How Safe Are Radiation Doses in Diagnostic Radiology? A Historical Perspective and Review of Current Evidence

The “no dose is safe” linear no-threshold (LNT) model forms the basis for radiation safety in radiology practice. This model has its origins in observations of germline mutations in fruit flies exposed to X-rays. After World War II, quantitative risk estimates of radiation injury are primarily derived from the atomic bomb survivor Life Span Study. Current understanding of tissue response to radiation has raised doubts about the validity of LNT model at low doses encountered in the practice of diagnostic radiology. This article traces the evolution of basic radiation safety concepts and provides a bird's eye view of the Life Span Study and other studies which throw light on the matter. The arguments for an alternative, threshold, or even hermetic models of dose response are examined. The relevance of these developments to the nuclear power industry is also outlined.

Modeling of Molecular Mechanisms of Radiation Adaptive Response Formation

The phenomenon of adaptive response is expressed in the increase of resistance of a biological object to high doses of mutagens under the conditions of previous exposure to these (or other) mutagens in low doses. Low doses of mutagen activate a number of protective mechanisms in a living object, which are called hormetic. Thus, the adaptive response and hormesis are links in the same chain. Radiation hormesis refers to the generally positive effect of low doses of low LET radiation on biological objects. The phenomenology of radiation-induced adaptive response and radiation hormesis for biological objects of different levels of organization is considered; the review of existing theories describing the dose-effect relationship has been reviewed. The hypothesis proposing one of the mechanisms of formation of radiation adaptive response of cells taking into account the conformational structure of chromatin has been submitted. The analysis of modern concepts of the phenomenon of hormesis on the basis of modeling of molecular mechanisms of formation of hormetic reactions to low-dose low LET radiation has been carried out. The parameters that can be used for quantitative and graphical evaluation of the phenomenon of hormesis was considered, and a formula for calculating the coefficient of radiation-induced adaptive response has been proposed. A review of mathematical models describing the radiation relative risk of gene mutations and neoplastic transformations at low-dose irradiation of cohorts has been performed. The following conclusions have been made: radiation hormesis and adaptive response are generally recognized as real and reproducible biological phenomena, which should be considered as very important phenomena of evolutionarily formed biological protection of living organisms from ionizing radiation. The hormesis model of dose-response relationship makes much more accurate predictions of a living object's response to radiation (or other stressors) in the low-dose range than the linear threshold (LNT) model does. The LNT model can adequately describe reactions only in the region of high doses of radiation, and, therefore, extrapolation modeling of biological object’s reactions from the zone of high doses to low doses is not correct.

Underground Radiobiology: A Perspective at Gran Sasso National Laboratory

Scientific community and institutions (e. g., ICRP) consider that the Linear No-Threshold (LNT) model, which extrapolates stochastic risk at low dose/low dose rate from the risk at moderate/high doses, provides a prudent basis for practical purposes of radiological protection. However, biological low dose/dose rate responses that challenge the LNT model have been highlighted and important dowels came from radiobiology studies conducted in Deep Underground Laboratories (DULs). These extreme ultra-low radiation environments are ideal locations to conduct below-background radiobiology experiments, interesting from basic and applied science. The INFN Gran Sasso National Laboratory (LNGS) (Italy) is the site where most of the underground radiobiological data has been collected so far and where the first in vivo underground experiment was carried out using Drosophila melanogaster as model organism. Presently, many DULs around the world have implemented dedicated programs, meetings and proposals. The general message coming from studies conducted in DULs using protozoan, bacteria, mammalian cells and organisms (flies, worms, fishes) is that environmental radiation may trigger biological mechanisms that can increase the capability to cope against stress. However, several issues are still open, among them: the role of the quality of the radiation spectrum in modulating the biological response, the dependence on the biological endpoint and on the model system considered, the overall effect at organism level (detrimental or beneficial). At LNGS, we recently launched the RENOIR experiment aimed at improving knowledge on the environmental radiation spectrum and to investigate the specific role of the gamma component on the biological response of Drosophila melanogaster.

Dismantling Fixations on Failed Fictions: A-Bomb Survivor Study Denies The Low-Dose Radiogenic Cancer Narrative

The linear no-threshold (LNT) model of low dose ionizing radiation's (LDIR) role in radiogenic cancer incidence has long served as a pseudo-scientific belief arising from evidence that has never been proven, but has been contested. One source of current evidence that favors the LNT model is the Radiation Effects Research Foundation’s (RERF) Life Span Study (LSS) cohort of Japanese atomic bomb survivors. The RERF has managed the input data, model development, and data analyses for the LSS cohort for 45 years, publishing research papers and reports updating the RERF’s progress. In recent years, the RERF has attempted to identify other cancer risk factors that may have played a role in the cancer incidence of cohort survivors, and this effort has drawn attention to the fact that many earlier years of papers and reports from the RERF have never considered these risk factors, making such publications of questionable merit. This investigation examines two recent papers from the RERF that denominate how the RERF now analyzes specific cancer incidence for cohort members, how it treats lifestyle and other risk factors for various cancers that have arisen in the cohort, and how it continues to find and assert that bomb-blast LDIR remains a distinguishable source of radiogenic cancer in the cohort. The investigation observes that the cohort input data and modeling have extensive deficiencies and defects, many having been identified by RERF authors themselves, that substantially compromise the findings of these two papers, and offers concluding evidence that the LDIR radiogenic cancer model is highly implausible if not impossible. From such evidence, a final conclusion must arise that supports a threshold model for the dose–response relationship between LDIR exposure and radiogenic cancer.

Until There Is a Resolution of the Pro-LNT/Anti-LNT Debate, We Should Head Toward a More Sensible Graded Approach for Protection From Low-Dose Ionizing Radiation

Current regulation of ionizing radiation is based on the linear no-threshold (LNT) model where any radiation dose increases cancer risk and is independent of dose rate, resulting in large amounts of time and money being spent protecting from extremely small radiation exposures and hence extremely small risk. There are animal studies which demonstrate that LNT is incorrect at low doses, supporting a threshold or hormesis model and thus indicating that there is no need to protect from very low doses. This has led to a sometimes bitter debate between pro-LNT and anti-LNT camps, and the debate has been at a stalemate for some time. This commentary is not aimed at taking either side of the debate. It is likely that the public, workers, and the environment are adequately protected under current regulation, which is the most important outcome. Until those on one side of the debate can convince the other, it would be sensible to move forward toward a graded (risk-based) approach to regulation, where the stringency of control is commensurate with the risk, resulting hopefully in more sensible practical thresholds. This approach is gradually being put forward by international radiation protection advisory bodies.

Replacing LNT: The Integrated LNT-Hormesis Model

Many scientists and regulators utilize the linear no-threshold (LNT) relationship to estimate the likelihood of carcinogenesis. The LNT model is incorrect and was adopted based upon false pretenses. The use of the model has been corrupted by many to claim that even the smallest ionizing radiation dose may initiate carcinogenesis. This claim has resulted in societal harm.

What Can Chemical Carcinogenesis Shed Light on the LNT Hypothesis in Radiation Carcinogenesis?

To protect the public’s health from exposure to physical, chemical, and microbiological agents, it is important that any policy be based on rigorous scientifically based research. The concept of “linear no-threshold” (LNT) has been implemented to provide guideline exposures to these agents. The practical limitation to testing this hypothesis is to provide sufficient samples for experimental or epidemiological studies. While there is no universally accepted understanding of most human diseases, there seems to be better understanding of cancer that might help resolve the “LNT” model. The public’s concern, after being exposed to radiation, is the potential of producing cancer. The most rigorous hypothesis of human carcinogenesis is the “multistage, multimechanism” chemical carcinogenesis model. The radiation carcinogenesis LNT model, rarely, if ever, built it into their support. It will be argued that this multistage, multimechanism model of carcinogenesis, involving the “initiation” of a single cell by a mutagen event, followed by chronic exposure to threshold levels of epigenetic agents or conditions that stimulate the clonal expansion of the “initiated” cell, can convert these benign cells to become invasive and metastatic. This “promotion” process can be interrupted, thereby preventing these initiated cells from transitioning to the “progression” process of invasion and metastasis.