Environmental Pollution

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.

One of the effects of the intensified agricultural activities involves environmental pollution by pesticides, which are bound to get into the soil and ultimately into the water sources through leaching. The recurrent exposure of soil microbiota to these poisonous substances facilitates the process of adaptive resistance and catabolic functions. In the current research, bacterial cultures taken in Karuppur and Salem pesticide-contaminated agricultural soils were filtered on their capability to decompose organophosphate pesticides. Two strong isolates, which were referred to as Bacillus sp. and Micrococcus sp. had a great level of tolerance and degradation capacity. Significant biomolecular changes in these isolates were observed after long-term exposure (three months) to organophosphate pesticides. A protein estimation showed a strong rise in the overall total protein content indicating the activation of stress-related and degradative enzymes. Genomic DNA damage was identified by DNA ladder assay, which is a genotoxic stress caused by pesticides. Thus, plasmid profiling also revealed a rise of copy number and change of the size of plasmids, implying potential adaption through plasmids and greater degradation potential. This evidence indicates that long-term exposure to pesticides leads to microbial adaptation in terms of physiological and genetic changes to allow survival in adverse environments. The isolates identified have great potential to be used in bioremediation strategies that will be used in detoxifying the soils that have been contaminated with organophosphate.

Fine particulate matter (PM2.5) was found to be associated with elevated blood lipids, but fewer studies have examined the associations with specific constituents of PM2.5. We studied the associations between exposure to annual PM2.5 and its 14 constituents, and repeated blood lipid measurements among general responders enrolled in the World Trade Center Health Program between 2003 and 2019 (n = 44,876). We used generalized additive mixed effect models to investigate the single-pollutant associations with repeated measures of blood total cholesterol (TC), high and low-density lipoprotein (HDL-C and LDL-C) levels. We then used linear generalized weighted quantile sum regression with a random intercept for participant ID to account for the clustering of repeated measures and evaluate the combined associations with the component mixture. A decile increase in the mixture of 14 PM2.5 chemical components was associated with 0.375 mg/dL increase in TC levels (95% confidence Interval (CI): 0.174-0.577) and 0.302 mg/dL increase in LDL-C (95% CI: 0.063, 0.540). Lead, organic carbon, and iron were major drivers of both associations. Component-specific models also show higher TC and LDL levels associated with interquartile range increases in organic carbon (0.472, 95% CI [0.027, 0.918] and 0.648 95% CI [0.136, 1.160]) and iron exposure (1.081, 95% CI [0.630, 1.532] and 0.748, 95% CI [0.318, 1.178]). In conclusion, we found PM2.5 exposure to be associated with elevated lipid levels. The associations differed by PM2.5 composition, highlighting organic carbon, lead, and iron and major drivers. These findings are highly significant for a population exposed to extreme air pollution event and susceptible to lipid alterations that might trigger cardiovascular events.

Perfluorooctanesulfonic acid (PFOS) is a persistent environmental contaminant widely detected in human serum and follicular fluid and has been associated with reduced implantation rates and female fertility. However, its direct effects on mammalian oocyte maturation remain poorly understood. Here, we developed a microinjection-based single-oocyte toxicological assay to directly evaluate how physiologically relevant PFOS concentrations affect mouse oocyte maturation and early embryonic development. Microinjection of PFOS at follicular-fluid level (5.6 nM) and occupational exposure level (60 nM) significantly reduced germinal vesicle breakdown (GVBD) and polar body extrusion (PBE) rates compared with water-injected controls. Notably, all tested concentrations (2.4 nM serum level, 5.6 nM, and 60 nM) induced abnormal polar-body formation, disrupted meiotic spindle morphology, and increased the proportion of unhealthy oocytes. PFOS exposure also significantly elevated intracellular reactive oxygen species (ROS) levels and mitochondrial membrane potential at 5.6 nM, indicating oxidative stress and mitochondrial dysfunction. Cytological analyses revealed chromosome misalignment and widened metaphase I plates, suggesting chromosome missegregation and subsequent prometaphase II arrest with defective polar bodies. Single-cell RNA sequencing of PFOS-treated oocytes exhibiting abnormal small polar bodies identified distinct transcriptional signatures, including dysregulation of genes involved in mRNA processing, chromosome segregation, mitochondrial function, and cell division. Functionally, these oocytes failed to progress beyond the 2-cell stage following in vitro fertilization, indicating loss of developmental competence. Collectively, these findings demonstrate that PFOS directly disrupts meiotic progression through spindle defects, oxidative stress, and transcriptional dysregulation, ultimately compromising oocyte quality even at environmentally relevant exposure levels. Environmental ImplicationPFOS is a persistent environmental contaminant widely detected in human serum and follicular fluid. Our findings demonstrate that PFOS at physiologically relevant levels can impair oocyte maturation, disrupt meiotic chromosome segregation, and compromise early embryonic development. By using a single-oocyte toxicological assay, we reveal that even low-dose PFOS exposure can induce oxidative stress and transcriptional dysregulation. These results highlight the potential reproductive risks of chronic PFOS exposure and underscore the importance of stricter environmental monitoring and regulation to protect female reproductive health and fertility. This novel assay also has the potential to redefine safety thresholds for other environmental toxicants.

Exposure to higher levels of ambient air pollution during pregnancy has been linked to multiple adverse pregnancy outcomes. However, studies on acute exposures and reduced gestation length have reported inconsistent findings. This project aims to examine the acute association between ambient air pollution and preterm (28-36 gestational weeks) or early-term (37-38 gestational weeks) births. Daily concentrations of 12 air pollutants, based on bias-corrected numerical model outputs, were linked to vital records of singleton live preterm and early-term births from 2005-2017 in California, Florida, Georgia, Kansas, Nevada, New Jersey, North Carolina (2005-2015), and Oregon. Under a time-stratified case-crossover design, odds ratios (OR) were estimated via conditional logistic regression with adjustment for risks among ongoing pregnancies, meteorology, time trends and federal holidays. We estimated cumulative associations up to a 6-day lag using distributed lag models. Risk estimates per interquartile range (IQR) increase in exposure were pooled across states using inverse-variance weighting. Our study included 1,085,162 preterm and 3,901,185 early-term births. We observed positive associations between 0-2 day cumulate exposure to several air pollutants and early-term births, including NO2 (OR: 1.0023, 95% CI:1.0010, 1.0037 per 7.1 g/m3 increase), PM2.5 (OR=1.0022, 95% CI: 1.006, 1.0038 per 4.6 g/m3 increase), PM2.5 organic carbon (OR= 1.0026, 95% CI: 1.0013, 1.0039 per 1.7 g/m3 increase) and PM2.5 elemental carbon (OR=1.0025, 95% CI: 1.0014, 1.0035 per 0.26 g/m3 increase). Associations with preterm birth were mostly null. In conclusion, we found positive associations between short-term air pollution exposure, including PM and major PM2.5 components, and risks of early-term birth.

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.

Concerns raised by ubiquitate plastic contamination are urging to develop alternative materials. In the recent years, bio-sourced polymers also coined as "bioplastics" have been proposed to mitigate plastic pollution while meeting industrial and commercial expectations. Like petro-sourced plastics, they are expected to break-down in the environment into fragments down to sub-micron size. However, only scarce data are available on the impacts of such biosourced nanoplastics once released into the environment. This study examines the effects on aquatic species of model nanoplastics made from several bio-sourced polymers (Bio-NPs) that are either already on market (PHA, PLA, PA11) or still under development (NIPU, PCAR). We exposed three species of micro-algae (at 10, 100, and 1000 {micro}g/L, for 24 and 48 hours, and one week) to test the effects of Bio-NPs on algal growth. We also exposed freshwater bivalves C. fluminea (at 1, 10 and 100 {micro}g/L, for one week) to test the filtration activity and gene expressions in response to Bio-NPs exposure. All five Bio-NPs tested generated growth inhibitions in at least one of the three algae tested. PLA and PA11 were the most deleterious ones for algal growth among the five tested Bio-NPs. The highest growth inhibitions were observed on the fresh water species D. subspicatus. Each Bio-NP tested resulted in significant decreases of the filtration rates of C. fluminea. PHA impaired filtration at the lowest concentrations tested (1 {micro}g/L), whereas PCAR, PA11 and NIPU led to significant effects only at higher concentrations (10 and 100 {micro}g/L). The results from gene expressions in C. fluminea showed strong inductions of all gene functions tested for all the five bio-NPs tested. These Bio-NPs triggered endocytosis and detoxification mechanisms. They impaired the mitochondrial metabolism and triggered oxidative stress and immune responses. PA11, NIPU and PHA exposures resulted in the strongest gene regulations. The present study brings brand new findings about a kind of nanoplastics that may be released into the environment in a near future as the use of bioplastics is growing fast. It will help better understanding the impacts of such fragmented bioplastic NPs on aquatic species.

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

Quaternary ammonium compounds (QACs) are high production volume biocidal compounds increasingly scrutinized for their potential to promote antimicrobial resistance spread. This study compared the release of QACs, QAC resistance indicator genes (qacE/qacE{Delta}1), and QAC tolerant bacteria from livestock and human waste streams into the environment. Five livestock farms with on-farm biogas plants (BGPs), a rural and an urban municipal wastewater treatment plant (WWTP) were studied in parallel. In WWTPs, <1% of incoming QACs were discharged with treated wastewater but 10-20% were transferred to sewage sludge. QAC concentrations in sewage sludge far exceeded those in raw and digested manure. The qacE/qacE{Delta}1 genes were detected in all samples with a higher relative abundance in solid than liquid samples. Relative abundances of QAC tolerant fast growing heterotrophic bacteria cultivated under high nutrient conditions at 37{degrees}C were higher in human than livestock waste streams. Providencia and Pseudomonas dominated the cultivated QAC tolerant bacteria in both systems but showed higher QAC tolerance when originating from human waste streams. Additionally, Enterobacteriaceae with higher QAC tolerance were cultivated from human waste streams. Most QAC tolerant strains carried antibiotic resistances without strong system differences. Only few strains carried the qacE/qacE{Delta}1 gene indicating that other mechanisms must be responsible for the increased QAC tolerance. In conclusion, QACs, qacE/qacE{Delta}1, and viable QAC tolerant bacteria including potential pathogenic bacteria were released from livestock and human waste streams into the environment with highest abundances in a post-pandemic sewage sludge sample. Highlights- QACs most abundant in human waste streams, especially biosolids - Higher relative abundance of QAC tolerant bacteria in human waste streams - Pseudomonas and Providencia dominated QAC tolerant bacteria in both waste streams - Enterobacteriaceae with higher QAC tolerance abundant in human waste streams - Most QAC tolerant strains carried additional antibiotic resistances Environmental implicationMunicipal wastewater treatment plants (WWTPs) and livestock farms are hotspots for antimicrobial resistance (AMR) propagation. We compared the simultaneous occurrence of quaternary ammonium compounds (QACs), resistance genes (RGs), QAC-tolerant bacteria, and their multidrug-resistance status in livestock and human waste streams. QACs, indicators of QAC tolerance and AMR occurred in both systems but were higher in WWTPs, especially sewage sludge. Our findings highlight the need for prudent disinfectant use and enhanced waste treatments to reduce the risks of spreading micropollutants, pathogens, and AMR via organic fertilizers or treated wastewater recycled in circular agricultural practice.

Metals and per- and polyfluoroalkyl substances (PFAS) represent a significant environmental concern, yet their association with epigenetic age acceleration (EAA) remain largely understudied in marine mammals. Here, associations between EAA in common dolphins (Delphinus delphis) and life history (sex and sexual maturity), trace metals, and PFAS were investigated. EAA was calculated as the residual in the regression of epigenetic age vs chronological age, hence providing a direct measure of the deviation of the epigenetic age of an organism (positive or negative) by comparison with expectation, given their actual chronological age. Sixteen trace elements were quantified in hepatic and renal tissues (n = 53). In addition, 28 PFAS were quantified in hepatic tissue (n = 58). Associations between EAA and explanatory variables were assessed using regression-based and multivariate modelling approaches (linear models and canonical analysis of principal coordinates). No effect of sex was observed, although sexual maturity did significantly increase EAA. Exposure to metals was significantly associated with EAA, explaining 55.4% of the variation, with hepatic metals (Se, Zn, Cu, Al, Mn) driving this relationship. Although EAA was not significantly related to the total PFAS exposure overall, a subset of PFAS variables (PFBA, PFDA, PFHxS-B, PFNA) showed significant association with EAA after adjusting for sex and sexual maturity. Together, these subsets of metal and PFAS variables, in addition to the selenium-to-mercury (Se:Hg) molar ratio, explained 66.7% of the variation in EAA. Our results identify sexual maturity and specific contaminant mixtures as key potential drivers of EAA in common dolphins, highlighting the possible use of EAA as a biomarker of environmental and physiological stress in marine mammals.

Antibiotic residues exceeding selective concentrations for antibiotic-resistant bacteria have been detected in various environments, including manure, wastewater, and effluents from wastewater treatment plants. When these residues come into contact with soils, for instance, due to wastewater irrigation or fertilization with manure, they interact with soil constituents. Soil colloids (1-1000 nm), such as montmorillonite, have been observed to adsorb pharmaceuticals, including antibiotics. We investigated the effect of colloids on the bioavailability of ciprofloxacin and found, that added to bacterial growth medium, montmorillonite reduces, but does not completely prevent, the growth-inhibitory effect of the antibiotic. The bacteria were able to grow at up to roughly double the concentration of ciprofloxacin in the presence of montmorillonite. We show that the incomplete deactivation of ciprofloxacin was most probably caused by medium components that decreased the adsorption of ciprofloxacin to montmorillonite. We conclude that a selective potential of this highly active antibiotic in contaminated soils, which also contain nutrients enabling bacterial growth, cannot be ruled out. Environmental implicationAntibiotics such as ciprofloxacin are frequently detected in water bodies and soils due to wastewater irrigation or manure application. These residues raise concerns about environmental toxicity and antibiotic resistance. This study demonstrates that montmorillonite, a common clay mineral in soils, significantly reduces the antimicrobial efficacy of environmental ciprofloxacin concentrations by sorption. The findings reveal a natural attenuation mechanism that may influence the environmental fate and bioavailability of antibiotics. Understanding such interactions is critical for predicting antibiotic behavior in terrestrial systems and for designing more accurate environmental risk assessments.

Waste mismanagement and metal pollution are high in countries in the global south and often create challenging, extreme conditions for soil microbial communities, which might lead to selection for antibiotic resistance. However, soils from polluted sites in Sub-Saharan areas are rarely sampled. Thus, it remains unclear whether the potential for dissemination of antibiotic resistance exists in these areas. In the present study, we performed genome-resolved metagenomics on samples across a gradient around an area impacted by a copper-nickel mine in Botswana to identify the potential for co-selection for antibiotic resistance due to mine pollution. Specifically, we sampled over a gradient across a mine area in Botswana and performed genome-resolved metagenomics. In general, pollution increased with proximity to the mine, while prokaryotic diversity increased with increasing distance from the mine, and we could identify a few taxa that significantly correlated with the metal concentrations. Moreover, our assembled contigs indicate a potential for co-selection due to the dual function of these genes as both antibiotic resistance genes (ARGs) and metal resistance genes (MRGs), as they act as multidrug efflux pumps. In contrast, some ARGs co-occurred in the same region as MRGs, indicating the potential for co-selection due to co-localization. However, we could not detect any co-localization of ARGs/MRGs with horizontal gene transfer (HGT) markers at the contig level. We binned the contigs to MAGs, and we found several MAGs of high quality and completeness, belonging to taxa such as Actinobacteriota, Chloroflexota, Acidobacteriota, and Dormibacterota, that possess ARGs, MRGs, and HGT-markers. Moreover, we found ARGs, MRGs, and HGT-markers in eight MAGs, after binning, indicating no direct association of HGT-markers with ARG and MRG occurrence. In summary, our metagenomic analysis indicates that pollution in mines can lead to co-selection of AMR, specifically ARGs with a broad spectrum of substrates (e.g., efflux pumps) that can act as MRGs, in an under-sampled location such as Sub-Saharan countries. IMPORTANCEThis study indicates the potential role of metal pollution from mismanaged mining activities in facilitating the selection for antibiotic resistance in soil microbial communities in a Sub-Saharan area located in Botswana. In combination with the lower amount of health regulations and hygiene standards, the dissemination of antibiotic resistance poses risks to human health through the environment in many Sub-Saharan countries. By performing genome-resolved metagenomics and identifying antibiotic resistance genes (ARGs) as metal resistance genes (MRGs) across diverse assembled genomes or co-localization, this work highlights the potential for antimicrobial resistance dissemination due to mine activities. Thus, these findings underscore the urgent need to understand the potential side effects of mine pollution on the spread of antimicrobial-resistant bacteria (ARB) and associated ARGs in Sub-Saharan countries.

Riverine ecosystems particularly in industrialized environment are subjected to chronic press disturbances, resulting from the decadal release of synthetic organic compounds and other xenobiotics. While indigenous microbial communities are highly sensitive to such stressors, the resulting metabolic restructuring and functional reshaping of the microbiome, driven by these long-term anthropogenic pressures remains poorly characterized. In this study, a microbial ecology of Bhadar River flowing across the Jetpur Industrial Estate, (Jetpur) were studied. Using a cross-sectional comparative approach, soil/sediment samples were collected from the diverse polluted and non-polluted sites from the estate. The taxonomic profiling using 16S rRNA gene amplicon sequencing, taxo-phenomic shifts (through metaphenomics) was studied, while the functional potential of metabolic pathways was validated using high-resolution shot-gun metagenomic study. Due to prolong pollution, the samples were rich in sulphur (9809 to 12391 mg/L), where polluted samples were having elevated COD (2432 to 4150 mg/L) as well as BOD (1000 to 1420 mg/L) values, along with the presence of heavy metals (e.g., Fe, Mg). Results revealed a distinct taxonomic shift at both the bacterial and archaeal levels. In non-polluted sites Proteobacteria (33 to 57%) dominated along with Acidobacteria and Actinobacteria, with diverse genera like Alcaligenes and Serratia. Whereas, polluted sites exhibited marked increase in Bacteroidetes (13 to 29%), Firmicutes, and Synergistetes and genera like Alkalitalea, Mesotoga and Desulfomicrobium, reflecting anaerobic, fermentative, and sulfate-reducing phenotypes. The archaeal communities at polluted sites were dominated by Euryarchaeota (78 to 99%), specifically methanogenic genera of Methanosaeta and Methanocalculus, contrasting with the Methanomassiliicoccus dominance in non-polluted areas. The alpha-diversity was marginally higher in polluted sites (Shannon: 4.11 to 4.81 vs. 3.81 to 5.39 (non-polluted)), but beta-diversity underscored clear separation (94% variance explained by pollution). The shot-gun metagenomic analysis indicated a substantial enhancement in anaerobic metabolic capacities within the polluted microbiome, primarily in sulphur respiration (dissimilatory sulfate reduction), methanogenesis (elucidating biogenic pathways), along with nitrogen cycling (identifying key denitrification and ammonification genes). The polluted microbiome have developed the potential to metabolise/degrade complex aromatic compounds (pcaK for benzoate/protocatechuate transport) and heavy metal resistance. The strong positive co-occurrences among anaerobic phyla (Thermotogae, Synergistetes, Bacteroidetes) in polluted sites was established, indicating syntrophic interactions for xenobiotic metabolism. These findings provide a theoretical ecological model for perturbed industrial ecosystems, emphasizing the role of habitat selection in shaping microbial functional diversity and demonstrate the remarkable adaptation of autochthonous communities to persistent press disturbances.

BackgroundCoarse particulate matter (PM10) deposits at the vocal fold (VF) mucosa, yet upper airway responses remain poorly characterized. Existing in vitro VF models use monocultures that lack the stratified epithelium, lamina propria, and physiological perfusion. We developed a chip-based co-culture model of human VF mucosa and applied it to acute PM10 exposure. MethodsVocal fold organ-on-chip (VF-OOC) paired primary VF fibroblasts with either immortalized laryngeal epithelial cells (iLEC) or induced pluripotent stem cells (iPSC)-derived VF epithelial cells. Transwell and 2D chip cultures were controls. Epithelia matured at an air-liquid interface on fibroblast-embedded collagen over a perfused microchannel. PM10 urban dust (0 to 400 {micro}g/mL) was applied for 24 hours. Responses were assessed by histology, immunofluorescence, transmission electron microscopy, qPCR, and ELISA. ResultsVF-OOC produced a thicker stratified epithelium with upregulated barrier, mucin, and extracellular matrix genes versus transwell controls. Intercellular junctions and basement membrane matched adult human VF mucosa. PM10 remained at the epithelial surface across all doses. TranswelliLEC downregulated basal markers (TP63, KRT5, KRT14). VF-OOCiLEC upregulated MUC1 and HAS3, consistent with an adaptive mucosal response. VF-OOCiPSC additionally induced suprabasal, junctional, extracellular matrix, and cytokine genes largely absent in iLEC and transwell formats. ConclusionsVF-OOC reproduced key features of native human VF mucosa and captured distinct, platform-specific responses to PM10 that differed by epithelial cell source. By introducing new approach methodologies (NAMs) into laryngology, this platform extends respiratory toxicology to the upper airway beyond bronchial and alveolar compartments and allows mechanistic studies of exposure-linked diseases such as laryngitis.

Compact poultry raising has turned poultry litter into an environmental problem, as it may all be packed with heavy metals and drug-resistant germs. Of all the metals, chromium contamination not only disturbs the general environment but is also a source of concern for public health. Poultry litters were taken from 14 farms in different places, and the bacteria characters from different places were tested for their capacity to tolerate Cr(VI). A total of 31 bacterial isolates were initially screened, and three of them (AH-2, AZ-1, and AMF-3) appeared to be very resistant to chromium. The isolates were able to survive at the highest concentration, 800 mg/L of the Cr(VI); however, AH-2 was the most resistant one (MIC: 900 mg/L; MBC: 1000 mg/L). Chromium reduction tests showed that AMF-3 at high concentration showed the maximum chromium reduction, while AH-2 achieved higher chromium reduction at medium concentration. Phenotypic and biochemical analysis showed that the isolates were Staphylococcus spp., which was confirmed by 16S rRNA gene sequencing as S. cohnii, S. saprophyticus, and S. gallinarum. Moreover, chromium was detected at higher levels in poultry litter compared to the feed, with the highest accumulation in AZ farm litter (4464.0 {micro}g/kg). The highlighting feature of our article is the presence of chromium-tolerant and reducing bacteria in poultry environments. Besides that, the level of chromium in poultry litter is really high, and it points to the need for better waste management.

Pregnant women are frequently exposed to various endocrine-disrupting chemicals (EDCs), such as bisphenol A (BPA), causing harm to both the developing placenta and fetus. BPA can promote placental dysfunction by altering key cellular processes such as differentiation, invasion, and migration in trophoblast cells. These cellular processes are also tightly managed by the ubiquitin proteasomal system via maintenance of the ubiquitinated protein pool. However, the BPA-mediated dysregulation of this ubiquitin proteasomal homeostasis is poorly understood. Therefore, we identified 19 deubiquitinases (DUBs) and a dynamic ubiquitinome profile of extravillous trophoblast cells (HTR8/SVneo), which reduced trophoblast cell migration post-BPA exposure. Further investigation using an integrated substrate-ligase-deubiquitinase network shows that BPA binding to PPAR-alpha or indirect regulation of its E3 Ligase MuRF1 and DUB USP5 via BPA resulted in hyper-ubiquitination of PPAR-alpha, triggering its nuclear localization. In the nucleus, the ubiquitinated PPAR-alpha can deregulate its migration-associated target gene expression, causing a reduction in the migration of HTR8/SVneo cells. This physiological alteration of extravillous trophoblast cells (EVTs) through BPA can disrupt placental homeostasis. Hence, we assumed that BPA-induced cellular alteration in EVTs can promote placental defects, which might contribute to adverse pregnancy outcomes.

Since the 1950s, micro- and nanoplastics (MNPs) have become omnipresent, representing a novel environmental hazard which continually deposits in our airways. Pulmonary macrophages (pMacs) orchestrate the balance between inflammation and tolerance required for homeostasis of the lung and are among the first immune cells to encounter inhaled MNPs. Yet, how pMacs react to plastic deposition in the lung and implications for disease remain unknown. Here, we exposed mice in vivo, human precision-cut lung slices (hPCLS) ex vivo, and monocyte-derived macrophages and cell lines to polystyrene MNPs in vitro. MNP deposition in the lung and extrapulmonary tissues was determined over a 1-week period and pMacs from MNP-laden lungs isolated for RNA-sequencing. We compared the effects of MNPs or diesel exhaust particulate exposures on hPCLS viability and metabolism, monocyte-derived macrophage transcription, and macrophage mitochondrial function, inflammation, and antigen presentation. MNPs readily translocated the lung and were observed in all organs examined within 1-day. pMacs from MNP-exposed mice expressed transcriptional pathways associated with endocrine system disorders, tissue remodeling, and malignant disease. Macrophage phagocytosis was impaired through decreased mitochondrial function which could be rescued pharmacologically. MNPs inhibited the ability of macrophages to effectively present OVA-antigen preventing TCR-specific activation, an effect that could be restored by blocking PD-1/PD-L1. These findings indicate that MNPs impair macrophages via unique mechanisms linking phagocytic and bioenergetic dysfunction. Loss of antigen-presenting capabilities in MNP-laden macrophages may compromise immunosurveillance. As such, MNPs have the potential to increase susceptibility to lung disease independent of the conventional mechanisms of inflammation and oxidative stress. Clinical relevanceO_LIBioaccumulation of micro- and nanoplastics in macrophages impairs their ability to function as antigen-presenting cells increasing susceptibility to pathogenic and malignant disease. C_LIO_LIPulmonary macrophages residing in micro- and nanoplastic laden lungs possess transcriptional profiles associated with endocrine system disorders, gastrointestinal disease, and cancers. C_LI

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.

ABTRACT Background Children from low- and middle-income countries are particularly vulnerable to air pollution, a major environmental health risk, due to the immaturity of their lungs and their proximity to sources of household pollution. This study aimed to investigated the effect of exposure to biomass combustion through domestic and maternal occupational activities on respiratory health of children living in disadvantaged urban areas of Abidjan, Cote dIvoire. Methods Between February and December 2023, we conducted a cross-sectional observational study among children <16 years from households of women using biomass fuel for cooking (Group (G) 1), engaged in occupational fish smoking activities (G2), or primarily using gas for domestic cooking (G3). We assessed reported respiratory symptoms through standardized questionnaires and the presence of lung function impairments (LFI) though pulmonary function tests (spirometry and Rint). We assessed the association between study groups and key covariates with respiratory symptoms and LFI using mixed-effects regression models. Results Of 210 children enrolled - 119 (56.8%) female, median age 9 (6-12) years, 82 (39.0%) in G1, 47 (22.4%) in G2, and 81 (38.6%) in G3 - 15 (7.1%) reported wheezing in the last 12 months, 82 (39.0%) reported dry cough at night, 9 (4.9%) presented with dyspnea and 5 (2.7%) had chest pain on clinical examination, for an overall proportion of children with reported respiratory symptoms of 43.8% (92/210). Of 176 children who underwent pulmonary function testing, 59 (33.5%) had LFI detected, including 34 (45.9%) in G1, 8 (22.2%) in G2, and 17 (25.8%) in G3 (p = 0.011). Study group was associated with respiratory symptoms (G1 vs G3; aOR 3.82, 95% CI 1.68-8.68; p < 0.001), as well as with LFI (p = 0.042). Girls were at greater risk of LFI than boys (aOR 2.69, 95% CI 1.24-5.80; p = 0.012). Children whose mothers used charcoal or wood as cooking fuel had higher odds of respiratory symptoms (OR 2.61, 95% CI 1.22-5.58; p = 0.013) but no association was found with LFI (p = 0.459) compared with unexposed children. Conclusion Respiratory symptoms and lung function impairments were highly prevalent among children living disadvantaged, especially when mothers cook with wood or charcoal. Targeted maternal awareness and broader interventions to reduce household air pollution in disadvantaged urban areas are urgently needed to protect long-term respiratory health.

Background: Particulate matter (PM) exposure is associated with increased risk and exacerbation of chronic rhinosinusitis (CRS), yet underlying mechanisms remain poorly understood. Methods: Human nasal epithelial cells obtained from ethmoid tissue of CRS (n = 5) and control donors (n = 4) were cultured at an air-liquid interface and exposed to PM. Single-cell RNA sequencing was performed to characterize PM-induced cellular and transcriptional changes. Protein expression, epithelial barrier integrity, cell death, and intracellular PM uptake were evaluated using biochemical, imaging, and ultrastructural approaches. Results: Unsupervised clustering identified seven epithelial cell populations. Gene set analysis revealed baseline enrichment of inflammatory and keratinization pathways and reduced ciliogenesis in CRS compared with controls. Although PM induced inflammation and squamous differentiation in controls, the pathogenic responses were significantly amplified in CRS, including uniquely enhanced IL-1 signaling. Transcriptional changes were validated by ELISA, transepithelial electrical resistance, and immunofluorescence, demonstrating increased inflammation, epithelial barrier disruption, and cell death following PM exposure. Transmission electron microscopy revealed increased intracellular PM within membrane-bound organelles. Pre-treatment with an endocytosis inhibitor rescued PM-induced epithelial barrier dysfunction and inflammation. Conclusion: CRS epithelium exhibits baseline dysfunction that may predispose it to environmental injury. PM exposure both induces CRS-like epithelial changes in controls and exacerbates disease-associated phenotypes.