Dataset Information

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

ABSTRACT: 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.

SUBMITTER: Zhou T

PROVIDER: S-EPMC6344747 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

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

Zhou Tianyu T Yu Qing Q Sun Chao C Wang Yunxia Y Zhong Yijue Y Wang Guangfa G

Journal of thoracic disease 20181201 12

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 C ...[more]

PMID: 30746254

Similar Datasets

Project description:BACKGROUND:Long-term exposure to particulate matter (PM) air pollution may increase blood pressure and the risk of hypertension. However, epidemiological evidence is scarce and inconsistent. OBJECTIVES:We investigated the associations between long-term exposure to PM with an aerodynamic diameter <2.5?m (PM2.5), blood pressure, and incident hypertension in a large Taiwanese cohort. METHODS:We studied 361,560 adults ?18y old from a large cohort who participated in a standard medical examination program during 2001 to 2014. Among this group, 125,913 nonhypertensive participants were followed up. A satellite-based spatiotemporal model was used to estimate the 2-y average PM2.5 concentrations at each participant's address. Multivariable linear regression was used in the cross-sectional data analysis with the 361,560 participants to investigate the associations between PM2.5 and systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse pressure (PP), and Cox proportional hazard regression was used in the cohort data analysis with the 125,913 participants to investigate the associations between PM2.5 and incident hypertension. RESULTS:Each 10-?g/m3 increment in the 2-y average PM2.5 concentration was associated with increases of 0.45?mmHg [95% confidence interval (CI): 0.40, 0.50], 0.07?mmHg (95% CI: 0.04, 0.11), and 0.38?mmHg (95% CI: 0.33, 0.42) in SBP, DBP, and PP, respectively, after adjusting for a wide range of covariates and possible confounders. Each 10-?g/m3 increment in the 2-y average PM2.5 concentration was associated with an increase of 3% in the risk of developing hypertension [hazard?ratio=1.03 (95% CI: 1.01, 1.05)]. Stratified and sensitivity analyses yielded similar results. CONCLUSIONS:Long-term exposure to PM2.5 air pollution is associated with higher blood pressure and an increased risk of hypertension. These findings reinforce the importance of air pollution mitigation strategies to reduce the risk of cardiovascular disease. https://doi.org/10.1289/EHP2466.

Project description:BackgroundFine particulate matter (PM2.5) related mild inflammation, altered autonomic control of cardiovascular function, and changes to cell function have been observed in controlled human exposure studies.MethodsTo measure the systemic and cardiopulmonary impacts of low-level PM exposure, we exposed 20 healthy, young volunteers to PM2.5, in the form of concentrated ambient particles (mean: 37.8 μg/m3, SD 6.5), and filtered air (mean: 2.1 μg/m3, SD 2.6). In this double-blind, crossover study the exposure order was randomized. During the 4 h exposure, volunteers (7 females and 13 males) underwent light intensity exercise to regulate ventilation rate. We measured pulmonary, cardiac, and hematologic end points before exposure, 1 h after exposure, and again 20 h after exposure.ResultsLow-level PM2.5 resulted in both pulmonary and extra-pulmonary changes characterized by alterations in systematic inflammation markers, cardiac repolarization, and decreased pulmonary function. A mean increase in PM2.5 concentration (37.8 μg/m3) significantly increased serum amyloid A (SAA), C-reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1), and soluble vascular cell adhesion molecule-1 (sVCAM-1), 1 h after exposure by 8.7, 9.1, 10.7, and 6.6%, respectively, relative to the filtered air control. SAA remained significantly elevated (34.6%) 20 h after PM2.5 exposure which was accompanied by a 5.7% decrease in percent neutrophils. Decreased pulmonary function was observed 1 h after exposure through a 0.8 and 1.2% decrease in forced expiratory volume in 1 s (FEV1) and FEV1/ forced vital capacity (FEV1/FVC) respectively. Additionally, sex specific changes were observed in repolarization outcomes following PM2.5 exposure. In males, P-wave and QRS complex were increased by 15.4 and 5.4% 1 h after exposure.ConclusionsThis study is the first controlled human exposure study to demonstrate biological effects in response to exposure to concentrated ambient air PM2.5 particles at levels near the PM2.5 US NAAQS standard.Clinical trial registration informationclinicaltrials.gov ; Identifier: NCT03232086 . The study was registered retrospectively on July 25, 2017, prior to final data collection on October 25, 2017 and data analysis.

Dataset Information

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

Publications

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

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets