Due to worldwide production, sales and application, neonicotinoids dominate the global use of insecticides. While, neonicotinoids are considered as pinpoint neurotoxicants that impair cholinergic neurotransmission in pest insects, the sublethal effects on nontarget organisms and other neurotransmitters remain poorly understood. Thus, we investigated long-term neurological outcomes in the decomposer nematode Caenorhabditis elegans. In the adult roundworm the neonicotinoid thiacloprid impaired serotonergic and dopaminergic neuromuscular behaviors, while respective exposures to thiamethoxam showed no effects. Thiacloprid caused a concentration-dependent delay of the transition between swimming and crawling locomotion that is controlled by dopaminergic and serotonergic neurotransmission. Age-resolved analyses revealed that impairment of locomotion occurred in young as well as middle-aged worms. Treatment with exogenous serotonin rescued thiacloprid-induced swimming deficits in young worms, whereas additional exposure with silica nanoparticles enhanced the reduction of swimming behavior. Delay of forward locomotion was partly caused by a new paralysis pattern that identified thiacloprid as an agent promoting a specific rigidity of posterior body wall muscle cells and peripheral neuropathy in the nematode (lowest-observed-effect-level 10 ng/ml). On the molecular level exposure with thiacloprid accelerated protein aggregation in body wall muscle cells of polyglutamine disease reporter worms indicating proteotoxic stress. The results from the soil nematode Caenorhabditis elegans show that assessment of neurotoxicity by neonicotinoids requires acknowledgment and deeper research into dopaminergic and serotonergic neurochemistry of nontarget organisms. Likewise, it has to be considered more that different neonicotinoids may promote diverse neural end points.

Many communities around the country are undergoing contentious battles over the installation of artificial turf. Opponents are concerned about exposure to hazardous chemicals leaching from the crumb rubber cushioning fill made of recycled tires, the plastic carpet, and other synthetic components. Numerous studies have shown that chemicals identified in artificial turf, including polycyclic aromatic hydrocarbons (PAHs), phthalates, and per- and polyfluoroalkyl substances (PFAS), are known carcinogens, neurotoxicants, mutagens, and endocrine disruptors. However, few studies have looked directly at health outcomes of exposure to these chemicals in the context of artificial turf. Ecotoxicology studies in invertebrates exposed to crumb rubber have identified risks to organisms whose habitats have been contaminated by artificial turf. Chicken eggs injected with crumb rubber leachate also showed impaired development and endocrine disruption. The only human epidemiology studies conducted related to artificial turf have been highly limited in design, focusing on cancer incidence. In addition, government agencies have begun their own risk assessment studies to aid community decisions. Additional studies in in vitro and in vivo translational models, ecotoxicological systems, and human epidemiology are strongly needed to consider exposure from both field use and runoff, components other than crumb rubber, sensitive windows of development, and additional physiological endpoints. Identification of potential health effects from exposures due to spending time at artificial turf fields and adjacent environments that may be contaminated by runoff will aid in risk assessment and community decision making on the use of artificial turf.

The environmental neurotoxin β-methylamino-L-alanine (BMAA) may represent a risk for human health in case of chronic exposure or after short-term exposure during embryo development. BMAA accumulates in freshwater and marine organisms consumed by humans. It is produced by marine and freshwater phytoplankton species, but the range of producers remains unknown. Therefore, analysing the phytoplankton composition is not sufficient to inform about the risk of freshwater contamination by BMAA. Filter-feeders mussels have accumulation capacities and therefore appear to be relevant to monitor various pollutants in aquatic ecosystems. We investigated the suitability of the freshwater mussels Dreissena polymorpha and Anodonta anatina for monitoring BMAA in water. Both species were exposed to 1, 10, and 50 μg of dissolved BMAA/L daily for 21 days, followed by 42 days of depuration in clean water. On days 0, 1, 7, 14, and 21 of exposure and 1, 7, 14, 21 and 42 of depuration, whole D. polymorpha and digestive glands of A. anatina were sampled, and the total BMAA concentration was measured. D. polymorpha accumulated BMAA earlier (from day 1 at all concentrations) and at higher tissue concentrations than A. anatina, which accumulated BMAA from day 14 when exposed to 10 μg BMAA/L and from day 7 when exposed to 50 μg BMAA/L. As BMAA accumulation by D. polymorpha was time and concentration-dependent, with a significant elimination during the depuration period, this species may be able to reflect the levels and dynamics of water contamination by dissolved BMAA. The species A. anatina could be used for monitoring water concentrations above 10 μg BMAA/L.

Excessive exposure to cobalt (Co) is known to make adverse impact on the nervous system, but its detailed mechanisms of neurotoxicity have yet to be determined. In this study, C57BL/6 mice (0, 4, 8, 16 mg/kg CoCl₂, 30 days) and human neuroblastoma H4 cells (0, 100, 400, 600 μM CoCl₂) were used as in vivo and in vitro models. Our results revealed that CoCl₂ intraperitoneal injection caused significant impairments in learning and memory, as well as pathological damage in the nervous system. We further certificated the alteration of m⁶A methylation induced by CoCl₂ exposure. Our findings demonstrate for the first time, significant differences in the degree of m⁶A modification, the biological function of m⁶A-modified transcripts between cortex and H4 cell samples. Specifically, MeRIP-seq and RNA-seq elucidate that CoCl₂ exposure results in differentially m⁶A-modified and expressed genes, which were enriched in pathways involving synaptic transmission, and central nervous system (CNS) development. Mechanistic analyses revealed that CoCl₂ remarkably changed m⁶A modification level by affecting the expression of m⁶A methyltransferase and demethylase, and decreasing the activity of demethylase. We observed variation of m⁶A modification in neurodegenerative disease-associated genes upon CoCl₂ exposure and identified regulatory strategy between m⁶A and potential targets mRNA. Our novel findings provide novel insight into the functional roles of m⁶A modification in neurodegenerative damage caused by environmental neurotoxicants and identify Co-mediated specific RNA regulatory strategy for broadening the epigenetic regulatory mechanism of RNA induced by heavy metals.

Samples from two reservoirs with eutrophication problems, located in Pontevedra and Ourense (Northwestern Spain), were cultured, along with a third crop from a reservoir with no problems detected in Ourense (Northwestern Spain). The samples were grown under the same conditions (with an average temperature of 21 ± 2 °C, and a 3000 lux light intensity) in triplicate, and their growth, absorbance and pH were studied. High correlation values were obtained for pH and cellular growth (R² ≥ 95%). The water from Salas showed the greatest microalgal growth (0.15 × 10⁶ cells/ml to 31.70 × 10⁶ cells/ml of Microcystis sp. for the last day of culturing) and the greatest increase in pH (5.72–9.02). In all the cultures studied here, the main species that reproduced was Microcystis sp., which can produce neurotoxins and hepatotoxins. In addition, water samples were cultured with sediments of their own reservoir and with others to observe their evolution. The sediments studied in this case were rich in biotites, which can lead phosphate to be a limiting factor for phytoplankton due to the formation and sedimentation of insoluble salts of ferric phosphate. In crops grown with sediments from the Salas reservoir, actinobacteria developed which can inhibit microalgal growth. The study of the growth of cyanobacteria and possible methods of inhibiting them directly concerns the quality of water and its ecosystems, avoiding pollution and impact on ecosystems.

Mercury (Hg) is a potent neurotoxicant known to induce important adverse effects on fish, but a deeper understanding is lacking regarding how environmental exposure affects the brain morphology and neural plasticity of specific brain regions in wild specimens. In this work, it was evaluated the relative volume and cell density of the lateral pallium, hypothalamus, optic tectum and molecular layer of the cerebellum on wild Liza aurata captured in Hg-contaminated (LAR) and non-contaminated (SJ) sites of a coastal system (Ria de Aveiro, Portugal). Given the season-related variations in the environment that fish are naturally exposed, this assessment was performed in the winter and summer. Hg triggered a deficit in cell density of hypothalamus during the winter that could lead to hormonal dysfunctions, while in the summer Hg promoted larger volumes of the optic tectum and cerebellum, indicating the warm period as the most critical for the manifestation of putative changes in visual acuity and motor-dependent tasks. Moreover, in fish from the SJ site, the lateral pallium relative volume and the cell density of the hypothalamus and optic tectum were higher in the winter than in summer. Thus, season-related stimuli strongly influence the size and/or cell density of specific brain regions in the non-contaminated area, pointing out the ability of fish to adapt to environmental and physiological demands. Conversely, fish from the Hg-contaminated site showed a distinct seasonal profile of brain morphology, presenting a larger optic tectum in the summer, as well as a larger molecular layer of the cerebellum with higher cell density. Moreover, Hg exposure impaired the winter-summer variation of the lateral pallium relative size (as observed at SJ). Altogether, seasonal variations in fish neural morphology and physiology should be considered when performing ecotoxicological studies in order to better discriminate the Hg neurotoxicity.

Albatrosses (Diomedeidae) are iconic pelagic seabirds whose life-history traits (longevity, high trophic position) put them at risk of high levels of exposure to methylmercury (MeHg), a powerful neurotoxin that threatens humans and wildlife. Here, we report total Hg (THg) concentrations in body feathers from 516 individual albatrosses from 35 populations, including all 20 taxa breeding in the Southern Ocean. Our key finding is that albatrosses constitute the family of birds with the highest levels of contamination by Hg, with mean feather THg concentrations in different populations ranging from moderate (3.8 μg/g) to exceptionally high (34.6 μg/g). Phylogeny had a significant effect on feather THg concentrations, with the mean decreasing in the order Diomedea > Phoebetria > Thalassarche. Unexpectedly, moulting habitats (reflected in feather δ13C values) was the main driver of feather THg concentrations, indicating increasing MeHg exposure with decreasing latitude, from Antarctic to subtropical waters. The role of moulting habitat suggests that the majority of MeHg eliminated into feathers by albatrosses is from recent food intake (income strategy). They thus differ from species that depurate MeHg into feathers that has been accumulated in internal tissues between two successive moults (capital strategy). Since albatrosses are amongst the most threatened families of birds, it is noteworthy that two albatrosses listed as Critical by the World Conservation Union (IUCN) that moult and breed in temperate waters are the most Hg-contaminated species (the Amsterdam and Tristan albatrosses). These data emphasize the urgent need for robust assessment of the impact of Hg contamination on the biology of albatrosses and they document the high MeHg level exposure of wildlife living in the most remote marine areas on Earth.

Methylmercury (MeHg), a neurotoxin, is a global concern because of its potential risk to human and ecological health. Elevated mercury (Hg) concentrations were recently reported in the Tibetan Plateau (TP) due to increasing Hg input from distant regions, yet little is known about MeHg production and distribution in the terrestrial ecosystems of the TP. Here, we report longitudinal occurrence of MeHg and the factors regulating net MeHg production in 23 grassland sites from eastern to western TP. The soil MeHg content varied from 0.002 to 0.058 ng g−1, with different distribution patterns between the eastern and western TP. There was a positive correlation between the MeHg concentration and the longitude after 90 °E, which is similar to the distribution patterns of the total mercury (THg), water and organic carbon in this region. Average MeHg concentration in topsoil is generally higher than that in subsoil. Our results show that MeHg concentration in soils of the TP is directly affected by soil water, potential microbial methylators and THg, while indirectly regulated by soil organic carbon through the microbial community and the longitude-dependent precipitation through soil water. Our study suggests that soil water is the most important driver regulating net MeHg production in the grasslands of the TP. These findings have important implications for unraveling the mechanism of net production of MeHg in high-altitude environments.

Thousands of hectares of wetlands are created annually because wetlands provide beneficial ecosystem services. Wetlands are also key sites for production of the bioaccumulative neurotoxin methylmercury (MeHg), but little is known about MeHg production in created systems. Here, we studied methylmercury in sediment, water, and invertebrates in created wetlands of various ages. Sediment MeHg reached 8 ng g⁻¹ in the newest wetland, which was significantly greater than in natural, control wetlands. This trend was mirrored in several invertebrate taxa, whose concentrations reached as high as 1.6 μg g⁻¹ in the newest wetland, above levels thought to affect reproduction in birds. The MeHg concentrations in created wetland invertebrate taxa generally decreased with increasing wetland age, possibly due to a combination of deeper anoxia and less organic matter accumulation in younger wetlands. A short-term management intervention and/or improved engineering design may be necessary to reduce the mercury-associated risk in newly created wetlands.

Bioassays using Daphnia pulex and Moina micrura were designed to detect cyanobacterial neurotoxins in raw water samples. Phytoplankton and cyanotoxins from seston were analyzed during 15 months in a eutrophic reservoir. Effective time to immobilize 50% of the exposed individuals (ET50) was adopted as the endpoint. Paralysis of swimming movements was observed between ∼0.5-3 h of exposure to lake water containing toxic cyanobacteria, followed by an almost complete recovery of the swimming activity within 24 h after being placed in control water. The same effects were observed in bioassays with a saxitoxin-producer strain of Cylindrospermopsis raciborskii isolated from the reservoir. Regression analysis showed significant relationships between ET50vs. cell density, biomass and saxitoxins content, suggesting that the paralysis of Daphnia in lake water samples was caused by saxitoxins found in C. raciborskii. Daphnia bioassay was found to be a sensitive method for detecting fast-acting neurotoxins in natural samples, with important advantages over mouse bioassays.