Avermectin (AVM) has been widely used in agriculture and animal husbandry based on its broad spectrum of effective anthelmintic activity and specificity targets. However, AVM induction of cytotoxicity in human liver is largely unknown. In this study, we investigate the cytotoxic effects of AVM on HepG2 cells in vitro. The results revealed that AVM inhibited the viability of HepG2 cells and enhanced apoptosis. Established assays of cytotoxicity were performed to characterize the mechanism of AVM toxicity on HepG2 cells. Typical apoptosis morphological changes were shown in AVM-treatment cells including chromatin condensation and DNA fragmentation. We demonstrated that AVM-induced apoptosis of HepG2 cells were mediated by generated ROS. Moreover, a decrease in mitochondrial membrane potential (MMP) and up-regulating the Bax/Bcl-2 ratio, resulted in a release of cytochrome-c as well as activation of caspase-9/-3. In conclusion, our experimental results show that AVM has a potential threat to human health which may be induce apoptosis of human hepatocyte cells via caspase-dependent mitochondrial pathways.

Microcystin-LR is the most poisonous and commonly encountered hepatotoxin produced by cyanobacteria in an aquatic ecosystem, and it may cause thyroid dysfunction in fish. The present study aimed to reveal the effects of transgenerational toxicity of MCLR on the thyroid endocrine system under sub-chronic exposure conditions. Adult zebrafish (F0) were exposed to environmentally relevant concentrations (1, 5 and 25 μg/L) of MCLR for 45 days. The produced F1 embryos were then tested without further MCLR treatment. In the F0 generation, exposure to 25 μg/L MCLR reduced thyroxine (T4) but not 3, 5, 3′-triiodothyronine (T3) levels in females, while the T4 and T3 levels were unchanged in males. After parental exposure to MCLR, we observed a decreased hatching and growth retardation correlated with reduced thyroid hormone levels in the F1 offspring. The gene transcription and protein expression along the hypothalamic-pituitary-thyroid axis were detected to further investigate the possible mechanisms of MCLR-induced thyroid disruption. Our results indicated MCLR could disturb the thyroid endocrine system under environmentally relevant concentrations and the disrupting effects could be remarkably transmitted to its F1 offspring. We regard these adverse effects as a parental transgenerational toxicity of MCLR.

Mercury is a toxic compound to which humans are exposed by consumption of fish. Current fish consumption advisories focus on minimizing the risk posed by the species that are most likely to have high levels of mercury. Less accounted for is the variation within species, and the potential role of the geographic origin of a fish in determining its mercury level. Here we surveyed the mercury levels in 117 yellowfin tuna caught from 12 different locations worldwide. Our results indicated significant variation in yellowfin tuna methylmercury load, with levels that ranged from 0.03 to 0.82 μg/g wet weight across individual fish. Mean mercury levels were only weakly associated with fish size (R2 < 0.1461) or lipid content (R2 < 0.00007) but varied significantly, by a factor of 8, between sites. The results indicate that the geographic origin of fish can govern mercury load, and argue for better traceability of fish to improve the accuracy of exposure risk predictions.

Antimicrobial resistance represents a growing and significant public health threat, which requires a global response to develop effective strategies and mitigate the emergence and spread of this phenomenon in clinical and environmental settings. We investigated, therefore, the occurrence and abundance of several antibiotics and antibiotic resistance genes (ARGs), as well as bacterial community composition in wastewater effluents from different hospitals located in the Cluj County, Romania. Antibiotic concentrations ranged between 3.67 and 53.05 μg L−1, and the most abundant antibiotic classes were β-lactams, glycopeptides, and trimethoprim. Among the ARGs detected, 14 genes confer resistance to β-lactams, aminoglycosides, chloramphenicol, macrolide-lincosamide-streptogramin B (MLSB) antibiotics, sulfonamides, and tetracyclines. Genes encoding quaternary ammonium resistance and a transposon-related element were also detected. The sulI and qacEΔ1 genes, which confer resistance to sulfonamides and quaternary ammonium, had the highest relative abundance with values ranging from 5.33 × 10−2 to 1.94 × 10−1 and 1.94 × 10−2 to 4.89 × 10−2 copies/16 rRNA gene copies, respectively. The dominant phyla detected in the hospital wastewater samples were Proteobacteria, Bacteroidetes, Firmicutes, and Actinobacteria. Among selected hospitals, one of them applied an activated sludge and chlorine disinfection process before releasing the effluent to the municipal collector. This conventional wastewater treatment showed moderate removal efficiency of the studied pollutants, with a 55–81% decrease in antibiotic concentrations, 1–3 order of magnitude lower relative abundance of ARGs, but with a slight increase of some potentially pathogenic bacteria. Given this, hospital wastewaters (raw or treated) may contribute to the spread of these emerging pollutants in the receiving environments. To the best of our knowledge, this study quantified for the first time the abundance of antibiotics and ARGs in wastewater effluents from different Romanian hospitals.

Pyrethroid pesticides were analysed in liver of striped dolphin (Stenella coeruleoalba) from the Alboran Sea (south of Spain, Mediterranean Sea). The occurrence and bioaccumulation of pyrethroid insecticides in marine mammal tissues from the northern hemisphere had never been determined before. Pyrethroids were detected in 87% of the specimens with a mean total concentration of 300 ng g-1 lw ± 932 (range 2.7–5200 ng g-1 lw). Permethrin and tetramethrin were the main contributors to the pyrethroid profiles, with enantiospecific accumulation for the first and isomer specific accumulation for the latter. Bioaccumulation of pyrethroids was unlike that of persistent organic pollutants (POPs), as pyrethroid concentrations were not correlated to the maturity stage of the specimens. Concentrations slightly increased from calves to juveniles, whereas juveniles presented similar concentrations to adults. Metabolization of pyrethroids after achieving sexual maturity might account for this pattern.

Vehicle emissions have become one of the key factors affecting the urban air quality and climate change in the Pearl River Delta (PRD) region, so it is important to design policies of emission reduction based on quantitative Co-benefits for air pollutants and greenhouse gas (GHG). Emissions of air pollutants and GHG by 2020 was predicted firstly based on the no-control scenario, and five vehicle emissions reduction scenarios were designed in view of the economy, technology and policy, whose emissions reduction were calculated. Then Co-benefits between air pollutants and GHG were quantitatively analyzed by the methods of coordinate system and cross-elasticity. Results show that the emissions reduction effects and the Co-benefits of different measures vary greatly in 2015–2020. If no control scheme was applied, most air pollutants and GHG would increase substantially by 20–64% by 2020, with the exception of CO, VOC and PM2.5. Different control measures had different reduction effects for single air pollutant and GHG. The worst reduction measure was Eliminating Motorcycles with average reducing rate 0.09% for air pollutants and GHG, while the rate from Updated Emission Standard was 41.74%. Eliminating Yellow-label Vehicle scenario had an obvious reduction effect for every single pollutant in the earlier years, but Co-benefits would descent to zero in later by 2020. From the perspective of emission reductions and co-control effect, Updated Emission Standard scenario was best for reducing air pollutants and GHG substantially (tanα=1.43 and Els=1.77).

In this study, we demonstrated an assay with turn-on fluorescence for monitoring cerebrospinal acetylcholinesterase (AChE) fluctuation as a biomarker for organophosphorus pesticides (OPs) poisoning and management based on single layer MnO2 nanosheets with graphene quantum dots (GQDs) as signal readout. Initially, the fluorescence of GQDs was quenched by MnO2 nanosheets mainly due to the inner filter effect (IFE). However, with the presence of reductive thiocholine (TCh), the enzymatic product, hydrolyzed from acetylthiocholine (ATCh) by AChE, the redox reaction between MnO2 and TCh occurred, leading to the destruction of the MnO2 nanosheets, and thereby IFE was diminished gradually. As a consequence, the turn-on fluorescence of GQDs with the changes in the spectrum of the dispersion constituted a new mechanism for sensing of cerebrospinal AChE. With the method developed here, we could monitor cerebrospinal AChE fluctuation of rats exposed to OPs before and after therapy, and could thereby open up the pathway to a new sensing platform for better understanding the mechanism of brain dysfunctions associate with OPs poisoning.

The complex QDs-Indolicidin (QDs-Ind) has been previously shown to be a good antimicrobial system with a low acute toxicity on Daphnia magna (D. magna). However, multigenerational effects caused by exposure to QDs-Ind and after subsequent recovery are still unknown. In this study, we performed multigenerational exposure tests and we evaluated individual fitness, population growth, DNA alteration, expression of Dhb (haemoglobin), Vtg (vitellogenin), CYP4 (cytochrome P450s CYP4 family), and CYP314 (cytochrome P450s mitochondrial family 314) genes on three generation of D. magna. Results showed that the total amount of eggs produced per female and total number of brood per female and body lengths were significantly decreased, Dhb, CYP4 were upregulated while Vtg was down-regulated except at reproduction days when it was slightly up-regulated under QDs-Ind exposure. Random Amplification of Polymorphic DNA (RAPD) method has proven to be useful to qualitative assess of DNA damage during generation and to underline modification in somatic or germinal cells. The results of the study suggest that effects of chronic exposure cannot be ignored.

Bisphenol A (BPA), a suspected endocrine disruptor, can modify normal plant growth and development. Photosynthesis provides material and energy for the growth and development of plants, in which chlorophyll (Chl) plays a significant role. Many studies have shown that the growth and metabolism of plants vary at different growth stages. Thus the sensitivity of plant's responses to environmental pollution is correspondingly different. We studied the effects of BPA on the Chl contents of soybean (Glycine Max L.) at different growth stages (seedling, flowering and podding, seed-filling and maturation) by measuring the contents of essential intermediates (5-aminolevulinic acid, porphobilinogen, protoporphyrin IX, magnesium protoporphyrin and protochlorophyll) and the activities of key enzymes (5-aminolaevulinic acid dehydratase, porphobilinogen deaminase, uroporphyrinogen III synthase, magnesium chelatase) in chlorophyll synthesis. Low-dose (1.5 mg/L) BPA exposure increased the activities of key enzymes in addition to the contents of intermediates in Chl synthesis at different growth stages, resulting in increases in Chl contents and net photosynthetic rate. In contrast, medium and high-dose (17.2, 50.0 mg/L) BPA exposure produced inhibitory effects on the indices. Following the withdrawal of BPA exposure, the indices recovered to a degree that was related to the plant growth stage. The effect level (high to low) of BPA on these indices at different growth stages was: seedling stage > maturation stage > flowering and podding stage > seed-filling stage. The reverse effect was observed following the withdrawal of BPA exposure. The responses of key enzymes in plant Chl synthesis to BPA illustrate how BPA affects Chl contents. The effects of BPA show clear differences at different plant growth stages.

Cities and contaminated areas can be primary or secondary sources of polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and other chemicals, into air and soil and can influence the regional level of some of these pollutants. In a contaminated site, the evaluation of such emissions can be crucial in the choice of the remediation technology to be adopted. In the city of Brescia (Northern Italy), more than 100 ha of agricultural areas were contaminated with PCBs, PCDD/Fs and heavy metals, originating from the activities of a former PCB factory. In order to evaluate the current emissions of PCBs and PCDD/Fs from the contaminated site, in a location where other current sources are present, we compared measured and predicted air concentrations, resulting from chemical volatilization from soils as well as fingerprints of Brescia soils and of soils contaminated by specific sources. The results confirm that the contaminated area is still a current and important secondary source of PCBs to the air, and to a lesser extent of PCDFs (especially the more volatile), but not for PCDDs. PCBs in soils have fingerprints similar to highly chlorinated mixtures, indicating contamination by these mixtures and/or a long weathering process. PCB 209 is also present at important levels. PCDD fingerprints in soil cannot be related to current emission sources, while PCDFs are compatible to industrial and municipal waste incineration, although weathering and/or natural attenuation may have played a role in modifying such soil fingerprints. Finally, we combined chemical and microbiological analyses to provide an integrated approach to evaluate soil fingerprints and their variation in a wider perspective, which accounts for the mutual effects between contamination and soil microbiota, a pivotal hint for addressing in situ bioremediation activities.