Toxics最新文献

Phosphogypsum (PG) is a byproduct of wet-process phosphoric acid production and contains soluble phosphorus (P), fluorine (F), and other harmful impurities in addition to calcium sulfate. Its acidic leachate enriched with P and F poses long-term risks to soil and surrounding water bodies. Owing to the incorporation of soluble P and F within calcium sulfate crystal interlayers, these contaminants are gradually released during storage, making it difficult to achieve an economically efficient and environmentally benign treatment of PG at an industrial scale. In this study, a low-cost and sustainable process for the effective and long-term immobilization of soluble P and F in PG was developed using sulfuric acid-activated red mud (RM), an industrial waste rich in Fe and Al. After pulping PG with water, activated RM was added, followed by pH adjustment with Ca(OH)₂, leading to the in situ formation of amorphous calcium aluminate and calcium ferrite polymers with strong adsorption affinity toward soluble P and F. The immobilization mechanism and phase evolution were systematically investigated using inductively coupled plasma optical emission spectroscopy (ICP-OES, PS-6PLASMA SPECTROVAC, BAIRD, USA), on a Rigaku Miniflex diffractometer (Rigaku Corporation, Tokyo, Japan), scanning electron microscopy coupled with energy-dispersive spectroscopy (SEM-EDS), and zeta potential analysis. The leachate of PG treated with activated RM and Ca(OH)₂ contained P < 0.5 mg/L and F < 10 mg/L at pH 8.5-9.0, meeting environmental requirements (pH = 6-9, P ≤ 0.5 mg/L, F ≤ 10 mg/L). Moreover, the immobilized P and F exhibited enhanced stability during long-term stacking, indicating the formation of durable immobilization products. This study demonstrates an effective "treating waste with waste" strategy for the large-scale, environmentally safe utilization of phosphogypsum.

While the adverse health effects of bisphenol A (BPA) or high-fat diet (HFD) exposure alone have been relatively well documented, the mechanisms underlying their combined impact on insulin resistance and type 2 diabetes remain poorly understood. In this study, we observed the effects of 90 days of treatment with BPA and an HFD on insulin resistance in mouse gastrocnemius muscle, as well as the expression of signaling molecules and proteins potentially associated with glucose transporter type 4 (GLUT4) translocation. Additionally, C2C12 myotubes were co-treated with BPA and palmitic acid (PA) to observe the effects on insulin signaling molecules, GLUT4 translocation, and insulin resistance. Specifically, in vitro cellular experiments further demonstrated that BPA and PA inhibited GLUT4 translocation from the nucleus to the cell membrane. Taken together, co-exposure to BPA and an HFD (or PA) treatment significantly altered the expression of insulin signaling molecules in both gastrocnemius muscle and C2C12 cells, suggesting a potential link to their impacts on insulin resistance and GLUT4 translocation.

Isothiazolinones are commonly used biocides that are extensively used in industrial areas and household products. The extensive usage of isothiazolinones raises concerns regarding their adverse human health effects. Isothiazolinones are readily absorbed and enter circulation. However, the potential systemic effects of isothiazolinones on the circulatory system remain unclear. Here, we examined whether the isothiazolinones, benzisothiazolinone (BIT) and octylisothiazolinone (OIT) affected platelets. In isolated platelets, BIT and OIT depleted intracellular glutathione, which led to mitochondrial reactive oxygen species (ROS) accumulation. Excessive mitochondrial ROS led to mitochondrial dysfunction, altering intracellular calcium and adenosine triphosphate homeostasis. These intracellular events activated phospholipid scramblase, externalizing phosphatidylserine, thereby enhancing procoagulant activity, as evidenced by thrombin generation. Overall, OIT showed a more potent effect than BIT. Notably, supplementation with N-acetyl-L-cysteine mitigated BIT- and OIT-induced effects, suggesting a thiol-dependent mechanism. Taken together, BIT and OIT stimulated the platelet-mediated coagulation pathway, which may increase prothrombotic risk and contribute to cardiovascular disease. These results could improve our understanding of the systemic adverse effects after isothiazolinone exposure.

The increased mobilization of Rare Earth Elements (REEs), due to emerging technologies, could impact human health. The study assessed the effects of CeO₂ nanopowder (100 μg/mL) in human intestinal cells (HT-29) following both acute (24 h) and, a novelty for in vitro study, sub-chronic exposure, treating subcultures of exposed cells to CeO₂ NP up to 35 days. Recovery was also examined in exposed cells' progeny. CeO₂ NP internalization and acute cytotoxicity were dose and time dependent. A significant pro-oxidant effect was observed for up to 14 days. The highest mitochondrial impairment was detected after 7 days, but in post-exposure experiments the recovery was observed. Conversely, genotoxicity highlighted the saturation of the DNA repair mechanisms. The irreversible cell damage of sub-chronic exposure was highlighted by the percentage of death cells (p = 0.011) and by the weekly cell replication index (5.68 vs. 7.41). The homeostatic mitophagy pathway was able to counteract ROS-induced mitochondrial dysfunction, as shown by overexpression of ATG5, LC3, and BECN1 genes throughout the examined times. Instead, the overexpression of the pro-apoptotic gene Bax was very brief, highlighting that prolonged exposure might cause more widespread adverse effects, also involving cells that are not directly exposed to nanoceria.

Agricultural watersheds are undergoing rapid rural-urban transitions, yet the relative contributions of diffuse agricultural runoff versus rural domestic and point sources to organophosphate esters (OPEs) pollution remain poorly understood. This study investigated the occurrence, spatiotemporal distribution, and potential risks of 17 legacy and emerging OPEs in the Dalongdong River, China. Combined non-target and target analyses revealed mean OPE concentrations of 111.94 ng/L in water and 8.76 ng/g in sediments. Spatially, total OPE concentrations increased progressively from upstream to downstream, with pronounced hotspots downstream of townships and near wastewater treatment facilities, indicating that rural domestic effluents and urban runoff, alongside agricultural activities, are critical contributors to OPE pollution in this watershed. Seasonally, concentrations of six legacy OPEs were significantly higher during the wet season. Furthermore, high-throughput phenotypic screening using Caenorhabditis elegans, combined with toxicological priority index analysis, showed that emerging OPEs generally pose higher integrated health and ecological risks, although certain legacy compounds, such as triphenyl phosphate, still display substantial toxic potential. These findings clarify the potential biological hazards of these compounds and provide baseline data on the fate of OPEs in riverine systems influenced by mixed agricultural and rural-urban anthropogenic activities.

This study presents the first systematic investigation of Volatile Organic Compounds (VOC) source profiles from key industrial sectors in Chongqing, China. Source-specific emission data were collected from fifteen representative facilities encompassing furniture manufacturing, automobile production, and chemical industries through a combination of on-site sampling and comprehensive literature review. Our results reveal distinct chemical signatures and regional variations among different source categories: furniture manufacturing emissions are dominated by alkanes (65%), chemical industries exhibit 51% alkane contribution, while automobile manufacturing demonstrates a remarkably high aromatic hydrocarbon content (64%), significantly exceeding other investigated sectors. Notably, aromatic hydrocarbons-particularly benzene derivatives-emitted from automotive manufacturing facilities pose potential carcinogenic and chronic health risks to both occupational workers and surrounding populations, necessitating prioritized regulatory intervention. These locally derived emission profiles fill a critical knowledge gap in regional VOC source characterization for Chongqing, providing essential scientific evidence for accurate source apportionment and formulation of sector-specific emission reduction strategies.

Cement production exerts a significant negative impact on the environment through the emission of greenhouse gases, particulate matter (PM), heavy metals, and other toxic substances into the atmosphere, soil, and bodies of water, degrading the environment and affecting the population's health. This study reviews different solutions to reduce pollution and mitigate its effects. Particular attention is given to Carbon Capture, Utilization, and Storage (CCUS) technologies and their ability to significantly reduce CO₂. Biomass and waste-derived fuels were identified as viable substitutes for fossil fuels, although challenges related to supply chain reliability and secondary environmental impacts remain. The study further examined mitigation strategies for non-gaseous pollutants, including noise pollution control measures such as sound barriers and vibration isolation systems, soil remediation techniques such as phytoremediation and the recycling of cement kiln dust (CKD), and water pollution control technologies, including filtration, chemical precipitation, biological treatment, and Zero Liquid Discharge (ZLD) systems. Key research gaps were identified, particularly concerning the long-term durability, scalability, and cost-effectiveness of these mitigation approaches. Overall, the review emphasizes the need for integrated pollution control strategies to support the transition toward a more sustainable cement industry and recommends future research focused on developing mitigation technologies that are efficient, economically viable, and adaptable to large-scale industrial applications.

Silicosis, an irreversible occupational lung disease resulting from prolonged exposure to respirable crystalline silica, faces challenges due to limitations in existing mammalian models. This study evaluated whether laboratory-prepared respirable α-quartz silica could induce immune cell-inflammatory-fibrotic initiation related to silicosis in zebrafish embryos as a tool for early toxicity assessment. Zebrafish embryos at 48 h post-fertilization (hpf) were microinjected into hindbrain ventricle with respirable α-quartz silica (test material 3.056 μm vs. standard material 3.217 μm) derived from natural α-quartz ore. The results indicated a significant decrease in zebrafish survival rates and an increase in malformation rates following exposure respirable α-quartz silica materials. Additionally, alterations in midbrain and hindbrain lengths were observed, while body length remained unaffected. Behavioral assessments revealed reduced touch response rates, decreased average speed, and less time spent in the central zone during open field tests in the treatment groups. In vivo imaging demonstrated sequential recruitment of neutrophils (peak at 18 h post-injection) and macrophages (peak at 24 h post-injection). qPCR analysis revealed upregulation of inflammation-related genes (tnf-α, il-6, il-1β) and fibrosis-related genes (tgf-β, acta-2, collagen). Moreover, the hydroxyproline content, a marker for fibrosis, was significantly elevated, although no mature fibrosis was observed histologically. These findings demonstrate that respirable α-quartz silica elicits pathophysiological changes associated with silicosis early initiation in zebrafish embryos. This supports the utility of the zebrafish embryo as a practical tool for early toxicity assessment and mechanistic studies of silica-induced immune-inflammatory-fibrotic initiation, with potential implications for silica exposure early risk warning.

Background: Exposure to environmental pollutants, especially endocrine-disrupting chemicals, disproportionately affects vulnerable populations like pregnant women, lactating mothers, and preterm infants. This study aimed to assess the detection patterns of DiNP-, DEP-, and DEHP-related metabolites in maternal urine and breast milk, examine agreement between matrices, and explore maternal factors associated with phthalate exposure.

Methods: Fifty-five mothers who delivered at ≤32 gestational weeks and whose infants were hospitalized in the Neonatal Intensive Care Unit (NICU) were enrolled. Breast milk and urine samples were analyzed using a validated isotope-dilution LC-MS/MS method. Urinary phthalate metabolite concentrations were adjusted for specific gravity. Linear mixed-effects models with a random intercept for mother were used to examine associations between urinary and breast milk phthalate metabolite concentrations, assess temporal changes, and evaluate the influence of breast milk lipid content.

Results: DEHP and DiNP metabolites were detected in nearly all maternal urine samples. Breast milk contained predominantly primary metabolites (MEHP and MiNP), while secondary oxidative metabolites were rarely detected. Urine concentrations consistently exceeded breast milk concentrations. Urinary and breast milk phthalate concentrations were not correlated across sampling periods, indicating limited matrix concordance.

Conclusions: Mothers of very preterm infants experience sustained phthalate exposure in the postpartum period; however, limited metabolite transfer to breast milk indicates that maternal urine remains the preferred biomonitoring matrix for assessing systemic phthalate exposure. Breast milk phthalate profiles exhibit compound-specific temporal changes and appear largely independent of concurrent urinary exposure biomarkers.

Background: Evidence linking chlorinated polyfluoroalkyl ether sulfonic acids (Cl-PFESAs) to preterm birth (PTB) is limited, and their relationships with the metabolome remain unexplored. Aims: Our study aimed to explore the role of the metabolome in the associations between Cl-PFESAs exposure and PTB. Methods: We conducted a nested case-control study in the Shenyang birth cohort, which included 206 spontaneous preterm birth cases and 206 full-term controls, matched for maternal age and pre-pregnancy BMI. We used conditional logistic regression models to analyze the associations between Cl-PFESAs exposure in umbilical cord blood and PTB. Moreover, the metabolomics of maternal blood (44 cases) between the preterm and control groups was analyzed using the interaction analysis. Results: We observed that a higher natural log-transformed 6:2 Cl-PFESA level was associated with greater odds of PTB in conditional multivariable-adjusted logistic regression models (OR = 1.738, 95% CI: 1.320, 2.287). The results of metabolomics pathway analysis showed that histidine metabolism pathways may modify the above risk. When stratified by histidine levels, the association between cord blood 6:2 Cl-PFESA and PTB was different. Conclusions: Intrauterine exposure to 6:2 Cl-PFESA was associated with increased PTB. Also, for the first time, our study illustrates that maternal plasma metabolite profiles may modify the associations of 6:2 Cl-PFESA with PTB. More research is needed to elucidate the mechanism underlying the reproductive toxicity of 6:2 Cl-PFESA in pregnant women following exposure.