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Microplastics in pediatric asthma: Clinical associations with disease severity
Summary
Researchers found tiny plastic particles (microplastics) in the lung mucus of every single child with asthma they tested, and kids with worse-controlled asthma had higher levels of these particles in their airways. Lab experiments on lung tissue models suggested these plastics may trigger harmful cell stress and inflammation, though more research is needed to confirm this actually causes the asthma symptoms rather than just being linked to them. This study is a reminder that the air we breathe, and the plastic particles in it, may be quietly affecting respiratory health, especially in children.
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.