Leaching of herbicides in cropping soils not only impacts the groundwater sources but also reduces their effect in controlling weeds. Leaching studies were carried out in two cropping soils and two forestry biowaste media, wood pulp and sawdust with two herbicides, atrazine and bromacil in a packed lysimeter with simulated rainfall. The hypothesis was that high organic matter forestry biowaste soil amendments reduce the leaching of herbicides through the soil profile. Results from the experimental setups varied due to the impact of the simulated rainfall on the surface structure of the media. Organic carbon content, pH and structure of the media were all factors which affected the leaching of the two herbicides. The hypothesis was true for wood pulp, but for sawdust, organic matter content had less bearing on the leaching of the herbicides than other over-riding factors, such as pH, that were media specific. In sawdust, its large particle size and related pore volume allowed preferential flow of herbicides. Overall, the data indicated that both forestry biowastes were retentive to herbicide leaching, but the effect was more pronounced with wood pulp than sawdust.

The plasticizer di(2-ethylhexyl) phthalate (DEHP) is frequently detected in the environment due to the abundance of its use. These levels might be hazardous to human health and ecosystems. Phthalates have been associated with neurological disorders, yet whether chronic DEHP exposure plays a role in Parkinson's disease (PD) or its underlying mechanisms is unknown. We investigated the effects of chronic DEHP exposure less than an environmentally-relevant dose on PD hallmarks, using Caenorhabditis elegans as a model. We show that developmental stage and exposure timing influence DEHP-induced dopaminergic neuron degeneration. In addition, in response to chronic DEHP exposure at 5 mg/L, mitochondrial fragmentation became significantly elevated, reactive oxygen species (ROS) levels increased, and ATP levels decreased, suggesting that mitochondrial dysfunction occurs. Furthermore, the data show that mitochondrial complex I (nuo-1 and gas-1) and complex II (mev-1) are involved in DEHP-induced dopaminergic neuron toxicity. These results suggest that chronic exposure to DEHP at levels less than an environmentally-relevant dose causes dopaminergic neuron degeneration through mitochondrial dysfunction involving mitochondrial complex I and II. Considering the high level of genetic conservation between C. elegans and mammals, chronic DEHP exposure might elevate the risk of developing PD in humans.

Lead (Pb) is a toxic element which is released as a result of anthropogenic activities, and Pb stable isotope ratios provide a means to distinguish sources and transport pathways in receiving environments. In this study, isotopes of bioaccumulated Pb (²⁰⁴Pb, ²⁰⁶Pb, ²⁰⁷Pb, ²⁰⁸Pb) were examined for diverse terrestrial and aquatic biota from three areas in western Canada: (a) otter, marten, gulls, terns, and wood frogs in the Alberta Oil Sands Region (AOSR), (b) fish, plankton, and gulls of Great Slave Lake (Yellowknife, Northwest Territories), and (c) wolverine from the Yukon. Aquatic and terrestrial biota from different habitats and a broad geographic area showed a remarkable similarity in their Pb isotope composition (grand mean ± 1 standard deviation: ²⁰⁶Pb/²⁰⁷Pb = 1.189 ± 0.007, ²⁰⁸Pb/²⁰⁷Pb = 2.435 ± 0.009, n = 116). Comparisons with Pb isotope ratios of local sources and environmental receptors showed that values in biota were most similar to those of atmospheric Pb, either measured in local aerosols influenced by industrial activities in the AOSR or in lichens (an aerosol proxy) near Yellowknife and in the Yukon. Biotic Pb isotope ratios were different from those of local geogenic Pb. Although the Pb isotope measurements could not unambiguously identify the specific anthropogenic sources of atmospheric Pb in biota, initial evidence points to the importance of fossil fuels currently used in transportation and power generation. Further research should characterize bioavailable chemical species of Pb in aerosols and important emission sources in western Canada.

The recently recognized adverse environmental and toxic effects of neonicotinoid insecticides (NNIs) on non-target organisms are alarming. A comprehensive design, screening, and regulatory system was developed to generate NNI derivatives and mutant receptors with selective-ecotoxicological effects to overcome such adverse effects. For ligand design, taking ACE-09 derivative as an example, the toxicity on non-target animals (aboveground: bees; underground: earthworms), plant absorption, and soil absorption decreased by 4.80% and 13.7%, 10.0%, and 121%, while the toxicity on target animals (aboveground: aphids; underground: B. odoriphagas), plant metabolism, and soil degradation increased by 70.2% and 51.7%, 5.08%, and 8.28%. For receptor modification, the ability of mutants to absorb ACE-09 derivative decreased by 31.0%, while the ability of mutants to metabolize ACE-09 derivative increased by 28.0% in scenario 2 (mainly plant selectivity); the ability of mutants to degrade ACE-09 derivative increased by 11.6% in scenario 3 (mainly soil selectivity). The above results indicated that the selective-ecotoxicological effects of ligand design and receptor modification were both improved. Additionally, the combined effects of the ACE-09 derivative on plant absorption and metabolic mutants improved by 31.1% and 31.4% in scenario 2, respectively, while the effect on microbial degradation mutant improved by 14.9%, indicating that there was a synergistic effect between ligand design and receptor modification. Finally, based on the interaction between the ACE-09 derivative and mutants, the optimal environmental factors that improved the selectivity of their ecotoxicological effects were determined. For example, alternate application of nitrogen and phosphorus fertilizers effectively reduced the oxidative damage to plants caused by NNI residues. The novel ligand-receptor joint modification method, combined with the regulation of environmental factors under multiple scenarios, can biochemically address the ecotoxicological concern and highlight the harmful effects of pesticides on the environment and non-target organisms.

Direct application of contaminated-rice straw (CRS) to soil can cause the secondary pollution in agricultural land because of high content of Cd in rice straw. This study employed biochar or modified biochar technique to reduce the potential pollution risk of Cd in CRS. In the pot experiment, the CRS, straw biochar prepared at 300 °C (B300) and 500 °C (B500), and phosphorus modified biochar pyrolyzed at 300 °C (PB300) and 500 °C (PB500) were added at dosage of 5% into three typical paddy soils. The results showed that CRS and its derived biochar could enhance soil pH, EC, Eh, organic carbon, exchangeable base cations (K⁺, Na⁺, Ca²⁺ and Mg²⁺), and available phosphate. The application of CRS, biochar and phosphorus modified biochar significantly increased the contents of total Cd in soils relative to control soil. Compared to CRS, the biochar application (especially the PB500) decreased the contents of 0.01M CaCl₂-extractable Cd. The application of CRS significantly increased the content of exchangeable Cd fraction (F1), whereas biochar increased residual Cd content (F4). The biochar and phosphorous modified biochar significantly decreased the contents of bioavailable Cd in soils compared to CRS application. The increased soil pH and dissolve organic matter were found to be the main factors in reducing the release of Cd in biochar. The possible mechanisms of biochar in reducing bioavailability of Cd were to significantly increase soil pH, enhance the complexation of Cd ions, and promote the transformation of Cd from easily available to stable (residual) forms. It could conclude that conversion of contaminated rice straw into biochar was an efficient way to minimize Cd availability in soil and reduce the pollution risk of Cd in rice straw.

Androstenedione (ADSD) was the main androgen detected in wastewaters. Chlorella was the most widely used plant in biological wastewater treatment process. In order to understand the toxicological response of chlorella to ADSD contamination, we used the weighted gene co-expression network analysis (WGCNA) method to systematically analyze the gene regulatory networks of chlorella after ADSD treatments. Total of 25 modules was identified from gene co-expression networks, and the turquoise module were selected for GO and KEGG enrichment analysis. Results showed that most hub genes were associated with chloroplast organizations or photosystems processes. Among them, the expressions profiles of hcar, nol, pao and sgr genes were highly correlated to the content fluctuations of chlorophylls after different ADSD treatments. All these results demonstrated that chlorophylls play a key role in preventing cell damage of chlorella caused by ADSD contamination. Besides, we proposed a possible chlorophyll metabolism pathway in chlorella response to ADSD contamination.

Estimating the burden of diseases induced by overexposure to solar ultraviolet radiation (SUVR) can help to prioritize environmental health interventions. The age-sex specific and cause-specific mortality and disability-adjusted life years (DALYs) attributable to overexposure to SUVR at the national and subnational levels in Iran, 2005–2019 were estimated. The burden of disease induced by overexposure to SUVR was quantified in four steps as follows: (1) estimating exposure to SUVR, (2) estimating total incidences and deaths of target causes, (3) assessing population attributable fractions of the target causes for the SUVR, and (4) calculating the attributable burden of disease. The attributable DALYs, deaths, age-standardized DALY rate, and age-standardized death rate at the national level were determined to be respectively 21896, 252, 42.59, and 0.56 in 2005 and were respectively changed to 28665, 377, 38.76, and 0.53 in 2019. The contributions of causes in the attributable DALYs at the national level were different by year and sex and for both sexes in 2019 were as follows: 46.15% for cataract, 20.36% for malignant skin melanoma, 16.07% for sunburn, 12.41% for squamous-cell carcinoma, and 5.01% for the other five causes. The contributions of population growth, population ageing, risk exposure, and risk-deleted DALY rate in the temporal variations of the attributable burden of disease in the country were +20.73%, +20.68%, +2.01%, and −12.51%. The highest and lowest provincial attributable age-standardized DALY rates in 2019 were observed in Fars (46.8) and Ardebil (32.7), respectively. The burden of disease induced by exposure to SUVR caused relatively low geographical inequality in health status in Iran. Due to increasing trends of the SUVR as well as the attributable burden of disease, the preventive interventions against the SUVR overexposure should be considered in the public health action plan all across the country.

Benzene is a common environmental carcinogen that induces leukemia. Studies suggest that metabolic disorder has a relationship with the toxicity of benzene. Pyruvate kinase M2 (PKM2) is a key rate-limiting enzyme in glycolysis. However, the upstream and downstream regulatory mechanisms of PKM2 in benzene-induced hematotoxicity and the therapeutic effects of targeting PKM2 in vivo are unclear. This study aims to provide insights into the new mechanism of benzene-induced hematotoxicity and reveal the therapeutic significance of targeting PKM2. Herein, we demonstrated that PKM2-dependent glycolysis contributes to benzene-induced hematotoxicity by regulating inflammation reaction. Mechanistically, acetylated proteomics revealed that 1,4-benzoquinone (1,4-BQ) induced acetylation of PKM2 at position K66, and this modification contributed to the increase of PKM2 expression and can be inhibited by inhibition of acetyltransferase GCN5. Meanwhile, the elevated PKM2 was shown to prompt the activation of nuclear phosphorylated Stat3 (p-Stat3) and IL17A. Clinically, pharmacological inhibition of PKM2 alleviated the blood toxicity induced by benzene, which was mainly characterized by an increase in routine blood parameters and improvement of hematopoietic imbalance. Besides, elevated PKM2 is a promising biomarker in people occupationally exposed to benzene. Overall, we identified PKM2/p-Stat3/IL-17A axis participates in the hematotoxicity of benzene, and targeting PKM2 has certain therapeutic implications in hematologic diseases.

In the current investigation, we presented the success of the modified hydrothermal method for synthesizing the iron-oxide nanoparticles (Fe₂O₃-NPs) efficiently. These NPs were further characterized by using different techniques such as X-ray diffraction (XRD), scanning electron microscope (SEM) micrographs, energy-dispersive X-ray spectroscopy (EDAX)/Mapping pattern, Raman Spectroscopy Pattern, ultra violet (UV) and Photoluminescence (PL). All these analyses revealed highly pure nature of Fe₂O₃-NPs with no internal defects, and suggested its application for plant growth improvement. Therefore, we further investigated the separate as well as combined effects of the Fe₂O₃-NPs and citric acid (CA) in the alleviation of arsenic (As) toxicity in the soybean (Glycine max L.), by evaluating the different plant growth and metabolic attributes. Results of our study revealed that As-induced growth inhibition, reduction of photosynthesis, water use efficiency (WUE), and reactive oxygen species (ROS) accumulation whereas application of the Fe₂O₃-NPs and CA significantly reversed all these adverse effects in soybean plants. Moreover, the As-stress induced malondialdehyde (MDA) and hydrogen peroxide (H₂O₂) production were partially reversed by the Fe₂O₃-NPs and CA in the As-stressed plants by 16% and 10% (MDA) and 29% and 12% (H₂O₂). This might have resulted due to the Fe₂O₃-NPs and CA induced activities of the antioxidant defense in plants. Overall, the Fe₂O₃-NPs and CA supplementation separately and in combination positively regulated the As tolerance in soybean; however, the effect of the combined application on the As tolerance was more profound relative to the individual application. These results suggested the synergetic effect of the Fe₂O₃-NPs and CA on the As-tolerance in soybean. However, in-depth mechanism underlying the defense crosstalk between the Fe₂O₃-NPs and CA needs to be further explored.

Metals may affect adversely cardiovascular system, but epidemiological evidence on the associations of priority-controlled metals including antimony (Sb), arsenic (As), cadmium, lead, and thallium with children's blood pressure (BP) was scarce and inconsistent. We conducted two panel studies with 3 surveys across 3 seasons among 144 and 142 children aged 4–12 years in Guangzhou and Weinan, respectively. During each seasonal survey, urine samples were collected for 4 consecutive days and BP was measured on the 4th day. We obtained 786 BP values and urinary metals measurements at least once within 4 days, while 773, 596, 612, and 754 urinary metals measurements were effective on the health examination day (Lag 0), and the 1ˢᵗ, 2ⁿᵈ, and 3ʳᵈ day preceding BP measurement (Lag 1, lag 2 and lag 3), respectively. We used linear mixed-effect models, generalized estimating equations and multiple informant models to assess the associations of individual metal at each lag day and accumulated lag day (4 days averaged, lag 0–3) with BP and hypertension, and Bayesian Kernel Machine Regression to evaluate the relations of metals mixture at lag 0–3 and BP outcomes. We found Sb was positively and consistently related to systolic BP (SBP), mean arterial pressure (MAP), and odds of having hypertension within 4 days, which were the strongest at lag 0 and declined over time. And such relationships at lag 0–3 showed in a dose-response manner. Meanwhile, Sb was the only contributor to the relations of mixture with SBP, MAP, and odds of having hypertension. Also, synergistic interaction between Sb and As was significant. In addition, modification effect of passive smoking status on the association of Sb and SBP was more evident in passive smokers. Accordingly, urinary Sb was consistently and dose-responsively associated with increased BP and hypertension, of which Sb was the major contributor among children.