Nanoscale characterization of PM2.5 airborne pollutants reveals high adhesiveness and aggregation capability of soot particles.
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ABSTRACT:
SUBMITTER: Shi Y
PROVIDER: S-EPMC4503936 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Epidemiological and experimental studies have documented that long-term exposure to fine particulate matter (PM2.5) increases the risk of respiratory diseases. However, the details of the underlying mechanism remain unclear. In this study, male C57BL/6 mice were exposed to ambient PM2.5 (mean daily concentration ~64 µg/m³) for 12 weeks through a "real-world" airborne PM2.5 exposure system. We found that PM2.5 caused severe lung injury in mice as evidenced by histopathological examination. Then, tandem mass tag (TMT) labeling quantitative proteomic technology was performed to analyze protein expression profiling in the lungs from control and PM2.5-exposed mice. A total of 32 proteins were differentially expressed in PM2.5-exposed lungs versus the controls. Among these proteins, 24 and 8 proteins were up- and down-regulated, respectively. Gene ontology analysis indicated that PM2.5 exerts a toxic effect on lungs by affecting multiple biological processes, including oxidoreductase activity, receptor activity, and protein binding. Furthermore, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that extracellular matrix (ECM)⁻receptor interaction, phagosome, small cell lung cancer, and phosphatidylinositol 3-kinase(PI3K)-protein kinase B (Akt) signaling pathways contribute to PM2.5-induced pulmonary fibrosis. Taken together, these results provide a comprehensive proteomics analysis to further understanding of the molecular mechanisms underlying PM2.5-elicited pulmonary disease.
| S-EPMC6339163 | biostudies-literature
Project description:BackgroundCurrent air quality standards for particulate matter (PM) use the PM mass concentration [PM with aerodynamic diameters ≤ 10 μm (PM(10)) or ≤ 2.5 μm (PM(2.5))] as a metric. It has been suggested that particles from combustion sources are more relevant to human health than are particles from other sources, but the impact of policies directed at reducing PM from combustion processes is usually relatively small when effects are estimated for a reduction in the total mass concentration.ObjectivesWe evaluated the value of black carbon particles (BCP) as an additional indicator in air quality management.MethodsWe performed a systematic review and meta-analysis of health effects of BCP compared with PM mass based on data from time-series studies and cohort studies that measured both exposures. We compared the potential health benefits of a hypothetical traffic abatement measure, using near-roadway concentration increments of BCP and PM(2.5) based on data from prior studies.ResultsEstimated health effects of a 1-μg/m3 increase in exposure were greater for BCP than for PM(10) or PM(2.5), but estimated effects of an interquartile range increase were similar. Two-pollutant models in time-series studies suggested that the effect of BCP was more robust than the effect of PM mass. The estimated increase in life expectancy associated with a hypothetical traffic abatement measure was four to nine times higher when expressed in BCP compared with an equivalent change in PM(2.5) mass.ConclusionBCP is a valuable additional air quality indicator to evaluate the health risks of air quality dominated by primary combustion particles.
| S-EPMC3261976 | biostudies-literature
Project description:Mitochondria have small mitochondrial DNA (mtDNA) molecules independent from the nuclear DNA, a separate epigenetic machinery that generates mtDNA methylation, and are primary sources of oxidative-stress generation in response to exogenous environments. However, no study has yet investigated whether mitochondrial DNA methylation is sensitive to pro-oxidant environmental exposures.We sampled 40 male participants (20 high-, 20 low-exposure) from each of three studies on airborne pollutants, including investigations of steel workers exposed to metal-rich particulate matter (measured as PM1) in Brescia, Italy (Study 1); gas-station attendants exposed to air benzene in Milan, Italy (Study 2); and truck drivers exposed to traffic-derived Elemental Carbon (EC) in Beijing, China (Study 3). We have measured DNA methylation from buffy coats of the participants. We measured methylation by bisulfite-Pyrosequencing in three mtDNA regions, i.e., the transfer RNA phenylalanine (MT-TF), 12S ribosomal RNA (MT-RNR1) gene and "D-loop" control region. All analyses were adjusted for age and smoking.In Study 1, participants with high metal-rich PM1 exposure showed higher MT-TF and MT-RNR1 methylation than low-exposed controls (difference = 1.41, P = 0.002); MT-TF and MT-RNR1 methylation was significantly associated with PM1 exposure (beta = 1.35, P = 0.025); and MT-RNR1 methylation was positively correlated with mtDNA copy number (r = 0.36; P = 0.02). D-loop methylation was not associated with PM1 exposure. We found no effects on mtDNA methylation from air benzene (Study 2) and traffic-derived EC exposure (Study 3).Mitochondrial MT-TF and MT-RNR1 DNA methylation was associated with metal-rich PM1 exposure and mtDNA copy number. Our results suggest that locus-specific mtDNA methylation is correlated to selected exposures and mtDNA damage. Larger studies are needed to validate our observations.
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Project description:Atmospheric pollution is mainly composed of volatile pollutants and particulate matter that strongly interact. However, their specific roles in the induction of cellular toxicity, in particular the impact of the vectorization of atmospheric pollutants by ultrafine particles, remains to be fully elucidated. For this purpose, non-toxic poly-lactic co-glycolic acid (PLGA) nanoparticles were synthesized and three pollutants (benzo(a)pyrene, naphthalene and di-ethyl-hexyl-phthalate) were adsorbed on the surface of the nanoparticles in order to evaluate the toxicity (cytotoxicity, genotoxicity and ROS induction) of these complexes to a human airway epithelial cell line. The adsorption of the pollutants onto the nanoparticles was confirmed by HPLC analysis. Interestingly, the cytotoxicity assays (MTT, LDH and CellTox Green) clearly demonstrated that the vectorization by nanoparticles decreases the toxicity of the adsorbed pollutants. Genotoxicity was assessed by the micronucleus test and the comet assay and showed no increase in primary DNA damage or in chromosomal aberrations of nanoparticle vectorized pollutants. Neither cytotoxicity nor genotoxicity was correlated with ROS induction. To conclude, our results indicate that the vectorization of pollutants by nanoparticles does not potentiate the toxicity of the pollutants studied and that, on the contrary, adsorption onto nanoparticles could protect cells against pollutants' toxicity.
| S-EPMC5557588 | biostudies-other
Project description:Heavy fuel oil (HFO) particulate matter (PM) emitted by marine engines is known to contain toxic heavy metals, including vanadium (V) and nickel (Ni). The toxicity of such metals will depend on the their chemical state, size distribution, and mixing state. Using online soot-particle aerosol mass spectrometry (SP-AMS), we quantified the mass of five metals (V, Ni, Fe, Na, and Ba) in HFO-PM soot particles produced by a marine diesel research engine. The in-soot metal concentrations were compared to in-PM2.5 measurements by inductively coupled plasma-optical emission spectroscopy (ICP-OES). We found that <3% of total PM2.5 metals was associated with soot particles, which may still be sufficient to influence in-cylinder soot burnout rates. Since these metals were most likely present as oxides, whereas studies on lower-temperature boilers report a predominance of sulfates, this result implies that the toxicity of HFO PM depends on its combustion conditions. Finally, we observed a 4-to-25-fold enhancement in the ratio V:Ni in soot particles versus PM2.5, indicating an enrichment of V in soot due to its lower nucleation/condensation temperature. As this enrichment mechanism is not dependent on soot formation, V is expected to be generally enriched within smaller HFO-PM particles from marine engines, enhancing its toxicity.
| S-EPMC5990929 | biostudies-literature
Project description:Animal and epidemiological studies have suggested that exposure to airborne particulate matter (PM) with an aerodynamic diameter less than 2.5 μm (PM2.5) is associated with the risk of developing type 2 diabetes. However, the mechanism underlying this risk is poorly understood. In the present study, we investigated the effects of PM2.5 exposure on glucose homeostasis and related signaling pathways in mice. Wild-type and nuclear factor erythroid 2-related factor 2 (Nrf2) knockout (Nrf2-/-) C57BL/6 male mice were exposed to either ambient concentrated PM2.5 or filtered air (FA) for 12 weeks through a whole-body PM exposure system. At the end of the exposure, we assessed liver damage, and performed metabolic studies, gene expressions, as well as molecular signal transductions to determine the signaling pathways involving oxidative responses, insulin signaling, and glucose metabolism. Our results indicated that PM2.5 exposure for 12 weeks caused significant liver damage as evidenced by elevated levels of aminotransferase (AST) and alanine aminotransferase (ALT). Furthermore, PM2.5 exposure induced impaired glucose tolerance and inhibited glycogen synthesis, leading to hepatic insulin resistance indicated by higher glucose levels, higher area under the curve (AUC), and homeostasis model assessment of insulin resistance (HOMA-IR) values. We further found that PM2.5 exposure significantly increased the expressions of Nrf2 and Nrf2-regulated antioxidant genes. Moreover, PM2.5 exposure activated the c-Jun N-terminal kinase (JNK) signaling pathway and increased insulin receptor substrate-1 (IRS-1) phosphorylation at Ser307, but reduced protein kinase B phosphorylation at Ser473. Taken together, our study demonstrated PM2.5 exposure triggered Nrf2-mediated oxidative responses and activated the JNK-mediated inhibitory signaling pathway, resulting in hepatic insulin resistance.
| S-EPMC5551225 | biostudies-other
Project description:Objectives: To explore the molecular mechanisms of PM2.5-induced dysfunction in human corneal epithelial cells (HCECs). Methods: RNA-Seq was performed to identify the differentially expressed genes (DEGs) in PM2.5-exposed HCECs compared to unexposed condition, which was followed by validation via real-time PCR (qRT-PCR). Results: A total of 434 DEGs—240 up-regulated and 194 down-regulated—were identified in PM2.5-exposed HCECs rather than unexposed HCECs. The expression of a few genes related to proliferation, inflammation, and aryl hydrocarbon stimulation were significantly altered by PM2.5 exposure, which may contribute to PM2.5-related corneal diseases. Conclusion: The present study identified the altered expression of hundreds of genes in HCECs exposed to PM2.5, which suggests the importance of PM2.5 for cornea health.
2022-08-01 | GSE135262 | GEO
Project description:Medical procedures that produce aerosolized particles are under great scrutiny due to the recent concerns surrounding the COVID-19 virus and increased risk for nosocomial infections. For example, thoracostomies, tracheotomies and intubations/extubations produce aerosols that can linger in the air. The lingering time is dependent on particle size where, e.g., 500 μm (0.5 mm) particles may quickly fall to the floor, while 1 μm particles may float for extended lengths of time. Here, a method is presented to characterize the size of <40 μm to >600 μm particles resulting from surgery in an operating room (OR). The particles are measured in-situ (next to a patient on an operating table) through a 75mm aperture in a ∼400 mm rectangular enclosure with minimal flow restriction. The particles and gasses exiting a patient are vented through an enclosed laser sheet while a camera captures images of the side-scattered light from the entrained particles. A similar optical configuration was described by Anfinrud et al.; however, we present here an extended method which provides a calibration method for determining particle size. The use of a laser sheet with side-scattered light provides a large FOV and bright image of the particles; however, the particle image dilation caused by scattering does not allow direct measurement of particle size. The calibration routine presented here is accomplished by measuring fixed particle distribution ranges with a calibrated shadow imaging system and mapping these measurements to the in-situ imaging system. The technique used for generating and measuring these particles is described. The result is a three-part process where 1) particles of varying sizes are produced and measured using a calibrated, high-resolution shadow imaging method, 2) the same particle generators are measured with the in-situ imaging system, and 3) a correlation mapping is made between the (dilated) laser image size and the measured particle size. Additionally, experimental and operational details of the imaging system are described such as requirements for the enclosure volume, light management, air filtration and control of various laser reflections. Details related to the OR environment and requirements for achieving close proximity to a patient are discussed as well.
| S-EPMC8021156 | biostudies-literature
Project description:This paper concerns the effect of unsaturation of hydrocarbons (single, double, and triple bonds) on soot particle characteristics (mass, number, and size) and on the carcinogenicity of soot particles. The soot particles were produced from oxygen-free pyrolysis of five hydrocarbons, namely: propane, propylene, ethane, ethylene, and acetylene. The characteristics of soot particles were measured with the aid of a differential mobility spectrometer (Cambustion-DMS-500) and measurement of soot mass concentration was confirmed using gravimetric filter measurements. The soot particle carcinogenicity was estimated from the emission quantities of total polyaromatic hydrocarbons (PAHs) and the toxicity equivalent factor (TEF) of each PAH. Oxygen-free pyrolysis of the hydrocarbon fuels was conducted in a laminar tube reactor within the temperature range of 1050 -1350oC at a constant nitrogen flow rate of 20 L/min and constant fuel flow rate of 1% (vol) on carbon-1 basis. The experimental results showed that increasing unsaturation of fuels from single to double and to triple bonds increased the mass concentration, particle size, number concentration, and carcinogenicity of soot particle notably at the initial temperature of 1050 oC. Increase in the pyrolysis temperature of the tube reactor from 1050 - 1350oC, increased the mass concentration and sizes of the soot particle while the number concentration and carcinogenicity of the soot particle decreased. There was a positive correlation between the soot particle number and the corresponding soot particle carcinogenicity, while a negative correlation was observed between the soot particle mass and size with soot particle carcinogenicity regardless of the pyrolysis temperature examined. The potential implication of these observations is that, low-temperature combustion (LTC) applications, aimed at reducing emissions of soot and NOx, could produce higher soot particle number concentration of higher carcinogenicity.
| S-EPMC7419260 | biostudies-literature