The effect of passive smoking on asthma symptoms,atopy,and airway hyperresponsiveness in schoolchildren

Passive smoking is a major cause of respiratory morbidity, and is associated with increased bronchial responsiveness in children. To evaluate the effect of smoking by a parent on asthma symptoms, atopy, and airway hyperresponsiveness (AHR), we conducted a cross-sectional survey of 503 schoolchildren...

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Veröffentlicht in:Journal of Korean medical science 2004, 19(2), , pp.214-217
Hauptverfasser: Jang, An-Soo, Choi, In-Seon, Lee, Soong, Nam, Hae-Sung, Kweon, Sun-Seok, Son, Myung-Ho, Lee, June-Hyuk, Park, Sung Woo, Kim, Do-Jin, Uh, Soo Taek, Kim, Yong-Hoon, Park, Choon-Sik
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Sprache:eng
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Zusammenfassung:Passive smoking is a major cause of respiratory morbidity, and is associated with increased bronchial responsiveness in children. To evaluate the effect of smoking by a parent on asthma symptoms, atopy, and airway hyperresponsiveness (AHR), we conducted a cross-sectional survey of 503 schoolchildren that involved questionnaires, spirometry, allergy testing, and a bronchial challenge test. If the PC20 methacholine was less than 16 mg/mL, the subject was considered to have AHR. The prevalence of a parent who smoked was 68.7%. The prevalence of AHR was 45.0%. The sensitization rate to common inhalant allergens was 32.6%. Nasal symptoms such as rhinorrhea, sneezing, nasal itching, and nasal obstruction were present in 42.7%. Asthma symptoms such as cough and wheezing were present in 55.4%. The asthma symptoms were significantly more prevalent in children who had a parent who smoked than in those whose parents did not. The nasal symptoms, atopy, and AHR did not differ according to whether a parent smoked. In a multiple logistic regression model, the asthma symptoms and atopy were independently associated with AHR, when adjusted for confounding variables. Passive smoking contributed to asthma symptoms in schoolchildren and was not an independent risk factor of airway hyperresponsiveness in an epidemiological survey.
ISSN:1011-8934
1598-6357
DOI:10.3346/jkms.2004.19.2.214