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.
Contamination of the air by tobacco smoke.
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.
Inhaling and exhaling the smoke of burning TOBACCO.
The clear, viscous fluid secreted by the SALIVARY GLANDS and mucous glands of the mouth. It contains MUCINS, water, organic salts, and ptylin.
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)
A class of compounds that contain a -NH2 and a -NO radical. Many members of this group have carcinogenic and mutagenic properties.
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.
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.
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.
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)
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 used to the detriment of a person's health or social functioning. Tobacco dependence is included.
Discontinuation of the habit of smoking, the inhaling and exhaling of tobacco smoke.
A willingness to reveal information about oneself to others.
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.
A piperidine botanical insecticide.
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)
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.
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.
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.
Items used to aid in ending a TOBACCO habit.
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.
Chromatographic techniques in which the mobile phase is a liquid.
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.

(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)

Cotinine is the major metabolite of nicotine, which is formed in the body after exposure to tobacco smoke or other sources of nicotine. It is often used as a biomarker for nicotine exposure and can be measured in various biological samples such as blood, urine, saliva, and hair. Cotinine has a longer half-life than nicotine, making it a more reliable indicator of long-term exposure to tobacco smoke or nicotine products.

Tobacco smoke pollution is not typically defined in medical terms, but it refers to the presence of tobacco smoke in indoor or outdoor environments, which can have negative effects on air quality and human health. It is also known as secondhand smoke or environmental tobacco smoke (ETS). This type of smoke is a mixture of sidestream smoke (the smoke given off by a burning cigarette) and mainstream smoke (the smoke exhaled by a smoker).

The medical community recognizes tobacco smoke pollution as a serious health hazard. It contains more than 7,000 chemicals, hundreds of which are toxic and about 70 that can cause cancer. Exposure to tobacco smoke pollution can cause a range of adverse health effects, including respiratory symptoms, lung cancer, heart disease, and stroke. In children, it can also lead to ear infections, asthma attacks, and sudden infant death syndrome (SIDS).

Therefore, many laws and regulations have been implemented worldwide to protect people from tobacco smoke pollution, such as smoking bans in public places and workplaces.

Nicotine is defined as a highly addictive psychoactive alkaloid and stimulant found in the nightshade family of plants, primarily in tobacco leaves. It is the primary component responsible for the addiction to cigarettes and other forms of tobacco. Nicotine can also be produced synthetically.

When nicotine enters the body, it activates the release of several neurotransmitters such as dopamine, norepinephrine, and serotonin, leading to feelings of pleasure, stimulation, and relaxation. However, with regular use, tolerance develops, requiring higher doses to achieve the same effects, which can contribute to the development of nicotine dependence.

Nicotine has both short-term and long-term health effects. Short-term effects include increased heart rate and blood pressure, increased alertness and concentration, and arousal. Long-term use can lead to addiction, lung disease, cardiovascular disease, and reproductive problems. It is important to note that nicotine itself is not the primary cause of many tobacco-related diseases, but rather the result of other harmful chemicals found in tobacco smoke.

Smoking is not a medical condition, but it's a significant health risk behavior. Here is the definition from a public health perspective:

Smoking is the act of inhaling and exhaling the smoke of burning tobacco that is commonly consumed through cigarettes, pipes, and cigars. The smoke contains over 7,000 chemicals, including nicotine, tar, carbon monoxide, and numerous toxic and carcinogenic substances. These toxins contribute to a wide range of diseases and health conditions, such as lung cancer, heart disease, stroke, chronic obstructive pulmonary disease (COPD), and various other cancers, as well as adverse reproductive outcomes and negative impacts on the developing fetus during pregnancy. Smoking is highly addictive due to the nicotine content, which makes quitting smoking a significant challenge for many individuals.

Saliva is a complex mixture of primarily water, but also electrolytes, enzymes, antibacterial compounds, and various other substances. It is produced by the salivary glands located in the mouth. Saliva plays an essential role in maintaining oral health by moistening the mouth, helping to digest food, and protecting the teeth from decay by neutralizing acids produced by bacteria.

The medical definition of saliva can be stated as:

"A clear, watery, slightly alkaline fluid secreted by the salivary glands, consisting mainly of water, with small amounts of electrolytes, enzymes (such as amylase), mucus, and antibacterial compounds. Saliva aids in digestion, lubrication of oral tissues, and provides an oral barrier against microorganisms."

Pyrrolidinones are a class of organic compounds that contain a pyrrolidinone ring, which is a five-membered ring containing four carbon atoms and one nitrogen atom. The nitrogen atom is part of an amide functional group, which consists of a carbonyl (C=O) group bonded to a nitrogen atom.

Pyrrolidinones are commonly found in various natural and synthetic compounds, including pharmaceuticals, agrochemicals, and materials. They exhibit a wide range of biological activities, such as anti-inflammatory, antiviral, and anticancer properties. Some well-known drugs that contain pyrrolidinone rings include the pain reliever tramadol, the muscle relaxant cyclobenzaprine, and the antipsychotic aripiprazole.

Pyrrolidinones can be synthesized through various chemical reactions, such as the cyclization of γ-amino acids or the reaction of α-amino acids with isocyanates. The unique structure and reactivity of pyrrolidinones make them valuable intermediates in organic synthesis and drug discovery.

Nitrosamines are a type of chemical compound that are formed by the reaction between nitrous acid (or any nitrogen oxide) and secondary amines. They are often found in certain types of food, such as cured meats and cheeses, as well as in tobacco products and cosmetics.

Nitrosamines have been classified as probable human carcinogens by the International Agency for Research on Cancer (IARC). Exposure to high levels of nitrosamines has been linked to an increased risk of cancer, particularly in the digestive tract. They can also cause DNA damage and interfere with the normal functioning of cells.

In the medical field, nitrosamines have been a topic of concern due to their potential presence as contaminants in certain medications. For example, some drugs that contain nitrofurantoin, a medication used to treat urinary tract infections, have been found to contain low levels of nitrosamines. While the risk associated with these low levels is not well understood, efforts are underway to minimize the presence of nitrosamines in medications and other products.

Ganglionic stimulants are a type of medication that act on the ganglia, which are clusters of nerve cells located outside the central nervous system. These medications work by stimulating the ganglia, leading to an increase in the transmission of nerve impulses and the activation of various physiological responses.

Ganglionic stimulants were once used in the treatment of conditions such as asthma, bronchitis, and cardiovascular disease. However, their use has largely been discontinued due to the development of safer and more effective treatments. These medications can have significant side effects, including increased heart rate and blood pressure, dizziness, headache, and in rare cases, seizures and coma.

It's important to note that the medical community no longer recommends the use of ganglionic stimulants due to their potential for serious harm. If you have any questions about medications or treatments for a particular condition, it's best to consult with a qualified healthcare professional.

Nicotinic agonists are substances that bind to and activate nicotinic acetylcholine receptors (nAChRs), which are ligand-gated ion channels found in the nervous system of many organisms, including humans. These receptors are activated by the endogenous neurotransmitter acetylcholine and the exogenous compound nicotine.

When a nicotinic agonist binds to the receptor, it triggers a conformational change that leads to the opening of an ion channel, allowing the influx of cations such as calcium, sodium, and potassium. This ion flux can depolarize the postsynaptic membrane and generate or modulate electrical signals in excitable tissues, such as neurons and muscles.

Nicotinic agonists have various therapeutic and recreational uses, but they can also produce harmful effects, depending on the dose, duration of exposure, and individual sensitivity. Some examples of nicotinic agonists include:

1. Nicotine: A highly addictive alkaloid found in tobacco plants, which is the prototypical nicotinic agonist. It is used in smoking cessation therapies, such as nicotine gum and patches, but it can also lead to dependence and various health issues when consumed through smoking or vaping.
2. Varenicline: A medication approved for smoking cessation that acts as a partial agonist of nAChRs. It reduces the rewarding effects of nicotine and alleviates withdrawal symptoms, helping smokers quit.
3. Rivastigmine: A cholinesterase inhibitor used to treat Alzheimer's disease and other forms of dementia. It increases the concentration of acetylcholine in the synaptic cleft, enhancing its activity at nicotinic receptors and improving cognitive function.
4. Succinylcholine: A neuromuscular blocking agent used during surgical procedures to induce paralysis and facilitate intubation. It acts as a depolarizing nicotinic agonist, causing transient muscle fasciculations followed by prolonged relaxation.
5. Curare and related compounds: Plant-derived alkaloids that act as competitive antagonists of nicotinic receptors. They are used in anesthesia to induce paralysis and facilitate mechanical ventilation during surgery.

In summary, nicotinic agonists are substances that bind to and activate nicotinic acetylcholine receptors, leading to various physiological responses. These compounds have diverse applications in medicine, from smoking cessation therapies to treatments for neurodegenerative disorders and anesthesia. However, they can also pose risks when misused or abused, as seen with nicotine addiction and the potential side effects of certain medications.

A biological marker, often referred to as a biomarker, is a measurable indicator that reflects the presence or severity of a disease state, or a response to a therapeutic intervention. Biomarkers can be found in various materials such as blood, tissues, or bodily fluids, and they can take many forms, including molecular, histologic, radiographic, or physiological measurements.

In the context of medical research and clinical practice, biomarkers are used for a variety of purposes, such as:

1. Diagnosis: Biomarkers can help diagnose a disease by indicating the presence or absence of a particular condition. For example, prostate-specific antigen (PSA) is a biomarker used to detect prostate cancer.
2. Monitoring: Biomarkers can be used to monitor the progression or regression of a disease over time. For instance, hemoglobin A1c (HbA1c) levels are monitored in diabetes patients to assess long-term blood glucose control.
3. Predicting: Biomarkers can help predict the likelihood of developing a particular disease or the risk of a negative outcome. For example, the presence of certain genetic mutations can indicate an increased risk for breast cancer.
4. Response to treatment: Biomarkers can be used to evaluate the effectiveness of a specific treatment by measuring changes in the biomarker levels before and after the intervention. This is particularly useful in personalized medicine, where treatments are tailored to individual patients based on their unique biomarker profiles.

It's important to note that for a biomarker to be considered clinically valid and useful, it must undergo rigorous validation through well-designed studies, including demonstrating sensitivity, specificity, reproducibility, and clinical relevance.

"Tars" is not a recognized medical term. However, "tarso-" is a prefix in anatomy that refers to the ankle or hind part of an organ. For example, the tarsal bones are the bones that make up the ankle and the rear part of the foot. Additionally, tarsus can refer to the thickened portion of the eyelid which contains the eyelashes. It is important to ensure you have the correct term when seeking medical information.

Environmental exposure refers to the contact of an individual with any chemical, physical, or biological agent in the environment that can cause a harmful effect on health. These exposures can occur through various pathways such as inhalation, ingestion, or skin contact. Examples of environmental exposures include air pollution, water contamination, occupational chemicals, and allergens. The duration and level of exposure, as well as the susceptibility of the individual, can all contribute to the risk of developing an adverse health effect.

Tobacco Use Disorder is a clinical diagnosis described in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), used by healthcare professionals to diagnose mental health conditions. It is defined as a problematic pattern of tobacco use leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month period:

1. Tobacco is often taken in larger amounts or over a longer period than was intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control tobacco use.
3. A great deal of time is spent on activities necessary to obtain or use tobacco, or recover from its effects.
4. Craving, or a strong desire or urge to use tobacco, occurs.
5. Recurrent tobacco use results in a failure to fulfill major role obligations at work, school, or home.
6. Important social, occupational, or recreational activities are given up or reduced because of tobacco use.
7. Tobacco use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by tobacco.
8. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of tobacco to achieve intoxication or desired effect.
b. Markedly diminished effect with continued use of the same amount of tobacco.
9. Characteristic withdrawal syndrome for tobacco, or tobacco is taken to relieve or avoid withdrawal symptoms.

The diagnosis excludes nicotine withdrawal that is a normal response to the cessation of tobacco use, intoxication, or substance/medication-induced disorders. Tobacco Use Disorder can be further specified as mild, moderate, or severe based on the number of criteria met.

Smoking cessation is the process of discontinuing tobacco smoking. This can be achieved through various methods such as behavioral modifications, counseling, and medication. The goal of smoking cessation is to improve overall health, reduce the risk of tobacco-related diseases, and enhance quality of life. It is a significant step towards preventing lung cancer, heart disease, stroke, chronic obstructive pulmonary disease (COPD), and other serious health conditions.

In a medical or healthcare context, self-disclosure generally refers to the act of a patient voluntarily sharing personal, relevant information about themselves with their healthcare provider. This could include details about their lifestyle, thoughts, feelings, experiences, or symptoms that may be pertinent to their health status or treatment. The purpose of self-disclosure is to enhance the provider's understanding of the patient's condition and facilitate more effective care planning, monitoring, and management. It is essential for building trust, fostering open communication, and promoting a strong therapeutic relationship between patients and healthcare providers.

It is important to note that self-disclosure should be encouraged in a safe, respectful, and confidential environment, where the patient feels comfortable sharing personal information without fear of judgment or negative consequences. Healthcare providers must maintain appropriate professional boundaries while still fostering an atmosphere of trust and collaboration with their patients.

Aryl hydrocarbon hydroxylases (AHH) are a group of enzymes that play a crucial role in the metabolism of various aromatic and heterocyclic compounds, including potentially harmful substances such as polycyclic aromatic hydrocarbons (PAHs) and dioxins. These enzymes are primarily located in the endoplasmic reticulum of cells, particularly in the liver, but can also be found in other tissues.

The AHH enzymes catalyze the addition of a hydroxyl group (-OH) to the aromatic ring structure of these compounds, which is the first step in their biotransformation and eventual elimination from the body. This process can sometimes lead to the formation of metabolites that are more reactive and potentially toxic than the original compound. Therefore, the overall impact of AHH enzymes on human health is complex and depends on various factors, including the specific compounds being metabolized and individual genetic differences in enzyme activity.

Anabasine is a type of toxic alkaloid that can be found in certain plants, including the leaves of the tobacco plant Nicotiana glauca (also known as tree tobacco). It has a similar structure to nicotine and can have similar physiological effects, such as stimulating the nervous system and increasing heart rate. However, anabasine is generally considered to be more toxic than nicotine.

Anabasine can also be produced synthetically in a laboratory. It has been used in research as a tool for studying the mechanisms of nicotinic acetylcholine receptors, which are important targets for drugs that affect the nervous system.

In terms of medical definitions, anabasine is not a term that is commonly used in clinical medicine. It is more likely to be encountered in the context of research or toxicology.

Carbon monoxide (CO) is a colorless, odorless, and tasteless gas that is slightly less dense than air. It is toxic to hemoglobic animals when encountered in concentrations above about 35 ppm. This compound is a product of incomplete combustion of organic matter, and is a major component of automobile exhaust.

Carbon monoxide is poisonous because it binds to hemoglobin in red blood cells much more strongly than oxygen does, forming carboxyhemoglobin. This prevents the transport of oxygen throughout the body, which can lead to suffocation and death. Symptoms of carbon monoxide poisoning include headache, dizziness, weakness, nausea, vomiting, confusion, and disorientation. Prolonged exposure can lead to unconsciousness and death.

Carbon monoxide detectors are commonly used in homes and other buildings to alert occupants to the presence of this dangerous gas. It is important to ensure that these devices are functioning properly and that they are placed in appropriate locations throughout the building. Additionally, it is essential to maintain appliances and heating systems to prevent the release of carbon monoxide into living spaces.

Glucuronides are conjugated compounds formed in the liver by the attachment of glucuronic acid to a variety of molecules, including drugs, hormones, and environmental toxins. This process, known as glucuronidation, is catalyzed by enzymes called UDP-glucuronosyltransferases (UGTs) and increases the water solubility of these compounds, allowing them to be more easily excreted from the body through urine or bile.

Glucuronidation plays a crucial role in the detoxification and elimination of many substances, including drugs and toxins. However, in some cases, glucuronides can also be hydrolyzed back into their original forms by enzymes called β-glucuronidases, which can lead to reabsorption of the parent compound and prolong its effects or toxicity.

Overall, understanding the metabolism and disposition of glucuronides is important for predicting drug interactions, pharmacokinetics, and potential adverse effects.

"Maternal exposure" is a medical term that refers to the contact or interaction of a pregnant woman with various environmental factors, such as chemicals, radiation, infectious agents, or physical environments, which could potentially have an impact on the developing fetus. This exposure can occur through different routes, including inhalation, ingestion, dermal contact, or even transplacentally. The effects of maternal exposure on the fetus can vary widely depending on the type, duration, and intensity of the exposure, as well as the stage of pregnancy at which it occurs. It is important to monitor and minimize maternal exposure to potentially harmful substances or environments during pregnancy to ensure the best possible outcomes for both the mother and developing fetus.

Meconium is the first stool passed by a newborn infant, typically within the first 48 hours of life. It is composed of materials ingested during fetal development, including intestinal epithelial cells, lanugo (fine hair), amniotic fluid, mucus, bile, and water. The color of meconium is usually greenish-black, and its consistency can range from a thick paste to a liquid. Meconium staining of the amniotic fluid can occur when the fetus has passed meconium while still in the uterus, which may indicate fetal distress and requires careful medical attention during delivery.

Tobacco use cessation products are a type of pharmacological or nicotine replacement therapy (NRT) designed to help individuals stop using tobacco products, such as cigarettes, cigars, and smokeless tobacco. These products include:

1. Nicotine gum: A chewing gum that delivers nicotine to the body through the lining of the mouth.
2. Nicotine lozenges: Similar to nicotine gum, but in the form of a small tablet that dissolves slowly in the mouth.
3. Nicotine patch: A transdermal patch that delivers a steady dose of nicotine through the skin.
4. Nicotine inhaler: A device that looks like a cigarette and delivers nicotine vapor to be inhaled.
5. Nicotine nasal spray: A spray that delivers nicotine through the nostrils.
6. Non-nicotine prescription medications: Such as bupropion (Zyban) and varenicline (Chantix), which help reduce cravings and withdrawal symptoms.

These products are intended to help manage nicotine dependence and make it easier for individuals to quit tobacco use by alleviating the unpleasant symptoms of withdrawal. It is important to note that these products should be used as part of a comprehensive cessation plan, which may also include counseling and behavioral support.

Tandem mass spectrometry (MS/MS) is a technique used to identify and quantify specific molecules, such as proteins or metabolites, within complex mixtures. This method uses two or more sequential mass analyzers to first separate ions based on their mass-to-charge ratio and then further fragment the selected ions into smaller pieces for additional analysis. The fragmentation patterns generated in MS/MS experiments can be used to determine the structure and identity of the original molecule, making it a powerful tool in various fields such as proteomics, metabolomics, and forensic science.

Liquid chromatography (LC) is a type of chromatography technique used to separate, identify, and quantify the components in a mixture. In this method, the sample mixture is dissolved in a liquid solvent (the mobile phase) and then passed through a stationary phase, which can be a solid or a liquid that is held in place by a solid support.

The components of the mixture interact differently with the stationary phase and the mobile phase, causing them to separate as they move through the system. The separated components are then detected and measured using various detection techniques, such as ultraviolet (UV) absorbance or mass spectrometry.

Liquid chromatography is widely used in many areas of science and medicine, including drug development, environmental analysis, food safety testing, and clinical diagnostics. It can be used to separate and analyze a wide range of compounds, from small molecules like drugs and metabolites to large biomolecules like proteins and nucleic acids.

Glucuronates are not a medical term per se, but they refer to salts or esters of glucuronic acid, a organic compound that is a derivative of glucose. In the context of medical and biological sciences, glucuronidation is a common detoxification process in which glucuronic acid is conjugated to a wide variety of molecules, including drugs, hormones, and environmental toxins, to make them more water-soluble and facilitate their excretion from the body through urine or bile.

The process of glucuronidation is catalyzed by enzymes called UDP-glucuronosyltransferases (UGTs), which are found in various tissues, including the liver, intestines, and kidneys. The resulting glucuronides can be excreted directly or further metabolized before excretion.

Therefore, "glucuronates" can refer to the chemical compounds that result from this process of conjugation with glucuronic acid, as well as the therapeutic potential of enhancing or inhibiting glucuronidation for various clinical applications.

Salivary cotinine concentrations are highly correlated to blood cotinine concentrations, and can detect cotinine in a low range ... At steady state, plasma cotinine levels are determined by the amount of cotinine formation and the rate of cotinine removal, ... Cotinine was developed as an antidepressant as a fumaric acid salt, cotinine fumarate, to be sold under the brand name Scotine ... Some work suggests that cotinine may be a positive allosteric modulator of α7 nAChRs. If this is true, cotinine would ...
Cotinine is an active metabolite of nicotine that remains in the blood with a half-life of 18-20 hours, making it easier to ... Urinary or salivary cotinine concentrations are frequently measured for the purposes of pre-employment and health insurance ... Bhalala O (Spring 2003). "Detection of Cotinine in Blood Plasma by HPLC MS/MS". MIT Undergraduate Research Journal. 8: 45-50. ... Grizzell JA, Echeverria V (October 2015). "New Insights into the Mechanisms of Action of Cotinine and its Distinctive Effects ...
Serum cotinine levels (a metabolite of nicotine) have been found to be similar in bystanders exposed to either e-cigarette ... Serum cotinine levels are comparable to that of traditional cigarettes, but are inharmonious and rely upon the user and the ... Moreover, cotinine did also enhance tumor growth. Nicotine may inhibit antitumor immune response. It has also been reported ... People living with e‐cigarette users had increased salivary concentrations of cotinine. A small number of e-cigarette studies ...
"Plasma cotinine, smoking, and lung cancer in China". The Lancet. 335 (8699): 1225-1226. doi:10.1016/0140-6736(90)92752-4. PMID ...
Chen G, Blevins-Primeau AS, Dellinger RW, Muscat JE, Lazarus P (October 2007). "Glucuronidation of nicotine and cotinine by ... It is responsible for glucuronidation of nicotine and cotinine. UGT2B17 ENSG00000109181 GRCh38: Ensembl release 89: ...
Dempsey, Delia; Jacob, Peyton; Benowitz, Neal L. (2002-05-01). "Accelerated metabolism of nicotine and cotinine in pregnant ... load among Aka hunter-gatherers that treatment with commercial anthelmintics was associated with a decrease in cotinine ...
"Time to first cigarette after waking predicts cotinine levels". Cancer Epidemiology, Biomarkers & Prevention. 18 (12): 3415- ...
Cotinine: Cotinine, a metabolite of nicotine, is present in smokers. Like carbon monoxide, a cotinine test can be a reliable ... Cotinine levels can be tested through urine, saliva, blood, or hair samples. One of the main concerns of cotinine testing is ... For example, breath CO monitoring is non-invasive, while cotinine testing relies on bodily fluid. For instance, these two ...
Bajanowski T, Brinkmann B, Mitchell EA, Vennemann MM, Leukel HW, Larsch KP, Beike J (January 2008). "Nicotine and cotinine in ...
Bajanowski T, Brinkmann B, Mitchell EA, Vennemann MM, Leukel HW, Larsch KP, Beike J (January 2008). "Nicotine and cotinine in ...
Nakajima M, Tanaka E, Kwon JT, Yokoi T (2003). "Characterization of nicotine and cotinine N-glucuronidations in human liver ... Kuehl GE, Murphy SE (2004). "N-glucuronidation of nicotine and cotinine by human liver microsomes and heterologously expressed ...
"A selective molecularly imprinted polymer-carbon nanotube sensor for cotinine sensing". Journal of Molecular Recognition. 27 (1 ...
However, cotinine levels found in the urine reflect exposure only over the preceding 48 hours. Cotinine levels of the skin, ... Cotinine, the metabolite of nicotine, is a biomarker of secondhand smoke exposure. Typically, cotinine is measured in the blood ... Urinary cotinine levels have been a reliable biomarker of tobacco exposure and have been used as a reference in many ... Cotinine accumulates in hair during hair growth, which results in a measure of long-term, cumulative exposure to tobacco smoke ...
Sodium, potassium, iodine and cotinine will be assessed in the urine samples. This sub-study is supported by an agreement with ...
... is the primary enzyme responsible for the oxidation of nicotine and cotinine. It is also involved in the metabolism of ...
Barreto GE, Iarkov A, Moran VE (2014). "Beneficial effects of nicotine, cotinine and its metabolites as potential agents for ...
... and nicotine and cotinine levels in professional baseball players". American Journal of Public Health. 82 (3): 417-21. doi: ...
Barreto GE, Iarkov A, Moran VE (January 2015). "Beneficial effects of nicotine, cotinine and its metabolites as potential ...
For example, the fingerprints of tobacco smokers contain traces of cotinine, a nicotine metabolite; they also contain traces of ... By treating the fingerprint with gold nanoparticles with attached cotinine antibodies, and then subsequently with a fluorescent ... agent attached to cotinine antibodies, the fingerprint of a smoker becomes fluorescent; non-smokers' fingerprints stay dark.[ ...
Cotinine is an active metabolite of nicotine that remains in the blood for 18-20 hours, making it easier to analyze due to its ... Increased nicotine or cotinine (the nicotine metabolite) is detected in urine or blood, or serum nicotine concentrations ... Bhalala O (Spring 2003). "Detection of Cotinine in Blood Plasma by HPLC MS/MS". MIT Undergraduate Research Journal. 8: 45-50. ( ...
Pyridyl functional groups present in minute amounts include anabasine, myosmine, cotinine and 2, 3′-bipyridyl. Indole alkaloids ...
Compared with the reported rates, the actual rates, which were measured using urinary cotinine concentration (UCC) methods, ... discrepancies in smoking rates between self-reports and urinary cotinine level". BMC Women's Health. 14: 156. doi:10.1186/ ...
The concentration of cotinine in the waters of Fishing Creek was measured eight times in 2008 and 2009. All of these times, the ...
A variety of pharmaceutical drugs are 2-pyrrolidone derivatives, including cotinine, doxapram, povidone, and ethosuximide, and ...
... such as cotinine or nicotine. PVP is typically prepared by free radical polymerization of 4-vinylphenol or a protected form of ...
One study found that higher levels of cotinine in children were correlated with a decreased ability to perform in reading and ... and cotinine in the blood. When comparing sidestream and mainstream condensate, sidestream has 2-6 times more condensate per ...
Serum cotinine levels (a metabolite of nicotine) have been found to be similar in bystanders exposed to either e-cigarette ...
... she joined a research project which discovered that CYP2A6 was responsible for the oxidation of nicotine to cotinine, as ...
... cotinine MeSH D03.383.773.812.226 - doxapram MeSH D03.383.773.812.498 - oxotremorine MeSH D03.383.773.812.555 - piracetam MeSH ...
Cosmegen CosmoFer Cosopt Cotazym cotinine (INN) Cotrim cotriptyline (INN) Coumadin. Redirects to Warfarin. coumafos (INN) ...
Salivary cotinine concentrations are highly correlated to blood cotinine concentrations, and can detect cotinine in a low range ... At steady state, plasma cotinine levels are determined by the amount of cotinine formation and the rate of cotinine removal, ... Cotinine was developed as an antidepressant as a fumaric acid salt, cotinine fumarate, to be sold under the brand name Scotine ... Some work suggests that cotinine may be a positive allosteric modulator of α7 nAChRs. If this is true, cotinine would ...
Measuring cotinine is preferred to measuring nicotine because cotinine remains in the body longer. ... Levels of Cotinine in the Nonsmoking U.S. Population. In the Fourth National Report on Human Exposure to Environmental ... Cotinine is a product formed after the chemical nicotine enters the body. Nicotine is a chemical found in tobacco products, ... Measuring cotinine in peoples blood is the most reliable way to determine exposure to nicotine for both smokers and nonsmokers ...
LBXCOT - Cotinine (ng/mL). Variable Name: LBXCOT. SAS Label: Cotinine (ng/mL). English Text: Cotinine (ng/mL). Target: Both ... Cotinine concentrations are derived from the ratio of native to labeled cotinine in the sample by comparisons to a standard ... Cotinine may be measured in serum, urine or saliva - the half-life of cotinine in all three fluids is essentially the same. ... Cotinine is a major metabolite of nicotine that may be used as a marker for both active smoking, and as an index to ...
Get more information on the procedure and preparation for an urine cotinine test. ... Cotinine urine test is a simple urine test conducted at labs. ... Cotinine Urine Test. A cotinine urine test is conducted to ... Cotinine is detected in the urine for two to four days after the use of tobacco. It is important to know that cotinine levels ... Cotinine urine test is an immunoassay test that qualitatively detects cotinine in the urine of an individual at a sensitivity ...
We conducted a whole-genome linkage analysis to search for candidate regions influencing quantitative variation in cotinine ... Characterizing cotinine pharmacokinetics is a useful way to study nicotine metabolism because the same liver enzyme is ... We conducted a whole-genome linkage analysis to search for candidate regions influencing quantitative variation in cotinine ... Genome-Wide Linkage of Cotinine Pharmacokinetics Suggests Candidate Regionson Chromosomes 9 and 11. ...
Tag: cotinine. * Quitting smoking without help is hard: Effects of motivation and other personality factors. Quitting smoking ...
The 10-Panel Cotinine Drug Test In Houston Will Identify Tobacco Usage Over The Past Several Days. ... 10 Panel Drug Test Plus Cotinine (Nicotine Metabolite) (Urine). The 10 Panel Drug Test Plus Cotinine (Urine) will identify the ... The 10 Panel Drug Test Plus Cotinine (Nicotine Metabolite) (Urine) is recommended for consumers seeking a drug test for ... The 10 Panel Drug Test Plus Cotinine (Nicotine Metabolite) (Urine) is recommended for employers looking for an expanded ...
Results There was a significant decrease in the mean cotinine levels from 35.9 ng/ml to a non-quantifiable value (p,0.001), and ... The impact of Michigans Dr Ron Davis smoke-free air law on levels of cotinine, tobacco-specific lung carcinogen and severity ... The impact of Michigans Dr Ron Davis smoke-free air law on levels of cotinine, tobacco-specific lung carcinogen and severity ... The main outcome measures were urine samples for total cotinine and total NNAL and data from a self-administered respiratory ...
Urinary cotinine will not necessarily improve the validity of studies of the relationship of passive smoking to LRI in infants. ... Urinary Cotinine and Parent History (Questionnaire) as Indicators of Passive Smoking and Predictors of Lower Respiratory ... Smoke absorption by the infants was measured by the urinary cotinine/ creatinine ratio. Of the 485 infants in the study, 325 ( ... Home / Resources / Publications / Urinary Cotinine and Parent History (Questionnaire) as Indicators of Passive Smoking and ...
The 10-Panel Cotinine Drug Test In Houston Will Identify Tobacco Usage Over The Past Several Days. ... 10 Panel Drug Test Plus Cotinine (Nicotine Metabolite) (Urine). The 10 Panel Drug Test Plus Cotinine (Urine) will identify the ... The 10 Panel Drug Test Plus Cotinine (Nicotine Metabolite) (Urine) is recommended for consumers seeking a drug test for ... The 10 Panel Drug Test Plus Cotinine (Nicotine Metabolite) (Urine) is recommended for employers looking for an expanded ...
"Any detectable cotinine" indicates blood cotinine levels at or above 0.05 ng/mL, the detectable level of cotinine in the blood ... NOTE: Cotinine levels are reported for nonsmoking children only (a non-smoker is defined as someone with a cotinine level less ... PHY2.B Secondhand smoke: Percentage of children ages 4-17 with any detectable blood cotinine level by age, race and Hispanic ...
Only a minor fraction of the generated cotinine is excreted by the kidneys, but cotinine is further metabolised to more polar ... The principal fragment ions (98 and 176 for cotinine, 91 for pyribenzamine) were monitored. The cotinines coefficient of ... of nicotine seems to be converted to cotinine. Cotinine is the major plasma metabolite of nicotine and persists for a ... The cotinine level cut off points to determine smoking has varied from 3 ng/ml to 40.5 ng/ml among studies.8 The most commonly ...
Cotinine concentrations in maternal serum and amniotic fluid during pregnancy and risk of testicular germ cell cancer in the ... Cotinine was quantified by liquid chromatography tandem mass spectrometry. An adapted cox regression model estimated the risk ... Cotinine was quantified by liquid chromatography tandem mass spectrometry. An adapted cox regression model estimated the risk ... Cotinine was quantified by liquid chromatography tandem mass spectrometry. An adapted cox regression model estimated the risk ...
The urinary cotinine concentration in Korean non-smoking adults living in smoking homes was higher than that in adults living ... Urinary cotinine concentrations were different significantly by home smoking status in most socio-demographic subgroups. Data ... The geometric mean of urinary cotinine concentrations for non-smoking adults living in smoking homes was 2.1 μg/L (95% ... This study examined differences in urinary cotinine concentrations in the Korean non-smoking adult population between living in ...
Results: Cotinine concentrations reduced by 69%, from 1.6 ng/ml to 0.5 ng/ml median (SD 1.29; p , 0.005). Overall 74% of ... Home , Secondhand smoke exposure and risk following the Irish smoking ban: an assessment of salivary cotinine concentrations in ... Main Outcome Measures: Salivary cotinine concentrations (ng/ml), duration of self reported exposures to secondhand smoke, air ... an assessment of salivary cotinine concentrations in hotel workers and air nicotine levels in bars. Tobacco Control, 14, (6), ...
Expired air- co and urinary cotinine levels of the electronic cigarette users: Descriptive study from Turkey. Dilek Aslan, ...
A cotinine-assisted smoking intervention programme managed from a central location as an adjunct to a maternal serum AFP ... Cotinine-assisted intervention in pregnancy to reduce smoking and low birthweight delivery Br J Obstet Gynaecol. 1991 Sep;98(9 ... Conclusion: A cotinine-assisted smoking intervention programme managed from a central location as an adjunct to a maternal ... Objective: To investigate the feasibility and impact of integrating a cotinine-assisted smoking intervention programme with an ...
Results We found significant positive correlations for cotinine and oxytocin (P = .002), β‐endorphin (P = .008), and orexin (P ... Conclusion and Scientific Significance These preliminary results suggest a relationship between cotinine and oxytocin, β‐ ... salivary cotinine and serum γ‐glutamyl transferase [GGT]) as well as with self‐reported smoking and alcohol drinking. Methods ... We found significant positive correlations for cotinine and oxytocin (P = .002), β‐endorphin (P = .008), and orexin (P < .001 ...
Cotinine alone had no effect on withdrawal symptoms. However, when nicotine patch was combined with cotinine, the beneficial ... Cotinine alone had no effect on withdrawal symptoms. However, when nicotine patch was combined with cotinine, the beneficial ... Cotinine alone had no effect on withdrawal symptoms. However, when nicotine patch was combined with cotinine, the beneficial ... Cotinine alone had no effect on withdrawal symptoms. However, when nicotine patch was combined with cotinine, the beneficial ...
1993). Saliva cotinine and recent smoking--evidence for a nonlinear relationship.. 108(6). Swan, G E et al. "Saliva cotinine ... Estimating Cotinine Associations and a Saliva Cotinine Level to Identify Active Cigarette Smoking in Alaska Native Pregnant ... Title : Estimating Cotinine Associations and a Saliva Cotinine Level to Identify Active Cigarette Smoking in Alaska Native ... "Estimating Cotinine Associations and a Saliva Cotinine Level to Identify Active Cigarette Smoking in Alaska Native Pregnant ...
After smoking tobacco cotinine which is a metabolite of nicotine is created and can be tested for in urine. ... Cotinine Cotinine is a metabolite of nicotine that is produced after smoking tobacco. Cotinine will remain detectable in the ... The level of cotinine present in the body is an indicator of how much or how little a person smokes tobacco. An amount of 10 ng ... whereas heavy use of tobacco can produce up to and above 500 ng/ml of cotinine in the body. ...
This test measures cotinine, a chemical your body makes after exposure to nicotine. ...
This test measures cotinine, a chemical your body makes after exposure to nicotine. ... Cotinine is a chemical your body makes after you are exposed to nicotine. Measuring cotinine is better than measuring nicotine ... Nicotine Cotinine (Urine). Does this test have other names?. Cotinine urine test, nicotine urine test ... Cotinine levels in a light smoker or someone exposed to secondhand smoke are 11 ng/mL to 30 ng/mL. ...
Home / Products tagged "cotinine urine test". cotinine urine test. No products were found matching your selection. ...
cotinine positive recently Cotinine showed positive another showed positive ex user months wondering cotinine gotten system ... Why is my cotinine test positive?. I recently took a urine test for Cotinine which showed up positive. I later did another test ... I am and ex-user been sober for months and I was wondering if there was a way that cotinine could have gotten in my system. I ...
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Plasma cotinine levels and pancreatic cancer in the EPIC cohort study Leenders M., Chuang S-C., Dahm CC., Overvad K., Ueland PM ...
Samples were assayed for cotinine using a well established rapid gas liquid chromatography technique.25 Cotinine is a major ... Saliva cotinine. Saliva samples were collected using a dental roll which participants were asked to keep in the mouth until ... Cotinine concentrations above 30 ng/ml in self-reported ex-smokers or non-smokers who did not indicate use of nicotine ... In the absence of the use of nicotine replacement products, saliva cotinine concentrations above 15 ng/ml usually indicate ...
  • 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)
  • Secondhand smoke exposure and risk following the Irish smoking ban: an assessment of salivary cotinine concentrations in hotel workers and air nicotine levels in bars. (drugsandalcohol.ie)
  • Mulcahy, Maurice and Evans, David S and Hammond, SK and Repace, JL and Byrne, M (2005) Secondhand smoke exposure and risk following the Irish smoking ban: an assessment of salivary cotinine concentrations in hotel workers and air nicotine levels in bars. (drugsandalcohol.ie)
  • Main Outcome Measures: Salivary cotinine concentrations (ng/ml), duration of self reported exposures to secondhand smoke, air nicotine (microg/cubic metre). (drugsandalcohol.ie)
  • In this secondary analysis of a pilot clinical trial with individuals with alcohol and nicotine use disorders, we investigate the relationship between serum concentrations of oxytocin, β‐endorphin, melatonin, α‐melanocyte‐stimulating hormone, substance P, and orexin, with objective biomarkers (salivary cotinine and serum γ ‐glutamyl transferase [GGT]) as well as with self‐reported smoking and alcohol drinking. (bryant.edu)
  • Existing evidence suggests there is an association between the salivary cotinine levels and passive smoking. (farmaciajournal.com)
  • The aim of this study was the objectively evaluation of the passive smoking prevalence in non-smoking adults from Constanta, Romania, based on their salivary cotinine levels measured by NicAlert™ Saliva tests. (farmaciajournal.com)
  • In a cross-sectional study made on 286 subjects, the levels of salivary cotinine were measured, together with the evaluation of the self-reported smoking status on a questionnaire basis. (farmaciajournal.com)
  • After analysis of the salivary cotinine, only 16.4% of all subjects were not exposed to tobacco products. (farmaciajournal.com)
  • Using the salivary cotinine levels as standard, the real distribution of the subjects according to their smoker status comprised 44.06% active smokers (constant and occasional), 16.43% (n=47) non-smokers (non-exposed to tobacco smoke) and 39.50% (n=113) passive smokers. (farmaciajournal.com)
  • Third-hand exposure at homes: Assessment using salivary cotinine. (bvsalud.org)
  • The objective of this work is to characterize salivary cotinine concentrations among people who self -reported exposure to SHS and THS at home. (bvsalud.org)
  • and (d) lower salivary cotinine. (rand.org)
  • Hence, we planned the present study to evaluate the impact of cigarette smoke on salivary antioxidant levels and cotinine levels in smokers and nonsmokers. (thejcdp.com)
  • In the present study, we assessed and compared the salivary α-amylase, CAT, and cotinine levels in smokers and nonsmoker subjects. (thejcdp.com)
  • The primary outcome was the continuous abstinence rate (CAR) at weeks 21 to 24, biochemically validated using salivary cotinine testing. (jmir.org)
  • 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)
  • Cotinine is the major plasma metabolite of nicotine and persists for a considerable time period in plasma, with a half life of approximately 16 hours. (bmj.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 metabolite of nicotine that is produced after smoking tobacco. (drugtestkits.ca)
  • Design, Setting, and Participants: Before and after the smoking ban a cohort of workers (n = 35) from a sample of city hotels (n = 15) were tested for saliva cotinine concentrations and completed questionnaires. (drugsandalcohol.ie)
  • Saliva cotinine and recent smoking--evidence for a nonlinear relationship. (cdc.gov)
  • Detectable saliva cotinine levels in 8/20 moth- ers of neonates (1-2 days old) suggested in utero exposure. (who.int)
  • African American smokers generally have higher plasma cotinine levels than Caucasian smokers. (wikipedia.org)
  • 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)
  • Main results: Among self reported regular smokers, 97.2% of men and 94.9% of women had a cotinine concentration of 10 ng/ml or higher in serum. (bmj.com)
  • Among never smokers 2.5% of men and 2.7% of women had detectable level of cotinine in their serum. (bmj.com)
  • Conclusions: In a sample of the general population in Finland the validity of self reported smoking is high, and most of the few self reported non-smokers who had cotinine in their serum had only low or moderate levels. (bmj.com)
  • Among the 547 self reported smokers 12.1% were found to have serum cotinine levels less than 14 ng/ml and were possible misclassifications by self report. (bmj.com)
  • These preliminary results suggest a relationship between cotinine and oxytocin, β‐endorphin, and orexin, which opens up new potential hypotheses on the potential role of these endocrine pathways in tobacco smokers. (bryant.edu)
  • 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. (ox.ac.uk)
  • The urinary cotinine levels were reduced in non-smokers. (nih.gov)
  • In non-smokers cotinine concentrations were higher based on urine sampled the morning after a shift than based on urine sampled immediately post-shift. (nih.gov)
  • Currently, life insurance companies check people's blood for traces of the protein cotinine to find out whether they are smokers, he said. (startribune.com)
  • Any detectable cotinine" indicates blood cotinine levels at or above 0.05 ng/mL, the detectable level of cotinine in the blood in 1988-1994. (childstats.gov)
  • CDC data have shown a decrease in cotinine levels in nonsmokers. (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)
  • The aims were to assess the impact of a total smoking ban on the level of airborne contaminants and the urinary cotinine levels in the employees in bars and restaurants. (nih.gov)
  • Cross-sectional study examining the accuracy of self-reported smoking status as compared to urinary cotinine levels among workers at risk for chronic kidney disease of unknown origin in Guatemala. (cdc.gov)
  • Design: We evaluated self-reported smoking status against urinary cotinine levels, the gold standard biomarker of tobacco smoke exposure, among agricultural workers at four separate cross-sectional time points. (cdc.gov)
  • Primary outcome measures: Compared self-reported smoking status and urinary cotinine levels in two agricultural worker studies. (cdc.gov)
  • Urinary cotinine levels show that smoking prevalence is underestimated in this worker population. (cdc.gov)
  • An associated question is what would be the value of measuring serum cotinine concentrations in such surveys to obtain validated smoking data. (bmj.com)
  • Cotinine administration, with or without nicotine patch, produced serum cotinine concentrations 3-4 times higher than during ad lib 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)
  • Since CYP2A6 activity differs by sex (estrogen induces CYP2A6) and genetic variation, cotinine accumulates in individuals with slower CYP2A6 activity, resulting in substantial differences in cotinine levels for a given tobacco exposure. (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)
  • In the Fourth National Report on Human Exposure to Environmental Chemicals (Fourth Report) , CDC scientists measured cotinine in the serum (a clear part of blood) of 6,320 nonsmoking participants aged three years and older who took part in CDC's National Health and Nutrition Examination Survey (NHANES) during 2003-2004. (cdc.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)
  • In bivariate analyses, reported tobacco smoke exposure and urinary cotinine were associated with LRI. (unc.edu)
  • We performed a nested case-control study using cotinine measurements in maternal serum and amniotic fluid as a biomarker for tobacco exposure during pregnancy. (lu.se)
  • Circulating levels of the nicotine metabolite cotinine is a marker of recent smoking exposure. (ox.ac.uk)
  • Using cotinine as a biomarker for tobacco exposure allows more accurate quantitative analyses to be performed. (ox.ac.uk)
  • After this exposure, the researchers tested levels of cotinine , the product formed after nicotine enters the body, in the rats' urine, as well as recorded changes observed in testicular weight, sperm count, and other characteristics that are indicative of testicle health. (snopes.com)
  • A questionnaire on tobacco use and passive exposure was administered, and a saliva sample was collected for cotinine determination . (bvsalud.org)
  • We used log-linear models to compare the cotinine concentration of each exposed group with respect to the unexposed group, adjusting for sex , age, educational level , and tobacco exposure in other settings. (bvsalud.org)
  • Among nonsmokers, the presence of cotinine in serum indicates exposure to secondhand tobacco smoke. (cdc.gov)
  • The consequences of prolonged exposure in smoke, the present study aimed to assess close proximity to parental smoking are the prevalence of infant exposure to envi- exacerbated by infants' immature immune ronmental tobacco smoke and to measure and pulmonary systems [ 2 ], small body size the cotinine levels in infant urine. (who.int)
  • During 1988 to 1991, data showed that 87.9% of nonsmokers had measurable levels of cotinine in their bodies. (cdc.gov)
  • From 2007 to 2008, an estimated 40.1% of nonsmokers had cotinine in their bodies. (cdc.gov)
  • 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)
  • This test measures the amount of cotinine in your urine. (stillwater-medical.org)
  • 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. (bmj.com)
  • Mothers completed a questionnaire about smoking habits of household members, and urine samples were obtained from infants for analysis of cotinine levels. (who.int)
  • So, two lines on the strip indicate the presence of cotinine. (medicalhealthtests.com)
  • When there is only one line it's a negative result, which means there is no presence of cotinine in the urine. (medicalhealthtests.com)
  • Conclusions The reduction in the SHS biomarkers cotinine and NNAL and reported improvement in respiratory health demonstrates that the Michigan smoke-free workplace law is protecting bar employee health. (bmj.com)
  • We collected preshift and postshift urine samples on 114 NP casino dealers to determine whether levels of ETS biomarkers (Cotinine (COT) and 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL)) in their urine would increase over an 8-hour work shift. (cdc.gov)
  • Drug tests can detect cotinine in the blood, urine, or saliva. (wikipedia.org)
  • A cotinine urine test is conducted to detect cotinine (nicotine) levels in a person's body. (medicalhealthtests.com)
  • People who smoke menthol cigarettes may retain cotinine in the blood for a longer period because menthol can compete with enzymatic metabolism of cotinine. (wikipedia.org)
  • Cotinine will remain detectable in the body for up to one week, however, studies have shown that people who smoke menthol cigarettes have traces of cotinine in their system for longer periods that those who smoke regular cigarettes. (drugtestkits.ca)
  • Nonetheless, treatment with cotinine in humans was reported to have no significant physiologic, subjective, or performance effects in one study, though others suggest that this may not be the case. (wikipedia.org)
  • Measuring cotinine is preferred to measuring nicotine because cotinine remains in the body longer. (cdc.gov)
  • 1, 2 Mainly, three biological measurements have been used to validate self reported smoking: carbon monoxide, thiocyanate, and cotinine. (bmj.com)
  • Characterizing cotinine pharmacokinetics is a useful way to study nicotine metabolism because the same liver enzyme is primarily responsible for the metabolism of both, and the clearances of nicotine and cotinine are highly correlated. (sri.com)
  • The confidence level of the linkage between the three genome regions and cotinine pharmacokinetics is statistically significant with a genome-wide empirical probability of P = 0.029. (sri.com)
  • According to the American Association for Clinical Chemistry , it can take over 2 weeks for a person's blood to reach the same cotinine levels as someone who does not use tobacco. (medicalnewstoday.com)
  • Back in the early 1990s, NCEH's Tobacco Laboratory developed a method for measuring levels of cotinine in a person's bloodstream. (cdc.gov)
  • Cotinine is a product formed after the chemical nicotine enters the body. (cdc.gov)
  • When nicotine enters the body, it is broken down into more than 20 different substances , including cotinine, anabasine, and nornicotine. (medicalnewstoday.com)
  • Cotinine was developed as an antidepressant as a fumaric acid salt, cotinine fumarate, to be sold under the brand name Scotine but it was never marketed. (wikipedia.org)
  • A between-subject, 2 x 2 factorial design was used, with the daily administration of a 15-mg nicotine patch (Nicotrol) versus placebo patch as one factor and 80 mg of oral cotinine fumarate versus placebo drug as the other factor. (umn.edu)
  • According to recent human data the major metabolite found in urine is hydroxylated cotinine. (bmj.com)
  • The intervention group received an interpreted measurement of the serum cotinine, reported through the physician to the woman, along with a self-help smoking cessation booklet and a repeat serum cotinine measurement one month later, again interpreted and reported through the physician to the woman. (nih.gov)
  • Importance of baseline cotinine plasma values in smoking cessation: results from a double-blind study with nicotine patch. (bvsalud.org)
  • Only a minor fraction of the generated cotinine is excreted by the kidneys, but cotinine is further metabolised to more polar water soluble substances. (bmj.com)
  • 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. (bmj.com)
  • 0.001, respectively) but decreased lung cancer risk (P = 0.01 for both, after adjusting for cotinine). (ox.ac.uk)
  • Urinary cotinine will not necessarily improve the validity of studies of the relationship of passive smoking to LRI in infants. (unc.edu)
  • A total of 60.0% of infants were reported to be exposed to passive smoking at home and 36.4% had detectable levels of urine cotinine (mean 7.1 ng/mL, range 0.27-41 ng/mL). (who.int)
  • Overall, the concentrations of cotinine were comparable in maternal serum and amniotic fluid (medianserum/amniotic fluid : 2.1/2.6 ng/ml). (lu.se)
  • To investigate the feasibility and impact of integrating a cotinine-assisted smoking intervention programme with an existing antenatal maternal serum alpha-fetoprotein (AFP) screening service for open neural tube defects. (nih.gov)
  • A cotinine-assisted smoking intervention programme managed from a central location as an adjunct to a maternal serum AFP screening service can, with the cooperation of physicians responsible for antenatal care, lead to a significant and cost-effective reduction in the number of low birthweight babies. (nih.gov)
  • Smoke absorption by the infants was measured by the urinary cotinine/ creatinine ratio. (unc.edu)
  • Of those participants who reported to have smoked at any time during their life but not during the previous month, 6.3% of men and 5.2% of women had a serum cotinine concentration of at least 10 ng/ml. (bmj.com)
  • Males generally have higher plasma cotinine levels than females. (wikipedia.org)
  • The half-life of cotinine in plasma has been estimated to be about 15-20 hrs (Jarvis et al. (cdc.gov)
  • 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). (ox.ac.uk)
  • 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]. (ox.ac.uk)
  • This study is the first to show that plasma cotinine levels are strongly related to pancreatic cancer. (ox.ac.uk)
  • 3 The aim of our paper is to study the validity of self reported smoking in a cardiovascular risk factor population survey by comparing self reports with results of measurements of cotinine levels in serum. (bmj.com)
  • Birthweight, physician cooperation with study protocol (as measured by effectiveness in obtaining repeat serum samples for cotinine measurements). (nih.gov)
  • 95% CI+9 to +123 g) and to a 30% reduction in the rate of low birthweight in pregnancies managed by the 70 physicians who secured the highest rate of obtaining repeat serum samples for cotinine measurements in their intervention group. (nih.gov)
  • It is important to know that cotinine levels not only depend on how many cigarettes you smoke but also on the type. (medicalhealthtests.com)
  • You could smoke ten cigarettes only whereas another individual may have smoked 15, and yet your cotinine levels could be higher. (medicalhealthtests.com)
  • People with a cotinine level over 1187.8 nmol/L, a level comparable to smoking 17 cigarettes per day, have an elevated risk of pancreatic cancer, compared to people with cotinine levels below 55 nmol/L (OR: 3.66, 95% CI: 1.44-9.26). (ox.ac.uk)
  • Some studies say that vaping delivers less nicotine than cigarettes, while others say that the levels of cotinine and nicotine might be higher in people who use vapes. (medicalnewstoday.com)
  • By measuring cotinine in the serum, scientists can estimate the amount of nicotine that has entered people's bodies. (cdc.gov)
  • Measuring cotinine is better than measuring nicotine because nicotine disappears from your system within a few hours, but cotinine remains for a day or more. (stillwater-medical.org)
  • 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)
  • Cotinine was quantified by liquid chromatography tandem mass spectrometry. (lu.se)
  • The 10 Panel Drug Test Plus Cotinine (Nicotine Metabolite) (Urine) is recommended for employers looking for an expanded workplace drug testing panel and may also need information about the prevalence of nicotine use among employees for insurance reasons. (anylabtestnow.com)
  • More specifically, this study examined the effects of cotinine on physiological measures, subjective measures assessing craving, withdrawal symptoms and mood, and performance measures. (umn.edu)
  • IMPACT: This study is the largest to date investigating the effects of polymorphisms affecting smoking behavior on lung cancer risk using circulating cotinine measures as proxies for recent smoking behavior. (ox.ac.uk)
  • Cotinine levels in a light smoker or someone exposed to secondhand smoke are 11 ng/mL to 30 ng/mL. (stillwater-medical.org)
  • These systematic differences in cotinine levels were attributed to variation in CYP2A6 activity. (wikipedia.org)
  • The Fourth Report shows differences in cotinine levels among different racial groups. (cdc.gov)
  • No differences in cotinine levels were found between those exposed to second- hand and third- hand smoke at home. (bvsalud.org)
  • It is only the bad passing insurance cotinine testing ones programme will not. (tripod.com)
  • Therefore, serum was chosen for NHANES cotinine analyses. (cdc.gov)
  • The level of cotinine present in the body is an indicator of how much or how little a person smokes tobacco. (drugtestkits.ca)
  • If you haven't smoked or been exposed to nicotine in 7 to 10 days, your cotinine levels start to return to a normal level. (stillwater-medical.org)
  • serum cotinine level was positively associated with CD, especially for non-Hispanic white males. (medscape.com)