The Role of Air Nicotine in Explaining Racial Differences in Cotinine Among Tobacco-Exposed Children

Stephen E. Wilson, MD, MSc; Robert S. Kahn, MD, MPH; Jane Khoury, PhD; Bruce P. Lanphear, MD, MPH


CHEST. 2007;131(3):856-862. 

In This Article

Abstract and Introduction


Objective: African-American children have higher rates of tobacco-associated morbidity. Few studies have objectively measured racial differences in the exposure of children to tobacco smoke. The objective of this study was to test whether African-American children have higher levels of cotinine compared to white children while accounting for ambient measures of tobacco smoke.
Setting: Community-based sample of asthmatic children (n = 220) enrolled in an environmental tobacco smoke (ETS) reduction trial.
Participants: A biracial sample (55% African American) of children with asthma aged 5 to 12 years who were routinely exposed to ETS.
Measurements: We measured cotinine levels in serum and hair samples at baseline, 6 months, and 12 months. We measured the level of ETS exposure over a 6-month period by placing air nicotine dosimeters in the homes of the children at baseline and at 6-month study visits.
Results: African-American children had significantly higher levels of cotinine at all time points in the study. At the 12-month visit, African-American children had higher levels of serum cotinine (1.39 µg/dL vs 0.80 µg/dL, p = 0.001) and hair cotinine (0.28 ng/mg vs 0.08 ng/mg, p < 0.0001) when compared with white children. In a repeated-measures analysis, African-American children had significantly higher levels of serum cotinine (ß = 0.28, p = 0.04) and hair cotinine (ß = 1.40, p < 0.0001) compared with white children. Air nicotine levels and housing volume were independently associated with higher levels of cotinine.
Conclusions: Among children with asthma, African-American children have higher levels of serum and hair cotinine compared with white children.


Exposure to environmental tobacco smoke (ETS) has a substantial impact on the health of children.[1,2,3,4] Exposure to ETS has been linked to sudden infant death syndrome, asthma exacerbations, and upper respiratory tract infections, often resulting in an excess in school absences.[1,2,4,5,6] Mannino et al[5] found that ETS exposure (as measured by cotinine) doubled the risk of school absenteeism among children ages 4 to 16 years. ETS exposure has also been shown to increase the risk for the development of some childhood cancers. Boffetta et al[7] reported that children's exposure to paternal tobacco smoke increased the risk for brain tumors and lymphomas in childhood.

Despite lower reported exposures to ETS, African-American children have disproportionately higher rates of some tobacco-associated disorders such as sudden-infant death syndrome and asthma compared to white children.[3,8,9] It is unclear whether tobacco is causally related to these disparities because most studies relied on parent report as the measure of ETS exposure. Parents may underreport their smoking habits for reasons of social desirability. Reliance on parent-reported measures of ETS exposure could bias the results. To overcome this dilemma, investigators are increasingly using cotinine, a nicotine metabolite, to objectively measure ETS exposure. Previous investigations[10,11,12] have identified striking racial differences in cotinine among tobacco-exposed children. Moreover, studies[13,14] suggest that cotinine is toxic to vascular cells and neurons. To our knowledge, no studies in children have explored racial differences in cotinine using ambient measures of air nicotine to quantify ETS exposure.

The objective of this study was to test for racial differences in biological measures of cotinine over 12 months using household air nicotine as the "gold standard" measure of exposure instead of parent report. We hypothesized that serum and hair cotinine levels among African-American children would exceed those of white children even after accounting for levels of exposure to ETS.


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