Associations between air pollution and the onset of acute exacerbations of chronic obstructive pulmonary disease: A time-stratified case-crossover study in China.

BACKGROUND: Associations between air pollution and the acute exacerbations of chronic obstructive pulmonary disease (AECOPD) have been established primarily in time-series studies in which exposure and case data were at the aggregate level, limiting the identification of susceptible populations. RESEARCH QUESTION: Are air pollutants associated with the onset of AECOPD in China? Who is more susceptible to the effects of air pollutants? STUDY DESIGN AND METHODS: AECOPD data were obtained from the Acute Exacerbation of Chronic Obstructive Pulmonary Disease Registry study and air pollution data were assigned to individuals based on their residential address. We adopted a time-stratified case-crossover study design combined with conditional logistic regression models to estimate the associations between six air pollutants and AECOPD. Stratified analyses were performed by individual characteristics, disease severity, COPD types, and the season of exacerbations. RESULTS: A total of 5,746 patients were finally included. At a 2-day lag, for each interquartile range increase in PM2.5 and PM10 concentrations, odds ratios for AECOPD were 1.054 (95% CI: 1.012, 1.097) and 1.050 (95% CI: 1.009, 1.092), respectively. The associations were more pronounced in participants who were aged < 65 years, had experienced at least one severe AECOPD in the past year, were first diagnosed with COPD between the ages of 20 and 50, and experienced AECOPD in the cool seasons. By contrast, significant associations for NO2, SO2, and CO lost significance when excluding cases collected before 2020 or with larger distance from the monitoring station, and no significant association was observed for O3. INTERPRETATION: This study provides robust evidence that short-term exposure to PM2.5 and PM10 was associated with higher odds of AECOPD onset. Individuals who are young, have severe COPD or young COPD, and experience an exacerbation during the cooler seasons may be particularly susceptible. CLINICAL TRIAL REGISTRATION NUMBER: NCT2657525 (ClinicalTrials.gov).

Outdoor particulate matter exposure affects metabolome in chronic obstructive pulmonary disease: Preliminary study.

Introduction: The 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. Methods: Thirty-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. Results: Metabolomic 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. Discussion: PM2.5 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.

Short-term exposure to fine particulate matter and genome-wide DNA methylation in chronic obstructive pulmonary disease: A panel study conducted in Beijing, China.

Background: 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. Objective: To evaluate the association of personal exposure to PM2.5 and genome-wide DNA methylation changes in the peripheral blood of patients with COPD. Methods: 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. Results: 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. Conclusion: 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.

Exposure Response Relationship of Acute Effects of Air Pollution on Respiratory Diseases - China, 2013-2018.

WHAT IS ALREADY KNOWN ABOUT THIS TOPIC?: Short-term exposure to air pollutants has been associated with chronic obstructive pulmonary disease (COPD) and asthma, which needs continuous observation. WHAT IS ADDED BY THIS REPORT?: This study uses the longest time series data so far from 2013 to 2018 and adds additional data analysis for ozone (O3) to existing studies. WHAT ARE THE IMPLICATIONS FOR PUBLIC HEALTH PRACTICE?: This study suggests that air pollutants have certain acute effects on outpatient and hospital admission of patients with COPD and asthma, which can be combined with the disease diagnosis and treatment guidelines to guide clinical practice.