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.

Litter is omnipresent in the ocean where it can be ingested by marine biota. Although ingestion of microplastics (MPs) is abundantly reported, insights into how MP can influence predator-prey interactions currently limits our understanding of the ecological impact of MPs. Here we demonstrate trophic transfer of MPs from zooplankton to benthic filter feeders, through consumption of contaminated prey (i.e. prey with ingested MP). However, predation rates of contaminated prey were significantly lower as compared to predation rates of prey that had no MPs ingested. As filter feeder clearance rates were not affected by consumption of MPs, the lower predation rates of contaminated prey appear to be primarily explained by disruption in zooplankton swimming behaviour that reduces their filtration risk. This is the first study that shows how MPs can change predator-prey interactions that are involved in the coupling between the pelagic and seabed habitat.

Per- and polyfluoroalkyl substances (PFASs) have been used for decades within industrial processes and consumer products, resulting in frequent detection within the environment. Using zebrafish embryos, we screened 38 PFASs for developmental toxicity and revealed that perfluorooctanesulfonamide (PFOSA) was the most potent developmental toxicant, resulting in elevated mortality and developmental abnormalities following exposure from 6 to 24 h post fertilization (hpf) and 6 to 72 hpf. PFOSA resulted in a concentration-dependent increase in mortality and abnormalities, with surviving embryos exhibiting a >12-h delay in development at 24 hpf. Exposures initiated at 0.75 hpf also resulted in a concentration-dependent delay in epiboly, although these effects were not driven by a specific sensitive window of development. We relied on mRNA-sequencing to identify the potential association of PFOSA-induced developmental delays with impacts on the embryonic transcriptome. Relative to stage-matched vehicle controls, these data revealed that pathways related to hepatotoxicity and lipid transport were disrupted in embryos exposed to PFOSA from 0.75 to 14 hpf and 0.75 to 24 hpf. Therefore, we measured liver area as well as neutral lipids in 128-hpf embryos exposed to vehicle (0.1% DMSO) or PFOSA from 0.75 to 24 hpf and clean water from 24 to 128 hpf, and showed that PFOSA exposure from 0.75 to 24 hpf resulted in a decrease in liver area and increase in yolk sac neutral lipids at 128 hpf. Overall, our findings show that early exposure to PFOSA adversely impacts embryogenesis, an effect that may lead to altered lipid transport and liver development.

Endocrine-disrupting chemicals (EDCs) are compounds that interfere with the expression, synthesis, and activity of hormones in organisms. They are released into the environment from flame retardants and products containing plasticizers. Persistent pesticides, such as dichlorodiphenyltrichloroethane (DDT) and hexachlorobenzene, also disrupt the endocrine system through interaction with hormone receptors. Endogenous hormones, such as 17β-estradiol (E2), are released in the urine and feces of farm animals and seep into terrestrial and aquatic ecosystems through sewage. Pigs are widely used as animal models to determine the effects of EDCs because they are physiologically, biochemically, and histologically similar to humans. EDCs primarily disrupt the reproductive and nervous systems of pigs. Moreover, embryonic development during the prenatal and early postnatal periods is particularly sensitive to EDCs. Mycotoxins, such as zearalenone, are food contaminants that alter hormonal activities in pigs. Mycotoxins also alter the innate immune system in pigs, making them vulnerable to diseases. It has been reported that farm animals are exposed to various types of EDCs, which accumulate in tissues, such as those of gonads, livers, and intestines. There is a lack of an integrated understanding of the impact of EDCs on porcine reproduction and development. Thus, this article aims to provide a comprehensive review of literature regarding the effects of EDCs in pigs.

Recently, we reported that hypoxia disrupts the endocrine system and causes metabolic abnormalities in prawns. Although transgenerational impairment effects of hypoxia have become a hot topic in vertebrate, it is unknown whether hypoxia could exert cross-generational effects on testicular function crustaceans. The present study aimed to investigate hypoxia’s toxic effects on the testicular function of oriental river prawns (Macrobrachium nipponense) and offspring development. Hypoxia disrupted testicular germ cells quality, caused sex hormone imbalance (testosterone and estradiol), and delayed testicular development. The F1 generation derived from male prawns exposed to hypoxia showed retarded embryonic development, and reduced hatching success and larval development, despite not being exposed to hypoxia. Analysis of the transcriptome the F0 generation (exposed to hypoxia) showed that the impaired testicular functions were associated with changes to mitochondrial oxidative phosphorylation, apoptosis, and steroid biosynthesis. Interestingly, quantitative real-time PCR confirmed that hypoxia could significantly suppress the expression of antioxidant and gonad development-related genes in the testis of the F1 generations, with and without continued hypoxia exposures. In addition, paternal exposure to hypoxia could result in a higher production of reactive oxygen species in offspring testis tissue compared with those without hypoxia exposure. The cross-generational effects of testicular function implied that the sustainability of natural freshwater prawn populations would be threatened by chronic hypoxia.

Diclofop-methyl (DM) is one of the most widely used herbicides in agriculture production and has been frequently detected in both freshwater and environments, even agricultural products. However, the potential toxic effects of DM on organisms and the underlying mechanisms are still poorly understood. In this study, we utilized zebrafish to evaluate the toxicity of DM during the cardiovascular developmental process. Exposure of zebrafish embryos to 0.75, 1.0 and 1.25 mg/L DM induced cardiac defects, such as pericardial edema, slow heart rate and long SV-BA distance but the vascular development in zebrafish larvae was not influenced by DM treatment. The expression of cardiac-related genes were disordered and DM exposure initiated disordering cardiogenesis from the period of precardiac mesoderm formation. Moreover, the apoptosis and proliferation of cardiomyocytes were not influenced but the levels of oxidative stress were upregulated by DM exposure. Fullerenes and astaxanthin was able to rescue cardiac defects caused by DM via downregulating oxidative stress. Wnt signaling was downregulated after DM treatment and activation of Wnt signaling could rescue cardiac defects. Therefore, our results suggest that DM has the potential to induce cardiac developmental toxicity through upregulation of Wnt-Mediated (reactive oxygen species) ROS generation in zebrafish larvae.

Maternal exposure to air pollution is associated with poor reproductive outcomes in in vitro fertilization (IVF). However, the susceptible time windows are still not been known clearly. In the present study, we linked the air pollution data with the information of 9001 women receiving 10,467 transfer cycles from August 2014 to August 2019 in The Second Hospital of Hebei Medical University, Shijiazhuang City, China. Maternal exposure was presented as individual average daily concentrations of PM₂.₅, PM₁₀, NO₂, SO₂, CO, and O₃, which were predicted by spatiotemporal kriging model based on residential addresses. Exposure windows were divided to five periods according to the process of follicular and embryonic development in IVF. Generalized estimating equation model was used to evaluate adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for association between clinical pregnancy and interquartile range increased average daily concentrations of pollutants during each exposure period. The increased PM₂.₅ (adjusted OR = 0.95, 95% CI: 0.90, 0.99), PM₁₀ (adjusted OR = 0.93, 95% CI: 0.89, 0.98), NO₂ (adjusted OR = 0.89, 95% CI: 0.85, 0.94), SO₂ (OR = 0.94, 95% CI: 0.90, 0.98), CO (adjusted OR = 0.93, 95% CI: 0.89, 0.97) whereas decreased O₃ (OR = 1.08, 95% CI: 1.02, 1.14) during the duration from preantral follicles to antral follicles were the strongest association with decreased probability of clinical pregnancy among the five periods. Especially, women aged 20–29 years old were more susceptible in preantral-antral follicle transition stage. Women aged 36–47 years old were more vulnerable during post-oocyte retrieve period. Our results suggested air pollution exposure during preantral-antral follicle transition stage was a note-worthy challenge to conceive among females receiving IVF.

The emerging flame retardants pentabromobenzene (PBB) has been frequently detected in recent years and may pose exposure risks to wild animals and human beings. In this study, the inflation of posterior swim bladder of zebrafish larvae was used as an endpoint to study the developmental toxicity and putative mechanisms associated with PBB toxicity. Our results showed that embryonic exposure to PBB could significantly inhibit the inflation of posterior swim bladders. Reduced T3 levels and transcriptional changes of crh and pomc were observed in PBB treated zebrafish larvae at 120 hpf. However, key regulators of thyroid and adrenocortical system involved in the synthesis (tsh), biological conversion (ugt1ab, dio2) and functional regulation (trα, trβ, gr) showed no significant changes. Further data revealed that prlra was the only gene that was altered among the detected genes at 96 h post fertilization (hpf). At 120 hpf, the morphology of swim bladder indicated deflation in treatments at 0.25 μM and higher. In addition, the mRNA levels of anxa5, prlra, prlrb, atp1b2 and slc12a10 were all significantly changed at 120 hpf. Taken together, we suppose that embryonic exposure to PBB inhibited the inflation of swim bladder in zebrafish probably via prlra mediated pathways. The observed changes of thyroid and adrenocortical parameters might be indirect effects evoked by PBB exposure. Overall, our results provide important data and indications for future toxicological study and risk assessment of the emerging flame retardants PBB.

Despite the widespread use of the antiviral drug, Tamiflu®, little is known about the long-term toxic effects of drug or its metabolites in an aquatic ecosystem. This study integrated epidemiological and ecotoxicological methods to determine environmentally relevant concentrations of Tamiflu. A model based on the species medaka (Oryzias latipes) was then used to determine the health status and reproductivity of adults exposed to the drug as well as the embryonic development of offspring. The proposed ecotoxicological model was also used to quantitatively and qualitatively evaluate the toxicodynamic parameters related to egg production, hatchability, and development. Our results revealed that at an environmentally relevant exposure, Tamiflu and its metabolites had no adverse effects on growth, survival, or fecundity of adult medaka. Nonetheless, we observed a reduction in hatchability under exposure to 300 μg L⁻¹ and a reduction in body length under exposure exceeding 90 μg L⁻¹. Under exposure to 300 μg L⁻¹, the estimated spawning time to reach 50% of the maximum percentage of cumulative egg production (ET50) far exceeded that of the control group (without exposure to Tamiflu). We also observed a ∼ 3-fold decrease in maximum egg hatching (Eₘₐₓ). Based on an integrated epidemiological and ecotoxicological model, predictions of environmental concentrations of Tamiflu and its metabolites revealed that the influenza subtypes associated with increases in environmental concentrations: A(H3N2) > A(H1N1) > type B (in order of their effects). We also determined that A(H3N2) posed a potential risk to hatchability and development. Note however, the environmental concentrations of Tamiflu and its metabolites in most countries are lower than the effect concentrations derived in this study, indicating no hazards for aquatic environments. We recommend the use of hatchability and embryonic development as indicators in assessing the effects of long-term parental exposure to Tamiflu metabolites.

As glyphosate-based herbicides, sold under the commercial name Roundup®, represent the most used herbicides in the world, contamination of the freshwater environment by glyphosate has become a widespread issue. In Italy, glyphosate was detected in half of the surface waters monitoring sites and its concentrations were higher than environmental quality standards in 24.5% of them. It can last from days to months in water, leading to exposure for aquatic organisms and specifically to amphibians’ larvae that develop in shallow water bodies with proven effects to development and behaviour. In this study, we tested the effects of a 96 h exposure during embryonic development of marsh frog’s tadpoles to three ecologically relevant Roundup® Power 2.0 concentrations. As expected, given the low concentrations tested, no mortality was observed. Morphological measurements highlighted a reduction in the total length in tadpoles exposed to 7.6 mg a.e./L, while an increase was observed at lower concentrations of 0.7 and 3.1 mg a.e./L compared to control group. Tadpoles raised in 7.6 mg a.e./L also showed a smaller tail membrane than those raised in the control solution. Regarding behaviour, we tested tadpoles in two different sessions (Gosner stages 25 and 28/29) for lateralization, antipredator response and basal activity. Lower intensity of lateralization was detected in tadpoles raised at the highest Roundup® concentration in the first session of observation, while no significant difference among treatments was observed in the second one. In both sessions, effects of Roundup® Power 2.0 embryonic exposure on antipredator response, measured as the proportional change in activity after the injection of tadpole-fed predator (Anax imperator) cue, were not detected. Tadpoles exposed during embryonic development to Roundup® exhibited lower basal activity than the control group, with the strongest reduction for the 7.6 mg a.e./L treatment. Our results reinforce the concern of Roundup® contamination impact on amphibians.