Browse
Submit Data
Databases
API
Help

Dataset Information

17 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Qianjinweijing Decoction Protects Against Fine Particulate Matter Exposure-mediated Lung Function Disorder.

ABSTRACT: Fine particulate matter (PM_2.5) is well known to impair lung function. Strategies protecting against PM_2.5-exerted lung dysfunction have been less investigated. Qianjinweijing decoction (QJWJ), a decoction of a herbal medicine of natural origin, has been used to treat lung disorders as it inhibits oxidation and inflammation. However, no clinical trial has yet evaluated the role of QJWJ in PM_2.5-induced lung dysfunction. Therefore, we conducted a randomized, double-blind, placebo-controlled trial to assess whether QJWJ provided lung benefits against the adverse effects of PM_2.5 exposure among adults. Eligible participants (n = 65) were recruited and randomized to receive QJWJ decoction (n = 32) or placebo (n = 33) for 4 weeks. The restrictive ventilatory defect (RVD), lung function parameters, and induced sputum were analyzed. The PM_2.5 exposure concentration was significantly associated with the vital capacity (VC), peak expiratory flow (PEF), and forced expiratory flow at 75% of the forced vital capacity (FEF₇₅). The negative associations between PM_2.5 and the lung function parameters were eliminated in response to the QJWJ intervention. Additionally, the percentage of RVD (P = 0.018) and the proportion of eosinophils (Eo%) in induced sputum (P = 0.014) in the QJWJ group was significantly lower than that in the placebo group. This study demonstrated that QJWJ could alleviated PM_2.5-induced lung dysfunction and could be a potential treatment for air pollution-related chronic respiratory disease.

SUBMITTER: Chen R

PROVIDER: S-EPMC9263354 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

A pilot study of blood microRNAs and lung function in young healthy adults with fine particulate matter exposure.

Project description:Fine particulate exposure (PM2.5) is a risk factor of pulmonary diseases such as chronic obstructive pulmonary disease (COPD), but the mechanism underlying was not clear. Recent studies found blood microRNAs (miRNAs) are potential indicators of either COPD or PM2.5 exposure, but these results had no unified conclusions. We suggested it was more targeted to find disease related miRNAs first and then observe them during PM2.5 exposure. Firstly, in order to screen COPD associated miRNAs, we identified differentially expressed blood miRNAs contrasting COPD participants (n=6) without diagnose of COPD or related treatment before and matched control (n=6). In total, 21 miRNAs were differentially expressed in COPD individuals and expression of miR-495-3p, miR-223-5p and miR-194-3p were further validated using qRT-PCR. The results showed miR-495-3p and miR-223-5p significantly increased whereas miR-194-3p decreased marginally (P=0.058) in COPD participants. Secondly, in order to recognize the relevance between these miRNAs and PM2.5 exposure, we designed an independent time-series study nested within "low-high-low" pollution levels. The expression of blood miR-495-3p, miR-223-5p and miR-194-3p were detected before and after exposure (n=8). The results showed expression of miR-223-5p increased significantly while expression of miR-194-3p decreased significantly after exposure. The Pearson analysis showed only miR-194-3p showed a positive statistically correlation with lag0-1 forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) during exposure of PM2.5. So miR-194-3p might be a potential regulator in the toxicological pathways of both PM2.5 exposure and COPD. As this was a pilot study, formal and large-scale studies should be planned in the future.

| S-EPMC6344747 | biostudies-literature

Hepatic alterations associated with fine particulate matter exposure.

Project description:Several studies have pointed to fine particulate matter (PM2.5) as the main responsible for air pollution toxic effects. Indeed, PM2.5 may not only cause respiratory and cardiovascular abnormalities but it may also affect other organs such as the liver. Be that as it may, only a few studies have evaluated the PM2.5 effects on hepatic tissue. Moreover, most of them have not analyzed the relationship between particles composition and toxicological effects. In this study, healthy rats were subjected to urban levels of PM2.5 particles in order to assess their structural and functional effects on the liver. During the exposure periods, mean PM2.5 concentrations were slightly higher than the value suggested by the daily guideline of the World Health Organization. The exposed rats showed a hepatic increase of Cr, Zn, Fe, Ba, Tl and Pb levels. This group also showed leukocyte infiltration, sinusoidal dilation, hydropic inclusions and alterations in carbohydrates distribution. These histologic lesions were accompanied by serological changes, such as increase of total cholesterol and triglycerides, as well as genotoxic damage in their nuclei. We also observed significant associations between several biomarkers and PM2.5 composition. Our results show that exposure to low levels of PM2.5 might cause histologic and serological changes in liver tissue, suggesting that PM2.5 toxicity is influenced not only by their concentration but also by their composition and the exposure frequency.

| S-EPMC7099102 | biostudies-literature

Fine Particulate Matter Exposure Alters Pulmonary Microbiota Composition and Aggravates Pneumococcus-Induced Lung Pathogenesis.

Project description:Exposure to fine particulate matter (PM) with aerodynamic diameter ?2.5 ?m (PM2. 5) is closely correlated with respiratory diseases. Microbiota plays a key role in maintaining body homeostasis including regulation of host immune status and metabolism. As reported recently, PM2. 5 exposure causes microbiota dysbiosis and thus promotes disease progression. However, whether PM2. 5 alters pulmonary microbiota distribution and aggravates bacteria-induced pathogenesis remains unknown. In this study, we used mouse experimental models of PM2. 5 exposure combined with Streptococcus pneumonia infection. We characterized the airway microbiota of bronchoalveolar lavage fluid (BALF) by sequencing the 16S rRNA V3-V4 amplicon on the Illumina MiSeq platform, followed by a combination of bioinformatics and statistical analyses. Shannon-diversity index, observed ASVs, and Fisher's diversity index indicated that microbiota richness was significantly decreased in the mice treated with either PM2. 5 or pneumococcus when compared with the control group. The genera Streptococcus, Prevotella, Leptotrichia, and Granulicatella were remarkably increased in mice exposed to PM2. 5 combined with pneumococcal infection as compared to mice with pneumococcal infection alone. Histopathological examination exhibited that a more pronounced inflammation was present in lungs of mice treated with PM2. 5 and pneumococcus than that in mouse groups exposed to either PM2. 5 or pneumococcal infection alone. Our results demonstrate that PM2. 5 alters the microbiota composition, thereby enhancing susceptibility to pneumococcal infection and exacerbating lung pathogenesis.

| S-EPMC7649221 | biostudies-literature

Long-Term Fine Particulate Matter Exposure and Major Depressive Disorder in a Community-Based Urban Cohort.

Project description:Previous studies have associated short-term air pollution exposure with depression. Although an animal study showed an association between long-term exposure to particulate matter ? 2.5 ?m (PM2.5) and depression, epidemiological studies assessing the long-term association are scarce.We aimed to determine the association between long-term PM2.5 exposure and major depressive disorder (MDD).A total of 27,270 participants 15-79 years of age who maintained an address within the same districts in Seoul, Republic of Korea, throughout the entire study period (between 2002 and 2010) and without a previous MDD diagnosis were analyzed. We used three district-specific exposure indices as measures of long-term PM2.5 exposure. Cox proportional hazards models adjusted for potential confounding factors and measured at district and individual levels were constructed. We further conducted stratified analyses according to underlying chronic diseases such as diabetes mellitus, cardiovascular disease, and chronic obstructive pulmonary disease.The risk of MDD during the follow-up period (2008-2010) increased with an increase of 10 ?g/m3 in PM2.5 in 2007 [hazard ratio (HR) = 1.44; 95% CI: 1.17, 1.78], PM2.5 between 2007 and 2010 (HR = 1.59; 95% CI: 1.02, 2.49), and 12-month moving average of PM2.5 until an event or censor (HR = 1.47; 95% CI: 1.14, 1.90). The association between long-term PM2.5 exposure and MDD was greater in participants with underlying chronic diseases than in participants without these diseases.Long-term PM2.5 exposure increased the risk of MDD among the general population. Individuals with underlying chronic diseases are more vulnerable to long-term PM2.5 exposure.Kim KN, Lim YH, Bae HJ, Kim M, Jung K, Hong YC. 2016. Long-term fine particulate matter exposure and major depressive disorder in a community-based urban cohort. Environ Health Perspect 124:1547-1553;?http://dx.doi.org/10.1289/EHP192.

| S-EPMC5047772 | biostudies-other

Global Effect Factors for Exposure to Fine Particulate Matter.

Project description:We evaluate fine particulate matter (PM2.5) exposure-response models to propose a consistent set of global effect factors for product and policy assessments across spatial scales and across urban and rural environments. Relationships among exposure concentrations and PM2.5-attributable health effects largely depend on location, population density, and mortality rates. Existing effect factors build mostly on an essentially linear exposure-response function with coefficients from the American Cancer Society study. In contrast, the Global Burden of Disease analysis offers a nonlinear integrated exposure-response (IER) model with coefficients derived from numerous epidemiological studies covering a wide range of exposure concentrations. We explore the IER, additionally provide a simplified regression as a function of PM2.5 level, mortality rates, and severity, and compare results with effect factors derived from the recently published global exposure mortality model (GEMM). Uncertainty in effect factors is dominated by the exposure-response shape, background mortality, and geographic variability. Our central IER-based effect factor estimates for different regions do not differ substantially from previous estimates. However, IER estimates exhibit significant variability between locations as well as between urban and rural environments, driven primarily by variability in PM2.5 concentrations and mortality rates. Using the IER as the basis for effect factors presents a consistent picture of global PM2.5-related effects for use in product and policy assessment frameworks.

| S-EPMC6613786 | biostudies-literature

The effects of fine and coarse particulate matter on lung function among the elderly.

Project description:Impaired lung function is associated with morbidity and mortality in the elderly. However, there is a paucity of data regarding the long-term effects of particulate matter (PM) on lung function among the elderly. This study evaluated the exposure-response relationship between ambient PM and different lung function indices among the elderly in Taiwan. A cross-sectional survey of individuals aged ?65 years was conducted in Taiwan from October 2015 to September 2016. Those who attended the annual health examination for the elderly in five hospitals of varying background PM concentrations were enrolled. The long-term (2015 annual mean concentration) exposure to air pollution was estimated by the Kriging method at the residence of each subject. The association between ambient PM exposure and lung function was evaluated by linear regression modeling, with adjustments for age, sex, height, weight, educational attainment, presence of asthma or chronic obstructive pulmonary disease, smoking status, season, and co-pollutants. There were 1241 subjects (mean age, 70.5 years). The mean residential PM2.5 and PM2.5-10 in 2015 was 26.02 and 18.01??g/m3, respectively. After adjustments for confounders and co-pollutants, the FVC decrease was best associated with fine particles (PM2.5), whereas the FEV1, FEF25-75%, FEF25% and FEF50% decreases were best associated with coarse particles (PM2.5-10). An IQR (10??g/m3) increase in PM2.5 decreased FVC by 106.38?ml (4.47%), while an IQR (7.29??g/m3) increase in PM2.5-10 decreased FEV1 and FEF25-75% by 91.23?ml (4.85%) and 104.44?ml/s (5.58%), respectively. Among the Taiwanese elderly, long-term PM2.5 exposure mainly decreases the vital capacity of lung function. Moreover, PM2.5-10 has a stronger negative effect on the function of conductive airways than PM2.5.

| S-EPMC6794286 | biostudies-literature

RNA sequencing reveals particulate matter exposure-induced cholesterol metabolism disorder in ferret lung epithelial cells

Project description:We report the biological effect of particulate matter on ferret lung epithelial cells with different concentration 500 ug/mL and 250 ug/mL. Treatment time is 48 h.

2021-10-28 | GSE186322 | GEO

Long-Term Exposure to Ambient Fine Particulate Matter (PM2.5) and Lung Function in Children, Adolescents, and Young Adults: A Longitudinal Cohort Study.

Project description:BackgroundThe association between long-term exposure to ambient fine particulate matter with aerodynamic diameter ≤2.5μm (PM2.5) and lung function in young people remains uncertain, particularly in Asia, where air pollution is generally a serious problem.ObjectivesThis study investigated the association between long-term exposure to ambient PM2.5 and lung function in Taiwanese children, adolescents, and young adults.MethodsThis study comprised 24,544 participants 6-24 years of age, with 33,506 medical observations made between 2000 and 2014. We used a spatiotemporal model to estimate PM2.5 concentrations at participants' addresses. Spirometry parameters, i.e., forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), and maximum midexpiratory flow (MMEF), were determined. A generalized linear mixed model was used to examine the associations between long-term exposure to ambient PM2.5 and lung function. The odds ratios (ORs) of poor lung function were also calculated after adjusting for a range of covariates.ResultsEvery 10-μg/m3 increase in the 2-y average PM2.5 concentration was associated with decreases of 2.22% [95% confidence interval (CI): -2.60, -1.85], 2.94 (95% CI: -3.36, -2.51), and 2.79% (95% CI: -3.15, -2.41) in the FVC, FEV1, and MMEF, respectively. Furthermore, it was associated with a 20% increase in the prevalence of poor lung function (OR: 1.20; 95% CI: 1.12, 1.29).ConclusionsTwo-year ambient PM2.5 concentrations were inversely associated with lung function and positively associated with the prevalence of poor lung function in children, adolescents, and young adults in Taiwan. https://doi.org/10.1289/EHP5220.

| S-EPMC6957275 | biostudies-literature

Fine Particulate Matter Exposure and Cerebrospinal Fluid Markers of Vascular Injury.

Project description:BACKGROUND:Cerebrovascular diseases play an important role in dementia. Air pollution is associated with cardiovascular disease, with growing links to neurodegeneration. Prior studies demonstrate associations between fine particulate matter (PM2.5) and biomarkers of endothelial injury in the blood; however, no studies have evaluated these biomarkers in cerebrospinal fluid (CSF). OBJECTIVE:We evaluate associations between short-term and long-term PM2.5 exposure with CSF vascular cell adhesion molecule-1 (VCAM-1) and e-selectin in cognitively normal and mild cognitive impairment (MCI)/Alzheimer's disease (AD) individuals. METHODS:We collected CSF from 133 community volunteers at VA Puget Sound between 2001-2012. We assigned short-term PM2.5 from central monitors and long-term PM2.5 based on annual average exposure predictions linked to participant addresses. We performed analyses stratified by cognitive status and adjusted for key covariates with tiered models. Our primary exposure windows for the short-term and long-term analyses were 7-day and 1-year averages, respectively. RESULTS:Among cognitively normal individuals, a 5 ?g/m3 increase in 7-day and 1-year average PM2.5 was associated with elevated VCAM-1 (7-day: 35.4 (9.7, 61.1) ng/ml; 1-year: 51.8 (6.5, 97.1) ng/ml). A 5 ?g/m3 increase in 1-year average PM2.5, but not 7-day average, was associated with elevated e-selectin (53.3 (11.0, 95.5) pg/ml). We found no consistent associations among MCI/AD individuals. CONCLUSIONS:We report associations between short-term and long term PM2.5 and CSF biomarkers of vascular damage in cognitively normal adults. These results are aligned with prior research linking PM2.5 to vascular damage in other biofluids as well as emerging evidence of the role of PM2.5 in neurodegeneration.

| S-EPMC7147945 | biostudies-literature

Global chemical composition of ambient fine particulate matter for exposure assessment.

Project description:Epidemiologic and health impact studies are inhibited by the paucity of global, long-term measurements of the chemical composition of fine particulate matter. We inferred PM2.5 chemical composition at 0.1° × 0.1° spatial resolution for 2004-2008 by combining aerosol optical depth retrieved from the MODIS and MISR satellite instruments, with coincident profile and composition information from the GEOS-Chem global chemical transport model. Evaluation of the satellite-model PM2.5 composition data set with North American in situ measurements indicated significant spatial agreement for secondary inorganic aerosol, particulate organic mass, black carbon, mineral dust, and sea salt. We found that global population-weighted PM2.5 concentrations were dominated by particulate organic mass (11.9 ± 7.3 ?g/m(3)), secondary inorganic aerosol (11.1 ± 5.0 ?g/m(3)), and mineral dust (11.1 ± 7.9 ?g/m(3)). Secondary inorganic PM2.5 concentrations exceeded 30 ?g/m(3) over East China. Sensitivity simulations suggested that population-weighted ambient PM2.5 from biofuel burning (11 ?g/m(3)) could be almost as large as from fossil fuel combustion sources (17 ?g/m(3)). These estimates offer information about global population exposure to the chemical components and sources of PM2.5.

| S-EPMC4238642 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data