Studies of the effects of tobacco smoke often rely on reported exposure to cigarette smoke, a measure that is subject to bias.
We describe here the relationship between parental smoking exposure as assessed by urinary cotinine excretion and lung function in children with asthma.
We studied 90 children 4-14 years of age, who reported a confirmed diagnosis or symptoms of asthma.
In each child, we assessed baseline pulmonary function (spirometry) and bronchial responsiveness to carbachol stimulation.
Urinary cotinine was measured by HPLC with ultraviolet detection.
Urinary cotinine concentrations in the children were significantly correlated (P<0.001) with the number of cigarettes the parents, especially the mothers, smoked.
Bronchial responsiveness to carbachol (but not spirometry test results) was correlated (P<0.03) with urinary cotinine in the children.
Passive smoke exposure increases the bronchial responsiveness to carbachol in asthmatic children.
Mots-clés Pascal : Enfant, Homme, Tabagisme passif, Cotinine, Marqueur biologique, Urine, Etiopathogénie, Epidémiologie, France, Europe, Asthme, Liquide biologique, Appareil respiratoire pathologie, Bronchopneumopathie obstructive, Immunopathologie
Mots-clés Pascal anglais : Child, Human, Passive smoking, Cotinine, Biological marker, Urine, Etiopathogenesis, Epidemiology, France, Europe, Asthma, Biological fluid, Respiratory disease, Obstructive pulmonary disease, Immunopathology
Notice produite par :
Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 99-0244498
Code Inist : 002B06C02. Création : 16/11/1999.