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Noninvasive Sampling of Mucosal Lining Fluid for the Quantification of In Vivo Upper Airway Immune-mediator Levels
Published on: August 7, 2017
Microplastics in pediatric asthma: Clinical associations with disease severity
Qing Wang1, Rui Feng2, Yuan Yuan1
1Department of Respiratory Medicine, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai 201102, China.
Background:
Respiratory exposure to microplastics (MPs) is increasingly recognized as a potential contributor to chronic airway disease, but the MPs burden in children with asthma and its relationship to disease remain poorly defined.
Methods:
In this cross-sectional study, sputum samples from 46 children with asthma were analyzed by pyrolysis-gas chromatography/mass spectrometry (Py-GC/MS) to quantify six prevalent synthetic polymers. Associations between MPs burden, asthma control status, pulmonary function, and airway inflammation were examined. To explore epithelial responses, patient-derived human alveolar organoids were exposed to polyethylene (PE) particles and subjected to bulk RNA sequencing.
Results:
MPs were identified in all 46 sputum samples from children with asthma, with a median total concentration of 21.12 μg/mL. Polystyrene (PS) was the most frequently detected polymer, present in 100% of the samples, while PE exhibited the highest median mass concentration at 13.96 µg/mL. Children with poorly controlled asthma demonstrated significantly elevated total MP burdens compared to those with well-controlled asthma. The total MP concentration showed a negative correlation with FEV₁% predicted, FVC% predicted, and the Asthma Control Test score. Transcriptomic analysis of PE-exposed alveolar organoids revealed 1297 differentially expressed genes, with enrichment in pathways associated with ferroptosis, apoptosis, p53 signaling, and inflammatory cytokine networks.
Conclusions:
Respiratory MPs burden is universal in this pediatric asthma cohort and associates with poor disease control. Exploratory transcriptomic analysis nominates ferroptosis-associated and pro-inflammatory pathways as candidate mechanisms warranting functional validation in future work.
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