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

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 (TM) 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.

Automated summary

The study found significant associations between exposure to PM2.5 concentrations and transcriptome responses in both COPD patients and healthy participants. There were distinct differences in the top PM2.5-associated transcripts between the two groups, indicating varied biological pathways affected by air pollution exposure.