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      Effects of radioactive caesium on bull testes after the Fukushima nuclear plant accident

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          Abstract

          We aimed to investigate the effect of chronic radiation exposure associated with the Fukushima Daiichi Nuclear Plant accident on the testis from 2 bulls. Estimated dose of internal exposure in one bull was 0.7–1.2 mGy ( 134Cs) and 0.4–0.6 mGy ( 137Cs) and external exposure was 2.0 mGy ( 134Cs) and 0.8 mGy ( 137Cs) (196 days). Internal dose in the other was 3.2–6.1 mGy ( 134Cs) and 1.8–3.4 mGy ( 137Cs) and external dose was 1.3 mGy ( 134Cs) and 0.6 mGy ( 137Cs) (315 days). Sperm morphology and spermatogenesis were within normal ranges. 134, 137Cs radioactivity was detected but Cs was not detectable in the testis by electron probe microanalysis. Thus, adverse radiation-induced effects were not observed in bull testes following chronic exposure to the above levels of radiation for up to 10 months. Since we could analyse a limited number of testes, further investigation on the effects of ionizing radiation on spermatogenesis should be extended to more animals.

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          Assessment of individual radionuclide distributions from the Fukushima nuclear accident covering central-east Japan.

          A tremendous amount of radioactivity was discharged because of the damage to cooling systems of nuclear reactors in the Fukushima No. 1 nuclear power plant in March 2011. Fukushima and its adjacent prefectures were contaminated with fission products from the accident. Here, we show a geographical distribution of radioactive iodine, tellurium, and cesium in the surface soils of central-east Japan as determined by gamma-ray spectrometry. Especially in Fukushima prefecture, contaminated area spreads around Iitate and Naka-Dori for all the radionuclides we measured. Distributions of the radionuclides were affected by the physical state of each nuclide as well as geographical features. Considering meteorological conditions, it is concluded that the radioactive material transported on March 15 was the major contributor to contamination in Fukushima prefecture, whereas the radioactive material transported on March 21 was the major source in Ibaraki, Tochigi, Saitama, and Chiba prefectures and in Tokyo.
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            Isotopic evidence of plutonium release into the environment from the Fukushima DNPP accident

            The Fukushima Daiichi nuclear power plant (DNPP) accident caused massive releases of radioactivity into the environment. The released highly volatile fission products, such as 129mTe, 131I, 134Cs, 136Cs and 137Cs were found to be widely distributed in Fukushima and its adjacent prefectures in eastern Japan. However, the release of non-volatile actinides, in particular, Pu isotopes remains uncertain almost one year after the accident. Here we report the isotopic evidence for the release of Pu into the atmosphere and deposition on the ground in northwest and south of the Fukushima DNPP in the 20–30 km zones. The high activity ratio of 241Pu/239+240Pu (> 100) from the Fukushima DNPP accident highlights the need for long-term 241Pu dose assessment, and the ingrowth of 241Am. The results are important for the estimation of reactor damage and have significant implication in the strategy of decontamination.
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              Studies of the mortality of atomic bomb survivors. Report 12, Part I. Cancer: 1950-1990.

              This continues the series of periodic general reports on cancer mortality in the cohort of A-bomb survivors followed by the Radiation Effects Research Foundation. The follow-up is extended by the 5 years 1986-1990, and analysis includes an additional 10,500 survivors with recently estimated radiation doses. Together these extensions add about 550,000 person-years of follow-up. The cohort analyzed consists of 86,572 subjects, of which about 60% have dose estimates of at least 0.005 Sv. During 1950-1990 there have been 3086 and 4741 cancer deaths for the less than and greater than 0.005 Sv groups, respectively. It is estimated that among these there have been approximately 420 excess cancer deaths during 1950-1990, of which about 85 were due to leukemia. For cancers other than leukemia (solid cancers), about 25% of the excess deaths in 1950-1990 occurred during the last 5 years; for those exposed as children this figure is nearly 50%. For leukemia only about 3% of the excess deaths in 1950-1990 occurred in the last 5 years. Whereas most of the excess for leukemia occurred in the first 15 years after exposure, for solid cancers the pattern of excess risk is apparently more like a life-long elevation of the natural age-specific cancer risk. Taking advantage of the lengthening follow-up, increased attention is given to clarifying temporal patterns of the excess cancer risk. Emphasis is placed on describing these patterns in terms of absolute excess risk, as well as relative risk. For example: (a) although it is becoming clearer that the excess relative risk for those exposed as children has declined over the follow-up, the excess absolute risk has increased rapidly with time; and (b) although the excess relative risk at a given age depends substantially on sex and age at exposure, the age-specific excess absolute risk depends little on these factors. The primary estimates of excess risk are now given as specific to sex and age at exposure, and these include projections of dose-specific lifetime risks for this cohort. The excess lifetime risk per sievert for solid cancers for those exposed at age 30 is estimated at 0.10 and 0.14 for males and females, respectively. Those exposed at age 50 have about one-third these risks. Projection of lifetime risks for those exposed at age 10 is more uncertain. Under a reasonable set of assumptions, estimates for this group range from about 1.0-1.8 times the estimates for those exposed at age 30. The excess life-time risk for leukemia at 1 Sv for those exposed at either 10 or 30 years is estimated as about 0.015 and 0.008 for males and females, respectively. Those exposed at age 50 have about two-thirds that risk. Excess risks for solid cancer appear quite linear up to about 3 Sv, but for leukemia apparent nonlinearity in dose results in risks at 0.1 Sv estimated at about 1/20 of those for 1.0 Sv. Site-specific risk estimates are given, but it is urged that great care be taken in interpreting these, because most of their variation can be explained simply by imprecision in the estimates.
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                Author and article information

                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group
                2045-2322
                08 October 2013
                2013
                : 3
                : 2850
                Affiliations
                [1 ]Faculty of Agriculture, Niigata University , Niigata, Japan
                [2 ]Graduate School of Science and Engineering, Yamagata University , Yamagata, Japan
                [3 ]Graduate School of Agricultural Sciences, Tohoku University , Sendai, Japan
                [4 ]Department of Chemistry, Tohoku University , Sendai, Japan
                [5 ]National Institute of Radiological Sciences , Chiba, Japan
                [6 ]Institute of Development, Aging and Cancer, Tohoku University , Sendai, Japan
                [7 ]School of Food, Agricultural and Environmental Sciences, Miyagi University , Sendai, Japan
                [8 ]Graduate School of Dentistry, Tohoku University , Sendai, Japan
                Author notes
                Article
                srep02850
                10.1038/srep02850
                3792411
                24100305
                5db110d1-6bdc-431b-882e-468aebac82d8
                Copyright © 2013, Macmillan Publishers Limited. All rights reserved

                This work is licensed under a Creative Commons Attribution-NonCommercial-ShareALike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/

                History
                : 21 January 2013
                : 04 September 2013
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