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


While prior studies have explored racial differences in cotinine using parent-reported levels of ETS exposure, this is the first study to our knowledge that actively measured levels of tobacco smoke in the home. Using air nicotine as an objective measure of exposure, we confirmed and extended the findings of previous studies[10,12,16,28] that showed racial differences in serum cotinine among children exposed to ETS. In this cohort of ETS-exposed children with asthma, the African-American participants had significantly higher levels of cotinine in serum and hair compared with white children. Racial differences in both hair and serum cotinine were robust even after accounting for a number of demographic factors and exposure levels outside of the home. Specifically, African-American children lived in smaller homes when compared with white children, which could have concentrated their exposure to ETS. Even when household volume was included in the model, African-American race remained an independent predictor of higher cotinine levels. Using air nicotine as an objective measure of exposure enhances our confidence in these results.

There is convincing evidence for racial differences in the metabolism of tobacco toxins in the literature.[15,29,30,31] Benowitz et al[15] and Perez-Stable et al[32] demonstrated delayed excretion of cotinine among African-American smokers. Their results indicated that African-American smokers had a lower total cotinine clearance and nonrenal cotinine clearance. Of note, there were no significant differences in nicotine levels. The addition of menthol to tobacco products could impact racial differences in nicotine, carboxyhemoglobin, and cotinine. In a crossover trial, Benowitz et al[30] found that smoking mentholated tobacco products increased serum nicotine and carboxyhemoglobin concentrations in African Americans and lowered the levels in whites. Ahijevych et al[29] found that both African-American and white women who smoked mentholated tobacco products had higher serum cotinine levels than women who smoked nonmentholated products. Unfortunately, we did not collect data on whether children were exposed to mentholated cigarettes in this study.

Racial differences in cotinine were larger for hair than serum. There are at least two explanations for this striking difference. The greater differences in hair cotinine could reflect biological differences in nicotine metabolism that accumulate over a longer time period. As cotinine circulates in the vascular system, it is deposited in the hair shaft through the bulb artery, thus reflecting the cumulative serum cotinine concentration.[33,34] Therefore, hair cotinine would have less variability and provide a cumulative measure of systemic exposure. Alternative explanations include racial differences in the physical properties of hair or differential use of various hair products. It is unlikely that physical properties account for our results given the consistent findings in serum. However, differential use of various hair products could impact hair cotinine concentrations. Pichini et al[35] demonstrated that various hair dyes and shampoos can influence hair cotinine levels in young adults. The authors[35] found that the administration of various hair dyes actually reduced hair cotinine levels when compared with control hair samples. However, the latter study was conducted in young adults, and it is not clear that these results are applicable to children.

The implications from this study are significant. African-American children have higher levels of cotinine, a tobacco toxicant, than white children for a given level of ETS exposure. In studies of asthmatic children, higher levels of cotinine have been associated with poorer outcomes.[5,6] Among children, Mannino et al[5] demonstrated significant associations between higher serum cotinine levels, and asthma prevalence and increased school absence. Chilmonczyk et al[36] identified an inverse relationship between urine cotinine levels and pulmonary function. However, these studies did not identify differences in outcomes by race. The impact of higher cotinine levels on racial differences in pulmonary outcomes is speculative and requires further study.

Our study is subject to some limitations. First, our study included only children with asthma, which could limit the generalizability of our results. However, other studies of nonasthmatic children reported significant racial differences in cotinine. Second, we had no ambient measures of tobacco smoke outside of the home, and thus could not objectively account for racial differences in ETS exposure outside of the home. However, there is no a priori reason to expect racial differences in the amount of time children spend outside of the home. Moreover, our results indicate that African-American children spend less time in smoke-filled environments than white children. Lastly, our study sample included only African Americans and whites. It is unclear whether children from other racial and ethnic groups experience a similar phenomenon.

In summary, our results confirm, using ambient measures of ETS exposure, that African-American children have higher levels of both serum and hair cotinine compared with white children. These results raise questions as to whether there are racial differences in biological measures of other toxicants found in ETS. Differential metabolism of tobacco toxicants could explain the striking racial differences in tobacco-associated diseases.[3,9,37,38] Understanding racial differences in the response to ETS could provide momentum to implement policies that protect highly susceptible populations from ETS exposure.


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