Racial Differences in Exposure to Environmental Tobacco Smoke Among Children Stephen E
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Children’s Health | Article Racial Differences in Exposure to Environmental Tobacco Smoke among Children Stephen E. Wilson,1,2 Robert S. Kahn,2 Jane Khoury,2 and Bruce P. Lanphear 2 1Division of General Internal Medicine, University of Cincinnati, and 2Division of General and Community Pediatrics, Cincinnati Children’s Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, USA Americans had serum cotinine levels that Exposure to environmental tobacco smoke (ETS) is a major cause of morbidity and mortality were 32–45% higher than those of whites among U.S. children. Despite African-American children’s having a lower reported exposure to (Benowitz et al. 1999, 2002; Perez-Stable tobacco compared to whites, they suffer disproportionately from tobacco-related illnesses and have et al. 1998). In a nationally representative higher levels of serum cotinine than white children. The goal of this study was to test whether sample, African-American smokers had sig- African-American children have higher levels of serum and hair cotinine, after accounting for ETS nificantly higher serum cotinine levels com- exposure and various housing characteristics. We investigated the level of cotinine in both hair pared with white smokers, even though they and serum in a sample of 222 children with asthma. Using a previously validated survey for adult reported smoking fewer cigarettes (Caraballo smokers, we assessed each child’s exposure to ETS. We collected detailed information on the pri- et al. 1998). However, the data for children mary residence, including home volume, ventilation, and overall home configuration. Despite a and ETS exposure, rather than actual tobacco lower reported ETS exposure, African-American children had higher mean levels of serum coti- use, are more limited. In one Canadian study, nine (1.41 ng/mL vs. 0.97 ng/mL; p = 0.03) and hair cotinine (0.25 ng/mg vs. 0.07 ng/mg; black children had higher levels of urine and p < 0.001) compared with white children. After adjusting for ETS exposure, housing size, and hair cotinine than did white or East Indian other demographic characteristics, serum and hair cotinine levels remained significantly higher in children, despite a lower reported home ETS African-American children (β = 0.34, p = 0.03) than in white children (β = 1.06, p < 0.001). exposure (Knight et al. 1996). In contrast, Housing volume was significantly associated with both serum and hair cotinine but did not fully Mannino et al. (2001a) found no significant explain the race difference. Our results demonstrate that, despite a lower reported exposure to ETS, racial differences in serum cotinine among African-American children with asthma had significantly higher levels of both serum and hair coti- ETS-exposed children. Few studies involving nine than did white children. Identifying causes and consequences of increased cotinine may help children have systematically examined how explain the striking differences in tobacco-related illnesses. Key words: African American, asthma, key factors such as housing size, housing ven- cotinine, ETS, housing. Environ Health Perspect 113:362–367 (2005). doi:10.1289/ehp.7379 tilation, and out-of-home exposure might available via http://dx.doi.org/ [Online 9 December 2004] influence the relationship between race, reported ETS, and cotinine (Henschen et al. 1997). Smaller housing size, for example, Environmental tobacco smoke (ETS) is a with white smokers, even though they report could be more common among African- major cause of morbidity and mortality among smoking fewer cigarettes per day (Caraballo American children and thus concentrate their children. ETS increases the risk of sudden et al. 1998, 2004; CDC 1998). African- exposure to ETS and increase cotinine levels. infant death syndrome (SIDS), otitis media, American children experience higher rates of The goal of the present study was to test lower respiratory tract infections, and asthma low birth weight, SIDS, and asthma, even whether African-American children with (Cook and Strachan 1999; Larsson et al. though their reported exposure to ETS is less asthma have higher serum and hair cotinine 2001). Furthermore, ETS contains known car- than that of white children. Although this levels compared with white children with cinogens, such as polycyclic aromatic hydro- paradox is not completely understood, many asthma, even after accounting for reported ETS carbons and 4-aminobiphenyl, which react investigators hypothesize that racial differ- exposure both inside and outside of the home with DNA and proteins to form adducts ences in the metabolism of tobacco toxins as well as important housing characteristics (Sexton et al. 2004; Tang et al. 1999). These may explain these striking differences in such as home volume and home ventilation. compounds have been associated with the tobacco-related morbidity and mortality development of cancer (Perera et al. 2002; (Ahijevych and Garrett 2004; Ahijevych et al. Materials and Methods Tang et al. 2001). Data from the National 2002; Benowitz et al. 1999, 2004; Clark et al. Study design and subjects. Data for this study Health Interview Survey indicate that regular 1996a; Mannino et al. 2001b; Perez-Stable were drawn from the Cincinnati Asthma smoking occurs in 36% of homes in which et al. 1998; Tang et al. 1999). Prevention (CAP) study. The CAP study is an children reside, an estimate that far exceeds the Surprisingly, studies show that, despite ongoing double-blind, placebo-controlled trial, Healthy People 2010 goal of reducing the per- lower levels of reported tobacco use compared designed to test the efficacy of reducing ETS centage of children exposed to ETS to ≤ 10% with white smokers, African-American smok- [Schuster et al. 2002; U.S. Department of ers have higher levels of some biologic mark- Address correspondence to S.E. Wilson, Division of Health and Human Services (DHHS) 2000]. ers of tobacco exposure. Until recently, most General Internal Medicine, University of Cincinnati, There is a disparity between the reported studies have relied on self-report to assess French-East, Suite 275, 3202 Eden Ave., Cincinnati, level of tobacco use and tobacco-associated tobacco exposure. Increasingly, studies are OH 45267-0840 USA. Telephone: (513) 558-2763. Fax: (513) 558-2744. E-mail: [email protected] outcomes among African Americans. Despite incorporating biomarkers to objectively assess We thank R. Hornung and A. Leonard for their lower levels of reported tobacco use and expo- tobacco exposure (Al-Delaimy et al. 2001; helpful comments. sure than among whites, African-American Caraballo et al. 1998, 2004; Hecht et al. This work was supported by funding from a National adults and children experience significantly 2001; Klein and Koren 1999; Knight et al. Research Service Award (T32PE10027), National higher levels of tobacco-related morbidity and 1996; Mannino et al. 2002, 2003). The most Health Lung and Blood Institute (R01 Hl65731), and mortality [Centers for Disease Control and widely used biomarker is cotinine, which is a National Institute of Child Health and Development (K23 HD40362). Prevention (CDC) 1998]. African-American relatively stable product of nicotine metabo- The authors declare they have no competing smokers experience significantly higher rates lism. In laboratory experiments that con- financial interests. of smoking-related cancers when compared trolled for tobacco smoke exposure, African Received 2 July 2004; accepted 9 December 2004. 362 VOLUME 113 | NUMBER 3 | March 2005 • Environmental Health Perspectives Children’s Health | Racial differences in serum and hair cotinine exposure using carbon-permanganate-zeolite diluted according to the laboratory protocol. status, and maternal depressive symptoms. (CPZ) high-efficient particulate air (HEPA) Trichloroacetic acid was added to each speci- Maternal depressive symptoms were assessed cleaners among children with asthma. We used men followed by potassium hydroxide to neu- with the Beck Depression Inventory (Beck the baseline data of the CAP study for our tralize this mixture. Cotinine was extracted et al. 1996). We used a cutoff score of > 17 to analysis. We identified potential subjects by using methylene chloride and subsequently indicate moderate to severe levels of depressive using medical records and billing information injected into the HPLC column. The eluant symptoms. from a large tertiary care center and a regional was monitored by mass spectrometry. Statistical analysis. Serum and hair coti- managed care organization, yielding subjects We determined longer-term exposure to nine levels were both highly skewed. Thus, we from urban, suburban, and rural communities. ETS using hair cotinine. Cotinine enters the log-transformed these variables before con- After notifying the child’s health care provider, hair shaft through the hair-bulb blood supply, ducting any analyses. We compared subject we contacted the family by mail to describe the thus reflecting the average concentration in characteristics using t-tests for continuous study in detail. Families that were interested in blood over a longer period of time (Al-Delaimy variables and chi-square tests for categorical participating were contacted by telephone to 2002; Al-Delaimy et al. 2002). Approximately variables. All values for cotinine are presented determine their eligibility, and invited to par- 10 shafts of hair were cut at the root from the as geometric means. Using bivariate analysis, ticipate in the trial. Eligibility criteria included occipital region