Environmental Pollution最新文献

Viral diseases have been present throughout human history, with early examples including influenza (1500 B.C.), smallpox (1000 B.C.), and measles (200 B.C.). The term "virus" was first used in the late 1800s to describe microorganisms smaller than bacteria, and significant milestones include the discovery of the polio virus and the development of its vaccine in the mid-1900s, and the identification of HIV/AIDS in the latter part of the 20th century. The 21st century has seen the emergence of new viral diseases such as West Nile Virus, Zika, SARS, MERS, and COVID-19. Human activities, including crowding, travel, poor sanitation, and environmental changes like deforestation and climate change, significantly influence the spread of these diseases. Conversely, viral diseases can impact the environment by polluting water resources, contributing to deforestation, and reducing biodiversity. These environmental impacts are exacerbated by disruptions in global supply chains and increased demands for resources. This review highlights the intricate relationship between viral diseases and environmental factors, emphasizing how human activities and viral disease progression influence each other. The findings underscore the need for integrated approaches to address the environmental determinants of viral diseases and mitigate their impacts on both health and ecosystems.

Effective biomarkers are paramount importance for the early detection and prognosis prediction of malignant mesothelioma (MM) which mainly caused by asbestos exposure, and DNA methylation has been demonstrated to be a potentially powerful diagnostic tool. To elucidate the relationship between asbestos exposure and alterations in DNA methylation patterns, as well as the potential diagnostic and prognostic value of differentially methylated regions and CpG sites (DMRs/DMCs) in the progression of MM. The current study employed reduced representation bisulfite sequencing (RRBS) to examine the genome-wide DNA methylation profiles in the peripheral blood of individuals exposed to asbestos and those diagnosed with MM, in comparison to the controls, and DMRs/DMCs were subsequently validated by targeted bisulfite sequencing (TBS). Our results suggested that there were 12 DMRs/DMCs exhibiting a consistent change trend of DNA methylation in both RRBS and TBS results. Significant correlations were observed between DNA methylation levels of DMRs/DMCs and the duration of occupational asbestos exposure. The evaluation of the receiver operating characteristic (ROC) curve suggested that the DNA methylation status of FHIT, CCR12P and CDH15 may serve as diagnosis indicator in distinguishing MM patients from healthy controls and those exposed to asbestos. Our findings offer a foundation for the role of DNA methylation in the development of MM induced by asbestos exposure. The potential significance of FHIT, CCR12P and CDH15 DNA methylation alterations in the pathogenesis and advancement of MM disease suggests their potential as diagnostic and prognostic biomarkers.

This study examined the effects of solar light driven plastic degradation on carbon chemistry in the coastal waters of eastern Arabian Sea along the west coast of India. The research was conducted through experimental incubations exposed to natural sunlight at multiple locations between December 2023–February 2024. Photodegradation induced a significant pH decrease (up to 0.38 ± 0.02) between controls and plastic incubations ranging from 8.17 ± 0.01 to 7.54 ± 0.02 with the highest variation in the Mumbai coast ranging from 8.13 ± 0.01 to 7.75 ± 0.03. pH variations are primarily caused by the leaching of organic acids and CO₂ release during solar irradiated incubation. Plastic leaching due to natural light irradiation and subsequent changes in the water chemistry is of prime significance with dissolved organic carbon (DOC) leaching of 0.002–0.03% of plastic weight into the coastal waters. Our estimations suggest 15–75 metric tonnes (MT) of DOC release per year by plastic pollution in the eastern Arabian Sea coastal waters. Further, the fluorescent dissolved organic matter (FDOM) fragmentation, a part of DOC, may act as an organic source of synthetic contaminants and would promote heterotrophic microbial action in the coastal waters. Photodegradation of plastic and the interaction of natural DOC and plastic-derived DOC resulted in longer wavelengths FDOM, which may affect the penetration of photosynthetically active radiation in the water column, thereby impacting primary production. Finally, future research work focussing on the role of plastic pollution in coastal ocean acidification and vice-versa is essential and will be increasingly intense in the upcoming decades.

This paper analyzes the dynamic impact of economic, social, and governance factors on PM2.5 concentrations in 89 countries from 2006 to 2019. Using the GMM-PVAR approach and Impulse-Response Functions, we examine how shocks to specific variables affect PM2.5 concentrations over a 10-year period. Our findings reveal that the influence of these factors on PM2.5 levels varies over time. For example, a shock in urbanization has no effect on PM2.5 concentrations in the first year, but in the second year, pollution increases significantly. In the third period, PM2.5 levels decrease, but they rise again in the fourth period, albeit not significantly. By the fifth period, pollution decreases until a new equilibrium is reached in the sixth period. Additionally, a shock in financial development, government effectiveness, industrialization, trade openness, or GDP has no effect on PM2.5 concentrations in the initial period. However, during the second period, air pollution decreases, followed by an increase in the third period and a decrease again in the fourth period. These dynamic patterns highlight the need for environmental policies that consider the evaluation time horizon. Our analysis is supplemented by the Granger causality test, guiding specific policy recommendations based on our findings.

While previous studies suggested that phthalate exposure poses a risk to cardiovascular health, the results are mixed and indicated variability based on population characteristics and health outcomes assessed. Research that simultaneously investigates the association between urinary phthalate metabolites and multiple cardiovascular risk factors within a single study is relatively scarce. This study assessed human exposure to phthalates by determining urinary metabolite concentrations, and applied multiple statistical techniques to systematically evaluate the individual dose-response relationships and joint effects of phthalate exposure on blood lipids, blood pressure, and fasting blood glucose. The results revealed significant negative associations between urinary phthalate metabolites and low-density lipoprotein cholesterol, triglycerides, total cholesterol, diastolic blood pressure, systolic blood pressure, and fasting blood glucose. Significant nonlinear associations were obtained between specific individual metabolites and diastolic blood pressure. The oxidative stress biomarker 8-hydroxydeoxyguanosine levels in urine and thyroid hormone levels in paired serum were measured simultaneously. Then, we examined the indirect roles of thyroid hormones and oxidative stress in the association between urinary phthalate metabolites and cardiovascular risk factors by mediation and moderation analysis. While the mediation effect was not statistically significant, the negative associations of urinary phthalate metabolites with fasting blood glucose, triglyceride, and lipoprotein cholesterol were statistically significant at lower levels of thyroid hormones by moderation analysis. The association was also significant under certain levels of oxidative stress. The results demonstrated that phthalate exposure is associated with several cardiovascular risk factors, and maintaining appropriate oxidative stress levels and ensuring sufficient thyroid hormone levels may attenuate these associations.

The presence of excessive antibiotic residues poses a significant threat to human health and the environment. This study was designed to identify an effective oxytetracycline (OTC)-degrading strain through the screening of the intestine of black soldier fly larvae (BSFL). A strain designated “B2” was selected using a series of traditional microbial screening methods. It could be identified as Enterococcus faecalis by Gram staining and 16S rDNA sequencing, with a similarity of 99.93%. Its ability to degrade OTC was then assessed using high-performance liquid chromatography (HPLC). The degradation of the strain was characterized using a one-way test to assess the effects of the substrate concentration, inoculum amount, and initial pH on the degrading bacteria. The results indicate that strain B2 exhibited optimal OTC-degrading performance at a substrate concentration of 50 mg/L, with an inoculum amount of 6% and a pH value of 5.0. Specifically, strain B2 achieved degradation rates of 71.11%, 56.14%, and 45.03%. These findings demonstrate the effectiveness of strain B2 in degrading OTC, indicating its potential for use in environmental remediation efforts.

This study investigates the effects of environmentally-relevant concentrations of fluoxetine (FLX, commercial name: Prozac) on wound healing. Pollution of water systems with pharmaceutical and personal care products, including antidepressants such as FLX and other selective serotonin reuptake inhibitors, is a growing environmental concern. Environmentally-relevant FLX concentrations are known to impact physiological functions and behaviour of aquatic animals, however, the effects of exposure on humans are currently unknown. Using a combination of human skin biopsies and a human keratinocyte cell line, we show that exposure to environmental FLX promotes wound closure. We show dose-dependent increases in wound closure with FLX concentrations from 125 ng/l. Using several –omics and pharmaceutical approaches, we demonstrate that the mechanisms underlying enhanced wound closure are increased cell proliferation and serotonin signalling. Transcriptomic analysis revealed 350 differentially expressed genes after exposure. Downregulated genes were enriched in pathways related to mitochondrial function and metabolism, while upregulated genes were associated with cell proliferation and tissue morphogenesis. Kinase profiling showed altered phosphorylation of kinases linked to the MAPK pathway. Consistent with this, phosphoproteomic analyses identified 235 differentially phosphorylated proteins after exposure, with enriched GO terms related to cell cycle, division, and protein biosynthesis. Treatment of skin biopsies and keratinocytes with ketanserin, a serotonin receptor antagonist, reversed the increase in wound closure observed upon exposure. These findings collectively show that exposure to environmental FLX promotes wound healing through modulating serotonin signalling, gene expression and protein phosphorylation, leading to enhanced cell proliferation. Our results justify a transition from the study of behavioural effects of environmental FLX in aquatic animals to the investigation of effects of exposure on wound healing in aquatic and terrestrial animals, including direct impacts on human health.

Ammonia, a common toxic gas, posed a hazard to both human and chickens. The Golgi apparatus, an essential organelle, helped maintain the internal environment of the organism and supported the protein foundation for the endoplasmic reticulum to be involved in pyroptosis. Thus, the Golgi apparatus has garnered significant attention. The purpose of our research was to explore the mechanisms of Golgin A7 (Golga7) involved in pyroptosis after chicken exposure to ammonia. To reach our goal, we first created an in vitro ammonia model to study the effect of ammonia on chicken splenic lymphocyte pyroptosis. Then, leveraging this model, we established Golga7 and miR-32-5p knockdown and overexpression models to investigate their roles in ammonia-induced pyroptosis. We found the ultrastructural changes in the nucleus, Golgi apparatus, and mitochondria of chicken splenic lymphocytes exposure to ammonia. The damage of mitochondria increased the level of Reactive Oxygen Species (ROS), which caused the down-regulation of miR-32-5p. The miR-32-5p inhibitor increased the expression of Golga7 and pyroptosis-related genes (NOD-like receptor protein 3 (NLRP3), Cysteine aspartase-1 (Caspase-1), Golgin A3 (Golga3), Nuclear Factor-kappa B (NF-κB), and Tumor Necrosis Factor-alpha (TNF-α)), which induced the pyroptosis, but when miR-32-5p mimic/si-Golga7 (Golga7 inhibitor) was utilized, these effects were reduced. Our research demonstrated that miR-32-5p/Golga7 regulated NLRP3 involving in the pyroptosis of chicken splenic cells exposed to ammonia. Our study provided a valuable foundation for the prevention and treatment chickens ammonia poisoning in the livestock production.

Addressing the impacts of emerging contaminants within the context of climate change is crucial for understanding ecosystem health decline. Among these, the organic UV-filters 4-methylbenzylidenecamphor (4-MBC) and benzophenone-3 (BP-3) are widely used in cosmetics and personal care products. Their unique physico-chemical properties, along with their growing commercialization and consumption, have made them ubiquitous in aquatic environments through both direct and indirect releases, raising significant concerns about their potential threats to inhabiting biota. Additionally, increasing surface water temperatures exacerbate ecological risks, making it imperative to understand the implications for non-target species at different biological levels. This study investigated the short- and long-term effects of UV-filters 4-MBC or BP-3, at ecologically relevant concentrations, combined with current and predicted warming scenarios, on the performance and male reproductive health of Mytilus galloprovincialis mussel populations. Using biomarkers across sub-cellular, cellular, tissue, and individual levels, the study revealed significant physiological and biochemical impairments in both sperm cells and adults exposed to UV-filters. Temperature emerged as the primary driver influencing mussel responses and modulating the impacts of 4-MBC/BP-3, emphasizing their sensitivity to temperatures outside the optimal range and interactive effects between stressors. Specifically, sperm motility declined with increasing UV-filter concentrations, while temperature alone influenced ROS production, leading to compromised mitochondrial activity and DNA damage in the presence of combined stressors, indicative of potential reproductive impairments. Adults exhibited high UV-filter bioconcentration potential in whole tissues, compromised physiological status, morphophysiological changes in digestive glands, oxidative stress, and alterations in metabolic capacity, antioxidant defences, and biotransformation mechanisms, correlating with UV-filter exposure and temperature increase. Among the UV-filters tested, 4-MBC was the most detrimental, especially when combined with warming. Overall, this study underscores the vulnerability of M. galloprovincialis to cumulative stressors and highlights the importance of employing a multi-biomarker approach to assess and mitigate the impacts of stressors on coastal ecosystems.

Greenspaces are important components of our living environment and have been linked to various human health. However, the mechanisms underlying the linkages remain unclear. Enriching microbiota has emerged as a novel mechanism, but the corresponding evidence is still limited. We collected soil samples from forest land, grassland, and barren land in Zunyi City, southwestern China and prepared soil solutions. A total of 40 BALB/c mice were evenly divided into normal control group, model control group, forest soil group, grassland soil group, and barren land soil group. After establishing the pseudo germ-free mouse model, different soil solutions were administered through gavage, lasting for seven weeks. Fecal samples were collected and a 16S rRNA high-throughput sequencing analysis was performed. Then, alpha- and beta-diversity were calculated and employed to estimate the effects of soil exposures on mice gut microbial diversity and composition. Further, Linear Discriminant Analysis Effect Size (LEfSe) analysis was carried out to evaluate the effects of soil exposures on gut microbiota specific genera abundances and functional pathways. Compared to mice exposed to barren land soils, those exposed to soils sourced from forest land showed an increase of 0.43 and 70.63 units in the Shannon index and the Observed ASVs, respectively. In addition, exposure to soils sourced from forest land and grassland resulted in healthier changes (i.e., more short-chain fatty acids (SCFAs)-producing bacteria) in gut microbiota than those from barren land. Furthermore, mice exposed to forest soil and grassland soil showed enrichment in 5 and 3 pathways (e.g., butanoate metabolism) compared to those exposed to barren land soil, respectively. In conclusion, exposure to various greenspaces soils may modify the gut microbial communities of mice, potentially fostering a more beneficial microbiota profile. Further better-designed studies are needed to validate the current findings and to explore the effects of greenspace related gut microbiota on human health.