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[cdn-nucl-l] Research Shows Beneficial Effects of Low Doses of Radiation
I thought you might to read the article that just appeared in the CNS
newsletter, C-NEWS, Issue 2, Spring 2003.
Research Shows Beneficial Effects of Low Doses of Radiation
By Jerry Cuttler
Summary of the Work
Ron Mitchel, Senior Scientist in the Radiation Biology and Health Physics
Branch at Chalk River Laboratories, and three co-workers have just published
an outstanding paper in the journal Radiation Research.* It presents
convincing evidence that a single radiation dose of 10 or 100 milli-Gray**
(mGy) (1 or 10 rad) cobalt-60 gamma rays to cancer-prone,
radiation-sensitive young (~50 day) mice delays cancer death substantially.
The dose of 10 or 100 mGy is approximately 4 or 40 times the average natural
radiation dose in a year, but it was delivered at 0.5 mGy per minute.
The research employed genetically modified Trp53+/- mice whose cells lack
the cancer-fighting gene Trp53 in one of their two chromosomes. Such mice
get cancer in middle age instead of old age, as would happen in normal mice
(Trp53+/+ ones). Not only are Trp53+/- mice cancer prone, they are also
radiation sensitive. Such mice do model cancer-prone and
radiation-sensitive people who would be part of a workforce.
Normal mice have a mean life span of 578 ± 138 days (1.6 ± 0.4 y). Exposure
to the large dose of 4 Gy (400 rad) at a high dose rate results in a life
span loss of 125 days or 22% of their normal life. In comparison, Trp53+/-
mice with a life span of 375 ± 103 days (1.0 y), when exposed to 4 Gy, have
their life reduced by 148 days or 40%. So Trp53+/- mice are therefore more
sensitive than normal mice to a high dose.
Radiation in low doses does not significantly affect the normal life span of
these radiation-sensitive, cancer-prone mice; however, the effect on cancer
latency (the time between spontaneous initiation and progress to malignant
tumors, which cause death due to cancer) is important. Trp53+/- mice
spontaneously develop a variety of cancer types. Two types that provide a
good measure of latency are bone cancer in the spine (indicated by the onset
of paralysis) and lymphomas (leading rapidly to death). The research
demonstrated that the radiation exposures had little effect on tumor
frequency, indicating no effect on tumor initiation. The 10-mGy exposure
reduced the risk of both cancer types by increasing latency (by up to ~120
days for spine cancer); i.e., it reduced the rate at which spontaneously
initiated cells progressed to malignancy. The effect of this adaptive
response persisted for the entire life span of all the animals that
developed these tumors. Exposure to 100 mGy delayed lymphoma latency longer
than the 10-mGy dose, however, the 100-mGy dose increased spinal cancer risk
by decreasing latency compared to unexposed control mice. The higher dose
is in the transition zone between reduced and increased risk; the dose at
which the transition occurs varies with tumor type.
The Importance of This Work
Hormesis is an adaptive response of living organisms to low levels of
chemical, biological or radiological stress or damage - a modest
overcompensation to a disruption - resulting in improved fitness.
Observations of this reproducible phenomenon (low-dose stimulation and
high-dose inhibition) have been widely reported in the scientific biomedical
literature since the 1880s and form the basis for all immunology treatment.
Despite the growing body of evidence for adaptive response to low-level
radiation, epidemiological (population) studies are generally inconclusive.
The reason given is that the dose-response is lost against the "noise" of
background cancer incidence. Public and occupational health policies, which
rely on such studies, therefore revert to the Linear-No-Threshold (LNT)
hypothesis. Unfortunately, interpretation of the LNT hypothesis, that it
implies proof of a negative health effect at any level of radiation
exposure, has contributed societal radiophobia and anti-nuclear propaganda.
This Chalk River paper reports on quality research carried out on
radiation-sensitive animals, and demonstrates that a low dose of radiation,
while neither increasing the average life span nor reducing the frequency of
tumor initiation in the sample population, did provide protection against
spontaneous cancer by delaying death due to cancer. This and other related
research suggest the need to reconsider the conventional "ever lower is
better" criterion for low-dose radiation limits in favour of criteria which
consider the beneficial effects of radiation at low-dose levels. Such a
policy shift would also enable the possible use of low-dose radiation
therapy in many important medical applications.
* Mitchel RE, Jackson JS, Morrison DP, Carlisle SM. Low Doses of Radiation
Increase the Latency of Spontaneous Lymphomas and Spinal Osteosarcomas in
Cancer-Prone, Radiation-Sensitive Trp53 Heterozygous Mice, Radiat Res
159(3):320-7, 2003 March
** One Gray is one joule of radiation energy per kilogram of animal mass.