Cattle-derived biochar (CB), which is derived from industrial pyrolysis of cattle carcasses in harmless treatment plants, is a naturally occurring mineral form of carbonate-bearing hydroxyapatite (CHAP) with a small amount of elemental carbon. CB has 4.02% of carbonate content, which falls under the B-type substitution of CHAP. In this work, the Cd(II) sorption capacity of CB was determined to be 0.82 mmol/g, with 97.6% of the Cd(II) uptake contributing to CHAP and only 2.36% of the Cd(II) uptake contributing to the elemental carbon component. The calculation and linear combination fitting (LCF) of Cd L₃-edge X-ray absorption near-edge structure (XANES) analysis indicated that the contributions of Cd(II) species to CB presented the following order: ion exchange (57.6%–61.0%) > precipitation (24.4%–29.9%) > surface complexation (12.5%–13.4%). The depth dependent X-ray photoelectron spectroscopy (XPS) showed the presence of ion exchange, which is accompanied by intraparticle diffusion. LCF of XANES and Rietveld analysis of X-ray diffraction (XRD) demonstrated that Cd(II) was precipitated in the form of Cd₅H₂(PO₄)₄·4H₂O on the CB surface. Furthermore, the precipitate was directly observed and identified by scanning electron microscopy with energy-dispersive spectroscopy (SEM-EDS). Consequently, we revealed the intricate binding mechanism of Cd(II) to CHAP-rich CB and confirmed the importance of surface precipitation.

2,2′,4,4′-Tetrabromodiphenyl ether (BDE-47) is associated with various adverse human health effects; however, the knowledge of its toxicity is still very limited. Mitochondrial injury has been observed in liver cells exposed to BDE-47 in vitro. Mitophagy impairment causes the accumulation of dysfunctional mitochondria, contributing to the pathological mechanisms of liver injury. The aim of this study was to investigate whether BDE-47 impairs mitophagy to trigger mitochondrial dysfunction-related liver injury and the underlying mechanisms. This study revealed that BDE-47 elicited mitochondrial dysfunction and related oxidative liver injury by impairing mitophagy. Moreover, our results showed that NAD⁺ insufficiency is responsible for BDE-47-mediated mitophagy defect and mitochondrial dysfunction in mouse livers, which was associated with suppression of Sirt3/FoxO3a/PINK1 signaling. Furthermore, our results indicated a potential role of miR-34a-5p in the hepatotoxicity of BDE-47. Mechanistically, BDE-47 dramatically upregulated miR-34a-5p expression in mouse livers. The data from AAV-sponge-mediated miR-34a-5p inhibition suggested that miR-34a-5p diminished NAD⁺ level by directly targeting NAMPT expression in BDE-47-treated mouse livers, which was confirmed by luciferase reporter assay. Consequently, miR-34a-5p markedly abated Sirt3/FoxO3a/PINK1 signaling-mediated mitophagy to promote mitochondrial dysfunction in BDE-47-treated mouse livers. The present study provided in vivo evidence to reveal a potential mechanism for BDE-47-induced mitochondrial dysfunction and related liver injury and indicated that miR-34a-5p-mediated mitophagy impairment might be a therapeutic target for BDE-47 toxicity.

(±) - PEN is a chiral fungicide widely used to control powdery mildew in agriculture. Currently, only a few studies have investigated the toxic effects of (±) – penconazole ((±) – PEN) on non-target organisms, and whether (±) - PEN from the enantiomeric level have toxic effects remains unclear. In this study, we systematically evaluated the effects of exposure to (±) – PEN, (+) – PEN and (−) – PEN on liver function in mice. Biochemical and histopathological analyses showed that exposure to (±) – PEN and (−) – PEN led to significant liver damage and inflammation. However, exposure to (+) – PEN treatment did not cause no adverse effects on liver function and inflammation. ¹H-NMR-based metabolomics revealed that exposure to (±) – PEN, (+) – PEN and (−) – PEN led to the animals developing liver metabolic disorder that was caused by changes in glycolipid metabolism. Quantitative analysis of genes regulating glycolipid metabolism revealed that expression of gluconeogenesis and glycolytic pathway genes were altered in individuals exposed to (±) – PEN, (+) – PEN and (−) – PEN. We also found that (±) – PEN, (+) – PEN and (−) – PEN have different effects on lipid metabolism of the liver. Exposure to (±) – PEN and (−) – PEN resulted in significant accumulation of lipids by regulating fatty acid synthesis, triglyceride synthesis, and fatty acid β oxidation pathways. In summary, we found different toxicological effects in individuals exposed to (±) – PEN, (+) – PEN and (−) – PEN. The results of this study are important for assessing the potential health risks of (±) – PEN.

Fluorotelomer alcohols (FTOHs) are important precursors of perfluorocarboxylic acids (PFCAs) in the environment and biota. With the growing application of 6:2 FTOH [F(CF₂)₆CH₂CH₂OH] in product formulation, it is becoming increasingly urgent to investigate its biological fates in different species. In this study, biotransformation of 6:2 FTOH by young soybean plants (Glycine max L. Merrill) were investigated using hydroponic experiments. During the 144 h-exposure, 6:2 FTCA [F(CF₂)₆CH₂COOH], 6:2 FTUCA [F(CF₂)₅CFCHCOOH], 5:3 FTUCA [F(CF₂)₅CHCHCOOH], 5:3 FTCA [F(CF₂)₅CH₂CH₂COOH], PFHxA [F(CF₂)₅COOH] and PFPeA [F(CF₂)₄COOH] were phase I metabolites in soybean. At the end of exposure, 5:3 FTCA (5.08 mol%), PFHxA (2.34 mol%) and PFPeA (0.58 mol%) were three main metabolites in soybean-solution system. 5:3 FTCA was predominant in soybean roots and stems, while PFHxA was the most abundant product in leaves. PFBA [F(CF₂)₃COOH] and 4:3 FTCA [F(CF₂)₄CH₂CH₂COOH] detected in the hydroponic solution most-likely came from the transformation of 5:3 FTCA by root-associated microbes. Moreover, phase II metabolites of 6:2 FTOH were identified and monitored in soybean tissues. Alcohol dehydrogenase, aldehyde dehydrogenase and glutathione S-transferase were found to participate in 6:2 FTOH metabolism. Based on the phase I and phase II metabolism of 6:2 FTOH in soybean, this study for the first time provides evidences for the transformation pathways of 6:2 FTOH in plants.

The increase of gaseous ammonia (NH₃) concentration in the atmosphere significantly impacts the regional air quality, human health, and the nitrogen cycle of ecosystems. This study aims to verify the reanalyzed product of IASI NH₃ (the ANNI-NH₃-v2.1R-I, hereafter referred to as IASI_NH₃_R) and to analyze the spatial and temporal characteristics of atmospheric NH₃ during 2008–2016 and its underlying influencing factors. Our results show a good agreement between spatial pattern and temporal (annual and monthly) trend of the satellite-derived surface NH₃ concentrations and the measured near-ground NH₃ measurements over different land covers in Eastern China, suggesting the IASI_NH₃_R product can be used to investigate spatial and temporal trends of atmospheric NH₃ concentration. The annual mean NH₃ column concentrations peaked in the North China Plain (averaged 12 × 10¹⁵ mol cm⁻² yr⁻¹) and showed a significant increasing trend at a rate of 0.6 × 10¹⁵ mol cm⁻² yr⁻¹ during the entire period, which can be ascribed to densely populated, intensive agricultural activities and substantial reduction of SO₂ and NO₂ emissions since 2011. The NH₃ column concentrations show a slight increase in winter in most regions of China, probably due to less precipitation amount and increased uncertainty for lower NH₃ columns and the thermal contrast (TC). A large seasonal variation of NH₃ column concentrations was observed, with the highest values in summer and the lowest in autumn. Such seasonal variation is mainly affected by seasonal differences in NH₃ emissions and meteorological conditions. Our results suggest that the current control measures effectively decreased SO₂ and NO₂ pollution but are not yet apparent in the mitigation of atmospheric NH₃ pollution, which also merits more attention considering that no effective measures are being implemented for NH₃ emission control at a regional or national scale in China.

New environmental regulations are mandating cleaner fuels and lower emissions from all maritime operations. Natural gas (NG) is a fuel that enables mariners to meet regulations; however, emissions data from maritime operations with natural gas is limited. We measured emissions of criteria, toxic and greenhouse pollutants from a dual-fuel marine engine running either on diesel fuel or NG as well as engine activity and analyzed the impacts on pollutants, health, and climate change. Results showed that particulate matter (PM), black carbon (BC), nitric oxides (NOₓ), and carbon dioxide (CO₂) were reduced by about 93%, 97%, 92%, and 18%, respectively when switching from diesel to NG. Reductions of this magnitude provide a valuable tool for the many port communities struggling with meeting air quality standards. While these pollutants were reduced, formaldehyde (HCHO), carbon monoxide (CO) and methane (CH₄) increased several-fold. A health risk assessment of exhaust plume focused on when the vessel was stationary, and at-berth showed the diesel plume increased long-term health risk and the NG plume increased short-term health risk. An analysis of greenhouse gases (GHGs) and BC was performed and revealed that, on a hundred year basis, the whole fuel cycle global warming potential (GWP) per kWh including well-to-tank and exhaust was 50% to few times higher than that of diesel at lower engine loads, but that it was similar at 75% load and lower at higher loads. Mitigation strategies for further reducing pollutants from NG exhaust are discussed and showed potential for reducing short-term health risks and climate impacts.

Although several studies have linked PM₂.₅ (particulate matter with a diameter less than 2.5 μm) to ocular surface diseases such as keratitis and conjunctivitis, very few studies have previously addressed its effect on the retina. Therefore, the aim of this study was to evaluate the effect of PM₂.₅ on epithelial-mesenchymal transition (EMT), a process involved in disorders of the retinal pigment epithelial (RPE) on APRE-19 cells. PM₂.₅ changed the phenotype of RPE cells from epithelial to fibroblast-like mesenchymal, and increased cell migration. Exposure to PM₂.₅ markedly increased the expression of mesenchymal markers, but reduced the levels of epithelial markers. Moreover, PM₂.₅ promoted the phosphorylation of MAPKs and the expression of transforming growth factor-β (TGF-β)-mediated nuclear transcriptional factors. However, these PM₂.₅-mediated changes were completely reversed by LY2109761, a small molecule inhibitor of the TGF-β receptor type I/II kinases, and N-acetyl-L-cysteine (NAC), a reactive oxygen species (ROS) scavenger. Interestingly, NAC, but not LY2109761, effectively restored the PM₂.₅-induced mitochondrial defects, including increased ROS, decreased mitochondrial activity, and mitochondrial membrane potential disruption. Collectively, our findings indicate that the TGF-β/Smad/ERK/p38 MAPK signaling pathway is activated downstream of cellular ROS during PM₂.₅-induced EMT. The present study provides the first evidence that EMT of RPE may be one of the mechanisms of PM₂.₅-induced retinal dysfunction.

Bisphenol A (BPA) is a highly pervasive chemical in consumer products with its ascribed endocrine-disrupting properties. Several studies have shown the cytotoxic, genotoxic, and carcinogenic property of BPA over a multitude of tissues. Although BPA exposure has earlier been implicated in female infertility, the underlying molecular mechanisms explaining the toxicity of BPA in the ovary remains less understood. In the present study, a plausible correlation between redox balance or inflammatory signaling and reproductive fitness upon BPA exposure has been examined in zebrafish (Danio rerio) ovary. Congruent with significant alteration of major antioxidant enzymes (SOD1, SOD2, catalase, GPx1α, GSTα1) at the transcript level, 30 d BPA exposure at environmentally relevant concentrations (1, 10 and 100 μg L⁻¹) promotes ovarian ROS/RNS synthesis, lipid peroxidation but attenuates catalase activity indicating elevated stress response. BPA promotes a sharp increase in ovarian p38 MAPK, NF-κB phosphorylation (activation), inducible nitric oxide synthase (Nos2a), and pro-inflammatory cytokines (TNF-α and IL-1β) expression, the reliable markers for inflammatory response. Congruent to an increased number of atretic follicles, BPA-exposed zebrafish ovary reveals elevated Bax/Bcl2 ratio, activation of caspase-8, -3 and DNA breakdown suggesting heightened cell death. Importantly, significant alteration in nuclear estrogen receptor (ER) transcripts (esr1, esr2a, and esr2b) and proteins (ERα, ERβ), gonadotropin receptors, and markers associated with steroidogenesis and growth factor gene expression in BPA-exposed ovary correlates well with impaired ovarian functions and maturational response. Collectively, elevated oxidative/nitrosative stress-mediated inflammatory response and altered ER expression can influence ovarian health and reproductive fitness in organisms exposed to BPA environment.

In the present work, low-cost and efficient iron oxide nanoparticle incorporated on mesoporous biochar was prepared from effluent treatment plant (ETP) sludge collected from the textile industry. This sludge contains a higher amount of Fe due to the use of ferric chloride as a coagulant in the treatment of wastewater generated during the process. The raw sludge and prepared biochar was extensively examined by various sophisticated techniques like XRF, XRD, BET, TGA, XPS, RAMAN, FTIR, FESEM, TEM, and VSM. TEM and XRD analysis confirms the presence of iron oxide nanoparticles on mesoporous biochar. The prepared biochar was found to possess BET surface area of 91 m² g⁻¹. Several parameters like pH, dose, initial concentration, temperature and time were optimized for the adsorptive removal of ofloxacin (OFL) from aqueous solution. Biochar (named as BTSFe) achieved ≈96% removal efficiency of OFL with a maximum adsorption capacity (qₘ) of 19.74 mg g⁻¹ at optimum condition. π-π electron–donor-acceptor and H bonding were the major mechanisms responsible for the OFL adsorption. Kinetic and equilibrium thermodynamic study of showed that the adsorption of OFL was represented by the pseudo-second-order kinetics model, and the process was exothermic and spontaneous. Additionally, Redlich-Peterson and Freundlich isotherms best fitted the experimental data indicating multilayer adsorption phenomenon. Biochar was magnetically separated and thermally regenerated after each cycle for five times with a nominal overall decrease of ≈8% in removal efficiency. Leaching of iron during the adsorption process was also checked and found to be within the permissible limit. This study provides an alternative application of the textile industry sludge as an efficient, low-cost biochar for the removal of emerging pharmaceutical compounds.

The contamination of ground water with arsenic is a great public health concern. This paper discusses the possible formation mechanism of high As groundwater; identify the main influences of natural and anthropogenic factors on As occurrence in groundwater; and finally estimates As-induced potential health hazards in an intensive agricultural region, Datong Basin (Northern China). Our findings indicate that the predominant controlling factors of As in groundwater can be divided into natural factors and anthropogenic activities. Natural factors can be classified as natural potential source of As, environmental geological characteristics and hydrochemical conditions; anthropogenic activities are manifested in industrial coal mining, domestic coal burning, agricultural irrigation return flow and excessive application of fertilizers, and groundwater exploitation. Microbial and/or chemical reduction desorption of arsenate from Fe-oxide/hydroxide and/or clay minerals, As-bearing Fe-oxide/hydroxide reduction coupled with sulfate reduction, and competition with phosphorus are postulated to be the major process dominating As enrichment in the alkaline and anoxic groundwater. In addition, age-dependent human health risk assessment (HHRS) was performed, and high risk values reveal a high toxic and carcinogenic risk of As contaminate for population who is subject to the continuous and chronic exposure to elevated As.