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How much exposure to radiation affects the body, and in what ways?

　The Life Span Study (LSS), a longitudinal study of 100,000 radiation victims of the Hiroshima and Nagasaki bombings, examined the long-term effects of large doses of radiation exposure. This study and others have looked at gruesome historical events and nuclear accidents to uncover more about the epidemiological aspects of radiation exposure. Exposure to a few Gray (Gy), a measure of radiation dosage, causes deterministic effects (hair loss and infertility) commensurate to the amount of exposure. 7Gy of instantaneous exposure is enough to cause death. Exposure to over 100mGy has also been shown to linearly increase the risk of death from cancer.

　At the same time, we are exposed to low dosages of natural radiation over the course of our daily lives. For example, in Japan, average radiation exposure in a year is calculated at 2.11mSv (see notes). Seen globally, there are many examples of other regions where, for geological reasons, there are several orders of magnitude more radiation exposure than in Japan, yet people are healthy there.

Note: if we assume that all exposure is from gamma rays, 2.11mSv is equivalent to 2.11mGy. However, natural radiation also includes alpha radiation and other sources, so the amount of Gy is likely differ from 2.11mSv.

Our bodies come equipped with the ability to repair radiation damage.

　Let us consider the effects of radiation at the molecular and cellular scale in the body (See Figure 1). When radiation reaches the body, the various components making up the body are subject to the strong energy released. In particular, DNA chains are the most susceptible to damage from radiation. DNA chains contain a wealth of information crucial to genetics and health. If subject to radiation (see notes) and damaged, DNA chains have the inherent ability to repair damage from small amounts of radiation. In the event that DNA sustains considerable damage, cell death (apoptosis, necrosis) occurs, and the damaged cells are eliminated and replaced with new ones. Thanks to this system, we are able to lead healthy lives, protected from the natural radiation all around us. However, when radiation exposure exceeds that which this system can sustain (going beyond the body’s natural limit), a range of physical symptoms like those pictured in Figure 2 occur.

Note: Radiation is not the only cause of damage to DNA chains. Other causes of damage to DNA are chemicals, ultraviolet rays, metabolic products in the body, and replication errors caused when the body reproduces cellular material.

Figure 1: Radiation effects seen at cellular scale

Figure 2: What effects does the body sustain from radiation exposure?

To what extent is the body capable of repairing radiation damage?

So, to what extent is the body able to self-repair damage from radiation exposure? If one continued living in an environment in which one was subject to several hundreds more times the natural level of radiation, what would be the physical effect on the human body?

　If humanity goes on to evolve in space colonies in the future, this information will be something critical to be aware of. (See notes)

Note: according to JAXA public relations materials, the radiation to which Japanese astronauts have been exposed at the International Space Station (ISS) is approximately 1mSv per day. This is equivalent to half a year of exposure on Earth in Japan.

　Yet no answer to reconcile this seemingly contrasting data has been found in the LSS. Moreover, it would be out of the question to perform radiation experiments on humans in order to resolve this. To circumvent this, animal testing is used. Thus far, fruit flies, mice, and other animals have been used in radiation exposure tests to determine the impact.

　One historically famous animal test was the ORNL Mouse-Genetics Program conducted by William L. Russell et al at Oak Ridge National Laboratory (ORNL) in the late 1900s in the United States. In this study, they spent several years examining the genetic effects of radiation on a population of several tens of thousands of mice (subjecting male mice to radiation and measuring the effects on their children). (See notes) There have been no similar large-scale surveys past or present.

Note: Details of the experiment can be found in The Mouse House: A brief history of the ORNL mouse-genetics program, 1947-2009 (Mutation Research 753, 69-90 (2013)), a review written by Liane B. Russell, Russell’s wife and co-researcher.

Russell et al conducted tests in which male mice were exposed to gamma and X-rays. They found that the greater the cumulative amount of exposure, the greater the frequency of mutations (the rate at which children with some genetic changes were born). This is a phenomenon that has been confirmed in numerous other animal tests since then. In the experiment, Russell et al compared the effects of acute exposure to radiation (long-term exposure of 700mGy per minute in male mice) to mild exposure (long-term exposure of 7mGy per minute in male mice). They found that, while the frequency of mutations in male mice increased commensurate with the cumulative exposure, the rate was much less pronounced in the mild exposure population than in the acute population, a world-first discovery. This phenomenon is today known as the “dose rate effect.” The body’s ability to repair damage from radiation relates to the dose rate effect.

　In addition to animal testing, there have been several tests involving irradiating human cell cultures. These experiments have led to a range of findings being accumulated that demonstrate the dose rate effect. Today, there is research ongoing around the world in order to clarify the mechanisms behind it.

　International standards and Japanese law do not take into effect the dose rate effect as a measure of the body’s ability to repair damage from exposure.

　As mentioned above, a vast amount of research involving animal and cell testing has been undertaken over the years in order to elucidate the effects of radiation exposure. In spite of scientists having made considerable effort to elucidate the dose rate effect, international standards and Japanese laws do not take into effect. (See notes)。

Note: international bodies like the International Council on Radiation Protection stipulate a dose- and rose-rate-effectiveness factor (DDREF), but there remains as yet insufficient scientific grounds for how this coefficient is defined and calculated. Furthermore, the ICRP does not recommend the use of this coefficient for radiation protection purposes.

　International standards and regulation postulate that a probabilistic effect (cancer, leukemia, and genetic effects) exists no matter how small the dosage, with the impact increasing commensurate with the level of exposure. This is given as the LNT (linear non-threshold) hypothesis. In effect, in research into the risk of cancer in the Hiroshima and Nagasaki bombing victim populations, and in numerous experimental results concerning generational (genetic) effects on animals, the effects linearly increase commensurate with the amount of exposure. In other words, the LNT hypothesis appears plausible at first glance. However, exposure conditions in this data correspond to a high volume of dosage far in excess of the body’s natural healing ability. That is to say, the LNT hypothesis was sufficient because the amount of exposure was so vast that the dose rate effect was irrelevant.

　The LNT hypothesis is a meaningful approach in terms of thoroughly protecting people from the negative effects of radiation. International standards and legal regulations appear to adhere to the LNT hypothesis for these reasons. However, from the vantage point of scientists, it remains unclear whether the LNT hypothesis is in fact an accurate reflection of scientific facts.

　The LNT hypothesis fails to account for the fact that people living under natural radiation exposure remain unaffected. It does not account for why those in regions with high rates of radiation exposure, or those on space flights, do not suffer ill effects.

　Following the TEPCO Fukushima Dai-ichi nuclear reactor incident in the wake of the Great East Japan Earthquake, we have visited the disaster-stricken areas many times. We were often asked by those evacuated to temporary housing and residents of towns scheduled for return what the acceptable hourly μSv (microsievert) dosage is. If we follow the LNT hypothesis, even a small amount of exposure is hazardous. Yet the realities of low dosage exposure remain unelucidated, so there was no suitable answer for residents. We as scientists do not have a concrete answer as to how this applies in cases of 100mGy (100mSv) or less. In addition, the LNT model does not allow for using the dose rate effect to arrive at a concrete number. Wanting to at least highlight what is demonstrable by modern science, the focus on visits to regions with high exposure to natural radiation has thus far been on discussions with residents and on explaining the body’s ability to heal. We regretted our inability to provide a substantive figure that could clearly be used to indicate exactly what hourly μSv is acceptable, so we undertook to build a new model.

The WAM Model explained

　Following the nuclear incident, several theoretical physicists undertook a new challenge. This is a new attempt to construct a mathematical model of the effects of radiation exposure that fully incorporates the dose rate effect discovered from a wide range of animal testing results. The outcome of this venture is the WAM model (whac-a-mole model, whack-a-mole model), pictured in Figure 3.
　The foremost feature of this model is that it does not look at cumulative radiation exposure (total dose), but rather the dose rate. It thus allows for estimating what symptoms or genetic effects occur with the passage of time.

Figure 3: Formulae and basic concepts implicated in the WAM model, which incorporates the dose rate effect

Values arrived at using this model bear a striking resemblance to the genetic data obtained by Russell et al in animal tests, as well as other studies. Further, the model now allows us to express how mice do not see a marked increase in ill effects when exposed to continuous low dosages, such as from natural background radiation. This offers possibilities not possible with prevailing models like LNT.
　A video comparing the WAM model and LNT model in a review of the genetic effects in mice can be found below.

A wide range of doctors, biologists, information scientists, and other experts from diverse fields are joining these theoretical physicists in conducting a variety of research. We intend to continue pursuing a proven mathematical model that is reflective of scientific truths.

　(Article by: Yunoichi Tsunoyama)

WAM Model simulator usage precautions

The default parameter values used for the WAMSIM genetic effect evaluative version are calculated based on experimental results from mice. These data can be used to review radiation experiments and estimates in mice, but would require further review as to their applicability to humans.

WAM Model research team

Past research results pertaining to the WAM model:

Please refer to the site Low Dosage Radiation Research Society, managed by Dr. Yuichiro Manabe (Osaka University).
---- But sorry, only japanese website is now available. English version is under construction.
https://www.rcnp.osaka-u.ac.jp/~manabe/project.html

*Each simulator site also contains relevant sources pertaining to that simulator.

Please direct inquiries to the address below:
E-mail: tsunoyama.yuichi.5s@kyoto-u.ac.jp