Cited by 76Smoking Behavior and CessationToxic Organic Pollutants ImpactCarcinogens and Genotoxicity Assessment

Involuntary tobacco smoke exposure and urinary levels of polycyclic aromatic hydrocarbons in the United States, 1999 to 2002

Suwan-ampai, Plernpit, Navas-Acien, Ana, Strickland, Paul T., Agnew, Jacqueline·2009·Cancer Epidemiology, Biomarkers & Prevention

Abstract

Evidence supports active smoking as a major source of exposure to polycyclic aromatic hydrocarbons (PAH), compounds that are mutagenic and carcinogenic in humans. The influence of involuntary exposure to tobacco smoke on PAH exposure levels among nonsmokers, however, is unknown. This study evaluated the association between both active and involuntary tobacco smoke and biomarkers of PAH exposure in the general U.S. population. A cross-sectional analysis of 5,060 participants ≥6 years of age was done using data from the 1999-2002 National Health and Nutrition Examination Survey (NHANES). PAH exposure was measured by urinary concentrations of 23 monohydroxylated metabolites of nine PAH compounds. Tobacco smoke exposure was defined as no exposure, involuntary exposure, and active exposure by combining serum cotinine levels, smoking status, and presence of household smokers. PAH metabolite levels ranged from 33.9 ng/L for 9-hydroxyphenanthrene to 2,465.4 ng/L for 2-hydroxynaphthalene. After adjustment for age, sex, race/ethnicity, education, household income, and broiled/grilled food consumption, participants involuntarily and actively exposed to tobacco smoke had urinary metabolite concentrations that were increased by a factor of 1.1 to 1.4 and 1.5 to 6.9, respectively, compared with unexposed participants. Associations for involuntary smoking were stronger and statistically significant for 1-hydroxypyrene, 2-hydroxyfluorene, 3-hydroxyfluorene, 9-hydroxyfluorene, 1-hydroxyphenanthrene, 2-hydroxyphenanthrene, and 3-hydroxyphenanthrene compared with other metabolites. Involuntary exposure to tobacco smoke was associated with elevated urinary concentrations of most PAH metabolites in a representative sample of the U.S. population. Policy and educational efforts must continue to minimize PAH exposure through active and involuntary tobacco smoke exposure. (Cancer Epidemiol Biomarkers Prev 2009;18(3):884–93)

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Crossref · 10.1158/1055-9965.epi-08-0939

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Authors
Suwan-ampai, P., Navas-Acien, A., Strickland, P. T., & Agnew, J.
Affiliations
  • Johns Hopkins University (US)
  • Department of Environmental Health Sciences, The Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland
Venue
Cancer Epidemiology, Biomarkers & Prevention
Published
2009-03-01
Volume
18
Issue
3
Pages
884-893
ISSN
  • 1055-9965 (ISSN-L)
  • 1538-7755
OpenAlex
W2098748525
Cited by
76
References
0
Citations by year
2025: 1 · 2024: 5 · 2023: 2 · 2022: 2 · 2021: 1 · 2020: 4 · 2019: 3 · 2018: 5 · 2017: 14 · 2016: 7 · 2015: 6 · 2014: 7 · 2013: 6 · 2012: 7
FWCI
2.73
Type
journal article
Language
en
Open access
closed
Locations
  • Cancer Epidemiology Biomarkers & Prevention (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute for Occupational Safety and Health (T42OH0008428)
Topics
  • Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
Keywords
passive smoking, polycyclic aromatic hydrocarbons, urinary PAH metabolites, biomarkers of exposure, active smoking, serum cotinine, 9-hydroxyphenanthrene, 1-hydroxypyrene, carcinogen exposure, NHANES
MeSH terms
Adolescent, Adult, Aged, Aged, 80 and over, Child, Cross-Sectional Studies, Female, Humans, Male, Middle Aged, Nutrition Surveys, Polycyclic Aromatic Hydrocarbons, Risk Factors, Tobacco Smoke Pollution, United States, Biomarkers, Confounding Factors, Epidemiologic, Linear Models

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