PM2.5 induced neurodegenerative-like changes in mice and the antagonistic effects of vitamin E.
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ABSTRACT:
SUBMITTER: Liu X
PROVIDER: S-EPMC6425994 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:We present a newly developed approach to characterize the sources of fine particulate matter (PM2.5)-related premature deaths in Europe using the chemical transport model GEOS-Chem and its adjoint. The contributions of emissions from each individual country, species, and sector are quantified and mapped out at km scale. In 2015, total PM2.5-related premature death is estimated to be 449,813 (257,846-722,138) in Europe, 59.0% of which were contributed by domestic anthropogenic emissions. The anthropogenic emissions of nitrogen oxides, ammonia, and organic carbon contributed most to the PM2.5-related health damages, making up 29.6%, 23.2%, and 16.8%, respectively of all domestic anthropogenic contributions. Residential, agricultural, and ground transport emissions are calculated to be the largest three sectoral sources of PM2.5-related health risks, accounting for 23.5%, 23.0%, and 19.4%, respectively, of total anthropogenic contributions within Europe. After excluding the influence of extra-regional sources, we find eastern European countries suffered from more premature deaths than their emissions caused; in contrast, the emissions from some central and western European regions contributed premature deaths exceeding three times the number of deaths that occurred locally. During 2005-2015, the first decade of PM2.5 regulation in Europe, emission controls reduced PM2.5-related health damages in nearly all European countries, resulting in 63,538 (46,092-91,082) fewer PM2.5-related premature deaths. However, our calculation suggests that efforts to reduce air pollution from key sectors in some countries can be offset by the lag in control of emissions in others. International cooperation is therefore vitally important for tackling air pollution and reducing corresponding detrimental effects on public health.
| S-EPMC10027220 | biostudies-literature
Project description:Background & aimsEmerging evidence supports ambient fine particulate matter (PM2.5) exposure is associated with insulin resistance (IR) and hepatic lipid accumulation. In this study, we aimed to evaluate the sex-dependent vulnerability in response to PM2.5 exposure and investigate the underlying mechanism by which PM2.5 modulates hepatic lipid metabolism.MethodsBoth male and female C57BL/6 mice were randomly assigned to ambient PM2.5 or filtered air for 24?weeks via a whole body exposure system. High-coverage quantitative lipidomics approaches and liquid chromatography-mass spectrometry techniques were performed to measure hepatic metabolites and hormones in plasma. Metabolic studies, histological analyses, as well as gene expression levels and molecular signal transduction analysis were applied to examine the effects and mechanisms by which PM2.5 exposure-induced metabolic disorder.ResultsFemale mice were more susceptible than their male counterparts to ambient PM2.5 exposure-induced IR and hepatic lipid accumulation. The hepatic lipid profile was changed in response to ambient PM2.5 exposure. Levels of hepatic triacylglycerols (TAGs), free fatty acids (FFAs) and cholesterol were only increased in female mice from PM group compared to control group. Plasmalogens were dysregulated in the liver from PM2.5-exposed mice as well. In addition, exposure to PM2.5 led to enhanced hepatic ApoB and microsomal triglyceride transport protein expression in female mice. Finally, PM2.5 exposure inhibited hypothalamus-pituitary-adrenal (HPA) axis and decreased glucocorticoids levels, which may contribute to the vulnerability in PM2.5-induced metabolic dysfunction.ConclusionsAmbient PM2.5 exposure inhibited HPA axis and demonstrated sex-associated differences in its effects on IR and disorder of hepatic lipid metabolism. These findings provide new mechanistic evidence of hormone regulation in air pollution-mediated metabolic abnormalities of lipids and more personalized care should be considered in terms of sex-specific risk factors.
| S-EPMC7178763 | biostudies-literature
Project description:IntroductionDespite the London Underground (LU) handling on average 2.8 million passenger journeys per day, the characteristics and potential health effects of the elevated concentrations of metal-rich PM2.5 found in this subway system are not well understood.MethodsSpatial monitoring campaigns were carried out to characterise the health-relevant chemical and physical properties of PM2.5 across the LU network, including diurnal and day-to-day variability and spatial distribution (above ground, depth below ground and subway line). Population-weighted station PM2.5 rankings were produced to understand the relative importance of concentrations at different stations and on different lines.ResultsThe PM2.5 mass in the LU (mean 88??g?m-3, median 28??g?m-3) was greater than at ambient background locations (mean 19??g?m-3, median 14??g?m-3) and roadside environments in central London (mean 22??g?m-3, median 14??g?m-3). Concentrations varied between lines and locations, with the deepest and shallowest submerged lines being the District (median 4??g?m-3) and Victoria (median 361??g?m-3 but up to 885??g?m-3). Broadly in agreement with other subway systems around the world, sampled LU PM2.5 comprised 47% iron oxide, 7% elemental carbon, 11% organic carbon, and 14% metallic and mineral oxides. Although a relationship between line depth and air quality inside the tube trains was evident, there were clear influences relating to the distance from cleaner outside air and the exchange with cabin air when the doors open. The passenger population-weighted exposure analysis demonstrated a method to identify stations that should be prioritised for remediation to improve air quality.ConclusionPM2.5 concentrations in the LU are many times higher than in other London transport Environments. Failure to include this environment in epidemiological studies of the relationship between PM2.5 and health in London is therefore likely to lead to a large exposure misclassification error. Given the significant contribution of underground PM2.5 to daily exposure, and the differences in composition compared to urban PM2.5, there is a clear need for well-designed studies to better understand the health effects of underground exposure.
| S-EPMC6902242 | biostudies-literature
Project description:BackgroundStudies suggested that PM2.5 exposure could lead to adverse reproductive effects on male animals. However, the underlying mechanism is still not clear. Besides, animals in the majority of previous studies were exposed to PM2.5 through intratracheal instillation which should be improved. In addition, limited amount of research has been conducted in China where the PM2.5 concentration is higher and the PM2.5 components are different. The aim of this work is to explore the effects of concentrated ambient PM2.5 (CAP) on mice sperm quality and testosterone biosynthesis.MethodsA total of 12 male C57BL/6 mice were exposed to filtered air (FA) or CAP for 125 days using the Shanghai Meteorological and Environmental Animal Exposure System. The mice sperm concentration, sperm motility, DNA fragmentation index, high DNA stainability and plasma testosterone were analyzed. Testicular histology and sperm morphology were observed through optical microscope. Testosterone biosynthesis related gene expressions were analyzed using real-time PCR, including cytochrome P450 CHOL side-chain cleavage enzyme (P450scc), steroidogenic acute regulatory protein (StAR), 3?-hydroxysteroid dehydrogenase (3? HSD), 17?-hydroxysteroid dehydrogenase, cytochrome P450 aromatase (P450arom), estrogen receptor (ER), androgen receptor (AR) and follicle stimulating hormone receptor (FSHR).ResultsExposure to CAP resulted in disturbance of various stages of spermatogenesis and significant higher percentage of abnormal sperm (FA vs. CAP: 24.37% vs. 44.83%) in mice testis. CAP exposure significantly decreased sperm concentration (43.00 × 106 vs. 25.33 × 106) and motility (PR: 63.58% vs. 55.15%; PR + NP: 84.00% vs. 77.08%) in epididymis. Plasma testosterone concentration were significantly declined (0.28 ng/ml vs. 0.69 ng/ml) under CAP exposure. Notably, the levels of testosterone biosynthesis related genes, StAR, P450scc, P450arom, ER and FSHR were significantly decreased with CAP exposure.ConclusionConcentrated ambient PM2.5 exposure altered mice sperm concentration, motility and morphology, which might be mediated primarily by the decline in testosterone concentration and testosterone biosynthesis process.
| S-EPMC6885350 | biostudies-literature
Project description:Greater Cairo (Egypt) is a megalopolis where the studies of the air pollution events are of extremely high relevance, for the geographical-climatological aspects, the anthropogenic emissions and the health impact. While preliminary studies on the particulate matter (PM) chemical composition in Greater Cairo have been performed, no data are yet available on the PM's toxicity. In this work, the in vitro toxicity of the fine PM (PM2.5) sampled in an urban area of Greater Cairo during 2017-2018 was studied. The PM2.5 samples collected during spring, summer, autumn and winter were preliminary characterized to determine the concentrations of ionic species, elements and organic PM (Polycyclic Aromatic Hydrocarbons, PAHs). After particle extraction from filters, the cytotoxic and pro-inflammatory effects were evaluated in human lung A549 cells. The results showed that particles collected during the colder seasons mainly induced the xenobiotic metabolizing system and the consequent antioxidant and pro-inflammatory cytokine release responses. Biological events positively correlated to PAHs and metals representative of a combustion-derived pollution. PM2.5 from the warmer seasons displayed a direct effect on cell cycle progression, suggesting possible genotoxic effects. In conclusion, a correlation between the biological effects and PM2.5 physico-chemical properties in the area of study might be useful for planning future strategies aiming to improve air quality and lower health hazards.
| S-EPMC6829270 | biostudies-literature
Project description:To stop the spread of COVID-19 (2019 novel coronavirus), China placed lockdown on social activities across China since mid-January 2020. The government actions significantly affected emissions of atmospheric pollutants and unintentionally created a nationwide emission reduction scenario. In order to assess the impacts of COVID-19 on fine particular matter (PM2.5) levels, we developed a "conditional variational autoencoder" (CVAE) algorithm based on the deep learning to discern unsupervised PM2.5 anomalies in Chines cities during the COVID-19 epidemic. We show that the timeline of changes in number of cities with unsupervised PM2.5 anomalies is consistent with the timeline of WHO's response to COVID-19. Using unsupervised PM2.5 anomaly as a time node, we examine changes in PM2.5 before and after the time node to assess the response of PM2.5 to the COVID-19 lockdown. The rate of decrease of PM2.5 around the time node in northern China is 3.5 times faster than southern China, and decreasing PM2.5 levels in southern China is 3.5 times of that in northern China. Results were also compared with anomalous PM2.5 occurring in Chinese's Spring Festival from 2017 to 2019, PM2.5 anomalies during around Chinese New Year in 2020 differ significantly from 2017 to 2019. We demonstrate that this method could be used to detect the response of air quality to sudden changes in social activities.
| S-EPMC8247192 | biostudies-literature
Project description:BackgroundThe adverse health effects of fine particulate matter (PM2.5) exposure are associated with marked inflammatory responses. Adipose-derived stem cells (ADSCs) have immunosuppressive effects, and ADSC transplantation could attenuate pulmonary fibrosis in different animal disease models. However, whether ADSCs affect PM2.5-induced lung injury has not been investigated.MethodC57BL/6 mice were exposed to PM2.5 every other day via intratracheal instillation for 4 weeks. After that, the mice received tail vein injections of ADSCs every 2 weeks.ResultsADSC transplantation significantly attenuated systemic and pulmonary inflammation, cardiac dysfunction, fibrosis, and cell death in PM2.5-exposed mice. RNA-sequencing results and bioinformatic analysis suggested that the downregulated differentially expressed genes (DEGs) were mainly enriched in inflammatory and immune pathways. Moreover, ADSC transplantation attenuated PM2.5-induced cell apoptosis and pyroptosis in the lungs and hearts.ConclusionADSCs protect against PM2.5-induced adverse health effects through attenuating pulmonary inflammation and cell death. Our findings suggest that ADSC transplantation may be a potential therapeutic approach for severe air pollution-associated diseases.
| S-EPMC8214780 | biostudies-literature
Project description:BackgroundExposure to fine particulate matter (PM2.5) is associated with the risk of developing metabolic-associated fatty liver disease (MAFLD). Melatonin is the main secreted product of the pineal gland and has been reported to prevent hepatic lipid metabolism disorders. However, it remains uncertain whether melatonin could protect against PM2.5-induced MAFLD.Methods and resultsThe purpose of our study was to investigate the mitigating effects of melatonin on hepatic fatty degeneration accelerated by PM2.5 in vivo and in vitro. Histopathological analysis and ultrastructural images showed that PM2.5 induced hepatic steatosis and lipid vacuolation in ApoE-/- mice, which could be effectively alleviated by melatonin administration. Increased ROS production and decreased expression of antioxidant enzymes were detected in the PM2.5-treated group, whereas melatonin showed recovery effects after PM2.5-induced oxidative damage in both the liver and L02 cells. Further investigation revealed that PM2.5 induced oxidative stress to activate PTP1B, which in turn had a positive feedback regulation effect on ROS release. When a PTP1B inhibitor or melatonin was administered, SP1/SREBP-1 signalling was effectively suppressed, while Nrf2/Keap1 signalling was activated in the PM2.5-treated groups.ConclusionOur study is the first to show that melatonin alleviates the disturbance of PM2.5-triggered hepatic steatosis and liver damage by regulating the ROS-mediated PTP1B and Nrf2 signalling pathways in ApoE-/- mice. These results suggest that melatonin administration might be a prospective therapy for the prevention and treatment of MAFLD associated with air pollution.
| S-EPMC9200552 | biostudies-literature
Project description:The serious ambient fine particulate matter (PM2.5) is one of the key risk factors for lung cancer. However, existing studies on the health effects of PM2.5 in China were less considered the regional transport of PM2.5 concentration. In this study, we aim to explore the association between lung cancer and PM2.5 and then forecast the PM2.5-induced lung cancer morbidity and mortality in China. Ridge regression (RR), partial least squares regression (PLSR), model tree-based (MT) regression, regression tree (RT) approach, and the combined forecasting model (CFM) were alternative forecasting models. The result of the Pearson correlation analysis showed that both local and regional scale PM2.5 concentration had a significant association with lung cancer mortality and morbidity and compared with the local lag and regional lag exposure to ambient PM2.5; the regional lag effect (0.172~0.235 for mortality; 0.146~0.249 for morbidity) was not stronger than the local lag PM2.5 exposure (0.249~0.294 for mortality; 0.215~0.301 for morbidity). The overall forecasting lung cancer morbidity and mortality were 47.63, 47.86, 39.38, and 39.76 per 100,000 population. The spatial distributions of lung cancer morbidity and mortality share a similar spatial pattern in 2015 and 2016, with high lung cancer morbidity and mortality areas mainly located in the central to east coast areas in China. The stakeholders would like to implement a cross-regional PM2.5 control strategy for the areas characterized as a high risk of lung cancer.
| S-EPMC7293676 | biostudies-literature
Project description:PM2.5 and formaldehyde (FA) are major outdoor and indoor air pollutants in China, respectively, and both are known to be harmful to human health and to be carcinogenic. Of all the known chronic health effects, leukaemia is one of the most serious health risks associated with these two pollutants. To explore the influence and underlying mechanisms of exposure to formaldehyde and PM2.5 on hematopoietic toxicity, we systematically studied the toxicity induced in hematopoietic organs: bone marrow (BM); spleen; and myeloid progenitor cells (MPCs). Male Balb/c mice were exposed to: PM2.5 (20, 160 μg/kg·d) at a dose of 40 μL per mouse or formaldehyde (0.5, 3.0 mg/m3) for 8 h per day for 2 weeks or co-exposed to formaldehyde and PM2.5 (20 μg/kg·d PM2.5 + 0.5 mg/m3 FA, 20 μg/kg·d PM2.5 + 3 mg/m3 FA, 160 μg/kg·d PM2.5 + 0.5 mg/m3 FA, 160 μg/kg·d PM2.5 + 3 mg/m3 FA) for 2 weeks. Similar toxic effects were found in the formaldehyde-only and PM2.5-only groups, including significant decrease of blood cells and MPCs, along with decreased expression of hematopoietic growth factors. In addition, individual exposure of formaldehyde or PM2.5 increased oxidative stress, DNA damage and immune system disorder by destroying the balance of Th1/Th2, and Treg/Th17. DNA repair was markedly inhibited by deregulating the mammalian target of rapamycin (mTOR) pathway. Combined exposure to PM2.5 and formaldehyde led to more severe effects. Administration of Vitamin E (VE) was shown to attenuate these effects. In conclusion, our findings suggested that PM2.5 and formaldehyde may induce hematopoietic toxicity by reducing the expression of hematopoietic growth factors, increasing oxidative stress and DNA damage, activating the 'immune imbalance' pathway and suppressing the DNA-repair related mTOR pathway. The hematopoietic toxicity induced by combined exposure of PM2.5 and formaldehyde might provide further insights into the increased incidence of hematological diseases, including human myeloid leukaemia.
| S-EPMC7839661 | biostudies-literature