Biomarkers of Environmental Tobacco Smoke in Preschool Children and Their Mothers

Crawford, Florence G.; Mayer, Jack; Santella, Regina M.; Cooper, Thomas B.; Ottman, Ruth; Tsai, Wei‐Yann; Simón-Cereijido, Gabriela; Wang, Margaret; Tang, Deliang; Perera, Frederica P.

doi:10.1093/jnci/86.18.1398

Cited by 101 publications

(39 citation statements)

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“…However, we previously reported a significant increase in PAH-albumin adducts (a surrogate for PAH-DNA adducts) in children exposed to ETS (61). ETS exposure is high in Poland.…”

Section: Discussionmentioning

confidence: 94%

Relationship between ambient air pollution and DNA damage in Polish mothers and newborns.

Whyatt

Santella

Jędrychowski

et al. 1998

Environ Health Perspect

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Industrialized regions in Poland are characterized by high ambient pollution, including polycyclic aromatic hydrocarbons (PAHs) from coal burning for industry and home heating. In experimental bioassays, certain PAHs are transplacental carcinogens and developmental toxicants. Biologic markers can facilitate evaluation of effects of environmental PAHs on the developing infant. We measured the amount of PAHs bound to DNA (PAH-DNA adducts) in maternal and umbilical white blood cells. The cohort consisted of 70 mothers and newborns from Krakow, Poland, an industrialized city with elevated air pollution. Modulation of adduct levels by genotypes previously linked to risk of lung cancer, specifically glutathione S-transferase Ml (GSTM1) and cytochrome P4501A1 (CYP1A1) Mspl restriction fragment length polymorphism (RFLP), was also investigated. There was a dose-related increase in maternal and newborn adduct levels with ambient pollution at the women's place of residence among subjects who were not employed away from home (p<0.05). Maternal smoking (active and passive) significantly increased maternal (p<0.01) but not newborn adduct levels. Neither CYP1A1 Mspl nor GSTM1 polymorphisms was associated with maternal adducts. However, adducts were significantly higher in newborns heterozygous or homozygous for the CYP1A1 Mspl RFLP compared to newborns without the RFLP (p=0.04).Results indicate that PAH-induced DNA damage in mothers and newborns is increased by ambient air pollution. In the fetus, this damage appears to be enhanced by the CYP1A1 Mspl polymorphism.Environ Health Perspect 106(Suppl 3):821-826 (1998). http.//ehpnetl.niehs.nih.gov/docs/1998/ Suppl-3/821-826whyattlabstract html

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“…However, we previously reported a significant increase in PAH-albumin adducts (a surrogate for PAH-DNA adducts) in children exposed to ETS (61). ETS exposure is high in Poland.…”

Section: Discussionmentioning

confidence: 94%

Relationship between ambient air pollution and DNA damage in Polish mothers and newborns.

Whyatt

Santella

Jędrychowski

et al. 1998

Environ Health Perspect

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“…A variety of biomarkers of tobacco smoke exposure are proposed ( (9), urinary excretion of nicotine-derived nitrosoamines (10), urinary hydroxyproline or n-nitrosoproline excretion (11), and urinary mutagenicity (2,12). Also, solanesol has recently been proposed as perhaps the best marker of particle exposure in the air (13,14).…”

Section: Potential Biomarkers Of Environmental Tobacco Smokementioning

confidence: 99%

Biomarkers of Environmental Tobacco Smoke Exposure

Benowitz¹

1999

Environmental Health Perspectives

108

127

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Biomarkers are desirable for quantitating human exposure to environmental tobacco smoke (ETS) and for predicting potential health risks for exposed individuals. A number of biomarkers of ETS have been proposed. At present cotinine, measured in blood, saliva, or urine, appears to be the most specific and the most sensitive biomarker. In nonsmokers with significant exposure to ETS, cotinine levels in the body are derived primarily from tobacco smoke, can be measured with extremely high sensitivity, and reflect exposure to a variety of types of cigarettes independent of machine-determined yield. Under conditions of sustained exposure to ETS (i.e., over hours or days), cotinine levels reflect exposure to other components of ETS. Supporting the validity of cotinine as a biomarker, cotinine levels have been positively correlated to the risks of some ETSrelated health complications in children who are not cigarette smokers. -Environ Health Perspect 1 07(Suppl 2): 349-355 (1999). http.//ehpnetl.niehs.nih.gov/docs/1999/Suppl-2/ 349-355benowitz/abstract.html

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“…Sufficient evidence has shown higher PAH exposure levels among current smokers compared with nonsmokers (17)(18)(19)(20). Although the health effects among nonsmokers who live with or spend time in the proximity of smokers are well established (8), few studies have evaluated the contribution of involuntary tobacco smoke exposure (also known as secondhand smoke, passive smoke, or environmental tobacco smoke) to PAH levels (21,22).…”

Section: Introductionmentioning

confidence: 99%

Involuntary Tobacco Smoke Exposure and Urinary Levels of Polycyclic Aromatic Hydrocarbons in the United States, 1999 to 2002

Suwan-ampai

Navas‐Acien

Strickland

et al. 2009

Cancer Epidemiology, Biomarkers &Amp; Prevention

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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 z6 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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Biomarkers of Environmental Tobacco Smoke in Preschool Children and Their Mothers

Abstract: Given the relatively low level of ETS exposure in this study, these results reinforce the need for effective programs aimed at smoking prevention and cessation among women, particularly women of reproductive age and minorities.

Cited by 101 publications

References 0 publications

Relationship between ambient air pollution and DNA damage in Polish mothers and newborns.

Relationship between ambient air pollution and DNA damage in Polish mothers and newborns.

Biomarkers of Environmental Tobacco Smoke Exposure

Involuntary Tobacco Smoke Exposure and Urinary Levels of Polycyclic Aromatic Hydrocarbons in the United States, 1999 to 2002

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