Radionuclide contamination poses serious hazards for terrestrial ecosystems. Beyond the readily apparent damage to the biota at high doses, low doses of ionizing radiation produce stochastic effects: mutation, carcinogenesis, and genomic instability. The proposed chapter is a review of the biological and ecological effects of radionuclides. The authors discuss, beyond the Chernobyl accident, other contamination events. The review includes the biological and ecological effects of the three principal technogenic contaminants in terrestrial ecosystems: Cs-137, Sr-90, and I-131. Ecological risks to terrestrial small mammals are assessed in detail. In addition, the chapter provides some of the lesser-known methods of remediation and detoxification, including the use of modified natural zeolites as environmental remedies and bio-sorbents. Presented herein is little-known information on environmental protection against radioactive contamination.

Classical radiation biology as we understand it clearly identifies genomic DNA as the primary target of ionizing radiation. The evidence appears rock-solid: ionizing radiation typically induces DSBs with a yield of ~30 per cell per Gy, and unrepaired DSBs are a very cytotoxic lesion. We know very well the kinetics of induction and repair of different types of DNA damage in different organisms and cell lines. And yet, higher organisms differ in their radiation sensitivity—humans can be unpredictably radiosensitive during radiotherapy; this can be due to genetic defects (e.g., ataxia telangiectasia (AT), Fanconi anemia, Nijmegen breakage syndrome (NBS), and the xeroderma pigmentosum spectrum, among others) but most often is unexplained. Among other mammals, goats (Capra hircus) appear to be very radiosensitive (LD₅₀ = 2.4 Gy), while Mongolian gerbils (Meriones unguiculatus) are radioresistant and withstand quadruple that dose (LD₅₀ = 10 Gy). Primary radiation lethality in mammals is due most often to hematopoietic insufficiency, which is, in the words of Dr. Theodor Fliedner, one of the pioneers of radiation hematology, “a disturbance in cellular kinetics”. And yet, what makes one cell type, or one particular organism, more sensitive to ionizing radiation? The origins of radiosensitivity go above and beyond the empirical evidence and models of DNA damage and repair—as scientists, we must consider other phenomena: the radiation-induced bystander effect (RIBE), abscopal effects, and, of course, genomic instability and immunomodulation. It seems that radiosensitivity is not entirely determined by the mathematics of DNA damage and repair, and it is conceivable that radiation biology may benefit from an informed enquiry into physiology and organism-level signaling affecting radiation responses. The current article is a review of several key aspects of radiosensitivity beyond DNA damage induction and repair; it presents evidence supporting new potential venues of research for radiation biologists.

For the first time, this study investigates in vivo the potential of Na-modified natural clinoptilolite to mitigate cadmium toxicity in ICR mice, a model relevant to human health. We enhanced natural clinoptilolite to improve its cadmium (Cd) exchange capacity. Mice were exposed to environmentally realistic cadmium nitrate Cd(NO₃)₂ doses in their drinking water. The detoxification efficacy of the mineral was evaluated over 45 days in four groups: control (no supplementation), Cd(NO₃)₂ only, clinoptilolite only, and a combination of Cd(NO₃)₂ and clinoptilolite. We assessed Cd bioaccumulation in the liver and kidneys, genotoxicity (micronucleus assay), hematological parameters, and oxidative stress markers. Cd exposure resulted in significant bioaccumulation, reduced growth, changes in erythrograms, DNA damage, and oxidative stress. Mice receiving clinoptilolite alone showed a significant increase in body mass. Modified clinoptilolite led to a nearly 48% reduction in Cd accumulation and a 30% increase in Cd excretion in the Cd-plus-clinoptilolite group compared to the Cd-only group. Erythrogram and leukogram parameters returned to near-normal levels, with reductions in malondialdehyde (MDA) and increases in glutathione (GSH) observed by the end of the experiment. No elevated levels of micronuclei were found following clinoptilolite supplementation. These results suggest that modified clinoptilolite may be a cost-effective detoxifier in Cd-polluted regions.

Lead and cadmium are long established toxic and carcinogenic metals. Still, the mechanisms of their interaction with eukaryotic DNA are not unequivocally understood. New data provide evidence on the influence of both metals on DNA repair, particularly non-homologous end joining (NHEJ) and mismatch repair (MMR). This may help explain the weak direct mutagenicity of both Pb2+ and Cd2+ ions in the Ames test, as opposed to the proven carcinogenicity of both metals; it has long been proposed that lead and cadmium may induce an imbalance in mammalian systems of DNA damage repair and promote genomic instability. While new evidence for mechanistic interactions of metals with DNA repair emerges, some of the old questions involving dose distribution, pathways of exposure and bioaccumulation/detoxification kinetics still remain valid. To help place the current state of the art in the genetic toxicology of lead and cadmium within the context of ecotoxicology, the current authors propose an integrative approach and offer a review of other authors’ work as well as some of their own data on systemic and organ-specific toxicities in laboratory mice. The current chapter is a comparative analysis of the state of the art in the specific toxicity and genotoxicity of Pb and Cd, presenting some new and little-known information.

Modern organic chemistry is capable of synthesizing molecules with incredible structural and functional diversity. Since the Second Industrial Revolution (1870–1914), vast amounts of technogenic organic chemicals have been released into nature, either in waste streams, accidentally, or deliberately as fertilizers and pesticides. The early generation of organic pesticides, including aldrin/dieldrin, chlordane, dichlorodiphenyltrichloroethane (DDT), dicofol, lindane, and others, has been recognized as an environmental hazard due to broad-spectrum toxicities, extraordinary persistence in ecosystems, and tendencies for bioaccumulation and biomagnification in higher organisms. First-generation organic pesticides comprise 10 of the original 12 persistent organic pollutants (POPs) governed by the Stockholm Convention (2001). While the phase-out of most POP pesticides has attracted widespread publicity, several risks have not been addressed widely: (1) Residual risk of POP pesticides has diminished but not disappeared across Europe, North America, and Australia; (2) DDT continues to be deployed in areas with high risk of drug-resistant malaria; (3) consistent use of “modern” pesticides may necessitate expansions of the POP list; and (4) as demonstrated by the war in Ukraine, unforeseen events like the destruction of the Kakhovka Dam (6 June 2023) can create a risk of pesticide remobilization, necessitating new solutions. With the expected intensification of agriculture by 2050, pesticide use is foreseen to be a major driver of biodiversity loss and other irreversible environmental damage. The current chapter is a review of the state of the art in the ecotoxicology and monitoring of pesticide contamination in terrestrial and riverine ecosystems, presenting new and little-known information.