Copper oxide nanoparticles (CuO-NP) are used as an efficient alternative to conventional Cu in agriculture and might end up in soils. They show a high toxicity towards cells and microorganisms, but only low toxicity towards soil invertebrates. However, most existing soil ecotoxicological studies were conducted in a sandy reference soil and at test concentrations ≥100 mg Cu/kg soil. Therefore, there is a knowledge gap concerning the effect of soil texture on the toxicity of CuO-NP at lower, more realistic test concentrations. In our study, a sandy reference soil and three loamy soils were spiked with CuO-NP at up to four concentrations, ranging from 5 to 158 mg Cu/kg. We investigated 28-day reproduction as well as weight and Cu content after 14-day bioaccumulation and subsequent 14-day elimination for the springtail Folsomia candida. For the first time we analysed the size distribution of CuO-NP in aqueous test soil extracts by single particle-ICP-MS which revealed that the diameter of CuO-NP significantly increased with increasing concentration, but did not vary between test soils. Negative effects on reproduction were only observed in loamy soils, most pronounced in a loamy-acidic soil (−61%), and they were always strongest at the lowest test concentration. The observed effects were much stronger than reported by other studies performed with sandy soils and higher CuO-NP concentrations. In the same soil and concentration, a moderate impact on growth (−28%) was observed, while Cu elimination from springtails was inhibited. Rather than Cu body concentration, the diameter of the CuO-NP taken up, as well as NP-clay interactions might play a crucial role regarding their toxicity. Our study reports for the first time toxic effects of CuO-NP towards a soil invertebrate at a low, realistic concentration range. The results strongly suggest including lower test concentrations and a range of soil types in nanotoxicity testing.

Lindane persists in the environment and bioaccumulates as an organochlorine pesticide and can pose risks to ecological environments and human health. To explore the long-term toxicity and underlying mechanisms of lindane, Caenorhabditis elegans was chosen as an animal model for toxicological study. The indicators of physiological, oxidative stress and cell apoptosis were examined in nematodes chronically exposed to environmentally relevant concentrations of lindane (0.01–100 ng/L). The data suggested that exposure to lindane at doses above 0.01 ng/L induced adverse physiological effects in C. elegans. Significant increases of ROS production and lipofuscin accumulation were observed in 100 ng/L of lindane-exposed nematodes, suggesting that lindane exposure induced oxidative stress in nematodes. Exposure to 10–100 ng/L of lindane also significantly increased the average number of germ cell corpses, which indicated cell apoptosis induced by lindane in C. elegans. Moreover, chronic exposure to 100 ng/L lindane significantly influenced the expression of genes related to oxidative stress and cell apoptosis (e.g., isp-1, sod-3, ced-3, and cep-1 genes). These results indicated that oxidative stress and cell apoptosis could play an important role in toxicity induced by lindane in nematodes.

Pyriproxyfen is a juvenile hormone analogue insecticide used worldwide. At present, the potential threat of pyriproxyfen to aquatic organism has not been well explored. In this work, the bioaccumulation, metabolic profile and toxicity of pyriproxyfen and its metabolites to zebrafish were studied, and the enantioselectivity of pyriproxyfen and the major chiral metabolites were also determined. Sixteen metabolites of pyriproxyfen in zebrafish were identified. Hydroxylation, ether linkage cleavage and oxidation in phase I metabolism, followed by sulfate and glucuronic acid conjugation. The bioconcentration factors ranged from 1175 to 1246. Hydroxylation metabolites of pyriproxyfen showed enantioselective behavior in zebrafish with enantiomer fractions (EFs) of 4′–OH– pyriproxyfen and 5″–OH– pyriproxyfen ranged from 0.50 to 0.71. Toxicological indexes including acute toxicity, joint toxicity and oxidative stress were tested. Among all the metabolites, 4′–OH– pyriproxyfen was found 2 folds more toxic to zebrafish than pyriproxyfen. (−)-Pyriproxyfen was found 2 folds more toxic than rac- and (+)-pyriproxyfen. Antagonistic effects were found in binary joint toxicity of pyriproxyfen and its hydroxylated metabolites. Pyriproxyfen and its metabolites also showed oxidative stress damage by inhibiting the activity of CAT and SOD and increasing MDA. This work provided deep insight into the metabolism and the potential risks of pyriproxyfen to aquatic organisms.

Spatial variation of the levels of polycyclic aromatic hydrocarbons (PAHs) was evaluated within an urban-industrial district where the main anthropogenic pressures are a 15 MW biomass power plant (BPP) and road traffic. The use of a high-density lichen transplant network and wind quantitative relationships made it possible to perform a hierarchical analysis of contamination. Combined uni-bi and multivariate statistical analyses of the resulting databases revealed a dual pattern. In its surroundings (local scale), the BPP affected the bioaccumulation of fluoranthene, pyrene and total PAHs, although a confounding effect of traffic (mostly petrol/gasoline engines) was evident. Spatial variation of the rate of diesel vehicles showed a significant association with that of acenaphthylene, acenaphthene, fluorene, anthracene and naphthalene. The series of high-speed wind values suggests that wind promotes diffusion rather than dispersion of the monitored PAHs. At the whole study area scale, the BPP was a source of acenaphthylene and acenaphthene, while diesel vehicles were a source of acenaphthylene. PAHs contamination strongly promotes oxidative stress (a threefold increase vs pre-exposure levels) in lichen transplants, suggesting a marked polluting effect of anthropogenic sources especially at the expense of the mycobiont. The proposed monitoring approach could improve the apportionment of the different contributions of point and linear anthropogenic sources of PAHs, mitigating the reciprocal biases affecting their spatial patterns.

Fipronil, a phenyl-pyrazole insecticide, has a wide range of uses, from agriculture to veterinary medicine. Due to its large-scale applications, the risk of environmental and occupational exposure and bioaccumulation raises concerns. Moreover, relatively little is known about the intracellular mechanisms of fipronil in trophoblasts and the endometrium involved in implantation. Here, we demonstrated that fipronil reduced the viability of porcine trophectoderm and luminal epithelial cells. Fipronil induced cell cycle arrest at the sub-G1 phase and apoptotic cell death through DNA fragmentation and inhibition of DNA replication. These reactions were accompanied by homeostatic changes, including mitochondrial depolarization and cytosolic calcium depletion. In addition, we found that exposure to fipronil compromised the migration and implantation ability of pTr and pLE cells. Moreover, alterations in PI3K-AKT and MAPK-ERK1/2 signal transduction were observed in fipronil-treated pTr and pLE cells. Finally, the antiproliferative and apoptotic effects of fipronil were also demonstrated in 3D cell culture conditions. In summary, our results suggest that fipronil impairs implantation potentials in fetal trophectoderm and maternal endometrial cells during early pregnancy.

Tissue distribution of legacy and emerging per-and polyfluoroalkyl substances (PFASs) in several kinds of edible fishes collected from Meiliang bay of Taihu Lake, China were investigated and the related human health risks were assessed. Perfluorooctanesulfonate (PFOS), perfluorooctanesulfonamide (PFOSA) and 6:2 fluorotelomer phosphate diester (6:2 diPAP) were the most abundant legacy perfluoroalkyl acid (PFAA), PFOS related precursor (PreFOS), and the emerging PFASs in all fish tissues, respectively. Similar to the legacy PFAAs, 6:2 diPAP and 6:6 perfluorophosphinate (6:6 PFPiA) had the highest levels in the fish liver, whereas the highest level of PFOSA was in kidney, which might be due to its intensive transformation in fish liver. The concentrations of PFASs were generally positively correlated with the trophic levels. The profiles of PFASs were significantly different among bitterling, crucian and other fish, which might be related to their different metabolic capacities. Bioaccumulation factors (BAFs) of PreFOSs, 6:2 diPAP, and 6:6 PFPiA were lower than those of PFAAs with the same number of perfluorinated carbons. The calculated hazard ratios (HR) of PFOS (Range: 0.0100–0.655) and perfluorooctanoic acid (PFOA) (<0.00200) in all fish muscles were less than 1.0. However, the HR of the ∑PFASs in crucian muscle was 1.04, which implied that frequent consumption of crucian collected from Meiliang Bay might pose potential risks to human health.

Microplastic pollution is emerging as a global environmental issue, and its potential for transferring hazardous chemicals to aquatic organisms is gaining attention. Studies have investigated the transfer of chemicals, mainly sorbed chemicals, through ingestion of microplastics by organisms, but limited information is available regarding chemical additives and uptake via the aqueous route through plastic leaching. In this study, we compared two bioaccumulation pathways of the additive hexabromocyclododecane (HBCD) by exposing mussels (Mytilus galloprovincialis) to two different sizes of expanded polystyrene (EPS): inedible size (4.2–5.5 mm) for leachate uptake and edible size (20–770 μm) for particle ingestion and leachate uptake. Over 10 days, the HBCD concentration increased significantly in mussels in the EPS exposure groups, indicating that EPS microplastic acts as a source of HBCD to mussels. The concentration and isomeric profiles of HBCD in mussels show that uptake through the aqueous phase is a more significant pathway for bioaccumulation of HBCD from EPS to mussels than particle ingestion. HBCD levels measured in EPS, leachate and exposed mussels from this study are environmentally relevant concentration. The fate and effects of chemical additives leached from plastic debris in ecosystem requires further investigation, as it may affect numerous environments and organisms through the aqueous phase.

The flame retardants hexabromobenzene (HBB) and pentabromobenzene (PBB) have been extensively used and become ubiquitous pollutants in the aquatic environment and biota, but their potential toxic effects on wildlife remained unknown. In this study, by using zebrafish (Danio rerio) as a model, the bioconcentration and developmental neurotoxicity were investigated. Zebrafish embryos were exposed to HBB and PBB (0, 30, 100 and 300 μg/L) from 2 until 144 h post-fertilization (hpf). Chemical analysis showed bioconcentrations of both chemicals, while HBB is readily metabolized to PBB in zebrafish larvae. Embryonic exposure to both chemicals did not cause developmental toxicity, but induced locomotor behavioral anomalies in larvae. Molecular docking results indicated that both chemicals could bind to zebrafish acetylcholinesterase (AChE). Furthermore, HBB and PBB significantly inhibited AChE activities, accompanied by increased contents of acetylcholine and decreased choline in larvae. Downregulation of the genes associated with central nervous system (CNS) development (e.g., mbp, α1-tubulin, gfap, shha) as well as the corresponding proteins (e.g., Mbp, α1-Tubulin) was observed, but gap-43 was upregulated at both gene and protein levels. Together, our results indicate that both HBB and PBB exhibit developmental neurotoxicity by affecting various parameters related to CNS development and indications for future toxicological research and risk assessment of the novel brominated flame retardants.

The present study aims to explore the bioaccumulation and biotic transformations of inorganic (iHg) and monomethyl mercury (MMHg) by natural pico-nanoplankton community from eutrophic lake Soppen, Switzerland. Pico-nanoplankton encompass mainly bacterioplankton, mycoplankton and phytoplankton groups with size between 0.2 and 20 μm. Species-specific enriched isotope mixture of ¹⁹⁹iHg and ²⁰¹MMHg was used to explore the accumulation, the subcellular distribution and transformations occurring in natural pico-nanoplankton sampled at 2 different depths (6.6 m and 8.3 m). Cyanobacteria, diatoms, cryptophyta, green algae and heterotrophic microorganisms were identified as the major groups of pico-nanoplankton with diatoms prevailing at deeper samples. Results showed that pico-nanoplankton accumulated both iHg and MMHg preferentially in the cell membrane/organelles, despite observed losses. The ratios between the iHg and MMHg concentrations measured in the membrane/organelles and cytosol were comparable for iHg and MMHg. Pico-nanoplankton demethylate added ²⁰¹MMHg (~4 and 12% per day depending on cellular compartment), although the involved pathways are to further explore. Comparison of the concentrations of ²⁰¹iHg formed from ²⁰¹MMHg demethylation in whole system, medium and whole cells showed that 82% of the demethylation was biologically mediated by pico-nanoplankton. No significant methylation of iHg by pico-nanoplankton was observed. The accumulation of iHg and MMHg and the percentage of demethylated MMHg correlated positively with the relative abundance of diatoms and heterotrophic microorganisms in the pico-nanoplankton, the concentrations of TN, Mg²⁺, NO₃⁻, NO₂⁻, NH₄⁺ and negatively with the concentrations of DOC, K⁺, Na⁺, Ca²⁺, SO₄²⁻. Taken together the results of the present field study confirm the role of pico-nanoplankton in Hg bioaccumulation and demethylation, however further research is needed to better understand the underlying mechanisms and interconnection between heterotrophic and autotrophic microorganisms.

Mercury (Hg), a potent neurotoxic element, can biomagnify through food webs once converted into methylmercury (MeHg). Some studies have found that selenium (Se) exposure may reduce MeHg bioaccumulation and toxicity, though this pattern is not universal. Se itself can also be toxic at elevated levels. We experimentally manipulated the relative concentrations of dietary MeHg and Se (as selenomethionine [SeMet]) for an aquatic grazer (the mayfly, Neocloeon triangulifer) and its food source (diatoms). Under low MeHg treatment (0.2 ng/L), diatoms exhibited a quadratic pattern, with decreasing diatom MeHg concentration up to 2.0 μg Se/L and increasing MeHg accumulation at higher SeMet concentrations. Under high MeHg treatment (2 ng/L), SeMet concentrations had no effect on diatom MeHg concentrations. Mayfly MeHg concentrations and biomagnification factors (concentration of MeHg in mayflies: concentration of MeHg in diatoms) declined with SeMet addition only in the high MeHg treatment. Mayfly MeHg biomagnification factors decreased from 5.3 to 3.3 in the high MeHg treatment, while the biomagnification factor was constant with an average of 4.9 in the low MeHg treatment. The benefit of reduced MeHg biomagnification was offset by non-lethal effects and high mortality associated with ‘protective’ levels of SeMet exposure. Mayfly larvae escape behavior (i.e., startle response) was greatly reduced at early exposure days. Larvae took nearly twice as long to metamorphose to adults at high Se concentrations. The minimum number of days to mayfly emergence did not differ by SeMet exposure, with an average of 13 days. We measured an LC50SₑMₑₜ for mayflies of 3.9 μg Se/L, with complete mortality at concentrations ≥6.0 μg Se/L. High reproductive mortality occurred at elevated SeMet exposures, with only 0–18% emergence at ≥4.12 μg Se/L. Collectively, our results suggest that while there is some evidence that Se can reduce MeHg accumulation at the base of the food web at specific exposure levels of SeMet and MeHg, Se is also toxic to mayflies and could lead to negative effects that extend across ecosystem boundaries.