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9 (
1
); 25-36
doi:
10.25259/JHSR_36_2023

Overestimation of medical consequences of low-dose radiation exposures and overtreatment of cancer

1Department of Pathology, The Peoples’ Friendship University of Russia (RUDN), Moscow, Russian Federation
*Corresponding author: Dr. Sergei V. Jargin MD, Department of Pathology, RUDN University, 117198 Moscow, Russian Federation. sjargin@hotmail.com
Received: , Accepted: ,
© 2024 Published by Scientific Scholar on behalf of Journal of Health Science Research
Licence
This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

How to cite this article: Jargin SV. Overestimation of medical consequences of low-dose radiation exposures and overtreatment of cancer. J Health Sci Res. 2024;9:25–36. doi: 10.25259/JHSR_36_2023

Abstract

It is crucial in our time of international tensions that scientists preserve objectivity. Certain scientific writers acted in the interests of fossil fuel vendors. Most evident is this tendency regarding ionizing radiation, whereas the overestimation of medical side effects of a slight anthropogenic increase of the radiation background contributes to the strangulation of atomic energy. The use of nuclear energy for electricity production is on the agenda today due to the increasing energy needs of humankind. Health risks and environmental damage are maximal for coal and oil, lower for natural gas, and much lower for atomic energy. Counting dormant cancers and questionable cases found by screening exposed populations, overdiagnosis, and registering people from clean areas as Chernobyl victims jointly contributed to the elevation of registered thyroid cancer incidence after the accident. Many neglected malignancies found by the screening in Chernobyl and Urals areas were misinterpreted as aggressive radiogenic cancers and overtreated. The epidemiological research on radiation-related malignancies is valuable, but conclusions of certain studies should be revised considering that many cases, interpreted as aggressive radiogenic cancers, were neglected. A promising approach to the study of dose-response relationships is lifelong animal experiments.

Keywords

Nuclear energy
Ionizing radiation
Cancer
Cardiovascular diseases
Overtreatment

Introduction

It is vital in our time of international tensions that scientists preserve objectivity. Potential conflicts of interest should be discussed. For many years, we have tried to demonstrate that certain scientists’ act following the interests of companies and governments selling petroleum and natural gas.[1-3] Most evident is this tendency regarding ionizing radiation, whereas the overestimation of medical and environmental side effects of nuclear energy contributes to its strangulation,[4] supporting appeals to dismantle nuclear power plants (NPPs). The use of atomic energy for electricity production is on the agenda today due to the increasing energy needs of humankind. Properly managed NPPs bear fewer risks than those using fossil fuels. Health risks and environmental damage are maximal for coal and oil, lower for natural gas, and much lower for atomic energy - the cleanest, safest, and practically inexhaustible energy resource.[4-6] Admittedly, NPPs are possible targets during armed conflicts. Overestimation of the health-related impact of low-dose exposures contributes to the strangulation of atomic energy.

Many papers appeared during the last decades, where pathological conditions in populations exposed to low ionizing radiation were a priori deemed radiogenic;[7-9] others discussed previously.[1-3,10] Among the motives for overestimating the damage from the Chernobyl accident were foreign aid and participation in international scientific cooperation. Furthermore, economic interests have come to light: the strangulation of atomic energy.[4] Trimming and manipulation of numerical data have been common in post-Soviet science.[11] Other biases have been discussed elsewhere.[12-14] The selection and self-selection bias noticed in exposed populations are particularly significant.[15-17] The formal analysis indicated that there has been some selection bias for many endpoints, particularly solid cancer and leukemia.[18] Persons receiving relatively high doses would care more about their health and frequently ask for medical attention. The diagnostics would be averagely more thorough in such people as medics may be informed about the patients’ higher doses.

The following comparisons are of importance in this connection. Individual dose rates from the natural radiation background (NRB) are usually within the range of 1.0-10 mSv/year; mean values for some countries are above 10 mSv/year.[19,20] Effective doses among federal subjects of Russia ranged from 2.47 to 9.06 mSv/year, with an average of 4.18 mSv/year.[21] According to United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR), the mean cumulative dose for 1986-2005 to six million inhabitants of the areas recognized as contaminated after Chernobyl was ~9 mSv.[22] In the life span study (LSS) of atomic bomb survivors of Hiroshima and Nagasaki, there was a significant dose-effect association for cancer among persons who received ≤500 mSv. However, the statistical significance disappeared if only doses ≤200 mSv were considered.[23-25] The doses below 100 mGy at low rates induced adaptive responses.[26]

Radioactive contamination in the Urals

Consequences of the radioactive contamination in the Urals were summarily more significant than those after the Chernobyl disaster. The difference is that the latter was due to an accident, but the former was a contamination lasting over 70 years with several accidents. Apart from professional exposures, the disposal of radioactive substances into the river Techa, the 1957 Kyshtym accident, and dispersion by winds from Lake Karachay in 1967 led to residents’ exposure. The East Urals Radioactive Trace (EURT) cohort included people exposed after the Kyshtym accident. The Chernobyl disaster and some cancer-related aspects of EURT have been discussed in more detail.[1-3]

In earlier studies (until 2005-2010), Russian researchers found no cancer increase in populations with average exposures below 0.5 Sv or among general Mayak Production Association (MPA) employees.[27-32] The absolute risk of leukemia per 1 Gy and 10,000 person-years was 3.5-fold smaller in the Techa River cohort (TRC) than in LSS. A higher efficiency of acute exposure reasonably explained this compared to chronic and fractionated ones. Later on, the same experts reported comparable or even higher risks of cancer and other diseases in the cohorts from the Urals compared to LSS.[33-35] Analogously, an earlier study found reduced cancer mortality in the EURT populace.[30] A review confirmed the same cancer-related and all-cause mortality level in the EURT vs. control.[28] In a later report on the same cohort, the authors avoided direct comparisons but fitted the figures into a linear model. The configurations of dose-response curves depicted in this paper seem inconclusive, but an elevated cancer risk in the EURT population was claimed.[36] Along the same lines, earlier Russian publications pointed out a higher biological efficiency of acute exposures compared to chronic ones;[27] later on, the same researchers claimed that the International Commission on Radiological Protection (ICRP) underestimates health risks from chronic exposures, and recommended dose and dose-rate effectiveness factor (DDREF) = 1.0 for the use in safety regulations.[37] This recommendation is unfounded for dose rates comparable with those from NRB.[38,39] Potential motives behind this metamorphosis have been discussed: financing, publication pressure, and, most importantly, exaggeration of health risks from low-dose radiation, strangulation of atomic energy, and boosting fossil fuel prices.[1-3]

In earlier reports, a mortality increase was not accompanied by an incidence elevation of cardio- and cerebrovascular diseases in MPA, TRC, and EURT populations.[40-42] This can be reasonably explained by greater diagnostic effectiveness in exposed people, leading to the detection of mild and questionable cases. A similar tendency for cancer was noticed among Chernobyl emergency workers.[43] commented previously.[44] The mechanism was analogous: Chernobyl cleanup workers underwent repeated medical checkups. As a result, tumors were efficiently detected, including small, dormant cancers and nodules with uncertain malignant potential. The early detection and treatment of diseases contributed to the diminution of mortality. Besides, some differentiated and borderline tumors, statistically filed as cancers, did not lead to death. The overestimation of cardiovascular consequences of low-dose, low-rate ionizing radiation has been reviewed recently.[45]

The excess relative risk (ERR) of cerebrovascular conditions in MPA employees was claimed to be even greater than in LSS.[46] Of note, some LSS data analyses were compatible with hormesis.[47-49] As mentioned above, a dose-response correlation for solid cancers and leukemia was detected in LSS at doses ≤500 mSv but not ≤200 mSv.[23-25] Furthermore, the data on kidney cancer in males indicated hormesis: U-shaped dose-response with negative risk estimates at low doses.[49] A preceding article by the same researchers showed different shapes of dose-response curves for men and women.[50] Other studies found no significant risks for renal cancer from low radiation doses.[51-53] Apparently, epidemiological data have too many uncertainties for a reliable evaluation of hormesis; large-scale animal experiments would be more informative.

Considering the above, the EURT experts’ following statements may create a biased impression. The statements cited below, not specifying dose levels, are apparently inapplicable to the cohorts from the Urals and to low radiation doses in general. Here follow the examples:

“It was shown that ionizing radiation is one of the promoters of the development of atherosclerosis”[54]

“It is concluded that this study provides evidence for an association of lower extremity arterial disease incidence with dose from external gamma-rays.”[55]

“This study provides strong evidence of ischemic heart disease incidence and mortality association with external gamma-ray exposure and some evidence of ischemic heart disease incidence and mortality association with internal alpha-radiation exposure.”[56]

“A significant increasing trend in circulatory diseases mortality with increasing dose from internal alpha-radiation to the liver was observed.”[57]

“Significant associations were observed between doses from external gamma-rays and ischemic heart disease and cerebrovascular disease incidence and between internal doses from alpha-radiation and ischemic heart disease mortality and cerebrovascular disease incidence.”[58]

“Findings are that aortal atherosclerosis prevalence was higher in males and females underwent external gamma-irradiation of total dose over 0.5 Gy, in males and females underwent internal alpha-irradiation from incorporated plutonium of total absorbed radiation dose in the liver over 0.025 Gy”.[59]

“There was a significantly increasing trend (ERR/Gy) of ischemic heart disease mortality with the total absorbed dose to the liver from internal alpha-radiation due to incorporated plutonium.”[40]

“The incidence data point to higher risk estimates (of cerebrovascular disease in MPA workers) than those from the Japanese A-bomb survivors.”[60]

“The categorical analyses showed that cerebrovascular disease incidence was significantly higher among workers with total absorbed external gamma-ray doses greater than 0.1 Gy compared to those exposed to lower doses and that cerebrovascular disease incidence was also significantly higher among workers with total absorbed internal alpha-particle doses to the liver from incorporated plutonium greater than 0.01 Gy compared to those exposed to lower doses”.[46]

The risk estimates by Tamara Azizova and co-workers[59] were found to be significantly higher than those in other studies.[61] Among members of the MPA cohort who received gamma-ray doses ≥0.1 Gy, circulatory disease incidence was more significant than in people exposed to lower doses.[46,62] Cause-effect relationships are improbable at such a low dose level, considering dose comparisons quoted in this review. The UNSCEAR could not reach a conclusion concerning causality between exposures ≤1-2 Gy and cardiovascular diseases.[63] The level 1-2 Gy is an underestimation due to the screening effect, selection, and other biases in epidemiological research.

Dose levels associated with cardiac derangements in experimental animals and humans after radiotherapy have been much more significant than average in Chernobyl and Urals populations.[64-67] Results of animal experiments (apart from genetically modified animals) are generally compatible with hormesis. In some experimental and epidemiological studies, low doses were protective against cardiovascular diseases.[64] The evidence in favor of hormesis is considerable.[13,68-72] In humans, myocardial fibrosis developed after radiotherapy at doses above 30 Gy. An increased risk of coronary heart disease after radiotherapy was noticed after exposures to 7.6-18.4 Gy.[66] which is much higher than the mean doses in Chernobyl and the Urals cohorts. It should be stressed that unrealistic cardiovascular risks at low-dose exposures call into question cancer risks reported by the same and other researchers. Finally, the recall bias should be mentioned: cancer patients remember radiation-related facts more often than healthy controls,[73] which may lead to overestimation of doses and dose-effect correlations.

The author agrees that “certain studies[56,58,74,75] should probably not be used for epidemiologic analysis, particularly…the Russian worker studies”.[76] Russian national mortality data is likely to be unsound.[77] The contrast between the medical surveillance of nuclear workers and the rest of the population has caused bias in data analyses from MPA. About 41% of the MPA cohort migrated away by the end of 2005, and information on causes of death was derived from various regions. The largest number of deaths in 1998-2010 happened not in Ozyorsk (where the Mayak facility is located) but elsewhere in Russia[77] whereas the reliability of data and interpretations are questionable.[3]

Here follows an example of a questionable attribution of lesions to radiation: a significantly increased risk of epidermal carcinoma was found in workers of MPA after exposures to 2.0 Sv or more.[78] This formally agrees with the LSS data indicating a threshold of ~1.0 Sv.[79] However, an observation bias seems to be probable in this study.[78] The workers and some medical personnel knew the employment duration that correlated with radiation doses. The latter could have influenced the diagnostic quality. Doses absorbed within the epidermis were not specified in the paper.[78] The workers were exposed predominantly to gamma, i.e., low-linear energy transfer (LET) radiation, so the doses within the epidermis were probably not high. Accordingly, the premalignant (actinic) epidermal lesions were “very rare.”[78] It is known that radiation exposures may cause premalignant epidermal changes, including actinic keratosis[80,81] that was not observed in the studied cohort.[78]

Another citation to be commented on: “…important issue in the field of radiation protection is the hypothesis of a reduction of radiation-associated cancer risk per unit dose at low dose-rates.[82-84] Such a hypothesis was derived from observations of biological results and has been implemented in the system of radiation protection by the introduction of a dose and dose-rate effectiveness factor (DDREF)… For solid cancer mortality, summary estimates of ERR/Gy derived from the LSS and The International Nuclear Workers Study (INWORKS) were similar in magnitude, a finding that does not support the conclusion of a reduction of ERR/Gy at low dose-rates”.[85] The conclusions regarding DDREF based on the studies of nuclear workers receiving doses largely compatible with broad-range NRB are unfounded,[38,39] as well as the statements that the linear no-threshold theory (LNT) for low radiation doses is unrejectable:[86] to reject the LNT, it suffices to prove hormesis. Some mathematical models suggested DDREF values from two up to infinity;[87] the latter agrees with the hormesis concept.

One more comment: the risks of leukemia in MPA employees, excluding chronic lymphocytic leukemia (CLL), calculated using incidence figures, were significantly greater than those calculated based on mortality.[88] A more efficient screening in people with higher doses is a probable mechanism. CLL is a special matter, often diagnosed early because of enlarged lymph nodes.[89]

Thyroid cancer

It is widely agreed that the frequency of thyroid cancer (TC) in people exposed at a young age after the Chernobyl accident (hereafter accident) increased significantly. The cause-effect relationship between Chernobyl exposures and other cancers has not been convincingly demonstrated.[22,90] The dramatic elevation of TC 4-5 years after the accident coincided with the start of mass screening;[9] it could be predicted neither from LSS nor from experience with radiotherapy.[91-100] The evidence of correlations between radiation doses and cancer risks comes predominantly from the epidemiological research associated with bias discussed in this article and elsewhere.[3]

Before the Chernobyl accident, the registered incidence of childhood TC in the Soviet Union was lower than in other industrialized countries.[101-105] The predominant increase among children and adolescents can be explained by the fact that the youth, contrary to older people, was actively screened at schools and kindergartens after the accident. Despite the normalized radiation background, awareness about thyroid tumors among medics and the population contributed to the enhanced TC incidence decades after the accident.[106,107] The detection rate of TC is known to depend on the screening intensity due to the pool of undiagnosed, dormant, and borderline tumors.[4,108]

The considerations delineated above have been camouflaged. The period 1986-1990 (when the TC frequency started to grow after the accident) was chosen for comparison with post-accident figures[109] “Since 1986, and not earlier, specific data on thyroid cancer incidence have been specifically collected by local oncologists” (UNSCEAR Secretariat, e-mail communication, 2013). It was stated that the TC incidence in Belarus in the period 1971-1985 did not significantly differ from global statistics,[110] referring to the paper,[95] where no such information was found. The pre-accident TC incidence in children <10 years old in Belarus and Ukraine was claimed without references to be 2-4 per million per year,[111] which is much higher than statistics published earlier (0.3 in Belarus, 0.1 in the North of Ukraine).[102] Extensive screening after the Chernobyl disaster found small tumors and neglected malignancies misinterpreted as radiogenic cancers arising after a short latency. Besides, residents were preoccupied with their recognition as victims of the accident to gain access to compensation and other provisions.[112] Cases brought from non-contaminated territories tended to be more advanced because there had been no mass screening outside the Chernobyl area. Accordingly, TCs found ten years after the accident were, on average, more advanced than those detected later.[113,114] Many early patients had advanced TC with distant metastases.[115]

Counting dormant cancers and questionable cases among malignancies, false-positivity, and registering people from clean areas as Chernobyl victims jointly contributed to the elevation of the recorded TC incidence after the Chernobyl disaster.[1-3,116] The frequency of papillary microcarcinoma in the general population was estimated at 1/200 people ≥ 30 years old;[117] its finding by the screening would elevate the detection rate considerably. In this connection, the following statement is potentially misleading: “77% of primary tumors were larger than 1 cm, suggesting that these were not incidental TCs detected by screening”.[118] It should be noted that the screening can find small nodules and advanced tumors, especially if targeted medical examinations have not covered the populace.

A recent study reported, “dose-related increases in DNA double-strand breaks in human TCs developing after the Chernobyl accident”.[119] This is not surprising considering that people with higher doses were generally better examined, and advanced malignancies were misinterpreted as rapidly growing radiogenic cancers: mutations tend to accumulate along with the neoplastic progression.[120,121] As for the lower TC incidence among people born after the accident, there were no motives to inflate the statistics, while the screening exhausted the pool of latent and neglected cases. The understanding of these facts finds its way to the literature: a recent study negated phenotypic differences between sporadic and supposedly radiogenic TCs[122] in contrast with preceding papers by the same research group, e.g.,[8] Analogous suggestions published more than a decade before[123] are, however, not cited.

Overtreatment of supposedly radiogenic cancer and precancerous lesions

The misinterpretation of neglected cancers, found by the screening, as rapidly growing radiogenic malignancies gave rise to the concept that radiogenic cancers are generally more aggressive. This contributed to the excessive radicalism of thyroid cancer (TC) treatment. The following was recommended for post-Chernobyl TC in children: “Radical thyroid surgery including total thyroidectomy combined with neck dissection followed by radioiodine ablation”[101] and radiotherapy with 40 Gy.[124] Side effects of the radioiodine therapy included salivary gland dysfunction (44.8% of cases), xerostomia (36%), and depressive states (38%).[125] Certain experts deemed subtotal thyroidectomy “oncologically not justified” and recommended total thyroidectomy with prophylactic neck dissection.[126-129] Less radical surgery was “only acceptable in exceptional cases of very small solitary intrathyroidal carcinomas without evidence of neck lymph node involvement on surgical revision.”[130] It was claimed that bilateral neck dissection is indicated for all TCs irrespective of size (including microcarcinoma), histological type, and lymph node involvement.[131] A similar approach was applied to radiation-exposed TC patients in the Urals.[132]

According to a recent report from Belarus, 69% of post-Chernobyl pediatric patients underwent total thyroidectomy; among them, radioiodine therapy was carried out in 69% of cases. For comparison, in patients diagnosed with TC after the Fukushima Daiichi accident, hemithyroidectomy was performed in 92% and total thyroidectomy in 8% of cases only.[125] In a study from Ukraine, “given the presence of radiation exposure in the patients’ histories,” total thyroidectomy was performed in 405 out of 465 papillary thyroid microcarcinomas (87.1%) with postoperative radioiodine therapy in 76.1% of the cases. The neck dissection was performed in ~50% of the cases.[133] Of note, recurrences to lymph nodes were detected only in 1.3% of the patients (median follow-up of 5.2 years). At the same time, the authors noted that microcarcinomas in their series were “rather indolent” and advised “more frequent organ-preserving surgeries vs. total thyroidectomy even for potentially radiogenic papillary thyroid microcarcinomas.”[133] In another paper, the same authors rightly concluded that “internal irradiation does not affect tumor phenotype… and does not worsen prognosis in pediatric or young adult patients with papillary thyroid microcarcinoma, implying that radiation history may not be a pivotal factor for determining treatment strategy”.[122] The long-term overall survival of post-Chernobyl TC patients was designated as excellent: during the 1990-2014 period, 21 (1.9%) pediatric TC patients died, among them only 2 from advanced cancer, 3 from secondary malignancies, 3 from other internal diseases, 6 due to trauma; 7 TC patients committed suicide.[125] These figures indicate the overdiagnosis and overuse of total thyroidectomy, associated with complications: hypoparathyroidism and recurrent laryngeal nerve palsy. The neck dissection is also associated with adverse effects.

Epidemiologists issued warnings against false-positive diagnoses of malignancy in thyroid nodules.[117,134] Many experts argued that the worldwide increase in TC incidence (not only in children) is caused by screening, medical surveillance improvements, and technological diagnostics advancements.[125,135] The author agrees with the following conclusions: “After the Chernobyl and Fukushima nuclear accidents, thyroid cancer screening was implemented mainly for children, leading to case over-diagnosis;” “The existence of a natural reservoir of latent thyroid carcinomas, together with advancements in diagnostic practices leading to case overdiagnosis, explain, at least partially, the rise in TC incidence in many countries;” “Total thyroidectomy, as performed after the Chernobyl accident, implies that patients must live the rest of their lives with thyroid hormone supplementation. Additional treatment using radioactive iodine-131 therapy in some cases may result in potentially short- or long-term adverse effects”;[136] “The extent to which opportunistic thyroid cancer screening is converting thousands of asymptomatic persons to cancer patients without any known benefit to them needs to be examined carefully.”[135] Similar concerns were expressed by other experts. American Thyroid Association (ATA) guidelines indicate that thyroid nodules less than 1 cm should not be biopsied, nodules 1 cm to 1.5 cm should be biopsied only when features concerning a malignant tumor exist, and papillary thyroid cancer (PTC) nodules 1 cm or less should be managed with active surveillance or lobectomy.[137]

The sources[138-140] were quoted to corroborate the recommendation: “The most prevailing opinion calls for total thyroidectomy regardless of tumor size and histopathology.”[130] This is a misquoting: the talk is about subtotal resection in the cited sources, which is not the same.[139-140] Analogously, the sources[140-142] were misquoted in the paper.[127] Potential health-related, cosmetic, and social (stigmatization as a cancer patient) adverse effects of surgical hyper-radicalism are known.[117,143-145] Histological images from Russian textbooks, potentially conducive to false-positivity, were reproduced and discussed previously.[3,116,146] Chernobyl-associated radiophobia contributed to the false positivity and overtreatment: “Practically all thyroid nodules, independently of their size, were regarded at that time in children as potentially malignant tumors, requiring an urgent surgery.”[147]

Mechanisms of false-positivity have been discussed previously;[3,116,146] among others, the misinterpretation of nuclear pleomorphism as a malignancy criterion of thyroid nodules occurred in the former Soviet Union (SU) of the 1990s. If the screening finds a thyroid nodule, a fine-needle aspiration is usually performed. The thyroid cytology is accompanied by some percentage of inconclusive results when histological examination is indicated. This percentage was relatively high in the former SU due to insufficient experience with pediatric material, suboptimal quality of specimens, and insufficient use of modern literature. The surgical specimen is sent to a pathologist, who may be sometimes prone, after in toto resection of the nodule to confirm malignancy even in case of uncertainty. The fine-needle aspiration cytology was introduced into practice later than ultrasonography, contributing to the overdiagnosis of malignancy, especially during the 1990s.

Analogous overtreatment tendencies have been noticed regarding renal and bladder lesions.[148-158] Surgeons might overuse nephrectomy if they learn that renal-cell carcinoma from contaminated territories is, on average, more aggressive, while surrounding parenchyma contains “proliferative atypical nephropathy with tubular epithelial nuclear atypia and carcinoma in situ.”[148] The same Chernobyl experts found in patients with the benign prostatic disease and cystitis from contaminated territories and the city of Kyiv (not recognized as contaminated), severe dysplasia or carcinoma in situ in urinary bladders of 56%-73% randomly selected cases.[153-158] These percentages are unrealistic for overdiagnosis and hypertherapy. Histological images from the papers[153,154] were reprinted and commented previously;[159] neither malignancy nor severe dysplasia is recognizable. The clinical and morphological findings designated as “Chernobyl cystitis” or “irradiation cystitis” with “reactive epithelial proliferation associated with hemorrhage, fibrin deposits, fibrinoid vascular changes, and multinuclear stromal cells”[158] were contributed by repeated cystoscopy, “mapping” punch biopsies and electrocoagulation of vesical mucosa. The “marked activation of angiogenesis,” described in supposedly radiation-related cystitis,[154] could have resulted from iatrogenic injury. The microphotographs from the papers[160,161] (reproduced[159]) indicate that overdiagnosis and overtreatment also occurred back in the 1980s.

In conclusion, the following unreasonable claim should be commented on: “When considering the effects of irradiation on human health, it is necessary to clearly distinguish between the effects of increased background radiation to which adaptation can occur over many generations at the population level and the effects of irradiation as a result of accidents or medical procedures.”[162] Note that an equivalent dose is essential, no matter where it was received: from natural or anthropogenic sources.

Discussion

Mutations and DNA repair are in a permanent balance. There must be an optimal exposure level, as it is for many physical factors, chemical elements, and compounds, including water radiolysis products.[163] NRB has probably been decreasing on the Earth’s surface.[164] Therefore, an optimal exposure level may be even higher than today’s NRB. It can be reasonably assumed that the evolutionary adaptation would be operative at all ages, including embryogenesis. There are suggestions that, in utero, relative risks in LSS may be lower than those in some other groups.[18] although acute exposures are generally more effective than chronic and fractionated ones, overviewed previously.[38,39] This adds doubts about conclusions based solely on epidemiological research. The available literature does not provide direct evidence that low-dose prenatal exposures increase stochastic effects (excess cancer risk) or deterministic impact on the offspring.[165]

The optimal approach for radiation protection regulations is determining the threshold dose for the carcinogenic effect and establishing rules to ensure that professional exposures are kept well below.[47,61] According to a recent review, epidemiological data provide no convincing evidence of harm at doses ≤100 mSv, whereas some studies suggested hormesis.[166] The dose level of 200 mSv was mentioned in some reviews as a threshold below which radiation-related cancer risks are unproven.[23,167,168] Dose reconstructions in humans are often imprecise. Screening effect, selection, and ideological bias in epidemiological research may contribute to the appearance of new reports on enhanced cancer risks associated with a moderate increase in the radiation background. This would not prove causality. Large-scale animal experiments using different species are the most reliable tool to determine threshold doses. In utero, damage, and corresponding thresholds can also be studied in animals.

CONCLUSION

Certain scientific writers act following the interests of companies and governments selling petroleum and natural gas. Most evident is this tendency regarding ionizing radiation, whereas the overestimation of medical and environmental side effects of nuclear energy contributes to its strangulation, supporting appeals to dismantle nuclear power plants and boosting fossil fuel prices. The use of atomic energy for electricity production is on the agenda today due to the increasing energy needs of humankind. Health risks and environmental damage are maximal for coal and oil, lower for natural gas, and much lower for atomic energy - the cleanest, safest, and practically inexhaustible energy resource. The weightiest argument against NPPs is that they are potential targets in armed conflicts. Escalation of conflicts and nuclear threats contribute to the boosting of fossil fuel prices. This is probably one of the motives of the Ukraine war, nuclear threats, and other militaristic rhetoric. Finally, speculations about the extraordinary aggressiveness of radiogenic cancers have contributed to the overtreatment. Nuclear energy production should be developed under the guidance centered in developed countries.

Authors’ contributions

The entire article has been drafted by the author.

Ethical approval

The Institutional Review Board approval is not required.

Declaration of patient consent

Patient’s consent not required as there are no patients in this study.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

Use of artificial intelligence (AI)-assisted technology for manuscript preparation

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

References

  1. . Over-estimation of radiation-induced malignancy after the Chernobyl accident. Virchows Arch. 2007;451:105-6.
    [CrossRef] [PubMed] [Google Scholar]
  2. . Hormesis and radiation safety norms: Comments for an update. Hum Exp Toxicol. 2018;37:1233-43.
    [CrossRef] [PubMed] [Google Scholar]
  3. . The overestimation of medical consequences of low - dose exposure to ionizing radiation. In: 2nd Edition. Newcastle upon Tyne. Cambridge Scholars Publishing; .
    [Google Scholar]
  4. . Observations on the Chernobyl Disaster and LNT. Dose Response. 2010;8:148-71.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  5. , . Electricity generation and health. Lancet. 2007;370:979-90.
    [CrossRef] [PubMed] [Google Scholar]
  6. , , , , , . Energy and Health. In: , , , , eds. Global energy assessment. Cambridge: Cambridge University Press; . p. :102-300.
    [Google Scholar]
  7. , , , , , . The characteristics of the biological action of low doses of irradiation. Radiats Biol Radioecol. 1996;36:610-31.
    [PubMed] [Google Scholar]
  8. , , , , , . Comparative histopathologic analysis of “Radiogenic” and “Sporadic” papillary thyroid carcinoma: patients born before and after the Chernobyl accident. Thyroid. 2018;28:880-90.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  9. , , , , , . Morphological and clinical presentation of papillary thyroid carcinoma in children and adolescents of Belarus: the influence of radiation exposure and the source of irradiation. Exp Mol Pathol. 2015;98:527-31.
    [CrossRef] [PubMed] [Google Scholar]
  10. . Overestimation of Chernobyl consequences: poorly substantiated information published. Radiat Environ Biophys. 2010;49:743-5.
    [CrossRef] [PubMed] [Google Scholar]
  11. . Misconduct in medical research and practice. Hauppauge NY: Nova Science Publishers; .
  12. , , . Epidemiology without biology: False paradigms, unfounded assumptions, and specious statistics in radiation science. Biol Theory. 2016;11:69-101.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  13. , . Overview of biological, epidemiological, and clinical evidence of radiation hormesis. Int J Mol Sci. 2018;19:2387.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  14. , , , . Hiroshima survivors exposed to very low doses of A-bomb primary radiation showed a high risk for cancers. Environ Health Prev Med. 2008;13:264-70.
    [CrossRef] [PubMed] [Google Scholar]
  15. , , , , . The non-cancer mortality experience of male workers at British Nuclear Fuels plc, 1946-2005. Int J Epidemiol. 2008;37:506-18.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  16. , , , , , . Thyroid cancer risk in Belarus among children and adolescents exposed to radioiodine after the Chornobyl accident. Br J Cancer. 2011;104:181-7.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  17. , , , , , . Radiation and the risk of chronic lymphocytic and other leukaemias among Chernobyl cleanup workers. Environ Health Perspect. 2011;211:59-65.
    [Google Scholar]
  18. , , , , , . Review of the risk of cancer following low and moderate doses of sparsely ionising radiation received in early life in groups with individually estimated doses. Environ Int. 2022;159:106983.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  19. . Radiation, people and the environment. Vienna: IAEA; .
  20. . Annex B: Exposures from natural radiation sources. Annex G: Biological effects at low radiation doses. New York: United Nations; .
  21. , , , , , . Radiation doses to the population of the Russian Federation in. 2020. Radiatsionnaya Gygiena - Radiation Hygiene. 2021;14:103-13.
    [Google Scholar]
  22. . Health effects due to radiation from the Chernobyl accident. New York: United Nations; .
  23. , , . No evidence for increased tumour rates below 200 mSv in the atomic bomb survivors data. Radiat Environ Biophys. 1997;36:205-7.
    [CrossRef] [PubMed] [Google Scholar]
  24. , . Evidence for curvilinearity in the cancer incidence dose-response in the Japanese atomic bomb survivors. Int J Radiat Biol. 1996;70:83-94.
    [CrossRef] [PubMed] [Google Scholar]
  25. , . Curvature in the cancer mortality dose response in Japanese atomic bomb survivors: absence of evidence of threshold. Int J Radiat Biol. 1998;74:471-80.
    [CrossRef] [PubMed] [Google Scholar]
  26. , , . Oxford textbook of cancer biology Oxford. .
  27. , , , , , . Health status of population exposed to environmental contamination in the Southern Urals. Moscow: Radekon; . Russian
  28. , , . Medical and biological consequences of human’s chronic exposure to radiation. Med Tr Prom Ekol 2004:30-6.
    [Google Scholar]
  29. , , , , , . The medical sequelae of the radiation accident in the Southern Urals in 1957. Med Radiol (Mosk). 1990;35:11-5.
    [Google Scholar]
  30. , . Long-term irradiation effects in the population evacuated from the east-Urals radioactive trace area. Sci Total Environ. 1994;142:119-25.
    [CrossRef] [PubMed] [Google Scholar]
  31. , , , , , . Health status among the staff at the nuclear waste processing plant. Med Tr Prom Ekol 2000:10-4.
    [Google Scholar]
  32. , , , , , . Interaction of radiation and smoking in lung cancer induction among workers at the Mayak nuclear enterprise. Health Phys. 2002;83:833-46.
    [CrossRef] [PubMed] [Google Scholar]
  33. , . Carcinogenic risk in residents of the Techa riverside villages. Vestn Ross Akad Med Nauk 2010:34-9.
    [Google Scholar]
  34. , , , , , . Leukaemia incidence in the Techa river cohort: 1953–2007. Br J Cancer. 2013;109:2886-93.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  35. , , , , , , . Breast cancer incidence following low-dose rate environmental exposure: Techa river cohort, 1956-2004. Br J Cancer. 2008;99:1940-5.
    [CrossRef] [PubMed] [Google Scholar]
  36. , , , . Consequences of the radiation accident at the Mayak production association in 1957 (the ‘Kyshtym Accident’) J Radiol Prot. 2017;37:R19-42.
    [CrossRef] [PubMed] [Google Scholar]
  37. , , . Overall results and prospects of the cancer risk assessment in the Urals population affected by chronic low dose-rate exposure. Radiat Med Prot. 2022;3:159-66.
    [Google Scholar]
  38. . On the Dose and Dose Rate Effectiveness Factor (DDREF) Radiats Biol Radioecol. 2017;57:308-14.
    [Google Scholar]
  39. . Dose and dose-rate effectiveness of radiation: first objectivity then conclusions. J Environ Occup Sci. 2016;5:25-9.
    [Google Scholar]
  40. , , , , , . Mortality risk of cardiovascular diseases for occupationally exposed workers. Radiats Biol Radioecol. 2012;52:158-66.
    [PubMed] [Google Scholar]
  41. , , , , . Cerebrovascular diseases incidence and mortality in an extended Mayak worker cohort 1948–1982. Med Radiol Radiaton Safety (Moscow). 2015;60:43-61.
    [Google Scholar]
  42. , . On possible mistakes in the estimation of radiation risk non-cancer effects in Mayak plant workers. Med Radiol Radiaton Safety (Moscow). 2018;63:83-4.
    [Google Scholar]
  43. , , , , , . 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.
    [CrossRef] [PubMed] [Google Scholar]
  44. . Solid cancer increase among Chernobyl liquidators: alternative explanation. Radiat Environ Biophys. 2015;54:373-5.
    [CrossRef] [PubMed] [Google Scholar]
  45. . Overestimation of cardiovascular consequences of low dose low rate ionizing radiation. Life Sciences: an International Journal (LSIJ). 2023;1:51-9.
    [Google Scholar]
  46. , , , , . Cerebrovascular diseases incidence and mortality in an extended Mayak Worker Cohort 1948–1982. Radiat Res. 2014;182:529-44.
    [CrossRef] [PubMed] [Google Scholar]
  47. . Future of radiation protection regulations. Health Phys. 2016;110:274-5.
    [CrossRef] [PubMed] [Google Scholar]
  48. . Atomic bomb health benefits. Dose Response. 2008;6:369-82.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  49. , , , , , . Radiation risks for the incidence of kidney, bladder and other urinary tract cancers: 1958-2009. Radiat Res. 2021;195:140-8.
    [CrossRef] [PubMed] [Google Scholar]
  50. , , , , , . Solid Cancer Incidence among the Life Span Study of Atomic Bomb Survivors: 1958-2009. Radiat Res. 2017;187:513-37.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  51. , , , , , , . Mortality among U.S. military participants at eight aboveground nuclear weapons test series. Int J Radiat Biol. 2022;98:679-700.
    [Google Scholar]
  52. , , , , . Cancer mortality and incidence following external occupational radiation exposure: an update of the 3rd analysis of the UK national registry for radiation workers. Br J Cancer. 2018;119:631-7.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  53. , , , , , . Site-specific solid cancer mortality after exposure to ionizing radiation: A Cohort Study of Workers (INWORKS) Epidemiology. 2018;29:31-40.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  54. , . The influence of the ionizing radiation on the development of atherosclerosis. Radiats Biol Radioecol. 2016;56:44-55.
    [PubMed] [Google Scholar]
  55. , , , , . Risk of lower extremity arterial disease in a cohort of workers occupationally exposed to ionizing radiation over a prolonged period. Radiat Environ Biophys. 2016;55:147-59.
    [CrossRef] [PubMed] [Google Scholar]
  56. , , , , . Ischaemic heart disease incidence and mortality in an extended cohort of Mayak workers first employed in 1948–1982. Br J Radiol. 2015;88:20150169.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  57. , , , , . Risk of mortality from circulatory diseases in Mayak workers cohort following occupational radiation exposure. J Radiol Prot. 2015;35:517-38.
    [CrossRef] [PubMed] [Google Scholar]
  58. , , , . Risks of circulatory diseases among Mayak PA workers with radiation doses estimated using the improved Mayak Worker Dosimetry System 2008. Radiat Environ Biophys. 2014;53:469-77.
    [CrossRef] [PubMed] [Google Scholar]
  59. , , , , , , , , . Cerebrovascular diseases in nuclear workers first employed at the Mayak PA in 1948–1972. Radiat Environ Biophys. 2011;50:539-52.
    [CrossRef] [PubMed] [Google Scholar]
  60. , , , , , . Risk of cerebrovascular disease incidence in the cohort of Mayak production association workers first employed during 1948–1958. Radiats Biol Radioecol. 2012;52:149-57.
    [PubMed] [Google Scholar]
  61. , , , , , . Dose limits for occupational exposure to ionising radiation and genotoxic carcinogens: a German perspective. Radiat Environ Biophys. 2020;59:9-27.
    [CrossRef] [PubMed] [Google Scholar]
  62. , , , , , . Cerebrovascular diseases in workers at Mayak PA: The difference in radiation risk between incidence and mortality. PLoS One. 2015;10:e0125904.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  63. . Epidemiological evaluation of cardiovascular disease and other non-cancer diseases following radiation exposure. New York: United Nations; .
  64. , , , , , . ICRP publication 118: ICRP statement on tissue reactions and early and late effects of radiation in normal tissues and organs - threshold doses for tissue reactions in a radiation protection context. Ann ICRP. 2012;41:1-322.
    [Google Scholar]
  65. , , , , , . Effects of ionizing radiation on the heart. Mutat Res Rev Mutat Res. 2016;770:319-27.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  66. , , , , , . Impact of ionizing radiation on the cardiovascular system: A review. Radiat Res. 2017;188:539-46.
    [CrossRef] [PubMed] [Google Scholar]
  67. . Radiation-induced heart disease: review of experimental data on dose response and pathogenesis. Int J Radiat Biol. 1992;61:149-60.
    [CrossRef] [PubMed] [Google Scholar]
  68. , . Radiation hormesis: historical and current perspectives. J Nucl Med Technol. 2015;43:242-6.
    [CrossRef] [PubMed] [Google Scholar]
  69. . Linear no-threshold model vs. radiation hormesis. Dose Response. 2013;11:480-97.
    [Google Scholar]
  70. . It’s time for a new low-dose-radiation risk assessment paradigm - one that acknowledges hormesis. Dose Response.. 2008;6:333-51.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  71. . Radiation safety and hormesis. Front Public Health. 2020;8:278.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  72. , , , , , . Role of low-dose radiation in senescence and aging: A beneficial perspective. Life Sci. 2022;302:120644.
    [CrossRef] [PubMed] [Google Scholar]
  73. . Dental x-rays and risk of meningioma. Cancer. 2013;119:463.
    [CrossRef] [PubMed] [Google Scholar]
  74. , , , , . The risk of radiation-induced cerebrovascular disease in Chernobyl emergency workers. Health Phys. 2006;90:199207.
    [Google Scholar]
  75. , , , , . Radiation-epidemiological study of cerebrovascular diseases in the cohort of Russian recovery operation workers of the Chernobyl accident. Health Phys. 2016;111:192-7.
    [CrossRef] [PubMed] [Google Scholar]
  76. . Radiation and circulatory disease. Mutat Res. 2016;770:299-318.
    [Google Scholar]
  77. , , . Low- and moderate-dose non-cancer effects of ionizing radiation in directly exposed individuals, especially circulatory and ocular diseases: a review of the epidemiology. Int J Radiat Biol. 2021;97:782-803.
    [CrossRef] [PubMed] [Google Scholar]
  78. , , , . Risk of malignant skin neoplasms in a cohort of workers occupationally exposed to ionizing radiation at low dose rates. PLoS One. 2018;13:e0205060.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  79. , . The risk of non-melanoma skin cancer incidence in the Japanese atomic bomb survivors. Int J Radiat Biol. 1997;71:589-602.
    [CrossRef] [PubMed] [Google Scholar]
  80. . Occupational skin cancers. Occupation Medicine (London). 2004;54:458-63.
    [Google Scholar]
  81. , . Actinic keratosis: A clinical and epidemiological revision. Anais Brasileiros de Dermatologia.. 2012;87:425-34.
    [CrossRef] [PubMed] [Google Scholar]
  82. , , , , , . Is cancer risk of radiation workers larger than expected? Occup Environ Med. 2009;66:789-96.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  83. , , , , , . Dose and dose-rate efects of ionizing radiation: a discussion in the light of radiological protection. Radiat Environ Biophys. 2015;54:379-401.
    [CrossRef] [PubMed] [Google Scholar]
  84. , , , , , , . Dose-rate efects in radiation biology and radiation protection. Ann ICRP. 2015;45:262-79.
    [Google Scholar]
  85. , , , , , . Risk of cancer associated with low-dose radiation exposure: comparison of results between the INWORKS nuclear workers study and the A-bomb survivors study. Radiat Environ Biophys. 2021;60:23-39.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  86. , . It is time to move beyond the linear no-threshold theory for low-dose radiation protection. Dose Response. 2018;16:1559325818779651.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  87. , , , . The increase in animal mortality risk following exposure to sparsely ionizing radiation is not linear quadratic with dose. PLoS One. 2015;10:e0140989.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  88. . Overview of epidemiological studies of nuclear workers: opportunities, expectations, and limitations. J Radiol Prot 2021:41.
    [Google Scholar]
  89. . On the radiation-leukemia dose-response relationship among recovery workers after the Chernobyl accident. Dose Response. 2013;12:162-5.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  90. Report of the UN Chernobyl Forum Expert Group “Health”. In: , , , eds. Health effects of the Chernobyl accident. WHO: Geneva; .
    [Google Scholar]
  91. . Exposure and Effects of the Chernobyl Accident. New York: United Nations; .
  92. . Chernobyl and thyroid cancer. J Surg Oncol. 2006;94:670-7.
    [CrossRef] [PubMed] [Google Scholar]
  93. . Radiation carcinogenesis: Lessons from Chernobyl. Oncogene. 2008;27:S9-18.
    [CrossRef] [PubMed] [Google Scholar]
  94. . Radiation-induced thyroid cancer - what’s new? J Natl Cancer Inst. 2005;97:703-5.
    [CrossRef] [PubMed] [Google Scholar]
  95. . Effects of irradiation on the thyroid gland. Endocrinol Metab Clin North Am. 1993;22:607-15.
    [PubMed] [Google Scholar]
  96. , , , , . Thyroid cancer risk after thyroid examination with 131I: A population-based cohort study in Sweden. Int J Cancer. 2003;106:580-7.
    [CrossRef] [PubMed] [Google Scholar]
  97. , , , . Thyroid cancer after diagnostic administration of iodine-131 in childhood. Radiat Res. 2001;156:61-70.
    [CrossRef] [PubMed] [Google Scholar]
  98. . Thyroid cancer after exposure to radioactive 131I. Acta Oncol. 2006;45:1037-40.
    [CrossRef] [PubMed] [Google Scholar]
  99. . Radiation-induced thyroid neoplasia. Soz Praventivmed. 1991;36:266-75.
    [CrossRef] [PubMed] [Google Scholar]
  100. . Increasing world incidence of thyroid cancer: Increased detection or higher radiation exposure? Hormones (Athens). 2010;9:103-8.
    [CrossRef] [PubMed] [Google Scholar]
  101. , , . Childhood thyroid cancer in Belarus, Russia and Ukraine after Chernobyl and at present. Arq Bras Endocrinol Metabol. 2007;51:748-62.
    [CrossRef] [PubMed] [Google Scholar]
  102. , , , , . Childhood thyroid cancer since accident at Chernobyl. BMJ. 1995;310:801.
    [Google Scholar]
  103. , , , . Thyroid cancer in childhood: Management strategy, including dosimetry and long-term results. Hormones (Athens). 2007;6:269-78.
    [CrossRef] [PubMed] [Google Scholar]
  104. , , , . Differentiated thyroid cancer in childhood: A literature update. Hormones (Athens). 2017;16:381-7.
    [CrossRef] [PubMed] [Google Scholar]
  105. , , , , . Increase in the incidence of differentiated thyroid carcinoma in children, adolescents, and young adults: A population-based study. J Pediatr. 2014;164:1481-5.
    [CrossRef] [PubMed] [Google Scholar]
  106. , , , , , . Morphological features of spontaneous papillary carcinoma of the thyroid in children and adolescents in the Republic of Belarus. Vopr Onkol. 2012;58:578-81.
    [PubMed] [Google Scholar]
  107. , , , , . The increase of non-cancerous thyroid tissue in children and adolescents operated for papillary thyroid cancer: related factors. Vopr Onkol. 2013;59:121-5.
    [PubMed] [Google Scholar]
  108. , , . Thyroid cancer in the pediatric population. Genes (Basel). 2019;10:723.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  109. . Evaluation of Data on Thyroid Cancer in Regions Affected by the Chernobyl Accident. New York: United Nations; .
  110. , , , . Clinical and morphological features of papillary thyroid cancer in children and adolescents in the Republic of Belarus: Analysis of 936 post-Chernobyl carcinomas. Vopr Onkol. 2014;60:43-6.
    [PubMed] [Google Scholar]
  111. . Health and environmental effects of the Chernobyl accident presented in the UNSCEAR Report. 2008: Lessons for nuclear emergency response. Med Radiol Radiaton Safety (Moscow). 2011;56:15-23.
    [Google Scholar]
  112. , , . Social and economic effects. In: Chernobyl - Catastrophe and Consequences. Chichester: Springer; . p. :239-66.
    [Google Scholar]
  113. , , , , , . Thyroid carcinoma after Chernobyl latent period, morphology and aggressiveness. Br J Cancer. 2004;90:2219-24.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  114. , . The Chernobyl accident - an epidemiological perspective. Clin Oncol (R Coll Radiol). 2011;23:251-60.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  115. , , , , , . Twenty-five years after Chernobyl: outcome of radioiodine treatment in children and adolescents with very high-risk radiation-induced differentiated thyroid carcinoma. J Clin Endocrinol Metab. 2013;98:3039-48.
    [CrossRef] [PubMed] [Google Scholar]
  116. . Some aspects of thyroid neoplasia after Chernobyl. Hamdan Med J. 2020;13:69-77.
    [Google Scholar]
  117. . Overdiagnosis of juvenile thyroid cancer. Eur Thyroid J. 2020;9:124-31.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  118. , , . Clinical presentation and clinical outcomes in Chernobyl-related paediatric thyroid cancers: What do we know now? What can we expect in the future? Clin Oncol (R Coll Radiol). 2011;23:268-75.
    [Google Scholar]
  119. , , , , , . Radiation-related genomic profile of papillary thyroid carcinoma after the Chernobyl accident. Science. 2021;372:eabg2538.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  120. , . Regulation of error-prone DNA double-strand break repair and its impact on genome evolution. Cells. 2020;9:1657.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  121. , , , , , . Recent advances in the nucleolar responses to DNA double-strand breaks. Nucleic Acids Res. 2020;48:9449-61.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  122. , , , , , . The high degree of similarity in histopathological and clinical characteristics between radiogenic and sporadic papillary thyroid microcarcinomas in young patients. Front Endocrinol (Lausanne). 2022;13:970682.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  123. . Overestimation of thyroid cancer incidence after Chernobyl. Health Phys. 2009;96:186.
    [CrossRef] [PubMed] [Google Scholar]
  124. , . Surgical treatment of nodular goiter after the accident at the Chernobyl nuclear power station. Klin Khir. 1992;12:38-40.
    [Google Scholar]
  125. , , , , , . A search for causes of rising incidence of differentiated thyroid cancer in children and adolescents after Chernobyl and Fukushima: comparison of the clinical features and their relevance for treatment and prognosis. Int J Environ Res Public Health. 2021;18:3444.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  126. . Thyroid cancer: modern approaches to diagnostics and treatment. Moscow: Geotar-Media; .
  127. , . Repeat surgery for recurrent thyroid cancer in children. Vopr Onkol. 2003;49:366-9.
    [PubMed] [Google Scholar]
  128. , , . Consequences of Chernobyl accident. In: Thyroid carcinoma in children. Moscow: Meditsina; . Russian
    [Google Scholar]
  129. , , . Thyroid microcarcinoma. Moscow: Meditsina; . Russian
  130. , , , , , . Comprehensive clinical assessment of 740 cases of surgically treated thyroid cancer in children of Belarus. Ann Surg. 2006;243:525-32.
    [CrossRef] [PubMed] [Google Scholar]
  131. , . Thyroid tumors. Minsk: BelMAPO; . Russian
  132. . Surgery of thyroid and parathyroid. St. Petersburg: Vesti; . Russian
  133. , , , , , . The relationship of the clinicopathological characteristics and treatment results of post-Chornobyl papillary thyroid microcarcinomas with the latency period and radiation exposure. Front Endocrinol (Lausanne). 2022;13:1078258.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  134. . How to handle borderline/precursor thyroid tumors in management of patients with thyroid nodules. Gland Surg. 2018;7:S8-S18.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  135. , , , , , . Thyroid Cancer Screening in South Korea Increases Detection of Papillary Cancers with No Impact on Other Subtypes or Thyroid Cancer Mortality. Thyroid. 2016;26:1535-40.
    [CrossRef] [PubMed] [Google Scholar]
  136. , , , , , . Lessons learned from Chernobyl and Fukushima on thyroid cancer screening and recommendations in case of a future nuclear accident. Environ Int. 2021;146:106230.
    [CrossRef] [PubMed] [Google Scholar]
  137. , , , , . Physician Perspectives of Overdiagnosis and Overtreatment of Low-Risk Papillary Thyroid Cancer in the US. JAMA Netw Open. 2022;5:e228722.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  138. , , , , , . Differentiated thyroid cancer in children and adolescents. J Endocrinol Invest. 2002;25:18-24.
    [CrossRef] [PubMed] [Google Scholar]
  139. , , , , , . Differentiated thyroid carcinoma in children and adolescents: clinical characteristics, treatment and outcome of 15 patients. Horm Res. 2002;57:153-6.
    [CrossRef] [PubMed] [Google Scholar]
  140. , , , , , . Thyroid carcinoma in children and adolescents. Eur J Pediatr. 1997;156:190-4.
    [CrossRef] [PubMed] [Google Scholar]
  141. , , , , . Recurrence and morbidity in differentiated thyroid carcinoma in children. Surgery. 1988;104:1149-56.
    [PubMed] [Google Scholar]
  142. , , , , . Cancer of the thyroid in children and adolescents. Clin Otolaryngol Allied Sci. 1997;22:525528.
    [Google Scholar]
  143. , , , , , . Pediatric thyroid cancer in Europe: An overdiagnosed condition? A Literature Review. Diagnostics (Basel).. 2020;19;10:112.
    [CrossRef] [PubMed] [Google Scholar]
  144. , , , , , . Management Guidelines for children with thyroid nodules and differentiated thyroid cancer. Thyroid. 2015;25:716-59.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  145. , , , , , . Thyroid cancer in adolescents and young adults. Pediatr Blood Cancer. 2018;65:e27025.
    [CrossRef] [PubMed] [Google Scholar]
  146. . Back to Chernobyl: some aspects of cancer diagnostics. J Environ Stud. 2016;2:8.
    [Google Scholar]
  147. , , . Thyroid cancer in Russia after the Chernobyl. Moscow: Meditsina; .
  148. , , , , . Radiation sclerosing proliferative atypical nephropathy of peritumoral tissue of renal-cell carcinomas after the Chernobyl accdent in Ukraine. Virchows Arch. 2001;438:146-53.
    [CrossRef] [PubMed] [Google Scholar]
  149. , , , , . Pathology and proliferative activity of renal-cell carcinomas (RCCS) and renal oncocytomas in patients with different radiation exposure after the Chernobyl accident in Ukraine. Int J Cancer. 2000;87:880-3.
    [CrossRef] [PubMed] [Google Scholar]
  150. , , , , . Alteration of apoptotic regulatory molecules in conventional renal cell carcinoma influenced by chronic long-term low-dose ionizing radiation exposure in humans revealed by tissue microarray. Cancer Genomics Proteomics. 2006;3:107-12.
    [PubMed] [Google Scholar]
  151. , , , , , . Extracellular matrix alterations in conventional renal cell carcinomas by tissue microarray profiling influenced by the persistent, long-term, low-dose ionizing radiation exposure in humans. Virchows Arch. 2006;448:584-90.
    [CrossRef] [PubMed] [Google Scholar]
  152. , , , , , . Microvessel density is high in clear-cell renal cell carcinomas of Ukrainian patients exposed to chronic persistent low-dose ionizing radiation after the Chernobyl accident. Virchows Arch. 2012;460:611-9.
    [CrossRef] [PubMed] [Google Scholar]
  153. , , , , , . Increased oxidative stress with gene alteration in urinary bladder urothelium after the Chernobyl accident. Int J Cancer. 2000;86:790-8.
    [CrossRef] [PubMed] [Google Scholar]
  154. , , , , , . Urinary bladder carcinogenesis induced by chronic exposure to persistent low-dose ionizing radiation after Chernobyl accident. Carcinogenesis. 2009;30:1821-31.
    [CrossRef] [PubMed] [Google Scholar]
  155. , , , , , . DNA damage repair in bladder urothelium after the Chernobyl accident in Ukraine. J Urol. 2002;168:973-7.
    [CrossRef] [PubMed] [Google Scholar]
  156. , , , , , . Upregulation of fibroblast growth factor receptor 3 and epidermal growth factor receptors, in association with Raf-1, in urothelial dysplasia and carcinoma in situ after the Chernobyl accident. Cancer Sci. 2006;97:1168-74.
    [CrossRef] [PubMed] [Google Scholar]
  157. , , , , , . Involvement of ubiquitination and sumoylation in bladder lesions induced by persistent long-term low dose ionizing radiation in humans. J Urol. 2006;175:739-43.
    [CrossRef] [PubMed] [Google Scholar]
  158. , , , . Correspondence re: W Paile’s letter to the editor Cancer Res., 60:1146, 2000. Cancer Res. 2001;61:6964-5.
    [PubMed] [Google Scholar]
  159. . Urological concern after nuclear accidents. Urol Ann. 2018;10:240-2.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  160. , , . Leukoplakia of the bladder. Arkh Patol. 1985;47:52-8.
    [Google Scholar]
  161. . Chronic cystitis in the aspect of its relationship with precancerous conditions. Arkh Patol. 1982;44:52-8.
    [Google Scholar]
  162. , , . Low-dose ionizing radiation as a hormetin: experimental observations and therapeutic perspective for age-related disorders. Biogerontology. 2021;22:145-64.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  163. , , . Reactive oxygen species and redox compartmentalization. Front Physiol. 2014;5:285.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  164. , . Calculations of background beta-gamma radiation dose through geologic time. Health Phys. 1999;77:662-7.
    [CrossRef] [PubMed] [Google Scholar]
  165. , , , , , . Ionizing radiation exposure during pregnancy: Effects on postnatal development and life. Radiat Res. 2017;187:647-58.
    [CrossRef] [PubMed] [Google Scholar]
  166. . Low doses of radiation - impact on the environment and human. Medical Research Journal 2023
    [CrossRef] [Google Scholar]
  167. , , . Cancer risk atlow doses of ionizing radiation: artificial neural net-works inference from atomic bomb survivors. J Radiat Res. 2014;55:391-406.
    [CrossRef] [PubMed] [PubMed Central] [Google Scholar]
  168. . Radiation safety standards and their application: international policies and current issues. Health Phys. 2004;87:258-72.
    [CrossRef] [PubMed] [Google Scholar]

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