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Clinical Investigations: SMOKING |

Predictors of Cotinine Levels in US Children*: Data From the Third National Health and Nutrition Examination Survey

David M. Mannino, MD, FCCP; Ralph Caraballo, MD; Neal Benowitz, PhD; James Repace, MS
Author and Funding Information

*From the Air Pollution and Respiratory Health Branch (Dr. Mannino), Division of Environmental Hazards and Health Effects, National Center for Environmental Health, Atlanta, GA; Epidemiology Branch (Dr. Caraballo), Office on Smoking and Health, National Center for Chronic Disease Prevention and Health Promotion, Atlanta, GA; Division of Clinical Pharmacology (Dr. Benowitz), Department of Medicine, University of California, San Francisco, CA; and Repace Associates (Mr. Repace), Bowie, MD.

Correspondence to: David M. Mannino, MD, FCCP, National Center for Environmental Health, Centers for Disease Control and Prevention, 1600 Clifton Rd, MS E-17, Atlanta, GA 30333; e-mail: dmannino@cdc.gov



Chest. 2001;120(3):718-724. doi:10.1378/chest.120.3.718
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Study objective: To determine what factors predict cotinine levels in US children.

Design: Cross-sectional study.

Subjects: Nationally representative sample of 5,653 US children, both with and without reported tobacco smoke exposure in their homes.

Methods: We stratified the children into those with reported passive smoke exposure at home and those without this exposure. We used regression models to predict the log of the cotinine level of the participants with the following independent covariates: age; race/ethnicity; number of rooms in the home; sex; parental education; family poverty index; family size; region; and, among children with reported passive smoke exposure, the number of cigarettes smoked in the home.

Results: Children exposed to passive smoke had a mean cotinine level of 1.66 ng/mL, and children not exposed to passive smoke had a mean level of 0.31 ng/mL. Among children with reported smoke exposure, non-Mexican-American race/ethnicity, young age, low number of rooms in the home, low parental education, and an increasing number of cigarettes smoked in the home were predictors of increased serum cotinine levels. Among children with no reported smoke exposure, significant predictors of increased cotinine levels included black race, young age, Midwest region of the United States, low number of rooms in the home, low parental education, large family size, and low family poverty index.

Conclusion: While the reported number of cigarettes smoked in the home is the most important predictor of cotinine levels in children exposed to smoke and may provide an opportunity for clinical intervention, other demographic factors are important among children both with and without reported smoke exposure.

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