Urinary Cotinine Measurements Research Articles

Urinary biomarkers for secondhand smoke.

The use of a biomarker is mandatory for quantitative analysis of exposure to secondhand smoke (SHS). This article summarizes urinary biomarkers of smoke exposure which can be now quantified. The most reliable urinary biomarkers to assess the exposure to SHS are NNAL 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and NNAL-Glucuronides, which is metabolites of tobacco-specific nitrosamine. These substances were detected even in 50% of children who had undetectable level of cotinine (<0.5 ng/ml). Urinary cotinine, which is determined by a highly sensitive competing enzyme immunoassay, is also a useful biomarker. However, individual variability of CYP2A6 allele,in which nicotine is catalyzed to cotinine, affects the level of urinary cotinine. Approximately 20% of Japanese subjects have homozygotes or heterozygotes of the CYP2A6*4 allele, which has impaired nicotine metabolism and subsequently may underestimate the actual exposure to SHS. In assessing the exposure to SHS, therefore, individual variability of CYP2A6 gene polymorphism should be taken into consideration. The combination of urinary cotinine measurement and self-report of parents' smoking seems to be accurate to assess the exposure to SHS in mass screening.

The role of GSTP1 polymorphisms and tobacco smoke exposure in children with acute asthma

Background. The glutathione S-transferase enzymes (GSTs) play an important role in the detoxification of environmental tobacco smoke (ETS), which contributes to airway inflammation, a key component of asthma. Genetic variation in GST genes may influence individuals' ability to detoxify environmental pollutants. Objective. To examine the role of polymorphisms in GSTP1 (Ile105Val and Ala114Val), alone and in combination with ETS exposure, on atopy and asthma severity. Methods. GSTP1 Ile105Val and Ala114Val were genotyped and ETS exposure was assessed by parental questionnaire, which was validated by urinary cotinine measurements. Associations between ETS exposure, GSTP1 polymorphisms, and their interaction on atopy and asthma severity were investigated. Results. For the functional GSTP1 105 SNP, those with the Ile/Ile genotype had odds for atopy of 2.77 (p = .054) when assessed by genotype alone, which increased to 9.02 (p = .050) when ETS was included, relative to individuals with other genotypes. Likewise, compared to children with other GSTP1 114 genotypes, those with Ala/Ala genotype had a 5.47-fold (p = .002) increased risk of atopy (p = .020) when assessed by genotype alone, increasing to 9.17-fold when ETS was included. The 105 Ile/Ile individuals all had the AA (105 Ile/Ile and 114 Ala/Ala) haplotype group; therefore, the odds for atopy were the same. Individuals without any *C haplotype (105 Val and 114 Val allele) who were exposed to ETS had a 9.17-fold increased risk of atopy when compared with individuals with at least one *C haplotype and not exposed to ETS (p = .020). Conclusion. There were significant interactions between GSTP1 SNPs, atopy, and ETS exposure in this cohort.

Household Smoking Behavior: Effects on Indoor Air Quality and Health of Urban Children with Asthma

The goal of the study was to examine the association between biomarkers and environmental measures of second hand smoke (SHS) with caregiver, i.e. parent or legal guardian, report of household smoking behavior and morbidity measures among children with asthma. Baseline data were drawn from a longitudinal intervention for 126 inner city children with asthma, residing with a smoker. Most children met criteria for moderate to severe persistent asthma (63%) versus mild intermittent (20%) or mild persistent (17%). Household smoking behavior and asthma morbidity were compared with child urine cotinine and indoor measures of air quality including fine particulate matter (PM(2.5)) and air nicotine (AN). Kruskal-Wallis, Wilcoxon rank-sum and Spearman rho correlation tests were used to determine the level of association between biomarkers of SHS exposure and household smoking behavior and asthma morbidity. Most children had uncontrolled asthma (62%). The primary household smoker was the child's caregiver (86/126, 68%) of which 66 (77%) were the child's mother. Significantly higher mean PM(2.5), AN and cotinine concentrations were detected in households where the caregiver was the smoker (caregiver smoker: PM(2.5) μg/m(3): 44.16, AN: 1.79 μg/m(3), cotinine: 27.39 ng/ml; caregiver non-smoker: PM(2.5): 28.88 μg/m(3), AN: 0.71 μg/m(3), cotinine:10.78 ng/ml, all P ≤ 0.01). Urine cotinine concentrations trended higher in children who reported 5 or more symptom days within the past 2 weeks (>5 days/past 2 weeks, cotinine: 28.1 ng/ml vs. <5 days/past 2 weeks, cotinine: 16.2 ng/ml; P = 0.08). However, environmental measures of SHS exposures were not associated with asthma symptoms. Urban children with persistent asthma, residing with a smoker are exposed to high levels of SHS predominantly from their primary caregiver. Because cotinine was more strongly associated with asthma symptoms than environmental measures of SHS exposure and is independent of the site of exposure, it remains the gold standard for SHS exposure assessment in children with asthma.

Passive smoking is associated with lower serum HDL‐C levels in school children

In recent years, a number of studies have reported that exposure to environmental tobacco smoke (ETS) reduces high-density lipoprotein cholesterol (HDL-C) levels in children, as well as in adults. Further, a number of countries have indicated that passive smoking increases the risk of early arteriosclerosis onset. Here, to evaluate the effects of ETS exposure, we conducted a cross-sectional epidemiological study on primary school children in Japan using answers from a questionnaire survey, as well as urine cotinine and lipid metabolism-related variable measurements. A total of 121 sixth-grade primary school children participated in this study by completing a questionnaire about their food intake, lifestyle and family smoking habits. Early in the morning, we also measured height, weight, blood pressure, serum levels of total cholesterol, triglyceride, HDL-C, and blood sugar, as well as urine levels of cotinine and creatinine under unfed conditions. From the questionnaire, 40 and 81 children reported being exposed and not exposed to ETS, respectively. Serum HDL-C levels, which were adjusted for the degree of corpulence and exercise habits, were significantly lower in the passive smoker group than the non-passive-smoker group (65.3 and 72.1 mg/dL, respectively; P= 0.012). In addition, proportional differences in serum HDL-C levels were also observed based on the amount of cigarettes smoked at home by family members of the child. Results suggest that ETS exposure at home is associated in a dose-related manner with lower serum HDL-C levels in primary school children. In addition, our results suggest that smoking in the presence of children who are not usually exposed to ETS increases the risk of arteriosclerosis. Given these findings, we strongly recommend the establishment of anti-passive-smoking measures.

Self-reported Smoking and Urinary Cotinine Levels among Pregnant Women in Korea and Factors Associated with Smoking during Pregnancy

This study examined urinary cotinine levels and self-reported smoking among pregnant women in Korea and the factors associated with smoking during pregnancy. The subjects were selected from pregnant women who visited 30 randomly sampled obstetric clinics and prenatal care hospitals in Korea in 2006. Smoking status was determined by self-reporting and urinary cotinine measurement. A total of 1,090 self-administered questionnaires and 1,057 urine samples were analyzed. The percentage of smoking revealed by self-reporting was 0.55% (95% confidence interval [CI], 0.11-0.99) and that revealed by urinary cotinine measurement (>100 ng/mL) was 3.03% (95% CI, 1.99-4.06). The kappa coefficient of agreement between self-reported smoking status and urinary cotinine measurement was 0.20 (95% CI, 0.03-0.37). Multiple logistic regression analysis revealed that early gestational period, low educational level, and being married to a smoker were significant risk factors for smoking during pregnancy. Smoking among pregnant women in Korea is not negligible, and those who are concerned to maternal and child health should be aware of this possibility among pregnant women in countries with similar cultural background.

Exhaled carbon monoxide screening for environmental tobacco smoke exposure in preanesthetic children

Exposure to environmental tobacco smoke (ETS) is associated with an increased risk of perioperative adverse events in children. The purpose of this study was to evaluate exhaled carbon monoxide (CO) as a preoperative ETS screening tool in children. Five hundred and one children aged 6-15 years were enrolled. The child's guardian completed a questionnaire that surveyed environmental exposures to CO and ETS. A preoperative urine sample was obtained from children who assented and were able to void, and urine cotinine values were measured. Exhaled CO was measured using the EC50-Micro Smokerlyzer (Bedfont Scientific Ltd, UK). Four hundred and fifty-one subjects completed the study, and urine samples were obtained from 83. 25% of subjects were classified as exposed to ETS based on questionnaire results. Exhaled CO values did not correlate with either the qualitative (questionnaire) or quantitative (urine cotinine) measurements of ETS exposure. Exhaled CO predicted a urine cotinine/creatinine ratio >10 with a sensitivity of 10% and a specificity of 85%. Exhaled CO measured by this device is not a useful preoperative screening tool for ETS exposure in children. Because exhaled CO has been used successfully to monitor ETS exposure in adolescents, we believe that its failure in our population is as a result of the limited ability of small children to perform vital capacity maneuvers in order to provide an adequate endtidal sample.

Smoking cessation is challenging even for patients recovering from lung cancer surgery with curative intent

Background Although it is recommended that smokers undergoing surgery for lung cancer quit smoking to reduce post-operative complications, few studies have examined patterns of smoking in the peri-operative period. The goals of this study were to determine: (1) patterns of smoking during post-operative recovery, (2) types of cessation strategies used to quit smoking, and (3) factors related to smoking after lung cancer surgery. Methods Data were collected from 94 patients through chart review, tobacco, health status, and symptom questionnaires at 1, 2, and 4 months after surgery. Smoking status was assessed through self-report and urinary cotinine measurement. Results Eighty-four patients (89%) were ever-smokers and 35 (37%) reported smoking at diagnosis. Thirty-nine (46%) ever-smokers remained abstinent, 13 (16%) continued smoking at all time-points, and 32 (38%) relapsed. Ten (46%) of those who relapsed were former-smokers and had not smoked for at least 1 year. Sixteen (46%) of those who were smoking at diagnosis received cessation assistance with pharmacotherapy being the most common strategy. Factors associated with smoking during recovery were younger age and quitting smoking ≤6 months before the diagnosis of lung cancer. Factors that were marginally significant were lower educational level, male gender, lower number of comorbidities, and the presence of pain. Conclusion Only half of those who were smoking received assistance to quit prior to surgery. Some patients were unable to quit and relapse rates post-surgery were high even among those who quit more than 1 year prior. Innovative programs incorporating symptom management and relapse prevention may enhance smoking abstinence during post-operative care.

The dog as a passive smoker: Effects of exposure to environmental cigarette smoke on domestic dogs

Of the few studies available regarding the effects of smoking on animals, most of them involve animals actively smoking through the use of a mask or tracheostomy. The present study investigated the effects of passive smoke exposure on domestic dogs. The sample comprised 30 Yorkshire terriers (18 males) ranging in age from 27 to 106 months (M = 38.6+/-15.8) and weighing 1.9-4.0 kg (M = 3.04+/-0.48). Half of the dogs came from homes where residents smoked at least 20 cigarettes/day for a minimum of 24 months, and the other half were from homes without smokers. All animals were subjected to bronchoalveolar lavage to determine cell populations and the presence of anthracosis in macrophage cytoplasm; in addition, a carinal biopsy was obtained. To characterize environmental cigarette smoke exposure, urinary cotinine was determined by an immunochromatographic assay. Cotinine was not detected in the urine of dogs not exposed to cigarette smoke, whereas exposed dogs tested positive. In dogs exposed to cigarette smoke, macrophage and lymphocyte populations were significantly increased (p<.05) and anthracosis was present in the cytoplasm of macrophages. The measurement of urinary cotinine by an immunochromatographic assay is an effective method that can be used to confirm environmental tobacco exposure. Cytological analysis of bronchoalveolar lavage fluid demonstrated airway alterations triggered by passive exposure to tobacco smoke in domestic animals.

Measurement of cotinine in urine by liquid chromatography tandem mass spectrometry

Cotinine is the major metabolite of nicotine. It is also a specific biomarker for nicotine exposure in cigarette smokers. The measurement of urine cotinine concentration will enable: (1) the assessment of the smoking status of lung transplant patients and (2) tobacco abstinence to be studied in patients during treatment under smoking cessation programmes. We have developed and validated a method for the measurement of urinary cotinine using reversed phase high-performance liquid chromatography (HPLC) coupled to tandem mass spectrometry (LC-MS/MS). This technique utilizes online ion exchange coupled with an analytical column to eliminate ion suppression effects. The chromatography was performed using a Waters 2795 Alliance HT LC system. Cotinine and d3-cotinine had a retention time of 2.5 min and the cycle time from injection to injection was 4 min. The transition identified for cotinine was m/z 177.1>79.6 and for d3-cotinine m/z 180.2>79.6. This method was linear up to 1000 microg/L. Mean recovery of the assay was 112% with a range of 107-117% (n=9). The limit of quantitation for this assay was 2.5 microg/L and the limit of detection was 0.156 microg/L. The intra- and inter-assay imprecision was <12% and <10% respectively over a concentration range of 22-660 microg/L. We have developed a robust and rapid assay for measuring and analysing urine cotinine by LC-MS/MS, by utilizing a technique, which has reduced ion suppression effects. Ultimately, the method will facilitate the assessment of lung transplant patients' smoking status.

Validation of Self-Reported Smoking Status Using Saliva Cotinine: A Rapid Semiquantitative Dipstick Method

This study evaluated the performance characteristics of a novel rapid method for verifying smoking status in individuals by measurement of cotinine, the primary metabolite of nicotine, in saliva samples using an immunochromatographic strip in a "dipstick" format compared with liquid chromatography/mass spectrometry (LC/MS). A prospective comparison was made of smoking status as determined by measurement of cotinine in urine by LC/MS (the gold standard) and in saliva using a semiquantitative dipstick assay that uses cotinine-specific monoclonal antibodies attached to gold particles and a series of avidity traps to measure cotinine levels (saliva NicAlert). One hundred seventy-two individuals from a family practice/general medical setting agreed to participate after informed consent and institutional review board approval. Saliva NicAlert tests were done by untrained operators who followed written directions. Comparison of smoking status as determined by urine cotinine measurement by LC/MS (50 ng/mL cutoff) with the saliva strip test results, averaged over the two operators, indicated that the saliva test strip results had a sensitivity of 99% and a specificity of 96%. Saliva NicAlert also identified four smokers who reported being nonsmokers but were confirmed to be smokers by LC/MS. The saliva NicAlert assay seems to be a valid, highly sensitive, and specific method for validating self-reported smoking status and may have clinical applications in selected medical settings.

Evaluating environmental tobacco smoke exposure in a group of Turkish primary school students and developing intervention methods for prevention

BackgroundIn countries like Turkey where smoking is highly prevalent, children's exposure to tobacco smoke is an important public health problem. The goals of this study were to determine the self-reported environmental tobacco smoke exposure status of primary school students in grades 3 to 5, to verify self-reported exposure levels with data provided from a biomarker of exposure, and to develop methods for preventing school children from passive smoking.MethodsThe study was conducted on 347 primary school students by using a standard questionnaire and urinary cotinine tests. Children with verified ETS exposure were randomly assigned to 2 intervention groups. Two phone interviews were conducted with the parents of the first group regarding their children's passive smoking status and its possible consequences. On the other hand, a brief note concerning urinary cotinine test result was sent to parents of the second group. Nine months after the initial urinary cotinine tests, measurements were repeated in both groups.ResultsAccording to questionnaire data, 59.9% of the study group (208 of 347) were exposed to ETS. Urinary cotinine measurements of children were highly consistent with the self-reported exposure levels (P < 0.001). Two different intervention methods were applied to parents of the exposed children. Control tests suggested a remarkable reduction in the proportion of those children demonstrating a recent exposure to ETS in both groups. Proportions of children with urinary cotinine concentrations 10 ng/ml or lower were 79.5% in Group I and 74.2% in Group II (P > 0.05).ConclusionSelf-reported ETS exposure was found to be pretty accurate in the 9–11 age group when checked with urinary cotinine tests. Only informing parents that their childrens' ETS exposure were confirmed by a laboratory test seems to be very promising in preventing children from ETS.

Smoking cessation is challenging even after lung cancer surgery

19507 Background: It is recommended that patients undergoing lung cancer surgery quit smoking pre-operatively to reduce peri- operative complications. Smoking cessation after diagnosis is associated with improved clinical outcomes. Few studies have examined the behavior of surgical lung cancer patients who are smokers. We sought to 1) determine the smoking prevalence rate at diagnosis; 2) identify readiness to quit and cessation strategies, 3) describe patterns of smoking overtime, and 4) identify factors (demographic, tobacco-related, and health status) correlating with smoking relapse and/or continued smoking (SR) after surgery. Methods: Ninety-four patients were enrolled in a descriptive study. Data were collected through chart review and standardized tobacco and health status questionnaires. Smoking status was assessed through self-report and measurement of urinary cotinine. The primary endpoints were smoking status at 1, 2, and 4 months after surgery. Frequencies, t-tests, and chi-square were used for analysis. Results: Eighty-four patients (89%) were ever-smokers and 35 (42%) reported smoking at diagnosis. Twenty-nine (83%) current smokers attempted cessation at diagnosis and 18 (51%) received assistance with pharmacotherapy being the most common strategy. One month post-operatively, 20 (56%) self-reported smokers planned to quit within the following month. Fifty (60%) ever-smokers remained abstinent, 13 (15%) continued smoking, and 21 (25%) relapsed. Ten (48%) of those who relapsed were former smokers and had not smoked for at least a year before diagnosis. Factors significantly associated with SR included younger age, lower education and pain. Those who relapsed were on average 7 years younger (p=0.01). Those without high school education (HS) had a significantly higher rate of relapse as compared to those with at least HS (83% vs. 48%, p=0.04). Those with pain had a higher rate of relapse as compared to those who did not have pain (73% vs. 33%, p=0.03). Conclusions: Smoking relapse rates are high after lung cancer surgery even among those who previously quit. Former and current smokers are at high risk for relapse and will require smoking cessation programs incorporating symptom management and relapse prevention. No significant financial relationships to disclose.

HPLC Analysis of Cotinine in Urine After SPE with a Cholesterol-Modified Adsorbent

A one-step solid-phase extraction procedure, based on a new silica gel adsorbent modified with cholesterol groups, has been investigated for measurement of cotinine in urine. Cotinine is the main metabolite of nicotine in the human body and is analyzed as a biomarker for assessment of direct or passive exposure to tobacco smoke. New cholesterol-modified adsorbents have been obtained by chemical modification of silica gel of different porosity with cholesterol ligands. Although recovery by this extraction procedure were optimum over a relatively broad range of sample pH (3.1–8.0), analytical conditions such as sample loading, washing and elution conditions, concentration of cotinine to be extracted, and the type of adsorbent used for extraction were found to affect the efficiency of the procedure and had to be controlled for optimum recovery. When these conditions were controlled, recovery of cotinine from spiked human urine was reproducible and depended on compound ionization. Quantitative analysis of cotinine was performed by reversed-phase high-performance liquid chromatography with UV detection.

DNA adducts in human placenta exposed to ambient environment and passive cigarette smoke during pregnancy

The risk of human diseases and abnormal development under the relatively reduced toxic environmental exposure conditions of passive cigarette smoke and urban pollution is emerging as significant. To assess the genotoxic potential of such exposure, we analyzed the DNA adducts of polynuclear aromatic hydrocarbons (PAH), a proven marker of genotoxicity, in human placental DNA samples of pregnancies monitored for passive cigarette smoke exposure. Maternal exposure to active and passive cigarette smoke was evaluated by verbal disclosure and urinary nicotine and cotinine measurements. PAH-DNA adducts were assayed by ELISA using a polyclonal antibody against benzo[alpha]pyrene-diol-epoxide-DNA in placental DNA. Birth weights of infants were recorded in these monitored pregnancies. Urinary nicotine and cotinine values were reduced in the passive smoke-exposed group compared to smokers and similar to those in the nonsmoker ambient exposure group. PAH-DNA and nicotine/cotinine values were not correlated with birth weight of the infant. PAH-DNA adducts were present in approximately 25% of samples exposed to passive cigarette smoke and ambient environment. The study has revealed that a subpopulation of humans is predisposed to accumulating PAH adducts independent of high levels of PAH sources (e.g., maternal cigarette smoke exposure). Because DNA adducts promote genomic changes, it is likely that this subpopulation is susceptible to diverse changes in the genome that may influence human development.

Neonatal Urinary Cotinine Correlates With Behavioral Alterations in Newborns Prenatally Exposed to Tobacco Smoke

Altered behavior due to prenatal smoke exposure was examined in 25 neonates born from smoking mothers who consumed at least 5 cigarettes/d during the entire gestation. Data were compared with 25 matched neonates born from nonsmoking mothers. Neonatal behavior was evaluated using the Brazelton Neonatal Behavioral Assessment Scale (BNBAS). Antenatal exposure to tobacco smoke at the end of the pregnancy was determined by measurement of urinary cotinine. Newborns from smoking mothers showed significant lower scores in various BNBAS items compared with neonates from nonsmoking mothers. A strong correlation was observed between infant irritability and urinary cotinine in newborns from smoker and nonsmoking mothers and with number of daily smoked cigarettes and maternal nicotine daily intake of infants exposed to active maternal smoking. Linear regression analysis showed that urinary cotinine was the best predictor of infant irritability (r(2) = 0.727). The latter was also associated to the neonate's low level of attention and poor response to inanimate auditory stimuli. Among infants from nonsmoking mothers, paternal smoking significantly correlated with infant urinary cotinine and infant irritability, being also the best predictor of irritability (r(2) = 0.364). Neonatal behavior can be significantly altered in a dose-dependent manner even after modest prenatal exposure to tobacco smoke.

Comparison of parental reports of smoking and residential air nicotine concentrations in children

Background: Using questionnaires to assess children’s residential exposure to environmental tobacco smoke (ETS) may result in misclassification from recall and response bias. Questionnaire data have frequently been validated against urinary...

Environmental tobacco smoke exposure in school children: parent report and urine cotinine measures

Environmental tobacco smoke (ETS) in the home continues to be a major health risk for children around the world. Measuring ETS is a central feature of clinical and epidemiological studies, with children's exposure often assessed through parental estimates. The authors examined the relationship between parent-reported estimates of children's exposure to ETS and children's urinary cotinine levels and evaluated the ETS exposure and its effect on respiratory health in children. A total of 188 school children were included in the study. Parents were asked to complete a questionnaire about their smoking habits, their children's respiratory morbidity status and housing conditions. Urinary cotinine levels were measured in children. According to the responses, 72.3% of the children came from households with smokers, and 34.6% had daily exposure to ETS. When urine cotinine levels of >10 ng/mL were used as the yardstick of exposure, 76% of the children were identified as ETS exposed. No relation was detected between the symptoms of respiratory tract diseases and ETS exposure. To determine the amount of ETS exposure, the contribution of parental reports was low. To evaluate the level of ETS exposure of children, the parents' reports were not reliable. The addition of a biological measure results in a more informative estimate of ETS exposure in children.

A passive smoking screening program for children

Background. There has been no report to date on mass screening of passive smoking in children using biomarkers. Method. To identify children exposed to actual environmental tobacco smoke (ETS), 261 children were divided into the following 3 groups: (A) both parents smoke; (B) one parent smokes; and (C) no parent smokes. Child urinary cotinine measurement and a parent questionnaire were obtained. Results. Urinary cotinine was positive (> 10 ng/ml) in 92 (35.2%) of the 261 children. Of the 92 children, 29 were classified into group A, 47 into group B, and 16 into group C. The percentages of children who tested positive for urinary cotinine in groups A, B, and C were 56.9%, 31.1%, and 27.1%, respectively. However, in group B, the percentage of children who tested positive for urinary cotinine was significantly higher if only the mother smoked (47.1%) than if only the father smoked (29.1%) ( P < 0.05). The mean + SD urinary cotinine level in group A was 12.9 ± 6.5 ng/ml, and that in group B was 10.4 ± 3.8 ng/ml if the mother smoked and 5.4 ± 2.6 ng/ml if the father smoked. Conclusions. This smoking screening program may be useful in identifying children with actual ETS exposure and motivating their parents to either quit smoking or modify their smoking behavior around children.

A Controlled Trial of a Quit and Win Contest

To evaluate the impact of a state-of-the-art Quit and Win contest on tobacco quit rates at 3, 6, and 12 months after the 30-day quit period. Quasi-experimental with a volunteer sample of 494 Quit and Win contest registrants (treatment group) and 512 randomly selected tobacco users not exposed to the promotional media campaign (control group). Intervention included a 30-day quit period to be eligible for large cash prizes; provider advice via weekly mailings; online and telephone quit assistance; media campaign; and community support. Community-based intervention in Kentucky. A total of 1006 adult tobacco users. Quit rates were measured using 7-day point prevalence for tobacco use. Urine cotinine measurements confirmed self-reported quitting. Treatment group participants were significantly more likely than controls to experience quitting during the 1-year follow-up, as determined by both self-report and urine confirmation. After adjusting for baseline differences in demographics, tobacco use, and stage of change, those in the treatment group had 2.6 times the odds of reporting quitting in the postintervention period and 5.3 times the odds of experiencing quitting confirmed by urine cotinine, relative to controls. Women, minorities, and low-income tobacco users had equal odds of quitting as men, whites, and those with higher incomes. That the contest was minimally intensive and yielded a relatively high, quit rate demonstrates the potential effectiveness of the intervention.

Only two-week smoking cessation improves platelet aggregability and intraplatelet redox imbalance of long-term smokers

We investigated whether and how soon smoking cessation ameliorates the smoking-induced intracellular oxidative stress and platelet aggregability in long-term smokers. Smoking is a major risk factor of atherothrombosis. Smoking cessation reduces cardiac events. However, the underlying mechanisms of the beneficial effects remain to be elucidated. Twenty-seven male long-term smokers were divided into two groups. Group A (n = 14) quit smoking for four weeks whereas group B (n = 13) resumed smoking two weeks after quitting. Smoking status was monitored by measurement of urinary cotinine. Using gel-filtered platelets, agonist (adenosine diphosphate and collagen)-induced platelet aggregation, platelet-derived nitric oxide (PDNO), intraplatelet nitrotyrosine production, intraplatelet levels of the reduced form of glutathione (GSH) and its oxidized form (GSSG), and urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) and urinary 8-iso-prostaglandin F(2alpha) (8-iso-PGF(2alpha)), as markers of systemic oxidative stress, were measured. The baseline measurements were similar between the two groups. Smoking cessation quickly reduced agonist-induced platelet aggregations, intraplatelet nitrotyrosine level, and urinary productions of 8-OHdG and 8-iso-PGF(2alpha) by two weeks in both groups. In group A, they were maintained at the low levels until four weeks, whereas they were reversed by resmoking in group B; PDNO release and intraplatelet GSH/GSSG ratio were time-dependently increased by smoking cessation but reversed by resmoking. The present findings are the first demonstration that only two weeks of smoking cessation can ameliorate the enhanced platelet aggregability and intraplatelet redox imbalance in long-term smokers, possibly by decreasing oxidative stress. Our findings may strengthen the motivation for smokers to quit smoking.