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.

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

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.

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.

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.

Abstract2O_ST_ABSBackgroundC_ST_ABSSustained exposures to high atmospheric levels of PM2.5 at population scale are associated with increased risks for pulmonary inflammatory diseases. These are marked by activation of the TRPC6 (Transient Receptor Potential Canonical type 6) calcium channel, increased reactive oxygen species (ROS) and oxidative stress. Long term exposures are associated with reduced life span, and increased incidences of cardiovascular diseases, dementia, Parkinsons and Alzheimer disease, and increased risk of autism and autism spectrum disorders. It has been proposed that the PM2.5 toxin is benzo[a]pyrene (B[a]P) that is adsorbed to the surface of the PM2.5 particle.. But the mechanism by which B[a]P might drive pulmonary inflammatory diseases, or any other of the indications above, are not known. HypothesisB[a]P was recently reported to bind irreversibly and destructively to the {beta}2 Adrenergic Receptor ({beta}2AR) in the lung. We have therefore hypothesized that B[a]P is the adsorbed PM2.5 toxin, and that {beta}2AR is the B[a]P receptor responsible for TRPC6 activation in lung epithelial cells. ResultsTo test this hypothesis, we exposed a polarized organoid model of normal human lung epithelia, polarized lung epithelial 16HBE14o-cells, and tracheobronchial slice cultures from ferret lung to either PM2.5 or B[a]P. We found that both PM2.5 and B[a]P: (i) irreversibly activated of {beta}2AR signaling via Gi to PI3K/AKT; (ii) increased NF{kappa}B-activated release of proinflammatory cytokines through IKK{beta} activation by PI3K/AKT, which was suppressed by the PI3K inhibitor LY 294002 (iii) desensitized and destroyed the activated {beta}2AR receptor by endocytic recycling; (iv) also destroyed {beta}2ARs signalplex partner CFTR by the same process; (v) activated the CFTR-bound calcium channel protein TRPC6 due to loss of inhibitory CFTR; leading to (vi) increased cytosolic [Ca2+] concentration; (vii) increased ROS due to mitochondrial uncoupling; and (viii) increased expression of oxidative stress. Treatment with the TRPC6 inhibitor BI 749327 blocked steps (vi-viii), and preserved CFTR from endocytic loss. Treatment of tracheobronchial slice cultures of ferret lung with either PM2.5 or B[a]P resulted in increased secretion of IL-6, increased expression of TRPC6, and reduced expression of {beta}2AR and CFTR. Finally, we found that exposure of lung organoids to B[a]P significantly reduced expression of the same five microRNAs (miR-126a-3p, miR-30b-5p, miR-103a-3p, miR-26a-5p, and miR-766-3p) previously identified in sera from service members exposed to PM2.5 from burn pit emissions during deployment to Iraq and Afghanistan. ConclusionPM2.5 and the PM2.5 toxin benzo[a]pyrene (B[a]P) induce inflammation and oxidative stress in the airway by increased expression of TRPC6 and inactivation of {beta}2AR/CFTR signaling. These discoveries mark the first identification of a mechanism by which exposure to PM2.5 or the PM2.5 toxin B[a]P itself can induce inflammation and TRPC6-dependent oxidative stress in lung epithelia.

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.

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.

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.

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.