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Original Research: ENVIRONMENTAL HEALTH |

The Role of Air Nicotine in Explaining Racial Differences in Cotinine Among Tobacco-Exposed Children* FREE TO VIEW

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

*From the Department of Medicine (Dr. Wilson), Division of General Internal Medicine, University of Cincinnati College of Medicine; and Cincinnati Children’s Environmental Health Center (Drs. Kahn, Khoury, and Lanphear), Cincinnati Children’s Hospital Medical Center, Cincinnati, OH.

Correspondence to: Stephen E. Wilson, MD, MSc, University of Cincinnati, 231 Albert Sabin Way, Room 6603, Cincinnati, OH 45267; e-mail: Stephen.wilson@uc.edu



Chest. 2007;131(3):856-862. doi:10.1378/chest.06-2123
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Published online

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 (β = 0.28, p = 0.04) and hair cotinine (β = 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.

Figures in this Article

Exposure to environmental tobacco smoke (ETS) has a substantial impact on the health of children.14 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.12,46 Mannino et al5 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 al7 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.3,89 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 investigations1012 have identified striking racial differences in cotinine among tobacco-exposed children. Moreover, studies1314 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.

Overview

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.35,1518 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.1920 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.2225 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.2224,26 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.

Race

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.

Analysis

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 χ2 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).

Sample Characteristics

The characteristics of this study population are outlined in Table 1 . African-American children were slightly older than white children, and resided in households with a smaller volume. African-American families used the HEPA air cleaners less frequently than white families during both the first 6 months and second 6 months of the study. There were no racial differences in the proportion of girls in the study, the season of enrollment, or the distribution of active filters. Also, there were no differences by race in the reported levels of ETS exposure in settings outside of the home.

Cotinine and Air Nicotine

African-American children had significantly higher levels of cotinine in both hair and serum compared to white children (Table 1). Racial differences in cotinine biomarkers persisted > 12 months (Fig 1,2 ) However, there were no significant racial differences in air nicotine levels at the 6-month (2.95 μg vs 2.55 μg, p = 0.62) and 12-month (3.27 μg vs 2.17 μg, p = 0.17) study visits.

Repeated-Measures Analysis

African-American race was independently associated with serum cotinine over time (Table 2 ). In the bivariate model, African-American race was significantly associated with serum cotinine. The addition of various covariates attenuated the relationship between race and cotinine, reducing the race estimate from 0.435 (p = 0.015) to 0.280 (p = 0.040), but African-American race and cotinine remained statistically significant. Transformation of the race coefficient in the adjusted model generated a value of 1.32, indicating the ratio of serum cotinine means between African-American children and white children. Other factors independently associated with serum cotinine included air nicotine, filter run time, home ETS exposure, and total home volume. Notably, age, gender, and season were not associated with serum cotinine levels.

Racial differences in hair cotinine were even more striking (Table 3 ). Adding potential confounders to the initial model increased the race estimate from 1.36 (p < 0.0001) to 1.40 (p < 0.0001). African-American race and air nicotine were independently associated with hair cotinine in the fully adjusted model. Transformation of the race coefficient provided a value of 3.9, indicating a fourfold difference in hair cotinine levels between African Americans and whites over the 12-month study period. Next, we tested for an interaction by introducing a race/air nicotine product term into both models. The p values for these product terms exceeded 0.80, indicating the absence of effect modification.

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 studies10,12,16,28 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.15,2931 Benowitz et al15 and Perez-Stable et al32 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 al30 found that smoking mentholated tobacco products increased serum nicotine and carboxyhemoglobin concentrations in African Americans and lowered the levels in whites. Ahijevych et al29 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.3334 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 al35 demonstrated that various hair dyes and shampoos can influence hair cotinine levels in young adults. The authors35 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.56 Among children, Mannino et al5 demonstrated significant associations between higher serum cotinine levels, and asthma prevalence and increased school absence. Chilmonczyk et al36 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.3,9,3738 Understanding racial differences in the response to ETS could provide momentum to implement policies that protect highly susceptible populations from ETS exposure.

Abbreviations: CAP = Cincinnati Asthma Prevention; ETS = environmental tobacco smoke; HEPA = high-efficiency particulate air

This work was performed with support from the National Heart, Lung, and Blood Institute grant H165731 (Drs. Lanphear and Khoury), Robert Wood Johnson Generalist Physician Faculty Scholars Award (Dr. Kahn), and the University of Cincinnati Department of Internal Medicine (Dr. Wilson).

The authors have no conflicts of interest to disclose.

This work was presented in part at the 2006 Pediatric Academic Societies Meeting in San Francisco, CA.

Table Graphic Jump Location
Table 1. CAP Study Population Characteristics*
* 

Data are presented as mean (SE) unless otherwise indicated.

Figure Jump LinkFigure 1. Geometric mean levels of serum cotinine over 12 months by race. The error bars represent the 95% confidence intervals around the mean.Grahic Jump Location
Figure Jump LinkFigure 2. Geometric mean levels of hair cotinine over 12 months by race. The error bars represent 95% confidence intervals around the mean.Grahic Jump Location
Table Graphic Jump Location
Table 2. Unadjusted and Adjusted Relationships Between African-American Race and Serum Cotinine*
* 

Final model adjusts for variables listed including age.

 

p< 0.05.

Table Graphic Jump Location
Table 3. Unadjusted and Adjusted Relationships Between African-American Race and Hair Cotinine*
* 

Final model adjusts for variables listed including age.

 

p < 0.05.

DiFranza, JR, Aligne, CA, Weitzman, M (2004) Prenatal and postnatal environmental tobacco smoke exposure and children’s health.Pediatrics113(4 suppl),1007-1015
 
Cook, DG, Strachan, DP Health effects of passive smoking: 10; Summary of effects of parental smoking on the respiratory health of children and implications for research.Thorax1999;54,357-366. [PubMed] [CrossRef]
 
US Department of Health and Human Services... Tobacco use among US racial/ethnic minority groups African Americans, American Indians and Alaska Natives, Asian Americans, and Pacific Islanders, Hispanics a report of the surgeon general. 1998; Centers for Disease Control and Prevention. Atlanta, GA:.
 
National Cancer Institute... Health effects of exposure to environmental tobacco smoke, etc., Monograph 10, August 1999. 1999; National Institutes of Health. Washington DC:.
 
Mannino, DM, Moorman, JE, Kingsley, B, et al Health effects related to environmental tobacco smoke exposure in children in the United States: data from the Third National Health and Nutrition Examination Survey.Arch Pediatr Adolesc Med2001;155,36-41. [PubMed]
 
Mannino, DM, Homa, DM, Redd, SC Involuntary smoking and asthma severity in children: data from the Third National Health and Nutrition Examination Survey.Chest2002;122,409-415. [PubMed]
 
Boffetta, P, Tredaniel, J, Greco, A Risk of childhood cancer and adult lung cancer after childhood exposure to passive smoke: a meta-analysis.Environ Health Perspect2000;108,73-82. [PubMed]
 
Akinbami, LJ, Schoendorf, KC Trends in childhood asthma: prevalence, health care utilization, and mortality.Pediatrics2002;110,315-322. [PubMed]
 
US Public Health Service, Office of the Surgeon General... The health consequences of involuntary exposure to tobacco smoke: a report of the surgeon general. 2006; US Department of Health and Human Services, Public Health Service, Office of the Surgeon General. Rockville, MD:.
 
Groner, J, Wadwa, P, Hoshaw-Woodard, S, et al Active and passive tobacco smoke exposure: a comparison of maternal and child hair cotinine levels.Nicotine Tob Res2004;6,789-795. [PubMed]
 
Wilson, SE, Kahn, RS, Khoury, J, et al Racial differences in exposure to environmental tobacco smoke among children.Environ Health Perspect2005;113,362-367. [PubMed]
 
Knight, JM, Eliopoulos, C, Klein, J, et al Passive smoking in children: racial differences in systemic exposure to cotinine by hair and urine analysis.Chest1996;109,446-450. [PubMed]
 
Carty, CS, Huribal, M, Marsan, BU, et al Nicotine and its metabolite cotinine are mitogenic for human vascular smooth muscle cells.J Vasc Surg Apr1997;25,682-688
 
Audesirk, T, Cabell, L Nanomolar concentrations of nicotine and cotinine alter the development of cultured hippocampal neurons via non-acetylcholine receptor-mediated mechanisms.Neurotoxicology1999;20,639-646. [PubMed]
 
Benowitz, NL, Perez-Stable, EJ, Fong, I, et al Ethnic differences in N-glucuronidation of nicotine and cotinine.J Pharmacol Exp Ther1999;291,1196-1203. [PubMed]
 
Mannino, DM, Caraballo, R, Benowitz, N, et al Predictors of cotinine levels in US children: data from the Third National Health and Nutrition Examination Survey.Chest2001;120,718-724. [PubMed]
 
Tricker, AR Nicotine metabolism, human drug metabolism polymorphisms, and smoking behaviour.Toxicology2003;183,151-173. [PubMed]
 
Centers for Disease Control and Prevention... Third national report on human exposure to environmental chemicals. 2005; National Center for Environmental Health. Atlanta, GA: publication No. 05–0570.
 
Bernert, JT, Jr, Turner, WE, Pirkle, JL, et al Development and validation of sensitive method for determination of serum cotinine in smokers and nonsmokers by liquid chromatography/atmospheric pressure ionization tandem mass spectrometry.Clin Chem1997;43,2281-2291. [PubMed]
 
Bernert, JT, Jr, McGuffey, JE, Morrison, MA, et al Comparison of serum and salivary cotinine measurements by a sensitive high-performance liquid chromatography-tandem mass spectrometry method as an indicator of exposure to tobacco smoke among smokers and nonsmokers.J Anal Toxicol2000;24,333-339. [PubMed]
 
Klein, J, Koren, G Hair analysis: a biological marker for passive smoking in pregnancy and childhood.Hum Exp Toxicol1999;18,279-282. [PubMed]
 
Marbury, MC, Hammond, SK, Haley, NJ Measuring exposure to environmental tobacco smoke in studies of acute health effects.Am J Epidemiol1993;137,1089-1097. [PubMed]
 
Hammond, SK, Sorensen, G, Youngstrom, R, et al Occupational exposure to environmental tobacco smoke.JAMA1995;274,956-960. [PubMed]
 
Eisner, MD, Katz, PP, Yelin, EH, et al Measurement of environmental tobacco smoke exposure among adults with asthma.Environ Health Perspect2001;109,809-814. [PubMed]
 
Emmons, KM, Hammond, SK, Fava, JL, et al A randomized trial to reduce passive smoke exposure in low-income households with young children.Pediatrics2001;108,18-24. [PubMed]
 
Glasgow, RE, Foster, LS, Lee, ME, et al Developing a brief measure of smoking in the home: description and preliminary evaluation.Addict Behav1998;23,567-571. [PubMed]
 
Harrell, F, Jr. Regression modeling strategies: with applications to linear models, logistic models, and survival analysis. 2001; Springer-Verlag. New York, NY:.
 
Sexton, K, Adgate, JL, Church, TR, et al Children’s exposure to environmental tobacco smoke: using diverse exposure metrics to document ethnic/racial differences.Environ Health Perspect2004;112,392-397. [PubMed]
 
Ahijevych, K, Tyndale, RF, Dhatt, RK, et al Factors influencing cotinine half-life during smoking abstinence in African American and Caucasian women.Nicotine Tob Res2002;4,423-431. [PubMed]
 
Benowitz, NL, Herrera, B, Jacob, IP Mentholated cigarette smoking inhibits nicotine metabolism.J Pharmacol Exp Ther2004;310,1208-1215. [PubMed]
 
Benowitz, NL, Perez-Stable, EJ, Herrera, B, et al Slower metabolism and reduced intake of nicotine from cigarette smoking in Chinese-Americans.J Natl Cancer Inst2002;94,108-115. [PubMed]
 
Perez-Stable, EJ, Herrera, B, Jacob, P, III, et al Nicotine metabolism and intake in black and white smokers.JAMA1998;280,152-156. [PubMed]
 
Al-Delaimy, WK Hair as a biomarker for exposure to tobacco smoke.Tob Control2002;11,176-182. [PubMed]
 
Al-Delaimy, WK, Crane, J, Woodward, A Is the hair nicotine level a more accurate biomarker of environmental tobacco smoke exposure than urine cotinine?J Epidemiol Commun Health2002;56,66-71
 
Pichini, S, Altieri, I, Pellegrini, M, et al Hair analysis for nicotine and cotinine: evaluation of extraction procedures, hair treatments, and development of reference material.Forensic Sci Int1997;84,243-252. [PubMed]
 
Chilmonczyk, BA, Salmun, LM, Megathlin, KN, et al Association between exposure to environmental tobacco smoke and exacerbations of asthma in children.N Engl J Med1993;328,1665-1669. [PubMed]
 
Cote, ML, Kardia, SL, Wenzlaff, AS, et al Risk of lung cancer among white and black relatives of individuals with early-onset lung cancer.JAMA2005;293,3036-3042. [PubMed]
 
Maurice, E, Trosclair, A, Merritt, R, et al Cigarette smoking among adults: United States 2004.MMWR Surveill Summ2005;54,1121-1124
 

Figures

Figure Jump LinkFigure 1. Geometric mean levels of serum cotinine over 12 months by race. The error bars represent the 95% confidence intervals around the mean.Grahic Jump Location
Figure Jump LinkFigure 2. Geometric mean levels of hair cotinine over 12 months by race. The error bars represent 95% confidence intervals around the mean.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1. CAP Study Population Characteristics*
* 

Data are presented as mean (SE) unless otherwise indicated.

Table Graphic Jump Location
Table 2. Unadjusted and Adjusted Relationships Between African-American Race and Serum Cotinine*
* 

Final model adjusts for variables listed including age.

 

p< 0.05.

Table Graphic Jump Location
Table 3. Unadjusted and Adjusted Relationships Between African-American Race and Hair Cotinine*
* 

Final model adjusts for variables listed including age.

 

p < 0.05.

References

DiFranza, JR, Aligne, CA, Weitzman, M (2004) Prenatal and postnatal environmental tobacco smoke exposure and children’s health.Pediatrics113(4 suppl),1007-1015
 
Cook, DG, Strachan, DP Health effects of passive smoking: 10; Summary of effects of parental smoking on the respiratory health of children and implications for research.Thorax1999;54,357-366. [PubMed] [CrossRef]
 
US Department of Health and Human Services... Tobacco use among US racial/ethnic minority groups African Americans, American Indians and Alaska Natives, Asian Americans, and Pacific Islanders, Hispanics a report of the surgeon general. 1998; Centers for Disease Control and Prevention. Atlanta, GA:.
 
National Cancer Institute... Health effects of exposure to environmental tobacco smoke, etc., Monograph 10, August 1999. 1999; National Institutes of Health. Washington DC:.
 
Mannino, DM, Moorman, JE, Kingsley, B, et al Health effects related to environmental tobacco smoke exposure in children in the United States: data from the Third National Health and Nutrition Examination Survey.Arch Pediatr Adolesc Med2001;155,36-41. [PubMed]
 
Mannino, DM, Homa, DM, Redd, SC Involuntary smoking and asthma severity in children: data from the Third National Health and Nutrition Examination Survey.Chest2002;122,409-415. [PubMed]
 
Boffetta, P, Tredaniel, J, Greco, A Risk of childhood cancer and adult lung cancer after childhood exposure to passive smoke: a meta-analysis.Environ Health Perspect2000;108,73-82. [PubMed]
 
Akinbami, LJ, Schoendorf, KC Trends in childhood asthma: prevalence, health care utilization, and mortality.Pediatrics2002;110,315-322. [PubMed]
 
US Public Health Service, Office of the Surgeon General... The health consequences of involuntary exposure to tobacco smoke: a report of the surgeon general. 2006; US Department of Health and Human Services, Public Health Service, Office of the Surgeon General. Rockville, MD:.
 
Groner, J, Wadwa, P, Hoshaw-Woodard, S, et al Active and passive tobacco smoke exposure: a comparison of maternal and child hair cotinine levels.Nicotine Tob Res2004;6,789-795. [PubMed]
 
Wilson, SE, Kahn, RS, Khoury, J, et al Racial differences in exposure to environmental tobacco smoke among children.Environ Health Perspect2005;113,362-367. [PubMed]
 
Knight, JM, Eliopoulos, C, Klein, J, et al Passive smoking in children: racial differences in systemic exposure to cotinine by hair and urine analysis.Chest1996;109,446-450. [PubMed]
 
Carty, CS, Huribal, M, Marsan, BU, et al Nicotine and its metabolite cotinine are mitogenic for human vascular smooth muscle cells.J Vasc Surg Apr1997;25,682-688
 
Audesirk, T, Cabell, L Nanomolar concentrations of nicotine and cotinine alter the development of cultured hippocampal neurons via non-acetylcholine receptor-mediated mechanisms.Neurotoxicology1999;20,639-646. [PubMed]
 
Benowitz, NL, Perez-Stable, EJ, Fong, I, et al Ethnic differences in N-glucuronidation of nicotine and cotinine.J Pharmacol Exp Ther1999;291,1196-1203. [PubMed]
 
Mannino, DM, Caraballo, R, Benowitz, N, et al Predictors of cotinine levels in US children: data from the Third National Health and Nutrition Examination Survey.Chest2001;120,718-724. [PubMed]
 
Tricker, AR Nicotine metabolism, human drug metabolism polymorphisms, and smoking behaviour.Toxicology2003;183,151-173. [PubMed]
 
Centers for Disease Control and Prevention... Third national report on human exposure to environmental chemicals. 2005; National Center for Environmental Health. Atlanta, GA: publication No. 05–0570.
 
Bernert, JT, Jr, Turner, WE, Pirkle, JL, et al Development and validation of sensitive method for determination of serum cotinine in smokers and nonsmokers by liquid chromatography/atmospheric pressure ionization tandem mass spectrometry.Clin Chem1997;43,2281-2291. [PubMed]
 
Bernert, JT, Jr, McGuffey, JE, Morrison, MA, et al Comparison of serum and salivary cotinine measurements by a sensitive high-performance liquid chromatography-tandem mass spectrometry method as an indicator of exposure to tobacco smoke among smokers and nonsmokers.J Anal Toxicol2000;24,333-339. [PubMed]
 
Klein, J, Koren, G Hair analysis: a biological marker for passive smoking in pregnancy and childhood.Hum Exp Toxicol1999;18,279-282. [PubMed]
 
Marbury, MC, Hammond, SK, Haley, NJ Measuring exposure to environmental tobacco smoke in studies of acute health effects.Am J Epidemiol1993;137,1089-1097. [PubMed]
 
Hammond, SK, Sorensen, G, Youngstrom, R, et al Occupational exposure to environmental tobacco smoke.JAMA1995;274,956-960. [PubMed]
 
Eisner, MD, Katz, PP, Yelin, EH, et al Measurement of environmental tobacco smoke exposure among adults with asthma.Environ Health Perspect2001;109,809-814. [PubMed]
 
Emmons, KM, Hammond, SK, Fava, JL, et al A randomized trial to reduce passive smoke exposure in low-income households with young children.Pediatrics2001;108,18-24. [PubMed]
 
Glasgow, RE, Foster, LS, Lee, ME, et al Developing a brief measure of smoking in the home: description and preliminary evaluation.Addict Behav1998;23,567-571. [PubMed]
 
Harrell, F, Jr. Regression modeling strategies: with applications to linear models, logistic models, and survival analysis. 2001; Springer-Verlag. New York, NY:.
 
Sexton, K, Adgate, JL, Church, TR, et al Children’s exposure to environmental tobacco smoke: using diverse exposure metrics to document ethnic/racial differences.Environ Health Perspect2004;112,392-397. [PubMed]
 
Ahijevych, K, Tyndale, RF, Dhatt, RK, et al Factors influencing cotinine half-life during smoking abstinence in African American and Caucasian women.Nicotine Tob Res2002;4,423-431. [PubMed]
 
Benowitz, NL, Herrera, B, Jacob, IP Mentholated cigarette smoking inhibits nicotine metabolism.J Pharmacol Exp Ther2004;310,1208-1215. [PubMed]
 
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    Print ISSN: 0012-3692
    Online ISSN: 1931-3543