BackgroundFine particulate matter (PM2.5) is a crucial risk factor for chronic obstructive pulmonary disease (COPD). However, the mechanisms whereby PM2.5 contribute to COPD risk have not been fully elucidated. Accumulating evidence suggests that epigenetics, including DNA methylation, play an important role in this process; however, the association between PM2.5 exposure and genome-wide DNA methylation in patients with COPD has not been studied.ObjectiveTo evaluate the association of personal exposure to PM2.5 and genome-wide DNA methylation changes in the peripheral blood of patients with COPD.MethodsA panel study was conducted in Beijing, China. We repeatedly measured and collected personal PM2.5 data for 72 h. Genome-wide DNA-methylation of peripheral blood was analyzed using the Illumina Infinium Human Methylation BeadChip (850 k). A linear-mixed effect model was used to identify the differentially methylated probe (DMP) associated with PM2.5. Finally, we performed a functional enrichment analysis of the DMPs that were significantly associated with PM2.5.ResultsA total of 24 COPD patients were enrolled and 48 repeated DNA methylation measurements were associated in this study. When the false discovery rate was < 0.05, 19 DMPs were significantly associated with PM2.5 and were annotated to corresponding genes. Functional enrichment analysis of these genes showed that they were related to the response to toxic substances, regulation of tumor necrosis factor superfamily cytokine production, regulation of photosensitivity 3-kinase signaling, and other pathways.ConclusionThis study provided evidence for a significant relationship between personal PM2.5 exposure and DNA methylation in patients with COPD. Our research also revealed a new biological pathway explaining the adverse effects of PM2.5 exposure on COPD risk.
IntroductionThe metabolomic changes caused by airborne fine particulate matter (PM2.5) exposure in patients with chronic obstructive pulmonary disease (COPD) remain unclear. The aim of this study was to determine whether it is possible to predict PM2.5-induced acute exacerbation of COPD (AECOPD) using metabolic markers.MethodsThirty-eight patients with COPD diagnosed by the 2018 Global Initiative for Obstructive Lung Disease were selected and divided into high exposure and low exposure groups. Questionnaire data, clinical data, and peripheral blood data were collected from the patients. Targeted metabolomics using liquid chromatography-tandem mass spectrometry was performed on the plasma samples to investigate the metabolic differences between the two groups and its correlation with the risk of acute exacerbation.ResultsMetabolomic analysis identified 311 metabolites in the plasma of patients with COPD, among which 21 metabolites showed significant changes between the two groups, involving seven pathways, including glycerophospholipid, alanine, aspartate, and glutamate metabolism. Among the 21 metabolites, arginine and glycochenodeoxycholic acid were positively associated with AECOPD during the three months of follow-up, with an area under the curve of 72.50% and 67.14%, respectively.DiscussionPM2.5 exposure can lead to changes in multiple metabolic pathways that contribute to the development of AECOPD, and arginine is a bridge between PM2.5 exposure and AECOPD.
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