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.Tobacco Smoke Pollution: Contamination of the air by tobacco smoke.Nicotine: 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.Smoking: Inhaling and exhaling the smoke of burning TOBACCO.Saliva: The clear, viscous fluid secreted by the SALIVARY GLANDS and mucous glands of the mouth. It contains MUCINS, water, organic salts, and ptylin.Pyrrolidinones: A group of compounds that are derivatives of oxo-pyrrolidines. A member of this group is 2-oxo pyrrolidine, which is an intermediate in the manufacture of polyvinylpyrrolidone. (From Merck Index, 11th ed)Nitrosamines: A class of compounds that contain a -NH2 and a -NO radical. Many members of this group have carcinogenic and mutagenic properties.Ganglionic Stimulants: Agents that mimic neural transmission by stimulation of the nicotinic receptors on postganglionic autonomic neurons. Drugs that indirectly augment ganglionic transmission by increasing the release or slowing the breakdown of acetylcholine or by non-nicotinic effects on postganglionic neurons are not included here nor are the nonspecific cholinergic agonists.Nicotinic Agonists: 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.Biological Markers: Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.Tars: Viscous materials composed of complex, high-molecular-weight compounds derived from the distillation of petroleum or the destructive distillation of wood or coal. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Environmental Exposure: The exposure to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals.Tobacco Use Disorder: Tobacco used to the detriment of a person's health or social functioning. Tobacco dependence is included.Smoking Cessation: Discontinuation of the habit of smoking, the inhaling and exhaling of tobacco smoke.Self Disclosure: A willingness to reveal information about oneself to others.Aryl Hydrocarbon Hydroxylases: A large group of cytochrome P-450 (heme-thiolate) monooxygenases that complex with NAD(P)H-FLAVIN OXIDOREDUCTASE in numerous mixed-function oxidations of aromatic compounds. They catalyze hydroxylation of a broad spectrum of substrates and are important in the metabolism of steroids, drugs, and toxins such as PHENOBARBITAL, carcinogens, and insecticides.Anabasine: A piperidine botanical insecticide.Carbon Monoxide: Carbon monoxide (CO). A poisonous colorless, odorless, tasteless gas. It combines with hemoglobin to form carboxyhemoglobin, which has no oxygen carrying capacity. The resultant oxygen deprivation causes headache, dizziness, decreased pulse and respiratory rates, unconsciousness, and death. (From Merck Index, 11th ed)Glucuronides: 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.Maternal Exposure: Exposure of the female parent, human or animal, to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals that may affect offspring. It includes pre-conception maternal exposure.Meconium: The thick green-to-black mucilaginous material found in the intestines of a full-term fetus. It consists of secretions of the INTESTINAL GLANDS; BILE PIGMENTS; FATTY ACIDS; AMNIOTIC FLUID; and intrauterine debris. It constitutes the first stools passed by a newborn.Tobacco Use Cessation Products: Items used to aid in ending a TOBACCO habit.Tandem Mass Spectrometry: A mass spectrometry technique using two (MS/MS) or more mass analyzers. With two in tandem, the precursor ions are mass-selected by a first mass analyzer, and focused into a collision region where they are then fragmented into product ions which are then characterized by a second mass analyzer. A variety of techniques are used to separate the compounds, ionize them, and introduce them to the first mass analyzer. For example, for in GC-MS/MS, GAS CHROMATOGRAPHY-MASS SPECTROMETRY is involved in separating relatively small compounds by GAS CHROMATOGRAPHY prior to injecting them into an ionization chamber for the mass selection.Chromatography, Liquid: Chromatographic techniques in which the mobile phase is a liquid.Glucuronates: 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.

*  IJERPH | Free Full-Text | Utility and Cutoff Value of Hair Nicotine as a Biomarker of Long-Term Tobacco Smoke Exposure,...

... compared with salivary cotinine, is still limited. We conducted a cross-sectional study with 289 participants (107 active ... while those for salivary cotinine were 181.0, 0.27, and 0.27 ng/mL, respectively. Hair nicotine concentrations for 10% of ... passive or non-smokers were higher than the 25th percentile value for active smokers while all corresponding salivary cotinine ... and hair nicotine characterizes tobacco exposure over a longer time period than blood or urine cotinine, information on its ...

*  ChemIDplus - 486-56-6 - UIKROCXWUNQSPJ-VIFPVBQESA-N - Cotinine [INN] - Similar structures search, synonyms, formulas, resource...

Cotinine [INN] - Similar structures search, synonyms, formulas, resource links, and other chemical information. ... Substance Name: Cotinine [INN]. RN: 486-56-6. UNII: K5161X06LL. InChIKey: UIKROCXWUNQSPJ-VIFPVBQESA-N. Note. *. The N- ... glucuronide conjugate of cotinine is a major urinary metabolite of NICOTINE. It thus serves as a biomarker of exposure to ...

*  Plus it

... or high serum cotinine levels. We used three definitions for secondhand smoke-maternal smoking during pregnancy, smoking in the ... and biomarkers such as serum cotinine levels were not available in this study. In particular, the prevalence of maternal ...

*  The Rest of the Story: Tobacco News Analysis and Commentary: Study on Cotinine Levels Among NYC Adults Being Used to Implicate...

Study on Cotinine Levels Among NYC Adults Being Used to Implicate Importance of Brief Tobacco Smoke Exposure on Sidewalks and ... The equipment used in the NYC NHANES had a level of detection of 0.05 ng/mL cotinine. The equipment used in NHANES was newer ... My point is not that the overall cotinine analysis was in any way invalid; it is simply that a conclusion drawn based on an ... In the national sample, the definition of exposure was a cotinine level of greater than 0.05 ng/mL.. These are two very ...

*  How long does it take to get cotinine out of your body? - Kgb Answers

The only way to reduce your cotinine level is to stop smoking. Depending on how high your level is to begin with, it could drop ... How long does it take to get cotinine out of your body? The KGB Agent answer: ... How long does it take to get cotinine out of your body?. kgb answers » Health & Body » Health & Fitness » How long does it take ... The only way to reduce your cotinine level is to stop smoking. Depending on how high your level is to begin with, it could drop ...

*  NIOSHTIC-2 Publications Search - 20042806 - Serum cotinine levels and prehypertension in never smokers.

... measured objectively by serum cotinine levels, and high blood pressure in never smokers. Methods. We examined never smokers ... Compared to those with cotinine levels in the lowest quartile (.0.024 ng/mL), the multivariable odds ratio (95% confidence ... Our exposure of interest was the secondhand smoke exposure estimated by serum cotinine level and our outcome was ... We found that, in never smokers, serum cotinine levels were positively associated with prehypertension. ...

*  Exposure to secondhand smoke and cognitive impairment in non-smokers: national cross sectional study with cotinine measurement ...

However, cotinine levels have proved to be a useful marker of general levels of exposure to secondhand smoke.37 38 We analysed ... Cotinine measurements were obtained for most of the eligible non-smoking participants in the Health Survey for England waves ... Median salivary cotinine levels were low. The patterns of potential confounders observed were in keeping with the general ... We used levels of salivary cotinine (ng/ml) measured in the Health Survey for England as a biomarker for recent exposure to ...

*  LC-MS-MS Measurements of Urinary Creatinine and the Application of Creatinine Normalization Technique on Cotinine in Smokers'...

LC-MS-MS Measurements of Urinary Creatinine and the Application of Creatinine Normalization Technique on Cotinine in Smokers' ... "LC-MS-MS Measurements of Urinary Creatinine and the Application of Creatinine Normalization Technique on Cotinine in Smokers' ...

*  Nicotine and Cotinine, LC/MS/MS, Serum/Plasma - Quest Diagnostics Nichols Institute of Valencia

Cotinine, the major nicotine metabolite, has a half-life of 24 hours and is detectable for several days after cessation of ... This assay is used for the detection of nicotine and cotinine in serum and plasma to determine the tobacco exposure status of ...

*  cotinine in Chinese translation

... , English Chinese dictionary, English Chinese translation, with pronunciation, a lot of example ... Cotinine has a24- hour half-life, so you can test whether or not someone has been smoking in the past day or two by screening ...

*  Cotinine Testing

Maryland cotinine test for Tobacco. Some jobs or insurance test for tobacco use. Be proactive at ARCpoint Labs of Southern ... Cotinine and Nicotine. The word "cotinine" is an anagram of the word "nicotine." Cotinine is a substance produced in the liver ... Why Test for Cotinine?. Cotinine testing works to tell whether someone is a current tobacco user, and also whether they have ... So a test for cotinine is a way to test for nicotine use. Employers may test for cotinine to affirm an applicant's statement of ...

*  Exposure to tobacco smoke based on urinary cotinine levels among Israeli smoking and nonsmoking adults: a cross-sectional...

All participants, smokers and nonsmokers, had urinary cotinine levels , LOD. The distribution of cotinine concentration levels ... Urinary cotinine, especially when corrected for creatinine concentration, is highly correlated with plasma cotinine [9]. ... However, urinary cotinine levels give better estimates of ETS and we were able to confirm our findings by data from the 2010 ... Cotinine was shown in the past to be derived from exposure to tobacco smoking, while other sources, such as dietary sources, ...

*  S)-(-)-Cotinine | C10H12N2O | ChemSpider

Cotinine;(S)-Co. tinine;NIH-10498 (5S)-(-)-1-Methyl-5. -(pyridin-3-yl)pyrr. olidin-2-one; 3-[(2. S)-(-)-1-Methyl-5-o. ... Cotinine is an alkaloid found in tobacco and is also the predominant metabolite of nicotine, used as a biomarker for exposure ...

*  "Comparison of Serum Cotinine Concentration within and across Smokers of Menthol and Nonmenthol Cigarette Brands among Non...

Comparison of Serum Cotinine Concentration within and across Smokers of Menthol and Nonmenthol Cigarette Brands among Non- ... "Comparison of Serum Cotinine Concentration within and across Smokers of Menthol and Nonmenthol Cigarette Brands among Non- ...

*  The Association of Pipe and Cigar Use With Cotinine Levels, Lung Function, and Airflow ObstructionA Cross-sectional Study |...

The Association of Pipe and Cigar Use With Cotinine Levels, Lung Function, and Airflow Obstruction: A Cross-sectional Study ... The Association of Pipe and Cigar Use With Cotinine Levels, Lung Function, and Airflow Obstruction: A Cross-sectional Study. ... Pipe and cigar smoking increased urine cotinine levels and was associated with decreased lung function and increased odds of ... To determine whether pipe and cigar smoking was associated with elevated cotinine levels, decrements in lung function, and ...

*  Cotinine-d3 - Alfa Chemistry

Cotinine-d3/AFI110952700 can be provided in Alfa Chemistry. We are dedicated to provide our customers the best products and ...

*  Cotinine-4-BSA (1 MG) - BioSell Solutions

Thank you for visiting bioSell Solutions Inc., we look forward to working with you to solve problems, in addition to provide excellent products and services. ...

*  Cotinine-N-alpha-D-glucuronide - Alfa Chemistry

Cotinine-N-alpha-D-glucuronide/AFI139427579 can be provided in Alfa Chemistry. We are dedicated to provide our customers the ...

Smokefree Environments Amendment Act 2003: The Smokefree Environments Amendment Bill was passed by the Parliament of New Zealand on 3 December 2003. The smoking ban legislation calls for progressive introduction of various clauses to totally ban smoking in all workplaces including offices, clubs, pubs, restaurants, airports, schools etc.Nicotine replacement therapySaliva testing: Saliva testing is a diagnostic technique that involves laboratory analysis of saliva to identify markers of endocrine, immunologic, inflammatory, infectious, and other types of conditions. Saliva is a useful biological fluid for assaying steroid hormones such as cortisol, genetic material like RNA, proteins such as enzymes and antibodies, and a variety of other substances, including natural metabolites, including saliva nitrite, a biomarker for nitric oxide status (see below for Cardiovascular Disease, Nitric Oxide: a salivary biomarker for cardio-protection).Nitrosamine: Nitrosamines are chemical compounds of the chemical structure R1N(-R2)-N=O, that is, a nitroso group bonded to an amine. Most nitrosamines are carcinogenic.SIB-1553ABiomarkers of aging: Biomarkers of aging are biomarkers that better predict functional capacity at a later age than chronological age. Stated another way, biomarkers of aging would give the true "biological age", which may be different from the chronological age.Lights (cigarette type): Cigarettes labeled as “Lights,” “Milds,” or “Low-tar,” are considered to have a “lighter,” less pronounced flavour than regular cigarettes. These cigarette brands may also contain lower levels of tar, nicotine, or other chemicals inhaled by the smoker.Tobacco cessation clinicAnatabineBreath carbon monoxide: Breath carbon monoxide is the level of carbon monoxide in a person's exhalation. It can be measured in a breath carbon monoxide test, generally by using a carbon monoxide breath monitor (breath CO monitor), such as for motivation and education for smoking cessation and also as a clinical aid in assessing carbon monoxide poisoning.Tandem mass spectrometry: 300 px|right|thumb|A [[Quadrupole mass analyzer|quadrupole time-of-flight hybrid tandem mass spectrometer.]]

(1/809) (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.

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)

(2/809) 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)

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)

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

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)

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

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)

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

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)

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

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)

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

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)

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

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)



serum cotinine

  • Serum cotinine levels and prehypertension in never smokers. (cdc.gov)
  • 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. (cdc.gov)
  • We found that, in never smokers, serum cotinine levels were positively associated with prehypertension. (cdc.gov)

nicotine

  • Our studies will use the nicotine metabolite ratio (NMR) (the ratio between the nicotine metabolites 3'hydroxycotinine and cotinine)as a simple and clinically feasible biomarker for the rate of nicotine metabolism. (clinicaltrials.gov)
  • While hair samples are easier to collect and less expensive to store and transport than biological fluids, and hair nicotine characterizes tobacco exposure over a longer time period than blood or urine cotinine, information on its utility, compared with salivary cotinine, is still limited. (mdpi.com)
  • Hair nicotine concentrations for 10% of passive or non-smokers were higher than the 25th percentile value for active smokers while all corresponding salivary cotinine concentrations for them were lower than the value for active smokers. (mdpi.com)
  • Urinary levels of cotinine, total NNAL, total NNN, and 1-hydroxypyrene (1-HOP) - biomarkers of exposure to nicotine, NNK, NNN, and polycyclic aromatic hydrocarbons (PAH), respectively - were measured at baseline and after one week of smoking MVB. (aacrjournals.org)
  • Cotinine, the primary proximate metabolite of nicotine, is used most frequently as a biomarker of tobacco smoke exposure, as its half-life is longer (approximately 16-18 hours) and levels remain fairly constant during the day. (biomedcentral.com)

smokers

  • We calculated creatinine-adjusted urinary cotinine geometric means (GM) among smokers and nonsmokers, and by socio-demographic, smoking habits and dietary factors. (biomedcentral.com)

Urinary

  • We analyzed urinary cotinine data from the first Israeli human biomonitoring study conducted in 2011. (biomedcentral.com)
  • We analyzed associations, in a univariable and multivariable analysis, between socio-demographic variables and proportions of urinary cotinine ≥1 μg/l (Limit of Quantification = LOQ) or ≥4 μg/l. (biomedcentral.com)

Exposure

  • Cotinine levels provide a valid measure of exposure to environmental tobacco smoke (ETS). (biomedcentral.com)

levels

  • Cotinine levels were measured using a gas chromatography-mass spectrometry procedure. (biomedcentral.com)