Without specific empirical evidence and reference, Sergej V. Jargin insinuates a possible cause of the observed long-term increases in perinatal mortality in contaminated prefectures after Fukushima: "It is not surprising that cataclysms with evacuation of people, associated with stress, temporary derangements of perinatal care services, of diets, etc., are accompanied by an increase in the perinatal mortality." Our data clearly show that in highly tsunami-impacted regions there is indeed a more than 50% increase in perinatal mortality, but this is confined to March and April 2011 only. From May through December 2011, nowhere in Japan perinatal mortality remained elevated. Moreover, the perinatal mortality increase in Chiba, Saitama, and Tokyo 10 months after the natural and technical catastrophes cannot be explained by "derangements of perinatal care" as the general infrastructure had not been compromised at all in these 3 prefectures.
Sergej V. Jargin compares the first-year radiation dose due to the Fukushima nuclear accident with the annual natural exposure worldwide. He concludes: "Additional doses to the residents of the most contaminated Fukushima prefecture have thus remained during the first year after the accident within the limits of the natural radiation background, being far below the limits for professional exposures."
The dose (Gray or Sievert) in the radiation sciences is a surprisingly old and crude concept developed long before the discovery of the molecular structure of the DNA. The basis of this concept is unit energy deposited per unit mass (Joule/kilogram). Therefore, dose can only be physically meaningful for energy deposits in volumes of at least a few milliliters, e.g. of water, and not for the interaction of photons, electrons, a-particles, and neutrons by external or internal emitters with cellular and sub-cellular structures like cells, DNA, and proteins in animate beings. Therefore, comparing the additional radiation exposure of human populations after radiological incidents and accidents with the natural background radiation level is misleading in principle as the specific physicochemical and microbiological consequences of artificial external and internal ionizing radiation and radionuclides are ignored. Jargin's view that the annual natural background radiation is trivial and that even multiples of this dose after nuclear accidents were acceptable points to a key dissent in science: The doubling of the background radiation level, say, from 1 mSv/a to 2 mSv/a, represents a doubling of an important physical environmental parameter relevant for the development of life on earth, and cannot as such be considered a 'low dose' and of no effect. It is hard to imagine any 'environmental parameter' relevant for human health a doubling or halving of which would have no consequences, be it the exposure to the sun, the oxygen and the carbon dioxide contents in the air, or the individual cigarette and alcohol consumption per year. With a case-control study of natural background radiation and incidence of childhood leukemia in Great Britain during 1980-2006, Kendall et al. have furnished evidence that there is a significant excess relative risk of childhood leukemia per millisievert of cumulative red bone marrow dose from gamma radiation1. In their review article "Future development of biologically relevant dosimetry", Palmans et al.2 emphasize that the "current approach … is based on the product of the absorbed dose to water and a biological weighting factor (=Sievert), but this is found to be insufficient for providing a generic method to quantify the biological outcome of radiation".
The carefree claim by Sergej V. Jargin "Health risks including perinatal mortality have never been proven for the doses discussed above" ignores powerful epidemiologic studies. It has been shown that radiation induced genetic effects like increases in stillbirths, increases in congenital malformations, and sex ratio shifts occur following radiological incidents and accidents 3-13. More recent investigations document increased cancers in the vicinity of nuclear power plants 14,15, in the workplace 16, in areas of high background radiation 17, and following computerized tomography examinations as well as cardiac imaging 18-20. "The association between the low dose of ionizing radiation received by the fetus in utero from diagnostic radiography, particularly in the last trimester of pregnancy, and the subsequent risk of cancer in childhood provides direct evidence against the existence of a threshold dose below which no excess risk arises, and has led to changes in medical practice. Initially reported in 1956, a consistent association has been found in many case-control studies in different countries. The excess relative risk obtained from combining the results of these studies has high statistical significance and suggests that, in the past, a radiographic examination of the abdomen of a pregnant woman produced a proportional increase in risk of about 40%. A corresponding causal relationship is not universally accepted and this interpretation has been challenged on four grounds. On review, the evidence against bias and confounding as alternative explanations for the association is strong. Scrutiny of the objections to causality suggests that they are not, or may not be, valid. A causal explanation is supported by evidence indicating an appropriate dose-response relationship and by animal experiments. It is concluded that radiation doses of the order of 10 mGy received by the fetus in utero produce a consequent increase in the risk of childhood cancer. The excess absolute risk coefficient at this level of exposure is approximately 6% per gray, although the exact value of this risk coefficient remains uncertain" 21.
All of the studies described in our paper and many more investigations in the international radiation science literature show that radiation risks, especially genetic reproductive risks and cancer risks, have been systematically underestimated in the past, due to inadequate scientific concepts and underpowered or poorly designed experimental and human studies.
a Hagen Scherb
b Kuniyoshi Mori
c Keiji Hayashi
a Dr. rer. nat. (Corresponding Author), Helmholtz Zentrum München, German Research Center for Environmental Health, Institute of Computational Biology, Ingolstädter Landstr. 1, D-85764 Neuherberg, Germany, firstname.lastname@example.org
b Medical Doctor (MD), Higashiosaka Health Center 4-3-22 Iwatachou, Higashiosakacity 578-0941 Osaka, Japan
c Medical Doctor (MD), Hayashi Children's Clinic, 4-6-11-1F Nagata, Joto-ku Osaka-Shi 536-0022 Osaka, Japan
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