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1.
Health Phys ; 125(6): 450-451, 2023 Dec 01.
Article in English | MEDLINE | ID: mdl-37874604
2.
Health Phys ; 125(3): 207-227, 2023 09 01.
Article in English | MEDLINE | ID: mdl-37294947

ABSTRACT

ABSTRACT: The purpose of this paper is to address the public fear that is usually associated with low-level radiation exposure situations. Its ultimate objective is to provide persuasive assurances to informed but skeptical members of the public that exposure situations involving low-level radiation are not to be feared. Unfortunately, just acquiescing to an unsupportive public fear of low-level radiation is not without consequences. It is causing severe disruptions to the benefits that harnessed radiation can produce for the well-being of all humanity. In this pursuit, the paper provides the scientific and epistemological basis needed for regulatory reform by reviewing the history in quantifying, understanding, modeling, and controlling radiation exposure, including some of the evolving contributions of the United Nations Scientific Committee on the Effects of Atomic Radiation, the International Commission on Radiological Protection, and the myriad of international and intergovernmental organizations establishing radiation safety standards. It also explores the various interpretations of the linear no-threshold model and the insights gained from radiation pathologists, radiation epidemiologists, radiation biologists, and radiation protectionists. Given that the linear no-threshold model is so deeply imbedded in current radiation exposure guidance, despite the lack of a solid scientific base on the actually proven radiation effects at low-doses, the paper suggests near-term ways to improve regulatory implementation and better serve the public by excluding and/or exempting trivial low-dose situations from the regulatory scope. Several examples are given where the unsubstantiated public fear of low-level radiation has resulted in crippling the beneficial effects that controlled radiation offers to a modern society.


Subject(s)
Radiation Exposure , Radiation Injuries , Radiation Protection , Humans , Radiation Injuries/prevention & control , Radiation Exposure/adverse effects , Background Radiation , Radiation Dosage
4.
Dose Response ; 18(3): 1559325820949729, 2020.
Article in English | MEDLINE | ID: mdl-32913426

ABSTRACT

Prior to observing low-dose-induced cell signaling and adaptive protection, radiogenic stochastic effects were assumed to be linearly related to absorbed dose. Now, abundant data prove the occurrence of radiogenic adaptive protection specifically at doses below ∼ 200 mGy (with some data suggesting such protection at a dose even higher than 200 mGy). Moreover, cells do not thrive properly when deprived of radiation below background dose. Two threshold doses need be considered in constructing a valid dose-response relationship. With doses beginning to rise from zero, cells increasingly escape radiation deprivation. The dose at which radiation-deprived cells begin to function homeostatically provides dose Threshold A. With further dose increase, adaptive protection becomes prominent and then largely disappears at acute doses above ∼ 200 mGy. The dose at which damage begins to override protection defines Threshold B. Thresholds A and B should be terms in modeling dose-response functions. Regarding whole-body responses, current data suggest for low-LET acute, non-chronic, irradiation a Threshold B of about 100 mGy prevails, except for leukemia and probably some other malignancies, and for chronic, low dose-rate irradiation where the Threshold B may well reach 1 Gy per year. A new Research and Development Program should determine individual Thresholds A and B for various radiogenic cell responses depending on radiation quality and target.

6.
Health Phys ; 114(6): 623-626, 2018 06.
Article in English | MEDLINE | ID: mdl-29521814

ABSTRACT

There is considerable controversy regarding risk of health detriment after low-level exposure to ionizing radiation. This stems in part from a sort of distance between radiation biologists, epidemiologists, and radiation protection professionals, as well as regulatory institutions. Also, there is a lack of overview of the relevant data and their origins regarding health risks at low doses of ionizing radiation. This feeds seriously into a somewhat hazy fear of ionizing radiation that besets large portions of the public. The current synopsis aims at presenting a holistic view in a concise yet comprehensive manner in order to help people understand the full extent of inputs into attempting to relate low-dose radiation exposure to health risk. It emerges again that different approaches must be found for optimal radiation protection replacing the use of the linear no-threshold (LNT) model.


Subject(s)
Dose-Response Relationship, Radiation , Neoplasms, Radiation-Induced/prevention & control , Radiation Protection/standards , Radiation, Ionizing , Risk Assessment/methods , Humans , Maximum Allowable Concentration , Radiation Dosage
7.
Dose Response ; 16(4): 1559325818820211, 2018.
Article in English | MEDLINE | ID: mdl-30627069

ABSTRACT

Our return to a study on dogs exposed lifelong to cobalt-60 γ-radiation was prompted by a comment that data in dog studies have large statistical errors due to the small number of dogs. We located an earlier article on the same study that had a better mortality curve for the dogs in each dose-rate group. The median life span of the dogs in each group was tabulated, and the standard error of each was calculated. No statistically significant shortening of median life span was observed for the lowest dose-rate group at any reasonable significance level (P value: .005-.05), whereas for dogs with higher irradiation rates, life span shortening was statistically significant at highest reasonable significance level (P value: .005). The results were entered on a graph of life span versus dose rate, assuming a threshold dose-response model. The fitted line indicates that the dose-rate threshold for γ-radiation induced life span reduction is about 600 mGy per year, which is close to the value we found previously. Making allowance for the calculated standard errors, we conclude that this threshold is in the range from 300 to 1100 mGy per year. This evidence is relevant for emergency measures actions (evacuation of residents) and for nuclear waste management.

9.
Antioxid Redox Signal ; 27(9): 596-598, 2017 Sep 20.
Article in English | MEDLINE | ID: mdl-28699353

ABSTRACT

Hydrogen peroxide (H2O2) is a stable product of water radiolysis, occurring at nanomolar concentration upon low-dose ionizing radiation (LDIR) (<100 mGy). In view of the recent recognition of H2O2 as a central redox signaling molecule that, likewise, is maintained in the nanomolar range in cells, we propose a role for H2O2 in radiation hormesis. LDIR is capable of utilizing known molecular redox master switches such as Nrf2/Keap1 or NF-κB/IκB to effect adaptive resistance. This leads to the hypothesis that, as a normal component of the exposome, LDIR mediates hormetic effects by H2O2 signaling. Antioxid. Redox Signal. 27, 596-598.


Subject(s)
Hormesis/radiation effects , Hydrogen Peroxide/metabolism , Oxidants/metabolism , Oxidative Stress/radiation effects , Signal Transduction
11.
Dose Response ; 15(1): 1559325817692903, 2017.
Article in English | MEDLINE | ID: mdl-28321175

ABSTRACT

After the 1956 radiation scare to stop weapons testing, studies focused on cancer induction by low-level radiation. Concern has shifted to protecting "radiation-sensitive individuals." Since longevity is a measure of health impact, this analysis reexamined data to compare the effect of dose rate on the lifespans of short-lived (5% and 10% mortality) dogs and on the lifespans of dogs at 50% mortality. The data came from 2 large-scale studies. One exposed 10 groups to different γ dose rates; the other exposed 8 groups to different lung burdens of plutonium. Reexamination indicated that normalized lifespans increased more for short-lived dogs than for average dogs, when radiation was moderately above background. This was apparent by interpolating between the lifespans of nonirradiated dogs and exposed dogs. The optimum lifespan increase appeared at 50 mGy/y. The threshold for harm (decreased lifespan) was 700 mGy/y for 50% mortality dogs and 1100 mGy/y for short-lived dogs. For inhaled α-emitting particulates, longevity was remarkably increased for short-lived dogs below the threshold for harm. Short-lived dogs seem more radiosensitive than average dogs and they benefit more from low radiation. If dogs model humans, this evidence would support a change to radiation protection policy. Maintaining exposures "as low as reasonably achievable" (ALARA) appears questionable.

14.
Int J Radiat Biol ; 92(11): 617-632, 2016 11.
Article in English | MEDLINE | ID: mdl-26926313

ABSTRACT

To identify the emergence of the recognition of the potential of the Auger effect for clinical application, and after tracing the salient milestones towards that goal, to evaluate the status quo and future prospects. It was not until 40 years after the discovery of Auger electrons, that the availability of radioactive DNA precursors enabled the biological power, and the clinical potential, of the Auger effect to be appreciated. Important milestones on the path to clinical translation have been identified and reached, but hurdles remain. Nevertheless the potential is still evident, and there is reasonable optimism that the goal of clinical translation is achievable.


Subject(s)
Cell Survival/radiation effects , Electrons/therapeutic use , Neoplasms/pathology , Neoplasms/radiotherapy , Animals , Dose-Response Relationship, Radiation , Evidence-Based Medicine , Humans , Radiotherapy Dosage , Treatment Outcome
16.
Health Phys ; 110(3): 276-80, 2016 Mar.
Article in English | MEDLINE | ID: mdl-26808882

ABSTRACT

The question whether low doses and low dose-rates of ionizing radiation pose a health risk to people is of public, scientific and regulatory concern. It is a subject of intense debate and causes much fear. The controversy is to what extent low-dose effects, if any, cause or protect against damage such as cancer. Even if immediate molecular damage in exposed biological systems rises linearly with the number of energy deposition events (i.e., with absorbed dose), the response of the whole biological system to that damage is not linear. To understand how initial molecular damage affects a complex living system is the current challenge.


Subject(s)
Adaptation, Physiological/radiation effects , Cell Physiological Phenomena/radiation effects , Disease Models, Animal , Dose-Response Relationship, Radiation , Models, Biological , Radiation Injuries/physiopathology , Absorption, Radiation , Animals , Cell Survival/radiation effects , Computer Simulation , Humans
17.
Dose Response ; 13(3): 1559325815592391, 2015.
Article in English | MEDLINE | ID: mdl-26674931

ABSTRACT

There are many places on the earth, where natural background radiation exposures are elevated significantly above about 2.5 mSv/year. The studies of health effects on populations living in such places are crucially important for understanding the impact of low doses of ionizing radiation. This article critically reviews some recent representative literature that addresses the likelihood of radiation-induced cancer and early childhood death in regions with high natural background radiation. The comparative and Bayesian analysis of the published data shows that the linear no-threshold hypothesis does not likely explain the results of these recent studies, whereas they favor the model of threshold or hormesis. Neither cancers nor early childhood deaths positively correlate with dose rates in regions with elevated natural background radiation.

18.
Dose Response ; 13(1)2015.
Article in English | MEDLINE | ID: mdl-26675366

ABSTRACT

Several studies on the effect of inhaled plutonium-dioxide particulates and the incidence of lung tumors in dogs reveal beneficial effects when the cumulative alpha-radiation dose is low. There is a threshold at an exposure level of about 100 cGy for excess tumor incidence and reduced lifespan. The observations conform to the expectations of the radiation hormesis dose-response model and contradict the predictions of the LNT hypothesis. These studies suggest investigating the possibility of employing low-dose alpha-radiation, such as from (239)PuO2 inhalation, as a prophylaxis against lung cancer.

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