BACKGROUND: Outdoor and indoor air pollutants are suspected to induce harmful effects on respiratory health, raising the question of their involvement in allergic asthma and rhinitis. OBJECTIVE: The potential effect of short-term personal exposure to particulate matter with a diameter of less than 2.5 microm (PM2.5) on nasal inflammation was examined in children living in the Paris area. METHODS: Forty-one children with allergic asthma and 44 healthy children participated in this study. They were monitored during 48 hours for their personal exposure to PM2.5. At the end of the measurement period, children underwent one nasal lavage. Nasal lavage fluid was investigated for cellular (neutrophils and eosinophils) and soluble (albumin, urea, elastase, alpha1-antitrypsin, IL-6, and IL-8) mediators. RESULTS: Pollutant concentrations did not differ between the 2 groups. In asthmatic subjects, but not in healthy children, personal PM2.5 levels were correlated to nasal percentage of eosinophils and to albumin, urea, and alpha1-antitrypsin concentrations after adjustment for confounders (age, sex, house dust mites, pollens, cat, environmental tobacco smoke through urinary cotinine, barometric pressure, and respiratory infection). CONCLUSION: The association observed with the percentage of eosinophils supports recent speculations on fine particle involvement in allergic phenotype overexpression. CLINICAL IMPLICATIONS: This study highlights the link between personal fine particle exposures and nasal inflammation in asthmatic allergic children living in urban areas. Because the view of united airways is still not completely understood, the question of pulmonary inflammation in such a situation deserves further investigation.
BACKGROUND: Outdoor and indoor air pollutants are suspected to induce harmful effects on respiratory health, raising the question of their involvement in allergic asthma and rhinitis. OBJECTIVE: The potential effect of short-term personal exposure to particulate matter with a diameter of less than 2.5 microm (PM2.5) on nasal inflammation was examined in children living in the Paris area. METHODS: Forty-one children with allergic asthma and 44 healthy children participated in this study. They were monitored during 48 hours for their personal exposure to PM2.5. At the end of the measurement period, children underwent one nasal lavage. Nasal lavage fluid was investigated for cellular (neutrophils and eosinophils) and soluble (albumin, urea, elastase, alpha1-antitrypsin, IL-6, and IL-8) mediators. RESULTS: Pollutant concentrations did not differ between the 2 groups. In asthmatic subjects, but not in healthy children, personal PM2.5 levels were correlated to nasal percentage of eosinophils and to albumin, urea, and alpha1-antitrypsin concentrations after adjustment for confounders (age, sex, house dust mites, pollens, cat, environmental tobacco smoke through urinary cotinine, barometric pressure, and respiratory infection). CONCLUSION: The association observed with the percentage of eosinophils supports recent speculations on fine particle involvement in allergic phenotype overexpression. CLINICAL IMPLICATIONS: This study highlights the link between personal fine particle exposures and nasal inflammation in asthmatic allergicchildren living in urban areas. Because the view of united airways is still not completely understood, the question of pulmonary inflammation in such a situation deserves further investigation.
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