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

Methods and Materials


This study was a longitudinal analysis of data from the Cincinnati Asthma Prevention (CAP) Study. The CAP Study was an institutional review board-approved year-long, double-blinded, placebo-controlled trial that aimed to test the efficacy of reducing ETS exposure among children with asthma using high-efficiency particulate air (HEPA) air cleaners. The objective of this was to test for racial differences in biological measures of cotinine while accounting for ambient measures of nicotine. The primary outcomes were serum cotinine and hair cotinine measured at baseline, 6 months, and 12 months of the study. The primary exposures were parent-reported race and household air nicotine. Other variables of interest included age, gender, home volume, air cleaner run time, and reported ETS exposure outside of the home.

Study Population

The study cohort consisted of a biracial community-based sample (55% African American) of tobacco-exposed children (n = 220) with asthma. We recruited children aged 5 to 12 years with physician-diagnosed asthma and symptoms consistent with persistent asthma. The child's primary caregiver had to concur with the asthma diagnosis. For participation in this study, we required moderate levels of ETS exposure defined as ≥ 5 cigarettes per day in or around the home. We excluded individuals with coexisting pulmonary disease (ie, cystic fibrosis), congenital heart disease, or neuromuscular disease (ie, muscular dystrophy).

Measures of Cotinine

We measured cotinine in serum samples collected at baseline, 6 months, and 12 months of the study. Cotinine is a stable metabolite of nicotine, and is the most widely used biomarker to measure tobacco use and exposure.[3,4,5,15,16,17,18] Serum cotinine has a half-life of 15 to 25 h and reflects tobacco exposure in the prior 3 to 5 days. Serum samples were analyzed at the National Center for Environmental Health using a validated protocol.[19,20] Serum samples were analyzed for cotinine using high-performance liquid chromatography linked to atmospheric pressure chemical ionization tandem mass spectrometry. Cotinine levels were reported in units of nanograms per milliliter with a limit of detection of 0.05 ng/mL.

To capture long-term ETS exposure, we measured cotinine in hair samples. Approximately 10 hairs were cut at the root from the occipital region of the head and collected at baseline, 6 months, and 12 months of the study. The root end was labeled, and the specimens were transported to the Division of Clinical Pharmacology at the University of Toronto. Using a validated procedure, the hair samples were analyzed for cotinine using radioimmunoassay.[12,21] Hair cotinine values were reported in nanograms of cotinine per milligram of hair with a limit of detection of 0.005 ng/mg.

Air Nicotine

We measured ETS exposure in the home using nicotine dosimeters. Nicotine, a major component of tobacco, provides an objective measure of ambient tobacco smoke exposure.[22,23,24,25] The dosimeters used in this study consisted of a filter treated with sodium bisulfate and contained in a 4-cm polystyrene cassette. Nicotine passively diffuses to the dosimeter and binds the filter. The dosimeter was housed in a metal compartment on the HEPA carbon-permanganate-zeolite air cleaner (Austin Air; Buffalo, NY) in the main activity room of each housing unit. Dosimeters were placed at the baseline and 6-month visits, and subsequently retrieved at the 6-month and 12-month visits, respectively. The nicotine dosimeters were analyzed using a standardized protocol.[22,23,24,26] Nicotine levels were reported in micrograms per filter. The passive monitors have a limit of detection of 0.01 µg per filter.[24]

Duration of ETS exposure likely impacts cotinine levels in children. To capture this information, we asked the primary caregiver to estimate the total time the child spent with someone smoking in the same room. Then we asked the parent to recall the level of tobacco exposure to the child in settings outside of the home: car, day care, and other homes.


We surveyed the primary caregiver about the child's race. The primary caregiver of each subject was offered a list of seven racial categories from which to select: African American (black), white, Asian or Asian American, Asian Indian, Native American, Native Hawaiian/Pacific Islander, and Middle Eastern. Because the cohort was primarily African American and white (95%), we excluded other racial and ethnic groups for the purpose of this analysis.

Other Variables

We measured HEPA air cleaner run time using electric counters. Each air cleaner was equipped with a counter that recorded the number of hours used. We recorded these values at 6 months and 12 months of the study. In addition, we collected demographic and housing information including the child's age and gender, household income, insurance status, and the season of enrollment. Finally, we measured the dimensions of each room using an electronic tape measure and calculated room volumes. Then, we summed these measures to obtain an overall housing volume.


We determined the longitudinal relationship between African-American race and biological measures of cotinine while accounting for measures of air nicotine. Since measures of air nicotine and cotinine followed a log-normal distribution, we transformed these variables using natural logarithms. We estimated the means, variance, proportions for all variables of interest. Then, we tested for racial differences using t tests and X2 tests as appropriate. First, we tested for racial differences in cotinine and nicotine using the baseline, 6-month, and 12-month data. After identifying variables that were associated with African-American race (p < 0.25), we employed a repeated measures analysis using a mixed-effects linear model (Proc Mixed in SAS; SAS Institute; Cary, NC) to determine the longitudinal relationship between race and cotinine, while adjusting for air nicotine and other factors.[27] All values of air nicotine and cotinine are presented as geometric means. Coefficients obtained from the repeated measures model are presented on the log scale. Exponentiation of the race coefficient would provide a ratio of cotinine means between African Americans and whites. We tested for effect modification by incorporating a race/air nicotine product in the final model. All analyses were completed using statistical software (SAS version 9.1; SAS Institute).


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