Procymidone (PCM), a fungicide widely used to control gray mold and Sclerotinia rot in agricultural production, is known for its hepatotoxic and endocrine-disrupting effects; however, its potential myotoxicity remains largely unexplored. To evaluate muscle toxicity and underlying mechanisms, zebrafish embryos were exposed to PCM (1, 1.25, 1.5 mg/L) until 72 h post-fertilization (hpf). Transgenic models revealed that PCM exposure was associated with myopathic phenotypes, including muscle atrophy and aberrant muscle cell fusion. Transcriptomic analysis identified extensive dysregulation of genes involved in muscle development, differentiation, fusion, and motor function. PCM exposure was accompanied by increased reactive oxygen species (ROS) levels and elevated apoptosis in affected tissues. Gene Set Enrichment Analysis (GSEA) suggested enrichment of Toll-like receptor and apoptosis signaling pathways, which have been associated with muscle atrophy. Integrative analyses suggested that PCM-induced muscular toxicity is associated with coordinated alterations in TNF-α/NF-κB signaling and oxidative stress. Notably, co-treatment with an NF-κB inhibitor partially alleviated PCM-induced muscle atrophy. Together, these findings indicate that PCM exposure induces muscular toxicity in developing zebrafish, which is associated with oxidative stress and inflammation-related apoptotic responses. This study provides mechanistic insight into procymidone-associated skeletal muscle toxicity and contributes to the understanding of its potential impacts on aquatic organisms.
Per- and polyfluoroalkyl substances (PFAS) are organofluorine chemicals with widespread global occurrence. Despite over 4700 known compounds, only a small fraction is regularly monitored, leading to potential underestimation of PFAS pollution, particularly perfluoroalkyl acid (PFAA) precursors. To address this analytical challenge, this study employed a comprehensive analytical approach, combining target analysis, oxidative conversion of PFAS precursors, and extractable organofluorine (EOF) mass balance analysis on surface sediment samples collected from the coastal South China Sea (n = 18) and eight major Pearl River outlets (n = 8) in 2021 and 2020, respectively, to investigate unidentified PFAA precursors and EOF levels for the first time. Target analysis revealed a ten-fold increase of mean PFAS concentrations in the estuary compared to a previous study on samples collected in 2018. PFAA precursors, including N-ethyl perfluorooctane sulfonamide phosphate diesters, perfluorooctane sulfonamidoacetic acids, and polyfluoroalkyl phosphate diesters, were more frequently detected at estuarine outlets. C4-C6 short-chain perfluoroalkyl carboxylic acids and perfluorooctanoic acid emerged as the predominant oxidation products, with a different composition between estuarine outlet and coastal sediment samples. Multiple regions with occurrence of C6 electrochemical fluorination precursors were identified, and 6:2 fluorotelomer sulfonic acid was detected as an unexpected oxidation product near an airport, suggesting the potential contribution from aqueous film-forming foams. A substantial fraction of extractable organofluorine was not explained by targeted PFAS analysis, indicating the presence of unidentified fluorinated compounds in the investigated coastal sediments.
Background: Exposure to fine particulate matter (PM2.5) is associated with increased arterial stiffness, yet the constituent-specific effects and mechanisms remain unclear.
Objectives: To assess the effects of short-term exposure to PM2.5 and its constituents on arterial stiffness and explore the potential mediation through inflammation and lipid pathways.
Methods: We conducted a longitudinal panel study in 32 healthy adults in Shanghai, China, with five follow-up visits between December 2020 and November 2021. Concentration of PM2.5 and its constituents (elemental carbon [EC], organic carbon [OC], ammonium [NH4+], nitrate [NO3-], and sulfate [SO42-]) were collected 24 h before each follow-up. Arterial stiffness indicators and biomarkers of inflammation and lipid metabolism were assessed. Linear mixed-effect models were applied to examine exposure-outcomes associations. Mediation analysis was employed to evaluate the potential mediating effects on the association of PM2.5 constituents and arterial stiffness.
Results: Short-term exposure to PM2.5 and its constituents was significantly associated with increased arterial stiffness. EC and OC demonstrated stronger effects. For example, each interquartile increase in EC (1.2 μg/m3) was associated with increments of 10.62 %, 2.13 %, and 13.75 % in augmentation index (AI), AI normalized to the heart rate of 75 beats per minute, and augmentation pressure, respectively. These effects were robust after adjusting for total PM2.5. Interleukin-6 could mediate the effects of EC and OC on elevating arterial stiffness, with mediation proportions of 32.02 % and 26.90 %, respectively.
Conclusion: Our findings highlight that short-term exposure to PM2.5 carbonaceous constituents may promote arterial stiffness, which may occur through inflammatory pathways, providing mechanistic insights into PM2.5-related cardiovascular effects.
Fungal species are known to shape the elemental composition of their fruiting bodies, but the extent to which broader taxonomic ranks show consistent patterns remains uncertain. We analyzed 19 ectomycorrhizal mushroom species belonging to four genera (Amanita, Cortinarius, Lactarius, and Russula) and the soils beneath their fruiting bodies (174 paired samples) collected in a mixed forest in central-western Poland. Concentration of 18 elements, grouped as major essential elements (MEEs), essential trace elements (ETEs), and trace elements with detrimental health effects (TEWDHE), were determined in both matrices. Species within the same genus often shared partially similar multielement profiles, yet each species retained a distinct accumulation pattern. On average, Amanita species contained the highest levels of MEEs and many ETEs, whereas some Lactarius species were particularly enriched in As, Cd, and Hg. Multielement heatmaps indicated that genus-associated patterns emerged against a background of considerable within-genus and between-site variability driven by soil properties and mycorrhizal partners. For the four (out of six) edible species assessed (A. fulva, A. rubescens, C. caperatus, and L.delicious), estimated daily intake and target hazard quotient values for As and Cd approached or exceeded unity, indicating potential non-carcinogenic health risk under frequent consumption scenarios. Overall, our results show that genus can be a useful proxy for predicting elemental accumulation in forest mushrooms, but the observed patterns should be interpreted as associations shaped by shared traits and the local environments rather than deterministic taxonomic effects. Broader, multi-regional datasets are still needed to test how general these patterns are.
The health risks associated with exposure to polystyrene nanoplastics (PS-NPs) and bisphenol A (BPA) are a recognized global concern, yet their individual and combined toxic effects on the mammalian thyroid remain poorly defined. This integrated in vivo and in vitro study demonstrates that in mice, four-week exposure to PS-NPs alone induced dose-dependent thyroid hormone disruption and structural damage, while co-exposure with BPA resulted in clearly exacerbated injury, indicating an additive toxic interaction. This additive effect was characterized by markedly worsened histopathology and a distinct shift in the thyroid transcriptome from pathways such as cytoplasmic translation toward extracellular matrix (ECM) organization and collagen fibril assembly. Mechanistically, although each pollutant downregulated core circadian genes (Per3 and Dbp), co-exposure did not produce further suppression. Instead, in vivo analysis revealed that PS-NPs enhanced BPA's inhibitory effect on specific ECM-related genes (Col1a2, Col5a1 and Col5a2). Notably, this transcriptional synergy was not observed in human thyroid cells in vitro, where co-exposure failed to amplify BPA's inhibitory action. These findings indicate that the additive thyroid toxicity is not driven by amplification of shared intracellular stress pathways in thyrocytes, but more likely stems from complex tissue-level interactions, with dysregulation of the extracellular matrix playing a central role. Overall, our results reveal an additive effect between PS-NPs and BPA and underscore the environmental risks posed by the co-occurrence of emerging pollutants and nanoparticles.
Hillringsberg, a former sawmill site in Sweden, is severely contaminated with polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs). This study collected site-specific data to assess the human health risks associated with locally produced food. To evaluate potential exposure, samples of salmon, perch, cow's milk, cattle, and sheep were collected near the site and analyzed for PCDD/Fs. The findings reveal that the most frequently detected congeners in the food samples corresponded with the most abundant congeners in the soil, underscoring the impact of contaminated sites on PCDD/F concentrations in locally produced food. Particularly concerning is the level of PCDD/Fs in sheep meat, which was found to be 11 times higher than the Tolerable Weekly Intake (TWI) for adults and 26 times higher for children. Comparing food samples from the sawmill site to those from the National Swedish Control Programme revealed that all food samples from Hillringsberg exhibited some level of contamination, even though the concentrations of PCDD/Fs remained below the European Maximum Limits (MLs) and Action Limits (ALs). The concentrations and patterns of contaminants in nearly all samples, particularly those from sheep, cattle and perch, were influenced by local contamination from the historical use of pentachlorophenol (PCP) at the old sawmill site. PCA showed that sheep and soil samples from the storage area exhibited strong covariance. Perch and sediment samples from the sawmill pond were also grouped together. These findings highlight the necessity of evaluating food production activities near contaminated sites during the initial stages of site-specific risk assessments. Ensuring food safety in these areas is crucial, and if necessary, relocating grazing lands, fish farms, and similar operations can help mitigate health risks associated with contaminated food.

