Exposure to Environmental Tobacco Smoke Among Children
Exposure to Environmental Tobacco Smoke Among Children
Exposure to environmental tobacco smoke (ETS) is a major cause of morbidity and mortality among U.S. children. Despite African-American children's having a lower reported exposure to tobacco compared to whites, they suffer disproportionately from tobacco-related illnesses and have higher levels of serum cotinine than white children. The goal of this study was to test whether African-American children have higher levels of serum and hair cotinine, after accounting for ETS exposure and various housing characteristics. We investigated the level of cotinine in both hair and serum in a sample of 222 children with asthma. Using a previously validated survey for adult smokers, we assessed each child's exposure to ETS. We collected detailed information on the primary residence, including home volume, ventilation, and overall home configuration. Despite a lower reported ETS exposure, African-American children had higher mean levels of serum cotinine (1.41 ng/mL vs. 0.97 ng/mL; p = 0.03) and hair cotinine (0.25 ng/mg vs. 0.07 ng/mg; p < 0.001) compared with white children. After adjusting for ETS exposure, housing size, and other demographic characteristics, serum and hair cotinine levels remained significantly higher in African-American children (β = 0.34, p = 0.03) than in white children (β = 1.06, p < 0.001). Housing volume was significantly associated with both serum and hair cotinine but did not fully explain the race difference. Our results demonstrate that, despite a lower reported exposure to ETS, African-American children with asthma had significantly higher levels of both serum and hair cotinine than did white children. Identifying causes and consequences of increased cotinine may help explain the striking differences in tobacco-related illnesses.
Environmental tobacco smoke (ETS) is a major cause of morbidity and mortality among children. ETS increases the risk of sudden infant death syndrome (SIDS), otitis media, lower respiratory tract infections, and asthma (Cook and Strachan 1999; Larsson et al. 2001). Furthermore, ETS contains known carcinogens, such as polycyclic aromatic hydrocarbons and 4-aminobiphenyl, which react with DNA and proteins to form adducts (Sexton et al. 2004; Tang et al. 1999). These compounds have been associated with the development of cancer (Perera et al. 2002; Tang et al. 2001). Data from the National Health Interview Survey indicate that regular smoking occurs in 36% of homes in which children reside, an estimate that far exceeds the Healthy People 2010 goal of reducing the percentage of children exposed to ETS to ≤ 10% [Schuster et al. 2002; U.S. Department of Health and Human Services (DHHS) 2000].
There is a disparity between the reported level of tobacco use and tobacco-associated outcomes among African Americans. Despite lower levels of reported tobacco use and exposure than among whites, African-American adults and children experience significantly higher levels of tobacco-related morbidity and mortality [Centers for Disease Control and Prevention (CDC) 1998]. African-American smokers experience significantly higher rates of smoking-related cancers when compared with white smokers, even though they report smoking fewer cigarettes per day (Caraballo et al. 1998, 2004; CDC 1998). African-American children experience higher rates of low birth weight, SIDS, and asthma, even though their reported exposure to ETS is less than that of white children. Although this paradox is not completely understood, many investigators hypothesize that racial differences in the metabolism of tobacco toxins may explain these striking differences in tobacco-related morbidity and mortality (Ahijevych and Garrett 2004; Ahijevych et al. 2002; Benowitz et al. 1999, 2004; Clark et al. 1996a; Mannino et al. 2001b; Perez-Stable et al. 1998; Tang et al. 1999).
Surprisingly, studies show that, despite lower levels of reported tobacco use compared with white smokers, African-American smokers have higher levels of some biologic markers of tobacco exposure. Until recently, most studies have relied on self-report to assess tobacco exposure. Increasingly, studies are incorporating biomarkers to objectively assess tobacco exposure (Al-Delaimy et al. 2001; Caraballo et al. 1998, 2004; Hecht et al. 2001; Klein and Koren 1999; Knight et al. 1996; Mannino et al. 2002, 2003). The most widely used biomarker is cotinine, which is a relatively stable product of nicotine metabolism. In laboratory experiments that controlled for tobacco smoke exposure, African Americans had serum cotinine levels that were 32-45% higher than those of whites (Benowitz et al. 1999, 2002; Perez-Stable et al. 1998). In a nationally representative sample, African-American smokers had significantly higher serum cotinine levels compared with white smokers, even though they reported smoking fewer cigarettes (Caraballo et al. 1998). However, the data for children and ETS exposure, rather than actual tobacco use, are more limited. In one Canadian study, black children had higher levels of urine and hair cotinine than did white or East Indian children, despite a lower reported home ETS exposure (Knight et al. 1996). In contrast, Mannino et al. (2001a) found no significant racial differences in serum cotinine among ETS-exposed children. Few studies involving children have systematically examined how key factors such as housing size, housing ventilation, and out-of-home exposure might influence the relationship between race, reported ETS, and cotinine (Henschen et al. 1997). Smaller housing size, for example, could be more common among African-American children and thus concentrate their exposure to ETS and increase cotinine levels.
The goal of the present study was to test whether African-American children with asthma have higher serum and hair cotinine levels compared with white children with asthma, even after accounting for reported ETS exposure both inside and outside of the home as well as important housing characteristics such as home volume and home ventilation.
Exposure to environmental tobacco smoke (ETS) is a major cause of morbidity and mortality among U.S. children. Despite African-American children's having a lower reported exposure to tobacco compared to whites, they suffer disproportionately from tobacco-related illnesses and have higher levels of serum cotinine than white children. The goal of this study was to test whether African-American children have higher levels of serum and hair cotinine, after accounting for ETS exposure and various housing characteristics. We investigated the level of cotinine in both hair and serum in a sample of 222 children with asthma. Using a previously validated survey for adult smokers, we assessed each child's exposure to ETS. We collected detailed information on the primary residence, including home volume, ventilation, and overall home configuration. Despite a lower reported ETS exposure, African-American children had higher mean levels of serum cotinine (1.41 ng/mL vs. 0.97 ng/mL; p = 0.03) and hair cotinine (0.25 ng/mg vs. 0.07 ng/mg; p < 0.001) compared with white children. After adjusting for ETS exposure, housing size, and other demographic characteristics, serum and hair cotinine levels remained significantly higher in African-American children (β = 0.34, p = 0.03) than in white children (β = 1.06, p < 0.001). Housing volume was significantly associated with both serum and hair cotinine but did not fully explain the race difference. Our results demonstrate that, despite a lower reported exposure to ETS, African-American children with asthma had significantly higher levels of both serum and hair cotinine than did white children. Identifying causes and consequences of increased cotinine may help explain the striking differences in tobacco-related illnesses.
Environmental tobacco smoke (ETS) is a major cause of morbidity and mortality among children. ETS increases the risk of sudden infant death syndrome (SIDS), otitis media, lower respiratory tract infections, and asthma (Cook and Strachan 1999; Larsson et al. 2001). Furthermore, ETS contains known carcinogens, such as polycyclic aromatic hydrocarbons and 4-aminobiphenyl, which react with DNA and proteins to form adducts (Sexton et al. 2004; Tang et al. 1999). These compounds have been associated with the development of cancer (Perera et al. 2002; Tang et al. 2001). Data from the National Health Interview Survey indicate that regular smoking occurs in 36% of homes in which children reside, an estimate that far exceeds the Healthy People 2010 goal of reducing the percentage of children exposed to ETS to ≤ 10% [Schuster et al. 2002; U.S. Department of Health and Human Services (DHHS) 2000].
There is a disparity between the reported level of tobacco use and tobacco-associated outcomes among African Americans. Despite lower levels of reported tobacco use and exposure than among whites, African-American adults and children experience significantly higher levels of tobacco-related morbidity and mortality [Centers for Disease Control and Prevention (CDC) 1998]. African-American smokers experience significantly higher rates of smoking-related cancers when compared with white smokers, even though they report smoking fewer cigarettes per day (Caraballo et al. 1998, 2004; CDC 1998). African-American children experience higher rates of low birth weight, SIDS, and asthma, even though their reported exposure to ETS is less than that of white children. Although this paradox is not completely understood, many investigators hypothesize that racial differences in the metabolism of tobacco toxins may explain these striking differences in tobacco-related morbidity and mortality (Ahijevych and Garrett 2004; Ahijevych et al. 2002; Benowitz et al. 1999, 2004; Clark et al. 1996a; Mannino et al. 2001b; Perez-Stable et al. 1998; Tang et al. 1999).
Surprisingly, studies show that, despite lower levels of reported tobacco use compared with white smokers, African-American smokers have higher levels of some biologic markers of tobacco exposure. Until recently, most studies have relied on self-report to assess tobacco exposure. Increasingly, studies are incorporating biomarkers to objectively assess tobacco exposure (Al-Delaimy et al. 2001; Caraballo et al. 1998, 2004; Hecht et al. 2001; Klein and Koren 1999; Knight et al. 1996; Mannino et al. 2002, 2003). The most widely used biomarker is cotinine, which is a relatively stable product of nicotine metabolism. In laboratory experiments that controlled for tobacco smoke exposure, African Americans had serum cotinine levels that were 32-45% higher than those of whites (Benowitz et al. 1999, 2002; Perez-Stable et al. 1998). In a nationally representative sample, African-American smokers had significantly higher serum cotinine levels compared with white smokers, even though they reported smoking fewer cigarettes (Caraballo et al. 1998). However, the data for children and ETS exposure, rather than actual tobacco use, are more limited. In one Canadian study, black children had higher levels of urine and hair cotinine than did white or East Indian children, despite a lower reported home ETS exposure (Knight et al. 1996). In contrast, Mannino et al. (2001a) found no significant racial differences in serum cotinine among ETS-exposed children. Few studies involving children have systematically examined how key factors such as housing size, housing ventilation, and out-of-home exposure might influence the relationship between race, reported ETS, and cotinine (Henschen et al. 1997). Smaller housing size, for example, could be more common among African-American children and thus concentrate their exposure to ETS and increase cotinine levels.
The goal of the present study was to test whether African-American children with asthma have higher serum and hair cotinine levels compared with white children with asthma, even after accounting for reported ETS exposure both inside and outside of the home as well as important housing characteristics such as home volume and home ventilation.
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