Rivers play an important role in the overall transport of microplastic pollution (1 μm to 5 mm), with fluvial dynamics expected to influence biotic interactions, particularly for fish. So far, there have been few assessments of microplastics in freshwater salmonids. The prevalence (i.e. percentage occurrence) and burden (i.e. abundance per fish) of microplastics were assessed in the gastrointestinal tracts (GITs) and stomach contents (SCs) of 58 brown trout Salmo trutta Linnaeus, 1758 sampled at six sites along the River Slaney catchment in south-east Ireland. Sites were divided into two classifications (high and low exposure) based on proximity to microplastic pollution sources, comprising three sites each. Analysis of biological traits (e.g. fish length) and diet was performed on the same fish to determine possible factors explaining microplastic burden. Microplastics were found in 72% of fish having been recovered from 66% of GITs (1.88 ± 1.53 MPs fish⁻¹) and 28% of SCs (1.31 ± 0.48 MPs fish⁻¹). Fibres were the dominant particle type recovered from GITs (67%) and SCs (57%) followed by fragments. No difference in median microplastic burden was observed between fish collected in high and low exposure sites. Microplastic burden was unrelated to fish fork length, while microplastic size distribution (100 ≤ 350 μm, 350 μm to ≤ 5 mm) was unrelated to S. trutta age class estimates. Furthermore, microplastic burden was not explained by dietary intake. Though further research is necessary, this study showed the presence of microplastics in wild S. trutta collected from an Irish riverine system, which could have further implications for top-level consumers that feed on the species, including humans. Further analysis is required to determine possible trophic linkages for the species, with respect to microplastics, and to assess the suitability of S. trutta for monitoring microplastics in river systems.

Contamination of diverse environments and wild species by some contaminants is projected to continue and increase in coming decades. In the marine environment, large volumes of data to assess how concentrations have changed over time can be gathered from indicator species such as seabirds, including through sampling feathers from archival collections and museums. As apex predators, Flesh-footed Shearwaters (Ardenna carneipes) are subject to high concentrations of bioaccumulative and biomagnifying contaminants, and reflect the health of their local marine environment. We analysed Flesh-footed Shearwater feathers from Australia from museum specimens and live birds collected between 1900 and 2011 and assessed temporal trends in three trace elements of toxicological concern: cadmium, mercury, and lead. Concentrations of cadmium increased by 1.5% per year (95% CI: +0.6, +3.0), while mercury was unchanged through the time series (−0.3% per year; 05% CI: -2.1, +1.5), and lead decreased markedly (−2.1% per year, 95% CI: -3.2, −1.0). A reduction in birds’ trophic position through the 20th century, and decreased atmospheric emissions were the likely driving factors for mercury and lead, respectively. By combining archival material from museum specimens with contemporary samples, we have been able to further elucidate the potential threats posed to these apex predators by metal contamination.

Despite intensive ecotoxicological research, we still know relatively little about the ecological impacts of many environmental contaminants. Filling these knowledge gaps is particularly important regarding amphibians, because they play significant roles in freshwater and terrestrial ecosystems, and their populations are declining worldwide. In this study, we investigated two pollutants that have been poorly studied in ecotoxicology despite their widespread occurrence in surface waters: the herbicide terbuthylazine and the pharmaceutical drug carbamazepine. We exposed two anuran species throughout their larval development to each of two environmentally relevant concentrations of each pollutant, and recorded mortality and 17 sub-lethal endpoints up to several months after exposure. Mortality was low and unrelated to treatment. In agile frogs (Rana dalmatina), we found that treatment with 0.3 μg/L terbuthylazine decreased tadpole activity and reduced fat bodies in juveniles, whereas treatment with 50 μg/L carbamazepine decreased spleen size and increased spleen pigmentation. In common toads (Bufo bufo), treatment with 0.003 μg/L terbuthylazine increased body mass at metamorphosis, treatment with 0.3 μg/L terbuthylazine increased the size of optic tecta, and treatment with 0.5 μg/L carbamazepine decreased hypothalamus size. Treatment with 50 μg/L carbamazepine reduced the feeding activity of toad tadpoles, decreased their production of anti-predatory bufadienolide toxins, and increased their body mass at metamorphosis; juvenile toads in this treatment group had reduced spleen pigmentation. Neither treatments affected the time to metamorphosis, post-metamorphic body mass, or sex ratios significantly. These results show that environmental levels of both terbuthylazine and carbamazepine can have several sub-lethal effects on anurans, which may be detrimental to individual fitness and population persistence in natural conditions. Our findings further highlight that toxic effects cannot be generalized between chemicals of similar structure, because the terbuthylazine effects we found do not conform with previously reported effects of atrazine, a related and extensively studied herbicide.

Condensed organic matters (COM) with black carbon-like structures are considered as long-term carbon sinks because of their high stability. It is difficult to distinguish COM from general organic matter by conventional chemical analysis, thus the contribution by and interaction mechanisms of organo-mineral complexes in COM stabilization are unclear and generally neglected. Molecular markers related to black carbon-like structures, such as benzene polycarboxylic acids (BPCAs), are promising tools for the qualitative and quantitative analysis of COM. In this study, one natural soil and two cultivated soils with 25 y- or 55 y-tillage activities were collected and the distribution characteristics of BPCAs were detected. All the investigated soils showed similar BPCA distribution pattern, and over 60% of BPCAs were detected in clay fraction. The extractable BPCA contents were substantially increased after mineral removal. The ratios of BPCA contents before and after mineral removal indicate the extent of COM-mineral particle interactions, and our results suggested that up to 73% COM were protected by mineral particles, and more stronger interactions were noted on clay than on silt. The initial cultivation dramatically decreased COM-clay interactions, and this interaction was recovered only slowly after 55-y cultivation. Kaolinite and muscovite are important for COM protection. But a possible negative correlation between BPCAs and reactive iron oxides of the cultivated soils suggested that iron may promote COM degradation when disturbed by tillage activities. This study provided a new angle to study the stabilization of COM and emphasized the importance of organo-mineral complexes for COM stabilization.

Plastic pollution represents one of the major threats to the marine environment. A wide range of marine organisms has been shown to ingest microplastics due to their small dimensions (less than 1 mm). This negatively affects some biological processes, such as feeding, energy reserves and reproduction. Very few studies have been performed on the effect of microplastics on sea urchin development and virtually none on adults. The aim of this work was to evaluate the uptake and distribution of fluorescent labelled polystyrene microbeads (micro-PS) in the Mediterranean sea urchin Paracentrotus lividus and the potential impact on circulating immune cells. Differential uptake was observed in the digestive and water vascular systems as well as in the gonads based on microbeads size (10 and 45 μm in diameter). Treatment of sea urchins with particles of both sizes induced an increase of the total number of immune cells already after 24 h. No significant differences were observed among immune cell types. However, the ratio between red and white amoebocytes, indicative of sea urchin healthy status, increased with both particles. This effect was detectable already at 24 h upon exposure to smaller micro-PS (10 μm). An increase of intracellular levels of reactive oxygen and nitrogen species was observed at 24 h upon both micro-PS exposure, whereas at later time these levels became comparable to those of controls. A significant increase of total antioxidant capacity was observed after treatment with 10 μm micro-PS. Overall data provide the first evidence on polystyrene microbeads uptake and tissue distribution in sea urchins, indicating a stress-related impact on circulating immune cells.

As a promising fungicide, the potential environmental risk of trifloxystrobin (TFS) and its main metabolism trifloxystrobin acid (TFSA) in soil environment should be given special attention. The present study investigated the potential risks of TFS and TFSA in soil environment to earthworms (Eisenia fetida) through measuring several biomarkers. Residual analysis showed that TFSA was more stable than TFS in artificial soil with half-lives ranging from 138.6 to 231.0 d and 20.4–24.7 d, respectively. Additionally, the accumulation of TFS in earthworms increased in the beginning and then decreased from day 14, while that of TFSA continuously increased. At concentrations of 4.0 mg/kg and 10.0 mg/kg, the weight and lysosomal membrane stability of earthworms were reduced; however, the superoxide dismutase (SOD) activity, glutathione-S-transferase (GST) activity and malondialdehyde (MDA) content in earthworms were enhanced by TFS and TFSA. Moreover, the growth inhibition effect and the oxidative damage level induced by TFSA to earthworms were higher than those induced by TFS. The transcriptome analysis date indicated that the differentially expressed genes (DEGs) in both TFS and TFSA treatments were mainly enriched in ribosome pathway and lysosome pathway, finally affecting the protein synthesis and proteolysis in earthworms. The findings of the present study indicated that TFSA may pose a higher risk in the soil environment than TFS.

The widespread use of zinc oxide nanoparticles (ZnO-NPs) has led to their release into the environment, and they thus represent a potential risk for both humans and ecosystems. However, the negative impact of ZnO-NPs on the immune system, especially in relation to host defense against pathogenic infection and its underlying regulatory mechanisms, remains largely unexplored. This study investigated the effects of early-life long-term ZnO-NPs exposure (from L1 larvae to adults) on innate immunity and its underlying mechanisms using a host–pathogen Caenorhabditis elegans model, and this was compared with the effect of ionic Zn. The results showed that the ZnO-NPs taken up by C. elegans primarily accumulated in the intestine and that early-life long-term ZnO-NPs exposure at environmentally relevant concentrations (50 and 500 μg/L) decreased the survival of wild-type C. elegans when faced with pathogenic Pseudomonas aeruginosa PA14 infection. Early-life long-term ZnO-NPs (500 μg/L) exposure significantly increased (by about 3-fold) the accumulation of live P. aeruginosa PA14 colonies in the intestine of C. elegans. In addition, ZnO-NPs (500 μg/L) inhibited the intestinal nuclear translocation of SKN-1 and also downregulated gcs-1 gene expression, which is an SKN-1 target gene. Further evidence revealed that early-life long-term exposure to ZnO-NPs (500 μg/L) did not increase susceptibility to mutation among the genes (pmk-1, sek-1, and nsy-1) encoding the p38 mitogen-activated protein kinase (MAPK) cascade in response to P. aeruginosa PA14 infection, though ZnO-NPs significantly decreased the mRNA levels of pmk-1, sek-1, and nsy-1. This study provides regulatory insight based on evidence that ZnO-NPs suppress the innate immunity of C. elegans and highlights the potential health risks of certain environmental nanomaterials, including ZnO-NPs, in terms of their immunotoxicity at environmentally relevant concentrations.

The placenta is essential for sustaining the growth of the fetus. The aim of this study was to investigate the role of the placenta in MCLR-induced significant reduction in fetal weight, especially the changes in placental structure and function. Pregnant mice were intraperitoneally injected with MCLR (5 or 20 μg/kg) from gestational day (GD) 13 to GD17. The results showed MCLR reduced fetal weight and placenta weight. The histological specimens of the placentas were taken for light and electron microscopy studies. The internal space of blood vessels decreased obviously in the placental labyrinth layer of mice treated with MCLR. After the ultrastructural examination, the edema and intracytoplasmic vacuolization, dilation of the endoplasmic reticulum and corrugation of the nucleus were observed. In addition, maternal MCLR exposure caused a reduction of 11β-hydroxysteroid dehydrogenase type 2 (HSD11B2) expression in placentae, a critical regulator of fetal development. Several genes of placental growth factors, such as Vegfα and Pgf and several genes of nutrient transport pumps, such as Glut1 and Pcft were depressed in placentas of MCLR-treated mice, however nutrient transporters Fatp1 and Snat4 were promoted. Moreover, significant increases in malondialdehyde (MDA) revealed the occurrence of oxidative stress caused by MCLR, which was also verified by remarkable decrease in the glutathione levels, total antioxidant capacity (T-AOC) as well as the activity of antioxidant enzymes. Real-time PCR and western blot analysis revealed that GRP78, CHOP, XBP-1, peIF2α and pIRE1 were remarkable increased in placentas of MCLR-treated mice, indicating that endoplasmic reticulum (ER) stress pathway was activated by MCLR. Furthermore, oxidative stress and ER stress consequently triggered apoptosis which contributed to the impairment of placental development. Collectively, these results suggest maternal MCLR exposure results in reduced fetal body weight, which might be associated with ROS-mediated endoplasmic reticulum stress and impairment in placental structure and function.

Ambient air pollution, namely exposure to air particulate matter (PM), has been shown to be connected with a number of adverse health effects. At least part of the effects can be caused by organic pollutant mixtures associated with PM, which can elicit a wide range of specific toxic potentials. These potentials could be affected by seasonal variation of pollutant mixtures and PM size fraction. To examine this, six size subfractions of PM₁₀ were collected at rural and urban site in the Czech Republic in a year-long sampling campaign. The samples were assessed for aryl hydrocarbon (AhR)-mediated activity, estrogenicity and anti-androgenicity using mammalian cell models. The concentrations of detected toxic potentials differed among seasons. The greatest levels were observed in samples collected during winter when AhR-mediated effects and estrogenicity were at least 10-times greater than in summer. While the observed potentials were mostly less pronounced in samples from rural area, during winter, their AhR-mediated activity was twice as great as at the urban site. This was probably caused by the low-quality of fuel used for heating at the rural site. Assessed toxic potentials were associated mainly with PM size fractions with lesser aerodynamic diameters (<1 μm). Toxic potentials were compared with data from chemical analyses covering 102 chemicals from different pollutant groups to model their contribution to the observed effects. For AhR-mediated activity, chemical analyses explained on average 44% of the effect and the main identified effect-drivers were polycyclic aromatic hydrocarbons. For estrogenicity and anti-androgenicity, detected chemicals were able to explain on average less than 1.6% and 11% of the potentials, with their highest explicability reaching 13% and 57%, respectively. This was affected by the lack of data on specific toxic potency of some detected air pollutants, but also indicates a possible role of further not analyzed chemicals in these effects.

Polychlorinated biphenyls (PCBs) are persistent organic pollutants that are linked to adverse health outcomes. PCB tissue levels are determinants of PCB toxicity; however, it is unclear how factors, such as an altered metabolism and/or a fatty liver, affect PCB distribution in vivo. We determined the congener-specific disposition of PCBs in mice with a liver-specific deletion of cytochrome P450 reductase (KO), a model of fatty liver with impaired hepatic metabolism, and wild-type (WT) mice. Eight-week-old male WT (MWT, n = 3), male KO (MKO, n = 5), female WT (FWT, n = 4), and female KO mice (FKO, n = 4) were exposed orally to Aroclor 1254. PCBs were quantified in adipose, blood, brain, and liver tissues by gas chromatography-mass spectrometry. The ΣPCB levels followed the rank order adipose > liver ∼ brain > blood in WT and adipose ∼ liver > brain > blood in KO mice. PCB levels were much higher in the liver of KO than WT mice, irrespective of the sex. A comparison across exposure groups revealed minor genotype and sex-dependent differences in the PCB congener profiles (cos Θ > 0.92). Within each exposure group, tissue profiles showed small differences between tissues (cos Θ = 0.85 to 0.98). These differences were due to a decrease in metabolically more labile PCB congeners and an increase in congeners resistant to metabolism. The tissue-to-blood ratio of PCBs decreased for adipose, increased for the brain, and remained constant for the liver with an increase in chlorination. While these ratios did not follow the trends predicted using a composition-based model, the agreement between experimental and calculated partition coefficients was reasonable. Although the distribution of PCBs differs between KO and WT mice, the magnitude of the partitioning of PCBs from the blood into tissues can be approximated using composition-based models.