Toxics最新文献

Urban cyclists experience elevated traffic-related air pollutant (TRAP) exposures due to proximity to emissions and increased breathing rates during exercise. Conventional assessments rely on concentration summaries, which may misrepresent actual inhaled doses and misclassify individuals in health studies. Street-level concentrations exhibit high temporal variability, producing non-normal distributions that challenge conventional averaging approaches. This study compares concentration- and dose-based methods to characterize cyclist exposure during urban commuting. Fifty-seven healthy adults completed cycling trips on two 9-km routes (high- and low-traffic) using conventional or electrically assisted bicycles. Real-time monitoring measured black carbon, ultrafine particles, PM_2.5, and PM₁₀. Heart rate-derived breathing rates enabled individualized inhaled dose calculations using three temporal integration methods. Mean concentrations correlated strongly with time-integrated concentrations (r = 0.988-0.998). Simplified dose calculations closely approximated full temporal integration (r > 0.999), with median dose ratios of 0.99-1.01. However, correlations between mean concentrations and inhaled doses were weaker (r = 0.72-0.78). Between 29% and 50% of participants changed exposure quartiles when comparing concentration- and dose-based classifications, with the highest reclassification for ultrafine particles (46-50%). These findings demonstrate that physiological variability substantially influences exposure classification during active commuting, supporting the integration of inhaled dose metrics in cyclist exposure assessment and epidemiological studies.

(1) Background: The increasing environmental concentration of polystyrene nanoplastics (PS-NPs) may pose a risk of human exposure and health threats. Previous studies have demonstrated that exposure to PS-NPs poses a threat to neural synaptic plasticity, yet the underlying mechanisms remain unclear. (2) Methods: Hippocampal astrocytes and neurons were co-cultured, exposed to PS-NPs at concentrations of 10, 50, and 100 μg/mL, and cytotoxicity was assessed. We investigated PS-NP-induced impairment of synaptic plasticity by regulating the brain-derived neurotrophic factor (BDNF). (3) Results: Calmodulin-dependent protein kinase II (CaMKII) is a central molecular organizer of synaptic plasticity, learning, and memory, and its activity is intrinsically linked to intracellular calcium ion concentration. Our research indicates that PS-NPs may interfere with calcium ion signaling and CaMKIIα activity, thereby reducing CaMKIIα activity. This subsequently downregulates the expression of cAMP response element-binding protein (CREB), modulates BDNF expression, and impacts synaptic plasticity. (4) Conclusions: In summary, this study primarily focused on the effects of PS-NPs exposure on hippocampal synaptic plasticity.

The global pollinator decline is linked to intensive farming and the high use of plant protection products (PPPs), necessitating risk assessment and mitigation. This study investigates the potential negative impacts of agricultural practices on pollinator health, specifically focusing on the effects of PPPs used in viticulture on the honey bee, Apis mellifera, despite grapevines' lack of reliance on bee pollination. The beehives sampled were from two farms with vineyards under different management regimes: one transitioning from conventional to organic practices and an organic-biodynamic site with pollinator mitigation measures. Sampling was conducted during three phases, pre-, during, and post-PPP application, to evaluate biomarkers of neurotoxicity (AChE), detoxification enzymes (CaE, GST), metabolic stress (ALP), and immune markers (Lys, PO, proPO). Comparison between the organic-biodynamic farm and the transitioning one revealed a pattern suggesting significant neurotoxic effects in the transitioning farm characterised by a trend of decreased AChE activity during treatments and the subsequent induction of GST post exposure. Crucially, both PO and proPO were induced post treatment, but with a lower PO/proPO ratio compared to previous seasons, suggesting inefficient proPO activation and potentially weakened immune competence that could favour pathogen proliferation. Bee health appeared to deteriorate most at the transitioning farm post treatment, while the biodynamic site remained relatively stable; these differences are likely associated with legacy residues and drift, exacerbated by overwintering stress and summer heat. Given the specific environmental and management characteristics of these two farms, the results provide an indicative comparison of how different agronomic approaches may influence bee health. Moreover, these results support the multi-biomarker approach for detecting potential PPP impacts, suggesting that organic transitions and mitigation strategies could play a role in pollinator conservation.

Background: Fetal and postnatal development appears to be influenced in multiple ways by exposure to endocrine-disrupting chemicals (EDCs). We used hair biomonitoring to assess the burden of selected EDCs-bisphenol S (BPS), parabens (PBs), triclosan (TCS), and organochlorine pollutants-in pregnant women and their children at birth and at ten months of follow-up.

Methods: Hair samples were collected from pregnant women in Crete at delivery and from their infants shortly after birth and during follow-up. The assessment of EDCs' burden was performed using liquid and gas chromatography-mass spectrometry (LC-MS, GC-MS).

Results: Pregnant mothers had higher BPS levels than their infants at birth, whereas at 10 months' follow-up, infants exhibited markedly higher BPS concentrations than both their birth levels and the maternal levels, indicating increasing postnatal exposure. Infants at birth had higher TCS levels than their mothers; these levels then declined at follow-up. In contrast, mothers contained higher levels of MeP, EthP, BenP, and ButP levels than those of infants, either at birth or at ten months' follow-up. Organochlorine compounds were present at low but measurable levels. Significant pairwise comparisons were observed for some of the EDC analytes, mostly between mothers and their infants and between mothers and infants at follow-up.

Conclusions: These findings demonstrate constant, compound-specific, and time-dependent EDC burdens, highlighting the importance of prenatal EDC exposure in infants at birth and at ten months' follow-up compared to that of mothers.

Phthalates are a class of compounds commonly used as plasticizers in various industrial and consumer products. In line with the increasing environmental and biological exposure concerns regarding these compounds, this study investigated the dose-dependent effects of diethyl phthalate (DEP) on the liver in a subacute rat model. Diethyl phthalate (DEP) was given orally by gavage to female Wistar albino rats at doses of 100, 300, and 600 mg/kg body weight per day for 21 days in order to assess liver tissue and associated function test levels. Liver function was evaluated by analyzing serum biochemical data. Liver tissues were evaluated using histopathological staining (H&E and Masson's trichrome staining), immunohistochemical analysis of IL-1β and TGF-β, tissue ELISA for IL-6 and TNF-α, and comet assay to determine DNA damage. DEP exposure was found to cause significant, dose-dependent histopathological changes in liver tissue, including hepatocyte necrosis, cytoplasmic vacuolization, sinusoidal dilation, and vascular congestion. AST levels were significantly increased compared to the control group, while no significant changes were observed in other serum biochemical parameters. Compared to the control group, the expression of pro-inflammatory cytokines (IL-6 and TNF-α), IL-1β, and TGF-β was found to be elevated in the DEP-treated groups, and their levels increased with increasing exposure dose. DEP exposure also caused significant DNA damage in liver tissue. These findings indicate that despite an increase in AST levels observed in subacute DEP exposure, there were limited changes in serum biochemical parameters; serum liver enzymes alone may not fully reflect the extent of hepatic damage, and DEP can cause significant inflammatory, histopathological, and genotoxic effects in liver tissue.

Aluminum chloride (AlCl₃), a widely used inorganic polymeric coagulant in everyday products and industrial materials, has been associated with male reproductive toxicity, though its molecular mechanisms remain poorly understood. To investigate the complex molecular mechanisms underlying GC-1spg cells' responses to AlCl₃ exposure, transcriptome and small RNA (sRNA) sequencing analyses were performed. Transcriptome sequencing identified 1168 differentially expressed genes (DEGs), while sRNA sequencing detected 65 differentially expressed microRNAs (DEMs). An mRNA-miRNA regulatory network was established, and functional enrichment analysis showed that its target genes were significantly associated with multiple signaling pathways, particularly the p53 pathway. Further validation via Western blot and Hoechst 33342 staining assays confirmed that GC-1spg cells underwent apoptosis upon AlCl₃ exposure via the p53 signaling pathway. Among the identified DEMs, mmu-miR-503-5p was found to enhance GC-1spg cells' tolerance to AlCl₃-induced stress. Moreover, dual-luciferase reporter assays and RT-qPCR confirmed that mmu-miR-503-5p directly binds to the Islr gene, which plays a role in modulating GC-1spg cell tolerance to AlCl₃-induced stress. These findings provide critical insights into the molecular mechanisms governing GC-1spg cells' responses to AlCl₃ exposure.

Amidst rapid urbanization, fine particulate matter (PM_2.5) has emerged as a critical environmental challenge in China, posing substantial health risks due to its complex composition and diverse sources. This study provides a seasonally resolved analysis of PM_2.5 composition and multi-faceted toxicity in Hefei, a major Chinese manufacturing center. PM_2.5 samples collected across four seasons were chemically characterized for water-soluble ions, carbonaceous components, metals, and polycyclic aromatic hydrocarbons (PAHs) and derivatives. Their toxicological effects were evaluated through oxidative potential (OP), cytotoxicity, and reactive oxygen species (ROS) generation in the human bronchial epithelial cell line BEAS-2B. The results reveal significant seasonal variations in PM_2.5 concentration and composition. Winter exhibited the highest PM_2.5 levels (68.31 ± 17.12 μg/m³), with enrichment of secondary inorganic aerosols (SIAs), toxic metals (Pb, Cd, As), and high-molecular-weight PAHs. Spring showed elevated crustal elements (Al, Fe, Mn), while summer had the lowest pollutant concentrations. Toxicity assays reflected the following patterns: winter PM_2.5 demonstrated the highest OP (0.1423 ± 0.0368 nmol DTT/min/μg), strongest cytotoxicity (51.85% cell viability), and greatest ROS induction (2.28-fold increase). Statistical analyses identified distinct toxicity drivers: OP was associated with SIA (NO₃^-, NH₄⁺) and redox-active metals (Cu, Zn); cytotoxicity correlated with toxic metals and PAHs; whereas ROS showed weaker compositional correlations. This integrated "composition-toxicity" assessment reveals that the elevated health risk in winter stems from a synergistic mix of secondary aerosols and combustion-derived toxicants, urging a shift toward component-specific, risk-based air quality management strategies.

Environmental hazard-induced male infertility has become a major public health issue. The concealment and accumulation of environmental hazards, and their interactions with the endogenous immune network, have long been underappreciated. As the central organ for sperm maturation and motility acquisition, the epididymis plays a vital role in male fertility, and the homeostasis of the epididymal immune microenvironment (EIM) is essential. Nevertheless, a systematic synthesis of common environmental hazards and their impact on EIM, which can lead to male infertility, remains lacking. This review comprehensively summarizes the composition, functionality, and key characteristics of the EIM and underscores its critical role in preserving male reproductive health. We further evaluate and delineate the disruption of EIM homeostasis resulting from major categories of environmental exposures-including chemical, physical, biological, and behavioral hazards-and discuss their shared pathophysiological mechanisms. By integrating evidence linking environmental insults, EIM dysregulation, and male infertility, this work aims to identify pivotal molecular mechanisms from an immunological perspective. The findings provide a mechanistic foundation for the development of targeted interventions and preventive strategies against environmental hazard-induced male infertility.

Microplastics (MPs) are pervasive contaminants that enter the food chain and cause health issues. However, the size-dependent effects of MPs on lipid metabolism remain inadequately characterized. Using Caenorhabditis elegans (C. elegans), we investigated the size-dependent toxicity of polystyrene (PS)-MPs as model contaminants with sizes of 100 nm and 1 μm, respectively. We evaluated multiple phenotypic endpoints, including lifespan, growth (body length and width), locomotion (head thrashes and body bends), reproduction, and intestinal lipofuscin. The expression of representative lipid metabolism-related transcripts was validated by quantitative PCR. Untargeted metabolomics profiling detected 831 differential metabolites (451down-regulated and 380 up-regulated) across both PS particle exposure groups, with over-representation of lipid metabolic pathways. Integration of multi-omics (transcriptomics and metabolomics) highlighted acdh-1, ech-6, hach-1, and sur-5 as core lipid-metabolism genes; RNA interference confirmed that knockdown of these target genes abolished the size-dependent differences in fat accumulation induced by MPs. Notably, it revealed elevated linoleic acid and taurocholic acid, signature metabolites indicative of disrupted lipid turnover by our metabolomic profiling. Collectively, our findings demonstrate that exposure to PS-MPs disrupts lipid homeostasis in C. elegans by perturbing mitochondrial function and key metabolic pathways, which in turn impairs growth, development, feeding, and reproductive capacity. Critically, these disruptive effects exhibit a strong size dependency, with 100 nm PS particles inducing more severe perturbations than the 1 μm particles, and provide novel mechanistic insight into MP-induced metabolic abnormalities, underscoring the importance of considering particle size in assessing the environmental and health risks of MP contamination.

Unsymmetrical dimethylhydrazine (UDMH) serves as a high-performance liquid rocket propellant extensively utilized in the global aerospace industry, and its environmental release and leakage (particularly into soil systems) pose severe risks to ecological integrity and human health. As one of the few studies to quantitatively correlate soil physicochemical properties with UDMH degradation kinetics and pathway partitioning using controlled incubation experiments, this work aims to reveal the environmental hazards of UDMH in soil and provide a theoretical basis for subsequent remediation. The temporal degradation dynamics of UDMH in three comparative soil matrices (yellow-brown soil, red soil and black soil) were explored, correlations between soil physicochemical characteristics and UDMH degradation behavior were clarified, and UDMH degradation pathways were quantified. Headspace solid-phase microextraction (HS-SPME) was adopted as the pretreatment method, and gas chromatography-mass spectrometry (GC-MS) was used to identify UDMH and its transformation products (TPs) in soil incubation. From the GC-MS chromatogram, UDMH and its TPs-formaldehyde dimethylhydrazone (FDMH), acetaldehyde dimethylhydrazone (ADMH) and 1,1,4,4-tetramethyltetrazene (TMT)-were identified in the three soil matrices. UDMH underwent rapid degradation within the first 7 days of incubation, with degradation rates reaching 66.03%, 67.51% and 73.13% in yellow-brown soil (YS), red soil (RS) and black soil (BS), respectively. Degradation was most rapid in BS, followed by YS and RS. UDMH degraded completely and was undetectable within 30 days of soil incubation in the present study. Correlation analysis of soil physicochemical properties and UDMH degradation behavior revealed a significant influence of these edaphic properties on UDMH degradation dynamics across the tested soil matrices. The analysis of UDMH degradation pathways, including volatilization, photodegradation, microbiological degradation, and others (oxidation and self-degradation, etc.) demonstrated that other pathways (including catalytic transformation, induced transformation or unidentified biotic-abiotic coupled processes) acted as the dominant pathway governing its degradation (accounting for 68.75%). This study provides important insights and theoretical basis for unraveling the environmental fate of UDMH and remediating UDMH-contaminated soils.