Environmental analysis, health and toxicology最新文献

Bisphenol A diglycidyl ether (BADGE) is commonly used to stabilize products synthesized from epichlorohydrin and bisphenol A. Although recent studies suggest that BADGE may adversely affect the male reproductive system, its underlying mechanisms remain unclear. This study investigates the impact of BADGE exposure on steroidogenesis via DNA methylation changes in adult zebrafish gonads. Adult male zebrafish were exposed to BADGE (10 μM) for 21 days (n = 15 per group). Genomic DNA and mRNA were extracted from the testes. Whole-genome bisulfite sequencing revealed differentially methylated (DM) regions, and the expression levels of genes associated with these DM sites and steroidogenesis were analyzed using quantitative reverse transcription polymerase chain reaction. Among the 2,673 DM sites (1,311 hypomethylated and 1,362 hypermethylated), 1,533 were successfully annotated. Pathway enrichment analysis showed that DM sites were associated with the phosphatidylinositol signaling system, inositol phosphate metabolism, cardiac muscle contraction, insulin resistance, insulin signaling, and the forkhead box O signaling pathway. Notably, the gene expression of insulin receptor substrate 1 (irs1) was significantly upregulated in the BADGE-treated group. In addition, the mRNA expression of steroidogenic enzymes, including steroidogenic acute regulatory protein, cytochrome P450 family 17 subfamily A member 1, and cytochrome P450 family 11 subfamily A member 1, was significantly increased in BADGE-treated group compared to the control group. These findings suggest that while BADGE may directly influence steroidogenesis, DNA methylation of insulin signaling-related molecules, including irs1, may also contribute to this process.

This study determined reference values of per- and polyfluoroalkyl substance (PFAS) exposure in the general Korean population. Serum samples from 2,993 adults in the fourth Korean National Environmental Health Survey (KoNEHS) (2018 -2020) were analyzed for five PFAS: perfluorooctanoic acids (PFOA), perfluorooctane sulfonic acid (PFOS), perfluorohexane sulfonic acid (PFHxS), perfluorodecanoic acid (PFDA), and perfluorononanoic acid (PFNA). The geometric means (GMs) and 95th percentile concentrations of serum PFOA were 6.43 and 16.55 μg/L, respectively; those of PFOS were 15.07 and 43.96 μg/L; 4.17 and 14.91 μg/L for PFHxS; 2.06 and 5.98 μg/L for PFNA; and 0.91 and 2.40 μg/L for PFDA. Higher serum PFAS concentrations were observed in older adults, men, former smokers, and frequent seafood consumers. Exposure levels also varied based on socioeconomic factors such as income and education. Additionally, participants residing in coastal areas exhibited higher serum PFAS concentrations, whereas higher PFHxS levels were observed in those living near industrial complexes. Higher concentrations of PFDA and PFNA were detected in participants consuming local drinking water (GMs, 3.29, 2.86 and 2.82 μg/L for local-based water, tap water and purifier or mineral water for PFNA; 1.43, 1.22 and 1.20 μg/L for PFDA; p-values were <0.05). These findings suggest that the Korean PFAS exposure level is relatively high, and may be related with residential and lifestyle characteristics.

Carcinogenicity testing has traditionally been conducted using long-term animal studies, as specified in OECD TG 451 and 453 guidelines. These studies typically use rats and last for two years, requiring significant time and resources. Consequently, there is a pressing need to develop alternative toxicity testing methods that can efficiently predict lung cancer risks caused by chronic chemical exposure. In this study, we designed integrated testing strategies (ITS) to assess carcinogenesis by focusing on cell survival, clonal growth, and metastasis using the BEAS-2B cell model. Non-tumorigenic BEAS-2B cells were exposed to Benzo(a)pyrene (B(a)P), Ethyl carbamate (EC), Epichlorohydrin (ECH), and chloromethyl methyl ether (CMME) for 4 months (#40 passages). After treatment, the BEAS-2B cells showed enhanced anchorage-dependent and anchorage-independent colony formation. Furthermore, cell migration and invasion assays using transwell chambers revealed a significant increase in these malignant characteristics in treated BEAS-2B cells. Collectively, our findings demonstrate that prolonged exposure of non-tumorigenic BEAS-2B cells to B(a)P, EC, ECH, and CMME can lead to the acquisition of metastatic potential and multiple malignant characteristics. These integrated testing strategies for assessing carcinogenic potential could serve as a valuable tool for identifying unknown carcinogens.

Microplastic pollution is increasingly recognized as a potential environmental stressor for microorganisms. This study aimed to explore how surface-functionalized polystyrene (PS) microplastics influence selected cellular-level responses in two Gram-negative bacteria, Escherichia coli and Acinetobacter sp., focusing on growth, viability, biofilm formation, and membrane-associated stress. Bacterial cultures were exposed to PS microplastics with three surface chemistries: non-functionalized PS, aminated PS (PS-NH2), and carboxylated PS (PS-COOH). Exposure to PS microplastic induced species- and surface chemistry-dependent alterations in bacterial responses. Compared to the control, non-functionalized PS reduced E. coli growth and viability to 74.8% and 61.3%, respectively, while Acinetobacter sp. showed reductions to 72.1% and 69.3% following PS exposure. Biofilm formation increased significantly to 143.2% in E. coli with PS, and to 207.2% and 190.7% in Acinetobacter sp. with PS and PS-COOH, respectively. Cytotoxicity assays revealed distinct stress patterns: in E. coli, PS exposure elevated MDA and LDH levels to 155.3% and 120.5% of control levels, respectively, while ROS levels remained near baseline (100.2%), indicating predominant membrane rupture and lipid peroxidation. In contrast, Acinetobacter sp. exhibited markedly elevated ROS (118.5% and 123.5%) and MDA (190.7% and 212.8%) levels upon exposure to PS and PS-COOH, while LDH remained comparable to the control, suggesting sublethal oxidative stress and membrane perturbation. These findings demonstrate that even chemically inert PS microplastics can trigger biologically significant responses in bacteria through surface-mediated mechanisms. The observed interspecies and inter-surface variability underscores the complexity of microplastic-microbe interactions and highlights the need for microbial-level assessments in evaluating the ecological risks of microplastic pollution.

This study evaluates the concentrations and associated health risks of heavy metals in dumpsite effluents across selected locations in Enugu State, Southeastern Nigeria. Surface and groundwater samples were collected in and around active municipal dumpsites and analyzed using Atomic Absorption Spectrophotometry (AAS). Detected metals included lead (Pb), iron (Fe), cadmium (Cd), chromium (Cr), copper (Cu), zinc (Zn), manganese (Mn), and nickel (Ni), with measured values compared to WHO and Nigerian drinking water standards. Elevated levels of Pb and Cd were observed, with Pb ranging from 1.5 to 5.1 μg/L and Cd from 2.1 to 4.8 μg/L. Fe and Mn concentrations reached 14.4 μg/L and 14.2 μg/L, respectively. Cr and Ni levels varied between 0.8-2.5 μg/L and 0.1-4.3 μg/L. Principal Component Analysis (PCA) and Pearson correlation revealed anthropogenic sources, notably leachate infiltration and waste decomposition, as primary contributors. Human health risks were assessed using USEPA models, estimating both ingestion and dermal exposure for adults and children. Hazard quotient (HQ) and hazard index (HI) values indicated significant non-carcinogenic risks, particularly for children exposed to Pb and Cd. Carcinogenic risk levels for Cr and Pb in several locations exceeded the acceptable threshold of 1.0 × 10-4. Communities depending on shallow wells and surface water near dumpsites showed the highest risk levels. The findings highlight the urgent need for improved waste management, regular water quality surveillance, and community health interventions. This work provides essential baseline data for environmental health governance and demonstrates the utility of chemometric tools for pollution source tracking and policy development.

The study aimed to analyse data from epizootological monitoring, microbiological and molecular genetic studies to assess the genetic biodiversity of Yersinia pestis (Y. pestis) strains, to determine the effectiveness of using individual methods and to develop the necessary algorithm for evaluating genetic methods and creating a biorepository of natural isolates of these pathogens. As a result, the biodiversity of Y. pestis strains isolated in natural plague foci of Kazakhstan was analysed using classical and modern methods (polymerase chain reaction, Multi Locus Variable Number Tandem Repeat Analysis, VITEK 2 Compact, MiniION Oxford Nanopore, MiSeq sequencer) of research and geographic information system (GIS) technology. Spatial and temporal characteristics of plague infection in the plague-enriched areas of the country were described. The study summarised the characteristics of phenotypic and molecular genetic properties of 1220 Y. pestis strains isolated from different sites in natural plague foci of the country during the period 2010-2023. As a result, 94.8% of Y. pestis strains were typical of these plague foci, and 5.2% of strains had altered properties in some respects. To obtain information on genetic diversity and their geographical distribution, 82 DNA samples of Y. pestis strains were studied. Three phylogenetic trees were constructed, GIS maps were compiled and a gene bank, a biorepository of molecular characteristics was created to obtain specific genetic characteristics of strains and a complete picture of the genetic parameters of the plague pathogen isolated from various sites in natural foci of Kazakhstan.

Bisphenol A (BPA), a common endocrine-disrupting chemical, can cause oxidative damage, apoptosis, and necroptosis in various organs. However, the underlying mechanisms for BPA-induced neurotoxicity were not properly reported. Here, we have evaluated the possible ameliorative roles of astaxanthin (ASX) against BPA-induced brain apoptosis/necroptosis in male rats. Forty male rats were equally grouped (30 days) into control, ASX (75 mg/kg), BPA (50 mg/kg), and BPA/ASX (50 mg/kg/BAP+75 mg/kg/ASX). The present findings demonstrated that ASX could mitigate the diminished acetylcholinesterase (AchE) activity and the increased dopamine, serotonin, and norepinephrine levels, besides anxiety behaviors that resulted from BPA intoxication. Furthermore, ASX significantly reduced BPA-induced brain oxidative injury by mitigating malondialdehyde (MDA), glutathione (GSH), glutathione transferase (GST), superoxide dismutase (SOD), and catalase (CAT) levels. Moreover, ASX could alleviate the histopathological changes promoted by BPA and repair the transcript levels of p53, BcL2, caspase9, FADD, RIPK1/3, MLKL along with Bax, and caspase3 immunoreactivity. In conclusion, ASX reserved brain injury-induced apoptosis, and necroptosis following exposure to BPA through p53/Bcl2/Bax/caspase9/capasase3 and RIPK1/FADD/RIPK3/MLKL pathways.

Mosquito coil fume is a cheap and commonly used method of reducing malaria incidence in third-world countries. The effects of fumes from pyrethroid and D-allethrin-based mosquito coils available in the Nigerian market were assessed in male Wistar rats. The rats were exposed to the insecticide fumes for 7, 14, and 21 days, while another group served as a control. The experiment consisted of seven randomly divided groups of six weight-matched animals per group. Plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), cholesterol, phospholipids, high-density lipoprotein cholesterol (HDL-C), and high-density lipoprotein phospholipid (HDL-P) were evaluated. Lung-, liver- and kidney-reduced glutathione (GSH), glutathione peroxide (GPx), glutathione-S-transferase (GST), superoxide dismutase (SOD), malondialdehyde/lipid peroxidation (MDA) and lipid hydroperoxide (LOOH) were also evaluated. Histoimmunochemistry was used to assess lung p53 and Bcl-2 expressions. Pyrethroid and D-allethrin-based fumes induced a significant (p < 0.05) increase in plasma AST, LDH, cholesterol, phospholipids, and HDL-P, with a reduction of HDL-C levels. The fumes significantly and differently dysregulated antioxidant enzymes. The inhalations of the fumes induced significant (p < 0.05) increases in kidney MDA and LOOH levels, liver MDA by pyrethroid fume, and lung MDA by D-allethrin only, but lung LOOH by inhalations of both fumes. The increased expression of lung p53 and repression of Bcl-2 by both fumes were duration-dependent. The fume-induced disproportionate tissue function biomarkers, redox status, and apoptosis-related proteins. These effects are a possible panoply of divergent modes by which exposure to coil fumes can be deleterious to human health.

This review expands upon prior work, which established that 112 out of 114 (98.2%) epidemiological articles published between 2011 and 2018 supported an association between exposure to elevated indoor mold/dampness and various single/multi-system health symptoms. Focusing on fatigue, our review rigorously examined these studies for statistically significant associations with mold and dampness exposure. We analyzed six articles involving a collective cohort from five cross-sectional studies with 40,933 participants, and a case-control study comprising 95 cases and 110 controls. We introduced a six-point ranking scale to assess the evidence, categorizing the studies from very low to very high support based on their methodological rigor and findings. Our evaluation revealed one study with very low support, one with moderate support, three with moderately high support, and one with very high support. Two studies were considered reference only. Our systematic review supports the assertion that fatigue is associated with exposure to indoor mold and dampness, highlighting the need for enhanced awareness and interventions in affected environments.

Toxicology has evolved from an observational science to predictive science, driven by advances in computational methods and large-scale data generation. Advances in computing power and the rapid accumulation of toxicological big data have opened new opportunities to modernize chemical risk assessment through artificial intelligence (AI). This study explores the current status of toxicity databases and key methodologies of AI such as machine learning, deep learning, and large language models. The study further examines representative case studies, which leverage AI-based toxicity prediction models in chemical prioritization and others. Despite the advancements, critical challenges remain, including the limited availability of high-quality, homogeneous datasets and the black-box nature of AI models, which hinder regulatory acceptance. To address these issues, this study emphasizes the need for explainable AI and the integration of the adverse outcome pathway framework to enhance model interpretability. By outlining future research directions and advocating for transparent, reproducible AI models, this study contributes to advancing regulatory science, chemical safety assessment, and the broader adoption of AI as new approach methodologies (NAMs) for next generation risk assessment (NGRA).