Monoclonal antibody ELISA for cotinine in saliva and urine of active and passive smokers
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Cotinine
Tobacco smoke
Passive smoking
The residence times of nicotine and its metabolites in rat brain after acute peripheral nicotine administration were determined. We hypothesize that nicotine metabolites will reach pharmacologically significant concentrations in brain. Cotinine, nornicotine, and norcotinine were structurally identified by dual label radiochemical and gas chromatography-mass spectrometric analysis as biotransformation products of nicotine present in rat brain after s. c. injection of S(-)-nicotine. Two unidentified minor metabolites were also detected in brain. The half-lives in brain of nicotine metabolites were determined after a single s.c. injection of [2'-(14)C]-(+/-)nicotine (0.8 mg/kg) and analysis of radiolabeled metabolites by high pressure-liquid radiochromatography. The brain half-lives of nicotine, cotinine, and nornicotine were 52, 333, and 166 min, respectively. Peak brain concentrations of nicotine metabolites were 300, 70, and 7 nM for cotinine, nornicotine, and norcotinine, respectively. Even with potential accumulation of cotinine in brain after chronic nicotine administration, it is likely that the brain concentration of cotinine will be insufficient to produce neuropharmacological effects resulting from activation of nicotinic receptors to induce dopamine release. Conversely, the concentration of nornicotine in brain after acute nicotine approaches the range found to be neuropharmacologically active. It is likely that nornicotine will accumulate in brain on chronic nicotine administration based on the brain half-life of this metabolite. Importantly, nornicotine is also a major alkaloidal component of tobacco. Thus, as a consequence of tobacco use, alkaloidal and metabolically formed nornicotine may reach concentrations in brain sufficient to produce pharmacological effects.
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Benzoylecgonine
Anabasine
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Of the various biochemical markers used to validate the smoking status of a person, nicotine and continine are considered as good markers for both active and passive smoking. In the present study an attempt was made to estimate urinary levels of nicotine and cotinine in healthy individuals from north India using different types of tobacco to identify and validate the smoking status.Twenty four hour urine sample of 130 healthy volunteers (smokers=70, passive smokers=20, tobacco chewers=20, non smokers=20) were analyzed by high-pressure liquid chromatography (HPLC) assay. Smokers were divided into different groups, viz., cigarette, bidi and hooka smokers.The mean values of nicotine (ng/ml) and cotinine (ng/ml) in urine were highest in cigarette smokers (nicotine=703.50+/-304.34; cotinine=2736.20+/-983.29), followed by hooka smokers (nicotine 548.0+/-103.47 and cotinine 2379.0+/-424.25), and bidi smokers (nicotine=268.53+/-97.62, cotinine=562.60+/-249.38). There was no correlation of nicotine or cotinine values with smoking index. In passive smokers (nicotine=109.75+/-22.33, cotinine=280.75+/-86.30) and in nonsmokers, the values were much lower (nicotine=55.00+/-13.71, cotinine=7.30+/-2.47) compared to smokers. In tobacco chewers, the values for nicotine and cotinine were 447.75+/-145.09 and 2178.30+/-334.29 respectively.All forms of tobacco users had significantly higher values compared to passive smokers and nonusers. Thus, cotinine and nicotine levels in urine may be considered as good indicators to assess the exposure to tobacco in our population.
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Abstract Nicotine is the major alkaloid present in tobacco and the most frequently determined compound as a biomarker of tobacco exposure in both smokers and non-smokers exposed to environmental tobacco smoke. Current knowledge on the human metabolism and disposition kinetics of nicotine is reviewed, together with methods for the determination of nicotine and various metabolites in different human biological fluids and matrices. Only short-term biomarkers of nicotine exposure exist and long-term biomarkers of exposure such as the incorporation of nicotine and cotinine into human hair, toenails and deciduous teeth require further investigation. Determination of ‘nicotine boost’, the difference in blood nicotine concentrations that occur after smoking a single cigarette, provides an experimental indication of individual smoking behaviour, but is unsuitable for population studies. The determination of nicotine plus multiple phase I and phase II metabolites in 24-hour urine, often expressed as ‘nicotine equivalents’, provides the most accurate way to determine exposure to nicotine in smokers; however, few laboratories are equipped to perform the complex analysis required for this purpose. Nicotine equivalents can be used to estimate the uptake of nicotine from a cigarette in both individuals and in population studies. Despite recent advancements in analytical methodology and the possibility of determining multiple nicotine metabolites in various biological fluids, determination of cotinine, the major metabolite of nicotine, is likely to remain the most commonly used approach to assess exposure to tobacco smoke in both smokers and non-smokers. Representative data for cotinine in blood, saliva and urine of smokers and non-smokers are presented.
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Aim: Children are commonly affected by environmental tobacco smoke.The presence of exposure can be deduced from urinary urine kotinine/ creatinine ratio and history.The aim of this study was to investigate passive smoking in healthy children between one-month and five year old, and to determine the adverse effects of passive smoking on child health.Material and Methods: Children between one-month and five year old who were regularly monitored for health were included following informed consent given by their parents.The questionnaire method was used.Demographic variables, respiratory tract infections, recurrent infections were questioned.The levels of cotinine, creatinine were measured and the cotinine/creatinine ratios were calculated in urine specimens taken from the children.Growth status and infection frequency were determined using demographic data, cotinine/creatinine ratios in urine, exposure rate to second-hand tobacco smoke of the children. Results:The ratio of household smokers was 70.3%, the ratio of non-smokers was 29.7%.Fifty percent of the mothers were smokers.Urinary cotinine/creatinine ratios were found to be significantly higher in children of smokers compared with children of non-smokers (p=0.011).One third of the children was evaluated as passive smokers.The presence of a smoker at home and the increase in the number of cigarettes smoked during the day increased the frequency of acute respiratory infections (p=0.047). Conclusion:In these regularly-monitored preschool children, we found frequent exposure to cigarette smoke.This study contributes to national data and will aid in increasing the awareness for the deleterious effects of passive smoking on child health.
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Planarian
Nicotine withdrawal
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Nonsmoking females age 35–65 years from Bremen, Germany (91 women), and Opole, Poland (98 women), were interviewed about their recent passive smoking exposure. We obtained urine samples at the time of interview and determined the concentration of cotinine as an indicator of tobacco smoke exposure. In Poland and in Germany, the vast majority of nonsmoking women are involuntarily exposed to environmental tobacco smoke (ETS). Polish women had slightly higher exposure levels than German women, with overall means of 9.93 and 8.65 ng cotinine/mg creatinine, respectively. Smoking by the husband was the major source of exposure in both study groups. In the Polish group, the work place was also an important source of ETS exposure. The validity of self-reported passive smoking exposure was found to be generally good; it was somewhat better in the German study group. A negative attitude toward tobacco smoke was slightly stronger among the German women. The percentage of women misreporting their active smoking status was low. (Epidemiology 1992;3:509–514)
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Abstract Nicotine and a basic metabolite, cotinine, were determined in the urine by gas-liquid chromatography after intravenous administration of (—)-nicotine hydrogen (+)-tartrate to groups of male and female smokers and non-smokers in whom the urine was maintained at an acid pH. The urinary recoveries of nicotine and cotinine from male smokers fell in two groups. One showed a lower recovery of both alkaloids than was seen with male non-smokers. The other showed a similar recovery of nicotine but more cotinine than the male non-smokers. Female smokers excreted less nicotine but more cotinine than female non-smokers. More nicotine but less cotinine was excreted by female non-smokers than by male non-smokers. The results show sex dependent metabolism of nicotine occurs in non-smoking humans and that smoking causes alterations in nicotine metabolism.
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Passive smoking is a preventable and significant cause of many serious health problems, with children being particularly at risk. In the fifth German Environmental Survey (GerES V), conducted from 2014 to 2017, information reflecting the extent of passive smoke exposure in children and adolescents was collected by interview-based questionnaires and human biomonitoring (HBM) analyses of cotinine in urine from 2260 participants, aged 3-17 years. Based on these population-representative data, we describe current passive smoke exposure stratified by different subgroups and identify specific exposure determinants using multivariate logistic regression. The questionnaire data revealed that 42% of children and adolescents lived with at least one smoker in the household. Quantifiable concentrations of cotinine could be detected in 56% of the participants. The overall median concentration of cotinine was 0.2 μg/L, with children and adolescents of low socioeconomic status found to be a group particularly affected by passive smoke with higher cotinine concentrations (median = 1.2 μg/L). In the multiple analysis, the most significant predictor of cotinine levels derived from the questionnaire was passive smoking at home (odds ratio (OR) 13.07 [95CI: 4.65, 36.70]). However, parental smoking and passive smoking among friends and relatives could also be identified as independent factors influencing elevated cotinine levels. The comparison between the previous cycle GerES IV (2003-2006) on 3-14-year-olds and GerES V shows that tobacco smoke exposure of children decreased significantly. This decrease is likely an effect of extensive non-smoker protection laws being enforced 2007-2008 on federal and state level. This is reflected by a halving of urinary cotinine concentrations. Nevertheless, our results indicate that passive smoke is still a relevant source of harmful pollutants for many children and adolescents in Germany, and thus support the need for further efforts to reduce passive smoke exposure, especially in the private environment.
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Background: Studies on the oral route of nicotine administration in rodents make important contributions to our understanding of human nicotine use, and alternative approaches to smoking cessation. While environmental availability of oral nicotine contributes to voluntary intake and appears to drive consumption initially, solution concentration may exert more control over intake with continued exposure. Further, it is believed that female rodents consume more nicotine and show greater motivation to obtain it than males. Objectives: The purpose of our study was to determine voluntary oral nicotine intake patterns following continuous exposure to relatively high concentrations in male and female rats, employing a multiple bottle approach, and to describe the relationship between oral nicotine consumption and sera cotinine. Methods: Using five bottles, adult Sprague–Dawley rats were given continuous access to water and 15 μg/ml nicotine solutions or water and 15 and 30 μg/ml nicotine solutions for 2 weeks; blood serum was analyzed for cotinine. Results: Rats consistently consumed oral nicotine and female rats ingested more nicotine than males, even at relatively high concentrations. Yet, when both concentrations were presented simultaneously, oral nicotine intake did not exceed that of water, thus overriding an environmental, or multiple-bottle, effect. Cotinine was systemically circulated following first-pass hepatic metabolism of nicotine at early, but not at later stages of nicotine exposure. Conclusions: Our findings suggest rats will readily and voluntarily ingest considerably higher doses of nicotine than previously reported resulting in initial systemic cotinine, and trends toward sex differences are mitigated by solution concentration.
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Introduction: There are a few publications about the impact of tobacco smoke on the children's immune system. Material and Methods: The study group consisted of 43 children with asthma. The control group consisted of 37 healthy children. The exposure to tobacco smoke was assessed by the presence of the cotinine in the urine (metabolit of nicotine). Results: The group of children with asthma exposed to tobacco smoke had significantly higher levels of the IL-1 and lower levels IL-4 than children not exposed to the passive smoking. The children from the control group exposed to tobacco smoke had a significantly higher concentration of IL-4 than unexposed children. In the whole analyzed population, there was a significant positive correlation between cotinine-IL1 and cotinine-CRP. Conclusion: In this study we found that the passive exposure to tobacco smoke has the immunomodulatory effects on the immune system.
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