Natalie Nardone1, Shonul Jain2, Newton Addo3, Gideon St Helen4, Peyton Jacob5, Neal L Benowitz6. 1. Division of Cardiology, Department of Medicine, Program in Clinical Pharmacology, University of California San Francisco (N Nardone, N Addo, and G St.Helen). Electronic address: natalie.nardone@ucsf.edu. 2. Department of Pediatrics, University of California San Francisco (S Jain). 3. Division of Cardiology, Department of Medicine, Program in Clinical Pharmacology, University of California San Francisco (N Nardone, N Addo, and G St.Helen). 4. Division of Cardiology, Department of Medicine, Program in Clinical Pharmacology, University of California San Francisco (N Nardone, N Addo, and G St.Helen); Center for Tobacco Control Research and Education, University of California San Francisco (G St.Helen and NL Benowitz). 5. Division of Cardiology, Departments of Medicine and Psychiatry, Clinical Pharmacology Research Laboratory, University of California San Francisco (P Jacob). 6. Center for Tobacco Control Research and Education, University of California San Francisco (G St.Helen and NL Benowitz); Department of Medicine and Bioengineering and Therapeutic Sciences, University of California San Francisco (NL Benowitz).
Abstract
OBJECTIVE: In an urban adolescent population, we evaluated sources of exposure to secondhand smoke exposure (SHS), examined differences in exposure by race/ethnicity, age and sex, and determined the relationship between exposure source(s) and the biomarkers cotinine and NNAL. METHODS: Participants were recruited from a public hospital-based outpatient clinic in San Francisco, CA, USA. RESULTS: Of a sample of N = 298 adolescents screened, 235 were biologically confirmed to be exposed to tobacco smoke. Of those, N = 16 were active smokers and N = 219 were exposed to SHS; 91 (39%) were heavily SHS exposed (median cotinine = 0.76 ng/mL) and 128 (54%) had light SHS exposure (median cotinine = 0.11 ng/mL). Within those SHS exposed, the most common source of exposure was in a public area. No significant racial/ethnic differences were found, although African American adolescents were more likely to live in a home that allowed smoking. Older adolescents were more likely to be exposed across several difference sources, and females more likely to be exposed in a car and in public areas. Past 7-day exposure in the home, in a car, and current blunt use were significantly related to biomarkers of exposure. CONCLUSIONS: Urban adolescents are exposed to SHS across a variety of sources. Although exposure in a public area is most common, exposure in the home and in cars significantly influences tobacco biomarker levels. Interventions to reduce exposure would have the greatest impact in this population if they focused on reducing exposure in the home and in cars. History of blunt use is a strong determinant of tobacco exposure.
OBJECTIVE: In an urban adolescent population, we evaluated sources of exposure to secondhand smoke exposure (SHS), examined differences in exposure by race/ethnicity, age and sex, and determined the relationship between exposure source(s) and the biomarkers cotinine and NNAL. METHODS:Participants were recruited from a public hospital-based outpatient clinic in San Francisco, CA, USA. RESULTS: Of a sample of N = 298 adolescents screened, 235 were biologically confirmed to be exposed to tobacco smoke. Of those, N = 16 were active smokers and N = 219 were exposed to SHS; 91 (39%) were heavily SHS exposed (median cotinine = 0.76 ng/mL) and 128 (54%) had light SHS exposure (median cotinine = 0.11 ng/mL). Within those SHS exposed, the most common source of exposure was in a public area. No significant racial/ethnic differences were found, although African American adolescents were more likely to live in a home that allowed smoking. Older adolescents were more likely to be exposed across several difference sources, and females more likely to be exposed in a car and in public areas. Past 7-day exposure in the home, in a car, and current blunt use were significantly related to biomarkers of exposure. CONCLUSIONS: Urban adolescents are exposed to SHS across a variety of sources. Although exposure in a public area is most common, exposure in the home and in cars significantly influences tobacco biomarker levels. Interventions to reduce exposure would have the greatest impact in this population if they focused on reducing exposure in the home and in cars. History of blunt use is a strong determinant of tobacco exposure.
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