It is well known that induction of low or intermittent levels of repairable damage in cells and tissues is a good thing. It triggers more aggressive cellular maintenance for some period of time, and the end result is a net gain in the quality of the cellular environment: fewer damaged proteins and structures left to cause secondary issues. This effect is known as hormesis, and most common forms of molecular damage and stress to cells can trigger it. Exercise and calorie restriction produce hormetic effects, for example, as does exposure to heat and to most toxins at suitably low doses. Of interest for today is the hormesis produced by exposure to low levels of ionizing radiation, a process that has been studied in insects and to a lesser degree in short-lived mammals.
The next step after research involving short-lived mammals is to run studies in longer-lived mammals. The cost of such studies increases dramatically with species life span, which is why the history of any particular subject in the life sciences starts with worms and flies, works up to mice, and only then reaches dogs, pigs, and primates before clinical translation to human medicine. At each stage, compelling results are needed to raise the funding for the next and more expensive set of work. The large amount of data on various methods of modestly slowing aging in this range of species has made it quite clear that a given method becomes dramatically less effective in species of longer life spans. Calorie restriction can add 40% to the life span of mice, but certainly doesn’t do that in humans. Life span in our species is much less plastic in response to environmental circumstances and genetic alterations known to impact health and longevity than is the case in flies, worms, and mice.
In the paper noted below, researchers reassess the effects of radiation hormesis in a comparatively short-lived breed of dogs, in both younger and older individuals. The data they use was originally generated in the late 1980s. They claim a gain of remaining life expectancy of 15% or so in older dogs, and 50% or so in younger dogs. The size of the study is not enormous, so I’d certainly like to see that result replicated. The outcome is unexpectedly, even suspiciously large for a hormesis effect in a mammalian species of this life span.
The authors state that the original studies controlled well for confounding variables, but given that they ran in the 1980s, I think it quite plausible that those researchers did not adequately control for calorie restriction effects. This is a major issue with many of the life span studies conducted prior to the turn of the century, and even a sizable fraction of those carried out later. I looked through one of the referenced documents that discussed the experimental protocols, and didn’t find any mention of diet there. So I don’t think that this paper means we should all be getting low-intensity ionizing radiation sources for our bedrooms – the evidence would have to be far more extensive and bulletproof to start making that sort of suggestion. Taken together with the other animal evidence, however, it does indicate that the present zero tolerance approach to radiation exposure is probably mistaken.
The overall effects of ionizing radiation on organisms are well known at high doses. At high and low doses, the detailed cell response mechanisms are complicated and may involve all levels of biological organization. About 75% of the human body is water, and a principal effect of radiation is the creation of reactive oxygen species (ROS), including hydrogen peroxide. They are a double-edged sword. Depending on their concentrations, they may cause damage or signaling in terms of stress responses. Studies on experimental living systems and on humans have shown, depending on the individual genome, that low doses of radiation upregulate many biological protective mechanisms, which also operate against nonradiogenic toxins and produce beneficial effects, including a lower risk of cancer.
For more than a century, extensive studies have been carried out on the effects of radiation, which demonstrate that harmful effects, such as radiation illness, may arise after exposures above known threshold dose levels, whereas a range of beneficial effects may be observed following low-dose exposures. Although there appears to be an awareness among the prominent leaders of the radiation protection establishment that current radiation protection policy contradicts this biological evidence; there is a very broad consensus among them that it is impossible to attribute health effects to low radiation exposures, namely to exposures similar to the wide spectrum of background levels. This opinion does not consider the recent progress in biological research on the mechanisms that underlay the fact that living organisms are “complex adaptive systems.”
When people increasingly question whether low levels or low doses of radiation are really harmful, protection practitioners argue that “radiation-sensitive individuals” exist who are more vulnerable than average people to potential “health effects” and must be protected. This concern about protecting sensitive individuals and the suggestion that longevity may be the most appropriate measure of the effect of radiation on health led to this examination of the effect of dose rate on the lifespans of dogs. The authors reexamined data on the health effects of long-term irradiations in two large-scale studies on groups of beagle dogs. One exposed the dogs to whole-body cobalt-60 γ-radiation. The other evaluated dogs whose lungs were exposed to α-particle radiation from plutonium. Each group of dogs received a different dose rate.
These studies had been reviewed previously to determine the dependence of the lifespan of 50% mortality dogs on dose rate. The lifespans of dogs at 5%, 10%, and 50% mortality in the control group (background dose rate) were compared with the lifespans of the 5%, 10%, and 50% mortality dogs in each dose rate group. Analysis of the data of the first study suggested an increase in the lifespan of dogs exposed to 50 mGy of γ-radiation per year, compared to the control dogs. Analysis of the data of the second study suggested an increase in longevity for dogs with an initial plutonium lung burden of 0.1 kBq/kg, compared to the control dogs. These are very credible studies, carefully carried out by qualified and experienced scientists who bred the dogs and controlled all confounding factors. Interpolations of the study data suggest that the optimum dose rate for longevity is about 50 mGy per year for all mortality levels. The lifespan increase is about 15% for 50% mortality dogs and much greater for the more radiation-sensitive dogs. The shorter lived control dogs (5% mortality level) have a lifespan of about 3000 days, whereas the dogs in the group with an initial plutonium lung burden of 0.16 kBq/kg have a lifespan of about 4500 days, 50% longer.
If dogs model humans, then one should expect that radiation-sensitive individuals would benefit more from exposures to low-level radiation than average humans. So protecting sensitive people from low-dose γ- or α-radiation would be inappropriate because it would deprive them of the health benefit of a longer life. The results of this review suggest the need to change radiation protection policy. Obviously, maintaining exposures as low as reasonably achievable is very likely detrimental.