Environmental Pollution

O_LIIn this study, we demonstrate that Benzo[a]pyrene (B[a]P) induces keratinocyte senescence and p21Cip1-dependent keratinocyte differentiation. Atmospheric and environmental pollution are known to induce senescence and promote terminal differentiation in human primary keratinocytes, thus driving skin aging. However, much is still unknown about the underlying molecular mechanisms. We observed that B[a]P, a common atmospheric pollutant, induced senescence in primary keratinocytes in both two-dimensional and three-dimensional (reconstructed human epidermis) culture. This was accompanied by signs of DNA damage in B[a]P-treated cells. B[a]P-treated cells also underwent accelerated late-stage terminal differentiation, indicated by increased IVL and FLG expression from 48 to 96 hours post-exposure. While pharmacological and genetic attenuation of p21Cip1 did not rescue cellular senescence, it prevented the expression of IVL and FLG, suggesting that the late-stage terminal differentiation induced by B[a]P exposure was p21-dependent. Our data thus suggest a key role for the p21Cip1 in the keratinocyte response to pollution-induced damage, where p21Cip1 induces terminal differentiation to maintain skin barrier homeostasis. C_LI

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.

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.

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.

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.

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.

Background Childhood overweight and obesity represent major public health challenges, shaped by socio-economic and environmental factors. This study investigates the mediating and moderating role of urban environmental exposures in socio-economic disparities in childhood excess weight. Methods Data was drawn from a population-based sample of children (2-9 years) and adolescents (10-17 years) living in Geneva, Switzerland. Parents reported household financial situation and children's height and weight, from which excess weight (i.e. overweight or obesity) was derived. Residential exposures to air pollution (PM2.5, NO2), noise (daytime, nighttime), and neighborhood greenness (green areas, canopy coverage) were estimated based on geocoded residential addresses. The association between household financial situation and excess weight was evaluated, as well as the mediating and moderating roles of urban environmental exposures. Results The analysis included 1006 children and 1154 adolescents. Among children, an average-to-poor household financial situation was associated with higher odds of excess weight in children (adjusted odds ratio [aOR]: 1.79, 95% confidence interval [CI]: 1.13; 2.84). Higher noise exposure was associated with excess weight (daytime: aOR: 1.40, 95% CI: 1.10; 1.77, nighttime: aOR: 1.37, 95% CI: 1.08; 1.74), while the association with PM2.5 appeared stronger among socio-economically disadvantaged children, though the interaction did not reach statistical significance (financial situation x PM2.5 interaction: aOR: 1.59, 95% CI: 0.98; 2.59). No significant associations were observed among adolescents. Conclusion These findings highlight the joint influence of social and environmental inequalities on childhood excess weight and stress the need to address these interconnected determinants to design equitable, targeted public health interventions.

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.

Per- and polyfluoroalkyl substances (PFAS) are new pollutants in the environment whose effects on bacterias physiology is not well understood. In this study, we show that exposure to PFAS causes membrane depolarization in Salmonella enterica serovar Typhi. This works as a metabolic uncoupler that breaks down proton motive force without immediately killing the cells. This disturbance results in a significant elevation of intracellular NADH and NAD levels while preserving redox equilibrium, signifying an augmented metabolic flux. At the same time, we see that {beta}-oxidation pathways are turned on, which suggests that the cells are shifting toward breaking down fats to make up for the lack of energy. Even though there are more reducing equivalents, ATP levels go down, which is what happens when respiration is uncoupled. This puts the cells in a state of "pseudo-starvation." This metabolic stress triggers the SpoT-dependent stringent response, leading to the accumulation of (p)ppGpp. Genetic analysis employing {Delta}relA and {Delta}relA{Delta}spoT mutants confirm that SpoT is necessary for this adaptive response. Functionally, PFAS-treated populations show an enhanced proportion of persister-like cells, which connects exposure to environmental pollutant in the environment to antibiotic tolerance. Our findings reveal a previously unidentified mechanism by which PFAS alters bacterial metabolism and stress responses, facilitating persistence through membrane depolarization, metabolic reconfiguration, and stringent response activation. This study underscores the potential influence of environmental pollutants on bacterial survival mechanisms and antibiotic resistance.

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

Artificial light at night (ALAN) disrupts natural light cycles and interferes with light-dependent biological processes. However, the effect of ALAN on cellular processes in wildlife is unclear. We examined diel brain transcriptomic alterations in the diurnal damselfish Dascyllus aruanus by comparing fish exposed to three consecutive nights of ALAN with control fish, sampled during both the day and night. ALAN partially disrupted circadian regulation transcription, altering diel expression of the core clock regulator bmal1 and glucocorticoid-regulated genes. At night, ALAN triggered activation of genes indicative of neuronal activity and acute neural stress, along with suppression of restorative nocturnal processes. The following day, the transcriptomic divergence between ALAN-exposed and control fish expanded, with widespread downregulation of genes governing vascular homeostasis, coagulation, and immune function. Together, these findings indicate that ALAN reshapes brain transcriptomic programs across the entire diel cycle, identifying molecular signatures of physiological disruption in light-polluted marine environments.

In recent years, the synergistic role of endocrine-disrupting chemicals (EDCs) and gut microbiota in the development of diabetes has been increasingly documented in rodent models. However, most studies have focused on one or two EDCs with varying doses and exposure durations, limiting the identification of a shared microbial signature associated with EDC-induced glucose dysregulation. This meta-analysis aimed to identify a common gut microbiome pattern across rodent studies involving diverse EDC exposures linked to glucose dyshomeostasis. A systematic search yielded 3,748 studies, of which ten met the inclusion criteria, comprising sequence data from 189 samples. These studies evaluated gut microbiota alterations in diabetes induced by various EDCs, including pesticides, food additives, and heavy metals, across different exposure conditions. Meta-analysis revealed a consistent reduction in microbial diversity and an increased Firmicutes/Bacteroidetes ratio following EDC exposure. At the phylum level, Firmicutes, Proteobacteria, Desulfobacterota, and Patescibacteria were significantly enriched. Although beneficial genera such as Lactobacillus, Bifidobacterium, and Akkermansia showed a decreasing trend, these changes were not statistically significant. In contrast, xenobiotic-associated genera including Desulfovibrio, Pseudomonas, Parasutterella, and Candidatus Saccharimonas were significantly increased. Notably, sulfate-reducing bacteria were the only inflammation-associated group consistently elevated. These microbial alterations were distinct from those observed in high-fat diet-induced diabetic models. This study identifies a distinct gut microbiome signature associated with EDC exposure in rodent models of glucose imbalance. These findings suggest unique microbiome-mediated pathways in EDC-induced diabetes and highlight potential microbial targets for early intervention in environmentally driven metabolic disorders.

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.

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.

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.

Numerous studies have shown that the abundance of antibiotic-resistant bacteria (ARBs) or antibiotic-resistance genes (ARGs) in soil increases after irrigation with wastewater. However, it is unclear whether this increase is due to the selection effects of pharmaceutical residues in the irrigation water or the continuous introduction of ARBs and ARGs with the wastewater. Further, it is unclear how the binding of antibiotics to natural colloids (1-1000 nm) affects their biological effects compared to truly dissolved substances (< 1 nm). We conducted competition experiments with resistant and susceptible Acinetobacter baylyi BD413 strains in wastewater, as well as in colloidal and truly dissolved extracts of soils irrigated with wastewater. Although the concentrations of our six target antibiotics were far below the measured minimum selective concentrations of the tested strains, we demonstrate that the resistant strain was favored in the wastewater and the colloidal extracts. In contrast, the truly dissolved fractions exhibited weaker and more variable selective effects. A non-targeted analysis revealed the presence of 82 additional substances in our extracts, including further antibiotics, pesticides, and different non-antibiotic drugs that may influence the selection of our resistant A. baylyi BD413 strain. Our findings suggest that antibiotic resistance is selected for in wastewater and wastewater-irrigated soils. This cannot be explained by antibiotic concentrations alone, but may also arise from the effects of complex mixtures of co-occurring contaminants, particularly those associated with colloidal particles.

Introduction Air pollution is the largest environmental risk to human health. Children are disproportionately affected by air pollution and their exposure is amplified during physical activity. Observed concentrations of nitrogen dioxide in 1 in 4 London school playground exceeds the European limit, but the health impacts of air pollution exposure in London school playgrounds remain unexplored. Our study aims to assess and compare the acute changes in lung function and airway inflammation of primary school-aged children exercising in school playgrounds. Methods and analysis 330 children aged 8 to 11 years from ten London schools will be recruited to complete 90 minutes of physical activity and 90 minutes of rest in their school playground in a randomised crossover design. Pre-, post-, and 24-hour post-exposure oscillometry measurements will be performed with airway resistance at 5 Hz (R5) the primary physiological outcome. Nasal lavage samples will be collected pre-exposure and 24-hour post-exposure for analysis of inflammatory, oxidative, and vascular biomarkers, with IL-6 as the primary biological outcome. Mixed-effects regression models will examine associations between estimated pollutant exposures, exercise and physiological responses.

Cadmium, being a highly toxic metal, perturbs cellular homeostasis by forming stable complexes with numerous thiol-active proteins, ultimately leading to severe liver and lung damage. Despite its well-documented toxicity, the molecular mechanisms governing cadmium export remain poorly understood. Given the chemical similarity between cadmium and copper, we investigated whether the canonical copper-exporting ATPases, ATP7A and ATP7B participate in cadmium handling. Upon Cd treatment in hepatocytes, ATP7B undergoes trafficking to lysosomes via the retromer complex, as also observed in the case of elevated copper, accompanied by the upregulation of acidic lysosomal populations. In contrast, ATP7A expressed in lung adenocarcinoma cells, though exhibit vesicular redistribution upon Cd exposure, does not mediate lysosomal sequestration, suggesting distinct deployment of late secretory pathways by the two copper ATPases in response to cadmium. We have also observed that ATP7B-/- hepatocytes exhibit increased sensitivity to Cd exposure compared to wild-type cells. Whereas, overexpressing the ATP7B amino-terminal copper-binding domain in bacteria alleviates cadmium-induced stress, indicating its capacity to sequester Cd. Caenorhabditis elegans lacking copper-ATPase cua-1, displayed increased Cd sensitivity, while mutants (glo-1-/-), deficient in lysosome-related organelles (LRO), and (lmp-1-/-), deficient in lysosomal membrane glycoprotein, showed reduced resistance to cadmium toxicity. Treatment of the worm with cadmium increases the abundance of lysosomes marked by elevation in lysosomal biogenesis and functional genes, reinforcing the importance of lysosomal pathways in cadmium detoxification. To summarise, we delineated the non-canonical role of copper ATPases and lysosomes in cadmium-induced cellular toxicity.

Staphylococcus aureus (S. aureus) is the most common pathogen associated with skin infections worldwide. Significant efforts have been made to identify and develop innovative therapeutic strategies against S. aureus as alternatives to conventional antibiotics. Physical plasma has a broad range of potential uses, with non-destructive disinfection being one of its earliest applications. Although the literature emphasizes the antibacterial properties of cold atmospheric plasma (CAP), the effect of plasma on S. aureus on damaged skin susceptible to S. aureus invasion through the itch-scratch cycle has not been studied to date. Thus, we examined the effectiveness of CAP treatment on S. aureus bacteria in atopic dermatitis lesions using floating electrode dielectric barrier discharge devices, as well as helium and argon plasma jets. Heat distribution on the skin target, ultraviolet C radiation, and ozone generation of plasma jets for the operator of plasma sources were evaluated. Microbial tests confirmed the presence of S. aureus on the lesions of the groups before treatment. The groups exposed to plasma treatment showed a notable reduction in bacterial population compared to the model group (p<0.05). Furthermore, our investigation indicated that plasma treatment reduced pruritus behavior. The findings suggest that cold atmospheric plasma treatment may potentially target skin infections caused by S. aureus in addition to conventional therapies.

Agricultural fields in the Mezquital Valley, Mexico, were irrigated with untreated wastewater over several decades. Following the construction of a wastewater treatment plant (WWTP) in Atotonilco de Tula, WWTP effluent is used for irrigation. To evaluate the effects of changed irrigation, a soil incubation experiment was performed. Soils of the Mezquital Valley long-term irrigated with untreated wastewater were irrigated with WWTP influent or effluent, both unspiked and spiked with antibiotics and biocidal compounds and incubated four weeks. We investigated the effects of shifted irrigation on the abundance of cultivable total heterotrophic and resistant bacteria (RB). Additionally, RB were cultivated from Coriandrum sativum (cilantro) sown in soil of the incubation experiment. While wastewater treatment significantly reduced the bacterial abundance in effluent, spiking increased RB abundance in both wastewater types including ciprofloxacin (CIP) RB. Before wastewater addition, all soils contained cultivable RB. Irrigation increased the relative abundance of RB cultivated on Mueller Hinton (MH) agar in Leptosols and Phaeozems, compared to soils prior to wastewater addition irrespective of the water type, but not in Vertisols, suggesting the soil type rather than water qualities influenced the RB abundance. Diverse CIP RB were cultivated including strains of 14 genera of three phyla. Among those, Achromobacter spp. strains related to potentially pathogenic A. spanius originating from soil were abundant in both leaves and roots of cilantro. Our results showed that the implementation of wastewater treatment does not reduce the abundance of cultivable RB in Mezquital Valley soils and cilantro plants. Health risk associated monitoring should include long-term persistent RB colonizing plants cultivated in wastewater irrigated soils.