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This paper starts with a brief history of the birth of the field of radioecology during the Cold War with a focus on US activity. We review the establishment of the international system for radiation protection and the science underlying the guidelines. We then discuss the famous ICRP 60 statement that if "Man" is protected, so is everything else and show how this led to a focus in radioecology on pathways to "Man" rather than concern about impacts on environments or ecosystems. We then review the contributions of Radiation Research Society members and papers published in Radiation Research which contributed to the knowledge base about effects on non-human species. These fed into international databases and computer-based tools such as ERICA and ResRad Biota to guide regulators. We then examine the origins of the concern that ICRP 60 is not sufficient to protect ecosystems and discuss the establishment of ICRP Committee 5 and its recommendations to establish reference animals and plants. The review finishes with current concerns that reference animals and plants (RAPs) are not sufficient to protect ecosystems, given the complexity of interacting factors such as the climate emergency and discusses the efforts of ICRP, the International Union of Radioecologists and other bodies to capture the concepts of ecosystem services and ecosystem complexity modelling in radioecology., (© 2024 by Radiation Research Society. All rights of reproduction in any form reserved.)

The aim of this paper is to review the history surrounding the discovery of lethal mutations, later described as delayed reproductive death. Lethal mutations were suggested very early on, to be due to a generalised instability in a cell population and are considered now to be one of the first demonstrations of "radiation-induced genomic instability" which led later to the establishment of the field of "non-targeted effects." The phenomenon was first described by Seymour et al. in 1986 and was confirmed by Trott's group in Europe and by Little and colleagues in the United States before being extended by Mendonca et al. in 1989, who showed conclusively that the distinguishing feature of lethal mutation occurrence was that it happened suddenly after about 9-10 population doublings in progeny which had survived the original dose of ionizing radiation. However, many authors then suggested that in fact, lethal mutations were implicit in the original experiments by Puck and Marcus in 1956 and were described in the extensive work by Sinclair in 1964, who followed clonal progeny for up to a year after irradiation and described "small colony formation" as a persistent consequence of ionizing radiation exposure. In this paper, we examine the history from 1956 to the present using the period from 1986-1989 as an anchor point to reach into the past and to go forward through the evolution of the field of low dose radiobiology where non-targeted effects predominate., (© 2024 by Radiation Research Society. All rights of reproduction in any form reserved.)

Abstract: It is now well accepted that the mechanisms induced by low-dose exposures to ionizing radiation (LDR) are different from those occurring after high-dose exposures. However, the downstream effects of these mechanisms are unclear as are the quantitative relationships between exposure, effect, harm, and risk. In this paper, we will discuss the mechanisms known to be important with an overall emphasis on how so-called "non-targeted effects" (NTE) communicate and coordinate responses to LDR. Targeted deposition of ionizing radiation energy in cells causing DNA damage is still regarded as the dominant trigger leading to all downstream events whether targeted or non-targeted. We regard this as an over-simplification dating back to formal target theory. It ignores that last 100 y of biological research into stress responses and signaling mechanisms in organisms exposed to toxic substances, including ionizing radiation. We will provide evidence for situations where energy deposition in cellular targets alone cannot be plausible as a mechanism for LDR effects. An example is where the energy deposition takes place in an organism not receiving the radiation dose. We will also discuss how effects after LDR depend more on dose rate and radiation quality rather than actual dose, which appears rather irrelevant. Finally, we will use recent evidence from studies of cataract and melanoma induction to suggest that after LDR, post-translational effects, such as protein misfolding or defects in energy metabolism or mitochondrial function, may dominate the etiology and progression of the disease. A focus on such novel pathways may open the way to successful prophylaxis and development of new biomarkers for better risk assessment after low dose exposures., (Copyright © 2024 Health Physics Society.)