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Air Pollution Relates to Airway Pathology in Children with Wheezing

Rationale: Outdoor air pollution contributes to asthma development and exacerbations, yet its effects on airway pathology have not been defined in children. Objectives: To explore the possible link between air pollution and airway pathology, we retrospectively examined the relationship between envir...

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Detalles Bibliográficos
Autores principales: Bonato, Matteo, Gallo, Elisa, Bazzan, Erica, Marson, Giovanna, Zagolin, Luca, Cosio, Manuel G., Barbato, Angelo, Saetta, Marina, Gregori, Dario, Baraldo, Simonetta
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Thoracic Society 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8641808/
https://www.ncbi.nlm.nih.gov/pubmed/34004126
http://dx.doi.org/10.1513/AnnalsATS.202010-1321OC
Descripción
Sumario:Rationale: Outdoor air pollution contributes to asthma development and exacerbations, yet its effects on airway pathology have not been defined in children. Objectives: To explore the possible link between air pollution and airway pathology, we retrospectively examined the relationship between environmental pollutants and pathological changes in bronchial biopsy specimens from children undergoing a clinically indicated bronchoscopy. Methods: Structural and inflammatory changes (basement membrane [BM] thickness, epithelial loss, eosinophils, neutrophils, macrophages, mast cells, and lymphocytes) were quantified in biopsy specimens by using immunohistochemistry. The association between exposure to particulate matter less than 10 μm in aerodynamic diameter (PM(10)), SO(2) and NO(2) and biopsy findings was evaluated by using a generalized additive model with Gamma family to allow for overdispersion, adjusted for atmospheric pressure, temperature, humidity, and wheezing. Results: Overall, 98 children were included (age 5.3 ± 2.9 yr; 53 with wheezing/45 without wheezing). BM thickness increased with prolonged exposure to PM(10) (rate ratio [RR], 1.29; 95% confidence interval [CI], 1.09–1.52), particularly in children with wheezing. Prolonged exposure to PM(10) was also associated with eosinophilic inflammation in children with wheezing (RR, 3.16; 95% CI, 1.35–7.39). Conversely, in children without wheezing, increased PM(10) exposure was associated with a reduction of eosinophilic inflammation (RR, 0.12; 95% CI, 0.02–0.6) and neutrophilic inflammation (RR, 0.36; 95% CI, 0.14–0.89). Moreover, NO(2) exposure was also linked to reductions in neutrophil infiltration (RR, 0.57; 95% CI, 0.34–0.93) and eosinophil infiltration (RR, 0.33; 95% CI, 0.14–0.77). Conclusions: Different patterns of association were observed in children with wheezing and in children without wheezing. In children without wheezing, exposure to PM(10) and NO(2) was linked to reduced eosinophilic and neutrophilic inflammation. Conversely, in children with wheezing, prolonged exposure to PM(10) was associated with increased BM thickness and eosinophilic inflammation, suggesting that it might contribute to asthma development by promoting airway remodeling and inflammation.