Impact of PM2.5 Exposure Trajectories on Asthma and Airway Hyperresponsiveness in Children through S100 protein expression: The COCOA Study

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Background: Early-life PM2.5 exposure has been identified as a potential risk factor for childhood asthma. However, the impact of sustained PM2.5 exposure from pregnancy through childhood on asthma development remains unclear. Objectives: This study aims to investigate PM2.5 exposure trajectories and their association with asthma and airway hyperresponsiveness (AHR) in children, and to elucidate the underlying mechanisms based on proteome analysis. Methods: This study included 1,083 children from the COCOA birth cohort. PM2.5 exposure was estimated using LUR models, and exposure trajectories were identified through latent class trajectory analysis based on PM2.5 levels from pregnancy through age 7. Asthma and AHR via methacholine challenge tests were evaluated at age 7. Plasma proteome and cytokine analysis was performed to identify the underlying mechanisms of PM2.5-related asthma and AHR. Results: Three distinct PM2.5 exposure groups were identified; consistently low, moderate, and consistently high exposure. Consistently high PM2.5 exposure had a significantly increased risk of AHR and asthma (aOR: 1.94; 95% CI: 1.29–2.93 and aOR: 2.09; 95% CI: 1.18-3.72, respectively). In children with both consistently high PM2.5 exposure and AHR, neutrophil degranulation and the positive regulation of NF-κB activity were identified as the main pathways, with S100 family proteins being significantly elevated among the various proteins associated with these pathways. Conclusion: This study suggests that consistently high PM2.5 exposure may contribute to the development of asthma and airway AHR through increased inflammatory responses mediated by S100.

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