A bibliographic database that includes MEDLINE as its primary subset. It is produced by the National Center for Biotechnology Information (NCBI), part of the NATIONAL LIBRARY OF MEDICINE. PubMed, which is searchable through NLM's Web site, also includes access to additional citations to selected life sciences journals not in MEDLINE, and links to other resources such as the full-text of articles at participating publishers' Web sites, NCBI's molecular biology databases, and PubMed Central.
The N-glucuronide conjugate of cotinine is a major urinary metabolite of NICOTINE. It thus serves as a biomarker of exposure to tobacco SMOKING. It has CNS stimulating properties.
A publication issued at stated, more or less regular, intervals.
"The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing.
The premier bibliographic database of the NATIONAL LIBRARY OF MEDICINE. MEDLINE® (MEDLARS Online) is the primary subset of PUBMED and can be searched on NLM's Web site in PubMed or the NLM Gateway. MEDLINE references are indexed with MEDICAL SUBJECT HEADINGS (MeSH).
Publications in any medium issued in successive parts bearing numerical or chronological designations and intended to be continued indefinitely. (ALA Glossary of Library and Information Science, 1983, p203)
Contamination of the air by tobacco smoke.
Inhaling and exhaling the smoke of burning TOBACCO.
Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke.
Elements of limited time intervals, contributing to particular results or situations.
Discontinuation of the habit of smoking, the inhaling and exhaling of tobacco smoke.
The clear, viscous fluid secreted by the SALIVARY GLANDS and mucous glands of the mouth. It contains MUCINS, water, organic salts, and ptylin.
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.
A systematic collection of factual data pertaining to the nutritional status of a human population within a given geographic area. Data from these surveys are used in preparing NUTRITION ASSESSMENTS.
Method in which repeated blood pressure readings are made while the patient undergoes normal daily activities. It allows quantitative analysis of the high blood pressure load over time, can help distinguish between types of HYPERTENSION, and can assess the effectiveness of antihypertensive therapy.
A personality trait rendering the individual acceptable in social or interpersonal relations. It is related to social acceptance, social approval, popularity, social status, leadership qualities, or any quality making him a socially desirable companion.
A class of compounds that contain a -NH2 and a -NO radical. Many members of this group have carcinogenic and mutagenic properties.
Techniques for using whole blood samples collected on filter paper for a variety of clinical laboratory tests.
Substances that increase the risk of NEOPLASMS in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included.
Any deviation of results or inferences from the truth, or processes leading to such deviation. Bias can result from several sources: one-sided or systematic variations in measurement from the true value (systematic error); flaws in study design; deviation of inferences, interpretations, or analyses based on flawed data or data collection; etc. There is no sense of prejudice or subjectivity implied in the assessment of bias under these conditions.
Derivatives of GLUCURONIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that include the 6-carboxy glucose structure.
Insurance providing for payment of a stipulated sum to a designated beneficiary upon death of the insured.
Items used to aid in ending a TOBACCO habit.
Organizations which assume the financial responsibility for the risks of policyholders.
The application of suitable drug dosage forms to the skin for either local or systemic effects.
Drugs that bind to and activate nicotinic cholinergic receptors (RECEPTORS, NICOTINIC). Nicotinic agonists act at postganglionic nicotinic receptors, at neuroeffector junctions in the peripheral nervous system, and at nicotinic receptors in the central nervous system. Agents that function as neuromuscular depolarizing blocking agents are included here because they activate nicotinic receptors, although they are used clinically to block nicotinic transmission.
Glycosides of GLUCURONIC ACID formed by the reaction of URIDINE DIPHOSPHATE GLUCURONIC ACID with certain endogenous and exogenous substances. Their formation is important for the detoxification of drugs, steroid excretion and BILIRUBIN metabolism to a more water-soluble compound that can be eliminated in the URINE and BILE.
A stable, physiologically active compound formed in vivo from the prostaglandin endoperoxides. It is important in the platelet-release reaction (release of ADP and serotonin).
Liquid chromatographic techniques which feature high inlet pressures, high sensitivity, and high speed.
An analytical method used in determining the identity of a chemical based on its mass using mass analyzers/mass spectrometers.
Substances and products derived from NICOTIANA TABACUM.
Tobacco used to the detriment of a person's health or social functioning. Tobacco dependence is included.
Powdered or cut pieces of leaves of NICOTIANA TABACUM which are inhaled through the nose, chewed, or stored in cheek pouches. It includes any product of tobacco that is not smoked.
A plant genus of the family SOLANACEAE. Members contain NICOTINE and other biologically active chemicals; its dried leaves are used for SMOKING.
Persons living in the United States having origins in any of the black groups of Africa.
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.
Individuals whose ancestral origins are in the continent of Europe.

(S)-(-)-Cotinine, the major brain metabolite of nicotine, stimulates nicotinic receptors to evoke [3H]dopamine release from rat striatal slices in a calcium-dependent manner. (1/809)

Cotinine, a major peripheral metabolite of nicotine, has recently been shown to be the most abundant metabolite in rat brain after peripheral nicotine administration. However, little attention has been focused on the contribution of cotinine to the pharmacological effects of nicotine exposure in either animals or humans. The present study determined the concentration-response relationship for (S)-(-)-cotinine-evoked 3H overflow from superfused rat striatal slices preloaded with [3H]dopamine ([3H]DA) and whether this response was mediated by nicotinic receptor stimulation. (S)-(-)-Cotinine (1 microM to 3 mM) evoked 3H overflow from [3H]DA-preloaded rat striatal slices in a concentration-dependent manner with an EC50 value of 30 microM, indicating a lower potency than either (S)-(-)-nicotine or the active nicotine metabolite, (S)-(-)-nornicotine. As reported for (S)-(-)-nicotine and (S)-(-)-nornicotine, desensitization to the effect of (S)-(-)-cotinine was observed. The classic nicotinic receptor antagonists mecamylamine and dihydro-beta-erythroidine inhibited the response to (S)-(-)-cotinine (1-100 microM). Additionally, 3H overflow evoked by (S)-(-)-cotinine (10-1000 microM) was inhibited by superfusion with a low calcium buffer. Interestingly, over the same concentration range, (S)-(-)-cotinine did not inhibit [3H]DA uptake into striatal synaptosomes. These results demonstrate that (S)-(-)-cotinine, a constituent of tobacco products and the major metabolite of nicotine, stimulates nicotinic receptors to evoke the release of DA in a calcium-dependent manner from superfused rat striatal slices. Thus, (S)-(-)-cotinine likely contributes to the neuropharmacological effects of nicotine and tobacco use.  (+info)

The effect of cotinine or cigarette smoke co-administration on the formation of O6-methylguanine adducts in the lung and liver of A/J mice treated with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) (2/809)

4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a tobacco-specific nitrosamine, induces lung adenomas in A/J mice, following a single intraperitoneal (i.p.) injection. However, inhalation of tobacco smoke has not induced or promoted tumors in these mice. NNK-induced lung tumorigenesis is thought to involve O6-methylguanine (O6MeG) formation, leading to GC-->AT transitional mispairing and an activation of the K-ras proto-oncogene in the A/J mouse. NNK can be metabolized by several different cytochromes P450, resulting in a number of metabolites. Formation of the promutagenic DNA adduct O6MeG is believed to require metabolic activation of NNK by cytochrome P450-mediated alpha-hydroxylation of the methylene group adjacent to the N-nitroso nitrogen to yield the unstable intermediate, methanediazohydroxide. Nicotine, cotinine (the major metabolite of nicotine), and aqueous cigarette tar extract (ACTE) have all been shown to effectively inhibit metabolic activation of NNK to its mutagenic form, most likely due to competitive inhibition of the cytochrome P450 enzymes involved in alpha-hydroxylation of NNK. The objective of the current study was to monitor the effects of cotinine and cigarette smoke (CS) on the formation of O6MeG in target tissues of mice during the acute phase of NNK treatment. To test the effect of cotinine, mature female A/J mice received a single intraperitoneal injection of NNK (0, 2.5, 5, 7.5, or 10 mumole/mouse) with cotinine administered at a total dose of 50 mumole/mouse in 3 separate i.p. injections, administered 30 min before, immediately after, and 30 min after NNK treatment. To test the effect of whole smoke exposure on NNK-related O6MeG formation, mice were exposed to smoke generated from Kentucky 1R4F reference cigarettes at 0, 0.4, 0.6, or 0.8 mg wet total particulate matter/liter (WTPM/L) for 2 h, with a single i.p. injection of NNK (0, 3.75, or 7.5 mumole/mouse) midway through the exposure. Cigarette smoke alone failed to yield detectable levels of O6MeG. The number of O6MeG adducts following i.p. injection of NNK was significantly (p < 0.05) reduced in both lung and liver by cotinine and by cigarette smoke exposure. Our results demonstrate that NNK-induced O6MeG DNA adducts in A/J mice are significantly reduced when NNK is administered together with either cotinine, the major metabolite of nicotine, or the parental complex mixture, cigarette smoke.  (+info)

Detection of benzo[a]pyrene diol epoxide-DNA adducts in embryos from smoking couples: evidence for transmission by spermatozoa. (3/809)

Tobacco smoking is deleterious to reproduction. Benzo[a]pyrene (B[a]P) is a potent carcinogen in cigarette smoke. Its reactive metabolite induces DNA-adducts, which can cause mutations. We investigated whether B[a]P diol epoxide (BPDE) DNA adducts are detectable in preimplantation embryos in relation to parental smoking. A total of 17 couples were classified by their smoking habits: (i) both partners smoke; (ii) wife non-smoker, husband smokes; and (iii) both partners were non-smokers. Their 27 embryos were exposed to an anti-BPDE monoclonal antibody that recognizes BPDE-DNA adducts. Immunostaining was assessed in each embryo and an intensity score was calculated for embryos in each smoking group. The proportion of blastomeres which stained was higher for embryos of smokers than for non-smokers (0.723 versus 0.310). The mean intensity score was also higher for embryos of smokers (1.40+/-0.28) than for non-smokers (0.38+/-0.14; P = 0.015), but was similar for both types of smoking couples. The mean intensity score was positively correlated with the number of cigarettes smoked by fathers (P = 0.02). Increased mean immunostaining in embryos from smokers, relative to non-smokers, indicates a relationship with parental smoking. The similar levels of immunostaining in embryos from both types of smoking couples suggest that transmission of modified DNA is mainly through spermatozoa. We confirmed paternal transmission of modified DNA by detection of DNA adducts in spermatozoa of a smoker father and his embryo.  (+info)

Metabolites of a tobacco-specific carcinogen in urine from newborns. (4/809)

BACKGROUND: Cigarette smoking during pregnancy can result in fetal exposure to carcinogens that are transferred from the mother via the placenta, but little information is available on fetal uptake of such compounds. We analyzed samples of the first urine from newborns whose mothers did or did not smoke cigarettes for the presence of metabolites of the potent tobacco-specific transplacental carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). METHODS: The urine was collected and analyzed for two metabolites of NNK, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and its glucuronide (NNAL-Gluc). Gas chromatography and nitrosamine-selective detection, with confirmation by mass spectrometry, were used in the analyses, which were performed without knowledge of the origin of the urine samples. RESULTS: NNAL-Gluc was detected in 22 (71%) of 31 urine samples from newborns of mothers who smoked; NNAL was detected in four of these 31 urine samples. Neither compound was detected in the 17 urine samples from newborns of mothers who did not smoke. The arithmetic mean level of NNAL plus NNAL-Gluc in the 27 newborns of smokers for which both analytes were quantified was 0.14 (95% confidence interval [CI] = 0.083-0.200) pmol/mL. The levels of NNAL plus NNAL-Gluc in the urine from these babies were statistically significantly higher than those in the urine from newborns of nonsmoking mothers (geometric means = 0.062 [95% CI = 0.035-0.110] and 0.010 [considered as not detected; no confidence interval], respectively; two-sided P<.001). NNAL plus NNAL-Gluc levels in the 18 positive urine samples in which both analytes were quantified ranged from 0.045 to 0.400 pmol/mL, with an arithmetic mean level of 0.20 (95% CI = 0.14-0.26) pmol/mL, about 5%-10% of the levels of these compounds detected in the urine from adult smokers. CONCLUSIONS: Two metabolites of the tobacco-specific transplacental carcinogen NNK can be detected in the urine from newborns of mothers who smoked cigarettes during pregnancy.  (+info)

Urinary cotinine and exposure to parental smoking in a population of children with asthma. (5/809)

BACKGROUND: Studies of the effects of tobacco smoke often rely on reported exposure to cigarette smoke, a measure that is subject to bias. We describe here the relationship between parental smoking exposure as assessed by urinary cotinine excretion and lung function in children with asthma. METHODS: We studied 90 children 4-14 years of age, who reported a confirmed diagnosis or symptoms of asthma. In each child, we assessed baseline pulmonary function (spirometry) and bronchial responsiveness to carbachol stimulation. Urinary cotinine was measured by HPLC with ultraviolet detection. RESULTS: Urinary cotinine concentrations in the children were significantly correlated (P <0.001) with the number of cigarettes the parents, especially the mothers, smoked. Bronchial responsiveness to carbachol (but not spirometry test results) was correlated (P <0.03) with urinary cotinine in the children. CONCLUSION: Passive smoke exposure increases the bronchial responsiveness to carbachol in asthmatic children.  (+info)

Tobacco smoke exposure at one month of age and subsequent risk of SIDS--a prospective study. (6/809)

The aim of this investigation was to identify the sources of postnatal exposure to tobacco smoke at 1 month of age and to examine their relation to sudden infant death syndrome (SIDS). The Tasmanian Infant Health Survey was a prospective cohort study undertaken from 1988 to 1995. It involved 9,826 infants (89% of eligible infants) at higher risk of SIDS. Subsequently 53 eligible infants died of SIDS. Hospital interviews were available on 51 and home interviews on 35 SIDS infants. Urinary cotinine assays were conducted using gas-liquid chromatography (n = 100). Within a predictive model that explained 63% of urinary cotinine variance, the strongest predictor of cotinine and also of SIDS was maternal smoking, though the effects of prenatal and postnatal smoking could not be separated. However, for particular smoking-related behaviors, there was a discordance between prediction of cotinine concentration and prediction of risk of SIDS. If smoking mothers did not smoke in the room with the baby, the cotinine level in the infant's urine was reduced by a little more than a half (p = 0.009), but this was not associated with a reduction in SIDS risk (odds ratio = 1.09, 95% confidence interval 0.47-2.55). Similarly, the presence of other adult resident smokers was associated with a 63% increase in urinary cotinine (p = 0.047) but not with increased SIDS risk (odds ratio = 0.69, 95% confidence interval 0.34-1.40). However, the study lacked the power to detect modest effects, that is, those altering risk less than twofold.  (+info)

Minor tobacco alkaloids as biomarkers for tobacco use: comparison of users of cigarettes, smokeless tobacco, cigars, and pipes. (7/809)

OBJECTIVES: This study (1) determined levels of various tobacco alkaloids in commercial tobacco products. (2) determined urinary concentrations, urinary excretion, and half-lives of the alkaloids in humans; and (3) examined the possibility that urine concentrations of nicotine-related alkaloids can be used as biomarkers of tobacco use. METHODS: Nicotine intake from various tobacco products was determined through pharmacokinetic techniques. Correlations of nicotine intake with urinary excretion and concentrations of anabasine, anatabine, nornicotine, nicotine, and cotinine were examined. By using urinary excretion data, elimination half-lives of the alkaloids were calculated. RESULTS: Alkaloid levels in commercial tobacco products, in milligrams per gram, were as follows: nicotine, 6.5 to 17.5; nornicotine, 0.14 to 0.66; anabasine, 0.008 to 0.030; and anatabine, 0.065 to 0.27. Measurable concentrations of all alkaloids were excreted in the urine of most subjects smoking cigarettes, cigars, and pipes and using smokeless tobacco. Correlations between nicotine intake and alkaloid concentrations were good to excellent. CONCLUSIONS: Anabasine and anatabine, which are present in tobacco but not in nicotine medications, can be used to assess tobacco use in persons undergoing nicotine replacement therapy.  (+info)

Advising parents of asthmatic children on passive smoking: randomised controlled trial. (8/809)

OBJECTIVE: To investigate whether parents of asthmatic children would stop smoking or alter their smoking habits to protect their children from environmental tobacco smoke. DESIGN: Randomised controlled trial. SETTING: Tayside and Fife, Scotland. PARTICIPANTS: 501 families with an asthmatic child aged 2-12 years living with a parent who smoked. INTERVENTION: Parents were told about the impact of passive smoking on asthma and were advised to stop smoking or change their smoking habits to protect their child's health. MAIN OUTCOME MEASURES: Salivary cotinine concentrations in children, and changes in reported smoking habits of the parents 1 year after the intervention. RESULTS: At the second visit, about 1 year after the baseline visit, a small decrease in salivary cotinine concentrations was found in both groups of children: the mean decrease in the intervention group (0.70 ng/ml) was slightly smaller than that of the control group (0.88 ng/ml), but the net difference of 0.19 ng/ml had a wide 95% confidence interval (-0.86 to 0.48). Overall, 98% of parents in both groups still smoked at follow up. However, there was a non-significant tendency for parents in the intervention group to report smoking more at follow up and to having a reduced desire to stop smoking. CONCLUSIONS: A brief intervention to advise parents of asthmatic children about the risks from passive smoking was ineffective in reducing their children's exposure to environmental tobacco smoke. The intervention may have made some parents less inclined to stop smoking. If a clinician believes that a child's health is being affected by parental smoking, the parent's smoking needs to be addressed as a separate issue from the child's health.  (+info)

BACKGROUND: No prospective studies are available on serum cotinine level as a marker of lung cancer risk. METHODS: We analyzed serum cotinine level among 1,741 individuals enrolled since the 1970s in a prospective study of Norwegian volunteers who developed lung cancer during the follow-up and 1,741 matched controls free from lung cancer. Serum cotinine was measured with a competitive immunoassay. Regression dilution was corrected for based on repeated measures on samples from 747 subjects. RESULTS: Mean serum cotinine level was higher in cases than in controls. Compared with subjects with a cotinine level of | or = 5 ng/mL, the odds ratio of lung cancer was increasing linearly, reaching 55.1 (95% confidence interval, 35.7-85.0) among individuals with a serum cotinine level of | 378 ng/mL. There was no clear suggestion of a plateau in risk at high exposure levels. Odds ratios were very similar in men and women. We found no association between serum cotinine level (range, 0.1-9.9 ng/mL) and lung cancer
Smoking is an established risk factor for pancreatic cancer, previously investigated by the means of questionnaires. Using cotinine as a biomarker for tobacco exposure allows more accurate quantitative analyses to be performed. This study on pancreatic cancer, nested within the European Prospective Investigation into Cancer and Nutrition (EPIC cohort), included 146 cases and 146 matched controls. Using liquid chromatography-mass spectrometry, plasma cotinine levels were analyzed on average 8.0 years before cancer onset (5-95% range: 2.8-12.0 years). The relation between plasma cotinine levels and pancreatic cancer was analyzed with conditional logistic regression for different levels of cotinine in a population of never and current smokers. This was also done for the self-reported number of smoked cigarettes per day at baseline. Every increase of 350 nmol/L of plasma cotinine was found to significantly elevate risk of pancreatic cancer [odds ratio (OR): 1.33, 95% confidence interval (CI): 1.11-1.60].
For example, lets say that the child lives with parent 1, who also provides regular medical care to the child. If the child keeps getting respiratory illnesses after spending weekends with parent 2, then it would be reasonable to wonder if the child is exposed to something, such as second-hand smoke, at parent 2s home. This would be detrimental to the childs health, not to mention be very aggravating for the parent 1, who has to take care of the sick child during the week, only to have the child become ill again in the same pattern. In this example, if cotinine levels are to be used, then a combination approach may be useful. Parent 1 should document by testing that his or her cotinine level is 0 by serum and urine tests the day that the child goes to parent 2. The childs urine cotinine level, by serum and urine tests, should be measure on the same day. Ideally, the cotinine levels of parent 2 and the child would be measured, although I have never seen a parent 2 cooperate. On the day the ...
NHANES III was conducted in two phases: October 1988--September 1991 and October 1991--September 1994. Additional information is available at http://www.cdc.gov/nchs/nhanes.htm. Cotinine is a metabolite only of nicotine. Among nonsmokers, the presence of cotinine in serum indicates exposure to secondhand tobacco smoke. From 1988--1991 through 2001--2002, median serum cotinine levels decreased by 74% in children aged 4--11 years, 79% in persons aged 12--19 years, and 83% in persons aged ,20 years, suggesting a substantial reduction in the exposure of the U.S. population to secondhand tobacco smoke. SOURCE: Pirkle JL, Bernert JT, Caudill SP, Sosnoff CS, Pechacek TF. Trends in the exposure of nonsmokers in the U.S. population to secondhand smoke: 1988--2002. Environ Health Perspect 2006;114:853--8. ...
In humans, cotinine is metabolically formed from nicotine in a reaction catalyzed by CYP2A6 and is further metabolized to trans-3′-hydroxycotinine (3HC) by CYP2A6 (1, 2). Cotinine is routinely used as an objective index of tobacco and tobacco-derived carcinogen exposure. The use of cotinine is particularly useful because of the wide individual variability in the relationship between self-reported cigarettes smoked per day and systemic exposure to tobacco and tobacco-derived carcinogen (3). Higher plasma cotinine levels have been associated with increased lung cancer risk (4), and variation in cotinine levels have recently been used as evidence that the mechanism mediating the association between genetic variation in CHRNA5-A3-B4 and lung cancer risk is almost entirely through the modulation of tobacco consumption (5).. The systemic intake of nicotine is correlated with exposure to tobacco-derived carcinogen (3). When used as a biomarker of tobacco-derived carcinogen exposure, it is generally ...
Background. Few studies have shown that self-reported secondhand smoke exposure in never smokers is associated with high blood pressure. However, there are no studies investigating the relationship between secondhand smoke exposure, measured objectively by serum cotinine levels, and high blood pressure in never smokers. Methods. We examined never smokers (.. = 2027) from the National Health and Nu
article{5715d9e5-2014-4a6d-a62e-31686d90f70d, abstract = {To validate a detailed questionnaire for assessment of environmental tobacco smoke (ETS) exposure by the biomarker cotinine in various media, a population-based study in the urban area of Malmo, Sweden was performed in children aged 8-13 years with and without asthmatic symptoms. There were strong correlations between urinary and saliva cotinine concentrations and also, though to a lesser extent, between these media and plasma. Even a detailed questionnaire gave only a rough picture of the ETS exposure, as indicated by the biomarkers. In a multivariate model, the most significant questionnaire-derived predictor of the cotinine levels was the maternal smoking habits; other questionnaire variables gave only a minimal explained variance. Children with a history of asthmatic symptoms had statistically significantly lower median cotinine levels in urine and saliva compared to referent children, most likely because of the antismoking ...
Kim, I., Wtsadik, A., Choo, R., Jones, H., & Huestis, M. (2005). Usefulness of salivary trans-3 Hydroxycotinine concentration and trans-3 Hydroxycotinine / cotinine ratio as biomarkers of cigarette smoke in pregnant women. Journal of Analytical Toxicology, 29, 689 - 695 ...
One hundred thirty-two children who attended a research day-care center were studied to determine whether passive tobacco smoke exposure was associated with an increased rate of otitis media with effusion or with an increased number of days with otitis media with effusion during the first 3 years of life. Based on preliminary studies, a serum cotinine concentration of ≥2.5 ng/mL was considered indicative of exposure to tobacco smoke. Otitis media with effusion was diagnosed using pneumatic otoscopy by nurse practitioners and pediatricians who reviewed the childrens health status each weekday. The 87 children with serum cotinine concentrations ≥2.5 ng/mL had a 38% higher rate of new episodes of otitis media with effusion during the first 3 years of life than the 45 children with lower or undetectable serum cotinine concentrations (incidence density ratio = 1.38, 95% confidence interval 1.21 to 1.56). The average duration of an episode of otitis media with effusion was 28 days in the children ...
TY - JOUR. T1 - Did smokefree legislation in England reduce exposure to secondhand smoke among nonsmoking adults? Cotinine analysis from the health survey for England. AU - Sims, Michelle. AU - Mindell, Jennifer S.. AU - Jarvis, Martin J.. AU - Feyerabend, Colin. AU - Wardle, Heather. AU - Gilmore, Anna. PY - 2012/3. Y1 - 2012/3. N2 - Background: On 1 July 2007, smokefree legislation was implemented in England, which made virtually all enclosed public places and workplaces smokefree. Objectives: We examined trends in and predictors of secondhand smoke exposure among nonsmoking adults to determine whether exposure changed after the introduction of smokefree legislation and whether these changes varied by socioeconomic status (SES) and by household smoking status. Methods: We analyzed salivary cotinine data from the Health Survey for England that were collected in 7 of 11 annual surveys undertaken between 1998 and 2008. We conducted multivariate regression analyses to examine secondhand smoke ...
Bernert, J. T., Jacob, P., Holiday, D., Benowitz, N. L., Sosnoff, C. S., Doig, M. V., ... Langman, L. J. (2009). Interlaboratory comparability of serum cotinine measurements at smoker and nonsmoker concentration levels: A round-robin study. Nicotine and Tobacco Research, 11(12), 1458-1466 ...
A nationally representative survey of the US population used 85.2 nmol/l (15 ng/ml) serum cotinine as a cut off for distinguishing smokers from non-smokers.17 Heavy exposure to secondhand smoke, however, may produce saliva concentrations as high as 177.8 nmol/l (31.3 ng/ml).10 Given the high exposures in bar workers,9 10 and as salivary concentrations are 25% higher than serum concentrations,18 we defined non-smokers as those who reported being former smokers or who had never smoked and had salivary cotinine concentration , 113.6 nmol/l (20 ng/ml). We excluded people who claimed to be non-smokers but had salivary cotinine concentration ≥113.6 nmol/l as we considered them to be active smokers.. To measure any changes, we analysed symptoms individually, grouped into two dichotomous variables (any respiratory symptoms and any sensory symptoms), and as two symptom scores (total number of respiratory symptoms and total number of sensory symptoms reported by each individual).. Analyses (changes ...
A nationally representative survey of the US population used 85.2 nmol/l (15 ng/ml) serum cotinine as a cut off for distinguishing smokers from non-smokers.17 Heavy exposure to secondhand smoke, however, may produce saliva concentrations as high as 177.8 nmol/l (31.3 ng/ml).10 Given the high exposures in bar workers,9 10 and as salivary concentrations are 25% higher than serum concentrations,18 we defined non-smokers as those who reported being former smokers or who had never smoked and had salivary cotinine concentration , 113.6 nmol/l (20 ng/ml). We excluded people who claimed to be non-smokers but had salivary cotinine concentration ≥113.6 nmol/l as we considered them to be active smokers.. To measure any changes, we analysed symptoms individually, grouped into two dichotomous variables (any respiratory symptoms and any sensory symptoms), and as two symptom scores (total number of respiratory symptoms and total number of sensory symptoms reported by each individual).. Analyses (changes ...
To the Editor:. We read with interest the well-written article by Alshaarawy et al1 that investigated the association of hypertension with secondhand smoke in 2889 never smokers from the National Health and Nutrition Examination Survey. Authors demonstrated that serum cotinine was positively associated with both systolic blood pressure (BP) and prevalence of hypertension. Although the determinant as depicted by serum cotinine levels-at first sight-seems appropriate to evaluate the exposure of participants to passive smoke, there are some obscured points that need to be clarified.. It is not reported whether cotinine assessment was performed on the same day of BP measurements. We should acknowledge that beyond BP variability evaluation2 completely lacking in the present study, there might also be variability in cotinine levels.3 This latter phenomenon could not be ruled out by the design of the present study,1 as exposure was not evaluated by structured questionnaires examining the periodicity of ...
Title:Neuroinflammation: A Therapeutic Target of Cotinine for the Treatment of Psychiatric Disorders?. VOLUME: 22 ISSUE: 10. Author(s):Valentina Echeverria, J. Alex Grizzell and George E. Barreto. Affiliation:10,000 Bay Pines Blvd, Bay Pines, FL 33744, USA.. Keywords:Neuroinflammation, Major depression, cotinine, Post-traumatic stress disorder, Bipolar disorder, suicide, anxiety.. Abstract:Neuroinflammation is a common characteristic of several mental health conditions such as major depression, bipolar disorder, post-traumatic stress disorder (PTSD) and schizophrenia (SCHZ). Inflammatory processes trigger and/or further deteriorate mental functions and are regarded as targets for therapeutic drug development. Cotinine is an alkaloid present in tobacco leaves and the main metabolite of nicotine. Cotinine is safe, non-addictive and has pharmacokinetic properties adequate for therapeutic use. Research has shown that cotinine has antipsychotic, anxiolytic, and antidepressant properties and modulates ...
Cigarette smoke is a complex mixture containing, among other chemicals, pyridine alkaloids and N-nitrosamines. Carcinogenic tobacco-specific N-nitrosamines, N-nitrosodimethylamine (NDMA) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), are both activated by cytochrome P450 (CYP) 2E1 in rats. Previous reports indicate that nicotine and the main nicotine metabolite, cotinine, reduce the mutagenicity of both NNK and NDMA in Salmonella typhimurium. To study the mechanism of this effect, we examined inhibition of CYP 2E1 activity, as assessed by p-nitrophenol (pNP) hydroxylation, by nicotine, cotinine, and an aqueous cigarette tar extract (ACTE) in human 2E1-expressing microsomes. At all substrate concentrations (0-1.25 mM) nicotine was a significantly more potent inhibitor of CYP 2E1 activity compared to cotinine. Estimated Ki values for nicotine and cotinine (both at 10 mM) were 13 mM (2 mg/ml) and 308 mM (54 mg/ml) respectively. The Ki for ACTE was 0.2 mg/ml at a concentration of 0.32 mg/ml.
Cotinine (Nicotine Metabolite) Detection Cotinine is the predominant metabolite of nicotine and used as a biomarker for exposure to tobacco smoke. In the human body, cotinine has a half-life of 20 hours and can be detected up to a week after the use of tobacco. The level of cotinine in the saliva, urine and blood is pr
Methods This study used a pre/postintervention experimental design. The setting was bars in 12 Michigan counties. Subjects were bar employees, recruited through flyers and individual discussions with local health department staff. Participants completed a screening questionnaire to determine eligibility. A total of 40 eligible employees completed a demographic survey, provided urine samples for analysis of cotinine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and completed questionnaires on respiratory and general health status 6 weeks before and 6-10 weeks after the law went into effect. The main outcome measures were urine samples for total cotinine and total NNAL and data from a self-administered respiratory and general health status questionnaire collected during the pre-law and post-law study periods. ...
Foods, principally from plants in the family Solanaceae, and a number of teas were examined for the presence of nicotine. Dietary nicotine would give rise to cotinine in urine and compromise estimates of exposure to tobacco smoke that depend on urinary cotinine. All foods were homogenized, extracted …
Nicotine and cotinine in hair are good biomarkers for assessing long-term exposure to smoking. However, analytical devices such as GC/MS are associated with high cost and are not widely used. HPLC/UV is used widely in laboratories, but is unsuitable for measurement of minor constituents, except when using the column-switching method. Thus, we aimed to establish a simple, inexpensive and sensitive method based on HPLC/UV with column switching for measuring nicotine and cotinine in hair. First, we compared the presence and absence of a column selection unit. We then measured amounts of nicotine and cotinine in hair samples collected from the general population, and compared both the corresponding levels and the detection limits with those in previous studies. Finally, initial and running costs of HPLC/UV were compared with other analytical methods. As one of the results, the areas of nicotine and cotinine measured by HPLC/UV with column-switching method were 12.9 and 16.9 times greater,
In this study, we evaluated the associations of smoking and alcohol intake, both independently and collectively, with sodium intake in Korean men. Subjects (6340 men) were from the fifth Korean National Health Examination Survey (2010-2012). Smoking-related factors included smoking status, urinary cotinine level, and pack-years of smoking. Food intake was assessed using a 24-h recall. The odds of excessive sodium intake were estimated using survey logistic regression analysis. The smoking rate was 44.1%. The geometric mean of the urinary cotinine level was 0.05 µg/mL, and the median (min-max) pack-years of smoking was 13.2 (0-180). When adjusted for related factors, the odds (95% confidence interval) of excessive sodium intake were 1.54 (1.00, 2.37), 1.55 (1.23, 1.94), 1.44 (1.07, 1.95), and 1.37 (1.11, 1.68) times higher in the group exposed to smoking and drinking than in the group that never smoked nor drank, the group that never smoked and drank <5 times per month, the group that did not
In this issue of Thorax a further paper from Dundee is published which explores a group of 438 children aged 2-12 years with asthma. In their first paper1 the authors investigated passive smoke exposure, as measured by salivary cotinine levels, and found that exposure to tobacco smoke was highest where housing conditions were crowded and where several heavy smokers smoked in the same room as the child. In a second paper2the authors reported that the intervention of asking the parents to reduce the exposure of their asthmatic children to tobacco smoke was ineffective.. The latest paper by Crombie et al 3 on page 9 investigates how often the 438 asthmatic children were taken to their family practitioners (GPs), either for asthma or non-asthma problems, and relates this to their smoke exposure. Smoke exposure was assessed both by salivary cotinine levels and also by the history of intensity of exposure as judged by the number of parents who smoked, how many cigarettes they smoked, and whether the ...
OBJECTIVES:. The primary objective of this study is to determine if providing urine cotinine feedback to caregivers in conjunction with standard education will be more effective than education alone in reducing patient SHS exposure.. The secondary objectives of this study are:. To determine whether urine cotinine feedback in conjunction with education provided to the caregiver is more effective in changing parental smoking behavior compared to education alone.. As an exploratory measure we will collect history and physical exam data to follow patients clinical complications during the study to determine if patients with a decrease in SHS exposure also have a decrease in clinical complications. ...
Leenders M., Chuang S-C., Dahm CC., Overvad K., Ueland PM., Midttun Ø., Vollset SE., Tjønneland A., Halkjær J., Jenab M., Clavel-Chapelon F., Boutron-Ruault M-C., Kaaks R., Canzian F., Boeing H., Weikert C., Trichopoulou A., Bamia C., Naska A., Palli D., Pala V., Mattiello A., Tumino R., Sacerdote C., Van Duijnhoven FJ., Peeters PH., Van Gils CH., Lund E., Rodriguez L., Duell EJ., Pérez M-JS., Molina-Montes E., Castaño JMH., Barricarte A., Larrañaga N., Johansen D., Lindkvist B., Sund M., Ye W., Khaw K-T., Wareham NJ., Michaud DS., Riboli E., Xun WW., Allen NE., Crowe FL., Bueno-de-Mesquita HB., Vineis P ...
April 9, 2009 - Some 56.7 percent of nonsmokers living in New York City were found to have elevated levels of the nicotine metabolite cotinine, compared with an average 44.9 percent of nonsmokers nationwide. Among the ethnic groups studied, nonsmokers of Asian descent were most often affected, with 68.7 percent of those examined showing elevated blood levels of cotinine (passive smoking, environmental tobacco smoke, ETS, secondhand smoke, sidestream smoke, involuntary smoking ...
When and how often laboratory tests are done may depend on many factors. The timing of laboratory tests may rely on the results or completion of other tests, procedures, or treatments. Lab tests may be performed immediately in an emergency, or tests may be delayed as a condition is treated or monitored. A test may be suggested or become necessary when certain signs or symptoms appear. Due to changes in the way your body naturally functions through the course of a day, lab tests may need to be performed at a certain time of day. If you have prepared for a test by changing your food or fluid intake, lab tests may be timed in accordance with those changes. Timing of tests may be based on increased and decreased levels of medications, drugs or other substances in the body. The age or gender of the person being tested may affect when and how often a lab test is required. Chronic or progressive conditions may need ongoing monitoring through the use of lab tests. Conditions that worsen and improve may ...
Previous studies report that low levels cognitive function and history of smoking are associated with increased mortality risk. Elderly smokers may have increased risk of dementia, but risk in former smokers is unclear. We tested the hypotheses that the harmful effect of impaired cognitive function as related to mortality is greater in persons smoking at baseline than in others. Further, we used serum cotinine levels to assess recall bias of smoking history by cognitive function level. Data were analyzed from a longitudinal mortality follow-up study of 4,916 American men and women aged 60 years and over, examined in 1988-1994 with complete data followed an average 8.5 years. Measurements at baseline included smoking history, a short index of cognitive function (SICF), serum cotinine and socio-demographics. Death during follow-up occurred in 1,919 persons. In proportional hazards regression analysis, a significant interaction of current smoking with cognitive function was not found; but there was a
Cigarette smoking is the foremost modifiable risk factor for adverse pregnancy outcomes. Nicotine is a suspected fetal neuroteratogen. There is concern that nicotine may achieve toxic levels during pregnancy if nicotine replacement therapies are prescribed at doses used in the nonpregnant state. Ten healthy, volunteer, pregnant smokers received infusions of deuterium-labeled nicotine and cotinine during pregnancy and again postpartum. From blood and urine measurements, the following were determined: clearance (renal and nonrenal) of nicotine and cotinine, clearance of nicotine via the cotinine pathway (an indicator of CYP2A6 activity), and daily intake of nicotine from smoking. The clearance of nicotine and cotinine was significantly higher (60 and 140%, respectively), and the half-life of cotinine was much shorter (8.8 versus 16.6 h, P , 0.01) during pregnancy. Although plasma levels of cotinine were lower during pregnancy (119 versus 202 ng/ml, P , 0.05), daily intake of nicotine from smoking ...
Cotinine is a metabolite (byproduct) of nicotine as it is processed by the human body. Cotinine is an indicator that nicotine has been inhaled or otherwi...
Cotinine: The N-glucuronide conjugate of cotinine is a major urinary metabolite of NICOTINE. It thus serves as a biomarker of exposure to tobacco SMOKING. It has CNS stimulating properties.
The iScreen OFD Cotinine Saliva Test detects the presence of cotinine (the main metabolite in nicotine) for up to 1-2 days after use. Limited quantity! Offer Expires: 5/31/2020
Background: Smoking is associated with decreased concentrations of several antioxidant vitamins. We sought to determine the relation between circulating concentrations of selected B vitamins and smoking status, with particular attention to longitudinal associations.. Methods: We used baseline data from 2 B-vitamin intervention trials that included 6837 patients with ischemic heart disease. Smoking habits were ascertained by interview. Vitamins and metabolites, including the nicotine metabolite cotinine, were measured in plasma and serum by microbiological assays or gas/liquid chromatography-tandem mass spectrometry.. Results: The highest circulating concentrations of folate and pyridoxal 5phosphate (PLP) and lowest concentrations of total plasma homocysteine, a functional marker of folate status, were observed for self-reported never smokers, followed by self-reported ex-smokers and current smokers (Ptrend , 0.001). Cobalamin and its functional marker methylmalonic acid were not associated with ...
Cytochrome P450 1B1 is a recently recognized phase I bioactivating enzyme with high affinity for both inhaled tobacco carcinogens and 17β-estradiol. We evaluated the human lung expression of this multifunctional member of the P450 superfamily across 16 individuals. Expression of CYP1B1 was evaluated by qualitative reverse transcription-polymerase chain reaction and Western immunoblots performed on human tumor and nontumor lung tissue. Expression at both mRNA and protein levels was then correlated with smoking history, plasma biomarkers of tobacco exposure (nicotine and cotinine), gender, and tumor histology. CYP1B1 mRNA and protein were detected in 94 and 100% of individuals, respectively. Multivariate analysis confirmed that there were more subjects displaying CYP1B1 mRNA expression in tumor than nontumor tissue (p = 0.0003). Correlation of CYP1B1 protein with plasma cotinine levels was statistically marginal (p = 0.027). Self-reported smoking history, gender, and tumor histology did not ...
Fu M, Martínez-Sánchez JM, Agudo A, Pascual JA, Borràs JM, Samet JM, et al. Association Between Time to First Cigarette After Waking Up and Salivary Cotinine Concentration. Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco. 2011;13(3):168-72. Abstract ...
Fu M, Martínez-Sánchez JM, Agudo A, Pascual JA, Ariza C, Moncada A, et al. Nicotine depedence and salivary cotinine concentration in daily smokers. European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP). 2012;21(1):96-102. Abstract ...
How the study was done. The study subjects were 16,046 people who had participated in the third National Health and Nutrition Survey in 1988-1994, and for whom demographic, smoke exposure, and serum TSH, antithyroid peroxidase (anti-TPO) antibody, and antithyroglobulin (anti-Tg) antibody results were available. Smoking or smoke exposure was determined by measuring serum cotinine, a metabolite of nicotine; people with concentrations ,15 ng/ml were designated as active smokers, and those with concentrations ≤15 ng/ml as nonsmokers.. The results of the study. There were 5134 active smokers (32 percent) and 10,912 nonsmokers (68 percent). More men than women were active smokers. Fewer active smokers than nonsmokers had high (,4.5 mU/L) serum TSH concentrations (2.6 vs. 5.4 percent). Serum TSH concentrations were low (,0.1 mU/L) in 0.6 percent of active smokers and 0.3 percent of nonsmokers, and the concentrations were slightly low (0.1 to 0.4 mU/L) in 2.2 and 1.2 percent, respectively. Fewer ...
The researchers in this study defined living a healthy lifestyle as meeting four parameters: being sufficiently active (150 mins of moderate-to-vigorous physical activity each week), eating a healthy diet (based on a 24-hour recall), being a nonsmoker (serum cotinine level) and having a recommended body-fat percentage (5%-20% for men, and 8%-30% for women). Researchers then examined the association between having different combinations of these characteristics and several biomarkers for cardiovascular disease. The results from the study came from a survey of 4,745 adults ...
Background and aims: In smoking treatment trials comparing varenicline with transdermal nicotine replacement therapy (NRT), stratified by nicotine metabolite (3-hydroxycotinine/cotinine) ratio (NMR), the relative benefit of varenicline is greater among normal rather than slow metabolizers. This study tested if the relative effectiveness of varenicline and NRT is associated with NMR status in a natural treatment setting. A secondary aim was to test if this relationship is moderated by behavioural support. Design: Prospective observational multi-centre study with 4-week and 52-week follow-up. Setting: Nine English Stop Smoking Services (SSS). Participants: Data came from 1556 smokers (aged ≥ 16 years) attending SSS between March 2012 and March 2013. Interventions: Participants received pharmacotherapy together with behavioural support. Measurements: The primary outcome was carbon monoxide-verified continuous abstinence at both follow-up times. Main explanatory variables were (1) NMR status [slow ...
The mean age±standard deviation (range) of the subjects was 42.8±6.2 (33-58). Subjects at a workplace with a current history of treatment for diabetes and/or subjects whose fasting plasma glucose level was ≥140 mg/dL were excluded from the analysis. Sampling of saliva was conducted using Salisoft® (Assist Co. Ltd., Tokyo). The analyses were performed by high-performance liquid chromatography using CAPCELL PAK MG II C18 (Shiseido Co. Ltd., Tokyo) columns under the 195temperature of 50℃ and wavelength of 262 nm. The detection limits for nicotine and cotinine were 5 ng/mL and 10 ng/mL, respectively. As an indicator of insulin resistance, the homeostasis model assessment for insulin resistance (HOMA-IR)5 was calculated as follows: HOMA-IR=(Fasting plasma glucose×Fasting serum insulin)/405. Units of glucose and insulin used for the calculation of HOMA-R were mg/dL and µIU/mL, respectively. Bernert et al.6 reported a regression line of salivary cotinine against the serum cotinine as Log10 ...
In most heavy smokers, cotinine levels fall below the detectable range after two weeks of abstinence, according to Mayo Clinic. This means that the laboratory test will show a value of less than 2...
In testing that included more than 1,200 children, researchers found that up to 15 percent of them had levels of cotinine, a byproduct of the bodys breakdown of nicotine, comparable with what would be found in an adult smoker.. Overall, about 63 percent of the babies and young children in the study had discernible levels of cotinine, evidence of significant exposure to second- and third-hand smoke, according to the study, published last week in the journal Nicotine & Tobacco Research. Previous similar research, focused on older children, detected cotinine in less than half of the children studied or did not document levels of cotinine, Medical Xpress reported.. For those who remain skeptical about the bodys susceptibility to passive smoke exposure, the study may serve as a wake-up call.. Were finding (as much as) 15 percent of the babies have levels as if they were smokers themselves, said Clancy Blair, senior study author and a professor of cognitive psychology at New York ...
Smoking and using tobacco products can be a difficult habit to qualm. Learn about nicotine drug testing, the difference between nicotine and cotinine, and more.
You may have this test to measure your progress in a program to quit smoking. This test can also help your doctor figure out the right dose for a nicotine patch to help you stop smoking.. You may need to take a cotinine test if youre applying for a job at a company that prohibits smoking. Some insurance companies may require this test as part of a health exam before approving a policy. ...
Looking for low cost nicotine/cotinine or alcohol test kits? Shop for tests that offer rapid and accurate results. Free shipping on orders $50+!
The N-glucuronide conjugate of cotinine is a major urinary metabolite of NICOTINE. It thus serves as a biomarker of exposure to tobacco SMOKING. It has CNS stimulating properties ...
, cotinine test for Tobacco. Some jobs or insurance test for tobacco use. Be proactive at ARCpoint Labs of Worcester, MA (508) 834-3760.
The Healthy Babies Project is an effectiveness trial designed to determine the effects of clinic-based behavioral counseling on environmental tobacco smoke (ETS) exposure among low-SES infants of smoking mothers, as measured by parent reports and babies urine cotinine values. One hundred and fifty women with children age three and younger have been recruited from two community clinic populations receiving well-baby care. Mothers were randomly assigned to a usual-treatment control group or to an experimental/counseling group which receives seven counseling sessions over six months. Counseling is administered by trained clinic staff. Mothers are assisted in setting personal goals for reducing their infants ETS exposure. Contingency contracting, shaping, and stimulus control are incorporated into individualized sessions which encourage mothers to decrease their babies exposure to ETS. All participants are interviewed at baseline, 3-months (mid-intervention), 6-months (post-intervention), and ...
Using data from the 1999-2012 National Health Nutrition and Examination Survey (NHANES), the researchers analyzed 25,522 individuals for the presence of five substances in the blood or urine that indicate tobacco exposure.. Three of these substances - lead, cadmium and arsenic - can be found in environmental sources, as well as tobacco. The other two substances - cotinine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) - are only found in tobacco.. Results of the analysis revealed that, compared with non-smokers, cigar smokers had much higher concentrations of cotinine and cadmium in their blood and NNAL in their urine. This result remained even after the team accounted for current cigarette smoking status.. Cotinine - an anagram of nicotine - is a compound produced after nicotine enters the body and is classed as the most reliable measurement of tobacco exposure. Cadmium is an element that has been linked to a number of health conditions in humans - such as kidney disease, inflammation ...
Sigma-Aldrich offers abstracts and full-text articles by [Andreas D Flouris, Maria S Chorti, Konstantina P Poulianiti, Athanasios Z Jamurtas, Konstantinos Kostikas, Manolis N Tzatzarakis, A Wallace Hayes, Aristidis M Tsatsakis, Yiannis Koutedakis].
  • Cotinine is the major metabolite of nicotine in man. (nih.gov)
  • Cotinine is an alkaloid found in tobacco and is also the predominant metabolite of nicotine. (wikipedia.org)
  • ETS exposure will also be assessed for examinees 3 years of age and older through the measurement of serum cotinine, a metabolite of nicotine. (cdc.gov)
  • The N-glucuronide conjugate of cotinine is a major urinary metabolite of NICOTINE. (curehunter.com)
  • A test for nicotine is designed to detect cotinine, the principal metabolite of nicotine, in urine and saliva specimens. (testcountry.com)
  • However, in recent years, new evidence has shown that cotinine, the main metabolite of nicotine, exhibits beneficial effects over psychiatric symptoms and may therefore promote smoking within this population. (frontiersin.org)
  • Recently, new studies have shown that the main metabolite of nicotine, an alkaloid named cotinine [(5 S )-1-methyl-5-(3-pyridyl)-pyrrolidin-2-one], has beneficial therapeutic properties, while not having nicotine's negative side-effects. (frontiersin.org)
  • Cotinine is the main metabolite of nicotine, and its serum or plasma level is a useful marker of tobacco smoking ( 9 , 19 ). (aacrjournals.org)
  • To date, nicotine or cotinine (a metabolite of nicotine) have not been measured in experienced ENDS users. (ersjournals.com)
  • Cotinine is the main metabolite of nicotine and is used as a biomarker for exposure to tobacco - both through first and secondhand smoke. (testcountry.com)
  • Use of cotinine, a metabolite of nicotine, has been proposed to detect active smokers who claim not to smoke. (scielo.org.za)
  • Purpose: This study evaluated the performance characteristics of a novel rapid method for verifying smoking status in individuals by measurement of cotinine, the primary metabolite of nicotine, in saliva samples using an immunochromatographic strip in a "dipstick" format compared with liquid chromatography/mass spectrometry (LC/MS). (aacrjournals.org)
  • Measurement of cotinine, a primary metabolite of nicotine that has a half-life of 16 to 18 h and that can be detected in urine, saliva, or serum, provides a reliable means of determining smoking status and other tobacco product use or exposure over a period of 2 to 3 days ( 20 - 22 ). (aacrjournals.org)
  • Cotinine is a metabolite of nicotine and is the primary biomarker for the determination of tobacco exposure. (calbiotech.com)
  • A: Cotinine is the first-stage metabolite of nicotine. (homehealthtesting.com)
  • This test is used to detect Cotinine , the primary metabolite of Nicotine in the urine. (requestatest.com)
  • Accurately screen for cotinine, the primary metabolite of nicotine, with this instant saliva drug test. (confirmbiosciences.com)
  • The NicAlert saliva and urine drug testing kit detects cotinine levels, the major metabolite of nicotine. (confirmbiosciences.com)
  • Extremely sensitive to cotinine, the principle metabolite of nicotine, the NicAlert™ test will detect 6 ranges of cotinine concentrations from 0 ng/ml through 2000+ ng/ml. (confirmbiosciences.com)
  • It rapidly detects the presence of cotinine, the major metabolite of nicotine, in urine. (drugtestingworld.com)
  • Cotinine is a metabolite of nicotine . (chemeurope.com)
  • The purpose of this study was to examine the effects of the metabolite of nicotine, cotinine, in comparison to the effects of the nicotine patch, and a combination thereof during cigarette abstinence. (umn.edu)
  • Cotinine is a major metabolite of nicotine and is used as a preferred target for assay in humans. (thebirdclinic.com)
  • Cotinine is a principal metabolite of nicotine with a substantially longer halflife. (johnyfit.com)
  • Notice that a principal or hours metabolite of nicotine, had a half existence of approximately 20 hours, while nicotine got a relatively shorter half health of nearly two cotinine. (johnyfit.com)
  • the swab test will detect the nicotine (or cotinine, its main metabolite) that is excreted in saliva , as well as that which comes directly in touch with oral mucosa if you are using snuff or chewing tobacco . (healthtap.com)
  • Infusion of cotinine to blood concentrations seen in moderately heavy smokers had no effect on heart rate, blood pressure, or skin temperature, measures that are sensitive to effects of nicotine. (nih.gov)
  • Salivary cotinine concentrations are highly correlated to blood cotinine concentrations, and can detect cotinine in a low range, making it the preferable option for a less invasive method of tobacco exposure testing. (wikipedia.org)
  • Urine cotinine concentrations average four to six times higher than those in blood or saliva, making urine a more sensitive matrix to detect low-concentration exposure. (wikipedia.org)
  • Cotinine concentrations are derived from the ratio of native to labeled cotinine in the sample by comparisons to a standard curve. (cdc.gov)
  • In order to compare maternal and fetal exposure to compounds of tobacco smoke at the end of pregnancy, concentrations of cotinine and thiocyanate were measured in cord serum and maternal serum collected from 24 daily smoking and four non-smoking women at the time of child birth. (nih.gov)
  • Saliva cotinine concentrations, demographic variables, self-reported smoking, presence or absence of smoking in the home, a composite index of social disadvantage derived from occupation, housing tenure and access to a car. (nih.gov)
  • Salivary cotinine concentrations in non-smoking children. (bmj.com)
  • Cotinine concentrations in all non-smoking children almost halved between 1988 and 1998, from a geometric mean of 0.96 (95% confidence interval 0.83 to 1.11) ng/ml in 1988 to 0.52 (0.43 to 0.62) ng/ml in 1998. (bmj.com)
  • We here report cotinine concentrations in children measured during school based surveys carried out since 1988. (bmj.com)
  • To exclude children who denied their smoking, we restricted our study to those with cotinine concentrations below 15 ng/ml, a suggested cutoff point for active smoking. (bmj.com)
  • Cotinine concentrations -Cotinine was assayed by gas chromatography with a detection limit of 100 pg/ml. 14 To check for drift in the assay over time, in 1994 we reanalysed 25 samples gathered and analysed in 1990. (bmj.com)
  • In children not living with a smoker, children living with one smoker, and children living with more than one smoker at home, median urinary cotinine concentrations (ng/mL) were 0.72, 2.97, and 4.46, respectively. (mdpi.com)
  • Subsequently the SMC were incubated with media containing 0.1% or 15% fetal bovine serum and nicotine or cotinine at concentrations ranging from 10(-9) mol/L to 10(-6) mol/L. Control samples were incubated with corresponding media but without the drugs. (biomedsearch.com)
  • Analyses of the relation between spirometric values and cotinine concentrations were based on 2511 children and of the relation between spirometric values and questionnaire measures on 2000 children. (bmj.com)
  • Salivary cotinine concentrations were strongly related to exposure to cigarette smoke at home but 88% of children who were from non-smoking households and not looked after by a smoker had detectable cotinine concentrations, 5% being in the top two fifths of the cotinine distribution. (bmj.com)
  • There were strong correlations between urinary and saliva cotinine concentrations and also, though to a lesser extent, between these media and plasma. (lu.se)
  • METHOD: Serum cotinine concentrations were measured in 1,943 smokers participating in the 2001 to 2006 National Health and Nutrition Examination Surveys (NHANES). (acs.org)
  • The objectives of this study were to determine urinary cotinine concentrations in non-smoking residents of smoke-free homes and to establish the relationship of urinary cotinine with housing type and other socio-demographic and secondhand smoke (SHS) exposure factors. (biomedcentral.com)
  • The urinary cotinine concentrations of residents living in attached [1.18 ng/mg creatinine (Cr)] and detached housing (1.23 ng/mg Cr) were significantly higher than those of residents who lived in apartments (0.69 ng/mg Cr). (biomedcentral.com)
  • In the multivariate regression analysis, housing type, sex, former smoking status, and frequency of experiencing SHS odor were associated with urinary cotinine concentrations ( R 2 = 0.14). (biomedcentral.com)
  • Housing type, sex, former smoking status, and frequency of experiencing SHS odor were predictors for urinary cotinine concentrations in the study participants. (biomedcentral.com)
  • One study that assessed the blood serum cotinine levels of US children who lived in homes where no one smoked indoors reported higher serum cotinine concentrations in children who lived in apartments than in those living in detached residences [ 18 ]. (biomedcentral.com)
  • At all substrate concentrations (0-1.25 mM) nicotine was a significantly more potent inhibitor of CYP 2E1 activity compared to cotinine. (usu.edu)
  • Cotinine administration, with or without nicotine patch, produced serum cotinine concentrations 3-4 times higher than during ad lib smoking. (umn.edu)
  • Therefore, cotinine appears to antagonize the effects of nicotine in the alleviation of withdrawal symptoms at concentrations higher than that attained from normal smoking. (umn.edu)
  • The level of cotinine in the blood, saliva, and urine is proportionate to the amount of exposure to tobacco smoke, so it is a valuable indicator of tobacco smoke exposure, including secondary (passive) smoke. (wikipedia.org)
  • On the other hand, the median level of cotinine (22 ng/ml) in maternal serum was less than half of the median level (51 ng/ml) in cord serum (P = 0.0009). (nih.gov)
  • The Janus serum bank offers the opportunity to investigate for the first time prospectively the association between lung cancer risk and serum level of cotinine. (aacrjournals.org)
  • 2) The post hoc analysis showed that urinary level of cotinine can be very helpful in the assessment of exacerbation of ophthalmological clinical symptoms before and after RIT particularly in smokers. (nel.edu)
  • For this reason alone, testing for tobacco is performed routinely, especially by health and insurance companies (standard cutoff level of cotinine (nicotine metabolite) is 200 ng/ml. (drugtestingworld.com)
  • Measuring cotinine in people's blood is the most reliable way to determine exposure to nicotine for both smokers and nonsmokers exposed to environmental tobacco smoke (ETS). (cdc.gov)
  • We studied cotinine disposition kinetics in 28 healthy habitual cigarette smokers. (nih.gov)
  • We conclude that, at levels to which cigarette smokers are generally exposed, cotinine exerts no cardiovascular activity and weak, if any, psychologic activity. (nih.gov)
  • Cotinine may also be measured in saliva and in hair, although hair testing is primarily used in a research setting, such as a study of non-smokers exposure to tobacco smoke. (labcorp.com)
  • African American smokers generally have higher plasma cotinine levels than Caucasian smokers. (wikipedia.org)
  • They used stored blood samples and measured serum cotinine to identify true smokers. (bmj.com)
  • In most heavy smokers, cotinine levels fall below the detectable range after two weeks of abstinence, according to Mayo Clinic. (reference.com)
  • Association of serum cotinine levels and hypertension in never smokers. (ahajournals.org)
  • 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. (biomedsearch.com)
  • Cotinine cut-points that are in use were derived from relatively small samples of smokers and non-smokers 20 or more years ago. (nih.gov)
  • The extent of non-smokers' exposure to other people's tobacco smoke is the principal factor driving optimal cotinine cut-points. (nih.gov)
  • In fact, prolonged exposure to Environmental Tobacco Smoke (ETS) may yield higher cotinine levels than would be present in firsthand smokers. (testcountry.com)
  • Serum cotinine level is a predictor of risk of lung cancer among smokers. (aacrjournals.org)
  • Cotinine at a concentration of 10(-9) mol/L, a level seen among passive smokers, was a statistically significant stimulus for DNA synthesis in both minimum serum and serum-supplemented media. (biomedsearch.com)
  • Validated for clinical use, and highly correlated with serum levels, Salimetrics Cotinine assay's high-sensitivity distinguishes between active smokers, non-smokers, and recent second-hand smoke exposure. (salimetrics.com)
  • It has been demonstrated that smokers who developed wound healing complications had higher levels of cotinine than those who did not when tested peri-operatively. (scielo.org.za)
  • Ten healthy, volunteer, pregnant smokers received infusions of deuterium-labeled nicotine and cotinine during pregnancy and again postpartum. (aspetjournals.org)
  • Lower cotinine levels observed during pregnancy do not necessarily reflect less smoke exposure, and cut-off levels used to classify nonsmokers, passive smokers, and active smokers need to be established for pregnancy. (aspetjournals.org)
  • Average cotinine level for adult non-smokers in the US: 0.1 ng/mL. (salimetrics.com)
  • Self-reported current pipe and cigar smokers had elevated urine cotinine levels compared with never-smokers. (annals.org)
  • This test could be an important adjunct for identifying smokers and treating smoking-related diseases by providing instantaneous results at a fraction of the cost of laboratory cotinine analysis. (ersjournals.com)
  • This study examined the relationship between smoking a menthol or nonmenthol cigarette brand on cotinine levels (adjusted by the number of cigarettes smoked per day) among non-Hispanic black and white U.S. adult smokers. (naquitline.org)
  • The study was an attempt to understand whether the preference for menthol cigarettes in black smokers accounts for their higher cotinine levels. (naquitline.org)
  • Results showed that smoking a menthol cigarette brand versus smoking a nonmenthol cigarette brand was not associated with mean serum cotinine concentration in either black or white smokers. (naquitline.org)
  • In this observational study, we intended to examine whether the use of high doses of radioiodine (RAI) [22 mCi (814 MBq)] with prophylaxis of oral glucocorticoids (oGCS) does not exacerbate Graves ophthalmopathy (GO) in smokers and non-smokers, especially regards to the urine level cotinine and ocular changes before and after RIT. (nel.edu)
  • There are many pharmacologic properties of menthol that may facilitate exposure to tobacco smoke, and it has been suggested that the preference for menthol cigarettes in black smokers accounts for their higher cotinine levels. (acs.org)
  • OBJECTIVE: To assess cigarettes smoked per day-adjusted cotinine levels in relation to smoking a menthol or nonmenthol cigarette brand among non-Hispanic black and white U.S. adult smokers under natural smoking conditions. (acs.org)
  • The effect of smoking a menthol brand on cigarettes smoked per day-adjusted serum cotinine levels in these two populations was modeled by adjusting for sex, age, number of smokers living in the home, body weight, time since last smoked, and FTC (Federal Trade Commission)-measured nicotine levels. (acs.org)
  • 0.05) with mean serum cotinine concentration in either black or white smokers. (acs.org)
  • CONCLUSIONS: The higher levels of cotinine observed in black smokers compared with white smokers are not explained by their higher preference for menthol cigarette brands. (acs.org)
  • Liquid-chromatographic determination of nicotine and cotinine in urine from passive smokers: comparison with gas chromatography with a nitrogen-specific detector. (aaccjnls.org)
  • We describe a simple, sensitive, and specific high-performance liquid-chromatographic method with ultraviolet detection (256 nm) for the simultaneous analysis of nicotine and cotinine in urine of passive smokers. (aaccjnls.org)
  • We assayed cotinine using a competitive immunoassay in NLF from 23 smokers, ten non smokers exposed to tobacco smoke and 60 nonsmokers who did not report smoke exposure. (johnyfit.com)
  • NLF cotinine levels were considerably higher in smokers than in 'nonsmokers', not even considering their exposure to ambient tobacco smoke. (johnyfit.com)
  • Our own results indicate that NLF cotinine is notably higher in smokers than in nonsmokers and established a cut of 0 ng/ml that might be used in future studies as an objective indicator of current smoking. (johnyfit.com)
  • In addition, sometimes cotinine levels are used to determine nicotine's presence in the body. (fastmed.com)
  • The Fourth Report shows differences in cotinine levels among different racial groups. (cdc.gov)
  • In the past 15 years, blood cotinine levels for nonsmokers in the U.S. population have decreased about 70%, indicating that public health interventions to reduce ETS exposure have been successful. (cdc.gov)
  • Males generally have higher plasma cotinine levels than females. (wikipedia.org)
  • These systematic differences in cotinine levels were attributed to variation in CYP2A6 activity. (wikipedia.org)
  • At steady state, plasma cotinine levels are determined by the amount of cotinine formation and the rate of cotinine removal, which are both mediated by the enzyme CYP2A6. (wikipedia.org)
  • Since CYP2A6 activity differs by sex (estrogen induces CYP2A6) and race (due to genetic variation), cotinine accumulates in individuals with slower CYP2A6 activity, resulting in substantial differences in cotinine levels for a given tobacco exposure. (wikipedia.org)
  • We measured serum and saliva cotinine levels with mass spectrometry. (nih.gov)
  • Detectable serum and salivary cotinine levels were common among children admitted for asthma and were associated with readmission, whereas caregiver report of tobacco exposure was not. (nih.gov)
  • Elevated levels of cotinine have been found in individuals exposed to second-hand smoking. (reference.com)
  • Levels as high as 8 nanograms per milliliter have been reported, and with 2 nanograms per milliliter being the cutoff, this will result in a positive cotinine test for someone exposed to tobacco smoke, according to Mayo Clinic. (reference.com)
  • Although the determinant as depicted by serum cotinine levels-at first sight-seems appropriate to evaluate the exposure of participants to passive smoke, there are some obscured points that need to be clarified. (ahajournals.org)
  • We should acknowledge that beyond BP variability evaluation 2 completely lacking in the present study, there might also be variability in cotinine levels. (ahajournals.org)
  • 4 The integration of passive smoking characteristics (ie, intensity, duration, environment of exposure) with cotinine levels would have provided a more integrated approach of passive smoking dynamics. (ahajournals.org)
  • 2 However, because BP measurement was performed 3 times during the same visit, it would be interesting to know the in-visit BP variability, given that subjects with high cotinine levels might demonstrate a higher variability with respect to those residing in the low cotinine levels group. (ahajournals.org)
  • 5 In these lines, the association of a clinically guided serum cotinine measurement with BP levels could not be definitive without ambulatory BP evaluation. (ahajournals.org)
  • Measurement of cotinine levels might not have clinical importance when measured separately of structured questionnaires evaluating smoking dynamics, but potentially could refine the clinical research in the field. (ahajournals.org)
  • Cotinine levels in a nonsmoker are generally less than 10 ng/mL. (baycare.org)
  • Cotinine levels in a light smoker or someone exposed to secondhand smoke are 11 ng/mL to 30 ng/mL. (baycare.org)
  • Cotinine levels in a heavy smoker may be more than 500 ng/mL. (baycare.org)
  • If you haven't smoked or been exposed to nicotine in seven to 10 days, your cotinine levels start to return to a normal level. (baycare.org)
  • The high correlation between measurements of cotinine in maternal serum and cord serum indicates that maternal cotinine levels can be used to describe interindividual differences in fetal exposure to tobacco smoke. (nih.gov)
  • Can cotinine levels be traced in nonsmokers? (testcountry.com)
  • Smoking also increases recovery time after surgical procedures, which is why it is necessary to delay elective aesthetic procedures until cotinine levels are diminished. (testcountry.com)
  • Can blood cotinine levels determine smoking frequency? (testcountry.com)
  • Although cotinine has an established half-life, it is not recommended to reference blood cotinine levels to determine smoking frequency. (testcountry.com)
  • Blood, urine, and saliva samples are analyzed for nicotine and cotinine (a product of nicotine metabolism) levels, and DNA will be collected studied for genes that are associated with nicotine and cotinine metabolism. (clinicaltrials.gov)
  • This oral drug screen detects cotinine levels (the main metabolite in nicotine) down to 30 ng/ml and can detect nicotine use for up to 2 day post consumption. (testcountry.com)
  • Salimetrics Salivary Cotinine ELISA provides researchers with a sensitive method to objectively quantify differences in individual cotinine levels (nicotine exposure), using an easy to collect, non-invasive saliva-sample. (salimetrics.com)
  • Companies may also evaluate salivary cotinine levels for tobacco use relative to employment, health, and life-insurance purposes. (salimetrics.com)
  • By contrast, Cotinine has an average half-life of 17 hours, and blood levels closely reflect the dose of nicotine absorbed from tobacco smoke. (salimetrics.com)
  • Many studies show that levels of Cotinine in saliva show large inter-individual differences. (salimetrics.com)
  • Tobacco Tests from QuickMedical screen for cotinine, a nicotine metabolite, in either urine or saliva and can identify levels of tobacco exposure or use. (quickmedical.com)
  • 0.001) effects on serum cotinine levels after active (60.6 ± 34.3 versus 61.3 ± 36.6 ng/ml) and passive (2.4 ± 0.9 versus 2.6 ± 0.6 ng/ml) smoking. (sigmaaldrich.com)
  • How long smoke free to pass a cotinine levels test? (healthtap.com)
  • To determine whether pipe and cigar smoking was associated with elevated cotinine levels, decrements in lung function, and increased odds of airflow obstruction. (annals.org)
  • The MESA Lung Study measured spirometry according to American Thoracic Society guidelines and urine cotinine levels by immunoassay on a subsample of MESA. (annals.org)
  • We then measured amounts of nicotine and cotinine in hair samples collected from the general population, and compared both the corresponding levels and the detection limits with those in previous studies. (scirp.org)
  • The same testing device was used, but the reagents were changed to improve sensitivity to detect the lower levels of cotinine found in saliva. (ersjournals.com)
  • The test detects elevated levels of cotinine (nicotine metabolite ) in oral fluid for accurate determination of smoking status. (confirmbiosciences.com)
  • The NicAlert nicotine test will detect six ranges of cotinine levels from 0 ng/ml through 2000+ ng/ml. (confirmbiosciences.com)
  • The CpG methylation levels were examined in relationship to prenatal exposure to cadmium and/or cotinine to identify genes and pathways influenced by in utero exposure. (rice.edu)
  • The test utilizes antibodies to selectively detect elevated levels of specific cotinine (nicotine) in human oral fluid. (drugtestingworld.com)
  • The test utilizes a monoclonal antibody to selectively detect elevated levels of Cotinine in urine. (drugtestingworld.com)
  • Children with a history of asthmatic symptoms had statistically significantly lower median cotinine levels in urine and saliva compared to referent children, most likely because of the antismoking information to their parents. (lu.se)
  • [1] Race may also play a role, as black people routinely register higher blood cotinine levels than white people. (chemeurope.com)
  • The factors associated with urinary cotinine levels in non-smoking residents were determined using multivariate regression analysis. (biomedcentral.com)
  • Use of Potentially Reduced Exposure Tobacco Products Among American Indian Smokeless Tobacco Users: Associations With Cessation Behaviors and Cotinine Levels. (ouhsc.edu)
  • Since this presentation, Dr. Nemetz has tested patients suspect of ETS poisoning and demonstrated cotinine levels as much as 100X normal. (thebirdclinic.com)
  • Despite the potential for a direct impact of tobacco smoke on the nasal epithelium and olfactory neurons, no prior studies have assessed cotinine levels in nasal mucus. (johnyfit.com)
  • We sought to determine whether cotinine levels in nasal lavage fluid will provide a reasonable estimate of smoke exposure. (johnyfit.com)
  • While in different situations where a noninvasive sample has always been desired and saliva was probably not accessible or safe, significant data concerning cotinine levels in people NLF with varying degrees of exposure to tobacco smoke was probably of clinical importance for studies evaluating impact of tobacco smoke on nasal and olfactory pathophysiology. (johnyfit.com)
  • We conducted multivariate regression analyses to examine secondhand smoke exposure as measured by the proportion of nonsmokers with undetectable levels of cotinine and by geometric mean cotinine. (bath.ac.uk)
  • Some of the behavioral effects of cotinine compared to nicotine are discussed here. (frontiersin.org)
  • Altogether, the new evidence suggests that the pharmacological and behavioral effects of cotinine may play a key role in promoting tobacco smoking in individuals that suffer from psychiatric conditions and represents a new potential therapeutic agent against psychiatric conditions such as AD and PTSD. (frontiersin.org)
  • The decrease in neuroinflammation induced by the stimulation of the cholinergic system seems to be a key element explaining the beneficial effects of cotinine in a diverse range of neurological and psychiatric conditions. (eurekaselect.com)
  • There is some research being done on the effects of cotinine on memory and cognition. (chemeurope.com)
  • The presence of cotinine is depicted on easy to read, color labeled test strips. (testcountry.com)
  • How long after smoking cigarettes can this test detect the presence of cotinine? (testcountry.com)
  • The presence of cotinine in saliva or urine is a reliable indicator for tobacco use within the past several days. (confirmbiosciences.com)
  • Among nonsmokers, the presence of cotinine in serum indicates exposure to secondhand tobacco smoke. (cdc.gov)
  • Since 1988 these have incorporated measures of saliva cotinine concentration in a random half of the schools surveyed. (bmj.com)
  • A weak mitogenic effect was observed at a low serum concentration for cotinine but not nicotine. (biomedsearch.com)
  • Measuring tobacco smoke exposure: Quantifying nicotine/cotinine concentration in biological samples by colorimetry, chromatography and immunoassay methods. (salimetrics.com)
  • Serum cotinine concentration and wound complication in head and neck reconstruction. (scielo.org.za)
  • Upon the addition of the substrate, the intensity of color is inversely proportional to the concentration of Cotinine in the samples obtained with the Cotinine blood test. (calbiotech.com)
  • A standard curve is prepared relating color intensity to the concentration of the Cotinine. (calbiotech.com)
  • Relation of passive smoking as assessed by salivary cotinine concentration and questionnaire to spirometric indices in children. (bmj.com)
  • The effects of passive exposure to smoke on lung function were assessed by means of both salivary cotinine concentration and questionnaire measurements of exposure. (bmj.com)
  • RESULTS: Cotinine concentration was negatively associated with all spirometric indices after adjustment for confounding variables, which included age, sex, body size, and social class. (bmj.com)
  • In children aged 5-7 years the use of a single salivary cotinine concentration as a marker of passive exposure to smoke resulted in clear relationships between exposure and FVC and FEV1, whereas the associations were much weaker and not significant when based on the questionnaire score. (bmj.com)
  • The associations between exposure and mid or end expiratory flow rates were of similar magnitude for cotinine concentration and the questionnaire score. (bmj.com)
  • The use of salivary cotinine concentration in longitudinal studies may help to determine the extent to which these effects are cumulative or reversible. (bmj.com)
  • Urinary cotinine concentration was used as a biomarker for SHS exposure. (biomedcentral.com)
  • In the present study, urinary cotinine concentration data from the Korean National Environmental Health Survey (KoNEHS) I, conducted by the National Institute of Environmental Research and the Ministry of Environment as a national bio-monitoring program, were used. (biomedcentral.com)
  • The half-life of cotinine in plasma has been estimated to be about 15-20 hrs (Jarvis et al. (cdc.gov)
  • 1990). Cotinine may be measured in serum, urine or saliva - the half-life of cotinine in all three fluids is essentially the same. (cdc.gov)
  • The average half-life of nicotine is two hours, while the half-life of cotinine is 15 hours. (reference.com)
  • Cotinine can also be easily detected with a cotinine saliva drug test such as our iScreen OFD Saliva Cotinine Test Kit , which can be administered with or without a private bathroom. (testcountry.com)
  • If you're in need of a cotinine test kit for zero tolerance policies or for use in your law enforcement agency, you'll love the iScreen OFD Saliva Cotinine Test Kit. (testcountry.com)
  • When you need an accurate cost-effective nicotine drug test, try the iScreen OFD Saliva Cotinine Test Kit. (testcountry.com)
  • Drug tests can detect cotinine in the blood, urine, or saliva. (wikipedia.org)
  • Which drug test methods can detect cotinine? (testcountry.com)
  • The same immunoassay technology that is used to detect illicit drugs in urine can also be used to detect cotinine in urine. (homehealthtesting.com)
  • Cotinine is actually a more reliable way to detect nicotine use than actually testing nicotine itself. (homehealthtesting.com)
  • The present study is unique, because the urine cotinine measurement was employed to detect nicotine exposure, also in regard to smoking intensity. (nel.edu)
  • Some years ago, while evaluating a novel 5-minute point-of-care urine test for cotinine and the other nicotine metabolites called SmokeScreen, I attended two hospital antenatal clinics in Birmingham and gathered information about smoking-habit from 800+ pregnant women at their 'booking' visit. (bmj.com)
  • Drug tests for nicotine use will screen for cotinine metabolites as the most reliable indicator of exposure to tobacco. (testcountry.com)
  • Cotinine metabolites produced by the body can be traced in urine and saliva specimens. (testcountry.com)
  • Exposure to tobacco smoke can be detected by measuring nicotine and its metabolites using a Cotinine test. (calbiotech.com)
  • When a person uses tobacco, the body immediately breaks nicotine down into about 97 different metabolites, the most stable of which is cotinine. (homehealthtesting.com)
  • Nicotine metabolites, such as cotinine, are judged to be the best biochemical test for smoking behaviour [ 2 ]. (ersjournals.com)
  • We would like to take this opportunity to describe a new point of care saliva test, which measures cotinine and the other nicotine metabolites. (ersjournals.com)
  • Cotinine, the most common biomarker for nicotine exposure analysis, and is primarily measured in smoking cessation studies, e-cigarette and public health research, and to assess second-hand smoke exposure in children. (salimetrics.com)
  • Cotinine is a preferred biomarker to evaluate tobacco use, because it maintains a half-life of up to 16-hours, as opposed to nicotine's half-life of just several hours. (salimetrics.com)
  • Cotinine as a biomarker of environmental tobacco smoke exposure. (salimetrics.com)
  • To validate a detailed questionnaire for assessment of environmental tobacco smoke (ETS) exposure by the biomarker cotinine in various media, a population-based study in the urban area of Malmo, Sweden was performed in children aged 8-13 years with and without asthmatic symptoms. (lu.se)
  • Cotinine is used as a biomarker for exposure to tobacco smoke. (ammonlabs.com)
  • A donor might test positive for cotinine or nicotine if they frequently use smoking cessation products, e.g. patches, gum, nasal sprays, electronic cigarettes, etc. (testcountry.com)
  • Will tobacco users and nicotine users (like e cigs) test positive for cotinine? (healthtap.com)
  • If no line appears at all in the 'T' Region then the sample is positive for cotinine, or in other words, positive for nicotine. (homehealthtesting.com)
  • Incorporation of a point-of-care cotinine test into routine community care to reduce smoking in pregnancy - a pilot study. (bmj.com)
  • VALLEY COTTAGE, N.Y. - According to a new market research report by Future Market Insights, the global cotinine screening devices market was valued at ~US$ 375 Mn in 2018, and is expected to increase at a CAGR of ~5% during the forecast period of 2019-2029. (pharmiweb.com)
  • As per the findings of the report, the global cotinine screening devices market is projected to experience a significant growth over the forecast period, which will be set in motion by a slew of factors such as growing focus on 'value-driven' healthcare services and high demand for effective screening techniques. (pharmiweb.com)
  • However, developing markets are expected to project lucrative growth in the global cotinine screening devices market in the forecast period of 2019-2029. (pharmiweb.com)
  • By device type, the cassettes are expected to hold prominent value shares of the global cotinine screening devices market. (pharmiweb.com)
  • The global cotinine screening devices market is significantly consolidated with a chunk of players commanding prominent shares of the market. (pharmiweb.com)
  • The global cotinine screening devices market size in 2018 was ~US$ 375 Mn. (futuremarketinsights.com)
  • The global cotinine screening devices market is expected to grow at a CAGR of ~5% in the forecast period 2019-2029. (futuremarketinsights.com)
  • The iScreen Cotinine Test Kit provides results in as little as 10 minutes. (testcountry.com)
  • The iScreen OFD Cotinine test device is a rapid, oral fluid drug test that can be performed anytime and almost anywhere. (confirmbiosciences.com)
  • The iScreen cotinine saliva test requires minimal training to use and the results are accurate and easy to interpret. (confirmbiosciences.com)
  • The iScreen® OFD - Cotinine device is a rapid, oral fluid screening test that can be performed anytime without the use of an instrument. (confirmbiosciences.com)
  • For example, if the measurement of cotinine (plasma half-life of 19-24 hours) was performed on the first working day after a weekend in a subject exposed to secondhand smoke only at workplace, the measurement might be by far different of another performed in a midweek working day. (ahajournals.org)
  • Cotinine also permits the measurement of exposure to second-hand smoke (passive smoking). (depression-guide.com)
  • The Salimetrics Cotinine Enzyme Immunoassay Kit is a competitive immunoassay specifically designed and validated for the quantitative measurement of salivary Cotinine. (salimetrics.com)
  • The detection of exposure to tobacco smoke by measurement of Cotinine is the preferred method. (salimetrics.com)
  • At this time, cotinine measurement has not been routinely used in clinical settings mainly due to the time involved, the methods required to collect the sample, and the cost and inconvenience of sending samples to laboratories. (aacrjournals.org)
  • With saliva providing very readily obtained source, measurement of salivary or even urinary cotinine values were used to validate 'self reported' smoking status. (johnyfit.com)
  • We found no association between serum cotinine level (range, 0.1-9.9 ng/mL) and lung cancer risk among self-reported nonsmokers and long-term quitters (79 cases and 350 controls). (aacrjournals.org)
  • Measuring cotinine is preferred to measuring nicotine because cotinine remains in the body longer. (cdc.gov)
  • You may need to take a cotinine test if you're applying for a job at a company that prohibits smoking. (baycare.org)
  • The factors such as growing prevalence of smoking, screening employees for illicit drugs, sporting events, and deciding the health plan premium are anticipated to surge the sales of cotinine screening devices in developing counties. (pharmiweb.com)
  • Adoption of screening techniques during the employee hiring process and to calculate insurance plans is increasing the demand for compact portable diagnostic kits, and subsequently driving the sales of cotinine screening devices. (futuremarketinsights.com)
  • The rate of metabolism of nicotine and cotinine depends on the genetic makeup of the individual. (reference.com)
  • 1. Collect DNA for exploratory analyses regarding genetic causes of differences in metabolism of nicotine and cotinine. (clinicaltrials.gov)
  • Biomonitoring studies of serum cotinine will help physicians and public health officials in monitoring population exposure to tobacco smoke and assessing the effectiveness of public health interventions to reduce smoking. (cdc.gov)
  • Urine cotinine testing is the preferred method to measure passive exposure to tobacco. (testcountry.com)
  • Fetal exposure to tobacco was studied by measuring cotinine in cord blood by radioimmunoassay (RIA). (biomedcentral.com)
  • Serum cotinine is measured by an isotope dilution-high performance liquid chromatography / atmospheric pressure chemical ionization tandem mass spectrometry (ID HPLC-APCI MS/MS). Briefly, the serum sample is spiked with methyl-D3 cotinine as an internal standard, and after an equilibration period, the sample is applied to a basified solid-phase extraction column. (cdc.gov)
  • Blood samples obtained at enrollment were tested for total cotinine using gas chromatography/mass spectrometry. (biomedsearch.com)
  • Paper spray tandem mass spectrometry (PS-MS/MS) is proposed and validated as a simple and rapid method for quantification of nicotine and cotinine in complex matrices to support tobacco-related research. (rsc.org)
  • Methods: We analyzed salivary cotinine data from the Health Survey for England that were collected in 7 of 11 annual surveys undertaken between 1998 and 2008. (bath.ac.uk)
  • When using the Salimetrics Cotinine EIA cut points should be adjusted accordingly. (salimetrics.com)
  • Among children whose caregivers reported no tobacco exposure, 39.1% had detectable serum cotinine and 69.9% had detectable salivary cotinine. (nih.gov)
  • Of the children with reported exposure, 87.6% had detectable serum cotinine and 97.7% had detectable salivary cotinine. (nih.gov)
  • We tested DBS from 10 infants whose mothers had detectable serum cotinine at baseline and 10 control infants whose mothers had none. (biomedsearch.com)
  • Cotinine has a longer plasma half-life than nicotine and showed no addictive or cardiovascular effects in humans. (frontiersin.org)
  • Furthermore, the use of serum cotinine rather than questionnaire data to measure tobacco exposure integrates different aspects of the exposure, including tobacco composition, uptake, distribution, and individual differences in metabolism ( 9 ). (aacrjournals.org)
  • A composite questionnaire score based on the number of regular sources of exposure was as strongly related to mid and end expiratory flow rates as the single cotinine measure. (bmj.com)
  • Upon receipt, vials were stored at -4°C for a few days and then shipped by express mail to ABS Laboratories (Welwyn Garden City, UK) for cotinine analysis by gas chromatography. (ersjournals.com)
  • Scanning electron microscopy is used to study the morphology of the film compared with the unimprinted control, and gas chromatography quantitatively confirms that the imprinted film selectively detects cotinine while discriminating against the structurally similar alkaloid, nicotine. (scienceopen.com)
  • Detection of cotinine in newborn dried blood spots. (biomedsearch.com)
  • The Calbiotech Cotinine Direct ELISA Kit is designed for the detection of Cotinine in serum and urine. (calbiotech.com)
  • This has majorly resulted from the cost effectiveness, ease of screening, quick detection, and portability of these compact cotinine screening devices. (pharmiweb.com)
  • The detection period for cotinine (the nicotine metabolite tested) can be as long as 15 days or more depending on the sensitivity of the specific testing method used by the laboratory. (justanswer.com)
  • Although the contribution of nicotine to ACTE-mediated 2E1 inhibition is probably modest, pyridine alkaloid-mediated CYP 2E1 inhibition is a possible mechanism for the observed inhibition of NNK and NDMA mutagenicity by nicotine and cotinine in vitro. (usu.edu)
  • Cotinine remains in the body for an extended period of time as a result of direct or secondhand smoke exposure. (testcountry.com)
  • PURPOSE: This randomized study will compare education only to education plus cotinine feedback in decreasing secondhand smoke exposure in pediatric patients with cancer that reside with a household smoker. (clinicaltrials.gov)
  • Those randomized to the active intervention will receive education about secondhand smoke exposure and feedback using the cotinine test strip. (clinicaltrials.gov)
  • When a person has reported that he or she is using nicotine replacement products but is no longer smoking, nicotine, cotinine, and urine anabasine measurements may sometimes be ordered. (labcorp.com)
  • This study demonstrated that cotinine measurements could be carried out rapidly and easily in an antenatal setting and repeat measurements were carried out at subsequent appointments to monitor changes to smoking behaviour following advice to quit. (bmj.com)
  • It is not reported whether cotinine assessment was performed on the same day of BP measurements. (ahajournals.org)
  • Since cotinine can be made only from nicotine, and since nicotine enters the body with cigarette smoke, cotinine measurements can show how much cigarette smoke enters your body. (depression-guide.com)
  • From blood and urine measurements, the following were determined: clearance (renal and nonrenal) of nicotine and cotinine, clearance of nicotine via the cotinine pathway (an indicator of CYP2A6 activity), and daily intake of nicotine from smoking. (aspetjournals.org)
  • However, cotinine measurements are largely confined to sophisticated laboratory tests, which are expensive and time consuming. (ersjournals.com)
  • When a person enters a smoking cessation program, blood or urine cotinine tests may be ordered to evaluate his or her compliance. (labcorp.com)
  • Since smoking cessation products contain trace amounts of nicotine, they can trigger positive results on a nicotine/cotinine drug test. (testcountry.com)
  • Cotinine, due to its longer half life, has been used in research as a reliable marker for smoking status and smoking cessation studies. (calbiotech.com)
  • Cotinine screening devices are used in the insurance sector, for smoking cessation programs, and at rehabilitation centres. (futuremarketinsights.com)
  • This can have a significant impact on the rate of cotinine metabolism. (reference.com)
  • This test measures the amount of cotinine in your urine. (baycare.org)
  • The amount of Cotinine Enzyme Conjugate detected is inversely proportional to the amount of Cotinine present in the sample. (salimetrics.com)

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