Urine cotinine as an index of smoking status in smokers during 96-hr abstinence: Comparison between gas chromatography/mass spectrometry and immunoassay test strips
ABSTRACT Biomarkers such as carbon monoxide (CO) and cotinine (a nicotine metabolite) are used in tobacco cessation studies to assess smoking status. CO is easy to assess, is inexpensive, and provides immediate results. However, the short half-life of CO may limit its ability to identify smokers who have abstained for several hours. Quantitative methods (e.g., gas chromatography/mass spectrometry, or GC/MS) for measuring urine cotinine, which has a longer half-life, are valid and reliable, though costly and time consuming. Recently developed semiquantitative urine cotinine measurement techniques (i.e., urine immunoassay test strips, or ITS) address these disadvantages, though the value of ITS as a means of identifying abstaining smokers has not been evaluated. The present study examined ITS as a measure of smoking status in temporarily abstaining smokers. A total of 236 breath and urine samples were collected from smokers who participated in two separate studies involving three independent, 96-hr (i.e., Monday-Friday), Latin-square-ordered, abstinence or smoking conditions; a minimum 72-hr washout separated each condition. Each urine sample was analyzed with GC/MS and ITS. Under these study conditions, CO demonstrated moderate sensitivity (83.1%) and strong specificity (100%), whereas ITS assessment showed strong sensitivity (98.5%) and weak specificity (58.5%). In this study of short-term abstinence, ITS classified as nonabstinent nearly half of the samples collected from abstaining smokers. However, it classified nearly all nonabstinent smokers as currently smoking. Validation of ITS using GC/MS results from smokers undergoing more than 96 hr of abstinence may be valuable.
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ABSTRACT: AimsTo investigate the relationship between cannabis and tobacco use by age 15 and subsequent educational outcomes.DesignBirth cohort studySettingEnglandParticipantsThe sample was drawn from the Avon Longitudinal Study of Parents and Children; a core sample of 1,155 individuals had complete information on all the variables.MeasurementsMain exposures were cannabis and tobacco use at age 15 assessed in clinic by computer assisted questionnaire and serum cotinine. Main outcomes were performance in standardised assessments at 16 (Key Stage Four, GCSE) in English and mathematics (mean scores), completion of five or more assessments at grade C level or higher and leaving school having achieved no qualifications. Analyses were sequentially adjusted for multiple covariates using a hierarchical approach. Covariates considered were: maternal substance use (ever tobacco or cannabis use, alcohol use above recommended limits) ; life course socio-economic position (family occupational class, maternal education, family income); child sex; month and year of birth; child educational attainment prior to age 11 (Key Stage 2); child substance use (tobacco, alcohol and cannabis) prior to age 15 and child conduct disorder.FindingsIn fully adjusted models both cannabis and tobacco use at age 15 were associated with subsequent adverse educational outcomes. In general the dose response effect seen was consistent across all educational outcomes assessed. Weekly cannabis use was negatively associated with English GCSE results (Grade Point Difference [GPD], −5.93, 95% CI, −8.34, −3.53) and with mathematics GCSE results (GPD, −6.91, 95% CI, −9.92, −3.89). Daily tobacco smoking was negatively associated with English GCSE (GPD, −11.90, 95% CI, −13.47, −10.33) and with mathematics GCSE (GPD, −16.72, 95% CI, −18.57, −14.86). The greatest attenuation of these effects was seen on adjustment for other substance use and conduct disorder. Following adjustment tobacco appeared to have a consistently stronger effect than cannabis.Conclusions Both cannabis and tobacco use in adolescence are strongly associated with subsequent adverse educational outcomes. Given the non-specific patterns of association seen and the attenuation of estimates on adjustment it is possible that these effects arise through non-causal mechanisms, although a causal explanation cannot be discounted. This article is protected by copyright. All rights reserved.Addiction 12/2014; 110(4). DOI:10.1111/add.12827 · 4.60 Impact Factor
Article: Peter macklem.Canadian respiratory journal: journal of the Canadian Thoracic Society 01/2011; 18(2):65. · 1.66 Impact Factor
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ABSTRACT: Background: We investigated ATP-binding cassette transporters A1/G1 expression and function in mediating cholesterol efflux by examining the macrophages of cigarette-smoking patients with coronary artery disease (CAD) before and after smoking abstinence. Methods and Results: Peripheral blood monocyte cells were collected from non-smokers (n=17) non-CAD (NCAD) smokers (n=35), and CAD smokers (n=32) before and after 3 months smoking cessation. We found that the ABCA1 expression level was lower in macrophages from both NCAD and CAD smokers than for non-smokers at baseline. The ABCA1 function of mediating cholesterol efflux was reduced in NCAD and CAD smokers as compared with non-smokers. After 3 months smoking cessation, ABCA1 expression and function were improved in CAD smokers. However, ABCG1 expression and function did not change after smoking cessation. Furthermore, ABCA1 expressions were inhibited by tar in THP-1-derived macrophages through the inhibition of Liver X receptors. Nicotine and carbon monoxide did not inhibit ABCA1 expression. Conclusion: Our results indicate that chronic cigarette smoking impaired ABCA1-mediated cholesterol efflux in macrophages, and tobacco abstinence reversed the function and expression of ABCA1, especially in CAD patients. It was tobacco tar, rather than nicotine or carbon monoxide, that played a major role in the tobacco-induced disturbance of cellular cholesterol homeostasis. Copyright © 2015, The American Society for Biochemistry and Molecular Biology.The Journal of Lipid Research 01/2015; 56(3). DOI:10.1194/jlr.P055491 · 4.73 Impact Factor