Chemosphere

Pollution of aquatic environments poses an increasingly severe threat to ecosystems worldwide, and understanding its molecular consequences for aquatic organisms requires extensive research and the development of advanced analytical tools. Phosphoproteomics can be particularly valuable for this purpose, as shifts in phosphorylation states can serve as early molecular indicators of toxic exposure. The cladoceran Daphnia is a keystone species in aquatic ecosystems, linking lower and higher trophic levels, and is therefore widely used as a model organism in ecotoxicology to study biological consequences of pollution. Here, we present a simple and effective strategy to analyse the phosphoproteome of Daphnia magna, a commonly used Daphnia species in ecotoxicology. Following TiO2-based phosphopeptide enrichment and LC-MS/MS analysis, we identified a comprehensive dataset of 3,532 phosphorylation sites across 1,329 phosphoproteins. These proteins were especially involved in signaling pathways and cellular structure and the vast majority have not yet been demonstrated in other Daphnia species. In conclusion, our results demonstrate that a straightforward phosphoproteomic LC-MS/MS workflow in D. magna can serve as a powerful tool for investigating adverse molecular effects caused by anthropogenic pollution, such as microplastics or pharmaceuticals. Statement of significanceThe dataset presented here demonstrates the feasibility of a simple yet effective strategy to perform phosphoprotemics in Daphnia magna, and it will be particularly valuable for future ecotoxicoproteomics research using this model organism.

Aroma perception during food consumption results from the combined effects of food composition, oral processing (such as chewing and saliva action), the release and transport of volatile compounds toward the olfactory epithelium, followed by cognitive integration in the brain. Recent advances in real-time analytical techniques, particularly Proton Transfer Reaction-Time-of-Flight Mass Spectrometry (PTR-ToF-MS), enable in vivo monitoring of aroma release with high temporal resolution and have become widely used for analyzing the composition of exhaled air. However, the interpretation of aroma release kinetics remains challenging due to substantial intra- and inter-individual variability caused by differences in physiology, anatomy, oral behavior, and respiratory patterns. In this context, the present study was designed to quantify aroma release associated with different food oral processing (FOP) mechanisms, such as chewing and swallowing, using simple model matrices containing a single aroma compound, and to document inter- and intra-individual variability among subjects. Real-time PTR-MS measurements were combined with self-reported oral events and simultaneous respiratory monitoring to analyze aroma release from aqueous solutions and gummy discs flavored with isoamyl acetate. The results showed that inter-individual variability was higher than intra-individual variability and allowed its quantification in aroma release. Significant differences in aroma release kinetics were observed depending on FOP protocols. The importance of considering swallowing events when analyzing aroma release data was also highlighted.

The ubiquitously occurring food contaminants altenuene (ALT) and tentoxin (TEN) are recognized as emerging Alternaria mycotoxins, yet substantial data gaps remain when it comes to their toxicological behavior and toxicokinetic characteristics. This study aimed to compare and generate quantitative data on their hepatic metabolism and to obtain semi-quantitative insights into their metabolite profiles. To this end, primary rat and human hepatocytes were incubated with 10 {micro}M ALT or TEN over multiple time points up to 4 h. Both substrate depletion and metabolite identification revealed pronounced interspecies differences. The extent of ALT metabolism was significant, with an 88% and 57% decrease in rat and human hepatocytes after 4 h, respectively. In contrast, TEN showed extensive biotransformation in rats (67%) but only modest turnover in humans (27%) over the same period. Hepatocellular clearances were consistently higher for ALT than TEN, with hepatic extraction ratios indicating intermediate extraction for ALT and low extraction for TEN. High-resolution mass spectrometry combined with targeted analysis of selected metabolites annotated phase II conjugation as the predominant metabolic pathway for ALT and phase I oxidative metabolism for TEN, including mono- and double-metabolized species for the latter. Overall, these results provide a comprehensive characterization of ALT- and TEN-metabolism in hepatocytes, offering a foundation for future studies on their toxicological relevance and impact on human health.

The foodborne mycotoxins alternariol (AOH) and alternariol monomethyl ether (AME) have been associated with several adverse effects, including cytotoxicity, genotoxicity, endocrine disruption, and immunomodulation. As these endpoints are typically observed in vitro at micromolar concentrations, the question arises whether such levels are attainable in exposed humans. To address this data gap in chemical risk assessment, a physiologically based kinetic (PBK) model was developed to predict internal exposure doses to AOH and AME in humans. As input parameters, kinetic constants for hepatic glucuronidation were obtained in vitro by incubating Sprague Dawley rat and human liver S9 fractions with 0.5-50 M AOH and 0.5-20 M AME, demonstrating rapid biotransformation in both species. Intestinal absorption of AME and physicochemical parameters were estimated using quantitative structure-activity relationship (QSAR) models. Sensitivity analysis identified parameters describing hepatic glucuronidation and gastrointestinal uptake as among the most influential, confirming the importance of their reliable estimation. The PBK model was evaluated against available rodent toxicokinetic data and subsequently extrapolated to humans. Ultimately, the currently available exposure estimates published by EFSA in 2016 were applied to predict target tissue concentrations, which were compared to points of departure (PoDs) for relevant toxicological endpoints. Even in the most susceptible group of male toddlers, predicted internal concentrations (10-4 M range) were approximately four orders of magnitude below the respective PoDs. Consequently, under the applied exposure assumptions and considering the compounds as isolated chemicals, AOH and AME are not expected to reach systemic or tissue concentrations associated with the investigated effects.

Widespread exposure to multiple pesticides might potentially represent a genotoxic risk to humans. However the effects of these mixtures are largely unknown. Genotoxicity is a key characteristic of carcinogens, and its assessment represents an important component of the overall safety assessment of pesticides. In the present study, in vitro micronucleus test on intestinal Caco-2 human cells was performed according to OECD TG 487 in order to ascertain the genotoxicity of ten commonly used pesticides (dose range 0-100 mg L-1), tested as individual pesticides or mixtures. Significant dose-related increases in micronuclei were observed for exposures to lambda-cyhalothrin, tebuconazole, glyphosate, deltamethrin, fluopyram and the synergist piperonyl butoxide. Significant increases of micronuclei were also observed at different doses for cypermethrin, acetamiprid and cyprodinil, however these increases were not dose-dependent. Imazalil genotoxicity could not be analyzed due to confounding of high cytotoxicity even at low doses. Results show that the co-formulant piperonyl butoxide was genotoxic to human cell lines at all tested doses. Moreover, glyphosate, acetamiprid and fluopyram showed genotoxic effects at concentrations of 0.01-1.0 mg L-1. Although previously reported to be not genotoxic cyprodinil and deltamethrin were observed to be genotoxic to Caco-2 cells. A combination of 3 prioritzided pesticides (acetamiprid, glyphosate, tebuconazole) showed genotoxic effects even at the lowest dose. A combination of 8 prioritized pesticides showed genotoxicity at the highest dose. No synergistic interactions in micronuclei formation were evident in either the mixture of 3 or 8 prioritized pesticides. This study provides important information on the genotoxicity of different widely used pesticides and confirms the validity of a component-based approach in genotoxicity assessment of pesticide mixtures. This study was performed as part of the EU SPRINT (Sustainable Plant Protection Transition: A Global Health Approach) project.

Bone is a highly durable biological tissue widely used in forensic, archaeological, and anthropological investigations; however, efficient protein recovery and understanding of protein stability over time remain major challenges in skeletal proteomics. Here, we systematically evaluated three bone protein extraction workflows and integrated them with data-independent acquisition (DIA) mass spectrometry to assess proteome coverage, reproducibility, and temporal protein dynamics under environmentally exposed conditions. Comparative analysis demonstrated that extraction strategy is a primary determinant of detectable proteome composition. EDTA-based demineralization followed by SDS extraction provided the deepest proteome coverage and highest reproducibility, whereas guanidine hydrochloride extraction preferentially enriched collagen and extracellular matrix proteins. In contrast, acid-based extraction yielded limited protein recovery. Temporal profiling of bone samples collected at 10 and 45 days post-exposure revealed two distinct protein classes. A temporally stable module, enriched in collagens and extracellular matrix proteins including COL1A2, COL5A2, BGN, SPARCL1, and NID2, exhibited minimal abundance change, indicating resistance to environmental degradation. In contrast, temporally dynamic proteins, enriched in mitochondrial, metabolic, and intracellular pathways such as ACO2, OGDH, PDHA1, ATP5PO, and PFKM, showed marked decline over time. These findings support a two-compartment model of bone protein preservation in which matrix-embedded proteins are preferentially retained while exposed intracellular proteins undergo progressive degradation. Collectively, this study establishes an integrated framework linking extraction methodology with temporal proteome stability and identifies candidate markers for skeletal preservation assessment and temporal biomarker development in forensic and archaeological applications.

Lead is a toxic metal ubiquitous in our environment. While dramatic reductions in lead sources have paralleled equivalent decreases in lead-poisoning rates, chronic lead exposure remains a critical public health concern. Childhood lead exposure (at its lowest levels) is liked to changes in cognitive development but less is known about lead's effects on children's brain structure, especially as a result of in utero exposure. We measured prenatal and early-postnatal lead exposure in shed deciduous teeth of 448 9- and 10-year-old children (from 20 United States cities) and linked those lead levels to childhood brain structure, cognition/behavior, and neighborhood- and family-level socioeconomic characteristics. Here we show negative associations between tooth-lead levels and the thickness of the brain's cortex, particularly in regions linked to language processing. With increasing tooth-lead levels, children of lower-income (versus higher-income) families showed steeper declines in receptive vocabulary. Caregiver-reported behavioral problems exhibited similar associations. With in utero exposure linked to adverse neurodevelopmental outcomes (well before lead exposure and its risks are evaluated by healthcare professionals), prenatal screening of maternal lead levels/exposure, coupled with recommended strategies to reduce its placental transmission, may help reduce lead's effects on future generations.

Silver has been used as a biocide for centuries, mostly in health-oriented applications. However, as a biocide, silver is toxic not only to its intended targets, mainly bacteria and fungi, but also to all living cells. Because of this toxicity, it is desirable to use forms of silver that maximize the required biocidal activity while minimizing the amount of silver that will be released in the environment at the end of life of the product. Silver nano objects are a good compromise for such requirements. The high surface to volume ratio allows for good reactivity and thus good biocidal activity, while the small amount of silver present in nano objects allows for a limited environmental release at the product end of life. In this work, we tested three types of silver nano objects. The first type, polyvinylpyrrolidone-coated silver nanoparticles (nAg-PVP) were used as a control nanoparticle, as this type of nanoparticle is now widespread. We also manufactured and tested maltodextrin-coated silver nanoparticles (nAg-MD) and micrometric (20 {micro}m in two dimensions and a few nanometers in the third one) silver flakes ({micro}AgSF). For these three silver nano objects, we investigated the biocidal activity by stringent tests using both Staphylococcus aureus and Escherichia coli as target bacteria. In addition, we investigated toxicity on mammalian macrophages or keratinocytes cell lines, as well as on an insect hemocyte cell line. Our results showed that the two innovative silver nano objects (nAg-MD and even more {micro}AgSF), showed both a better bactericidal activity and a lesser toxicity than the reference nAg-PVP nanoparticles. In addition, we also checked that beyond toxicity, the silver nano objects did not induce an inflammatory reaction, making them safer to use.

Pesticides are ubiquitous in agroecosystems and pose substantial risks to non-target organisms. Traditional ecotoxicological assessments focus on survival, reproduction, or overt behavior, yet these endpoints may fail to detect subtle, molecular-level stress. Here, we investigated the effects of sublethal deltamethrin exposure on the head proteome of field-collected European earwig (Forficula auricularia) females, sampled at two life stages (pre-oviposition and post-family life) to account for physiological context. Our results reveal that deltamethrin induces a robust proteomic response shared across developmental stages, including the regulation of key detoxification enzymes (NADPH- cytochrome P450 reductase, arginine kinase). In parallel, stage-specific responses were observed, involving proteins related to metabolism, stress response, and cellular organization. Strikingly, these molecular perturbations occurred without detectable changes in reproductive traits, highlighting a disconnect between cellular stress and organismal phenotypes. Several uncharacterized proteins were consistently regulated, representing promising targets for future studies on pesticide adaptation and potential detoxification pathways. Overall, these findings suggest that classical phenotypic assays may underestimate sublethal pesticide effects, and that proteomic profiling provides a sensitive framework to uncover underlying molecular responses. By integrating natural variability, realistic exposure, and reproductive physiology, our study emphasizes the need for molecular approaches in environmental risk assessment and offers a new perspective on the subtle, cryptic effects of agrochemicals.

Until now, there has been no animal-free alternative method for predicting chronic inflammation and delivering the associated dose responses, the timing of onset, and the duration of inflammation, as required by regulatory agencies. We present the results of pre-validation of an in-vitro-learned digital twin (InFiniteLungDT) capable of predicting chronic neutrophilic lung inflammation for regulatory use. The method is based on measuring the dynamics of early biological effects in vitro induced by respirable materials or their mixtures, without the need to know their intrinsic properties. We constructed the digital twin(s) for each of the material, for which we have in vivo exposure data. The instillation data set, comprising 49 different nanomaterials, was used as the primary anchor to calibrate the model. Inhalation data set, comprising 7 different nanomaterials, compliant with OECD TG 412, was used to show the general applicability of the method across species and for different exposure scenaria. In total, about 3094 single mouse exposures and 364 rat exposures (and approx. 775/225 non-exposed mouse/rat controls) were used to predict concentration-dependent time-evolved neutrophil influx into the lung. The accuracy (predictive capacity) of LOAEL determination is 93% for instillation and 84% for inhalation exposure. Taking into account the time-to-deliver-result being less than 1 week, this proves that the effect of inhaled material from acute to chronic conditions can be assessed orders of magnitude faster and cheaper than in a reference animal study.

Endocrine disrupting chemicals (EDCs) are ubiquitous environmental contaminants capable of dysregulating the production of thyroid hormones. Traditional thyroid toxicological assays rely on 2D cell cultures and animal models, both of which fail to accurately recapitulate human thyroid physiology and provide limited mechanistic insight into EDC toxicity. To overcome these limitations, we report a novel thyroid-on-chip platform integrating mouse embryonic stem cell-derived thyroid organoids with advanced organ-on-chip (OoC) technology and downstream multi-omics analysis. The platform leverages a reversibly-sealed microphysiological flow battery (MFB) to allow scale up of dynamic organoid culture and controlled chemical exposure while reducing operational complexity. Upon EDC exposure, transcriptomic and proteomic analysis revealed new molecular signatures of thyroid disruption across four different EDC classes, even at very low EDC concentrations (1nM), validating the capacity of this system to mechanistically dissect EDC-induced responses. This represents an integrated platform consists of an advanced physiologically relevant assay framework for next-generation endocrine toxicity testing, bridging the gap between in vitro screening and in vivo thyroid physiology.

The early developmental environment plays a critical role in the etiology of cardiovascular diseases (CVDs), but underlying molecular mechanisms are poorly understood. Exposure to per and polyfluoroalkyl substances (PFAS) are linked to various CVDs, but effects of developmental PFAS exposures on the human heart remain unclear. Using human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CM), the objective of this study was to investigate the effects of PFAS exposure during cardiac differentiation on gene expression and function of cardiomyocytes. We exposed two hiPSC lines (one male and one female donor) to perfluorooctanoic acid (PFOA), a common and ubiquitous PFAS (0.05, 0.5, 5, 50, 100, 150, 200 M), followed by assessment of cellular number and pluripotency marker expression. PFOA exposure for 72 hours had no significant effects on hiPSC pluripotency, and modest inhibition of proliferation was observed only at the highest concentration. hiPSCs were then differentiated into ventricular cardiomyocytes in the continued presence or absence of PFOA (0, 0.5, 5, 50 M) using an established small molecules protocol. Optical mapping studies using voltage and calcium-sensitive dyes revealed dose and cell line-specific effects of PFOA on cardiomyocyte voltage and calcium dynamics that were still present 10 days after cessation of exposure. Patch clamping studies demonstrated small but significant reductions in repolarizing IKr currents with 5{micro}M PFOA exposure in cardiomyocytes from both donors. Using RNA-seq, we found that exposure to PFOA led to significant changes in transcriptional pathways related to lipids and lipoproteins in the female hiPSC-CM. In the male hiPSC-CM, we observed significant effects on developmental pathways and calcium homeostasis. Thus, we found that environmentally relevant PFOA exposure during cardiomyocyte differentiation affects the electrophysiological properties and transcriptome of hiPSC-CM even after cessation of exposure, with effects that differ by donor cell line. These findings provide direct experimental evidence that transient developmental exposure to PFOA can durably reprogram human cardiomyocyte function, supporting a developmental origin of PFAS-associated cardiovascular risk. Impact StatementThese studies demonstrate that exposure to environmentally relevant levels of PFOA during the differentiation of hiPSCs into cardiomyocytes alters cardiac gene expression and function, with effects that persist beyond cessation of exposure.

Fluorinated chemicals are increasingly prevalent in pharmaceuticals and agrochemicals, yet their influence on the human gut microbiome and the potential for microbial biotransformation to alter therapeutic and toxicological profiles remain poorly understood. Here, we investigated the bidirectional relationship between 15 structurally diverse fluorinated chemicals and the gut microbiota by using an ex vivo high-throughput fermentation system. Screening revealed that flutamide, fluazinam, and pretomanid were consistently biotransformed across the donor microbiomes, while other compounds showed substantial inter-individual variability in degradation. Furthermore, exposure to fluorinated chemicals induced compound-specific shifts in microbial diversity and community composition, demonstrating their capacity to alter gut microbial ecology. Using a computational workflow combining in silico biotransformation predictions with untargeted LC-MS/MS analysis, we identified nitroreduction as the primary gut microbial transformation across all three compounds. Single-strain experiments confirmed that the nitroreduction of flutamide to flu-6, previously attributed only to hepatic metabolism, is a widespread capacity among gut bacterial strains. Finally, in vitro cytotoxicity assays and in silico modelling further revealed flu-6 to be a less hepatotoxic derivative than the parent compound, suggesting a potential detoxifying role for the gut microbiota. Together, these findings establish an integrated ex vivo, in vitro, and in silico approach for assessing the bidirectional interactions between fluorinated chemicals and the gut microbiome.

Railway catenary sparking generates airborne ultrafine particles (UFPs) that may pose health risks due to their metallic composition and ability to penetrate deep into the alveolar region of the lungs. Copper, widely used in wires and pantographs, is a major component of these emissions, making copper-rich particles common in railway environments such as subways. However, exposure levels and health impacts remain poorly characterized, and localized hotspots may represent an underrecognized risk in densely populated areas. This study investigated the toxicity of copper UFPs under realistic dosimetry and deposition conditions. Copper UFPs were generated using a spark discharge generator and applied to two in vitro lung models: a 3D co-culture of Calu-3 epithelial cells, THP-1-derived macrophages, and EA.hy926 endothelial cells, and a monoculture of A549 alveolar epithelial cells. Cells were exposed at the air-liquid interface (ALI) using an automated platform to mimic inhalation exposure and UFPs deposition. Copper deposition ranged from 6.5 to 41 ng/cm2, within occupationally relevant levels. A549 cells showed cytotoxic responses consistent with previous studies, whereas the 3D co-culture model revealed broader adverse effects, including inflammation, impaired epithelial barrier integrity, oxidative stress, and early DNA damage. Inflammatory activation also differed between models: A549 cells mainly exhibited transcriptional responses, while the 3D model showed significant secretion of IL-6 and IL-8, associated with interferon signaling. These findings highlight the potential health risks of copper UFPs from railway systems and emphasize the need for improved characterization of UFP exposure in environmental and occupational railway settings.

Phthalates are pervasive endocrine-disrupting chemicals widely used in consumer products. The wide use of many phthalates results in chronic human exposure to complex mixtures rather than single compounds. Despite extensive studies on individual compounds, the combined effects of phthalate metabolites on oogenesis remain poorly understood. Here, we developed a precise microinjection-based single-oocyte toxicological assay to examine the impact of a defined phthalate metabolite mixture on meiotic progression. Phthalate mixture exposure markedly impaired oocyte maturation, as most oocytes failed to extrude the first polar body. Mechanistic analyses revealed severe meiotic defects, including disrupted spindle morphology, chromosome misalignment, disorganized actin cytoskeleton, and impaired mitochondrial function, accompanied by excessive reactive oxygen species (ROS) accumulation and DNA damage. Single-cell transcriptomic profiling further identified differentially expressed genes enriched in biological processes related to exocytosis, secretory pathway regulation, and cytoskeletal organization, as well as in MAPK, JAK-STAT, cGMP-PKG, and GnRH signaling pathways that are essential for follicular development and oocyte maturation. Together, these findings demonstrate that combined phthalate exposure directly compromises female gamete quality and underscore the importance of evaluating mixture effects when assessing risks to womens reproductive health.

Neonatal meconium provides a non-invasive matrix for assessing prenatal or near-birth exposure to environmental contaminants. Although microplastics and metals have each been reported in human biological samples, integrated assessments of concurrent particle and metal exposure in meconium remain scarce, particularly in South Asia. In this cross-sectional biomonitoring study, meconium from 30 Cesarean-delivered neonates born in Dhaka, Bangladesh, was analyzed for microplastic occurrence, morphology, and polymer composition using stereomicroscopy, scanning electron microscopy, and Raman spectroscopy, and for fifteen metals using inductively coupled plasma mass spectrometry. Maternal breast milk from a subset of lactating mothers was analyzed as a complementary maternal exposure context. Microplastics were detected in all analyzable meconium samples (n=28), with a median burden of 149 particles/g wet weight, dominated by polyethylene terephthalate fragments and nylon fibers. All fifteen measured metals were also detected in all analyzable meconium samples, with median Pb and Cr concentrations of 1.18 and 3.92 ug/g dry weight, respectively. No microplastic-metal associations remained significant after multiple-testing correction, suggesting partly distinct exposure or accumulation pathways. Here, we show that neonatal meconium captures concurrent microplastic and metal exposure in an urban South Asian birth cohort. This study provides one of the first integrated meconium-based assessments of concurrent microplastic and metal exposure from the region and highlights meconium as a practical matrix for early-life biomonitoring.

The gut microbiome plays a pivotal role in overall host health, yet the extent at which diet-derived microbial metabolites affect neurodevelopment and inflammation remains unclear. Here, we employed the robogut bioreactor system seeded with fecal samples from two healthy pediatric donors to generate microbial communities exposed to four different diets: low fiber Western (LFW), high fiber Western (HFW), Mediterranean (MED), and Yanomami (YAN), as well as three fiber supplements: fruit and vegetable fiber (FVF), cereal fiber (CRF), and resistant starch fiber (RSF). Metabolites produced by these microbial communities were isolated and applied to germ-free zebrafish (Danio rerio) embryos to assess their effects on neurodevelopment and inflammatory gene expression under basal and stress-induced conditions. Despite minimal changes in microbial composition across diets and fiber sources, significant differences in short-chain fatty acid concentrations were observed. Metabolite treatments had limited effects on the expression of neural and inflammatory genes under basal conditions. Under stress conditions, metabolites from any diet mitigated stress-induced bdnf expression, suggesting a possible modulatory role of microbial metabolites on stress responses. Overall, these findings highlight the resilience of microbial communities to dietary changes and underscore the importance of microbial metabolite output and its donor-specific nature in influencing host neurodevelopment and immune responses.

Organohalide-respiring bacteria (OHRB), such as Dehalobacter, play key roles in the bioremediation of anoxic environments contaminated with chlorinated aromatic compounds. These obligate anaerobes rely on syntrophic interactions to obtain essential resources--hydrogen, acetate, and corrinoid cofactors--from acetogens and fermenters. However, the metabolic interactions enabling complete reductive dehalogenation of compounds like 1,2,4-trichlorobenzene (1,2,4-TCB) to benzene remain incompletely understood. In this study, we asked: (1) What are the key microbial taxa and their functional roles within a Dehalobacter-containing anaerobic microbial community detoxifying chlorinated benzenes? (2) How do syntrophic interactions enable complete dehalogenation of 1,2,4-TCB to benzene under anaerobic conditions? (3) Can genome-resolved metagenomics and genome-scale metabolic modeling elucidate the metabolic dependencies supporting organohalide respiration in complex consortia? To address these questions, we cultivated microbial communities in batch reactors using methanol as electron donor and either 1,2,4-TCB or monochlorobenzene (MCB) as electron acceptor. In active MCB-fed cultures, benzene increased from 0 to 62.3{micro}mol per bottle while MCB decreased from 88.3 to 22.0{micro}mol per bottle over 120 days, with this pattern repeating across multiple substrate additions. Using genome-resolved metagenomics to identify dominant taxa and select 12 high-quality metagenome-assembled genomes (MAGs) for modeling, we reconstructed genome-scale metabolic models (GEMs) to identify candidate metabolic interactions and predict syntrophic dependencies that may support organohalide respiration in these consortia. Community flux sampling predicted that methanol, H2, acetate, and CO2 formed the dominant exchange backbone of the modeled community, while also indicating competition for shared electron donors between the two Dehalobacter populations. Model-guided minimal-community analysis further identified a narrow dechlorinating core in which all feasible minimal consortia retained a Dehalobacter member together with Methanothrix. These results provide a modeling-informed framework for hypothesis generation and future experimental validation of anaerobic consortia relevant to bioremediation.

Ethylene oxide is a widely used industrial chemical,yet evidence linking its exposure to Parkinsons disease remains limited.Using data from participants in the United States,we examined whether exposure to ethylene oxide is associated with Parkinson's disease.This cross-sectional study included 8,430 adults from the National Health and Nutrition Examination Survey (NHANES) collected between 2013 and 2020.Information on demographic characteristics,socioeconomic factors,lifestyle behaviors,body mass index,sedentary time and major chronic conditions was analyzed. Levels of hemoglobin ethylene oxide adducts,a biomarker of ethylene oxide exposure, were evaluated in relation to Parkinsons disease using statistical modeling approaches.After accounting for potential confounding factors,higher levels of ethylene oxide exposure were associated with an increased likelihood of Parkinson's disease.The association followed a positive and linear pattern.These findings provide new population-based evidence suggesting that ethylene oxide may be linked to Parkinsons disease and highlight the need for further studies to confirm causality and to better understand the biological mechanisms involved.

Microplastics (MP) are ubiquitous environmental contaminants with diverse physicochemical characteristics. Many studies have shown that size, shape, and polymer type are responsible for their toxicity, but this also seems to differ among MP from the same plastic type. One parameter likely contributing to these differences is plastic chemicals, a broad class of compounds intentionally or unintentionally added to plastics during their production and manufacturing. However, knowledge on the composition of plastic chemicals and their effects remains scarce. Therefore, to elucidate the chemical aspect of MP toxicity, we exposed Daphnia magna individuals to MP (PET, PBS, and PDLLA), cellulose, extracted particles (eMP), and methanol-based extracts of these particles for 10 days. Chemicals within such extracts were analyzed via GC-MS. This study was conducted with reduced food availability to investigate plastic effects in an environmentally relevant scenario. The introduction of a high-food control suggests that a more realistic feeding regime might exacerbate the plastic effects of the selected treatments. Our results indicated that, depending on the polymer type, plastic chemicals determine MP toxicity, which varies according to the endpoint investigated (i.e., body length, reproduction, levels of ROS and LPO). Body length, in particular, was significantly impaired by PET and PDLLA extracts, whereas reproduction was affected by most treatments. The investigated biochemical parameters (ROS and LPO) were not affected by the exposure. These results suggest that MP toxicity strongly depends on their chemical composition, whereas adverse effects due to physical properties are present independently of chemical composition across all MP types. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=80 SRC="FIGDIR/small/724551v1_ufig1.gif" ALT="Figure 1"> View larger version (23K): org.highwire.dtl.DTLVardef@3c2d4forg.highwire.dtl.DTLVardef@c2ccd7org.highwire.dtl.DTLVardef@116721dorg.highwire.dtl.DTLVardef@9df888_HPS_FORMAT_FIGEXP M_FIG C_FIG