Dr Sergei Jargin, Clementovski per 6-82, 115184 Moscow, Russia
Dr Sergei Jargin, Clementovski per 6-82, 115184 Moscow, Russia
Dr Sergei Jargin
Peoples’ Friendship University of Russia
Dr. Sergei Jargin, RADIATION SAFETY STANDARDS AND HORMESIS(2017)SDRP Journal of Earth Sciences & Environmental Studies 2(3)
Strictly observed realistic safety standards are more helpful for the public health than excessive restrictions that would be disregarded. Today’s radiation safety standards are based on the linear no-threshold theory (LNT): extrapolation of dose-response relationships down to low doses, where such relationships are unproven and can be inverse due to hormesis. Hormesis is theoretically founded for environmental factors causing adaptation to a background level or some average from the past when the natural background was higher. According to this concept, the harm caused by anthropogenic radiation would tend to zero with a dose rate decreasing down to a wide range level of the natural background. Hormesis concept should be applied with caution as hormetic stimuli may act without threshold on pre-damaged or atrophic tissues or act synergistically with other noxious agents. Experimental evidence in favor of hormesis is considerable but further studies are needed. Low doses should be analyzed separately from higher doses, which would prevent unfounded LNT-based extrapolations. Some reviews and metaanalises have analyzed studies of uneven quality. Questionable data on Chernobyl accident, Techa river and Mayak workers cohorts are discussed here along with motives to exaggerate consequences of low-dose low-rate exposures. Among the biases of epidemiological research, dose-dependent self-selection and recall bias are pointed out. In conclusion, current radiation safety standards are excessively restrictive and should be revised to become more realistic and workable. Revision of the limits should be based on reliable experiments and accompanied by measures guaranteeing observance.
Standards are only effective if they are properly applied in practice . Unrealistic laws and regulations are often violated, which contributes to the disrespect for the law in general. Today’s radiation safety standards are based on the linear no-threshold theory (LNT): extrapolations of a dose-response relationship down to the low doses, where such relationship is unproven and can become inverse due to hormesis [2-6]. According to the current standards, an equivalent effective dose to individual members of the public should not exceed 1 mSv/year. The limits of effective dose for exposed workers are 100 mSv in a consecutive 5-year period, with a maximum effective dose of 50 mSv in any single year . For comparison, worldwide annual exposures to natural radiation sources are generally expected to be in the range of 1-10 mSv, 2.4 mSv being a current estimate of the global average .
For solid cancers and leukemia, significant dose-response relationships were found in survivors of atomic explosions exposed to <500 mSv but not for doses < 200 mSv [7-10]. According to UNSCEAR, a statistically significant elevation of the cancer risk was observed in epidemiological studies at the doses >100-200 mGy . There were also reports on dose-response relationships for lower doses [12,13] but validity was questioned . Practical thresholds can in fact be higher due to biases in epidemiological research on stochastic effects of low doses [14-17]. The value 200 mSv has been regarded as a level, below which no excess cancers were proven [10,18]. Some reports contain poorly substantiated information (details are in [19,20]). The quality of the research is uneven; data trimming according to a preconceived idea appears to be probable in some studies . Reviews and metaanalises discuss together studies of uneven quality [e.g., 22]; although in the latter review the unreliability of mortality data from the former Soviet Union (SU) was pointed out. We agree  with Prof. Little that “such data should therefore probably not be used for epidemiologic analysis, in particular for the Russian worker studies considered here [24-27]” . This recommendation pertains apparently also to some other studies by the same and other researchers, discussed below. Today, when the literature is so abundant, research quality, possible biases and conflicts of interest should be taken into account defining inclusion criteria into metaanalyses and reviews.
Using the LNT, Chernobyl accident was predicted to result in a “virtual epidemic” of radiation-induced cancer. Instead, there was no cancer increase provably caused by radiation except for thyroid cancer (TC) [28,29]. TC in people exposed at a young age has been the only oncologic sequel of the Chernobyl accident widely believed to be proven . It should be commented that the incidence of pediatric TC was much lower in the contaminated areas of the former SU compared to more developed countries obviously due to differences in diagnostic quality and coverage of the population by medical checkups (discussed in ). The mass screening after the accident detected not only small cancers but also advanced neglected TC accumulated in the population, classified as aggressive radiogenic cancers. Besides, some TC cases were brought from non-contaminated areas and registered as Chernobyl victims. As there was no screening outside the contaminated areas, such cases tended to be more advanced. These phenomena were confirmed by the fact that the ‘first wave’ TC after the accident were on average larger and less differentiated than later ones [32,33]. The following citation is illustrative: ‘The tumors were randomly selected (successive cases) from the laboratories of Kiev and Valencia... [The cancers were] clearly more aggressive in the Ukrainian population in comparison with the Valencian cases’ . There is an explanation: averagely earlier cancer diagnostics in Valencia. Further details and references are in .
In the meantime, there continue to appear reports on Chernobyl material, where the cause-effect relationship between dose estimates and a cancer risk is discussed as a matter-of-fact [35-38]. Without repeating the previously published arguments [20,31], the following should be stressed. Among the motives of the exaggeration of Chernobyl consequences were writing of numerous dissertations, financing, international help and scientific cooperation with overseas voyages, etc. Moreover, Chernobyl accident was misused to strangle the nuclear power  thus contributing to higher fossil fuel prices. Furthermore, the mechanisms of false-positive diagnosis of malignancy have been discussed previously [40,41]. Among others, misinterpretation of cellular pleomorphism as a malignancy criterion of thyroid nodules was not uncommon in the 1990s. In the urinary bladder, inflammatory reactive atypia was obviously misinterpreted as dysplasia or carcinoma in situ [40,43,44]. On the basis of morphological descriptions and images from Russian-language editions on tumor pathology of that time, no reliable differential diagnosis could be made; some images were reproduced in [43,45]. In the author’s opinion, based also on interviews with pathologists and other experts involved in the diagnostics of Chernobyl-related cancer, trimming of statistics contributed to the overestimation of Chernobyl consequences. A circumstantial evidence thereof is the large number of papers reporting unrealistic data, partly referenced in  and commented in .
The exaggeration of Chernobyl consequences may lead to the overestimation of carcinogenicity of certain radionuclides. Moreover, the exaggeration caused anxiety contributing to enhanced abortion rate . Chernobyl accident has been exploited to strangle the worldwide development of nuclear power, the cleanest, safest and practically inexhaustible means to meet the global energy needs [41,48]. However, it was necessary for the time being: the nuclear technology should have been prevented from spreading to densely populated regions, where conflicts and terrorism are not excluded. The worldwide introduction of nuclear energy will be possible only after a concentration of authority in the most developed parts of the world. It will make possible the construction of nuclear reactors in optimally suitable places, considering all sociopolitical, geographical, and geological conditions, attitudes of workers and engineers to their duties , which would prevent accidents like Fukushima and Chernobyl.
TECHA RIVER, MAYAK FACILITY AND OTHER EPIDEMIOLOGICAL RESEARCH
There is a tendency to exaggerate cause-effect relationships between radiation and certain diseases in studies of the Techa river and Mayak workers cohorts in the Ural region of Russia . It should be noted that dimensions of radiocontamination in the Urals were larger than that after Chernobyl. The Mayak complex, located 70 km to the north from the million city of Chelyabinsk, included the Facility A, the reactor, and Facility B, a radiochemical plant. The main source of exposure at the Facility A was gamma radiation, while overage total doses for workers in the period 1949-1954 were estimated to be 1220 mSv. The major radiation components at Facility B were external gamma irradiation and 229Pu aerosols. The average total doses for workers of this facility in the period 1949-1953 were 2450 mSv . Waste disposal into the Techa river system, the Kyshtym accident (1957), resuspension by winds from the waste repository lake Karachai (1967) and other accidents contributed to exposures of surrounding population. About 7500 evacuees from the Techa river area received average doses in the range 35-1700 mSv. Especially high doses were received in the village Metlino, where some residents obtained red bone marrow doses 3000-4000 mSv . The relatively large discharges of radioactive materials into the Techa river occurred between the years 1949 and 1956. The Techa river cohort consists of over 30,000 people who were born before the start of exposure in 1949 and lived along the Techa river; more details and references are in . The difference between Chernobyl and the East Urals radioactive trace is that the former was an accident, but the latter - a contamination tolerated over decades, with several accidents in between.
The tendency to exaggerate medical consequences of the East Urals radioactive trace seems to be rather new: in earlier papers no increase in cancer incidence was reported at the doses <0.52 Sv  or among all studied Mayak workers , while existence of a threshold was regarded possible . It was pointed out that excessive absolute risk of leukemia had been 3.5 times lower in the Techa river cohort than among A-bomb survivors [54,55] i.e. the risk from acute exposure had been higher than that from protracted exposures at comparable doses. However, later works by the same scientists have repeatedly stressed comparability of the data from Japan and the Ural region and, correspondingly, a similar level of cancer risk from acute and protracted exposures both for leukemia and for solid cancers [56-58]. An unofficial directive could have been behind this metamorphosis. Along with the elevated cancer risk, an increased risk of non-neoplastic diseases (circulatory, respiratory, gastrointestinal) has been reported by the same and other researchers [24-27, 59-69]. For example, cerebrovascular disease incidence was significantly elevated in workers with a total external dose 0.1 Gy protracted over years . This can be seen as a circumstantial evidence in favor of biases e.g. self-selection: dose-related differences in self-reporting and medical surveillance, a phenomenon noticed also by other researchers in exposed populations [71,72], discussed in . Individuals knowing their higher doses would probably be more motivated to visit medical institutions, being on average given more attention. Besides, studies in humans may be prone to a recall bias: cases would recollect facts related to the exposure better than controls. The dose-effect relationships between low-dose low-rate exposures and non-neoplastic diseases [24-27,59-69] call in question such relationships for cancer reported by the same and other scientists e.g. [74-80]. Although there may be some risk of cardiovascular disease at high dose and dose-rate exposures , existing data do not confirm a cause-effect relationship between radiation and cardiovascular diseases at doses <1-2 Gy, while plausible biological mechanisms are unknown . The latter value seems to be an underestimation due to the biases in the epidemiological research. Note that patients treated by radiotherapy who received doses >40 Gy to parts of the heart may develop cardiovascular complications later in life; some sources mention also lower doses [82,83], which are still much higher than the average doses in Chernobyl and Ural cohorts. The doses associated with cardiovascular alterations in animal experiments have been also considerably higher [84,85].
Average total doses to male workers of the Mayak facility were 0.91 Gy ; over 90% of the Techa river cohort received < 0.1 Gy  protracted over many years. A relationship of aortic atherosclerosis and cerebrovascular diseases with low-dose exposures was reported from the Mayak facility, where both conditions were increased in workers exposed to external gamma-rays at total doses >0.5 Gy protracted over years [59,65]. The excess relative risk (ERR) per Gy for cerebrovascular diseases in the cohort of Mayak workers was reportedly even higher than that in A-bomb survivors , where the self-selection bias could have been active as well.
Epidemiological studies have a limited statistical power to detect the risk of cardiovascular disease after exposures <0.5 Gy . In particular, the research based on the best fitting of mathematical models e.g. [57,58,86] does not necessarily prove a cause-effect relationship. For example, a study of atomic bomb survivors concluded that the estimated lowest dose range with a significant ERR for all solid cancers was 0 to 0.20 Gy, while a dose-threshold analysis indicated no threshold . This conclusion was questioned as the analysis had restricted possible functional forms using only linear and linear-quadratic dependences [87-89]. If a more generalized functional form had been used to fit the data, the lower bounds of the 95% confidence intervals would have been under zero for low doses i.e. a threshold cannot be excluded. The artificial neural networks, applied to the cancer databases of A-bomb survivors, demonstrated the presence of thresholds for the ERR varying with organs, gender and age at exposure .
Furthermore, biases and limitations of epidemiological studies have included a priori classification of spontaneous diseases as radiation-induced, discussion of doses disregarding natural radiation background, conclusions about incidence increase without adequate comparisons with a control, “dose lagging, odds averaging over wide dose ranges when evaluating odds ratios, and forcing a positive slope to the relative risk dose-response curve” , data trimming etc., commented in [20,21]. Some experiments, where no effects had been found in exposed animals, were excluded from databases ; other studies with negative results have not been cited in reviews  etc. All that contributed to overestimation of the low dose effects.
HORMESIS AND RADIATION SAFETY NORMS
Hormesis describes any process in which a cell or organism(s) exhibit a biphasic response to exposure to increasing amounts of a substance or condition; typically, low-dose exposures elicit a beneficial response, whereas high doses cause toxicity . Among hormetic agents (hormetins) are numerous chemical substances and elements, vitamins, heat, light, ultraviolet, ionizing radiation and products of water radiolysis , exercise, and different kinds of stress . For factors that are present in the natural environment, hormesis is generally conceivable as it can be caused by adaptation to an environmental level. This pertains also to ionizing radiation. Nonetheless, the LNT has been used as a basis of the safety standards. The LNT is based on the idea that cells are randomly altered by ionizing radiation events causing mutations: the more particle tracks go through cell nuclei, the higher would be the risk of malignant transformation [28,96]. This concept does not take into account that DNA damage and repair are permanent processes in dynamic equilibrium. Natural background radiation has been decreasing over the time of life existence on the Earth among others due to the decay of radionuclides and formation of the ozone layer. It was reported, for example, that the radiation dose from internal 40K has decreased by a factor of about eight over the past 4 billion years. Radiation exposure from geologic materials has decreased from about 1.6 mGy/year to 0.66 mGy/year over the same period; while exposure to an organism with a potassium concentration of 250 mmol/liter has decreased from about 5.5 to about 0.70 mGy/year. Accordingly, background radiation exposure from these two sources has dropped from about 7.0 to 1.35 mGy/year during the time of the life existence . The conservative nature of mutation repair mechanisms in modern organisms suggest that these mechanisms may have evolved in the distant past and that organisms may retain some of the capability of efficiently repairing damage from higher radiation levels than exist at present . By analogy with other environmental factors, there may be adaptation  i.e. an optimal impact level. The natural selection is a slow process; therefore, current adaptation would correspond to some average from the past when the natural radiation background was higher. Exposure levels corresponding to the maximal adaptation may be expected to act as hormetic stimuli.
Hormesis cannot be used in the radiation safety regulations without unequivocal experimental evidence from large-scale animal experiments. Current evidence in favor of hormesis is, however, considerable [87,91,98,99], which means that a part of experimental data is at variance with epidemiological studies cited above. Admittedly, some animal experiments did not support hormesis e.g. showing no life lengthening of mice continuously exposed to low dose radiation . Other researchers did report life lengthening of mice in low dose rate experiments [e.g., 101]. In small animals, minimal doses associated with carcinogenesis are generally higher than those in the Chernobyl and Ural cohorts, being in the range of hundreds or thousands of mGy [7,102-104]. Hormesis is assumed to work on molecular (stimulating DNA repair) and cellular levels. Eukaryotic cells display cell-type-specific adaptive responses enhancing their radioresistance after a low-dose priming irradiation [3,4,105-107]; details of these mechanisms are outside the scope of this review.
Although the value of experiments for extrapolation to humans is controversial , for such a universal mechanism as DNA repair the extrapolation would probably be permissible if various animal species are used. Further work can quantify sensitivity of different species enabling more precise extrapolations to humans . Outstanding data e.g. that “above doses of 50-100 mSv (protracted exposure) or 10-50 mSv (acute exposure), direct epidemiological evidence from human populations demonstrates that exposure to ionizing radiation increases the risk of some cancers” , or four-fold increase in the incidence of thyroid cancer and twofold increase of benign thyroid tumors in children linked to a thyroid dose of 90 mGy  should be verified by experiments. The same applies to the data on the excess radiation-related cancer deaths related to the doses below the occupational limits . In any case, the hormesis concept should be applied cautiously as hormetic stimuli may act without threshold on pre-damaged or atrophic tissues and/or synergistically with other noxious agents including carcinogens [112-115].
The benefit from a moderate exposure to ionizing radiation was demonstrated epidemiologically among survivors of atomic explosions , although these data might be not free from biases e.g. due to a better medical surveillance of the survivors. Occupational exposures were repeatedly shown to be associated with better health [3,4], which, however, can at least in part be explained by the healthy worker effect . The cancer mortality was found to be lower in high-elevation areas, where the natural radiation background is increased due to the higher intensity of cosmic rays [3,117]. However, better medical surveillance, increasing attention of people to their health, and biased research may cause one day enhanced registered cancer incidence in the areas with high natural radiation background, which would prove no cause-effect relationship. Certainly, knowledge on hormesis is incomplete. The most promising way to reliable data on the dose-effect relationships for low doses would be large-scale experiments. Note that animal experiments are ethically inadmissible without integrity of all participants of the research.
Discussing the exclusion of hormesis from the risk assessment, Zbigniew Jaworowski wrote: “It seems to me that the driving force was (and still is) ... the antinuclear power lobby, concerned that demonstration of the beneficial effects of small radiation doses, and thus of the existence of a threshold for harmful effects occurring near this dose region, will destroy their raison d'être” . The raison d'être should probably be replaced by cui bono (for whose benefit?): strangulation of the nuclear power in the wake of Chernobyl contributed to higher prices for fossil fuels. The motives for overestimation of Chernobyl consequences in the former SU were discussed above and in [20,31]. In many countries, among the motives were antinuclear sentiments supported by the Green movement, well in agreement with the interests of fossil fuel producers. Today, however, there are no alternatives to the nuclear power: in the long run, nonrenewable fossil fuels will become increasingly expensive, contributing to the uncontrolled population growth in oil-producing countries and poverty in the rest of the world.
Summarizing the above and previously published arguments [118,119], the harm caused by anthropogenic radiation would tend to zero with a dose rate decreasing down to a wide range level of the natural background. Within a certain range, the dose-effect relationship would be inverse in accordance with hormesis. A corresponding graph, plotted on the basis of experimental data, with a sagging of the dose-effect curve below the background cancer risk in the range 0.1-700 mGy, is depicted in . However, hormesis cannot be used in radiation safety regulations without consistent experimental evidence obtained in large-scale experiments using different animal species, under controlled conditions to exclude biases and conflicts of interest. Low doses should be analyzed separately from higher doses [120,121], which would prevent unfounded LNT-based extrapolations such as prediction of millions of deaths from nuclear accidents, e.g. .
The current radiation safety standards are exceedingly restrictive and should be revised to become more realistic and workable. Elevation of the limits must be accompanied by measures guaranteeing their strict observance, and by openness of dosimetric data. We found no contraindications to an elevation of the total equivalent effective doses to individual members of the public up to 5 mSv/year. The dose rate would remain within the range of the natural background radiation. Considering inevitable global spread of the nuclear power to meet the energy needs of the mankind [41,123], elevation of the limits for professional exposures should be considered as well. The revision must be based on reliable experiments and accompanied by measures guaranteeing observance. Strictly observed realistic safety standards are more helpful for the public health than excessive restrictions that would be disregarded.
IAEA Safety Standards Series No. GSR Part 3. Radiation protection and safety of radiation sources: International Basic Safety Standards. Vienna: International Atomic Energy Agency, 2014.
Jaworowski Z. Radiation hormesis - a remedy for fear. Hum Exp Toxicol 2010;29:263-270. PMid:20332170View Article PubMed/NCBI
Prekeges JL. Radiation hormesis, or, could all that radiation be good for us? J Nucl Med Technol 2003;31:11-17. PMid:12624121PubMed/NCBI
Jolly D, Meyer J. A brief review of radiation hormesis. Australas Phys Eng Sci Med 2009;32:180-187. PMid:20169836View Article PubMed/NCBI
Cui J, Yang G, Pan Z, et al. Hormetic response to low-dose radiation: Focus on the immune system and its clinical implications. Int J Mol Sci 2017;18(2).View Article
Mattson MP, Calabrese EJ (Editors). Hormesis. A Revolution in Biology, Toxicology and Medicine. New York etc.: Springer, 2010.
UNSCEAR 2000 Report. Sources and effects of ionizing radiation. Annex B: Exposures from natural radiation sources. Annex G: Biological effects at low radiation doses.
Little MP, Muirhead CR. Evidence for curvilinearity in the cancer incidence dose-response in the Japanese atomic bomb survivors. Int J Radiat Biol 1996;70:83-94.View Article
Little MP, Muirhead CR. Curvature in the cancer mortality dose response in Japanese atomic bomb survivors: absence of evidence of threshold. Int J Radiat Biol 1998;74:471-480.View Article
Heidenreich WF, Paretzke H, Jacob P. No evidence for increased tumor rates below 200 mSv in the atomic bomb survivors data. Radiat Environ Biophys 1997;36:205-207. PMid:9402638View Article PubMed/NCBI
UNSCEAR 2010 Report. Scientific report: summary of low-dose radiation effects on health.
Cardis E, Vrijheid M, Blettner M, et al. Risk of cancer after low doses of ionising radiation: retrospective cohort study in 15 countries. BMJ 2005;331:77. PMid:15987704 PMCid:PMC558612View Article PubMed/NCBI
Pierce DA, Shimizu Y, Preston DL, et al. Studies of the mortality of atomic bomb survivors. Report 12, Part I. Cancer: 1950-1990. Radiat Res 1996;146:1-27. PMid:8677290View Article PubMed/NCBI
Tubiana M, Feinendegen LE, Yang C, Kaminski JM. The linear no-threshold relationship is inconsistent with radiation biologic and experimental data. Radiology 2009;251:13-22. PMid:19332842 PMCid:PMC2663584View Article PubMed/NCBI
UNSCEAR 1972 Report. Ionizing radiation: levels and effects. Annex G: Experimental induction of neoplasms by radiation; Annex H: Radiation carcinogenesis in man.
UNSCEAR 2006 Report. Annex A: Epidemiological studies of radiation and cancer. Annex B: Epidemiological evaluation of cardiovascular disease and other non-cancer diseases following radiation exposure.
Watanabe T, Miyao M, Honda R, Yamada Y. Hiroshima survivors exposed to very low doses of A-bomb primary radiation showed a high risk for cancers. Environ Health Prev Med 2008;13:264-270. PMid:19568913 PMCid:PMC2698250View Article PubMed/NCBI
Gonz?lez AJ. Radiation safety standards and their application: international policies and current issues. Health Phys 2004;87:258-272. PMid:15303062View Article PubMed/NCBI
Jargin SV. Overestimation of Chernobyl consequences: poorly substantiated information published. Radiat Environ Biophys 2010;49:743-745. PMid:20640449View Article PubMed/NCBI
Jargin SV. Thyroid cancer after Chernobyl: obfuscated truth. Dose Response 2011;9(4):471-6. PMid:22461757 PMCid:PMC3315168View Article PubMed/NCBI
Jargin SV. Scientific misconduct and related topics. Am J Exp Clin Res 2017;4(1):197-201.
Little MP. Radiation and circulatory disease. Mutat Res 2016;770(Pt B):299-318.
Jargin SV. Cardiovascular mortality in Russia: a comment. Cardiovasc Diagn Ther 2017. doi: 10.21037/cdt.2017.08.03.
Ivanov VK, Maksioutov MA, Chekin SY, et al. The risk of radiation-induced cerebrovascular disease in Chernobyl emergency workers. Health Phys 2006;90(3):199-207. PMid:16505616View Article PubMed/NCBI
Kashcheev VV, Chekin SY, Maksioutov MA, et al. Radiation-epidemiological study of cerebrovascular diseases in the cohort of Russian recovery operation workers of the Chernobyl accident. Health Phys 2016;111(2):192-197. PMid:27356064View Article PubMed/NCBI
Azizova TV, Grigoryeva ES, Haylock RG, et al. Ischaemic heart disease incidence and mortality in an extended cohort of Mayak workers first employed in 1948-1982. Br J Radiol 2015;88(1054):20150169. PMid:26224431 PMCid:PMC4730965View Article PubMed/NCBI
Moseeva MB, Azizova TV, Grigoryeva ES, Haylock R. Risks of circulatory diseases among Mayak PA workers with radiation doses estimated using the improved Mayak Worker Dosimetry System 2008. Radiat Environ Biophys 2014;53(2):469-477. PMid:24482017View Article PubMed/NCBI
Raabe OG. Toward improved ionizing radiation safety standards. Health Phys 2011;101(1):84-93. PMid:21617395View Article PubMed/NCBI
Anspaugh LR, Catlin RJ, Goldman M. The global impact of the Chernobyl reactor accident. Science 1988;242:1513-1519. PMid:3201240View Article PubMed/NCBI
UNSCEAR 2008 Report. Sources and Effects of Ionizing Radiation. Annex D: Health effects due to radiation from the Chernobyl accident.
Jargin SV. Debate on the Chernobyl Disaster. Int J Health Serv 2017;47(1):150-159. PMid:27956579View Article PubMed/NCBI
Williams ED, Abrosimov A, Bogdanova T, et al. Thyroid carcinoma after Chernobyl latent period, morphology and aggressiveness. Br J Cancer 2004;90(11):2219-2224.View Article
Nikiforov Y, Gnepp DR. Pediatric thyroid cancer after the Chernobyl disaster. Pathomorphologic study of 84 cases (1991-1992) from the Republic of Belarus. Cancer 1994;74(2):748-766. 74:2<748::AID-CNCR2820740231>3.0.CO;2-HView Article
Romanenko A, Morell-Quadreny L, Ramos D, et al. Author reply to: overestimation of radiation-induced malignancy after the Chernobyl accident. Virchows Arch 2007;451(1):107-108.View Article
Ivanov VK, Gorsky AI, Kashcheev VV, et al. Latent period in induction of radiogenic solid tumors in the cohort of emergency workers. Radiat Environ Biophys 2009;48:247-252. PMid:19326138View Article PubMed/NCBI
Kashcheev VV, Chekin SY, Maksioutov MA, et al. Incidence and mortality of solid cancer among emergency workers of the Chernobyl accident: assessment of radiation risks for the follow-up period of 1992-2009. Radiat Environ Biophys 2015;54:13-23. PMid:25315643View Article PubMed/NCBI
Tronko M, Brenner AV, Bogdanova T, et al. Thyroid neoplasia risk is increased nearly 30 years after the Chernobyl accident. Int J Cancer 2017; doi: 10.1002/ijc.30857.View Article
Zablotska LB, Nadyrov EA, Rozhko AV, et al. Analysis of thyroid malignant pathologic findings identified during 3 rounds of screening (1997-2008) of a cohort of children and adolescents from belarus exposed to radioiodines after the Chernobyl accident. Cancer 2015;121:457-466. PMid:25351557 PMCid:PMC4433039View Article PubMed/NCBI
Derizhanova IS. The Pulmonary-Renal Syndrome among Chernobyl Nuclear Accident Liquidators. XXIII International Congress of the International Academy of Pathology and 14th World Congress of Academic and Environmental Pathology; 15-20 October 2000; Nagoya, Japan. Pathol Int 2000;50(Suppl):A73.
Romanenko A, Fukushima S. Prediction of urinary bladder cancer induction in Ukraine after the Chernobyl accident. XXIII International Congress of the International Academy of Pathology and 14th World Congress of Academic and Environmental Pathology; 15-20 October 2000; Nagoya, Japan. Pathol Int 2000;50(Suppl):A70.
Jaworowski Z . Observations on the Chernobyl disaster and LNT. Dose Response 2010;8:148-171. PMid:20585443 PMCid:PMC2889503View Article PubMed/NCBI
Jargin SV. Thyroid carcinoma in children and adolescents resulting from the Chernobyl accident: possible causes of the incidence increase overestimation. Cesk Patol 2009;45:50-52. PMid:19534395PubMed/NCBI
Jargin SV. Back to Chernobyl: Some aspects of cancer diagnostics. J Environ Stud 2016;2(1):8.
Jargin SV. Chernobyl-related bladder lesions: New interpretation required. J Interdiscipl Histopathol 2014;2:96-97.View Article
Jargin SV. Pathology in the former Soviet Union: scientific misconduct and related phenomena. Dermatol Pract Concept 2011;1:75-81. PMid:24396725 PMCid:PMC3881088PubMed/NCBI
Yablokov AV, Nesterenko VB, Nesterenko AV. Consequences of the catastrophe for people and the environment. Ann NY Acad Sci 2009;1181.
Jargin SV. Consequences of the Fukushima nuclear accident with special reference to the perinatal mortality and abortion rate. J Environ Occup Sci 2016;5(4):82-85.View Article
Jargin SV. Re: The high price of public fear of low-dose radiation. J Radiol Prot. 2017; 2017;37:797-799. PMid:28675752View Article PubMed/NCBI
Jargin SV. Leukemia and cardiovascular diseases in the Techa River Cohort: New interpretation required. J Environ Occup Sci 2014;3:63-64.View Article
Mould RF. The Chernobyl record. The definite history of Chernobyl catastrophe. Philadelphia: Institute of Physics; 2000.View Article
Buldakov LA, Demin SN, Kosenko MM, et al. The medical sequelae of the radiation accident in the Southern Urals in 1957. Med Radiol (Mosk) 1990;35(12):11-15.
Okladnikova ND, Pesternikova VS, Azizova TV, et al. Health status among the staff at the nuclear waste processing plant. Med Tr Prom Ekol 2000;(6):10-14. PMid:10934848PubMed/NCBI
Tokarskaya ZB, Scott BR, Zhuntova GV, et al. Interaction of radiation and smoking in lung cancer induction among workers at the Mayak nuclear enterprise. Health Phys 2002;83(6):833-846. PMid:12467291View Article PubMed/NCBI
Akleev AV, Preston D, Krestinina LIu. Medical and biological consequences of human's chronic exposure to radiation. Med Tr Prom Ekol 2004;(;3):30-36.
Akleyev AV, Kossenko MM, Krestinina LIu, et al. Health status of population exposed to environmental contamination in the Southern Urals. Moscow: Radekon; 2001. (in Russian)
Akleev AV, Krestinina LIu. Carcinogenic risk in residents of the Techa riverside villages. Vestn Ross Akad Med Nauk 2010;(6):34-39. PMid:20698304PubMed/NCBI
Krestinina LY, Davis FG, Schonfeld S, et al. Leukaemia incidence in the Techa River Cohort: 1953-2007. Br J Cancer 2013;109(11):2886-28893. PMid:24129230 PMCid:PMC3844904View Article PubMed/NCBI
Ostroumova E, Preston DL, Ron E, et al. Breast cancer incidence following low-dose rate environmental exposure: Techa River Cohort, 1956-2004. Br J Cancer 2008;99(11):1940-1945. PMid:19002173 PMCid:PMC2600704View Article PubMed/NCBI
Azizova TV, Kuznetsova KV, Bannikova MV, et al. Prevalence of aortal atherosclerosis in workers underwent occupational irradiation. Med Tr Prom Ekol 2014;(11):1-6. PMid:25845141PubMed/NCBI
Azizova TV, Bannikova MV, Moseeva MV, et al. Cerebrovascular disease incidence in workers occupationally exposed to radiation over prolonged time periods. Zh Nevrol Psikhiatr Im S S Korsakova 2014;114(12):128-132. PMid:25726792View Article PubMed/NCBI
Moseeva MB, Azizova TV, Muirhed CR, et al. Risk of cerebrovascular disease incidence in the cohort of Mayak production association workers first employed during 1948-1958. Radiats Biol Radioecol 2012;52(2):149-157. PMid:22690577PubMed/NCBI
Azizova TV, Muirhead CR, Moseeva MB, et al. Cerebrovascular diseases in nuclear workers first employed at the Mayak PA in 1948-1972. Radiat Environ Biophys 2011;50:539-552. PMid:21874558View Article PubMed/NCBI
Azizova TV, Haylock R, Moseeva MB, et al. Cerebrovascular diseases incidence and mortality in an extended Mayak Worker Cohort: 1948-1982. Med Radiol Radiaton Safety (Moscow) 2015;(4):43-61.
Azizova TV, Haylock RG, Moseeva MB, et al. Cerebrovascular diseases incidence and mortality in an extended Mayak Worker Cohort 1948-1982. Radiat Res 2014;182(5):529-544. PMid:25361397View Article PubMed/NCBI
Azizova TV, Muirhead CR, Druzhinina MB, et al. Cardiovascular diseases in the cohort of workers first employed at Mayak PA in 1948-1958. Radiat Res 2010;174(2):155-168. PMid:20681782View Article PubMed/NCBI
Azizova TV, Zhuntova GV, Haylock RG, et al. Chronic bronchitis in the cohort of Mayak workers first employed 1948-1958. Radiat Res 2013;180(6):610-621. PMid:24219326View Article PubMed/NCBI
Krestinina LY, Epifanova S, Silkin S, et al. Chronic low-dose exposure in the Techa River Cohort:risk of mortality from circulatory diseases. Radiat Environ Biophys 2013;52(1):47-57. PMid:23124827View Article PubMed/NCBI
Yablokov AV. Nonmalignant diseases after the Chernobyl catastrophe. Ann N Y Acad Sci 2009;1181:58-160. PMid:20002045PubMed/NCBI
Jargin SV. Focused review of mathematical modeling of radiation-related abnormalities in the Techa River cohort. J Environ Occup Sci 2015;4(2):114-117.View Article
Simonetto C, Sch?llnberger H, Azizova TV, et al. Cerebrovascular Diseases in Workers at Mayak PA: The Difference in Radiation Risk between Incidence and Mortality. PLoS One 2015;10:e0125904. PMid:25933038 PMCid:PMC4416824View Article PubMed/NCBI
Zablotska LB, Bazyka D, Lubin JH, et al. Radiation and the risk of chronic lymphocytic and other leukemias among chornobyl cleanup workers. Environ Health Perspect 2013;121(1):59-65. PMid:23149165PubMed/NCBI
McGeoghegan D, Binks K, Gillies M, et al. The non-cancer mortality experience of male workers at British Nuclear Fuels plc, 1946-2005. Int J Epidemiol 2008;37:506-518. PMid:18319298 PMCid:PMC2409051View Article PubMed/NCBI
Jargin SV. On the radiation-leukemia dose-response relationship among recovery workers after the Chernobyl accident. Dose Response 2013;12(1):162-165. PMid:24659940 PMCid:PMC3960961PubMed/NCBI
Krestinina LY, Davis FG, Schonfeld S, et al. Leukaemia incidence in the Techa River Cohort: 1953-2007. Br J Cancer 2013;109(11):2886-2893. PMid:24129230 PMCid:PMC3844904View Article PubMed/NCBI
Krestinina LY, Davis F, Ostroumova E, et al. Solid cancer incidence and low-dose-rate radiation exposures in the Techa River cohort: 1956 2002. Int J Epidemiol 2007;36(5):1038-1046. PMid:17768163View Article PubMed/NCBI
Sokolnikov ME, Gilbert ES, Preston DL, et al. Lung, liver and bone cancer mortality in Mayak workers. Int J Cancer 2008;123(4):905-911. PMid:18528867 PMCid:PMC4020282View Article PubMed/NCBI
Sokolnikov M, Preston D, Gilbert E, et al. Radiation effects on mortality from solid cancers other than lung, liver, and bone cancer in the Mayak worker cohort: 1948-2008. PLoS One 2015;10(2):e0117784. PMid:25719381 PMCid:PMC4342229View Article PubMed/NCBI
Azizova TV, Korobkin AV, Osovets SV, Bannikova MV. Latency period of acute leukemia in the cohort of Mayak workers. In: Chronic radiation exposure: low-dose effects. Abstracts of the 4th International Conference, November 9-11, 2010, Chelyabinsk, Russia; 2010; pp. 14-15.
Yablokov AV. Oncological diseases after the Chernobyl catastrophe. Ann N Y Acad Sci 2009;1181:161-191. PMid:20002046PubMed/NCBI
Ivanov VK, Gorski AI, Tsyb AF, et al. Solid cancer incidence among the Chernobyl emergency workers residing in Russia: estimation of radiation risks. Radiat Environ Biophys 2004;43(1):35-42. PMid:14762668View Article PubMed/NCBI
National Research Council of the National Academies. Health risks from exposure to low levels of ionizing radiation (BEIR VII Phase 2). Washington, D.C.: National Academy Press, 2006.
Baselet B, Rombouts C, Benotmane AM, et al. Cardiovascular diseases related to ionizing radiation: The risk of low-dose exposure (Review). Int J Mol Med 2016;38(6):1623-1641. PMid:27748824 PMCid:PMC5117755View Article PubMed/NCBI
Darby SC, Cutter DJ, Boerma M, et al. Radiation-related heart disease: Current knowledge and future prospects. Int J Radiat Oncol Biol Phys 2010;76:656-665. PMid:20159360 PMCid:PMC3910096View Article PubMed/NCBI
UNSCEAR 1962 Report. Annex D: Somatic effects of radiation.
Schultz-Hector S. Radiation-induced heart disease: review of experimental data on dose response and pathogenesis. Int J Radiat Biol 1992;61:149-160. PMid:1351901View Article PubMed/NCBI
Ozasa K, Shimizu Y, Suyama A, et al. Studies of the mortality of atomic bomb survivors, Report 14, 1950-2003: an overview of cancer and noncancer diseases. Radiat Res 2012;177(3):229-243. PMid:22171960View Article PubMed/NCBI
Doss M. Linear no-threshold model vs. radiation hormesis. Dose Response 2013;11:480-497. PMid:24298226 PMCid:PMC3834742View Article PubMed/NCBI
Doss M, Egleston BL, Litwin S. Comments on "Studies of the mortality of atomic bomb survivors, report 14, 1950-2003: an overview of cancer and noncancer diseases" (Radiat Res 2012; 177:229-43). Radiat Res 2012;178(3):244-245. PMid:22817395 PMCid:PMC3662863View Article PubMed/NCBI
Cuttler JM. Remedy for radiation fear - discard the politicized science. Dose Response 2014;12(2):170-184. PMid:24910587 PMCid:PMC4036393View Article PubMed/NCBI
Sasaki MS, Tachibana A, Takeda S. Cancer risk at low doses of ionizing radiation: artificial neural networks inference from atomic bomb survivors. J Radiat Res 2014;55(3):391-406. PMid:24366315 PMCid:PMC4014156View Article PubMed/NCBI
Scott BR. It's time for a new low-dose-radiation risk assessment paradigm - one that acknowledges hormesis. Dose Response 2008;6(4):333-351. PMid:19088900 PMCid:PMC2592992View Article PubMed/NCBI
Duport P, Jiang H, Shilnikova NS, et al. Database of radiogenic cancer in experimental animals exposed to low doses of ionizing radiation. J Toxicol Environ Health B Crit Rev 2012;15(3):186-209. PMid:22458255View Article PubMed/NCBI
Dreicer M. Book review. Chernobyl: Consequences of the catastrophe for people and the environment. Environ Health Perspect 2010;118:A500. PMCid:PMC2974725View Article
Kaludercic N, Deshwal S, Di Lisa F. Reactive oxygen species and redox compartmentalization. Front Physiol 2014;5:285. PMid:25161621 PMCid:PMC4130307View Article PubMed/NCBI
Le Bourg ?, Rattan SI. Hormesis and trade-offs: a comment. Dose Response 2014;12(4):522-524. PMid:25552954 PMCid:PMC4267446View Article PubMed/NCBI
Brenner DJ, Doll R, Goodhead DT, et al. Cancer risks attributable to low doses of ionizing radiation: assessing what we really know. Proc Natl Acad Sci U S A 2003;100(24):13761-13766. PMid:14610281 PMCid:PMC283495View Article PubMed/NCBI
Karam PA, Leslie SA. Calculations of background beta-gamma radiation dose through geologic time. Health Phys 1999;77(6):662-667.View Article
Baldwin J, Grantham V. Radiation hormesis: historical and current perspectives. J Nucl Med Technol 2015;43(4):242-246. PMid:26584616View Article PubMed/NCBI
Calabrese EJ. Model uncertainty via the integration of hormesis and LNT as the default in cancer risk assessment. Dose Response 2015;13(4):1559325815621764. PMid:26740815 PMCid:PMC4679205View Article PubMed/NCBI
Tanaka S, Tanaka IB 3rd, Sasagawa S, et al. No lengthening of life span in mice continuously exposed to gamma rays at very low dose rates. Radiat Res 2003;160(3):376-379. PMid:12926996View Article PubMed/NCBI
Caratero A, Courtade M, Bonnet L, et al. Effect of a continuous gamma irradiation at a very low dose on the life span of mice. Gerontology 1998;44(5):272-276. PMid:9693258View Article PubMed/NCBI
UNSCEAR 1986 Report. Genetic and somatic effects of ionizing radiation. Annex B. Dose-response relationships for radiation-induced cancer.
Mitchel RE. The dose window for radiation-induced protective adaptive responses. Dose Response 2009;8:192-208. PMid:20585438 PMCid:PMC2889505PubMed/NCBI
Moskalev I. Biological effects of low radiation doses. Moscow: Institute of Biophysics, 1983. (in Russian).
Klammer H, Zhang LH, Kadhim M, Iliakis G. Dependence of adaptive response and its bystander transmission on the genetic background of tested cells. Int J Radiat Biol 2012;88(10):720-726. PMid:22574641View Article PubMed/NCBI
Ojima M, Eto H, Ban N, Kai M. Radiation-induced bystander effects induce radioadaptive response by low-dose radiation. Radiat Prot Dosimetry 2011;146(1-3):276-279. PMid:21561936View Article PubMed/NCBI
Nenoi M, Wang B, Vares G. In vivo radioadaptive response: a review of studies relevant to radiation-induced cancer risk. Hum Exp Toxicol 2015;34(3):272-283. PMid:24925363 PMCid:PMC4442823View Article PubMed/NCBI
van der Worp HB, Howells DW, et al. Can animal models of disease reliably inform human studies? PLoS Med 2010;7(3):e1000245. PMid:20361020 PMCid:PMC2846855View Article PubMed/NCBI
Higley KA, Kocher DC, Real AG, Chambers DB. Relative biological effectiveness and radiation weighting factors in the context of animals and plants. Ann ICRP 2012;41(3-4):233-245. PMid:23089022View Article PubMed/NCBI
Ron E, Modan B, Preston D, et al. Thyroid neoplasia following low-dose radiation in childhood. Radiat Res 1989;120(3):516-531. PMid:2594972View Article PubMed/NCBI
Wing S, Richardson D, Stewart A. The relevance of occupational epidemiology to radiation protection standards. New Solut 1999;9(2):133-151. PMid:17208790View Article PubMed/NCBI
Little JB. Low-dose radiation effects: interactions and synergism. Health Phys 1990;59(1):49-55. PMid:2193003View Article PubMed/NCBI
Tidd MJ. The big idea: polonium, radon and cigarettes. J R Soc Med 2008;101(3):156-157. PMid:18344474 PMCid:PMC2270238View Article PubMed/NCBI
Zhang R, Li J, Burns FJ, Huang C. Ionizing radiation synergistic induction of cyclooxygenase-2 with benzo[a]pyrene diol-epoxide through nuclear factor of activated T cells in mouse epidermal Cl 41 cells. Oncol Rep 2006;15(3):721-727.View Article
Jargin SV. Hormetic use of stress in gerontological interventions requires a cautious approach. Biogerontology. 2016;17(2):417-420. PMid:26712317View Article PubMed/NCBI
Luckey TD. Atomic bomb health benefits. Dose Response 2008;6:369-382. PMid:19088902 PMCid:PMC2592990View Article PubMed/NCBI
Hart J. Cancer mortality in six lowest versus six highest elevation jurisdictions in the U.S. Dose Response 2010;9(1):50-58. PMid:21431077 PMCid:PMC3057635PubMed/NCBI
Jargin SV. Hormesis and radiation safety norms. Hum Exp Toxicol 2012;31(7):671-675. PMid:22249392View Article PubMed/NCBI
Jargin SV. Dose and dose-rate effectiveness of radiation: first objectivity then conclusions. J Environ Occup Sci 2016;5(1):25-29.View Article
Rozhdestvenskii LM. Radiobiological analysis of cancerogenic risk values in radioepidemiological investigations. Radiats Biol Radioecol 2008;48(4):389-408. PMid:18825986PubMed/NCBI
Rozhdestvenskii LM. The threshold for radiation stochastic effects: arguments "pro" and "contra". Radiats Biol Radioecol 2011;51(5):576-594. PMid:22279771PubMed/NCBI
Bertell R Behind the cover-up. Assessing conservatively the full Chernobyl death toll. Pacific Ecologist 2006;(Winter):35-40.
Jargin SV. Nuclear facilities and nuclear weapons as a guarantee of peace. J Def Manag 2016;6:146. doi:10.4172/2167-0374.1000146View Article