The overexpressed RP11-86H7.1 could directly sponge miR-9-5p, enhance the expression levels of NFKB1, IL-6, IL-8, and tumor necrosis factor (TNF)-α, and promote the inflammatory response in TRAPM2.5-treated 16HBE cells, providing further insights into lncRNA–miRNA interactions regarding new treatment strategies for airway inflammatory diseases caused by PM2.5 exposure, such as COPD (Zhao et al., 2020). This evidence concerns the gene IL6 and chronic obstructive pulmonary disease.