Pyraclostrobin is a widely used and highly efficient fungicide that also has high toxicity to aquatic organisms, especially fish. Although some research has reported the toxic effects of pyraclostrobin on fish, the main toxic pathways of pyraclostrobin in fish remain unclear. The present study has integrated histopathological, biochemical and hematological techniques to reveal the main toxic pathways and mechanisms of pyraclostrobin under different exposure routes. Our results indicated that pyraclostrobin entered fish mainly through the gills. The highest accumulation of pyraclostrobin was observed in the gills and heart compared with accumulation in other tissues and gill tissue showed the most severe damage. Hypoxia symptoms (water jacking, tummy turning and cartwheel formation) in fish were observed throughout the experiment. Taken together, our results suggested that the gills are important target organs. The high pyraclostrobin toxicity to gills might be associated with oxidative damage to the gills, inducing alterations in ventilation frequency, oxygen-carrying substances in blood and disorders of energy metabolism. Our research facilitates a better understanding of the toxic mechanisms of pyraclostrobin in fish, which can promote the ecotoxicological research of agrochemicals on aquatic organisms.

Water treatment and reuse initiatives are essential to combat declining water supplies in a changing climate, especially in arid and semi-arid regions. Pollution of water resources intensifies the search for strategies to provide water for potable and non-potable reuse that mitigates detrimental ecological and human health effects. Fipronil and synthetic pyrethroids are common urban-use insecticides that exert aquatic toxicity at trace levels and have been often found in urban surface streams. In this study, samples were collected from the 182 ha Prado Wetlands in Southern California for seven months to assess the occurrence of fipronil and its degradation products as well as pyrethroids (bifenthrin and cyfluthrin) in water, sediment, and plants in a 4.45 ha vegetated surface flow constructed wetland (CW). Concentration-based removal values and changes in mass flux were calculated to determine the efficacy of CW treatment. Observed water concentrations were further used to calculate toxic units for the invertebrates Hyalella azteca and Chironomus dilutus. Pesticide concentrations in water, sediment, and plant samples consistently decreased during passage through the CW at all time points. Removal values for fipronil desulfinyl, fipronil sulfide, fipronil, fipronil sulfone, bifenthrin, and cyfluthrin were 100%, 99.7–100%, 57.8–88.1%, 75.6–100%, 74.7–100%, and 36.6–82.2%, respectively, and there was a general net deposition of pesticides into CW compartments. Toxic unit values decreased in every instance for both aquatic invertebrates. Settling of contaminated particles, adsorption to sediment, plant uptake or adsorption, and subsequent degradation contributed to the effective removal of these urban-use insecticides, which highlights the potential of CWs for protecting urban water quality.

Carbon disulfide (CS₂) has been reported to induce disorder of glucose metabolism. However, the associations of CS₂ exposure with plasma glucose levels and risk of diabetes have not been explored in general population, and the underlying mechanisms remain unclear. We aim to examine the relationships between CS₂ exposure and fasting plasma glucose (FPG) levels, as well as diabetes, and assess the potential role of oxidative stress among the abovementioned relationships in Chinese general adults. The concentrations of urinary biomarkers of CS₂ exposure (2-thiothiazolidin-4-carboxylic acid, TTCA), and biomarkers for lipid peroxidation (8-isoprostane, 8-iso-PGF₂α) and DNA oxidative damage (8-oxo-7,8-dihydro-20-deoxyguanosine, 8-OHdG) were measured among 3338 urban adults from the Wuhan-Zhuhai cohort. Additionally, FPG levels were tested promptly. Generalized linear models and logistic regression models were used to quantify the associations among urinary TTCA, oxidative damage markers, FPG levels and diabetes risk. Mediation analysis was employed to estimate the role of oxidative damage markers in the association between urinary TTCA and FPG levels. We discovered a significant relationship between urinary TTCA and FPG levels with regression coefficient of 0.080 (95% CI: 0.002,0.157). Besides, the risk of diabetes was positively related to urinary TTCA (OR:1.282, 95% CI: 1.055,1.558), particularly among those who did not exercise regularly. Each 1% increase of urinary TTCA concentration was associated with a 0.096% and 0.037% increase in urinary 8-iso-PGF₂α and 8-OHdG, respectively. Moreover, we found an upward trend of FPG level as urinary 8-iso-PGF₂α gradually increased (Pₜᵣₑₙd<0.05), and urinary 8-iso-PGF₂α mediated 21.12% of the urinary TTCA-associated FPG increment. Our findings indicated that urinary CS₂ metabolite was associated with increased FPG levels and diabetes risk in general population. Lipid peroxidation partly mediated the association of urinary CS₂ metabolite with FPG levels.

Polycyclic aromatic hydrocarbons (PAHs) are compounds with two or more benzene rings whose hydroxylated metabolites (OH-PAHs) are excreted in urine. Human PAH exposure is therefore commonly estimated based on urinary OH-PAH concentrations. However, no study has compared PAH exposure estimates based on urinary OH-PAHs to measurements of PAH levels in blood samples. Estimates of PAH exposure based solely on urinary OH-PAHs may thus be subject to substantial error. To test this hypothesis, paired measurements of parent PAHs in serum and OH-PAHs in urine samples from 480 participants in Guangzhou, a typical developed city in southern China, were used to investigate differences in the estimates of human PAH exposure obtained by sampling different biological matrices. The median PAH concentration in serum was 4.05 ng mL⁻¹, which was lower than that of OH-PAHs in urine (8.33 ng mL⁻¹). However, serum pyrene levels were significantly higher than urinary levels of its metabolite 1-hydroxypyrene. Concentrations of parent PAHs in serum were not significantly correlated with those of their metabolites in urine with the exception of phenanthrene, which exhibited a significant negative correlation. Over 28% of the participants had carcinogenic risk values above the acceptable cancer risk level of 10⁻⁶. Overall, estimated human exposure and health risks based on urinary 1-hydroxypyrene levels were only 13.6% of those based on serum pyrene measurements, indicating that estimates based solely on urine sampling may substantially understate health risks due to PAH exposure.

Polyhalogenated carbazoles (PHCZs) are well-known as emergent environmental contaminants. Given their wide distribution in the environment and structural similarity with dioxins and dioxin-like chemicals (DLCs), the environmental behavior and ecological risks of these chemicals have become the major issue concerned by the governments and scientists. Since the initial report of PHCZ residues in the environment in the 1980s, over 20 PHCZ congeners with different residual levels had been identified in various environmental media all over the world. Nevertheless, researches concerning the toxicological effects of PHCZs are of an urgent need for the relatively lagging study of their ecological risks. Currently, only limited evidence has indicated that PHCZs would pose dioxin-like toxicity, including developmental toxicity, cardiotoxicity, etc; and their toxicological effects were partially consistent with AhR activation. And yet, much remains to be done to fill in the knowledge gaps of their toxicological effects. In this review, the research progresses in environmental behavior and toxicology study of PHCZs were remarked; and the lack of current research, as well as future research prospects, were discussed.

(S,S)-ethylenediaminedisuccinic acid (EDDS) has a strong capacity to mobilize potentially toxic elements (PTEs) in phytoextraction. It can release NH₄⁺-N via biodegradation, which can enhance N supply to soil thereafter promote plant growth and plant resistance to PTEs. However, the advanced feature of released N in the EDDS-enhanced phytoextraction remains unclear. In the current study, the effects of N supply released from EDDS on ryegrass phytoextraction and plant resistance to PTEs were investigated in detail by a comparison with urea. Our results supported that the addition of both EDDS and urea increased N concentration in soil solution, yet EDDS needed more time to release available N for plant uptake and transported more N from root to shoot. Additionally, EDDS significantly increased the concentration of all targeted PTEs, i.e. Cu, Zn, Cd, and Pb, in the soil solution, which results in higher levels of their occurrence in plant biomass compared with urea. By contrast, the supply of N slightly enhanced the ryegrass uptake of micro-nutrients, i.e. Cu and Zn, yet it caused negligible effects on nonessential elements, i.e. Cd and Pb. The mobilized PTEs by EDDS lead to elevated oxidative stress because higher levels of malondialdehyde and O₂•⁻ were observed. The supply of N attenuated oxidative stress caused by O₂•⁻ and H₂O₂, which was associated with enhanced activities of superoxide dismutase and peroxidase. Our results advanced the understanding of the exogenous N supply and metal resistance mechanisms in the EDDS-enhanced phytoextraction. This study also highlighted that EDDS can serve as a N source to ease N-deficient problems in PTEs-contaminated soils.

Plants can take up and transform brominated flame retardants (BFRs) and organophosphate flame retardants (OPFRs) from soil, water and the atmosphere, which is of considerable significance to the geochemical cycle of BFRs and OPFRs and their human exposure. However, the current understanding of the plant uptake, translocation, accumulation, and metabolism of BFRs and OPFRs in the environment remains very limited. In this review, recent studies on the accumulation and transformation of BFRs and OPFRs in plants are summarized, the main factors affecting plant accumulation from the aspects of root uptake, foliar uptake, and plant translocation are presented, and the metabolites and metabolic pathways of BFRs and OPFRs in plants are analyzed. It was found that BFRs and OPFRs can be taken up by plants through partitioning to root lipids, as well as through gaseous and particle-bound deposition to the leaves. Their microscopic distribution in roots and leaves is important for understanding their accumulation behaviors. BFRs and OPFRs can be translocated in the xylem and phloem, but the specific transport pathways and mechanisms need to be further studied. BFRs and OPFRs can undergo phase I and phase II metabolism in plants. The identification, quantification and environmental fate of their metabolites will affect the assessment of their ecological and human exposure risks. Based on the issues mentioned above, some key directions worth studying in the future are proposed.

Mining activities in the world's largest platinum mining area in South Africa have resulted in environmental contamination with Pt (e.g., the Hex River's vicinity). The present study compared a Pt mining area with a non-mining area along this river in terms of (1) metal concentrations in different grain size fractions from soils and aquatic sediments; (2) the toxicological potential of aquatic sediments based on the Consensus-Based Sediment Quality Guideline (CBSQG); and (3) the chronic toxicity of aqueous eluates from soils and sediments to Caenorhabditis elegans. Platinum concentrations were higher in the mining area than in the non-mining area. For most metals, the sediment silt and clay fraction contained the highest metal concentrations. Based on the CBSQG, most sampling sites exhibited a high toxicological potential, driven by Cr and Ni. Eluate toxicity testing revealed that C. elegans growth, fertility, and reproduction inhibition were not dependent on mining activities or the CBSQG predictions. Toxicity was instead likely due to Cd, Fe, Mn, Ni, Pt, and Pb. In conclusion, the investigated region is loaded with a high geogenic background resulting in high reproduction inhibition. The mining activities lead to additional environmental metal contamination (particularly Pt), contributing to environmental soil and sediment toxicity.

Tropospheric ozone (O₃) affects isoprenoid emissions, and floral emissions in particular, which may result in potential impacts on the interactions of plants with other organisms. The effects of ozone (O₃) on isoprenoid emissions have been investigated for many years, while knowledge on O₃ effects on floral emissions is still scarce and the relevant mechanism has not been clarified so far. We investigated the effects of O₃ on floral and foliar isoprenoid emissions (mainly isoprene, monoterpenes and sesquiterpenes) and their synthase substrates from three rose varieties (CH, Rosa chinensis Jacq. var. chinensis; SA, R. hybrida ‘Saiun’; MO, R. hybrida ‘Monica Bellucci’) at different exposure durations. Results indicated that the O₃-induced stimulation after short-term exposure (35 days after the beginning of O₃ exposure) was significant only for sesquiterpene emissions from flowers, while long-term O₃ exposure (90 days after the beginning of O₃ exposure) significantly decreased both foliar and floral monoterpene and sesquiterpene emissions. In addition, the observed decline of emissions under long-term O₃ exposure resulted from the limitation of synthase substrates, and the responses of emissions and substrates varied among varieties, with the greatest variation in the O₃-sensitive variety. These findings provide important insights on plant isoprenoid emissions and species selection for landscaping, especially in areas with high O₃ concentration.

Effective and fair mitigation measures hinge on the identification of hotspots and tracking provenance on reactive nitrogen (Nr) loss at a high spatial resolution. We assessed the Nr loss intensity in China at 1 km spatial resolution from 1980 to 2015. The total Nr loss increased from 20.2 to 54.5 Tg N yr⁻¹, with hotspots (>100 kg N ha⁻¹ yr⁻¹) concentrated in the North China Plain, the Middle and Lower Yangtze River and the Sichuan Basin. The Nr loss hotspots covered less than 20% of the Chinese territory but contributed more than 90% of total Nr loss since 1990. Geographical disparity in Nr loss has increased and calls for a fair regional policy synergy. Compared to managing Nr loss based only on production, we demonstrate that the estimation of Nr loss responsibility driven by consumption has greater potential to allocate a fair share of responsibility for reducing Nr loss.