Large ammonia (NH₃) emissions contribute approximately 8–30% to the fine particle pollution in China and highlight the need for understanding the emission trends and mitigation effects of NH₃ in the future. The purpose of this study is to predict the NH₃ emissions and analyze the mitigation potential up to year 2040 by scenario analysis based on the established new NH₃ emission inventory from anthropogenic sources for the Beijing–Tianjin–Hebei (BTH) region. The results showed that the total NH₃ emission in the BTH region was estimated at 966.14 Gg in 2016. Under the Business-as-Usual (BAU) scenario, the total NH₃ emissions in 2030 and 2040 would increase by 13% and 26% compared with 2016 levels, with average annual growth rates of 0.9% and 1.0%, respectively. Livestock will continue to dominate NH₃ emissions in the future, with the proportions of total emissions increasing from 57% in 2016 to 64% in 2030 and 68% in 2040. The share of the second-largest NH₃ emission source, synthetic fertilizer application, will decrease from 36% in 2016 to 31% in 2030 and 27% in 2040. Among five other sources, the largest change occurred in waste disposal, increasing notably by 3.31 times from 2016 to 2040 owing to rapid urbanization. Under the Combined Options (CO) scenario, the total NH₃ emissions could be reduced by as much as 34% by 2030 and 50% by 2040 compared with the BAU scenario, which is attributed to livestock (24% in 2030, 37% in 2040) and synthetic fertilizer application (10% in 2030, 13% in 2040), respectively. This study can give a reliable estimation of anthropogenic NH₃ emission in the BTH region during 2020–2040 and provide a valuable reference for effective mitigation measures and control strategies for policy makers.

Despite the now well recognised impact of diclofenac on vultures across the Indian subcontinent, this non-steroidal anti-inflammatory drug (NSAID) was registered in 2013 for livestock treatment in Spain, Europe’s main vulture stronghold. We assessed the risk of exposure to diclofenac and nine other NSAIDs in avian scavengers in the Iberian Peninsula (Spain and Portugal) after the onset of diclofenac commercialization. We sampled 228 livestock carcasses from vulture feeding sites, primarily pig (n = 156) and sheep (n = 45). We also sampled tissues of 389 avian scavenger carcasses (306 Eurasian griffon vultures, 15 cinereous vultures, 11 Egyptian vultures, 12 bearded vultures and 45 other facultative scavengers). Samples were analysed by liquid chromatography with mass spectrometry (LCMS). Seven livestock carcasses (3.07%) contained NSAID residues: flunixin (1.75%), ketoprofen, diclofenac and meloxicam (0.44% each). NSAID residues were only detected in sheep (4.44%) and pig (3.21%) carcasses. Fourteen dead avian scavengers (3.60%) had NSAID residues in kidney and liver, specifically flunixin (1.03%) and meloxicam (2.57%). Flunixin was associated with visceral gout and/or kidney damage in three (0.98%) dead Eurasian griffons. To date, diclofenac poisoning has not been observed in Spain and Portugal, however, flunixin would appear to pose an immediate and clear risk. This work supports the need for well managed carrion disposal, alongside appropriate risk labelling on veterinary NSAIDs and other pharmaceuticals potentially toxic to avian scavengers.

Tris(1,3-dichloro-2-propyl) phosphate (TDCIPP) has been demonstrated to be transferred from parental animals to their offspring. However, whether parental exposure to environmental concentrations of TDCIPP show neurodevelopmental toxicity in the F1 generation and the possible underlying mechanism remain unclear. Therefore, in this study, zebrafish embryos were exposed to environmental concentrations of TDCIPP (3, 30 and 300 ng L⁻¹) for 120 days. The effects of exposure on motor behaviors, neurotransmitter levels, DNA methylation, and gene expression of F1 larvae were investigated. Parental exposure left TDCIPP residues in F1 eggs as well as reduced body length of F1 larvae. Moreover, parental exposure significantly reduced swimming activity in F1 5 dpf larvae, although it did not significantly alter serotonin, dopamine, 3,4-dihydroxyphenylacetic acid, γ-aminobutyrate, and acetylcholine levels. Genes encoding DNA methylation transferases (dnmt3aa and dnmt1) were downregulated in F1 larvae. Reduced representation bisulfite sequencing analysis revealed 446 differentially methylated regions and enriched neuronal cell body Gene Ontology term in F1 generation. Correlation analysis between the expression of genes related to neural cell body and swimming speed indicated that solute carrier family 1 member 2b (slc1a2b) downregulation might be responsible for the inhibition of motor behaviors. Furthermore, bisulfite amplicon sequencing analysis confirmed hypermethylation of the promoter region of slc1a2b in F1 larvae following parental exposure to 300 ng L⁻¹ TDCIPP, which might have led to significant downregulation of gene expression and, in turn, influenced the motor behaviors. These results indicate that parental exposure to environmental concentrations of TDCIPP alters DNA methylation, downregulates gene expressions and, thus inducing developmental neurotoxicity, in F1 larvae.

PM2.5 pollution is an important and urgent problem in China that can increase mortality and hospital admissions. Traffic-originated PM2.5 organic component (tPo) mainly contains polycyclic aromatic hydrocarbons (PAHs). Research has shown that PAHs can promote invasion, metastasis, and cancer stem cell properties in lung adenocarcinoma cells, but the exact toxicological mechanism is unknown. In the present study, we investigated the effect of lncRNAs on the progression of lung adenocarcinoma induced by tPo and the underlying mechanisms mediated by lncRNA-signaling pathway interactions. We found that chronic tPo treatment upregulated the expression of loc107985872, which further promoted cell invasion and migration, EMT and cancer stem cell properties via notch1 pathway in lung adenocarcinoma cells. Meanwhile, activation of the notch1 signaling pathway through loc107985872 might be associated with abnormally high expression of its upstream proteins, such as ADAM17, PSEN1 and DLL1. Moreover, tPo exposure induced EMT and the acquisition of cancer stem cell-like properties via the notch1 signaling pathway in vivo. In summary, loc107985872 upregulated by tPo promoted lung adenocarcinoma progression via the notch1 signaling pathway.

2,3,3,3-Tetrafluoro-2-(heptafluoropropoxy)propanoate (known as GenX) has been used as an alternative to perfluorooctanoic acid (PFOA) which was phased out of formulations for industrial and consumer product applications in 2015. While the effects of GenX on lab animals have been studied, little is known about its effects on plants. This study examined and compared the accumulation and toxicity of GenX and PFOA in the model plants Arabidopsis thaliana and Nicotiana benthamiana. Both plants showed reduction in biomass and root growth following exposure to PFOA or GenX in a dosage-dependent manner. The bioaccumulation factors (BFs) of GenX and PFOA were plant species-dependent, with higher BFs in A. thaliana compared to N. bethanminana. Additionally, GenX and PFOA were more readily accumulated into shoot tissues of A. thaliana than in N. bethanminana. Exposure to GenX also caused a reduction in chlorophyll content (18%) and total phenolic compounds (26%). However, GenX exposure increased superoxide dismutase activity and H₂O₂ content (1.6 and 2.6 folds increase, respectively) in N. benthamiana. Overall, our result suggest that GenX is bioaccumulative, and that its accumulation likely inhibits plant growth and photosynthesis as well as inducing oxidative stress.

Legacy perfluoroalkyl and poly-fluoroalkyl substances (PFASs) are gradually phased out because of their persistence, bioaccumulation, toxicity, long-distance transport and ubiquity in the environment. Alternatively, emerging PFASs are manufactured and released into the environment. It is accepted that PFASs can impact microbiota, although it is still unclear whether emerging PFASs are toxic towards soil microbiota. However, it could be assumed that OBS could impact soil microorganisms because it had similar chemical properties (toxicity and persistence) as legacy PFASs. The present study aimed to explore the influences of an emerging PFAS, namely sodium p-perfluorous nonenoxybenzene sulfonate (OBS), on archaeal, bacterial, and ammonia-oxidizing archaea (AOA) and bacteria (AOB) communities and ammonia oxidation. Grassland soil was amended with OBS at different dosages (0, 1, 10 and 100 mg/kg). After OBS amendment, tolerant microorganisms (e.g., archaea and AOA) were promoted, while susceptive microorganisms (e.g., bacteria and AOB) were inhibited. OBS amendment greatly changed microbial structure. Potential nitrifying activity was inhibited by OBS in a dose-dependent manner during the whole incubation. Furthermore, AOB might play a more important role in ammonia oxidation than AOA. Overall, OBS influenced ammonia oxidation by regulating the activity, abundance and structure of ammonia-oxidizing microorganisms, and could also exert influences on total bacterial and archaeal populations.

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.

Melatonin is a hormone which is generated from pineal gland, and it is responsible for the regulation of wake-sleep cycle. Melatonin is a well-known antioxidant and free radical scavenger to protect against multiple type of tissue damage. While ochratoxin A (OTA) is a mycotoxin found widely in contaminated food and foodstuffs, which causes nephrotoxicity, hepatotoxicity, immunotoxicity, and reproductive damage in humans and animals. In present study we report the toxicity of OTA on porcine oocyte quality and the protective effects of melatonin on OTA-exposed oocytes. Using transcriptome analysis our results show that OTA exposure alters the expression of multiple genes in oocytes, indicating its effect on oocyte maturation. The cellular changes following OTA treatment are examined, and the results show that OTA adversely affects oocyte polar body extrusion, which is confirmed by the delay of Cdc2-mediated cell cycle progression. OTA exposure also disrupts meiotic spindle formation, which is confirmed by altered phosphorylated MAPK expression. RNA-seq screening and further fluorescence staining results show that OTA induces aberrant mitochondria distribution and oxidative phosphorylation defects, which then causes oxidative stress, followed by early apoptosis and autophagy. Treatment with melatonin significantly ameliorates oxidative stress and apoptosis, which further protects cell cycle and spindle formation in OTA-exposed oocytes. Collectively, these results show the protective effects of melatonin against defects induced by OTA during porcine meiotic oocyte maturation.

Microplastics are ubiquitous in natural waters and affect the environmental fate of hydrophobic organic micropollutants. This study evaluated the impacts of four microplastics, polypropylene (PP), polyethylene (PE), polystyrene (PS) and polymethyl methacrylate (PMMA), on the photodegradation of organotin compounds (OTCs) under UV₃₆₅ irradiation (2.3 ± 0.1 W m⁻²). The experiments were performed by mixing PP, PE, PS or PMMA microparticles with tri-organotins in artificial seawater. The photodegradation of OTCs in microplastic suspensions was influenced by the absorptivity onto microplastics. The decomposition rate of tributyltin (TBT) in UV-irradiated PP suspensions was greater than trimethyltin (TMT) and triphenyltin (TPhT) (p < 0.01). The adsorption capacities of OTCs (e.g., TBT) on PP particle surfaces were significantly lower than those on PE surfaces (p < 0.05) but similar with those on PMMA due to the different surface areas, shapes, and surface hydrophobicity of microplastics. TBT degraded faster (9.1%) in PS than in PMMA suspension (11.2%) within 240 min, respectively. However, only less than 5.4% was photodegraded in PP suspension due to the light scattering or absorption of the large sized PP particles. This study provided new insight into the impacts of microplastics on photodegradation of micropollutants in natural waters.

Thallium (TI) is one of the most toxic heavy metals and priority pollutant metals. The emerging TI environmental pollution worldwide has posed a great threat to human health. However, based on the World Health Organization (WHO), the risk and severity of adverse health effects of TI in the range of 5–500 μg/L are uncertain. Moreover, evidence regarding the adverse impacts of TI on children’s health is still insufficient. Herein, we aim to investigate the early adverse effects of TI on children’s health and provide references for the WHO to establish stricter safety limits of TI. From 2015 to 2019, urinary TI and many clinical laboratory parameters related to blood routine, hepatic, renal, myocardial, coagulation function and serum electrolyte were measured in six children aged 1–9 years. The urinary TI concentration ranged from 13.4 μg/L to 60.1 μg/L with a mean of 36.1 μg/L and a median of 34.8 μg/L in six children in 2015. Although only four children felt a little poor appetite, several laboratory abnormalities indicated early damage in liver, renal, and myocardial functions in all children in 2015. After treatment and following up for four years, although the children’s TI concentration decreased below 5 μg/L, their liver and renal functions did not completely recover, and their myocardial function worsened. Results indicated that impaired liver, renal, and myocardial functions were closely associated with elevated urinary TI concentration in children. Considering the increasing use of TI in high-technology industries and emerging TI environmental-contamination zones worldwide, establishing stricter safety limits of TI and paying more attention to the adverse health effects of TI on children are urgently required.We found that a relatively low concentration of thallium (13.4 μg/L to 60.1 μg/L) impaired liver, renal, and myocardial function in six children. After treatment and following up these children for four years, although their urinary TI concentration decreased below 5 μg/L, their liver and renal functions did not completely recover, and their myocardial function worsened.