PERSONAL EXPOSURE TO OUTDOOR URBAN AIR POLLUTION AND NASAL INFLAMMATION IN ASTHMATIC AND HEALTHY CHILDREN

Abstract

Introduction In urban areas, outdoor air pollutants such as particulate matter (PM) are suspected to induce harmful effects on respiratory health, rising the question of their involvement in allergic asthma and rhinitis, two inflammatory diseases. In the present study, the potential effect of the personal exposure to two major outdoor pollutants resulting from vehicle emissions, PM2.5 (diameter less than 2.5 μm) and nitrogen oxides (NOx) on nasal inflammatory biomarkers was examined in healthy and asthmatic allergic children living in Paris area. Methods Forty five children with allergic asthma and 46 healthy children participated in this prospective study. They were monitored during 48h for their personal exposure to PM2.5 with an active sampler and to NOx with a passive sampler. Environmental tobacco smoke exposure was assessed by urinary cotinine levels. In addition, indoor exposures were assessed for each child by measuring formaldehyde and acetaldehyde concentrations with an active sampler and house-dust mites levels at home. Total pollen counts and ozone exposures data were also collected from air quality monitoring networks. The next morning of the 48h measurement period, children underwent a nasal lavage. Nasal inflammation was assessed by measuring cellular biomarkers (neutrophils, eosinophils) and soluble biomarkers (albumin, urea, uric acid, elastase, alphal-antitrypsin, ECP, IL-4, IL-5, IL-6, IL-8, GM-CSF). Results There was no significant difference between the two groups for any of the pollutants concentrations nor pollen counts and house-dust mite levels were similar in both groups. The mean personal PM2.5 and NOx values were, respectively 30.6 +/− 25.0 μg/m3 and 57.2 +/− 35.5 μg/m3 for asthmatic children and 42.0 +/− 59.5 μg/m3 and 49.8 +/− 23.9 μg/m3 for healthy children. Nasal biomarkers were not different between the two populations, except for eosinophils counts mediane values (20.7 × 1000 for asthmatics and 3.1 × 1000 for healthy children, p = 0.02). In asthmatics, personal PM2.5 levels were highly significantly correlated to nasal neutrophils and eosinophils counts and to albumin, urea and alphal-antitrypsin concentrations. In healthy children, urinary cotinine was correlated with nasal epithelial cell counts, urea and IL-6 levels. Conclusion These results show for the first time that personal PM2.5 exposure, at levels commonly encountered in urban areas, is related to neutrophilic and eosinophilic inflammation in children with allergic asthma. The strongest association is observed with eosinophil counts, which support recent speculations on diesel exhaust particles involvement in allergic phenotype over-expression.