Considering Existing Factors That May Cause Radiation Hormesis at &lt;100 mSv and Obey the Linear No-Threshold Theory at ≥100 mSv

Kino, Katsuhito; Ohshima, Takayuki; Takeuchi, Hajime; Kobayashi, Tomomi; Kawada, Taishu; Morikawa, Masayuki; Miyazawa, Hiroshi

doi:10.3390/challe12020033

Cited by 5 publications

(7 citation statements)

References 17 publications

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“…We had previously reported a model that suppresses radiation-specific cancer development [38][39][40]. In this paper, we considered reaction kinetic models that suppress radiation-nonspecific cancer.…”

Section: Discussionmentioning

confidence: 99%

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The Theoretical Dose That Exerts the Maximum Hormesis Effect Is 20 mSv When the Risk Is Approximately Proportional to Dose above 100 mSv.

Kino

2023

Preprint

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To date, radiation adaptation response has been reported as a low-dose related phenomenon and has been associated with radiation hormesis. Well-known cancers are caused by non-radiation active reactants, in addition to radiation. A model of suppression for radiation-specific cancers was previously reported, but the model did not target radiation-nonspecific cancers. In this paper, we describe kinetic models of radiation-induced suppressors for general radiation non-specific cancers, estimating the dose that induces the maximum hormesis effect while satisfying the condition that the risk is approximately proportional to dose above 100 mSv. It was found that the radiation hormesis effect is maximal at about 20 mSv when the rate constant for generation is the same as the rate constant for decomposition. When the two rate constants are different, the dose at which the radiation hormesis effect is maximized depends on both rate constants, but the dose increases as the two rate constants approach each other, reaching a maximum of about 20 mSv. This conclusion may lead to the discovery of unknown cancer suppressors at low doses and the development of cancer suppression methods in the future.

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Section: Discussionmentioning

confidence: 99%

“…Our theory is based on the hypothesis that radiation risk is approximately proportional to dose above 100 mSv and that a hormesis effect occurs below 100 mSv [38][39][40]. If we assume that cancer is caused solely by radiation, then the radiation risk at 0 mSv must be zero [38].…”

Section: Introductionmentioning

confidence: 99%

The Theoretical Dose That Exerts the Maximum Hormesis Effect Is 20 mSv When the Risk Is Approximately Proportional to Dose above 100 mSv.

Kino

2023

Preprint

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“…We had previously reported a model that suppresses radiation-specific cancer development [69][70][71]. In this paper, we considered reaction kinetic models that suppress radiation-nonspecific cancer.…”

Section: Conclusion Problems and Implicationsmentioning

confidence: 99%

“…Our theory is based on the hypothesis that radiation risk is approximately proportional to doses above 100 mSv, and that a hormesis effect occurs below 100 mSv [69][70][71]. If we assume that cancer is caused solely by radiation, then the radiation risk at 0 mSv must be zero (Figure 2A,D of Ref.…”

Section: Introductionmentioning

confidence: 99%

Calculations of the Radiation Dose for the Maximum Hormesis Effect

Kino

2024

Radiation

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To date, the radiation-adaptive response has been reported as a low-dose-related phenomenon and has been associated with radiation hormesis. Well-known cancers are caused by non-radiation active reactants, in addition to radiation. A model of suppression for radiation-specific cancers was previously reported, but the model did not target radiation-nonspecific cancers. In this paper, we describe kinetic models of radiation-induced suppressors for general radiation non-specific cancers, estimating the dose M that induces the maximum hormesis effect while satisfying the condition that the risk is approximately proportional to a dose above NOAEL (No Observed Adverse Effect Level). The radiation hormesis effect is maximal when the rate constant for generation of a risk-reducing factor is the same as the rate constant for its decomposition. When the two rate constants are different, the dose M at which the radiation hormesis effect is maximized depends on both rate constants, but the dose M increases as the two rate constants approach each other, reaching a maximum dose. The theory proposed in this paper can only explain existing experiments with extremely short error bar lengths. This theory may lead to the discovery of unknown risk-reducing factor at low doses and the development of risk-reducing methods in the future.

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“…In spite of the popularity of the LNT, doubts about its correctness and in consequence reasonability and applicability have arisen for years. A number of researchers have expressed their doubts [7], [14], [15]. They found non-linear dose-response models that may also fit the data.…”

Section: Critique Of the Lnt And Alternative Modelsmentioning

confidence: 99%

A Contribution to the Current Debate About the Adequacy of The Linear-No-Threshold (Lnt) Model for the Risk Resulting From Radon Exposure

Elío,

Janik,

Bossew

2023

RAP Conference Proceedings

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The Linear-No Threshold Hypothesis (LNT) states that risk from ionizing radiation is linearly related to dose with no dose threshold below which there was no risk. The LNT is an important fundament in practical radioprotection and for assessment of population risk, e.g., of estimating lung cancer risk or incidence attributable to exposure to indoor radon. The popularity of the LNT stems largely from its mathematical simplicity and therefore, its practicability. It seems that this has obscured the question of whether it is physically true, or "only" a useful practical rule. Distribution of exposure and dose to radon through the population is strongly right-skew, with the bulk of dose low. Therefore, attribution of risk, i.e., mainly lung cancer incidence, depends strongly on the risk model for low dose. As long as no micro-dosimetric model exists which causally relates incident radiation flux or exposure to radon progeny to a sequence of effects, starting on sub-cellular level, which results in clinical evidence, it is impossible to make statements on the effect of very low doses, since it is in principle impossible to extend empirical epidemiological inference to arbitrarily small doses. Therefore, epidemiological findings are extrapolated towards low doses. The most quoted large-scale epidemiological radon meta-study is Darby et al. (2006), which concludes that the LNT model is statistically compatible with the findings. This has been essentially corroborated by newer studies. However, with availability or more data, there seems to be increasing evidence that the model may not be applicable to estimate risk for low doses, which represent the bulk of exposure, if the objective is assessment of population risk. We review literature about the strongly debated question about validity of the LNT. Data are not publicly available, therefore statistical re-analysis is impossible. However, published information in the form of graphs and statistics allows some hypotheses alternative to the LNT. The debate is so serious because of the political consequences regarding radon abatement policy. We refrain from stating any "alternative truth" but investigate the possible consequences for risk assessment and what they entail for radon regulation and policy, resulting from different risk models.

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Considering Existing Factors That May Cause Radiation Hormesis at <100 mSv and Obey the Linear No-Threshold Theory at ≥100 mSv

Cited by 5 publications

References 17 publications

The Theoretical Dose That Exerts the Maximum Hormesis Effect Is 20 mSv When the Risk Is Approximately Proportional to Dose above 100 mSv.

The Theoretical Dose That Exerts the Maximum Hormesis Effect Is 20 mSv When the Risk Is Approximately Proportional to Dose above 100 mSv.

Calculations of the Radiation Dose for the Maximum Hormesis Effect

A Contribution to the Current Debate About the Adequacy of The Linear-No-Threshold (Lnt) Model for the Risk Resulting From Radon Exposure

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