Pregnant women are widely exposed to organophosphate (OP) pesticides, which are potentially neurotoxicant for the developing fetus. We aimed to identify principal demographic and dietary predictors of OP pesticide exposure among 450 pregnant women participating in the New York University Children’s Health and Environment Study (enrolled 2016–19). Urinary concentrations of six dialkyl phosphate (DAP) metabolites (3 dimethyl (DM) metabolites and 3 diethyl (DE) metabolites) of OP pesticides were determined at three time points across pregnancy. At mid-gestation, the Diet History Questionnaire II was used to assess women’s dietary intake over the past year. Demographic characteristics were obtained using questionnaires and/or electronic health records. We used linear mixed models to evaluate the associations of demographic and food groups with DAP metabolite levels, and partial-linear single-index (PLSI) models to analyze the contribution proportions of food groups to DAP metabolite concentrations and the dose-response relationships between them. We observed that pregnant women in NYC had lower levels of OP pesticide metabolites than pregnant populations in Europe, Asia, and other regions in the U.S. Having lower pre-pregnancy body mass index and being Asian, employed, and single were associated with higher DAP metabolite concentrations. Fruit and grain intakes were associated with higher ∑DM, ∑DE, and ∑DAP levels. ∑DE concentrations increased 9.0% (95% confidence interval (CI) = 1.2%, 17.4%) per two-fold increase in dairy consumption, whereas ∑DE concentrations decreased 1.8% (95%CI = −3.1%, −0.4%) per two-fold increase in seafood consumption. The PLSI model indicated that among the food mixture, fruit and grains were the main food groups contributed to higher levels of ∑DAP, while meat contributed to lower levels of ∑DAP. The contribution proportions of fruit, grains, and meat were 18.7%, 17.9%, and 39.3%, respectively. Our results suggest that fruit, grains, and meat are major dietary components associated with OP pesticide exposure in urban pregnant women.

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.

Perfluorooctanoic acid (PFOA) is a widely used synthetic industrial chemical which accumulates in ecosystems and organisms. Our study have investigated the neurobehavioral effects of PFOA and the alleviation effects of PFOA-induced neurotoxicity by blueberry anthocyanins (ANT) in Dugesia japonica. The planarians were exposed to PFOA and ANT for ten days. Researchs showed that exposure to PFOA affected locomotor behavior and ANT significantly alleviated the reduction in locomotion induced by PFOA. The regeneration of eyespots and auricles was suppressed by PFOA and was promoted by ANT. Following exposure to PFOA, acetylcholinesterase activity continually decreased and was unaffected in the ANT group, but was elevated after combined administration of PFOA and ANT. Oxidative DNA damage was found in planarians exposed to PFOA and was attenuated after administration of ANT by the alkaline comet assay. Concentrations of three neurotransmitters increased following exposure to PFOA and decreased after administration of ANT. Furthermore, ANT promoted and PFOA inhibited neuronal regeneration. DjotxA, DjotxB, DjFoxG, DjFoxD and Djnlg associated with neural processes were up-regulated following exposure to PFOA. Our findings indicate that PFOA is a neurotoxicant while ANT can attenuate these detrimental effects.

Background: Amyotrophic lateral sclerosis (ALS) is a serious and rapidly fatal neurodegenerative disorder with an annual incidence of 1–2.6/100,000 persons. Few known risk factors exist although gene–environment interaction is suspected. We investigated the relationship between suspected neurotoxicant hazardous air pollutants (HAPs) exposure and ALS. Methods: A case–control study involving sporadic ALS cases (n = 51) and matched controls (n = 51) was conducted from 2008 to 2011. Geocoded residential addresses were linked to U.S. EPA NATA data (1999, 2002, and 2005) by census tract. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using conditional logistic regression. Results: Residential exposure to aromatic solvents significantly elevated the risk of ALS among cases compared to controls in 2002 (OR = 5.03, 95% CI: 1.29, 19.53) and 1999 (OR = 4.27, 95% CI: 1.09, 16.79) following adjustment for education, smoking, and other exposure groups. Metals, pesticides, and other HAPs were not associated with ALS. Conclusions: A potential relationship is suggested between residential ambient air aromatic solvent exposure and risk of ALS in this study.

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.

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.

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.

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.

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.

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.