Environmental Pollution

BackgroundEpidemiological studies suggest an interaction between air pollution including particulate matter <2.5 {micro}m (PM2.5) and coronavirus disease 2019 (COVID-19) mortality and morbidity; however, the underlying mechanisms are not clear. The aim of our study was to investigate effects of PM2.5 on viability, epithelial integrity, and cellular entry of SARS-CoV-2 into airway epithelial cells, and the mechanisms involved. MethodsWe exposed Calu-3 airway epithelial cell cultures to PM2.5 (10, 50, and100 {micro}g/ml) and SARS-CoV-2 (MOI 0.01) for 24 h. The viability of Calu-3 cells and epithelial barrier integrity were determined using MTT assay and immunofluorescence staining for Zonula Occludens-1, respectively. mRNA expression for viral entry-related genes such as angiotensin converting enzyme (ACE)2 and transmembrane protease, serine (TMPRSS)2, and inflammatory and inflammasomal genes, including interleukin (IL)-8,IL-6, nuclear factor (NF)-{kappa}B p65 (RELA), JNK, c-JUN, Caspase-1, IL-1{beta}, NLRP3, was analyzed by qRT-PCR. Intracellular viral spike protein intensity and RNA-dependent RNA polymerase (RdRP) expression were determined using immunofluorescence staining and qRT-PCR, respectively. ELISA was used to analyze the release of inflammatory cytokines (IL-8, IL-6, and GM-CSF). ResultsHigher concentrations of 100{micro}g/ml PM2.5 decreased Calu-3 cell viability (p=0.02) and deteriorated epithelial barrier integrity, while 50 {micro}g/ml of PM2.5 (p<0.01) induced mRNA expression for ACE2 and TMPRSS2. Although PM2.5 alone decreased c-JUN, it did not alter the expression of mRNA for JNK and RELA. In contrast, a combination of SARS-CoV-2 and PM2.5 led to a significant increase in mRNA for both JNK and RELA (p < 0.05 and p < 0.01, respectively) and attenuated c-JUN expression. Moreover, our results indicated an increase in the expression of IL-1{beta}, IL-6, and GM-CSF following exposure to PM2.5 and PM2.5 + SARS-CoV-2, whereas IL-8 was induced only by SARS-CoV-2 exposure. Co-incubation of Calu-3 cells with PM2.5 and SARS-CoV-2 leads to a decrease in IL-8, IL-1{beta}, Caspase-1 (CASP-1), and Interferon gamma (IFNG) expression. Finally, the viral load (RdRP) also increased in the presence of both PM2.5 and the SARS-CoV-2 group. ConclusionOur findings have demonstrated that PM2.5 impaired epithelial integrity and cell viability, whereas it increased the mRNA expression for ACE2 and TMPRSS2, and induced inflammatory changes in Calu-3 cells incubated with SARS-CoV-2. These findings suggest that PM2.5 can facilitate the entry of SARS-CoV-2 into airway epithelial cells, and that both PM2.5 and SARS-CoV-2 can decrease the inflammatory and antiviral responses of the host cell.

ObjectiveTo explore the underlying mechanism behind the fine particulate matters (PM2.5)-mediated regulation of reproductive function in male rats, and to determine the role of vitamins in this process. MethodsIn all, 32 male SD rats were randomized to a control cohort (normal saline), a Vit cohort (vitamin C at 100 mg/kg + vitamin E at 50 mg/kg), a PM2.5 cohort (PM2.5 10 mg/kg), and a PM2.5+Vit cohort (PM2.5 exposure + vitamin C at 100 mg/kg + vitamin E at 50 mg/kg), with eight rats in each cohort. After four weeks of exposure, mating experiments were carried out. Thereafter, rats were euthanized, and the testis and epididymis tissues were excised for hematoxylin-eosin (HE) staining and sperm quality analysis. Apoptosis of testis tissues was quantified via a terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Moreover, the testicular oxidative stress (OS)-, apoptosis- and mitochondrial unfolded protein response (UPRmt)-related essential protein expressions were measured via western blotting (WB). ResultsAfter PM2.5 exposure, the sperm count and motility decreased, while sperm abnormality and the apoptosis index increased. HE staining showed that the number of spermatogenic cells decreased. WB showed that the PM2.5 group had decreased expressions of superoxide dismutase (SOD), nuclear factor E2-related factor 2 (Nrf2), and B-cell lymphoma-2 (Bcl-2) (p < 0.05), increased expressions of malondialdehyde (MDA), Bcl-2 associated X protein (Bax), and Caspase3 (p < 0.05), and downregulated expressions of C/EBP homologous protein (CHOP), heat shock protein 60 (HSP60), and activating transcription factor 5 (ATF5) (p < 0.05). These were all reversed by vitamin intervention. ConclusionPM2.5 from automobile exhaust disrupts male reproductive function. A combination of vitamins may protect reproductive function via the reactive oxygen species (ROS)-UPRmt signaling pathway. HighlightsO_LIPM2.5 from vehicle exhaust can cause apoptosis of male germ cells. C_LIO_LIPM2.5 from vehicle exhaust induces germ cell apoptosis through the ROS-UPRmt signaling pathway. C_LIO_LICombined vitamin C and E can enhance UPRmt activity to alleviate the germ cell apoptosis caused by PM2.5 from vehicle exhaust. C_LI Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=134 SRC="FIGDIR/small/621651v1_ufig1.gif" ALT="Figure 1"> View larger version (30K): org.highwire.dtl.DTLVardef@d3f5edorg.highwire.dtl.DTLVardef@1b6daa1org.highwire.dtl.DTLVardef@1cba0b4org.highwire.dtl.DTLVardef@1a3c9f1_HPS_FORMAT_FIGEXP M_FIG C_FIG

Perfluorooctane sulfonic acid (PFOS), a per- and polyfluoroalkyl substance (PFAS), is a widespread persistent environmental pollutant that has been implicated in various human health conditions, including infertility and cancer. Here, we investigate the effects of acute exposure to PFOS on human fallopian tube epithelial (FNE) cells that are essential for fertility and increasingly recognized as the origin site for high-grade serous ovarian cancer. We show that acute PFOS exposure changes morphology, arrests proliferation, impairs adhesion, and compromises epithelial integrity of FNE cells. Using transcriptomic profiling of FNE cells exposed to PFOS, we found increased expression of genes associated with stress-response signal transduction, including KRAS, and decreased expression of genes related to cholesterol transport and lipid homeostasis. We show that inhibition of MEK/ERK or cholesterol supplementation rescued changes in cell morphology. Further, we performed membrane fluidity measurements of cells exposed to PFOS and found elevated membrane disorder and fluidity. Our results are consistent with a model in which PFOS perturbs plasma membrane, activates stress-response signaling pathways, and impairs epithelial cell function. These studies establish a framework for understanding the effects of PFAS on cell physiology.

The global industrialization and rapid urbanization elevated the risk of toxic pollutant exposure, which affects human health specially during pregnancy. Pregnant mothers are daily exposed to bisphenol-A (BPA), which is a common plastic leachate and a prominent toxic pollutant present in our environment. BPA act as an endocrine disrupting chemical (EDCs) by altering feto-placental homeostasis. This persistent and potent exposure of BPA during gestation can trigger placental damage affecting trophoblast cell function and survival. BPA even disrupts specific signalling cascades by altering post translational protein phosphorylation. However, this BPA mediated dysregulation of signalling nodes in early trimester placenta is still unexplored. Therefore, this study investigates the global proteome changes in post-BPA exposed extravillous trophoblast (EVTs) cells, which revealed a BPA mediated dynamic regulation of phosphoproteome-signatures and their associated kinases. Further inspection showed that the altered phosphorylation of c-JUN (S63) and GSK3 (Y279) is associated with BPA toxicity in EVTs and placenta. This altered phosphorylation affects the cellular signalling downstream, imparting damage upon the growing feto-placental unit. This highlights an altered phosphorylation mediated mechanism of BPA toxicity in placenta which can cause an onset of adverse pregnancy outcome. Data are available via ProteomeXchange with the identifiers PXD074780.

BackgroundEpidemiology has demonstrated a strong relationship between fine particulate matter (PM) exposure and cardiovascular disease. Whether PM aggravates myocardial ischemia/reperfusion (I/R) injury and its related mechanisms remain unclear. Our previous study showed that adipose stem cell-derived exosomes (ADSC-Exo) contain a large amount of miR-221/222. This study investigated the effects of PM exposure on I/R-induced cardiac injury through mitophagy and apoptosis, as well as the potential role of miR-221/222 in ADSC-Exo. MethodsWild-type, miR-221/222 knockout (miR-221/222 KO), and miR-221/222 overexpressed transgenic (miR-221/222 TG) mice were intratracheally injected with 100 g/kg PM for 24 h before I/R treatment. Ischemia was induced by temporarily occluding the left anterior descending (LAD) coronary artery with sutures for 30 min, followed by 3 h of reperfusion. In an in vitro model, H9c2 cells were exposed to 50 g/mL PM for 6 h and subjected to hypoxia (1% O2) at 37{degrees}C for 6 h, followed by 12 h reoxygenation. ResultsPM aggravates I/R (H/R)-induced cardiac injury by increasing ROS levels and causing mitochondrial dysfunction, leading to an increase in mitochondrial fission-related proteins like Drp1 and Mff, mitophagy-related proteins such as BNIP3 and LC3B, as well as apoptosis-related proteins like PUMA and p-p53 in vivo and in vitro studies. In comparison, transfection of ADSC-Exo and miR-221/222 mimics significantly reduced PM+I/R (H/R)-induced cardiac injury. Importantly, ADSC-Exo contains miR-221/222, which directly targets BNIP3, LC3B, and PUMA, decreasing their expression and ultimately reducing cardiomyocyte mitophagy and apoptosis. ConclusionsThe study showed that PM aggravates I/R or H/R-induced cardiac injury, and ADSC-Exo treatment significantly reduced this by regulating mitophagy and apoptosis through miR-221/222/BNIP3/LC3B/PUMA.

Phenanthrene (PHE), as one of the most frequently found polycyclic aromatic hydrocarbons can induce immunotoxicity, oxidative stress, and endocrine disruption in marine organisms. However, whether autophagy can be induced by PHE and the regulatory mechanism and cytoprotective roles of autophagy under PHE stress condition have not been unveiled. Our data first unveil a "E3 ubiquitin ligases-NF-{kappa}B-autophagy" axis, which play cytoprotective roles in Pacific oysters Crassostrea gigas exposed to PHE. The results of confocal laser scanning microscope, flow cytometry and transmission electron microscope confirmed that PHE could induce autophagy in the haemocytes of Pacific oysters, and the presence of autophagosomes was also confirmed. The proteomics results showed that the expression of the E3 ubiquitin ligase HUWE1, TRIM36, and autophagy-related protein 7 (ATG7) were significantly upregulated. The expression of genes of the "axis" were significantly upregulated, and the expression of genes of autophagy was downregulated after the inhibition of the NF-{kappa}B, indicating that the expression of the "axis"-related genes can be stimulated by PHE, and thus autophagy is activated. The upregulation of the expression of "axis"-related genes in mouse macrophages, further demonstrating the existence of the "axis" proposed by this study and the "axis" can be activated by PHE. Incorporating with changes of cell number, apoptosis rate, phagocytic capacity, and ROS levels of lymphocytes, we demonstrated that autophagy plays a cytoprotective role in cellular defence against PHE. This study proposed a novel pathway and supplied a comprehensive understanding of the protective role of autophagy in Pacific oysters to cope with pollutants.

AO_SCPLOWBSTRACTC_SCPLOWAmong the numerous questions about human impacts on ecosystems, there is a growing interest for acoustic pollution. First studies on underwater acoustic pollution focused, and showed effects, on vertebrates behaviours. Knowledge on the effects on invertebrates is more limited and there is a huge lack concerning zooplankton species, although widely used as bioindicators in chemical pollution. Consequently, it is critical to assess the impact of noise on zooplanktons fitness (survival and fecundity). Here, isolated water fleas, Daphnia magna, were reared from birth to death in the presence or absence of motorboat noises. Effects on lifespan and clonal offspring production (e.g., clutch size, number of offspring produced along life) were assessed and chronic exposure to boat noise did not affect Daphnias fitness. The spectral and temporal features of the sounds could explain the results. This study highlights the importance of integrating noise pollution into ecotoxicological research to understand, and prevent, human impacts on communities.

This symmetric bidirectional case-crossover study examined the association between short-term ambient air pollution exposure during weeks 3-8 of pregnancy and certain common congenital anomalies in Ulaanbaatar, Mongolia, between 2014 and 2018. Using predictions from a Random Forest regression model, authors assigned daily ambient air pollution exposure of particulate matter <2.5 um aerodynamic diameter, sulphur dioxide, nitrogen dioxide, and carbon monoxide for each subject based on their administrative area of residence. We used conditional logistic regression with adjustment for corresponding apparent temperature to estimate relative odds of select congenital anomalies per IQR increase in mean concentrations and quartiles of air pollutants. The adjusted relative odds of cardiovascular defects (ICD-10 subchapter: Q20-Q28) was 2.64 (95% confidence interval: 1.02-6.87) per interquartile range increase in mean concentrations of particulate matter <2.5 um aerodynamic diameter for gestational week 7. This association was further strengthened for cardiac septal defects (ICD-10 code: Q21, odds ratio: 7.28, 95% confidence interval: 1.6-33.09) and isolated ventricular septal defects (ICD-10 code: Q21.0, odds ratio: 9.87, 95% confidence interval: 1.6-60.93). We also observed an increasing dose-response trend when comparing the lowest quartile of air pollution exposure with higher quartiles on weeks 6 and 7 for Q20-Q28 and Q21 and week 4 for Q21.0. Other notable associations include increased relative odds of cleft lip and cleft palate subchapter (Q35-Q37) and PM2.5 (OR: 2.25, 95% CI: 0.62-8.1), SO2 (OR: 2.6, 95% CI: 0.61-11.12), and CO (OR: 2.83, 95% CI: 0.92-8.72) in week 4. Our findings contribute to the limited body of evidence regarding the acute effect of ambient air pollution exposure on common adverse birth outcomes.

We have previously shown that exposure to particulate air pollution, both from natural and anthropogenic sources, alters gene expression in the airways and increases susceptibility to respiratory viral infection. Additionally, we have shown that woodsmoke particulates (WSP) affect responses to influenza in a sex-dependent manner. In the present study, we used human nasal epithelial cells (hNECs) from both sexes to investigate how particulate exposure could modulate gene expression in the context of SARS-CoV-2 infection. We used diesel exhaust particulate (DEP) as well as WSP derived from eucalyptus or red oak wood. HNECs were exposed to particulates at a concentration of 22 g/cm2 for 2 h then immediately infected with SARS-CoV-2 at a MOI (multiplicity of infection) of 0.5. Exposure to particulates had no significant effects on viral load recovered from infected cells. Without particulate exposure, hNECs from both sexes displayed a robust upregulation of antiviral host response genes, though the response was greater in males. However, WSP exposure before infection dampened expression of genes related to the antiviral host response by 72 h post infection. Specifically, red oak WSP downregulated IFIT1, IFITM3, IFNB1, MX1, CCL3, CCL5, CXCL11, CXCL10, and DDX58, among others. After sex stratification of these results, we found that exposure to WSP prior to SARS-CoV-2 infection downregulated anti-viral gene expression in hNECs from females more so than males. These data indicate that WSP, specifically from red oak, alter virus-induced gene expression in a sex-dependent manner and potentially suppress antiviral host defense responses following SARS-CoV-2 infection.

Although the relationship between the environmental factors such as weather conditions and air pollution and COVID-19 case fatality rate (CFR) has been found, the impacts of these factors to which infected cases are exposed at different infectious stages (e.g., virus exposure time, incubation period, and at or after symptom onset) are still unknown. Understanding this link can help reduce mortality rates. During the first wave of COVID-19 in the United Kingdom (UK), the CFR varied widely between and among the four countries of the UK, allowing such differential impacts to be assessed. We developed a generalized linear mixed-effect model combined with distributed lag nonlinear models to estimate the odds ratio of the weather factors (i.e., temperature, sunlight, relative humidity, and rainfall) and air pollution (i.e., ozone, NO2, SO2, CO, PM10 and PM2.5) using data between March 26, 2020 and May 12, 2020 in the UK. After retrospectively time adjusted CFR was estimated using back-projection technique, the stepwise model selection method was used to choose the best model based on Akaike information criteria (AIC) and the closeness between the predicted and observed values of CFR. We found that the low temperature (8-11{degrees}C), prolonged sunlight duration (11-13hours) and increased PM2.5 (11-18 g/m3) after the incubation period posed a greater risk of death (measured by odds ratio (OR)) than the earlier infectious stages. The risk reached its maximum level when the low temperature occurred one day after (OR = 1.76; 95% CI: 1.10-2.81), prolonged sunlight duration 2-3 days after (OR = 1.50; 95% CI: 1.03-2.18) and increased P.M2.5 at the onset of symptom (OR =1.72; 95% CI: 1.30-2.26). In contrast, prolonged sunlight duration showed a protective effect during the incubation period or earlier. After reopening, many COVID-19 cases will be identified after their symptoms appear. The findings highlight the importance of designing different preventive measures against severe illness or death considering the time before and after symptom onset.

Air pollution remains a great challenge for public health, with the detrimental effects of air pollution on cardiovascular, rhinosinusitis, and pulmonary health increasingly well understood. Recent epidemiological associations point to the adverse effects of air pollution on cognitive decline and neurodegenerative diseases. Mouse models of subchronic exposure to PM2.5 (ambient air particulate matter < 2.5 {micro}m) provide an opportunity to demonstrate the causality of target diseases. Here, we subchronically exposed mice to concentrated ambient PM2.5 for 7 weeks (5 days/week; 8h/day) and assessed its effect on behavior using standard tests measuring cognition or anxiety-like behaviors. Average daily PM2.5 concentration was 200 {micro}g/m3 in the PM2.5 group and 10 {micro}g/m3 in the filtered air group. The novel object recognition (NOR) test was used to assess the effect of PM2.5 exposure on recognition memory. The increase in exploration time for a novel object versus a familiarized object was lower for PM2.5-exposed mice (42% increase) compared to the filtered air (FA) control group (110% increase). In addition, the calculated discrimination index for novel object recognition was significantly higher in FA mice (67 %) compared to PM2.5 exposed mice (57.3%). The object location test (OLT) was used to examine the effect of PM2.5 exposure on spatial memory. In contrast to the FA-exposed control mice, the PM2.5 exposed mice exhibited no significant increase in their exploration time between novel location versus familiarized location indicating their deficit in spatial memory. Furthermore, the discrimination index for novel location was significantly higher in FA mice (62.6%) compared to PM2.5 exposed mice (51%). Overall, our results demonstrate that subchronic exposure to higher levels of PM2.5 in mice causes impairment of novelty recognition and spatial memory.

Wild animals in urbanized environments face several unique challenges, including increased anthropogenic stressors, decreased natural food availability and quality, and increased pollutant exposure. While some work has shown that individual urbanization stressors can have negative impacts on aspects of wild bird physiology, other studies have demonstrated ambiguous or sometimes positive interactions. As such, the impact of multiple, coincident urban stressors on avian health still needs to be fully understood. Here, we addressed this knowledge gap by holistically measuring multiple physiological markers of American robin (Turdus migratorius) health across a gradient of urbanization throughout Chicagoland. We predicted that birds using highly urbanized habitats would experience higher heavy metal contamination, higher oxidative stress, lower body condition, higher avian malaria burden, and decreased measures of immune response compared to exurban birds in the Chicagoland area. Multiple linear models revealed that robins in more urbanized areas exhibited higher levels of heavy metal contamination and slightly elevated levels of associated physiological impairments compared to their counterparts in exurban sites. Additionally, noise and light pollution were significantly associated with oxidative stress and infection status, respectively, albeit in different directions. Overall, our findings underscore how the complex environmental changes that accompany urbanization can impact the health of urban bird populations.

Tropical fish are fast-growing and high energetic-demand organisms, which can be highly vulnerable to long-lasting effects of heat stress and pollution, particularly under food shortages. We tested this by assessing highly complex direct and delayed interactive effects of an extreme temperature (32{degrees}C) from a simulated marine heatwave (MHW), copper (Cu, 0, 100, 150 and 175 {micro}g L-1) and food availability (limited and saturated food) on larvae of a tropical, reef-associated seaperch (Psammoperca waigiensis). Cu, MHW, and food limitation independently reduced survival and growth, partly explained by reduced feeding. The negative effect of Cu on fish survival was more substantial under MHW, particularly under limited food. Delayed interactive effects of Cu, MHW, and food limitation were still lethal to fish larvae during the post-exposure period. These results indicate that reef-associated fish larvae are highly vulnerable to these dominant stressors, impairing their ecological function as predators in the coral reefs. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=101 SRC="FIGDIR/small/481600v1_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@1bc37aborg.highwire.dtl.DTLVardef@1eaedaeorg.highwire.dtl.DTLVardef@9a409eorg.highwire.dtl.DTLVardef@1087cc6_HPS_FORMAT_FIGEXP M_FIG C_FIG

BackgroundAir pollution, particularly from Diesel Exhaust Particles (DEP) and Wildfire Smoke (WFS), is increasingly recognised as a significant driver of neuroinflammation linked to brain diseases. However, the role of microglia in mediating these neuroinflammatory responses remains poorly understood. This study aimed to investigate the effects of air pollution on monocyte-derived microglia-like cells (MDMi) from both young (< 40 years of age), and (older > 60 years of age) healthy individuals, focusing on immune response, cytokine secretion, nitrosative stress, and phagocytic activity. ResultsOur study demonstrated that DEP and WFS extract (WFSE) significantly upregulated expression of the oxidative stress marker, heme-oxygenase-1 (HO-1) in MDMi after 24 hr, with levels normalising by 96 hr, indicating a transient oxidative stress response. Both DEP and WFSE elicited distinct inflammatory cytokine profiles. DEP induced a rapid response, increasing TNF-, IL-6, IL-23, and IL-33 within 2 hr in young MDMi and 24 hr in aged MDMi. In contrast, WFSE triggered a delayed but sustained inflammatory response, with TNF-, IFN-{gamma}, IL-23, and IL-33 levels persisting at 96 hr in aged MDMi, highlighting an age-related vulnerability to air pollutant-induced inflammation. Both pollutants activated p38, ERK, and NF-{kappa}B pathways, with p38 activity resolving by 96 hours and ERK activation persisting, reflecting their distinct roles in cellular stress and inflammation. NF-{kappa}B p65 nuclear translocation, observed at 24 hours, highlighted its critical role in cytokine release and inflammation following exposure to DEP and WFSE. This is the first report of NF-{kappa}B activation in human microglia exposed to air pollutants. ConclusionsThese results highlight the distinct and potentially harmful effects of DEP and WFSE on immune and inflammatory responses in MDMi, particularly in ageing populations, with significant implications for brain health. DEP triggers acute oxidative stress and inflammatory responses, while WFSE induces more prolonged effects, especially in aged microglia. Both pollutants activate the MAPK and NF-{kappa}B pathways and exhibit unique cytokine profiles, underscoring their overlapping yet distinct mechanisms of action. These findings advance our understanding of air pollutant-induced neuroinflammation and its contribution to neurodegeneration, providing a foundation for developing targeted interventions to mitigate the neurotoxic effects of air pollution.

Davao City airshed was selected for air quality mapping using particulate matter (PM) concentrations. PM data were taken from the regulatory office, Environmental Management Bureau XI, from 2016 to 2021 to understand annual variation and determine trends that may be attributed to seasonal changes in the region. PM concentrations were spatially interpolated using Inverse distance weighting (IDW) feature, an interpolation technique of ArcGIS. PM concentration and distribution over the years showed no similar patterns, both for PM10 and PM2.5. No annual similarities of PM concentration were observed, and distribution varies yearly. No seasonal trends were shown on the interpolated maps for PM. However, there was an overall PM concentration decrease and distribution covered fewer affected areas over time. PM concentration in 2016 were generally at a level within the defined limit of NAAQGV except for some AQMS locations and years but sparingly exceeding the NAAQGV limit over time. Results show that PM emissions were lower suggesting a possible success on the regulation policies in the Davao City airshed through reduction or better management of air pollutant emissions.

Iron is essential for almost all bacterial pathogens and consequently it is actively withheld by their hosts. However, the production of extracellular siderophores enables iron sequestration by pathogens, increasing their virulence. Another function of siderophores is extracellular detoxification of non-ferrous metals. Here, we experimentally link the detoxification and virulence roles of siderophores by testing whether the opportunistic pathogen Pseudomonas aeruginosa displays greater virulence after exposure to copper. To do this, we incubated P. aeruginosa under different environmentally relevant copper regimes for either two or twelve days. Subsequent growth in a copper-free environment removed phenotypic effects, before we quantified pyoverdine production (the primary siderophore produced by P. aeruginosa), and virulence using the Galleria mellonella infection model. Copper selected for increased pyoverdine production, which was positively correlated with virulence. This effect increased with time, such that populations incubated with high copper for twelve days were the most virulent. Replication of the experiment with a non-pyoverdine producing strain of P. aeruginosa demonstrated that pyoverdine production was largely responsible for the change in virulence. Therefore we here show a direct link between metal stress and bacterial virulence, highlighting another dimension of the detrimental effects of metal pollution on human health.

The escalating prevalence of infertility and reproductive malignancies in the youth demographic warrants thorough investigation. The escalating ubiquity of communication devices, such as mobile phones and Wi-Fi, exposes individuals to unprecedented levels of Radiofrequency Radiation (RFR), raising concerns about its potential association with reproductive issues and cancer. In this study, we endeavored to elucidate the impact of RFR exposure on the fertility of F0 male Swiss albino mice, as well as the consequential effects on sperm quality and testicular morphology in F1 male mice during adulthood. F0 male mice were subjected to RFR exposure for 3 hours per day, twice daily, over a span of 35 days, followed by mating with naive, unexposed females, culminating in a comprehensive endpoint evaluation. The repercussions of RFR exposure included a diminution in sperm count, heightened incidence of sperm defects, augmented DNA damage in both sperm and bone marrow cells, diminished sperm viability, and aberrations in testicular histology. Subsequent mating of exposed male mice with naive females revealed no discernible effects on pregnancy outcomes, as indicated by the fertility index, litter size, and copulation index.Nevertheless, F1 male offspring exhibited a noteworthy reduction in sperm count and depletion of the germinal epithelium within seminiferous tubules in the testes. These findings propose that RFR exposure to F0 males may precipitate diminished sperm count in subsequent F1 generations, implicating the potential role of epigenetic modulation through the male germline.

Ulaanbaatar city (UB), the capital and the home to half of Mongolias total population, has experienced extreme seasonal air pollution in the past two decades with levels of fine particulate matter with an aerodynamic diameter less than 2.5 micrometers (PM2.5) exceeding 500 g/m3 during winter. Based on monitoring data, (PM2.5), sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO) exposures were estimated for residential areas across UB using Random Forest models. We collected individual-level data on 1093 stillbirths from UB hospital records (2010-2013) and a surveillance database (2014-2018). Using a time-stratified case-crossover design, we investigated whether short-term increases in daily ambient air pollutants with different exposure lags (2 to 6 days) before delivery were associated with stillbirth. We estimated associations using conditional logistic regression and examined individual-level characteristics for effect modification. During the cold season (Oct-Mar) we observed significantly elevated relative odds of stillbirth per interquartile range increase in mean concentrations of PM2.5 (odds ratio [OR]=1.35, 95% confidence interval [CI]=1.07-1.71), SO2 (OR=1.71, 95% CI=1.06-2.77), NO2 (OR=1.30, 95% CI=0.99-1.72), and CO (OR=1.44, 95% CI=1.17-1.77) 6 days before delivery after adjusting for apparent temperature with a natural cubic spline. The associations of pollutant concentrations with stillbirth were significantly stronger among those younger than 25, nulliparous, and without comorbidities or pregnancy complications during stratified analyses. There was a clear pattern of increased risk for women living in areas of lower socioeconomic status. We conclude that acute exposure to ambient air pollution before delivery may trigger stillbirth, and this risk is higher for certain subsets of women.

Glyphosates primary metabolite, aminomethylphosphonic acid (AMPA), is the most detected pollutant in surface waters. Recent studies have raised concerns about its toxicity, yet underlying mechanisms remain poorly understood. A disruption of the gut microbiome, which plays a crucial role in host health, could mediate most of the adverse effects. We investigated the impact of AMPA exposure on the gut microbiome of spined toad tadpoles (Bufo spinosus). We hypothesized that AMPA could alter the gut microbiota composition and that these effects could depend on the microbiota source. We exposed tadpoles to minute concentrations of AMPA and analyzed their faecal microbiota using 16S rRNA gene sequencing as a proxy of the gut microbiota. AMPA exposure decreased the gut bacterial biomass and affected the bacterial community composition of tadpoles faeces. Furthermore, we observed interactions between AMPA exposure and maternal body condition on the Bacteroidota and Actinobacteriota phyla abundances. This suggests a maternal effect on early-life microbial colonizers that could influence the response of the gut microbiome to AMPA. These findings highlight the importance of considering the gut microbiome when studying the effects of environmental contaminants. Further research is needed to elucidate the long-term implications of this microbiome alteration for amphibian health.

Over the last decades, environmental pollution with polycyclic aromatic hydrocarbons (PAH) has risen due to human development and industrial activities. The consequences of potential contamination with oil or any of its components must be evaluated. Here, we faced the effects on cell growth and detoxification that might arise from the exposure to hydrocarbons sourced from contaminated waters. MCF-7 and MDA-MB-231 human breast cancer cells and/or MCF-10A epithelial non-tumorigenic cells were exposed to water-accommodated oil fraction (WAF) or anthracene as a PAH currently found in the environment to evaluate clonogenicity, viability, GST and CAT activities. WAF decreased MDA-MB-231 cells clonogenicity and MDA-MB-231 and MCF-7 cells viability. Anthracene significantly reduced non-tumorigenic cells viability and clonogenicity, without affecting the survival of tumorigenic cells. Both tumorigenic cells responded mainly by activating the antioxidant system through the increment of CAT when exposed to low concentrations of WAF. In both cell lines, WAF also increased GST. Anthracene exposure significantly decreased CAT activity of the three cell lines evaluated. GST activity decreased 38% after 28 {micro}M anthracene exposure in MDA-MB-231 cells (p<0.05) and 15, 17 and 21% after 7 (p<0.05), 14 and 28 {micro}M (p<0.01) in MCF-10A cells, while in MCF-7 cells 28 {micro}M anthracene increased GST activity by 75% (p<0.001). We conclude that the sensitivity of cells to the different contaminants evaluated is affected by the degree of cellular tumorigenicity and exposure to WAF or anthracene may exacerbate malignant conditions. The integration of multiple parameters, analyzed through multivariate methods, offers a comprehensive evaluation of toxicant effects. HIGHLIGHTSO_LIWAF and anthracene affect tumorigenic mammary cells viability and clonogenicity C_LIO_LINon tumorigenic mammary cells show more sensitivity to anthracene exposure C_LIO_LIWAF activates antioxidant and detoxicant system in tumorigenic mammary cells C_LIO_LIAnthracene decreased CAT activity of tumorigenic and non-tumorigenic mammary cells C_LIO_LIAnthracene affected GST activity of tumorigenic and non-tumorigenic mammary cells C_LI