The Elimination Half-Life of Urinary Cotinine in Children of Tobacco-Smoking Mothers

Leong, Jcy; Dore, Nigel D.; Shelley, Kirk H.; Holt, E.J.; Laing, Ingrid A.; Palmer, Lyle J.; Lesouëf, Peter

doi:10.1006/pupt.1998.0153

Cited by 51 publications

(40 citation statements)

References 11 publications

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“…The median half-life of cotinine was 28 h in infants in one study (20), and most DBS are collected 12 to 48 h after birth (21). Cotinine in DBS must therefore represent tobacco exposure shortly before delivery and, as might be expected, identifies babies born to the most refractory smokers.…”

Section: Discussionmentioning

confidence: 99%

Detection of Cotinine in Newborn Dried Blood Spots

Spector

Hecht²,

Ognjanovic

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Maternal smoking while pregnant is a plausible risk factor for childhood cancers because many seem to initiate in utero and tobacco-specific carcinogens cross the placenta. Social desirability bias may affect maternal report of smoking in case-control studies and could explain inconsistently observed associations with offspring cancer. Detection of tobacco smoke biomarkers in dried blood spots (DBS), which are increasingly stored by newborn screening programs, may improve retrospective assessment of fetal tobacco exposure. As proof-of-principle, we examined cotinine in DBS of 20 infants enrolled in a pilot study of pregnancy among low-income women. We recruited 107 pregnant women (<30 weeks of gestation) from six Women, Infants, and Children clinics in Minneapolis and St. Paul in 1999. Blood samples obtained at enrollment were tested for total cotinine using gas chromatography/mass spectrometry. Women were then interviewed at 7 months of gestation to determine current smoking habits. DBS were obtained from the Minnesota Department of Health. We tested DBS from 10 infants whose mothers had detectable serum cotinine at baseline and 10 control infants whose mothers had none. One quarter of each DBS was assayed for cotinine using gas chromatography/mass spectrometry; levels were estimated assuming 50 ML blood per sample. Mean cotinine was 29 ng/mL (SD, 7.5), 45 ng/mL (SD, 9.7), and 9 ng/mL (SD, 7.4), respectively, among infants of all smokers, infants of four women who acknowledged smoking at 7 months of gestation, and infants of nonsmokers. These results suggest that DBS analysis may identify infants of women who smoke throughout pregnancy. (Cancer Epidemiol Biomarkers Prev 2007; 16(9):1902 -5)

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Section: Discussionmentioning

confidence: 99%

Detection of Cotinine in Newborn Dried Blood Spots

Spector

Hecht²,

Ognjanovic

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…Cotinine half-life is reported to be similar in neonates, older children, and adults in two studies (Leong et al, 1998;Dempsey et al, 2000), but two other studies found that half-life of urine cotinine was about 3 times longer in children less than 1 year old compared with the cotinine half-life in adults (Etzel et al, 1985;Collier et al, 1994). Urine cotinine half-life is prone to be influenced by variations in urine volume and excretion of creatinine.…”

Section: G Factors Influencing Nicotine Metabolismmentioning

confidence: 99%

Metabolism and Disposition Kinetics of Nicotine

2005

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“…24,27 The nicotine metabolite cotinine is the biomarker of choice because its halflife is much longer (17-24 hours) than nicotine (2-3 hours). 28,29 However, children with asthma may have lower clearance rates of nicotine, resulting in higher systemic exposure; African-American children differ in their rate of absorption and metabolism of nicotine, which further enhances the problems with obtaining these measurements. 30,31 One study determined that the use of 2 simple questions worked as well as cotinine screening among inner-city children with asthma.…”

Section: Assessment Of Shs Exposurementioning

confidence: 99%

Smoking and Asthma

Stapleton

Howard-Thompson²,

George³

et al. 2011

The Journal of the American Board of Family Medicine

139

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Background:The purpose of this review is to describe the current understanding of the prevalence and adverse effects of cigarette smoking and secondhand smoke (SHS) in asthmatics in terms of patient outcomes and response to inhaled corticosteroids.Methods: We searched the English biomedical literature via PubMed, Embase, and Scopus using the terms "smoking and asthma," "secondhand smoke and asthma," "environmental tobacco smoke and asthma," and "smoking/secondhand smoke and corticosteroids." We also reviewed reference lists of identified articles for relevant citations.Results: In asthmatic patients who smoke, disease control is poorer than in asthmatic nonsmokers. Of all forms of SHS, maternal exposure seems to have the largest impact on asthma by increasing the frequency and severity of the disease and decreasing lung function. Asthmatic children exposed to multiple household smokers face an increased risk for respiratory illness-related absences from school, and these effects persist during adolescence but weaken during adulthood. Airway mucosal permeability is increased in smokers, which could lead to increased clearance of inhaled corticosteroids from the airways. Smokers also have decreased histone deacetylase activity, which is necessary for corticosteroids to fully suppress cytokine production, and can lead to corticosteroid resistance.

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The Elimination Half-Life of Urinary Cotinine in Children of Tobacco-Smoking Mothers

Cited by 51 publications

References 11 publications

Detection of Cotinine in Newborn Dried Blood Spots

Detection of Cotinine in Newborn Dried Blood Spots

Metabolism and Disposition Kinetics of Nicotine

Smoking and Asthma

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