Exposure to radiation from different types of television sets was measured to ascertain the levels of hazards posed to the human biological system. Measurement of the annual radiation dose hazards was performed using a halogen-quenched GM tube with thin mica end window having a density of 1.5 mg/cm2, effective window diameter of 0.360 inch and side wall of 0.012 inch thick. The GM tube was placed for 180 minutes and the sensor faced the screens of the various TV sets, one meter apart. The annual radiation dose ranged from 0.012 ± 0.006 mSv/yr for plasma-SONY to 0.13 ± 0.012 mSv/yr for SHARP and SAMSUNG 24 inch TV sets, containing cathode ray tubes. The annual doses from the 15 and 24 inch-LG TVs (manufactured with cathode ray tubes) were relatively low, with values of 0.031 ± 0.017 and 0.035 ± 0.005 mSv/yr, respectively. The 21 inch THERMOCOOL and PROTECH (with cathode ray tubes), produced annual doses of 0.110 ± 0.052 Sv/yr and 0.063 ± 0.002 mSv/yr, respectively. This provides an insight into the amount of radiation generated by different TV sets in households, on an annual basis. After some years of exposure to TV radiation, health complications such as carcinogenesis or other adverse cellular events may occur, due to cumulated (but does not always) doses which may result in DNA damage, to the human biological system.

International audience | Estimating the consequences of environmental changes, specifically in a global change context, is essential for conservation issues. In the case of pollutants, the interest in using an evolutionary approach to investigate their consequences has been emphasized since the 2000s, but these studies remain rare compared to the characterization of direct effects on individual features. We focused on the study case of anthropogenic ionizing radiation because, despite its potential strong impact on evolution, the scarcity of evolutionary approaches to study the biological consequences of this stressor is particularly true. In this study, by investigating some particular features of the biological effects of this stressor, and by reviewing existing studies on evolution under ionizing radiation, we suggest that evolutionary approach may help provide an integrative view on the biological consequences of ionizing radiation. We focused on three topics: (i) the mutagenic properties of ionizing radiation and its disruption of evolutionary processes, (ii) exposures at different time scales, leading to an interaction between past and contemporary evolution, and (iii) the special features of contaminated areas called exclusion zones and how evolution could match field and laboratory observed effects. This approach can contribute to answering several key issues in radioecology: to explain species differences in the sensitivity to ionizing radiation, to improve our estimation of the impacts of ionizing radiation on populations, and to help identify the environmental features impacting organisms (e.g., interaction with other pollution, migration of populations, anthropogenic environmental changes). Evolutionary approach would benefit from being integrated to the ecological risk assessment process.

The effects of exposure to different levels of ionising radiation were assessed on the genetic, epigenetic and microbiome characteristics of the “hologenome” of earthworms collected at sites within the Chernobyl exclusion zone (CEZ). The earthworms Aporrectodea caliginosa (Savigny, 1826) and Octolasion lacteum (Örley, 1881) were the two species that were most frequently found at visited sites, however, only O. lacteum was present at sufficient number across different exposure levels to enable comparative hologenome analysis. The identification of morphotype O. lacteum as a probable single clade was established using a combination of mitochondrial (cytochrome oxidase I) and nuclear genome (Amplified Fragment Length Polymorphism (AFLP) using MspI loci). No clear site associated differences in population genetic structure was found between populations using the AFLP marker loci. Further, no relationship between ionising radiation exposure levels and the percentage of methylated loci or pattern of distribution of DNA methylation marks was found. Microbiome structure was clearly site dependent, with gut microbiome community structure and diversity being systematically associated with calculated site-specific earthworm dose rates. There was, however, also co-correlation between earthworm dose rates and other soil properties, notably soil pH; a property known to affect soil bacterial community structure. Such co-correlation means that it is not possible to attribute microbiome changes unequivocally to radionuclide exposure. A better understanding of the relationship between radionuclide exposure soil properties and their interactions on bacterial microbiome community response is, therefore, needed to establish whether these the observed microbiome changes are attributed directly to radiation exposure, other soil properties or to an interaction between multiple variables at sites within the CEZ.

A main challenge in ecological risk assessment is to account for the impact of multiple stressors. Nuclear facilities can release both radiological and chemical stressors in the environment. This study is the first to apply species sensitivity distribution (SSD) combined with mixture models (concentration addition (CA) and independent action (IA)) to derive an integrated proxy of the ecological impact of combined radiological and chemical stressors: msPAF (multisubstance potentially affected fraction of species). The approach was tested on the routine liquid effluents from nuclear power plants that contain both radioactive and stable chemicals. The SSD of ionising radiation was significantly flatter than the SSD of 8 stable chemicals (namely Cr, Cu, Ni, Pb, Zn, B, chlorides and sulphates). This difference in shape had strong implications for the selection of the appropriate mixture model: contrarily to the general expectations the IA model gave more conservative (higher msPAF) results than the CA model. The msPAF approach was further used to rank the relative potential impact of radiological versus chemical stressors.

Environmental reservoirs of antibiotic resistant bacteria are poorly understood. Understanding how the environment selects for resistance traits in the absence of antibiotics is critical in developing strategies to mitigate this growing menace. Indirect or co-selection of resistance by environmental pollution has been shown to increase antibiotic resistance. However no attention has been given to the effects of low-level ionizing radiation or the interactions between radiation and heavy metals on the maintenance or selection for antibiotic resistance (AR) traits. Here we explore the effect of radiation and copper on antibiotic resistance. Bacteria were collected from biofilms in two ponds – one impacted by low-level radiocesium and the other an abandoned farm pond. Through laboratory controlled experiments we examined the effects of increasing concentrations of copper on the incidence of antibiotic resistance. Differences were detected in the resistance profiles of the controls from each pond. Low levels (0.01 mM) of copper sulfate increased resistance but 0.5 mM concentrations of copper sulfate depressed the AR response in both ponds. A similar pattern was observed for levels of multiple antibiotic resistance per isolate. The first principal component response of isolate exposure to multiple antibiotics showed significant differences among the six isolate treatment combinations. These differences were clearly visualized through a discriminant function analysis, which showed distinct antibiotic resistance response patterns based on the six treatment groups.

Environmental contamination with radioactive materials of geogenic and anthropogenic origin is a global problem. A variety of mutagenicity test procedures has been developed which enable the detection of DNA damage caused by ionizing radiation which plays a key role in the adverse effects caused by radioisotopes. In the present study, we investigated the usefulness of the Tradescantia micronucleus test (the most widely used plant based genotoxicity bioassay) for the detection of genetic damage caused by environmental samples and a human artifact (ceramic plate) which contained radioactive elements. We compared the results obtained with different exposure protocols and found that direct exposure of the inflorescences is more sensitive and that the number of micronuclei can be further increased under “wet” conditions. The lowest dose rate which caused a significant effect was 1.2 μGy/h (10 h). Comparisons with the results obtained with other systems (i.e. with mitotic cells of higher plants, molluscs, insects, fish and human lymphocytes) show that the Tradescantia MN assay is one to three orders of magnitude more sensitive as other models, which are currently available. Taken together, our findings indicate that this method is due to its high sensitivity a unique tool, which can be used for environmental biomonitoring in radiation polluted areas.

Exposure to chemicals produced by petrochemical industrial complexes (PICs), such as benzene, ionizing radiation, and particulate matters, may contribute to the development of leukemia. However, epidemiological studies showed controversial results. This systematic review and meta-analysis aimed to summarize the association between residential exposure to PICs and the risk of leukemia incidence, focusing on exposure-response effects. We searched PubMed, Embase, Web of Science, and Cochrane Library databases for studies published before September 1st, 2019. Observational studies investigating residential exposure to PICs and the risk of leukemia were included. The outcome of interest was the incidence of leukemia comparing to reference groups. Relative risk (RR) was used as the summary effect measure, synthesized by characteristics of populations, distance to PICs, and calendar time in meta-regression. We identified 7 observational studies, including 2322 leukemia cases and substantial reference groups, in this meta-analysis. Residential exposure to PICs within a maximal 8-km distance had a 36% increased risk of leukemia (pooled RR = 1.36, 95% CI = 1.14–1.62) compared to controls, regardless of sex and age. In terms of leukemia subtypes, residential exposure to PICs was associated with the risks of acute myeloid leukemia (AML, pooled RR = 1.61, 95% CI = 1.12–2.31) and chronic lymphocytic leukemia (CLL, pooled RR = 1.85, 95% CI = 1.11–6.42). In meta-regression, the positive association occurred after 10 years of follow-up with a pooled RRs of 1.21 (95% CI = 1.02–1.44) and then slightly increased to 1.77 (95% CI = 1.35–2.33) at 30 years after follow-up. No effect modification was found by sex, age, and geographic locations.

The issue of potential long-term or hereditary effects for both humans and wildlife exposed to low doses (or dose rates) of ionising radiation is a major concern. Chronic exposure to ionising radiation, defined as an exposure over a large fraction of the organism's lifespan or even over several generations, can possibly have consequences in the progeny. Recent work has begun to show that epigenetics plays an important role in adaptation of organisms challenged to environmental stimulae. Changes to so-called epigenetic marks such as histone modifications, DNA methylation and non-coding RNAs result in altered transcriptomes and proteomes, without directly changing the DNA sequence. Moreover, some of these environmentally-induced epigenetic changes tend to persist over generations, and thus, epigenetic modifications are regarded as the conduits for environmental influence on the genome.Here, we review the current knowledge of possible involvement of epigenetics in the cascade of responses resulting from environmental exposure to ionising radiation. In addition, from a comparison of lab and field obtained data, we investigate evidence on radiation-induced changes in the epigenome and in particular the total or locus specific levels of DNA methylation. The challenges for future research and possible use of changes as an early warning (biomarker) of radiosensitivity and individual exposure is discussed. Such a biomarker could be used to detect and better understand the mechanisms of toxic action and inter/intra-species susceptibility to radiation within an environmental risk assessment and management context.

This paper summarizes the historical and scientific foundations of the Linear No-Threshold (LNT) cancer risk assessment model. The story of cancer risk assessment is an extraordinary one as it was based on an initial incorrect gene mutation interpretation of Muller, the application of this incorrect assumption in the derivation of the LNT single-hit model, and a series of actions by leading radiation geneticists during the 1946–1956 period, including a National Academy of Sciences (NAS) Biological Effects of Atomic Radiation (BEAR) I Genetics Panel (Anonymous, 1956), to sustain the LNT belief via a series of deliberate obfuscations, deceptions and misrepresentations that provided the basis of modern cancer risk assessment policy and practices. The reaffirming of the LNT model by a subsequent and highly influential NAS Biological Effects of Ionizing Radiation (BEIR) I Committee (NAS/NRC, 1972) using mouse data has now been found to be inappropriate based on the discovery of a significant documented error in the historical control group that led to incorrect estimations of risk in the low dose zone. Correction of this error by the original scientists and the application of the adjusted/corrected data back to the BEIR I (NAS/NRC, 1972) report indicates that the data would have supported a threshold rather than the LNT model. Thus, cancer risk assessment has a poorly appreciated, complex and seriously flawed history that has undermined policies and practices of regulatory agencies in the U.S. and worldwide to the present time.

Ionizing radiation causes a variety of effects, including DNA damage associated to cancers. However, the effects in progeny from irradiated parents is not well documented. Using zebrafish as a model, we previously found that parental exposure to ionizing radiation is associated with effects in offspring, such as increased hatching rates, deformities, increased DNA damage and reactive oxygen species. Here, we assessed short (one month) and long term effects (one year) on gene expression in embryonic offspring (5.5 h post fertilization) from zebrafish exposed during gametogenesis to gamma radiation (8.7 or 53 mGy/h for 27 days, total dose 5.2 or 31 Gy) using mRNA sequencing. One month after exposure, a global change in gene expression was observed in offspring from the 53 mGy/h group, followed by embryonic death at late gastrula, whereas offspring from the 8.7 mGy/h group was unaffected. Interestingly, one year after exposure newly derived embryos from the 8.7 mGy/h group exhibited 2390 (67.7% downregulated) differentially expressed genes. Overlaps in differentially expressed genes and enriched biological pathways were evident between the 53 mGy/h group one month and 8.7 mGy/h one year after exposure, but were oppositely regulated. Pathways could be linked to effects in adults and offspring, such as DNA damage (via Atm signaling) and reproduction (via Gnrh signaling). Comparison with gene expression analysis in directly exposed embryos indicate transferrin a and cytochrome P450 2x6 as possible biomarkers for radiation response in zebrafish. Our results indicate latent effects following ionizing radiation exposure from the lower dose in parents that can be transmitted to offspring and warrants monitoring effects over subsequent generations.