’s health by stimulating hypothetical reserve repair mechanisms on a cellular level. The reserve repair mechanisms are hypothesized to be sufficiently effective when stimulated as to not only cancel the detrimental effects of extra ionizing radiation but also protect from other damage.
We are all exposed to background radiation, the constant presence of cosmic rays from space, natural radiation from the Earth (in the form of radon gas) and objects that incorporate radiation into their structure, such as buildings and self-illuminating dials. Radiation hormesis theory does contend that exposure to large levels of ionizing radiation is harmful. It is directly opposed to the linear no-threshold (LNT) model of radiation exposure in relation to carcinogenic risk.
Some flaws do exist to the hormogenesis theory, including the requirement that the health-promoting cellular repair mechanisms are not activated in absence of additional, ongoing ionizing radiation.
The National Academies of Sciences, an institution formed by the US Congress in 1863 for the purpose of centralizing scientific efforts, has acknowledged studies that result in radiation hormesis, however, they caution it is not yet known if radiation hormesis occurs outside the laboratory, or in humans.
LNT contends that an accumulation of small doses equals the harmful effect of one large dose. It is easier to use for administration purposes, so the advocates of radiation hormesis are quick to point out it’s the only reason their theory is rejected by the scientific community.
Laboratory studies do prove the initiation of a variety of cellular repair mechanisms following exposure to ionizing radiation. This includes apoptosis and activation of enzymatic DNA repair. The doses are controlled, unlike what the experience would be in a nuclear fallout. And, the dosage can be repeated from additional exposure prior to the onset of the cellular repair mechanisms taking effect. For example, a study by Kensuka et al (2006) reported an increase in the gene expression of catalase and manganese superoxide, as well as an increase in the enzymatic activity of catalase equal to the gene expression to begin on day 23 after exposure to ionizing radiation.
Of value to this conversation is the difference between ionizing and non-ionizing radiation. Non-ionizing radiation does not break chemical bonds resulting in the formation of radioactive materials. Examples of this are microwaves, radio waves and infra-red waves.
Types of Radiation in the Electromagnetic Spectrum
http://en.wikipedia.org/wiki/Ionizing_radiation
Ionizing radiation DOES break chemical bonds, creating what is commonly called radiation or radioactive materials. There are three types of ionizing radiation. They are particulate (atomic or subatomic particles), waves (electromagnetic) and neutrons. Examples of this are x-rays and gamma rays.
http://www.who.int/ionizing_radiation/about/what_is_ir/en/index.html
Interesting, although the National Academy of Sciences acknowledges the confirmation of radiation hormogenesis in studies, its sister organization, the United States National Research Council does not accept the theory. Nor does the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR). They have published a statement as follows:
“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.”
In conclusion, 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.
Kensuke O, Takao K, Hiroshi T, Kazuo S. “Activation of Antioxidative Enzymes Induced by Low-Dose-Rate Whole‐Body γ Irradiation: Adaptive Response in Terms of Initial DNA Damage.” Radiation Research 2006. 166(3):474-478.
MORALES-RAMí¬REZ P, MENDIOLA-CRUZ MT. “Kinetics of the Early Adaptive Response to Gamma Rays: Induction of a Cellular Radioprotective Mechanism in Murine Leukocytes In vivo.” Bioscience Reports 2004. 24: 609–616.
Cao J, Wells RL, Elkind MM. “Enhanced sensitivity to neoplastic transformation by 137Cs gamma-rays of cells in the G2-/M-phase age interval.” Int J Radiat Biol. 1992 Aug;62(2):191-9.
Stewart GS, Maser RS, Stankovic T, Bressan BA, Kaplan MI, Jaspers NGJ, Raams A, Byrd PJ, Petrini JHJ, Taylor AMR. “The DNA Double-Strand Break Repair Gene
hMRE11 Is Mutated in Individuals
with an Ataxia-Telangiectasia-like Disorder”. Cell 1999, Vol. 99, 577–587.
Darby S, Hill D, Auvinen A, Barros-Dios JM, Baysson H, Bochcchio F, Deo H, Falk R, Forastiere F, Hakama H, Heid I, Kreienbrock L, Kreuzer M, Lagarde F, Makelainen I, Muirhead C, Oberaigner W, Pershagen G, Ruano-Ravina A, Ruosteenojo A, Schraffrath-Rosario A, Timarche M, Tomascaronek L, Whitley E, Wichmann H-E, Doll R. “Radon in homes and risk of lung cancer: collaborative analysis of individual data from 13 European case-control studies.” BMJ 2004. 330: 223.
http://en.wikipedia.org/wiki/Radiation_hormesis#cite_note-Stewart1-9
http://en.wikipedia.org/wiki/No_threshold
http://www.who.int/ionizing_radiation/about/what_is_ir/en/index.html
http://www.epa.gov/radiation/understand/ionize_nonionize.html
