Effect of air pollutants particulate matter (PM2.5, PM10), sulfur dioxide (SO2) and ozone (O3) on cognitive health
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ABSTRACT:
SUBMITTER: Meo S
PROVIDER: S-EPMC11343771 | biostudies-literature | 2024 Jan
REPOSITORIES: biostudies-literature
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Project description:Because air pollution is a complex mixture of pollutants consisting of both particulate and gaseous components, understanding the health risks from these pollutants requires an evaluation of their combined effects rather than predictions based on the toxicities of single chemicals alone. Particulate matter (PM2.5) and sulfur dioxide (SO2) commonly co-exist in the atmospheric environment, and epidemiological studies have linked air pollution to the development of neurodegenerative disorders, in addition to increased morbidity from cardiopulmonary diseases. However, few studies have examined the potential effects from combinations of these pollutants on neurodegeneration, especially at NOEC doses. In the present study, we first found that PM2.5 and SO2 co-exposure leads to neurodegeneration at low doses, including neuronal apoptosis, the reduction of synaptic structural protein postsynaptic density (PSD-95) and synaptic functional protein N-methyl-d-aspartate (NMDA) receptor subunits (NR2B), and the elevation of tau phosphorylation in vitro and in vivo, which did not induce clear effects when the compounds were tested separately. Furthermore, we clarified that the microRNA (miRNA) miR-337-5p, which is homologous to a human miRNA that targets tau, was involved in the combined effect and contributed to synergistic neurodegeneration. This work implies the potential risk of neuronal dysfunction from the co-existence of PM2.5 and SO2 in coal-burning areas and provides new insights into the molecular markers for the relevant diseases.
| S-EPMC6060696 | biostudies-literature
Project description:BackgroundSeveral observational studies reported on the association between particulate matter ≤2.5μm (PM2.5) and its absorbance with coronavirus (COVID-19), but none use Mendelian randomisation (MR). To strengthen the knowledge on causality, we examined the association of PM2.5 and its absorbance with COVID-19 risk using MR.MethodsWe selected genome-wide association study (GWAS) integration data from the UK Biobank and IEU Open GWAS Project for two-sample MR analysis. We used inverse variance weighted (IVW) and its multiple random effects and fixed effects alternatives to generally predict the association of PM2.5 and its absorbance with COVID-19, and six methods (MR Egger, weighted median, simple mode, weighted mode, maximum-likelihood and MR-PRESSO) as complementary analyses.ResultsMR results suggested that PM2.5 absorbance was associated with COVID-19 infection (odds ratio (OR) = 2.64; 95% confidence interval (CI) = 1.32-5.27, P = 0.006), hospitalisation (OR = 3.52; 95% CI = 1.05-11.75, P = 0.041) and severe respiratory symptoms (OR = 28.74; 95% CI = 4.00-206.32, P = 0.001) in IVW methods. We observed no association between PM2.5 and COVID-19.ConclusionsWe found a potential causal association of PM2.5 absorbance with COVID-19 infection, hospitalisation, and severe respiratory symptoms using MR analysis. Prevention and control of air pollution could help delay and halt the negative progression of COVID-19.
| S-EPMC10346132 | biostudies-literature
Project description:Fine particulate matter (PM2.5) is the leading environmental risk factor that requires regular monitoring and analysis for effective air quality management. This work presents the variability, trend, and exceedance analysis of PM2.5 measured at US Embassy and Consulate in five Indian megacities (Chennai, Kolkata, Hyderabad, Mumbai, and New Delhi) for six years (2014-2019). Among all cities, Delhi is found to be the most polluted city followed by Kolkata, Mumbai, Hyderabad, and Chennai. The trend analysis for six years for five megacities suggests a statistically significant decreasing trend ranging from 1.5 to 4.19 μg/m3 (2%-8%) per year. Distinct diurnal, seasonal, and monthly variations are observed in the five cities due to the different site locations and local meteorology. All cities show the highest and lowest concentrations in the winter and monsoon months respectively except for Chennai which observed the lowest levels in April. All the cities consistently show morning peaks (~08: 00-10:00 h) and the lowest level in late afternoon hours (~15:00-16:00 h). We found that the PM2.5 levels in the cities exceed WHO standards and Indian NAAQS for 50% and 33% of days in a year except for Chennai. Delhi is found to have more than 200 days of exceedances in a year and experiences an average 15 number of episodes per year when the level exceeds the Indian NAAQS. The trends in the exceedance with a varying threshold (20-380 μg/m3) suggest that not only is the annual mean PM2.5 decreasing in Delhi but also the number of exceedances is decreasing. This decrease can be attributed to the recent policies and regulations implemented in Delhi and other cities for the abatement of air pollution. However, stricter compliance of the National Clean Air Program (NCAP) policies can further accelerate the reduction of the pollution levels.
| S-EPMC7417276 | biostudies-literature
Project description:BackgroundParticulate matter (PM) is strongly linked to human health and has detrimental effects on the eye. Studies have, however, focused on the ocular surface, with limited research on the impact of PM2.5 on intraocular pressure (IOP).MethodsTo investigate the impact of PM2.5 on IOP and the associated mechanism, C57BL/6 mouse eyes were topically exposed to a PM2.5 suspension for 3 months, and human trabecular meshwork (HTM) cells were subjected to various PM2.5 concentrations in vitro. Cell viability, NLRP3/caspase-1, IL-1β, and GSDMD expression, reactive oxygen species (ROS) production and cell contractility were measured by western blot, ELISA, cell counting kit-8, ROS assay kit or a cell contractility assay. ROS scavenger N-acetyl-L-cysteine (NAC) and caspase-1 inhibitor VX-765 were used to intervene in PM2.5-induced damages.ResultsThe results revealed that the IOP increased gradually after PM2.5 exposure, and upregulations of the NLRP3 inflammasome, caspase-1, IL-1β, and GSDMD protein levels were observed in outflow tissues. PM2.5 exposure decreased HTM cell viability and affected contraction. Furthermore, elevated ROS levels were observed as well as an activation of the NLRP3 inflammasome and downstream inflammatory factors caspase-1 and IL-1β. NAC improved HTM cell viability, inhibited the activation of the NLRP3 inflammasome axis, and HTM cell contraction by scavenging ROS. VX-765 showed similar protection against the PM2.5 induced adverse effects.ConclusionThis study provides novel evidence that PM2.5 has a direct toxic effect on intraocular tissues and may contribute to the initiation and development of ocular hypertension and glaucoma. This occurs as a result of increased oxidative stress and the subsequent induction of NLRP3 inflammasome mediated pyroptosis in trabecular meshwork cells.
| S-EPMC7934500 | biostudies-literature
Project description:Air pollution exposure, especially particulate matter ≤2.5 μm in diameter (PM2.5), is associated with poorer kidney function in adults and children. Perinatal exposure may occur during susceptible periods of nephron development. We used distributed lag nonlinear models (DLNMs) to examine time-varying associations between early life daily PM2.5 exposure (periconceptional through age 8 years) and kidney parameters in preadolescent children aged 8-10 years. Participants included 427 mother-child dyads enrolled in the PROGRESS birth cohort study based in Mexico City. Daily PM2.5 exposure was estimated at each participant's residence using a validated satellite-based spatio-temporal model. Kidney function parameters included estimated glomerular filtration rate (eGFR), serum cystatin C, and blood urea nitrogen (BUN). Models were adjusted for child's age, sex and body mass index (BMI) z-score, as well as maternal education, indoor smoking report and seasonality (prenatal models were additionally adjusted for average first year of life PM2.5 exposure). We also tested for sex-specific effects. Average perinatal PM2.5 was 22.7 μg/m3 and ranged 16.4-29.3 μg/m3. Early pregnancy PM2.5 exposures were associated with higher eGFR in preadolescence. Specifically, we found that PM2.5 exposure between weeks 1-18 of gestation was associated with increased preadolescent eGFR, whereas exposure in the first 14 months of life after birth were associated with decreased eGFR. Specifically, a 5 μg/m3 increase in PM2.5 during the detected prenatal window was associated with a cumulative increase in eGFR of 4.44 mL/min/1.732 (95%CI: 1.37, 7.52), and during the postnatal window we report a cumulative eGFR decrease of -10.36 mL/min/1.732 (95%CI: -17.68, -3.04). We identified perinatal windows of susceptibility to PM2.5 exposure with preadolescent kidney function parameters. Follow-up investigating PM2.5 exposure with peripubertal kidney function trajectories and risk of kidney disease in adulthood will be critical.
| S-EPMC8678189 | biostudies-literature
Project description:Exposure to air pollution fine particulate matter (PM2.5) aggravates respiratory and cardiovascular diseases. It has been proposed that PM2.5 uptake by alveolar macrophages promotes local inflammation that ignites a systemic response, but precise underlying mechanisms remain unclear. Here, we demonstrate that PM2.5 phagocytosis leads to NLRP3 inflammasome activation and subsequent release of the pro-inflammatory master cytokine IL-1β. Inflammasome priming and assembly was time- and dose-dependent in inflammasome-reporter THP-1-ASC-GFP cells, and consistent across PM2.5 samples of variable chemical composition. While inflammasome activation was promoted by different PM2.5 surrogates, significant IL-1β release could only be observed after stimulation with transition-metal rich Residual Oil Fly Ash (ROFA) particles. This effect was confirmed in primary human monocyte-derived macrophages and murine bone marrow-derived macrophages (BMDMs), and by confocal imaging of inflammasome-reporter ASC-Citrine BMDMs. IL-1β release by ROFA was dependent on the NLRP3 inflammasome, as indicated by lack of IL-1β production in ROFA-exposed NLRP3-deficient (Nlrp3-/-) BMDMs, and by specific NLRP3 inhibition with the pharmacological compound MCC950. In addition, while ROFA promoted the upregulation of pro-inflammatory gene expression and cytokines release, MCC950 reduced TNF-α, IL-6, and CCL2 production. Furthermore, inhibition of TNF-α with a neutralizing antibody decreased IL-1β release in ROFA-exposed BMDMs. Using electron tomography, ROFA particles were observed inside intracellular vesicles and mitochondria, which showed signs of ultrastructural damage. Mechanistically, we identified lysosomal rupture, K+ efflux, and impaired mitochondrial function as important prerequisites for ROFA-mediated IL-1β release. Interestingly, specific inhibition of superoxide anion production (O2•-) from mitochondrial respiratory Complex I, but not III, blunted IL-1β release in ROFA-exposed BMDMs. Our findings unravel the mechanism by which PM2.5 promotes IL-1β release in macrophages and provide a novel link between innate immune response and exposure to air pollution PM2.5.
| S-EPMC10804998 | biostudies-literature
Project description:Temuco (Chile) is one of the most polluted cities in Chile and Latin America. Although the fine fraction of particulate matter (PM2.5) has been extensively studied and monitored due to its negative impact on public health, its microbiological components remain unknown. We explored, the airborne bacterial community in PM2.5 under good, moderate, alert, pre-emergency and emergency indices of air quality (AQIs) established by the Chilean government. Bacterial community relationship with environmental factors (PM2.5, PM10, carbon monoxide, among others), was also evaluated. Significant differences in PM2.5 bacterial community composition associated with AQIs were revealed, using 16S rRNA target sequences of denaturing gradient gel electrophoresis (DGGE) bands. Bacterial communities in PM2.5 were mainly clustered (80%) into emergency and pre-emergency samples. The dominant phylum was Proteobacteria and most abundant genus was Novosphingobium, traditionally related to opportunistic respiratory diseases. The main factors associated with community structure were PM2.5, PM10 and carbon monoxide concentrations. This study exposed that bacterial community composition in Temuco varies according to AQIs, with the occurrence of potential opportunistic bacteria on heavily polluted days.
| S-EPMC8776980 | biostudies-literature
Project description:The development of infrastructure, a rapidly increasing population, and urbanization has resulted in increasing air pollution levels in the African city of Addis Ababa. Prior investigations into air pollution have not yet sufficiently addressed the sources of atmospheric particulate matter. This study aims to identify the major sources of fine particulate matter (PM2.5) and its seasonal contribution in Addis Ababa, Ethiopia. Twenty-four-hour average PM2.5 mass samples were collected every 6th day, from November 2015 through November 2016. Chemical species were measured in samples and source apportionment was conducted using a chemical mass balance (CMB) receptor model that uses particle-phase organic tracer concentrations to estimate source contributions to PM2.5 organic carbon (OC) and the overall PM2.5 mass. Vehicular sources (28%), biomass burning (18.3%), plus soil dust (17.4%) comprise about two-thirds of the PM2.5 mass, followed by sulfate (6.5%). The sources of air pollution vary seasonally, particularly during the main wet season (June-September) and short rain season (February-April): From motor vehicles, (31.0 ± 2.6%) vs. (24.7 ± 1.2%); biomass burning, (21.5 ± 5%) vs. (14 ± 2%); and soil dust, (11 ± 6.4%) vs. (22.7 ± 8.4%), respectively, are amongst the three principal sources of ambient PM2.5 mass in the city. We suggest policy measures focusing on transportation, cleaner fuel or energy, waste management, and increasing awareness on the impact of air pollution on the public's health.
| S-EPMC8583055 | biostudies-literature
Project description:The health of humans has been negatively impacted by PM2.5 exposure, but the chemical composition and toxicity of PM2.5 might vary depending on its source. To investigate the toxic effects of particulate matter from different sources on lung epithelial cells (A549), PM2.5 samples were collected from residential, industrial, and transportation areas in Nanjing, China. The chemical composition of PM2.5 was analyzed, and toxicological experiments were conducted. The A549 cells were exposed using an air-liquid interface (ALI) exposure system, and the cytotoxic indicators of the cells were detected. The research results indicated that acute exposure to different sources of particulate matter at the air-liquid interface caused damage to the cells, induced the production of ROS, caused apoptosis, inflammatory damage, and DNA damage, with a dose-effect relationship. The content of heavy metals and PAHs in PM2.5 from the traffic source was relatively high, and the toxic effect of the traffic-source samples on the cells was higher than that of the industrial- and residential-source samples. The cytotoxicity of particulate matter was mostly associated with water-soluble ions, carbon components, heavy metals, PAHs, and endotoxin, based on the analysis of the Pearson correlation. Oxidative stress played an important role in PM2.5-induced biological toxicity.
| S-EPMC10821317 | biostudies-literature
Project description:Air pollution is linked to brain inflammation, which accelerates tumorigenesis and neurodegeneration. The molecular mechanisms that connect air pollution with brain pathology are largely unknown but seem to depend on the chemical composition of airborne particulate matter (PM). We sourced ambient PM from Riverside, California, and selectively exposed rats to coarse (PM2.5-10: 2.5-10 µm), fine (PM<2.5: <2.5 µm), or ultrafine particles (UFPM: <0.15 µm). We characterized each PM type via atomic emission spectroscopy and detected nickel, cobalt and zinc within them. We then exposed rats separately to each PM type for short (2 weeks), intermediate (1-3 months) and long durations (1 year). All three metals accumulated in rat brains during intermediate-length PM exposures. Via RNAseq analysis we then determined that intermediate-length PM2.5-10 exposures triggered the expression of the early growth response gene 2 (EGR2), genes encoding inflammatory cytokine pathways (IL13-Rα1 and IL-16) and the oncogene RAC1. Gene upregulation occurred only in brains of rats exposed to PM2.5-10 and correlated with cerebral nickel accumulation. We hypothesize that the expression of inflammation and oncogenesis-related genes is triggered by the combinatorial exposure to certain metals and toxins in Los Angeles Basin PM2.5-10.
| S-EPMC5890281 | biostudies-literature