BACKGROUND: Eosinophil activation is characteristic for allergic airways disease. However, eosinophilic airways inflammation has also been observed subsequent to ambient ozone exposure. METHODS: For a population sample of 877 children living at nine sites with different ozone exposure we measured urinary eosinophil protein X (U-EPX) as a marker of eosinophil activation. U-EPX was determined from a single spot urine sample during autumn 1997. Children were participants in a longitudinal study of ozone effects on lung function. RESULTS: The 5-95% percentiles of ozone exposure (30-day mean before test) were 11.8-51.5 p.p.b. (mean: 31.6 ppb). U-EPX was measured by radioimmunoassay and expressed as ratio to urinary creatinine (microg EPX/mmol creatinine). Log transformation was performed to achieve a normal distribution. LogU-EPX was associated with gender, a diagnosis of asthma and atopy (skin test sensitivity to any of seven aeroallergens). LogU-EPX increased with ozone exposure for all children. The medians of LogU-EPX according to the first-fourth quartiles of ozone exposure were: 1.82, 1.88, 1.95 and 2.03. For 172 non-asthmatic children who had spent the whole summer at their site corresponding figures were 1.57, 1.78, 2.07 and 2.13. In a multivariate model with logU-EPX being the dependent variable and adjusted for gender, site and atopy, ozone was found to be significant (estimate: 0.007 microg/mmol creatinine per ppb ozone; SE:0.02; P < 0.001). CONCLUSION: Our observation supports the hypothesis that ozone in healthy children is associated with eosinophil inflammation, most likely in the airways.
BACKGROUND: Eosinophil activation is characteristic for allergic airways disease. However, eosinophilic airways inflammation has also been observed subsequent to ambient ozone exposure. METHODS: For a population sample of 877 children living at nine sites with different ozone exposure we measured urinary eosinophil protein X (U-EPX) as a marker of eosinophil activation. U-EPX was determined from a single spot urine sample during autumn 1997. Children were participants in a longitudinal study of ozone effects on lung function. RESULTS: The 5-95% percentiles of ozone exposure (30-day mean before test) were 11.8-51.5 p.p.b. (mean: 31.6 ppb). U-EPX was measured by radioimmunoassay and expressed as ratio to urinary creatinine (microg EPX/mmol creatinine). Log transformation was performed to achieve a normal distribution. LogU-EPX was associated with gender, a diagnosis of asthma and atopy (skin test sensitivity to any of seven aeroallergens). LogU-EPX increased with ozone exposure for all children. The medians of LogU-EPX according to the first-fourth quartiles of ozone exposure were: 1.82, 1.88, 1.95 and 2.03. For 172 non-asthmatic children who had spent the whole summer at their site corresponding figures were 1.57, 1.78, 2.07 and 2.13. In a multivariate model with logU-EPX being the dependent variable and adjusted for gender, site and atopy, ozone was found to be significant (estimate: 0.007 microg/mmol creatinine per ppb ozone; SE:0.02; P < 0.001). CONCLUSION: Our observation supports the hypothesis that ozone in healthy children is associated with eosinophil inflammation, most likely in the airways.
Authors: Kinjal Maniar-Hew; Edward M Postlethwait; Michelle V Fanucchi; Carol A Ballinger; Michael J Evans; Jack R Harkema; Stephan A Carey; Ruth J McDonald; Alfred A Bartolucci; Lisa A Miller Journal: Am J Physiol Lung Cell Mol Physiol Date: 2010-12-03 Impact factor: 5.464
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