Environmental Pollution

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.

Photosymbiosis indicates a long-term association between animals and photosynthetic organisms. It has been mainly investigated in photosymbiotic cnidarians, while other photosymbiotic associations have been largely neglected. The acoel Symsagittifera roscoffensis lives in obligatory symbiosis with the microalgal Tetraselmis convolutae and has recently emerged as alternative model to study photosymbiosis. Here, we investigated the effects of Bisphenol A, a common plastic additive, on two pivotal stages of its lifecycle: aposymbiotic juvenile development and photosymbiogenesis. Based on our results, this pollutant altered the development of the worms and their capacity to engulf algae from the environment at concentrations higher than the levels detected in seawater, yet aligning with those documented in sediments of populated areas. Data provide novel information about the effects of pollutants on photosymbiotic associations and prompt the necessity to monitor their concentrations in marine environmental matrices.

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.

In many regions around the world, including the United States, inorganic arsenic (iAs) contaminates groundwater used for drinking, food production, and irrigation. Although the World Health Organization has set a safety limit of 10 {micro}g/L for arsenic in drinking water, an estimated 200 million people worldwide are still exposed to arsenic concentrations above this threshold. Eliciting a broad range of adverse health effects, arsenic is a known carcinogen classified by the International Agency for Research on Cancer (IARC) and causes increased susceptibility to infectious diseases, highlighting its role as an immunotoxicant. The purpose of this study is to elucidate the effects of arsenic on the innate immune system, namely macrophages, using in vitro exposure models. Bone marrow-derived macrophages (BMDMs) were cultured from adult male and female C57/BL6 mice. These naive macrophages ("M0" BMDMs) were exposed in vitro to a non-cytotoxic dose of iAs (0.1 {micro}M sodium (meta)arsenite) during the 7 day period of macrophage differentiation and stimulated for 24 hrs with LPS and IFN{gamma} (to induce "M1" pro-inflammatory activation) or IL-4 and IL-13 (to induce "M2" anti-inflammatory activation). In a parallel chronic exposure model, RAW 264.7 (RAW) macrophages were cultured in vitro with iAs for 70 days. Culture supernatant analysis for nitric oxide and cytokine secretion revealed sex-dependent differences in immune response between exposure models, as well as between iAs-exposed and nonexposed macrophages, with and without stimulation. Additionally, iAs-exposed macrophages exhibited increased lipid droplet formation and altered lipidomic and metabolomic profiles, as determined by LC/MS. Flow cytometric analysis further revealed changes in macrophage polarization markers in a sex- and stimulation-dependent manner, with M2-related markers being upregulated in iAs-exposed conditions. Finally, to assess the effects of iAs on macrophages in the context of cancer, we demonstrated that iAs-exposed macrophages displayed increased migration toward cancer cell-conditioned media, and promoted cancer cell proliferation. These results suggest that dysregulated macrophage polarization due to iAs exposure could impact susceptibility to diseases. This research contributes to our understanding of the full spectrum of adverse health effects of iAs exposure and may aid in the development of therapeutics for iAs-induced diseases, including cancer.

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

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.

Land snails are one of the most harmful agricultural pests to crops, causing economic devastation to a variety of plants. The purpose of this study is to determine the optimal food preference of land snails, Eobania vermiculata, and evaluate the mortality and biochemical activity of five pesticides using a leaf dipping technique against them in vitro. The findings revealed that in "no-choice feeding," it was observed that land snails consumed a significantly higher amount of Cos lettuce leaves compared to leaves from other plants. However, chicory leaves were found to be the least preferred by the snails. On the other hand, "free choice feeding," revealed that land snails showed a preference for Cos lettuce and cabbage leaves, which were consumed more frequently. Conversely, Komatsuna leaves had the lowest acceptance among the snails. Also, the results indicated the mortality rate increased with an increased concentration during exposure time. After three days, the lower concentrations of Sulfoxaflor and Fipronil caused a high mortality percentage in the animals compared with other pesticides, respectively. Moreover, after one month of exposure to 1000 ppm/100 ml, Chlorantraniliprole caused 46.43% mortality. But Sulfoxaflor and Fipronil exhibited (42.86%) mortality. They achieved LC50 (1010.48, 2501.93, and 1444.66 ppm/100ml), against tested snails, respectively. Nevertheless, Spinetoram and Spirotetramat caused a lower mortality rate. During seven days of exposure to LC25 for five pesticides by leaf dipping on E. vermiculata. They impacted some of the biochemical activity of two enzymes: alanine amino transaminase (ALT), aspartate amino transaminase (AST), total proteins (LP), and the lipid profile of E. vermiculata. The results showed that the activities of ALT, AST, and Triglycerides rose by 50%, with 108 u/l, 407 u/l, and 2064 mg/dl, respectively. Compared to the control and other compounds, Spirotetramat raised total cholesterol by 33 mg/dl. ALT and AST activity and Triglycerides lowered following Spinetoram and Fipronil treatment at 13 u/l, 32u/l, and (4 mg/dl) of TL, respectively. However, no substantial treatments or controls that influence TP, (Total cholesterol and LDH) or LP levels after the exposure period are available. Ultimately, the results indicated that both Cos lettuce and cabbage leaves were the preferred food choices for land snails, as observed in both feeding methods. However, it is important to note that these findings also highlight the need to consider the impact of insecticides on land snails. Incorporating these insecticides into a comprehensive management strategy to mitigate any negative effects of land snails while ensuring the overall well-being of the environment.

In vitro human cell models and new approach methodologies offer valuable alternatives to animal testing, providing human-relevant data for chemical risk assessment. However, the impact of exposure duration and biological levels on the sensitivity of responses in human cells in vitro remains underexplored. In this study, we employed benchmark concentration modeling to derive and compare points of departure (PODs) for apical (A-POD) and transcriptomic (T-POD) changes in human vascular endothelial cells EA.hy926 following short-term (48 h) and long-term (6 and 12 weeks) exposure to 1, 10, and 100 {micro}M and 1, 10, and 100 nM perfluorooctanoic acid (PFOA), respectively. We found that A-POD could not be calculated for short-term exposure; however, A-PODs after 6 and 12 weeks were determined to be 3.7 nM and 5.4 nM, respectively. mRNA sequencing revealed a significant number of differentially expressed genes in PFOA-exposed EA.hy926 cells across all time points. T-POD values after 6 and 12 weeks (4.1 nM and 22.1 nM, respectively) demonstrated greater sensitivity than the acute T-POD (6.3 {micro}M) and were comparable to the chronic A-POD. Functional gene analysis revealed that transcription was a sensitive, yet general molecular pathway affected by acute exposure, while the IL-17 pathway and extracellular matrix and cytokine-cytokine interactions were implicated after 6 and 12 weeks of exposure to PFOA, respectively. In conclusion, chronic PODs proved to be more informative than acute PODs for chemical risk assessment in PFOA-exposed human endothelial cells. Furthermore, transcriptomics data from long-term exposure can elucidate early molecular pathways associated with chemical exposure, highlighting their potential to connect toxicity effects across different biological levels.

Chlorpyrifos (CP) is a widely used insecticide that has been used extensively, contributing towards a negative impact on public health concerns and associated ecosystems. Bioremediation is one of the key biological methods used for reducing these environmental toxicants. The present study examined the effectiveness of a combined process including solar photo-Fenton process followed by bacterial degradation using Ochrobactrum sp. CPD-03 for effective CP degradation in wastewater. Results showed that solar photo-Fenton treatment had CP degradation efficiency of ~42% in 4 h with a final degradation efficiency of ~92% in 96 h upon combined bacterial degradation. Simultaneous survivability of zebrafish (Danio rerio) was also studied during CP degradation. Compared to control, adult zebrafishes showed increased survivability following the addition of CPD-03 in water resulting a reduced CP concentration. CP toxicity in wastewater had caused acetylcholinesterase inhibition in zebrafish; however, this inhibition is due to absence of CP degrading bacteria. Therefore, a combined approach would influence for regulating CP degradation in wastewater along with simultaneous survival of Danio rerio.

The present study has investigated the role of regional meteorology and air quality parameters in the outbreak pattern of COVID-19 pandemic in India. Using the remote sensing based dataset of 12 environmental variables we correlated infective case counts at a district level in India. Our investigation carried out on the circumstantial data from more than 300 major affected districts in India and found that air quality parameters are playing very crucial role in this outbreak. Among the air pollutants, O3 was better correlating with infection counts followed by AOD, CO, NO2, BC and SO2. We also observed that among the weather parameters air temperature, incoming shortwave radiation, wind speed are positively and significantly associate with outbreak pattern and precipitation and humidity are negatively correlated with confirmed cases; only cloud cover has no significant relation. We noted that coastal districts in the both coast of India and districts located in the plain and low-lying areas have experienced bitter situation during this pandemic. Our study suggests that improving air quality with proper strict regulations and complete lockdown during the peak of pandemic could reduce the misfortune in all over India.

The Coronavirus (COVID-19) epidemic, which was first reported in December 2019 in Wuhan, China, has caused 3,314 death as of March 31, 2020 in China. This study aimed to investigate the spatial associations of daily particulate matter (PM) concentrations with death rate of COVID-19 in China. We conducted a cross-sectional analysis to examine the spatial associations of daily PM2.5 and PM10 concentrations with death rate of COVID-19 in China through multiple linear regression method. We found that COVID-19 held higher death rates with increasing concentration of PM2.5 and PM10 levels in the spatial scale, which may affect the process of patients developed from mild to severe and finally influence the prognosis of COVID-19 patients.

Due to their broad-spectrum antimicrobial action and ease of synthesis, silver nanoparticles (AgNPs) are one of the most widely used nanomaterials in different industrial and ecological areas. AgNPs are released into marine ecosystems; however, their ecotoxicological effects have been overlooked. In this study, we evaluated the toxic effects of biogenic and synthesized AgNPs on sea urchin Echinometra lucunter embryos and compared them to those of AgNO3. Fertilized eggs were exposed to five concentrations of the test compounds and a negative control for 48 h under controlled conditions. The EC50-48h of biogenic and synthetic AgNPs and AgNO3 were 0.31, 4.095, and 0.01 g L-1, evidencing that AgNPs are less toxic than AgNO3, and that synthetic AgNP is less toxic. Toxicity to E. lucunter embryos could be explained by the fact that Ag affects DNA replication and induces the formation of pores in the cellular wall, leading to apoptosis.

BackgroundAir pollution has been recognized as an untraditional risk factor for myocardial infarction (MI). However, the MI risk attributable to long-term exposure to fine particulate matter (PM2.5) is unclear, especially in younger populations, and few studies represented the general population. MethodsWe applied the difference-in-differences approach to estimate the relationship between annual PM2.5 exposure and hospitalizations for MI among U.S. residents and further identified potential susceptible subpopulations. All hospital admissions for MI in ten U.S. states over the period 2002-2016 were obtained from the Healthcare Cost and Utilization Project State Inpatient Database. ResultsIn total, 1,914,684 MI hospital admissions from 8,106 ZIP codes in ten states from 2002 to 2016 were included in this study. We observed a 1.35% (95% CI: 1.11-1.59%) increase in MI hospitalization rate for 1 g/m3 increase in annual PM2.5 exposure. The estimate was robust to adjustment for surface pressure, relative humidity and co-pollutants. In the population with exposure at or below 12 g/m3, there was a larger increment of 2.17% (95% CI: 1.79-2.56%) in hospitalization rate associated with 1 g/m3 increase in PM2.5. Young people (0-34 years) and elderly people ([&ge;]75 years) were the two most susceptible age groups. Residents living in more densely populated or poorer areas and individuals with comorbidities were observed to be at a greater risk. ConclusionsThis study indicates long-term residential exposure to PM2.5 could lead to increased risk of MI among U.S. general population. The association persists below current standards. Clinical PerspectiveO_ST_ABSWhat is new?C_ST_ABSO_LILong-term exposure to PM2.5 increased the risk of myocardial infarction in the general U.S. population. C_LIO_LIYoung individuals aged 0-34 years had the highest relative risk from long-term exposure to PM2.5, and elderly people aged [&ge;]75 years were the second most susceptible to the effects. C_LIO_LIIndividuals with iron deficiency anemia, psychosis, and renal failure were more susceptible to the long-term effects of PM2.5 on MI. C_LI What are the clinical implications?O_LILong-term PM2.5 exposure is one of the important modifiable environmental risk factors for myocardial infarction, therefore, air pollution control and behavioral interventions should be taken to prevent the occurrence of myocardial infarction. C_LI

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.

Understanding the ecological toxicity of marine pollutants is essential for assessing marine environmental quality and developing effective protection strategies. This study presents a novel approach using the motility of the marine microalgae as a sensitive physiological indicator for rapid toxicity assessment. Results demonstrated that both copper (0{micro}mol l-1-4.4{micro}mol l-1) and phenol (0mmol l-1-9.1mmol l-1) significantly inhibited algal locomotory behavior parameters (movement patterns, mobility, and swimming speed) within 2 hours, exhibiting clear dose-response relationships. The 2 h-EC50 values determined by logistic regression were 2.2{micro}mol l-1-2.7{micro}mol l-1 for copper and 4.5{micro}mol l-1-5.7 mmol l-1 for phenol. Notably, combined exposure showed antagonistic effects (2 h-EC50 >1 TU). The motility-based assay showed strong correlation with traditional toxicity tests (72h growth inhibition, 24-48 h Daphnia immobilization, and 96h fish mortality), while providing significant advantages in speed and sensitivity. These findings establish microalgal motility as an efficient, ecologically relevant biomarker for comprehensive marine pollutant assessment, offering great potential for environmental monitoring and risk evaluation.

IntroductionThe human breast secretes three types of milk during lactation - colostrum, transitional milk and mature milk However, like any other biofluid, human breast milk is not pristine ObjectivesThe objectives of this study was to determine the levels of polychlorinated biphenyls congeners in colostrum, transitional milk and mature milk of mothers at the Ho Teaching Hospital to ascertain which portion contained the highest levels of PCPBs that could pose any significant health risks to neonates. MethodologyA cross-sectional study design was employed to conduct the study at the Ho Teaching Hospital. Protocol for the study was reviewed and approved by the University of Health and Allied Sciences Research Ethics Committee (UHAS-REC). The study recruited forty-seven (47) mothers using purposive sampling. About 10.0 g of each aliquot of colostrum, transitional milk and mature milk were treated using a modified form of QuEChERS to extract PCBs and the resulting extract analyzed for fourteen (14) PCB congeners using GC-MS/MS. ResultsFourteen (14) PCB congeners were examined in all the 141 breast samples, which represented three different types of human milk. All samples had levels that were below thresholds of detection. The lack of PCB residues in the examined samples may be viewed as positive news. It might suggest that the mothers were only minimally exposed to these industrial pollutants. ConclusionAt any stage of lactation, no PCBs were found in the breast milk samples. As a result, there were no obvious health concerns for breastfed infants from the levels of PCBs found in the samples of breast milk that were examined. The result is good news for international efforts to eliminate PCBs in the environment and on people.

Coral reefs are at risk of bleaching due to various environmental and anthropogenic stressors such as global warming and chemical pollutants. However, there is little understanding of stressor-specific mechanisms that cause coral bleaching. Therefore, conducting accurate ecotoxicological risk assessments and deciphering modes of action of potentially deleterious ultraviolet (UV) filters (sunscreen compounds) are crucial issues. In this study, we evaluated the toxicity and bleaching effect of benzophenone-3 (BP-3), which is widely used in sunscreen products, on the reef-building coral Acropora tenuis. Furthermore, to understand differences in UV filter- and temperature-induced bleaching, a comparative ecotoxicogenomic approach using RNA-seq was integrated into a toxicity test to clarify differences in gene expression changes induced by BP-3 and heat stress (31{degrees}C). The lethal concentration 50% (LC50) was calculated as 3.9 mg/L, indicating that emission level of BP-3 was properly controlled based on the risk assessment. Differentially expressed genes related to oxidative stress and extracellular matrix organization were involved in coral responses to both BP-3 and heat stress, but their patterns differed. Whereas immune and heat-shock responses were activated in response to heat stress, activation of a drug metabolism pathway and several signal transduction pathways were identified in BP-3 treatment groups. Our study enhances understanding of stress responses in corals induced by UV filters and thermal stress. Using potential gene markers identified in this study for eco-epidemiological surveys of stressed corals, we urgently need to develop effective countermeasures.

Chlorpyrifos is classified as an organophosphorus pesticide that exhibits properties of being a broad-spectrum insecticide, acaricide, and nematicide. It is characterized by its ability to degrade quickly and its non-persistent nature. The current investigation involved the determination of the LC50 value of chlorpyrifos on A. testudineus. The computed LC50 values were found to be 11.59, 8.82, 6.30, and 3.82 ppm for exposure durations of 24, 48, 72, and 96 hours, respectively. The levels of protein and glycogen in the stomach, gut, and muscle of A. testudineus, which were subjected to a concentration of 3.82 ppm (LC50 96 hours) chlorpyrifos for a duration of 96 hours, exhibited a notable reduction when compared to the control group. The stomach sections of A. testudineus, when subjected to a concentration of 3.82 ppm chlorpyrifos for a duration of 96 hours, exhibited degeneration of the mucosa layer and necrosis of the mucosa epithelium. The histopathological examination of the intestine revealed several notable findings, including the presence of a disintegrating serosa, a significantly enlarged muscularis layer, and observable damage to both the circular muscle layer and submucosa. Additionally, evidence of necrosis was observed within the mucosa layer. The muscle tissue exhibited degeneration inside the muscle bundles, characterized by the presence of discrete regions of necrosis and the development of vacuoles within the muscle bundles. The results of this study demonstrate that chlorpyrifos exhibits a significant level of toxicity towards A. testudineus, and it is important to note that the absence of mortality does not guarantee the maintenance of physiological well-being in this particular fish species.

This study investigated the cytotoxicity, genotoxicity, oxidative stress, and mitochondrial toxicity in human keratinocytes (HaCaT) caused by lead nitrate. An increase in lead nitrate concentration (50-800 {micro}M) showed a decrease in cell viability and the IC50 concentration was found to be 385.7 {micro}M. Lead nitrate at 250 {micro}M was also found to decrease the clonogenic potential, produce an increased number of binucleated cells with a micronucleus, increase the olive tail movement, reduce the thiol protein content, increase the intracellular and mitochondrial ROS levels, increase the mitochondrial mass and mitochondrial membrane potential. Which showed that Lead nitrate does indeed show cytotoxic, genotoxic effects as well as increase oxidative stress and alter mitochondrial functions. HIGHLIGHTSO_LILead nitrate causes cytotoxicity in keratinocytes with an IC50 conc. of 385.7 {micro}M. C_LIO_LIExposure to lead nitrate showed a significant increase in DNA damage. C_LIO_LILead nitrate increased the mitochondrial membrane potential and mass. C_LI

IntroductionThis study presents an observational analysis of acute poisoning cases admitted to Dhaka Medical College Hospital, Bangladesh, over a two-month period, highlighting key demographic, etiological, clinical, and outcome-based trends. ResultsA total of 611 cases were reviewed, with a predominant incidence among young adults aged 20-40 years. The highest fatality rate occurred in the 16-25-year-old cohort, with a secondary fatality peak noted among individuals aged 66-70, indicating varying vulnerability across age groups. Pesticide-related poisonings were common, with nearly equal distributions between organophosphorus compounds (51%) and non-organophosphorus compounds (49%). Commuter poisoning (31.2%) was notably the leading type of non-pesticide poisoning, primarily associated with criminal activities. Suicidal poisoning accounted for most cases at 57.4%, often linked to family disharmony as a frequent underlying factor. Additionally, snake bites (7.5%) emerged as a notable public health concern, especially in rural areas. Fatalities were highest among those who ingested kerosene (20%), despite its low incidence. Logistic regression analysis identified key predictors of mortality, including severely low Glasgow Coma Scale scores (GCS<9; OR=80.59, p<0.001), hypotension, tachycardia, and pupillary abnormalities. Non-organophosphorus poisonings displayed increased severity in terms of neurological impairment and hypotension compared to organophosphorus poisonings, which mainly resulted in pupillary constriction. Demographic analysis revealed a higher mortality risk among females, rural residents, and individuals with lower educational attainment, although the statistical significance was limited. ConclusionThis study identifies important gaps in managing and preventing acute poisoning in Bangladesh. It calls for structured clinical protocols, better training for healthcare providers, and targeted community interventions. Improving public awareness and timely medical responses is essential to reduce poisoning-related morbidity and mortality.