Estuaries provide critical habitat for food webs supporting fish and shellfish consumed by humans, but estuarine ecosystem health has been threatened by increases in nitrogen loading as well as inputs of the neurotoxin, mercury (Hg), which biomagnifies in food webs and poses risk to humans and wildlife. In this study, the effects of nutrient loading on the fate of Hg in shallow coastal estuaries were examined to evaluate if their interaction enhances or reduces Hg bioavailability in sediments, the water column, and concentrations in lower trophic level fish (Fundulus heteroclitus and Menidia menidia). Multiple sites were sampled within two human impacted coastal lagoons, Great South Bay (GSB) and Jamaica Bay (JB), on the southern coast of Long Island, NY, United States of America (U.S.A.). Carbon (C), nitrogen (N), sulfur (S), Hg, and methylmercury (MeHg) were measured in surface sediments and the water column, and total Hg (THg) was measured in two species of forage fish. Minimal differences were found in dissolved and particulate Hg, dissolved organic carbon (DOC), and salinity between the two bays. Across lagoons, concentrations of chlorophyll-a were correlated with total suspended solids (TSS), and water column THg and MeHg was largely associated with the particulate fraction. Methylmercury concentrations in particulates decreased with increasing TSS and chlorophyll-a, evidence of biomass dilution of MeHg with increasing productivity at the base of the food chain. Water column Hg was associated with THg concentrations in Atlantic silversides, while mummichog THg concentrations were related to sediment concentrations, reflecting their different feeding strategies. Finally, higher nutrient loading (lower C:N in sediments) while related to lower particulate concentrations coincided with higher bioaccumulation factors (BAF) for Hg in both fish species. Thus, in shallow coastal lagoons, increased nutrient loading resulted in decreased Hg concentrations at the base of the food web but resulted in greater bioaccumulation of Hg to fish relative to its availability in algal food.

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.

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.

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.

Risk assessments of the ecotoxicological effects insecticides impose on ectotherms have increasingly considered temperature. However, the changes toxicants induce in thermoregulatory behavioral traits may lead to a divergence of thermal selection and temperature-dependent changes of contaminant toxicity. This study demonstrated the interaction of behavioral thermoregulation and temperature-dependent toxicity of beta-cyfluthrin (BC) in the lizard Eremias argus. Based on the negative relationship between temperature and BC toxicity, seeking a warming environment was assumed to represent a self-rescue behavior (and vice versa). The results showed that BC-treated lizards (0–20 μg/g body weight (bw)) showed such self-rescue behavior, while lizards exposed to an extremely high BC dose (200 μg/g bw) sought a cooler environment. Biochemical assays showed that BC affected neurotransmitter systems, caused oxidative stress, and interfered with ion-transport in the central nervous system. Biomarkers of the cholinergic and glutamatergic system, ion-transport function, and oxidative stress were identified as potential biochemical variables related to thermoregulatory behavior. Apparently, seeking a warmer environment is a survival strategy with the aim to neutralize BC toxicity, while seeking a cooler environment aims to attenuate the harmful effects of metabolic and oxidative stress, and to decelerate internal BC diffusion. This phenomenon could be also explained by the concept of the “cooling trap”, i.e., a behavior where cooler temperatures are sought. This impairs survival after exposure to BC at it has a negative temperature coefficient, derived from a dysfunction of the central nervous system regarding thermoregulation caused by the high dosage of neurotoxicant and resulting temperature maladaptation. Implications of the interaction between thermoregulatory behavior and temperature-dependent toxicity are presented, which may aid further temperature-dependent risk assessments.

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.

Lead (Pb) is one of the predominant heavy metals in e-waste recycling arears and recognized as a notorious environmental neurotoxic substance. However, whether Pb at environmentally relevant concentrations could cause neurobehavioral alteration and even what kind of signaling pathway Pb exposure would disrupt in zebrafish were not fully uncovered. In the present study, 6 h postfertilization (hpf) zebrafish embryos were exposed to Pb at the concentrations of 0, 5, 10, and 20 μg/L until 144 hpf. Then the neurobehavioral indicators including locomotor, turnings and social behaviors, and the expressions of selected genes concerning brain-derived neurotrophic factor (BDNF) signaling were investigated. The results showed that significant changes were obtained under 20 μg/L Pb exposure. The hypoactivity of zebrafish larvae in locomotor and turning behaviors was induced during the dark period, while hyperactivity was observed in a two-fish social assay during the light period. The significantly downregulation of genes encoding BDNF, its receptor TrkB, and N-methyl-D-aspartate glutamate receptor (NMDAR) suggested the involvement of NMDAR-dependent BDNF signaling pathway. Overall, our study demonstrated that developmental exposure to Pb at environmentally relevant concentrations caused obvious neurobehavioral impairment of zebrafish larvae by disrupting the NMDAR-dependent BDNF signaling, which could exert profound ecological consequences in the real environment.

Methylmercury (MeHg) is a neurotoxic compound that is found in virtually all fish and biomagnifies in aquatic food webs. Although MeHg concentrations in marine and estuarine fish are often elevated, the impacts of MeHg on marine and estuarine fish have largely been understudied. To evaluate the impact of dietary MeHg on marine fish reproduction and effects on their offspring, female juvenile sheepshead minnows (Cyprinodon variegatus) at three months of age were experimentally exposed to MeHg-contaminated diets for two months and then paired with Hg-free males for spawning. Egg production, hatching success of embryos, time to hatching, survival of larvae, growth of larvae and swimming behavior of larvae were determined. Selenium (Se) was also measured and Se/Hg molar ratios were calculated to assess whether Se reduced MeHg toxicity. MeHg had no significant impact on fish reproduction or on survival and growth of larvae. Larvae produced by MeHg-exposed mothers had concentrations of Hg about 1 ppm (dry wt), or about 12% of that in the muscle of their mothers and consistently displayed 6–15% increased swimming speed relative to controls; the ecological significance of this moderate effect on swimming speed requires further study. The Se/Hg molar ratios in these fish, which were >1 in controls (adults and larvae) and MeHg-exposed larvae but <1 in Hg-exposed adults, did not correlate with MeHg effects. The sheepshead minnow, at a low trophic level, appears to have a high tolerance of MeHg; however, it can pass MeHg to higher trophic levels in marine ecosystems where upper level predators have MeHg concentrations sometimes exceeding US FDA safety limits of 1 ppm wet wt.

DCOIT (4,5-dichloro-2-n-octyl-4-isothiazolin-3-one) is the main active ingredient in an emerging water environment antifoulant, the toxicity and environmental impacts of which need to be further investigated. Thus, this study examined the toxicity of DCOIT on Nile tilapia (Oreochromis niloticus), including its effects on behavior, respiration and energy metabolism as well as the role of endoplasmic reticulum stress (ER stress) in mediating its toxicity and metabolic changes. The changes in fish behavior, respiration, neuronal signal transmission, energy metabolism, ER stress, and liver histology were examined via acute (4 days) and chronic (28 days) exposures to 0, 3, 15, 30 μg/L DCOIT in vivo. Additionally, ER stress levels were measured in 24-h periods of hepatocyte exposure to 0, 3, 15, 30 and 300 μg/L DCOIT in vitro. The hyper-locomotor activities decreased, but the respiration rate increased after a 4-day acute exposure period, indicating that DCOIT exposure altered fish energy metabolism. After acute exposure at a low DCOIT concentration, the activation of ER stress induced triglyceride accumulation in the liver. After chronic exposure for 28 days, the prolonged ER stress induced a series of pathological cellular changes. At the cellular level, exposure to a high DCOIT concentration induced ER stress in the hepatocytes. In addition, as a neurotoxin, DCOIT has the potential to disrupt the neurotransmission of the cholinergic system, resulting in motor behavior disruption. This study demonstrates that DCOIT plays a role in time- and concentration-dependent toxicity and that changes in lipid metabolism are directly related to endoplasmic reticulum function after exposure to an antifouling agent. This work advances the understanding of the toxic mechanism of DCOIT, which is necessary for its evaluation.