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Clinical Chemistry 45: 505-509, 1999;
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(Clinical Chemistry. 1999;45:505-509.)
© 1999 American Association for Clinical Chemistry, Inc.

Articles

Urinary Cotinine and Exposure to Parental Smoking in a Population of Children with Asthma

Christiane Oddoze1,a, Jean Christophe Dubus2, Monique Badier4, Xavier Thirion5, Anne Marie Pauli1, Jean Pastor1 and Bernard Bruguerolle3

1 Analytical Chemistry Laboratory, Faculty of Pharmacy, University of Aix-Marseille II, Bd J Moulin, 13005 Marseille Cedex 5, France.
Departments of
2 Pediatrics and
3 Medical and Clinical Pharmacology, Timone Hospital, 13385 Marseille Cedex 5, France.

4 Respiratory Function Laboratory and
5 Department of Medical Information, Ste Marguerite Hospital, 13274 Marseille Cedex 9, France.
a Address correspondence to this author at: Laboratoire de Chimie Analytique, Service du Pr. Pastor, Faculté de Pharmacie, 13385 Marseille Cedex 5, France. Fax (33)4 91 74 60 09; e-mail coddoze{at}ap-hm.fr

Background: 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.

Methods: 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.

Results: 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.

Conclusion: Passive smoke exposure increases the bronchial responsiveness to carbachol in asthmatic children.© 1999 American Association for Clinical Chemistry




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