Fine 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.
To evaluate the association of personal exposure to PM2.5 and genome-wide DNA methylation changes in the peripheral blood of patients with COPD.
A 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.
A 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.
This 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.