INTRODUCTION: The aim of this study was to investigate the effect of passive smoking on urine eosinophil cationic protein (u-ECP) in children with lower respiratory tract infections (LRTI). METHOD: This was a case-control study. The study cohort consisted of 150 children with LRTI (case group) and 150 healthy children (control), all from a urban setting. The statistical parameters were: a minimum of 139 children for a 95% confidence interval (95% CI), 80% power, and a possible exposure prevalence of 50%. The u-cotinine and u-ECP levels were measured by radioimmunoassay and fluoroimmunoassay methods, respectively. Data were analyzed by the McNemar chi-square test, t-test, and Pearson correlation. RESULTS: When the generally accepted cut-off level of 30 ng/mg urinary cotinine/creatinine was applied, 87.3% of the children with LRTI and 84.7% of healthy children were passive smokers. Using a cut-off level of 60 ng/mg, passive smoking increased the prevalence of LRTI by 4.7-fold (p=0.000). The mean u-ECP values were significantly higher in the case group than in the healthy control group (p=0.018). A positive association was found between u-cotinine and u-ECP values in children with LRTI (p=0.034). CONCLUSION: The results of this study indicate that passive smoking may play an important role in the development of respiratory infections and can cause airway inflammation in children with existing LRTI.
INTRODUCTION: The aim of this study was to investigate the effect of passive smoking on urine eosinophil cationic protein (u-ECP) in children with lower respiratory tract infections (LRTI). METHOD: This was a case-control study. The study cohort consisted of 150 children with LRTI (case group) and 150 healthy children (control), all from a urban setting. The statistical parameters were: a minimum of 139 children for a 95% confidence interval (95% CI), 80% power, and a possible exposure prevalence of 50%. The u-cotinine and u-ECP levels were measured by radioimmunoassay and fluoroimmunoassay methods, respectively. Data were analyzed by the McNemar chi-square test, t-test, and Pearson correlation. RESULTS: When the generally accepted cut-off level of 30 ng/mg urinary cotinine/creatinine was applied, 87.3% of the children with LRTI and 84.7% of healthy children were passive smokers. Using a cut-off level of 60 ng/mg, passive smoking increased the prevalence of LRTI by 4.7-fold (p=0.000). The mean u-ECP values were significantly higher in the case group than in the healthy control group (p=0.018). A positive association was found between u-cotinine and u-ECP values in children with LRTI (p=0.034). CONCLUSION: The results of this study indicate that passive smoking may play an important role in the development of respiratory infections and can cause airway inflammation in children with existing LRTI.