BACKGROUND: Daily variations in ambient particulate air pollution have been associated with respiratory mortality and morbidity. AIMS: To assess the associations between urinary concentration of lung Clara cell protein CC16, a marker for lung damage, and daily variation in fine and ultrafine particulate air pollution. METHODS: Spot urinary samples (n = 1249) were collected biweekly for six months in subjects with coronary heart disease in Amsterdam, Netherlands (n = 37), Erfurt, Germany (n = 47), and Helsinki, Finland (n = 47). Ambient particulate air pollution was monitored at a central site in each city. RESULTS: The mean 24 hour number concentration of ultrafine particles was 17.3x10(3) cm(-3) in Amsterdam, 21.1x10(3) cm(-3) in Erfurt, and 17.0x10(3) cm(-3) in Helsinki. The mean 24 hour PM2.5 concentrations were 20, 23, and 13 microg/m3, respectively. Daily variation in ultrafine particle levels was not associated with CC16. In contrast, CC16 concentration seemed to increase with increasing levels of PM2.5 in Helsinki, especially among subjects with lung disorders. No clear associations were observed in Amsterdam and Erfurt. In Helsinki, the CC16 concentration increased by 20.2% (95% CI 6.9 to 33.5) per 10 microg/m3 increase in PM2.5 concentration (lag 2). The respective pooled effect estimate was 2.1% (95% CI -1.3 to 5.6). CONCLUSION: The results suggest that exposure to particulate air pollution may lead to increased epithelial barrier permeability in lungs.
BACKGROUND: Daily variations in ambient particulate air pollution have been associated with respiratory mortality and morbidity. AIMS: To assess the associations between urinary concentration of lung Clara cell protein CC16, a marker for lung damage, and daily variation in fine and ultrafine particulate air pollution. METHODS: Spot urinary samples (n = 1249) were collected biweekly for six months in subjects with coronary heart disease in Amsterdam, Netherlands (n = 37), Erfurt, Germany (n = 47), and Helsinki, Finland (n = 47). Ambient particulate air pollution was monitored at a central site in each city. RESULTS: The mean 24 hour number concentration of ultrafine particles was 17.3x10(3) cm(-3) in Amsterdam, 21.1x10(3) cm(-3) in Erfurt, and 17.0x10(3) cm(-3) in Helsinki. The mean 24 hour PM2.5 concentrations were 20, 23, and 13 microg/m3, respectively. Daily variation in ultrafine particle levels was not associated with CC16. In contrast, CC16 concentration seemed to increase with increasing levels of PM2.5 in Helsinki, especially among subjects with lung disorders. No clear associations were observed in Amsterdam and Erfurt. In Helsinki, the CC16 concentration increased by 20.2% (95% CI 6.9 to 33.5) per 10 microg/m3 increase in PM2.5 concentration (lag 2). The respective pooled effect estimate was 2.1% (95% CI -1.3 to 5.6). CONCLUSION: The results suggest that exposure to particulate air pollution may lead to increased epithelial barrier permeability in lungs.
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