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RSH
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1999 > Hiroshi Tanooka 1999 |
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PROGRAM
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Ionizing radiation has been known to cause
cancer. Its carcinogenic effect is sometimes over-emphasized. How far down to the low dose
region does radiation still have a potential to cause cancer? This is a difficult
question. To estimate the cancer risk of low level radiation, it has been sometimes
assumed that the data obtained at a high dose region can be linearly extrapolated to the
low dose region. By this estimate, even a small dose of radiation can cause a significant
number of cancers if a large number of people is involved. This, however, is a
hypothetical calculation, not reality. In reality, what is the actual cancer risk from a
small dose of radiation? This is the main theme of this symposium. To tell the conclusion
first, the relation between radiation dose and cancer incidence varies depending upon the
manner of exposure to radiation. If radiation is given at a low dose rate, the
carcinogenic effect is decreased. The mechanism to explain this dose-rate effect is
currently being elucidated and includes the higher efficiency of DNA repair and apoptosis
to exclude molecular damage and injured cells operating at the lower dose-rate. 1. Human cases In proportion to radiation dose, damage to biological molecules is increased. However, the amount of damage is not necessarily proportional to the frequency of cancer. Table 1 shows various conditions of human exposure to radiation. The case of a single acute exposure is seen in A- bomb survivors. In this case, the first cancer to appear among various cancers with a relatively high frequency is leukemia, and for this reason it is the largest concern in considering the cancer risk of radiation. Its dose-response seems to approach the linear relation at high doses, but under 0.4 Gy no significant increase is recognized in Nagasaki cases where gamma rays are the major component.
ICRP recommendations are made on the assumption of the linear dose-response even at low doses. However, this is hypothesis, not reality. ICRP recommendations have been immediately incorporated into the nation's law in Japan and Sweden; however, the United States, Britain, and France have their own views on a radiation protection policy. Leaving unsolved the low dose problems in A-bomb survivors might make it difficult to estimate the cancer risk of radiation in the human environment directly from A-bomb data. The extreme case in contrast to the A-bomb case is dial painters who received continuous radiation from internally deposited radium. No bone-cancer dose extends close to 10 Gy of cumulative local dose and then with the increasing doses the cancer incidence rises sharply in a threshold manner (Rowland et al.). This indicates that when radiation is given in a protracted manner and when radiation is given to a part of the body as opposed to the whole, the cancer risk is much lower than in the case of acute whole body exposure. In areas in China with a high (3 -fold) natural radiation background and in India (10-fold), residents so far exhibit no recognizable increase of cancer mortality. It should not be forgotten that humans receive not only natural radiation, but also constantly undergo a considerably large amount of oxidative DNA damage which possesses a structure identical to the radiation-induced base damage. 2. Animal experimental data Animal experiments can be designed with accurate dosimetry. However, since animal experiments often employ sensitive strains to detect cancers more easily, care should be taken in extrapolating animal data to humans. Various types of dose-response relations for tumor induction have been reported depending on the animal system. Repeated beta-irradiation at 0.5 Gy per exposure on the backs of mice 3 times weekly do not result in mice that develop tumors, while with higher doses the tumor incidence increases to 100% in a threshold manner (Fig. 1). Such a threshold response is also obtained when rats are orally given tritiated water at various concentrations (Yamamoto et al.). Moreover, rats which inhaled radon at various concentrations exhibit a decreased lung cancer incidence at low concentrations with the same total dose (Monchaux et al.). It is important that high LET radiation has a dose-rate effect in its carcinogenic effect. The use of the unit Sv for radiation protection purposes may have to be revised, since it involves RBE, which was assumed to be independent of dose-rate.
3. Molecular mechanism of threshold dose-response of cancer induction DNA repair has been known to operate more efficiently when cells are irradiated at a low dose and low dose-rate than at a high dose and high dose-rate. Secondly, apoptosis which eliminates injured cells from the tissue operates more efficiently at a low dose and low dose-rate. Furthermore, the adaptive response and inducible-immunological activity are thought to contribute to the threshold response. Conclusion The risk of cancer from ionizing radiation is not necessarily proportional to the radiation dose given. A certain small amount of damage can be eliminated completely. When the tissue receives radiation at a low dose-rate, it can tolerate a considerably high dose. The key molecular mechanisms are DNA repair and apoptosis, efficiently operating at a low dose and low dose-rate.
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The
Seventh International Conference on Nuclear Engineering April 21, 1999 |
RSH > Documents > Tokyo 1999 >
Hiroshi Tanooka 1999
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