Urine nicotine metabolite concentrations in relation to plasma cotinine during low-level nicotine exposure

Benowitz, Neal L.; Dains, Katherine M.; Dempsey, Delia; Herrera, Brenda; Yu, Lisa; Jacob, Peyton

doi:10.1093/ntr/ntp092

Cited by 98 publications

(83 citation statements)

References 14 publications

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“…These metabolites are excreted in urine primarily [25]. Urinary levels of cotinine are higher than that of the blood levels [26]. Studies in animals showed a dose-dependent increase in cotinine levels in the urine.…”

Section: Discussionmentioning

confidence: 99%

The Role of Combined Nicotine and Caffeine Administration on the Histological Structure of the Rat Urinary Bladder with a Special Reference to P53

Allehaibi¹,

Abunasef²,

Zaki³

2017

J Cytol Histol

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Section: Discussionmentioning

confidence: 99%

The Role of Combined Nicotine and Caffeine Administration on the Histological Structure of the Rat Urinary Bladder with a Special Reference to P53

Allehaibi¹,

Abunasef²,

Zaki³

2017

J Cytol Histol

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“…Despite the demonstration of these adverse effects of secondhand smoke exposure, 40% of Americans are still exposed to secondhand smoke, including 54% of children between ages 3 and 11 years (35). In some of our analyses, we dichotomized passive smokers at the median into low-level (,0.19 ng/ml) and moderate-to high-level (>0.19 ng/ml) exposure; a plasma cotinine level of 0.20 ng/ml is roughly equivalent to spending 1 hour in a moderately smoky room, such as a bar or restaurant (43,44). Thus, the quantity of passive smoke exposure associated with increased risk of ALI in this study appears to be relatively modest, although this threshold for exposure will need to be further tested in other at-risk groups.…”

Section: Discussionmentioning

confidence: 99%

Active and Passive Cigarette Smoking and Acute Lung Injury after Severe Blunt Trauma

Calfee¹,

Matthay²,

Eisner³

et al. 2011

Am J Respir Crit Care Med

137

120

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Rationale: Cigarette smoking has been demonstrated in laboratory studies to have effects on lung epithelial and endothelial function similar to those observed in acute lung injury (ALI). However, the association between active and passive cigarette smoke exposure and susceptibility to ALI has not been prospectively studied. Objectives: We hypothesized that both active and passive cigarette smoke exposure would be associated with increased susceptibility to ALI after severe blunt trauma. Methods: We measured levels of cotinine, a metabolite of nicotine and validated biomarker of tobacco use, in plasma samples obtained immediately on arrival at the emergency department from 144 adult subjects after severe blunt trauma. Patients were then followed for the development of ALI. Measurements and Main Results: Increasing quartiles of plasma cotinine were associated with the development of ALI (odds ratio [OR] for developing ALI in highest cotinine quartile, 3.25; 95% confidence interval [CI], 1.22-8.68; P 5 0.017 for trend across quartiles). Moderate to heavy passive smoke exposure was associated with nearly the same odds of developing ALI as active smoking (OR for moderate to heavy passive smoking compared with no exposure or low level exposure, 3.03; 95% CI, 1.15-8.04; OR for active smoking, 2.77; 95% CI, 1. 28-5.99). This association persisted after adjusting for other predictors of ALI, including Injury Severity Score and alcohol abuse. Conclusions: Both moderate to heavy passive smoking and active smoking are independently associated with the development of ALI after severe blunt trauma. This finding has important implications both for public health and for understanding the pathogenesis of ALI.

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“…For comparison purposes, researchers must consider whether free cotinine or total (free plus conjugated) cotinine was measured. Free cotinine is preferable to use as it correlates better with plasma cotinine than total cotinine 7. Current state-of-the-art methods are GC-MS/MS and LC-MS/MS, with limits of detection (LOD) of 0.05 ng/ml,20 21 a sensitivity concentration needed in countries with low SHSe due to clean air regulations and lower air nicotine concentrations.…”

Section: Analytical Methods For Biomarkers Of Shsementioning

confidence: 99%

“…Blood's cotinine concentrations and saliva are highly correlated. Urine cotinine concentrations average fourfold to sixfold higher than those in blood or saliva, making urine a more sensitive matrix to detect low-concentration exposure 7. Six metabolites (nicotine, cotinine and trans-3′-hydroxycotinine (3-HC) and their respective glucuronide conjugates) account for about 85% to 90% of a nicotine dose, and the sum of these metabolites in urine provides an approximate estimate of daily nicotine intake.…”

Section: Selection Of Biomarkers Of Shsementioning

confidence: 99%

Assessing secondhand smoke using biological markers

et al. 2012

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Secondhand smoke exposure (SHSe) is a known cause of many adverse health effects in adults and children. Increasingly, SHSe assessment is an element of tobacco control research and implementation worldwide. In spite of decades of development of approaches to assess SHSe, there are still unresolved methodological issues; therefore, a multidisciplinary expert meeting was held to catalogue the approaches to assess SHSe and with the goal of providing a set of uniform methods for future use by investigators and thereby facilitate comparisons of findings across studies. The meeting, held at Johns Hopkins, in Baltimore, Maryland, USA, was supported by the Flight Attendant Medical Research Institute (FAMRI). A series of articles were developed to summarise what is known about self-reported, environmental and biological SHSe measurements. Non-smokers inhale toxicants in SHS, which are mainly products of combustion of organic materials and are not specific to tobacco smoke exposure. Biomarkers specific to SHSe are nicotine and its metabolites (eg, cotinine), and metabolites of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). Cotinine is the preferred blood, saliva and urine biomarker for SHSe. Cotinine and nicotine can also be measured in hair and toenails. NNAL (4-[methylnitrosamino]-1-[3-pyridyl]-1-butanol), a metabolite of NNK, can be determined in the urine of SHS-exposed non-smokers. The selection of a particular biomarker of SHSe and the analytic biological medium depends on the scientific or public health question of interest, study design and setting, subjects, and funding. This manuscript summarises the scientific evidence on the use of biomarkers to measure SHSe, analytical methods, biological matrices and their interpretation.

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Urine nicotine metabolite concentrations in relation to plasma cotinine during low-level nicotine exposure

Abstract: Measurement of urine cotinine corrected for creatinine concentration appears to be the best predictor of plasma cotinine.

Cited by 98 publications

References 14 publications

The Role of Combined Nicotine and Caffeine Administration on the Histological Structure of the Rat Urinary Bladder with a Special Reference to P53

The Role of Combined Nicotine and Caffeine Administration on the Histological Structure of the Rat Urinary Bladder with a Special Reference to P53

Active and Passive Cigarette Smoking and Acute Lung Injury after Severe Blunt Trauma

Assessing secondhand smoke using biological markers

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