摘要:This study compared susceptibility to respiratory morbidity in a cohort of 9-year-old children exposed congenitally and postnatally to environmental tobacco smoke (ETS) to susceptibility in a cohort of unexposed children. The epidemiologic study included 1129 children: 594 boys and 535 girls attending the second grade of grammar schools in Kraków, Poland. We found strong evidence that children exposed to ETS in their homes were more susceptible to acute respiratory tract illnesses than unexposed children. A dose-response relationship between degree of exposure [for lower ETS exposure, odds ratio (OR) = 1.32; for higher ETS exposure, OR = 1.74] supports a causal explanation for the association observed. The significant trend of increased risk of respiratory infections due to ETS level in nonatopic children whose mothers did not smoke cigarettes during pregnancy suggests a direct effect of ETS exposure on the child's respiratory health. ETS combined with allergy nearly tripled the risk of acute respiratory tract illness (OR = 3.39; 95% CI, 1.93-5.93), and maternal smoking during pregnancy had a modifying effect on the risk of respiratory illnesses due to ETS after accounting for atopy. The stronger effect of ETS in atopic children and in those whose mothers smoked during pregnancy may be result of biologic interaction of endogenous and environmental factors. The results of this study are of relevance to public health policy, as children with higher risk of respiratory infections may be more susceptible to environmental hazards later in adolescence or in adulthood. Respiratory infections also increase demands for medical interventions in terms of outpatient services and hospital administrations. In addition, respiratory illnesses cause missed school days, and caring for a sick child may lead to absenteeism from work. Full text Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (2.1M), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References . 302 303 304 305 306