Aqueous film-forming foam (AFFF) has historically contained high concentrations of long-chain per-and polyfluoroalkyl substances (PFAS), which have been linked with adverse health outcomes. However, the toxicity of historical AFFFs remains largely unknown, presenting uncertainties in their risk assessment. This study assessed the toxicity of historical AFFFs by exposing human liver cells (HepG2) to various dilutions of 3M Light Water AFFF or Ansulite AFFF (0.001%, 0.002%, 0.005%, 0.009%, 0.019%, 0.038%, 0.075%, 0.15%, and 0.3%) for 24 h. The effects of the two AFFF formulations on the cell viability, intracellular reactive oxygen species (ROS) production, Nrf2-ARE activity, and DNA damage were assessed by CellTiter 96® Aqᵤₑₒᵤₛ One Solution Cell Proliferation Assay (MTS kit), dichlorofluorescein diacetate assay, luciferase assay, and alkaline Comet assay, respectively. The results revealed that the two brands of AFFFs tested were toxic to HepG2 cells at dilutions lower than the recommended 3% application formulation. Specifically, exposure to 3M Light Water AFFF or Ansulite AFFF induced a dilution-dependent decrease in cell viability, increased intracellular ROS production, and increased Nrf2-ARE activity. However, except for the highest concentration (lowest dilution) of 3M Light Water AFFF tested (0.038%.), both 3M Light Water AFFF and Ansulite AFFF did not significantly induce cellular DNA damage. Overall, 3M Light Water AFFF was more toxic than Ansulite AFFF. The findings from this study provided valuable in vitro toxicity data that may better inform the health risk assessment of these historical AFFFs.

The main intent of the current research was to appraise if combined application of hydrogen sulfide (H₂S, 0.2 mM) and silicon (Si 2.0 mM) could improve tolerance of tomato plants to arsenic (As as sodium hydrogen arsenate heptahydrate, 0.2 mM) stress. Plant growth, chlorophylls (Chl), PSII maximum efficiency (Fv/Fm), H₂S concentration and L-cysteine desulfhydrase activity were found to be suppressed, but leaf and root As, leaf proline content, phytochelatins, malondialdehyde (MDA) and H₂O₂ as well as the activity of lipoxygenase (LOX) increased under As stress. H₂S and Si supplied together or alone enhanced the concentrations of key antioxidant biomolecules such as ascorbic acid, and reduced glutathione and the activities of key antioxidant system enzymes including catalase (CAT), superoxide dismutase (SOD), dehydroascorbate reductase (DHAR), glutathione reductase (GR), and glutathione S-transferase (GST). In comparison with individual application of H₂S or Si, the joint supplementation of both had better effect in improving growth and key biochemical processes, and reducing tissue As content, suggesting a putative collaborative role of both molecules in improving tolerance to As-toxicity in tomato plants.

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.