Environmental tobacco smoke and children's health
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Passive exposure to tobacco smoke significantly contributes to morbidity and mortality in children. Children, in particular, seem to be the most susceptible population to the harmful effects of environmental tobacco smoke (ETS). Paternal smoking inside the home leads to significant maternal and fetal exposure to ETS and may subsequently affect fetal health. ETS has been associated with adverse effects on pediatric health, including preterm birth, intrauterine growth retardation, perinatal mortality, respiratory illness, neurobehavioral problems, and decreased performance in school. A valid estimation of the risks associated with tobacco exposure depends on accurate measurement. Nicotine and its major metabolite, cotinine, are commonly used as smoking biomarkers, and their levels can be determined in various biological specimens such as blood, saliva, and urine. Recently, hair analysis was found to be a convenient, noninvasive technique for detecting the presence of nicotine exposure. Because nicotine/cotinine accumulates in hair during hair growth, it is a unique measure of long-term, cumulative exposure to tobacco smoke. Although smoking ban policies result in considerable reductions in ETS exposure, children are still exposed significantly to tobacco smoke not only in their homes but also in schools, restaurants, child-care settings, cars, buses, and other public places. Therefore, more effective strategies and public policies to protect preschool children from ETS should be consolidated. Key words: Tobacco smoke pollution, Nicotine, Cotinine, Child, HairKeywords:
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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Cotinine
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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To determine the concentrations of nicotine and nicotine metabolites in RBC units as a means to estimate the point prevalence of exposure within the healthy donor pool.Segments from 105 RBC units were tested for the presence of nicotine, cotinine, or trans-3'-hydroxycotinine by liquid chromatography-tandem mass spectrometry.Of the 20 (19%) units that contained detectable concentrations of nicotine, cotinine, or trans-3'-hydroxycotinine, 19 (18.1%) contained concentrations consistent with the use of a nicotine-containing product within 48 hours of specimen collection. One RBC unit contained nicotine concentrations consistent with passive exposure.Chemicals from nicotine-containing products are detectable within the US RBC supply. Further investigation is needed to determine the risks of transfusion-associated exposure to nicotine and other tobacco-associated chemicals among vulnerable patient populations such as neonates.
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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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Blood-brain barrier (BBB) nicotine transfer has been well documented in view of the fact that this alkaloid is a cerebral blood flow marker. However, limited data are available that describe BBB penetration of the major tobacco alkaloids after chronic nicotine exposure. This question needs to be addressed, given long-term nicotine exposure alters both BBB function and morphology. In contrast to nicotine, it has been reported that cotinine (the major nicotine metabolite) does not penetrate the BBB, yet cotinine brain distribution has been well documented after nicotine exposure. Surprisingly, therefore, the literature indirectly suggests that central nervous system cotinine distribution occurs secondarily to nicotine brain metabolism. The aims of the current report are to define BBB transfer of nicotine and cotinine in naive and nicotine-exposed animals. Using an in situ brain perfusion model, we assessed the BBB uptake of [3H]nicotine and [3H]cotinine in naive animals and in animals exposed chronically to S-(–)nicotine (4.5 mg/kg/day) through osmotic minipump infusion. Our data demonstrate that 1) [3H]nicotine BBB uptake is not altered in the in situ perfusion model after chronic nicotine exposure, 2) [3H]cotinine penetrates the BBB, and 3) similar to [3H]nicotine, [3H]cotinine BBB transfer is not altered by chronic nicotine exposure. To our knowledge, this is the first report detailing the uptake of nicotine and cotinine after chronic nicotine exposure and quantifying the rate of BBB penetration by cotinine.
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