© 1994 by Oxford University Press
Journal of the National Cancer Institute, Vol. 86, No. 18, 1398-1402,
September 21, 1994
© 1994 Oxford University Press
Biomarkers of Environmental Tobacco Smoke in Preschool Children and Their Mothers
Environmental Sciences Divison, School of Public Health, Columbia University New York, N. Y.
Epidemiology Division, School of Public Health, Columbia University New York, N. Y.
Biostatistics Division, School of Public Health, Columbia University New York, N. Y.
Pediatric Department, Columbia Presbyterian Medical Center New York, N. Y.
New York State Psychiatric Institute New York
Correspondence to: Frederica P. Perera, Dr. P. H., Program in Molecular Epidemiology, Environmental Sciences Divisions, School of Public Health, Columbia University, 60 Haven Ave., Rm. B-109, New York, NY 10032.
Background: Adverse health effects attributable to environmental tobacco smoke (ETS) include respiratory illness and lung cancer in nonsmokers. There is accumulating evidence that children may be at heightened risk of cancer later in life as a result of exposure to carcinogens during their early development. It is of concern that as many as 9 million American children under the age of 5 years may be exposed to ETS. Purpose: Our goal was to assess whether levels of cotinine and polycyclic aromatic hydrocarbon-albumin (PAH-albumin) are associated with ETS exposure in children and in women of reproductive age, after accounting for background exposures to PAHs in the diet, workplace, and the home environment. Methods: The study cohort was composed of 87 Hispanic and African-American mothers and 87 of their preschool children (2–5 years of age). Plasma cotinine was analyzed by gas chromatography; PAH-albumin adducts in peripheral blood were analyzed by enzyme-linked immuno-sorbent assay. Exposure data were obtained by interview-administered questionnaires. Results: Both cotinine and PAH-albumin were significantly higher in the children whose mothers smoked than in the children of nonsmoking mothers (P<. 001 and P<. 05, respectively). Among the children of nonsmoking mothers, cotinine levels were also significantly higher in those who had ETS exposure from others in the household compared with the unexposed children. By regression analysis, after adjustment for ethnicity, there was a significant dose-response relationship between cotinine and the number of cigarettes smoked per day by the mother, both in the children (partial r2 =. 23; P =. 01) and in the mothers (partial r2 =. 22; P =. 01). Among the non smoking mothers, regression of bio-markers against total passive smoking exposure also showed a significant association with cotinine (r2 =. 25; P =. 04). PAH-albumin did not show the same dose-related response with the smoking variables. Mothers‘ cotinine levels were significantly correlated with those of their children (r =. 76; P<. 001) as were PAH— albumin adducts (r =. 27; P =. 014). Conclusion: ETS exposure of young children via their mothers’ smoking is associated with increases not only in the internal dose of ETS (cotinine), which has been previously reported, but also in the biologically effective dose of the carcinogenic (PAH) components of ETS (PAH-albumin adducts). This observation underscores the carcinogenic and public health hazard of ETS. Implications: Given the relatively low level of ETS exposure in this study, these results reinforce the need for effective programs aimed at smoking prevention and cessation among women, particularly women of reproductive age and minorities. [J Natl Cancer Inst 86: 1398–1402, 1994]
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