Kim, Hoon;Kim, Seul Ki;Yu, Eun Jeong;Lee, Jung Ryeol;Jee, Byung Chul;Suh, Chang Suk;Kim, Seok Hyun
Clinical and Experimental Reproductive Medicine
/
v.42
no.4
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pp.136-142
/
2015
Objective: Smoking has been reported to harm nearly every organ of the body, but conflicting results have been reported regarding the effects of smoking on assisted conception. In this prospective cohort study, we aimed to investigate the prevalence of positive urinary cotinine tests in infertile couples and whether cotinine positivity was associated with infertility treatment outcomes. Methods: A qualitative urinary cotinine test was administered to 127 couples who underwent in vitro fertilization (IVF, n=92) or intrauterine insemination (IUI, n=35). Results: The overall prevalence of positive urinary cotinine test was 43.3% (55/127) in the male partners and 10.2% (13/127) in the female partners with similar prevalence rates in both genders in the IUI and IVF groups. Semen characteristics, serum markers of ovarian reserve, and number of retrieved oocytes were comparable among cotinine-positive and cotinine-negative men or women (with the exception of sperm count, which was higher among cotinine-positive men). The results of urinary cotinine tests in infertile couples were not associated with IVF and IUI outcomes. Conclusion: The presence of cotinine in the system, as indicated by a positive urinary cotinine test, was not associated with poorer outcomes of infertility treatment.
Objectives : This study was conducted to validate self-reported smoking among high school students using urinary cotinine. Methods : A self report of smoking behavior was collected together with urine sample for cotinine analysis from 130 male and female students in two vocational high school students in November, 2007. Validity and agreement between self-reported smoking and urinary cotinine was analyzed with STATA 9.0 for different definitions of current smokers, and frequent and daily smokers. Urinary cotinine concentration was measured by the DRI Cotinine Assay for urine (Microgenics Corp., Fremont, CA) on Toshiba 200FR. The cut-off point of urinary cotinine was 50 ng/dl. Results : The concentrations of urinary cotinine were significantly different according to the frequency and amount of smoking. Sensitivity and specificity was 90.9% and 91.8% respectively, and the Cohen s kappa value was 0.787 among the current smokers who smoked at least one day during one month preceding the survey. The comparable high sensitivity, specificity, and kappa value were shown also among the other definitions of current smokers, that is, subjective smokers, and weekly smokers. Conclusions : The results showed the high validity of self-reported smoking among high school students. However, due to the small sample size and limitation of the participants, it is cautious to generalize the results to overall high school students.
This study was conducted to evaluate the personal effects of tobacco smoke and environmental tobacco smoke(ETS) by measuring the concentration of nicotine and cotinine in the urine. While 129 urine samples were being collected, Personal characteristics such as sex, age, number of years since a Person has been a smoker, average consumption number of cigarettes per day, and number of smoker in family were also surveyed. Collected urine samples were used for analysis of nicotine and cotinine by GC/NPD after Passing the extrelut column. In the urine of the smoker, the average contents of nicotine and cotinine were 5.38$\mu\textrm{g}$/ml and 3.14 $\mu\textrm{g}$/ml, respectively. The average contents of nicotine and cotinine were 0.18$\mu\textrm{g}$/ml and 0.07$\mu\textrm{g}$/ml in the urine of male non-smoker, respectively. The contents of nicotine and cotinine in the non-smoker's urine were dependent on sex and age. On the other hand, the contents of nicotine and cotinine in smoker's urine were dependent on average consumption amount of cigarettes per day. Also, there was a direct relation between nicotine levels in the smoker's urine and the average consumption number of cigarettes Per day of smoker. The Possible sources of nicotine and cotinine in the non-smoker's urine seemed to be caused by food, beverage and En, Our results indicate that the number of smoker in family had no effect on increasing nicotine and cotinine contents in the urine of non-smoker.
Nicotine is one of the major hazardous components in cigarettc smoke. Nicotine deals a harmful effect to smokers and passive smokers due to its rapid conversion to various carcinogenic metabolites. Nitrosamine-4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is believed to cause lung cancers among the nicotine-derived carcinogens. Recent studies report that NNK synthesis can be inhibited by the metabolism pathway to produce a stable metabolite cotinine from nicotine. Tea polyphenols have been known to contain factors to prevent cancers and to retard progression of cancers. This study aims to correlate tea polyphenol's potential for cancer prevention with an accelerated formation of cotinine. The conversion from nicotine to cotinine in the presence of tea extracts or three polyphenols (Catechin, epicatechin gallate, epigallocatechin gallate) was measured in established cell lines and in Xenopus oocytes. Among three lines of cell used, PLC/PRF5 and HEK293 cells showed a fast turnover from nicotine to cotinine while HepG2 cell line showed a marginal difference between groups treated and non-treated with tea polyphenols. When Xenopus oocytes were microinjected with nicotine, tea polyphenols appear to accelerate the conversion of nicotine to cotinine. Among the polyphenols tested in this study, (+)-catechin showed the best efficiency overall in accelerating conversion from nicotine to cotinine both in the cell lines and in the oocytes. In summary, the present study indicated that tea polyphenols have a positive effect on conversion of nicotine to cotinine.
This study aims to find the correlation the low-molecule fucoidan for cancer prevention with an accelerated formation of cotinine. In the presence of fucoidan, a nicotine to cotinine coversion was studied in established assay, direct mixture method and Hep-G2 cell line method. Fucoidan of $1{\mu}g/mL$ showed the potential effect for converting nicotine to cotinine in the direct mixture method compared to control. Increase of conversion rate at the treatment of fucoidan is exhibited as 15 times compared to control. In Hep-G2 cell treatment, fucoidan showed the potential activity for converting nicotine to cotinine as 6 times compared to control. Therefore, fucoidan was shown to be effective in the conversion of nicotine into cotinine even though it is not higher content of polyphenol and flavonoid than its of green tea extract.
The purpose of the study was to assess relationship between smoking-related questionnaire and urinary cotinine. Seventy-five students of each one class of the first and second grade in one vocational school were administered the smoking-related items of the Youth Risk Behavior Survey October 2000, after which urine samples were collected. Urinary cotinine was detected by qualitative AccuSign Nicotine immunoassay. Positivity of urinary cotinine was detected in 29 of 75 students (38.7%). Kappa coefficients between self-reported smoking behaviors and positivity of urinary cotinine were all statistically significant, showing 0.41, 0.50, 0.28, 0.71 in lifetime smokers, regular smokers, current smokers, and current frequent smokers, respectively. These results showed that self-reported questionnaire may be useful in smoking-related survey and qualitative urinary cotinine may be used as validation of self-reported questionnaire.
The aim of the present study was to clarify whether cotinine affects the release of catecholamines (CA) from the isolated perfused rat adrenal gland, and to establish the mechanism of its action, in comparison with the response of nicotine. Cotinine (0.3∼3 mM), when perfused into an adrenal vein for 60 min, inhibited CA secretory responses evoked by ACh (5.32 mM), DMPP (a selective neuronal nicotinic agonist, 100 $\mu$M for 2 min) and McN-A-343 (a selective muscarinic $M_1 -agonist, 100 \mu$ M for 2 min) in dose- and time-dependent manners. However, cotinine did not affect CA secretion by high $K^+$ (56 mM). Cotinine itself also failed to affect basal CA output. Furthermore, in the presence of cotinine (1 mM), CA secretory responses evoked by Bay-K-8644 (an activator of L-type $Ca^{2+}$ channels, 10 $\mu$ M) and cyclopiazonic acid (an inhibitor of cytoplasmic $Ca^{2+}-ATPase, 10 \mu$ M) were relative time-dependently attenuated. However, nicotine (30$\mu$ M), given into the adrenal gland for 60 min, initially rather enhanced CA secretory responses evoked by ACh and high $K^+$, followed by the inhibition later, while it time-dependently depressed the CA release evoked by McN-A-343 and DMPP. Taken together, these results suggest that cotinine inhibits greatly CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors, but does fail to affect that by the direct membrane-depolarization. It seems that this inhibitory effect of cotinine may be exerted by the cholinergic blockade, which is associated with blocking both the calcium influx into the rat adrenal medullary chromaffin cells and $Ca^{2+}$ release from the cytoplasmic calcium store. It also seems that there is a big difference in the mode of action between cotinine and nicotine in the rat adrenomedullary CA secretion.
Background: In monitoring exposure to environmental smoke (ETS), biomarkers can overcome the subjectivity and inaccuracy of self-reporting measurements, and have the advantage of reflecting ETS exposure in all places. This study aims to evaluate the effectiveness of ETS exposure measurement using biomarkers such as urine cotinine. Methods: This study used the Korea National Health and Nutrition Survey data from 2009 to 2018. A total of 28,574 non-smokers with urine cotinine data were selected for the study. The cotinine concentration and ETS exposure rate using urine cotinine was estimated and then compared with the self-reporting measurements. The degree of agreement among measurements of ETS exposure was confirmed. Results: As a result of measuring ETS exposure with urine cotinine, 23,594 (83.8%) out of 28,574 subjects were classified as to exposure groups. This estimate differs significantly from measurements made by self-reporting. In addition, the average concentration of cotinine in non-smokers has decreased to a 10th level over the past 10 years. Based on the biomarker, the sensitivity of the self-reporting was 8.5%-29.0%, the specificity was 16.4%-19.5%, and the kappa value was 2.0%-5.8%. Conclusion: The findings of our study show that self-reporting measurement does not well reflect the extent to which non-smoker's exposure to smoking materials. Whereas cotinine concentration has decreased significantly over the past 10 years, the ETS exposure rate has not reduced. It strongly suggests the need for intervention in the group of non-smokers exposed to low concentrations of smoke. Therefore, an assessment using biomarkers such as cotinine-based measurement should be made in the Health Plan 2030.
Background: Smoking exposure may be objectively assessed through specific biomarkers. The most common biomarker for smoking is cotinine concentration in urine, and setting an optimal cut-off point can accurately classify smoking status. Such a cut-off point for Korean adolescents has never been studied. Objectives: The aim of this study was to determine a cut-off point for urinary cotinine concentration for the discrimination of smoking in adolescents. Methods: Participants were adolescents aged 13~18 years who participated in the third cycle of the Korean National Environmental Health Survey. We used urine samples to confirm the level of cotinine concentrations. Smoking status was determined by self-reported questionnaire. We identified the optimal cotinine cut-off point for discriminating smoking status using receiver operating characteristic curve analysis. Results: Of the 904 participants, 28 (3.1%) were smokers, among whom 20 (71.4%) were male. The median urinary cotinine concentrations in smokers was 218 ㎍/L (male: 215 ㎍/L, female: 303 ㎍/L), and that in non-smokers was 1.31 ㎍/L (male: 1.46 ㎍/L, female: 1.18 ㎍/L). We found significant differences in urinary cotinine concentration according to smoking status and sex (p<0.001). Urinary cotinine concentrations performed well for identifying smoking adolescents [area under the curve: 0.954 (male: 0.963, female: 0.908)]. The cut-off that optimally distinguished smokers from non-smokers was 39.85 ㎍/L (sensitivity: 89.3%, specificity: 97.4%). Male [39.85 ㎍/L (sensitivity: 90.0%, specificity: 94.9%)] had a different optimal cut-off point than female [26.26 ㎍/L (sensitivity: 87.5%, specificity: 99.6%)]. Conclusions: This study determined a cut-off point for urinary cotinine of 39.85 ㎍/L (male: 39.85 ㎍/L, female: 26.26 ㎍/L) to distinguish smokers from non-smokers in adolescents.
Desouky, Dalia El Sayed;Elnemr, Gamal;Alnawawy, Ali;Taha, Azza Ali
Asian Pacific Journal of Cancer Prevention
/
v.17
no.1
/
pp.139-145
/
2016
Environmental tobacco smoke (ETS) is a major public health problem for all ages. Despite the high prevalence of smoking among the Saudi population, there is limited information about levels of urinary cotinine in Saudi children exposed to SHS. The aim of the study was to assess the exposure of schoolchildren to ETS, and measure their urinary cotinine levels. Multistage cluster sampling was carried out, where schoolchildren from 4 schools were randomly chosen from primary schools in Taif city. A questionnaire including questions on SHS exposure and smoking rules in the residence were sent to students parents/guardians. Urine samples were taken and analyzed for total cotinine using chemiluminescent immunoassay. Of the studied children, 38.4% had a smoking father, 61.8%, 41.2% and 49.3% of them were exposed to ETS indoors, outdoors and both indoors and outdoors respectively. The mean urinary cotinine was significantly higher among children exposed to ETS compared to unexposed children. Urinary cotinine levels in children with both indoor and outdoor exposure was significantly higher compared with its level in children with single exposure. A significant positive correlation was found between urinary cotinine concentrations and the number of cigarette packs smoked by parents, and the number of smokers in the residence. The mean urinary cotinine level was significantly higher in children who reported no smoking rules at the residence.. The study revealed a high exposure of Saudi children to ETS. An antismoking media awareness campaign on the harmful effects of ETS should be carried out, in addition to family counseling programs targeted to parents to protect their children from ETS.
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