Search Results (1,541)

Zinc oxide (ZnO) nanoparticles are semiconductor nanomaterials widely used in biomedical, environmental, and catalytic applications due to their unique physicochemical properties. However, their increasing environmental release has raised concerns regarding potential toxicity in aquatic ecosystems. In this study, pure ZnO, 1% Au-modified ZnO, and 5% Au-modified ZnO nanoparticles were synthesized via a reflux-assisted method to evaluate the effects of Au incorporation on morphology, crystallinity, optical behavior, surface chemistry, and ecotoxicological responses, using Artemia salina as a marine bioindicator. Structural characterization was performed using high-resolution transmission electron microscopy (HRTEM), electron diffraction, high-angle annular dark-field scanning transmission electron microscopy (HAADF-STEM), and energy-dispersive X ray spectroscopy (EDS) elemental mapping, while optical and surface analyses were conducted using UV–Vis and Fourier-transform infrared (FT-IR) spectroscopy. Although Au-rich domains were identified, the available data do not allow definitive determination of whether Au is incorporated into the ZnO lattice or present as surface-associated metallic Au. Increasing Au content promoted greater nanoparticle agglomeration and broader particle size distributions while preserving the hexagonal wurtzite ZnO crystalline structure. UV-Vis and FT-IR analyses demonstrated that Au modification altered the optical response and surface chemical environment of the nanoparticles. Toxicological evaluations revealed concentration- and time-dependent toxicity. Pure ZnO nanoparticles exhibited LC₅₀ values of 531.25 ppm after 24 h and 65.15 ppm after 48 h exposure. In contrast, 1% Au-modified ZnO nanoparticles showed reduced toxicity, whereas 5% Au-modified ZnO nanoparticles exhibited increased toxicity after prolonged exposure. These findings demonstrate that Au modification significantly influences the physicochemical properties and biological interactions of ZnO nanoparticles. Full article

Global plastic production has led to widespread contamination by micro- and nanoplastics, with polystyrene nanoplastics (PSNPs) increasingly being detected in human biological samples, including blood and cardiac tissue. Given the critical role of mitochondria in cardiac energy metabolism, this study investigated whether 100 nm PSNPs interact with mitochondria and affect mitochondrial function in H9c2 cardiomyoblasts. Cellular uptake and intracellular distribution were examined, followed by an evaluation of mitochondrial ultrastructure, intracellular and mitochondrial reactive oxygen species (ROS) production, mitochondrial membrane potential, mitochondrial dynamics and mitophagy-related gene expression, mitochondrial DNA copy number, and metabolic function. PSNPs were internalized but did not directly localize to mitochondria within 24 h. No significant cytotoxicity, increase in intracellular or mitochondrial ROS production, or alteration in basal metabolic activity was observed. However, PSNP exposure resulted in intracellular accumulation, an altered mitochondrial ultrastructure characterized by crista loosening and vacuole-like structural changes. These changes were accompanied by reduced mitochondrial membrane potential; the upregulation of mitochondrial dynamics-related genes, including optic atrophy 1 (Opa1) and dynamin-related protein 1 (Drp1); the suppression of PTEN-induced kinase 1 (PINK1)/Parkin RBR E3 ubiquitin protein ligase (Parkin)-mediated mitophagy-related genes; and decreased maximal respiratory capacity. Lactate production and the extracellular acidification rate remained unchanged, suggesting that compensatory glycolysis was not activated. These findings indicate that PSNP exposure induces early mitochondrial structural and functional alterations without substantial cell damage, suggesting a potential reduction in cardiac adaptive capacity under PSNP-induced stress conditions. Full article

Despite their high effectiveness in reducing material flammability, modern brominated flame retardants (BFRs) remain poorly understood with respect to the toxic substances they generate during combustion. BFRs such as 1,2-bis(pentabromodiphenyl)ethane (DBDPE) and tetrabromophthalate diol (PHT4-DIOL) have been introduced following the limitations on legacy brominated additives. However, their thermal decomposition pathways and toxic product emission profiles under real fire conditions remain poorly characterized. Exposure to elevated temperatures may promote the formation of halogenated toxicants and environmentally persistent compounds, raising concerns that extend beyond conventional fire-safety performance. The combustion behavior of DBDPE-, PHT4-DIOL-, and BFR-containing epoxy resins was investigated using a steady-state tube furnace designed to reproduce realistic fire scenarios. Controlled temperature and ventilation conditions were applied to simulate representative stages of fire. Combustion emissions were comprehensively characterized using Fourier transform infrared spectroscopy (FT-IR) to analyze asphyxiant and irritant gases and solid-phase microextraction gas chromatography–mass spectrometry (SPME-GC-MS) for volatile and semi-volatile organic compounds. The results presented that the incorporation of BFRs substantially altered combustion emission profiles, promoting the formation of brominated and mixed-halogenated species alongside toxic gaseous products. Significant differences in the composition and distribution of combustion byproducts were observed between non-modified and BFR-containing materials, indicating that the environmental and toxicological consequences of these additives cannot be adequately assessed solely through flammability-reduction metrics. These conclusions provide new knowledge of the environmental impacts of brominated flame retardants and highlight the importance of integrated fire-safety assessment strategies that simultaneously consider flame-inhibition efficiency, combustion toxicity, and environmental persistence. Full article

Pharmaceutical residues are increasingly detected in aquatic environments and are recognized as contaminants of emerging concern. This systematic literature review compiled and evaluated published concentrations of pharmaceutical residues in bottled water, tap water, and surface water in Portugal, applying risk quotient (RQ) and screening-level risk quotient (RQ_screen) approaches to evaluate potential human health risks and prioritize contaminants. Assessment based on the compiled literature data across age groups showed bottled and tap water posed low risk, while surface water presented the highest concern, with compounds spanning the full risk spectrum. Key contributors to potential human health risk included hormones (17-alpha-ethinylestradiol, 17-beta-estradiol, estrone), ramipril, betamethasone, citalopram, and amoxicillin. RQ_screen highlighted compounds relevant for ongoing monitoring even in treated waters, such as carbamazepine, diclofenac, salicylic acid, warfarin, fluoxetine, and erythromycin, due to their persistence and toxicological significance. Both RQ and RQ_screen indicated higher risk values for infants and children, reflecting lower body weight and higher water intake per unit mass, underscoring the need for age-specific evaluations. The RQ_screen method proved useful for contaminant prioritization, identifying substances relevant for monitoring despite low concentrations. Overall, this systematic review highlights pharmaceutical residues as an emerging public and environmental health concern in Portugal and emphasizes the importance of targeted monitoring and risk-based management within a One Health framework. Full article

Bisphenol A (BPA) is a common industrial chemical primarily used in the manufacture of plastics, and it has been found in more than 90% of people worldwide. As an endocrine disruptor, BPA can impair reproduction, development, immunity, metabolism, and cognition; it also disturbs immune balance and thus fosters chronic inflammation. A number of population-based studies have indicated a link between environmental BPA exposure and atopic dermatitis (AD). Nevertheless, the detailed molecular pathways connecting BPA to AD remain poorly understood. AD is the leading chronic recurrent inflammatory skin disorder, characterized by severe itching and repeated eczema-like lesions. Its prevalence is roughly 13% among children and 5% among adults, and its global incidence continues to rise, imposing heavy health and economic burdens on societies. To clarify whether and how BPA may promote or worsen AD, we carried out a comprehensive computational study that integrated network toxicology, transcriptomic data, machine learning, molecular docking, and molecular dynamics simulations. From the CTD, ChEMBL, and SwissTargetPrediction databases, we collected 5701 potential BPA targets; from GeneCards and OMIM, we obtained 3270 genes linked to AD. The overlap between these two gene sets gave a group of common candidate genes. Enrichment analyses using GO and KEGG showed that these common genes were significantly overrepresented in the PI3K-Akt signaling pathway, Th17 cell differentiation, and the JAK-STAT signaling pathway—all central to immune and inflammatory regulation. We then built a protein–protein interaction (PPI) network by submitting the common genes to the STRING database and employed Cytoscape to extract hub genes from that network. By integrating human AD transcriptomic profiles with the hub genes and applying two machine learning techniques (LASSO and SVM), we identified six core toxic targets of BPA in AD: TIGIT, JAK3, IL22, S100A8, CCL2, and FCER1G. These six targets fall into two main functional categories: immune dysregulation and inflammatory cell infiltration. Subsequent molecular docking and molecular dynamics simulation experiments confirmed that BPA binds well to all six targets and can form stable complexes with them. Collectively, our findings offer a preliminary experimental foundation for future investigations into the pathogenesis of BPA-induced AD and provide important molecular evidence for understanding how environment–gene interactions contribute to complex inflammatory skin diseases such as AD. Full article

Ochratoxin A (OTA) is a prevalent foodborne mycotoxin that has been increasingly recognized as a potential environmental contributor to neurodegenerative diseases. Despite extensive research, a systematic integration of how OTA replicates the specific pathological hallmarks of Alzheimer’s Disease (AD) is currently lacking. This study provides a comprehensive systematic review of the mechanistic evidence linking OTA exposure to AD-related pathways, utilizing the Adverse Outcome Pathway (AOP) framework to categorize complex toxicological data into biological key events (KEs). A systematic literature search was conducted across PubMed, Scopus, and Web of Science. A total of 24 peer-reviewed articles were selected for synthesis, comprising 14 in vitro studies and 10 in vivo investigations. The integrated evidence demonstrates that OTA exposure triggers a robust toxicological cascade that replicates several key mechanistic pathways associated with AD in experimental models. Early molecular triggers involve significant redox imbalance and mitochondrial bioenergetic failure, which serve as catalysts for sustained neuroinflammation and microglial activation. In vivo data, from multiple animal models, consistently show that these cellular dysfunctions culminate in structural damage. This systematic integration provides a clearer roadmap for future risk assessment and emphasizes the urgent need for refined regulatory guidelines to protect neurological health from chronic mycotoxin exposure. Full article

Microplastics (MPs) are an emerging environmental pollutant, and their contamination has emerged as a pressing global environmental concern. Developmental processes exhibit heightened sensitivity to environmental perturbations, and MP exposure can induce long-term adverse effects on organismal health by disrupting fundamental cellular processes. This review focuses on the toxicity and developmental toxicity risks of microplastics investigated using stem cell models. The core section comprehensively summarizes the primary mechanisms through which MP exposure interferes with the biological functions of stem cells, including the impairment of self-renewal capacity and lineage specification, as well as the inhibition of tissue-specific differentiation and organogenesis. Finally, the integration and application of modern toxicological methods in deepening research and improving risk assessment capabilities are synthesized. This review aims to provide a systematic perspective to understand the developmental hazards of MPs and look forward to future risk studies based on stem cell modeling, providing theoretical basis and fundamental support. Full article

Polycyclic aromatic hydrocarbons (PAHs) represent a major class of ubiquitous environmental pollutants, posing significant risks to ecosystems and human health due to their persistence, toxicity, and potential for bioaccumulation. This review provides a comprehensive synthesis of current scientific knowledge on PAHs, integrating insights from chemical kinetics, environmental fate, and toxicological mechanisms. The fundamental structural chemistry of PAHs and its direct influence on their physicochemical properties and environmental properties are discussed. The major anthropogenic and natural sources of PAHs are detailed, alongside the chemical kinetics behind their formation during incomplete combustion and their transformation in environmental media. Unlike previous reviews that address PAH sources, remediation, or health effects as separate topics, this review uniquely traces the mechanistic continuum from molecular formation kinetics through physicochemical partitioning and environmental transport to toxicological endpoints, providing a causally linked framework for understanding how structural properties ultimately determine biological outcomes. A central focus is placed on the environmental fate and transport of PAHs across atmospheric, aquatic, and terrestrial compartments, highlighting processes such as gas–particle partitioning, sediment accumulation, and long-range transport. The review further elucidates the complex toxicological pathways of PAHs, including metabolic activation to reactive intermediates, DNA adduct formation, oxidative stress, and their roles in carcinogenesis and other systemic health effects. The analysis reveals strong scientific consensus on the carcinogenic mechanism of parent PAHs via CYP450-mediated metabolic activation to diol-epoxide intermediates while identifying critical areas of uncertainty: the current regulatory framework based on 16 priority PAHs underestimates total carcinogenic risk by a factor of 2–5, mixture toxicology remains poorly characterized, and dose–response relationships for non-cancer endpoints (cardiovascular, neurodevelopmental, immunotoxic) lack the quantitative data needed for robust risk assessment. Finally, human exposure pathways and health risk characterization approaches are discussed, highlighting the need for cumulative, mixture-based assessment frameworks. Full article

Landfill tire fires are complex environmental disasters generating toxic pollutants with severe health risks. This study quantified emission dynamics and toxicological consequences of a large-scale tire fire in an urban ecosystem. A comprehensive source-to-receptor approach was applied, integrating Hybrid Single-Particle Lagrangian Integrated Trajectory (HYSPLIT) atmospheric dispersion modeling with comparison against air quality monitoring data. Soil samples collected from the fireground and surrounding urban allotment gardens were analyzed for tire-specific tracers (Zn) and 16 priority polycyclic aromatic hydrocarbons (PAHs). Human health risks were assessed using Incremental Lifetime Cancer Risk (ILCR), Toxic Equivalency Quotient (TEQ), and Mutagenic Equivalency Quotient (MEQ) metrics. Fire emissions were dominated by particulate matter (PM₁₀: 1.34 t) and PAHs (17.7 kg). Soil at the fire site showed severe contamination (Σ PAHs: 148.9 mg/kg), with benzo[a]pyrene as the primary carcinogen. The cumulative ILCR for children reached 9.7 × 10⁻⁴, exceeding the commonly used upper regulatory benchmark of 10⁻⁴. Dermal contact was identified as the dominant exposure pathway for pyrogenic PAHs. Elevated risk levels persisted at distal residential sites (ILCR: 10⁻⁵–10⁻⁴), indicating long-term environmental contamination Ecological risk quotients (RQ) exceeded unity for PAHs across all fire-impacted locations and for Zn and Cu in the immediate vicinity of the fire scene. These findings demonstrate that acute tire fire events can evolve into persistent terrestrial health hazards, highlighting the critical role of dermal exposure in PAH uptake and the need for long-term environmental monitoring and adaptive land-use management strategies to mitigate chronic health risks in urban populations. Full article

Salmonella remains one of the most critical zoonotic pathogens in the poultry sector, linked to animal disease, foodborne illness, and the global crisis of antimicrobial resistance (AMR). Poultry acts as a major reservoir, enabling Salmonella transmission from hatchery to retail products through horizontal, vertical, and environmental routes. Despite the use of biosecurity, vaccination, antibiotics, and chemical decontamination, effective and sustainable control across the poultry value chain remains difficult, particularly in the face of rising multidrug-resistant strains and growing consumer concerns over chemical residues. Bacteriophages (phages), viruses that selectively infect and lyse bacteria, have emerged as a promising biological alternative for Salmonella control. Although many studies have reported the effectiveness of phages against bacterial species, including Salmonella, in the poultry industry, reports on their full potential to combat antimicrobial-resistant Salmonella across the entire poultry value chain remain limited. Therefore, this review synthesizes current evidence on the application of phages throughout the poultry value chain, including on-farm interventions, processing plant decontamination, and food packaging and storage. Findings from the reviewed articles indicate over a 90% reduction in Salmonella spp. in poultry farms and post-harvest meat, along with lower mortality in phage-treated groups compared to untreated groups; however, these outcomes depend on several factors (e.g., phage strains, concentrations, application methods, and environmental conditions). Laboratory, pilot, and field studies consistently demonstrate that phage preparations, especially when formulated as cocktails or combined with complementary interventions, can achieve substantial reductions in Salmonella, including antibiotic-resistant serovars, in live birds, eggs, poultry environments, and meat products. Unlike antibiotics and chemical sanitizers, phages act with high specificity, preserving beneficial microbiota and maintaining the sensory and nutritional quality of poultry products. Their safety has been supported by toxicological and genomic assessments, and several phage-based products have obtained regulatory approval, including Generally Recognized as Safe (GRAS) status for food applications in the United States. By integrating efficacy, safety, regulatory, and practical deployment data, this review highlights bacteriophages as a scientifically validated and One Health–aligned tool capable of reducing Salmonella transmission from farm to fork across the poultry value chain, thereby laying the foundation for their future adoption in the poultry industry. Phage-based interventions offer a sustainable pathway to enhance food safety, limit antimicrobial resistance (AMR) dissemination, and strengthen consumer confidence in poultry products. However, the major limitation is the emergence of phage-resistant bacterial strains, as well as the potential involvement of some phages in the transfer of resistance and virulence genes, which could raise public concern. Nevertheless, the use of phage cocktails and whole-genome sequencing, involving tools such as ResFinder and virulence finder, can facilitate the selection of safe phages for application. Full article

The accumulation of polylactic acid nano-plastics (PLA-NPs) in saline–alkali soils poses a potential threat to crop growth; however, the underlying toxicological mechanisms remain poorly understood. We conducted a hydroponic experiment to investigate the effects of polylactic acid (PLA) NPs (100 and 500 mg L⁻¹) under conditions both in the presence (50 mmol L⁻¹ NaCl) and absence of salt stress on maize seed germination, seedling growth, physiological characteristics, and transcriptomic responses. The results showed that exposure to PLA-NPs, particularly at a high concentration (500 mg L⁻¹), significantly inhibited seed germination and seedling growth. Compared to the low concentration (100 mg L⁻¹) of PLA-NPs, the high concentrations (500 mg L⁻¹) reduced the germination percentage by 25.0% and fresh weight by 25.8% and increased root MDA (6.7%), SOD (30.0%), POD (6.3%), ASA (13.4%), and GSH (13.1%). Under the same concentration of the PLA, PLA + NaCl treatments exerted stronger inhibitory effects than PLA-NPs alone, with the seed germination percentage and fresh weight reduced by an average of 52.7% and 6.6%, respectively. Notably, the inhibitory effects and integrated biomarker response (IBR) index of the PLA 500 + NaCl treatment were the highest. The presence of PLA-NPs in roots was confirmed using confocal laser scanning microscopy. GO enrichment analysis showed that pathways related to nutrient reservoir activity, oxidoreductase activity, hydrogen peroxide catabolic process, and hydrogen peroxide metabolic process were enriched under PLA-NP and PLA + NaCl treatments. KEGG analysis further indicated enrichment in phenylpropanoid biosynthesis, ABC transporters, and alpha-linolenic acid metabolism. The PLA-NP and PLA + NaCl treatments upregulated genes associated with oxidoreductase activity (Zm00001eb238800, Zm00001eb128620, and Zm00001eb020790). These findings suggest that synergistic toxicity of PLA-NPs and salinity stress in maize is primarily driven by the internalization of PLA-NPs and Na⁺ within maize roots, which negatively impacts maize seed germination and seedling growth by disrupting redox homeostasis and metabolic balance, thereby forcing plants to reallocate resources from growth toward oxidative stress defense. This study provides critical insights into the environmental risks of biodegradable nano-plastics in saline–alkali soil environments. Full article

Earthworms possess a highly developed innate immune system based on the coordinated activity of coelomocytes and humoral factors present in the coelomic fluid. These immune components play a central role in host defence against pathogens, maintenance of physiological homeostasis, and adaptation to environmental stressors. Coelomocytes exhibit remarkable functional and morphological diversity, including participation in phagocytosis, encapsulation, extracellular trap formation, cytotoxic responses, wound healing, and regulation of oxidative and osmotic stress. In addition, coelomic fluid contains numerous biologically active molecules, such as lysenin, coelomic cytolytic factor 1, perforin, serine proteases, lysozyme, antimicrobial peptides, and pattern recognition receptors, which contribute to cellular and humoral immune responses. Recent studies have demonstrated that earthworm coelomocytes are highly sensitive to environmental pollutants, including heavy metals, pesticides, nanomaterials, and microplastics, highlighting their importance in ecotoxicological research and soil biomonitoring. Furthermore, antifungal, antimicrobial, anti-inflammatory, antipyretic, and cytotoxic activities associated with coelomocytes and coelomic fluid suggest promising applications in agriculture, biotechnology, and pharmaceutical research. This review summarises current knowledge regarding the classification, characteristics, immune functions, toxicological responses, and applied significance of earthworm coelomocytes and coelomic fluid, with particular emphasis on their role in environmental monitoring and potential biomedical applications. Full article

Microplastics (MPs) have emerged as persistent environmental contaminants due to their persistence, widespread distribution, and potential risks to the environment and human health. This review focuses on the sources of MPs, their potential environmental risks, and human impacts, as documented in the recent literature from 2020 to 2026. Recent studies focusing on pathways, environmental weathering, and toxicity were evaluated and synthesized into the analysis. Previous studies have demonstrated that microplastics are transported across and between environmental compartments. Environmental degradation, driven by ultraviolet radiation, mechanical fragmentation, and oxidation, can alter microplastics’ surface characteristics, which may affect microplastic mobility, reactivity, and the solid-state adsorption of contaminants. Human exposure occurs primarily through ingestion and inhalation, with dermal and occupational exposure also contributing under certain conditions. Emerging evidence from in vitro, animal, and human tissue studies suggests that smaller particles, particularly nanoplastics, may contribute to oxidative stress, inflammation, and cellular injury; however, important uncertainties remain regarding environmentally realistic exposure levels, long-term health outcomes, and the extrapolation of experimental findings to real-world human health risk. Overall, the current literature highlights the need for standardized methodologies, improved integration of environmental monitoring and exposure assessment, and stronger evidence to support risk assessment and policy development. Full article

Per- and polyfluoroalkyl substances (PFASs) present a critical challenge to global public health and environmental integrity due to the exceptional stability of the carbon–fluorine (C–F) bond. This review synthesizes current knowledge on PFAS physicochemical properties, exposure pathways, and toxicological outcomes, while evaluating global regulatory efficacy. A central problem addressed in this review is the widening discrepancy between rigid, yet deeply fragmented, international regulatory frameworks and the increasingly complex, non-linear epidemiological data regarding PFAS health risks. While historical paradigms focused heavily on direct carcinogenicity, recent high-resolution data reveal significant heterogeneity and methodological inconsistencies in cancer links. Instead, robust evidence points to severe systemic toxicities—including hepatotoxicity, immunotoxicity, and maternal–fetal disruptions—frequently driven by mixture co-exposures and sex-specific metabolic dimorphisms. Furthermore, the industrial transition to short-chain substitutes has inadvertently compounded the crisis due to their high environmental mobility and resistance to conventional water treatment. By critically evaluating these toxicological and regulatory contradictions, this review demonstrates that current substance-by-substance legislative models fail to mitigate real-world pollution trends. Ultimately, we emphasize the urgent need to transition to holistic mixture modeling, implement unified class-based global regulations, and accelerate advanced destructive remediation technologies to mineralize the resilient C–F bond. Full article

Bismuth (Bi) is increasingly used as a substitute for lead (Pb) in several industrial applications, raising concerns about its potential environmental impact. However, the effects of Bi on early plant development and nutrient homeostasis remain poorly understood. In this study, toxicological and transcriptional responses were investigated in garden cress (Lepidium sativum L.) exposed in vitro to increasing Bi concentrations (0, 30, 60, 121, and 242 mg L⁻¹) under dark and light conditions. In darkness, Bi progressively reduced the germination index and root growth. In contrast, under light conditions, low Bi concentrations stimulated seedling growth, whereas this effect decreased at higher doses. Gene expression analyses showed that Bi differentially affected key genes involved in iron (Fe) uptake and homeostasis, including LsIRT1 and LsFRO2, which displayed divergent expression patterns in dark- and light-grown seedlings. Micro-X-ray fluorescence (µ-XRF) analysis revealed distinct Fe and Bi accumulation profiles under dark and light conditions. Moreover, LsPCS1 expression, a marker of heavy metal detoxification responses, was strongly induced in the shoots of light-grown seedlings, where Bi accumulation was detected. Taken together, these results show that Bi inhibits early seedling development in darkness by impairing Fe uptake and homeostasis, whereas light promotes tolerance to Bi by enhancing these processes. Full article