Tobacco Use Disorder
Aryl Hydrocarbon Hydroxylases
Tandem Mass Spectrometry
(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)
Tobacco use disorder refers to a condition where an individual engages in the excessive and compulsive consumption of tobacco products, despite the negative consequences it may have on their health and well-being. Tobacco use disorder is a common condition that affects millions of people worldwide, and it is characterized by a pattern of continued tobacco use despite harmful effects, as well as an increased tolerance to tobacco and withdrawal symptoms when trying to stop.
The Diagnostic and Statistical Manual of Mental Disorders (DSM-5) defines tobacco use disorder as a chronic condition that can manifest in different forms, including nicotine dependence and tobacco abuse. The criteria for diagnosing tobacco use disorder include:
1. Tolerance: A need to use more tobacco to achieve the desired effect.
2. Withdrawal: Experiencing symptoms such as irritability, anxiety, or depression when trying to stop using tobacco.
3. Loss of control: Consuming more tobacco than intended or for longer periods than intended.
4. Negative consequences: Continuing to use tobacco despite social, physical, or psychological problems caused by its use.
5. Increased time and effort spent on using tobacco.
6. Craving or a strong desire to use tobacco.
7. Failure to control or reduce tobacco use.
Tobacco use disorder can have severe consequences, including lung cancer, heart disease, respiratory problems, and other health issues. It can also lead to social and economic problems, such as lost productivity and strained relationships with family and friends. Treatment for tobacco use disorder includes behavioral therapies, medications, and support groups, and it is important for individuals struggling with this condition to seek professional help to quit using tobacco and improve their overall health and well-being.
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- Cotinine is a product formed after the chemical nicotine enters the body. (cdc.gov)
- 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)
- Measuring cotinine is preferred to measuring nicotine because cotinine remains in the body longer. (cdc.gov)
- By measuring cotinine in the serum, scientists can estimate the amount of nicotine that has entered people's bodies. (cdc.gov)
- 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 generally preferred over nicotine for such assessments because of its substantially longer half-life. (cdc.gov)
- In this study, we measured hair nicotine and cotinine levels as exposure biomarkers in non-smokers and assessed the risk from the actual situation of passive smoking in different lifestyle environments. (unboundmedicine.com)
- Nicotine and cotinine contents in hair samples of 110 non-smoker subjects were measured by in-tube solid-phase microextraction with on-line coupling to liquid chromatography-tandem mass spectrometry, and self-reported lifestyle questionnaires were completed by the subjects. (unboundmedicine.com)
- Nicotine and cotinine were detected at concentrations of 1.38 ng mg-1 and 12.8 pg mg-1 respectively in the hair of non-smokers, with levels significantly higher in subjects who reported being sensitive to tobacco smoke exposure. (unboundmedicine.com)
- Nicotine and cotinine in hair are useful biomarkers for assessing the effects of passive smoking on long-term exposure to environmental tobacco smoke, and our analytical methods can measure these exposure levels in people who are unaware of passive smoking. (unboundmedicine.com)
- Cotinine, the main metabolite of nicotine, has a long half-life and does not have cardiovascular or addictive side effects in humans. (nih.gov)
- Controlling for baseline demographic and smoking features, the association between reductions in nicotine exposure during the 6-week trial, assessed by urinary total cotinine and biomarker-confirmed smoking abstinence 1 month later, was tested. (bmj.com)
- Results Greater reductions in nicotine exposure while smoking VLNC cigarettes predicted abstinence independent of individual differences in baseline smoking, cotinine, dependence, gender and study. (bmj.com)
- Approximately 15 percent of children in the study tested positive for cotinine, a byproduct formed when the body breaks down nicotine, at levels comparable to those of adult smokers. (nih.gov)
- In multivariate analysis, participants with banked biospecimens were significantly more likely to self-identify as White, to be older, to have increased total nicotine equivalents per cigarette, decreased serum cotinine, and increased forced vital capacity, compared to participants without. (biomedcentral.com)
- Researchers also found elevated levels of cotinine, a byproduct of nicotine, in the samples. (ksl.com)
- When nicotine oxidizes, it will produce cotinine. (freedombeer.com)
- Cotinine is generated in the human body as a degradation product of nicotine. (bund.de)
- CYP2A6 encodes an enzyme that metabolizes several drugs, including nicotine and its metabolite cotinine. (biomedcentral.com)
- Eighty-seven percent of nonsmoking children ages 4 to 17 years had detectable levels (at or above 0.05 ng/mL) of cotinine in 1988-1991. (epa.gov)
- About 63 percent of children in the study had detectable levels of cotinine, suggesting widespread exposure to smoke. (nih.gov)
- Results: In total, 100% of children had detectable levels of cotinine and >96% had detectable NNAL and N-oxide levels. (nih.gov)
Excretion of cotinine2
- Child age negatively correlated with urinary cotinine (r = -0.202, p = 0.007) and log NNAL levels (r = -0.275, p (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)
- The relationship between household tobacco smoke exposure and wheezing and nonwheezing lower respiratory tract illnesses in young children was investigated using both a questionnaire and the urinary cotinine/creatinine ratio to assess passive smoking. (who.int)
- The current study was conducted therefore to investigate the relationship of household tobacco smoke exposure to wheezing and nonwheezing LRTIs in young children using both a questionnaire and the urinary cotinine/creatinine ratio (CCR) to assess passive smoking. (who.int)
- 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)
- 1990). Cotinine may be measured in serum, urine or saliva - the half-life of cotinine in all three fluids is essentially the same. (cdc.gov)
- Therefore, serum was chosen for NHANES cotinine analyses. (cdc.gov)
- 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)
- In 2013-2016, the median concentration of cotinine in blood serum for nonsmoking children living below the poverty level (0.07 ng/mL) was about 4 times the median for nonsmoking children living at or above the poverty level (0.02 ng/mL). (epa.gov)
- Serum cotinine was quantified to evaluate current smoking. (dovepress.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)
- Both NNAL and cotinine are specific to tobacco and were not found in the nonsmokers' urine before their casino visit. (ksl.com)
- Have a urine cotinine level corresponding to smoker status for the specific test being used, typically corresponding to a urine cotinine above about 200 ng/ml, and have been smoking for at least 1 year. (nih.gov)
- Daily water pipe consumption (one water pipe per day) leads to a cotinine level in 24-hour urine that corresponds to the consumption of 10 cigarettes a day. (bund.de)
- Urine Cotinine Screening Detect Nearly Ubiquitous Tobacco Smoke Exposure in Urban Adolescents. (famri.org)
- Comparison of Urine 4-(Methylnitrosamino)-1-(3)Pyridyl-1-Butanol and Cotinine for Assessment of Active and Passive Smoke Exposure in Urban Adolescents. (ucsf.edu)
- Cotinine concentrations are derived from the ratio of native to labeled cotinine in the sample by comparisons to a standard curve. (cdc.gov)
- The percentage of participants with saliva samples with measurable concentrations of cotinine fell from 92.4% to 64.2% after both Spanish smoking legislations. (bvsalud.org)
- There was a large reduction in the salivary cotinine concentration among adult non-smokers and higher cotinine concentrations among those declaring exposure to SHS at home after both legislations. (bvsalud.org)
- Thirty-six percent of nonsmoking children ages 3 to 17 years had levels at or above 0.05 ng/mL of cotinine in 2015-2016, although improvements in laboratory methods made it possible to detect cotinine at lower concentrations starting with the 2001-2002 survey cycle. (epa.gov)
- In 2013-2016, median concentrations of cotinine in blood for nonsmokers were approximately 0.12 ng/mL for Black non-Hispanic children, 0.02 ng/mL for White non- Hispanic children, and 0.02 ng/mL for Mexican-American children. (epa.gov)
- In 2013-2016, 95th percentile concentrations of cotinine in blood for nonsmokers were 1.9 ng/mL for White non-Hispanic children and 3.5 ng/mL for Black non-Hispanic children, while Mexican-American children had levels that were more than 3 times lower (0.6 ng/mL). (epa.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)
- CDC data have shown a decrease in cotinine levels in nonsmokers. (cdc.gov)
- 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)
- Objectives: Cotinine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), and N-oxides are biomarkers of tobacco smoke exposure (TSE) used to assess short- and longer-term TSE. (nih.gov)
- The decrease of the GM salivary cotinine concentration was statistically significant independently of the sociodemographic variables. (bvsalud.org)
- Assessment of salivary cotinine concentration among general non-smokers population: Before and after Spanish smoking legislations. (bvsalud.org)
- We used linear mixed effect models, with individuals as random effects, to model the percentage change in salivary cotinine concentration and their 95% confidence intervals . (bvsalud.org)
- Moreover, after both Spanish smoke -free laws salivary cotinine concentration was homogenized according to sociodemographic variables. (bvsalud.org)
- Cotinine values at the 95th percentile decreased by 50% from 1988-1991 to 2015-2016. (epa.gov)
- For the years 2013-2016, there were no significant differences between children's age groups in median levels of cotinine. (epa.gov)
- These values are higher than those seen in data previously reported in the National Health and Nutrition Examination Survey, which found that only one-third to one-half of children's blood samples had detectable cotinine. (nih.gov)
- Fluorosilicic acid and cotinine, separately and in combination, induce genotoxicity and telomeric reduction in human osteoblast cell line MG63. (fluoridealert.org)
- Cotinine is measured in blood samples obtained from individual survey participants. (epa.gov)
- Fifteen percent of the children were in the high exposure group, with cotinine levels comparable to active adult smokers (12ng/mL or higher), 48 percent were in the moderate exposure group (0.46 to 12ng/mL) and 37 percent were in the low exposure group (less than or equal to 0.46ng/mL). (nih.gov)
- The Fourth Report shows differences in cotinine levels among different racial groups. (cdc.gov)
- Children at the 95th percentile of cotinine levels had much higher levels than those at the median. (epa.gov)
- In every time period measured except for 2013-2014, children at the 95th percentile had higher levels of cotinine in their blood than women at the 95th percentile. (epa.gov)
- We found that infants had higher cotinine levels compared to toddlers," said Lisa M. Gatzke-Kopp, Ph.D., a professor at Pennsylvania State University and the lead author of the study. (nih.gov)
- Back in the early 1990s, NCEH's Tobacco Laboratory developed a method for measuring levels of cotinine in a person's bloodstream. (cdc.gov)
- In vitro studies confirmed the inhibitory effect of cotinine on Aβ1-42 aggregation. (nih.gov)
- The average increase in the amount of cotinine following the casino visit was 456 percent. (ksl.com)
- The half-life of cotinine in plasma has been estimated to be about 15-20 hrs (Jarvis et al. (cdc.gov)
- Cotinine stimulated Akt signaling, including the inhibition of glycogen synthase kinase 3β (GSK3β), which promotes neuronal survival and the synaptic plasticity processes underlying learning and memory in the hippocampus and cortex of wild type and Tg6799 AD mice. (nih.gov)
- We studied the effect of cotinine on amyloid-β (Aβ) aggregation as well as addressed its impact on working and reference memories. (nih.gov)