Air Pollution Relates to Airway Pathology in Wheezing Children.

Abstract

RATIONALE\nOutdoor air pollution contributes to asthma development and exacerbations; yet, its effects on airway pathology have not been defined in children.\n\n\nOBJECTIVES\nTo explore the possible link between air pollution and airway pathology, we examined retrospectively the relation between environmental pollutants and pathological changes in bronchial biopsies of children undergoing a clinically indicated bronchoscopy.\n\n\nMETHODS\nStructural and inflammatory changes (Basement Membrane-BM thickness, epithelial loss, eosinophils, neutrophils, macrophages, mast-cells, lymphocytes) were quantified in biopsies by immunohistochemistry. The association between exposure to PM10, SO2 and NO2 and biopsy findings was evaluated using a Generalized Additive Model with Gamma family to allow for overdispersion, adjusted for atmospheric pressure, temperature, humidity and wheezing.\n\n\nRESULTS\nOverall, 98 children were included (age 5.3±2.9 yrs; 53 wheezing/ 45 non-wheezing). BM thickness increased with prolonged exposure to PM10 [Rate ratio RR 1.29; CI 1.09-1.52], particularly in wheezing children. Prolonged exposure to PM10 was also associated with eosinophilic inflammation in wheezing children [RR 3.16; CI 1.35-7.39]. Conversely, in non-wheezers, increased PM10 exposure was associated with a reduction of eosinophilic [RR 0.12; CI 0.02-0.6] and neutrophilic inflammation [RR 0.36; CI 0.14-0.89]. Moreover, NO2 exposure was also linked to reductions in neutrophil [RR 0.57; CI 0.34-0.93] and eosinophil infiltration [RR 0.33; CI 0.14-0.77].\n\n\nCONCLUSION\nDifferent patterns of association were observed in wheezing and non-wheezing children. In non-wheezing children, exposure to PM10 and NO2 was linked to reduced eosinophilic/neutrophilic inflammation. Conversely, in wheezing children prolonged exposure to PM10 was associated with increased BM thickness and eosinophilic inflammation, suggesting that it might contribute to asthma development by promoting airway remodeling and inflammation.