ZnO nanoparticles (NPs) have been detected in various wastewater treatment plants. It is widely assumed that size has a crucial effect on the NPs toxicity. Concerns have been raised over probable size-dependent toxicity of ZnO NPs to activated sludge, which could eventually affect the treatment efficiencies of wastewater treatment facilities. The size-dependent influences of ZnO NPs on performance, microbial activities, and extracellular polymeric substances (EPS) from activated sludge were examined in sequencing batch reactor (SBR) in present study. Three different sizes (15, 50, and 90 nm) and five concentrations (2, 5, 10, 30, and 60 mg L⁻¹) were trialled. The inhibitions on COD and nitrogen removal were determined by the particle size, and smaller ZnO NPs (15 nm) showed higher inhibition effect than those of 50 and 90 nm, whereas the ZnO NPs with size of 50 nm showed maximum inhibition effect on phosphorus removal among three sizes of ZnO NPs. After exposure to different sized ZnO NPs, microbial enzymatic activities and removal rates of activated sludge represented the same trend, consistent with the nitrogen and phosphorus removal efficiency. In addition, apparent size- and concentration-dependent effects on EPS contents and components were also observed. Compared with the absence of ZnO NPs, 60 mg L⁻¹ ZnO NPs with sizes of 15, 50, and 90 nm increased the EPS contents from 92.5, 92.4, and 92.0 mg g⁻¹ VSS to 277.5, 196.8, and 178.2 mg g⁻¹ VSS (p < 0.05), respectively. The protein and polysaccharide contents increased with the decreasing particle sizes and increasing ZnO NPs concentrations, and the content of protein was always higher than that of polysaccharide.

Few studies have explored the links of air pollution and childhood lipid profiles and dyslipidemias. We aimed to explore this topic in Chinese children and adolescents. This study included 12,814 children aged 7–18 years who participated in a national survey in 2013. Satellite-based spatial-temporal model was used to predict 3-y (2011–2013) average particles with diameters ≤ 1.0 μm (PM₁), ≤2.5 μm (PM₂.₅), ≤10 μm (PM₁₀), and nitrogen dioxide (NO₂) concentrations. Generalized linear mixed models were employed to evaluate the relationships of air pollution and total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and dyslipidemias. Every 10 μg/m³ increase in PM₁, PM₂.₅, PM₁₀, and NO₂ was related to increases of 6.20% [95% confidence interval (CI): 2.44, 10.10], 5.31% (95%CI: 0.41, 10.44), 3.49% (95%CI: 0.97, 6.08), and 5.25% (95%CI: 1.56, 9.07) in TC, respectively. The odds ratio of hypercholesterolemia associated with a 10 μg/m³ increase in PM₁, PM₂.₅, and NO₂ was 2.15 (95%CI: 1.27, 3.65), 1.70 (95%CI: 1.12, 2.60), and 1.43 (95%CI: 1.05, 1.93), respectively. No associations were found for air pollution and other blood lipids. Long-term PM₁, PM₂.₅, PM₁₀, and NO₂ exposures were positively associated with TC levels and risk of hypercholesterolemia in children and adolescents.

In the marine environment, microplastic contamination and acidification may occur simultaneously, this study evaluated the effects of ocean acidification and microplastics on oxidative stress responses and digestive enzymes in mussels. The thick shell mussels Mytilus coruscus were exposed to four concentrations of polystyrene microspheres (diameter 2 μm, 0, 10, 10⁴ and 10⁶ particles/L) under two pH levels (7.7 and 8.1) for 14 days followed by a 7-day recovery acclimation. Throughout the experiment, we found that microplastics and ocean acidification exerted little oxidative stress to the digestive gland. Only catalase (CAT) and glutathione (GSH) showed a significant increase along with increased microplastics during the experiment, but recovered to the control levels once these stressors were removed. No significant effects of pH and microplastics on glutathione peroxidase (GPx) and superoxide dismutase (SOD) were observed. The responses of digestive enzymes to both stressors were more pronounced than antioxidant enzymes. During the experiment, pepsin (PES), trypsin (TRS), alpha-amylase (AMS) and lipase (LPS) were significantly inhibited under microplastics exposure and this inhibition was aggravated by acidification conditions. Only PES and AMS tended to recover during the recovery period. Lysozyme (LZM) increased significantly under microplastic exposure conditions, but acidification did not exacerbate this effect. Therefore, combined stress of microplastics and ocean acidification slightly impacts oxidative responses but significantly inhibits digestive enzymes in mussels.

Anti-sea lice pesticides, used in the salmonid aquaculture industry, are a growing environmental concern due to their potential to adversely affect non-target crustaceans. Azamethiphos and deltamethrin are two bath treatment pesticides used on salmon farms in Norway, however, limited information is available on their impact on European lobster (Homarus gammarus) larvae in the Norwegian marine environment. Here, we firstly report the lethal (LC₅₀) and effective (EC₅₀) concentrations of azamethiphos and deltamethrin for stage I and stage II larvae, following 1-h exposures. Using a hydrodynamic model, we also modelled the dispersal of both compounds into the marine environment around selected Norwegian farms and mapped the potential impact zones (areas that experience LC₅₀ and EC₅₀ concentrations) around each farm. Our data shows that azamethiphos and deltamethrin are acutely toxic to both larval stages, with LC₅₀ and EC₅₀ values below the recommended treatment concentrations. We also show that the azamethiphos impact zones around farms were relatively small (mean area of 0.04–0.2 km²), however deltamethrin impact zones covered much larger areas (mean area of 21.1–39.0 km²). These findings suggest that deltamethrin poses a significant risk to European lobster in the Norwegian marine environment while the impact of azamethiphos may be less severe.

Although huge interspecies differences in the response to dioxins have been acknowledged, toxic equivalency factors derived from rodent studies are often used to assess human health risk. To determine interspecies differences, we first developed a toxicokinetic model in humans by measuring dioxin concentrations in environmental and biomonitoring samples from Southern China. Significant positive correlations between dioxin concentrations in blood and age were observed for seven dioxin congeners, indicating an age-dependent elimination rate. Based on toxicokinetic models in humans, the half-lives of 15 dioxin congeners were estimated to be 1.60–28.55 years. In consideration that the highest contribution to total toxic equivalency in blood samples was by 12378-polychlorinated dibenzo-p-dioxin (P₅CDD), this study developed a physiologically based pharmacokinetic (PBPK) model of 12378-P₅CDD levels in the liver, kidney, and fat of C57/6J mice exposed to a single oral dose, and the half-life was estimated to be 26.1 days. Based on estimated half-lives in humans and mice, we determined that the interspecies difference of 12378-P₅CDD was 71, much higher than the default usually used in risk assessment. These results could reduce the uncertainty human risk assessment of 12378-P₅CDD, and our approach could be used to estimate the interspecies differences of other dioxin congeners.

Tropospheric ozone (O₃) impairs physiological processes of plants while nitrogen (N) deposition may cause imbalances in soil N and other nutrients such as phosphorus (P) suggesting an increase of P demand for plants. However, the combined effect of O₃, soil N and P on isoprene emission from leaves has never been tested. We therefore examined isoprene emission in leaves of Oxford poplar clone exposed to O₃ (ambient, AA [35.0 nmol mol⁻¹ as daily mean]; 1.5 × AA; 2.0 × AA), soil N (0 and 80 kg N ha⁻¹) and soil P (0, 40 and 80 kg P ha⁻¹) in July and September in a Free-Air Controlled Exposure (FACE) facility. We also investigated the response of isoprene emission to foliar N, P and abscisic acid (ABA) contents in September because the 2-C-methylerythritol-5-phosphate (MEP) pathway of isoprenoid biosynthesis produces ABA. We found that O₃ increased isoprene emission in July, which was associated to increased dark respiration, suggesting an activation of metabolism against O₃ stress as an initial response. However, O₃ decreased isoprene emission in September which was associated to reduced net photosynthesis. In September, isoprene emission was positively correlated with leaf N content and negatively correlated with leaf P content in AA. However, no response of isoprene emission to foliar N and P was found in elevated O₃, suggesting that the isoprene responses to foliar N and P depended on the O₃ exposure levels. Isoprene emission rate in 1.5 × AA and 2.0 × AA increased with increasing leaf ABA content, indicating accelerated senescence of injured leaves to favor new leaf growth when high O₃ and nutritional availability in the soil were combined. Even though foliar N and P usually act as a proxy for isoprene emission rate, the impact of recent abiotic factors such as O₃ should be always considered for modeling isoprene emission under climate change.

The active use of solid fossil fuels (coal) in the production of heat and electricity has led to significant pollution, climate change, environmental degradation, and an increase in morbidity and mortality. Many countries (in particular, European ones, China, Japan, the USA, Canada, etc.) have launched programs for using plant and agricultural raw materials to produce heat and electricity by burning them instead of or together with traditional fuels. It is a promising solution to produce slurry fuels, based on a mixture of coal processing, oil refining and agricultural waste. This paper presents the results of experimental research into the formation and assessment of the most hazardous emissions (sulfur and nitrogen oxides) from the combustion of promising coal slurry fuels with straw, sunflower and algae additives, i.e. the most common agricultural waste. A comparative analysis has been carried out to identify the differences in the concentrations of sulfur and nitrogen oxides from the combustion of typical coal, coal processing waste, as well as fuel slurries with and without plant additives. It has been shown that the concentration of sulfur and nitrogen oxides can be reduced by 62–87% and 12–57%, respectively, when using small masses of plant additives (no more than 10 wt%) and maintaining high combustion heat of the slurry fuel. However, the use of algae and straw in the slurry composition can increase the HCl emissions, which requires extra measures to fight corrosion. A generalizing criterion of slurry fuel vs. coal efficiency has been formulated to illustrate significant benefits of adding plant solid waste to coal-water slurries containing petrochemicals. Straw and sunflower waste (10 wt%) were found to be the best additives to reduce the air pollutant emissions.

Artificial light at night (ALAN) exposes us to prolonged illumination, that adversely affects female reproduction. However, it remains to be clarified how prolonged light exposure affects oocyte meiotic maturation and quality. To this end, we exposed female mice to a constant light (CL) of 250 lux for different durations. Our findings showed that CL exposure for 7 weeks reduced the oocyte maturation rate. Meanwhile, CL exposure caused greater abnormalities in spindle assembly and chromosome alignment and a higher rate of oocyte aneuploidy than the regular light dark cycle. CL exposure also induced oxidative stress and caused mitochondrial dysfunction, which resulted in oocyte apoptosis and autophagy. Notably, our results showed that CL exposure reduced the levels of α-tubulin acetylation, DNA methylation at 5 mC, RNA methylation at m⁶A and histone methylation at H3K4me2 but increased the levels of histone methylation at H3K27me2 in oocytes. In summary, our findings demonstrate that constant bright light exposure causes oocyte meiotic defects and reduces cytoplasmic quality. These results extend the current understanding of ALAN-mediated defects in female reproduction.

Pharmaceutical pollution is now recognised as a major emerging agent of global change. Increasingly, pharmaceutical pollutants are documented to disrupt ecologically important physiological and behavioural traits in exposed wildlife. However, little is known about potential impacts of pharmaceutical exposure on among-individual variation in these traits, despite phenotypic diversity being critical for population resilience to environmental change. Furthermore, although wildlife commonly experience multiple stressors contemporaneously, potential interactive effects between pharmaceuticals and biological stressors—such as predation threat—remain poorly understood. To redress this, we investigated the impacts of long-term exposure to the pervasive pharmaceutical pollutant fluoxetine (Prozac®) on among-individual variation in metabolic and behavioural traits, and the combined impacts of fluoxetine exposure and predation threat on mean metabolic and behavioural traits in a freshwater fish, the guppy (Poecilia reticulata). Using a mesocosm system, guppy populations were exposed for 15 months to one of two field-realistic levels of fluoxetine (nominal concentrations: 30 and 300 ng/L) or a solvent control. Fish from these populations were then tested for metabolic rate (oxygen uptake) and behaviour (activity), both before and after experiencing one of three levels of a predation treatment: an empty tank, a non-predatory fish (Melanotaenia splendida) or a predatory fish (Leiopotherapon unicolor). Guppies from both fluoxetine treatments had ∼70% lower among-individual variation in their activity levels, compared to unexposed fish. Similarly, fluoxetine exposure at the higher dosage was associated with a significant (26%) reduction in individual-level variation in oxygen uptake relative to unexposed fish. In addition, mean baseline metabolic rate was disrupted in low-fluoxetine exposed fish, although mean metabolic and behavioural responses to predation threat were not affected. Overall, our study demonstrates that long-term exposure to a pervasive pharmaceutical pollutant alters ecologically relevant traits in fish and erodes among-individual variability, which may be detrimental to the stability of contaminated populations globally.

Early-life exposure to toxicants may have lasting effects that adversely impact later development. Thus, although the production and use of a toxicant have been banned, the risk to previously exposed individuals may continue. BDE-47, a component of commercial penta-BDEs, is a persistent organic pollutant with demonstrated neurotoxicity. To investigate the persistent effects of BDE-47 and the mechanisms thereof, we employed a metabolomics approach to analyze the brain, blood and urine of mice exposed to BDE-47 for 28 days and then 3 months post-exposure. In the brain, BDE-47 was detectable just after exposure but was below the limit of detection (LOD) 3 months later. However, the metabolomic alterations caused by early-life exposure to BDE-47 persisted. Potential biomarkers related to these alterations included phosphatidylcholine, lysophosphatidylcholine, sphingomyelin and several amino acids and biogenic amines. The metabolic pathways involved in the response to BDE-47 in the brain were mainly those related to glycerophospholipid metabolism, sphingomyelin metabolism and neurotransmitter regulation. Thus, our study demonstrates the utility of metabolomics, as the omics most closely reflecting the phenotype, in exploring the mechanisms underlying the lasting effects induced by early-life BDE-47 exposure.