Differences in transcriptome response to air pollution exposure between adult residents with and without chronic obstructive pulmonary disease in Beijing: A panel study

Abstract

Ambient air pollution is a major risk factor for the prevalence and exacerbation of chronic obstructive pulmonary disease (COPD). Based on the COPDB (COPD in Beijing) panel study, whole-blood transcriptomes were repeatedly measured in 48 COPD patients and 62 healthy participants. Ambient mass concentrations of fine particulate matter (PM2.5), temperature, and relative humidity were continuously monitored at a monitoring station. The linear mixed-effects models were applied to estimate the associations between logarithmically transformed transcript levels and 1-day (d), 7-d, and 14-d average concentrations of PM2.5 before the start of follow-up visits. MetaCore™ was used to conduct the pathway enrichment analyses. Exposure to 1-, 7-, and 14-d average concentrations of PM2.5 was significantly associated with the transcriptome responses in both groups. The top 10, top 100, and top 1000 PM2.5-associated transcripts differed greatly between the two groups. Among COPD patients, role of alpha-6/beta-4 integrins in carcinoma progression, Notch signaling in breast cancer, and ubiquinone metabolism were the most significantly enriched PM2.5-associated biological pathways in the three time windows, respectively. In healthy participants, pro-opiomelanocortin processing was the most significant PM2.5-associated biological pathway in all three time windows. Our findings provide novel insights into the adverse health effects of air pollution exposure.