Air Pollution Exposure Impairs Airway Epithelium IFN-β Expression in Pre-School Children

Air pollution is a risk factor for respiratory infections and asthma exacerbations. We previously reported impaired Type-I and Type-III interferons (IFN-β/λ) from airway epithelial cells of preschool children with asthma and/or atopy. In this study we analyzed the association between rhinovirus-induced IFN-β/λ epithelial expression and acute exposure to the principal outdoor air pollutants in the same cohort.

We studied 34 children (17asthmatics/17non-asthmatics) undergoing fiberoptic bronchoscopy for clinical indications. Bronchial epithelial cells were harvested by brushing, cultured and experimentally infected with Rhinovirus Type 16 (RV16). RV16-induced IFN-β and λ expression was measured by quantitative real time PCR, as was RV16vRNA. The association between IFNs and the mean exposure to PM10, SO2 and NO₂ in the day preceding bronchoscopy was evaluated using a Generalized Linear Model (GLM) with Gamma distribution.

Acute exposure to PM10 and NO₂ was negatively associated to RV16-induced IFNβ mRNA. For each increase of 1ug/m³ of NO₂ we found a significative decrease of 2.3x10³ IFN-β mRNA copies and for each increase of 1ug/m³ of PM10 a significative decrease of 1x10³ IFN-β mRNA copies. No significant associations were detected between IFN-λ mRNA and NO₂ nor PM10. Increasing levels of NO₂ (but not PM10) were found to be associated to increased RV16 replication.

Short-term exposure to high levels of NO₂ and PM10 is associated to a reduced IFN-β expression by the airway epithelium, which may lead to increased viral replication. These findings suggest a potential mechanism underlying the link between air pollution, viral infections and asthma exacerbations.