Airborne fine particulate matter exposure induces transcriptomic alterations resembling asthmatic signatures: insights from integrated omics analysis.

Abstract

Fine particulate matter (PM_2.5), an atmospheric pollutant that settles deep in the respiratory tract, is highly harmful to human health. Despite its well-known impact on lung function and its ability to exacerbate asthma, the molecular basis of this effect is not fully understood. This integrated transcriptomic and epigenomic data analysis from publicly available datasets aimed to determine the impact of PM_2.5 exposure and its association with asthma in human airway epithelial cells. Differential gene expression and binding analyses identified 349 common differentially expressed genes and genes associated with differentially enriched H3K27ac regions in both conditions. Co-expression network analysis revealed three preserved modules (Protein Folding, Cell Migration, and Hypoxia Response) significantly correlated with PM_2.5 exposure and preserved in asthma networks. Pathways dysregulated in both conditions included epithelial function, hypoxia response, interleukin-17 and TNF signaling, and immune/inflammatory processes. Hub genes like TGFB2, EFNA5, and PFKFB3 were implicated in airway remodeling, cell migration, and hypoxia-induced glycolysis. These findings elucidate common altered expression patterns and processes between PM_2.5 exposure and asthma, helping to understand their molecular connection. This provides guidance for future research to utilize them as potential biomarkers or therapeutic targets and generates evidence supporting the need for implementing effective air quality management strategies.