Higher nicotine and carbon monoxide levels in menthol cigarette smokers with and without schizophrenia.

This study examined whether smoking menthol cigarettes was associated with increased biochemical measures of smoke intake. Expired carbon monoxide (CO) and serum nicotine and cotinine were measured in 89 smokers with schizophrenia and 53 control smokers immediately after smoking an afternoon cigarette. Serum nicotine levels (27 vs. 22 ng/ml, p = .010), serum cotinine levels (294 vs. 240 ng/ml, p = .041), and expired CO (25 vs. 21 ppm, p = .029) were higher in smokers of menthol compared with nonmenthol cigarettes, with no differences in 3-hydroxycotinine/cotinine ratios between groups when controlling for race. Backward stepwise linear regression models showed that, in addition to having a diagnosis of schizophrenia, smoking menthol cigarettes was a significant predictor of nicotine and cotinine levels. Individuals with schizophrenia or schizoaffective disorder smoked more generic or discount value brands (Basic, Doral, Monarch, USA, Wave, others) compared with control smokers (28% vs. 6%, p = .002) but did not smoke more brands with high nicotine delivery as estimated by the U.S. Federal Trade Commission method. Although rates of mentholated cigarette smoking were not higher in smokers with schizophrenia overall, they were significantly higher in non-Hispanic White people with schizophrenia compared with controls of the same ethnic/racial subgroup (51% vs. 28%, p<.0001). The higher exhaled CO in menthol smokers suggests that the higher nicotine levels are at least partly related to increased intake of smoke from menthol cigarettes, although menthol-mediated inhibition of nicotine metabolism also may be a factor. Menthol is an important cigarette additive that may help explain why some groups have lower quit rates and more smoking-caused disease.     

Salivary cotinine concentration versus self-reported cigarette smoking: Three patterns of inconsistency in adolescence.

The present study examined the extent and sources of discrepancies between self-reported cigarette smoking and salivary cotinine concentration among adolescents. The data are from household interviews with a cohort of 1,024 adolescents from an urban school system. Histories of tobacco use in the last 7 days and saliva samples were obtained. Logistic regressions identified correlates of three inconsistent patterns: (a) Pattern 1-self-reported nonsmoking among adolescents with cotinine concentration above the 11.4 ng/mg cutpoint (n = 176), (b) Pattern 2-low cotinine concentration (below cutpoint) among adolescents reporting having smoked within the last 3 days (n = 155), and (c) Pattern 3-high cotinine concentration (above cutpoint) among adolescents reporting not having smoked within the last 3 days (n = 869). Rates of inconsistency were high among smokers defined by cotinine levels or self-reports (Pattern 1 = 49.1%; Pattern 2 = 42.0%). Controlling for other covariates, we found that reports of nonsmoking among those with high cotinine (Pattern 1) were associated with younger age, having few friends smoking, little recent exposure to smokers, and being interviewed by the same interviewer as the parent and on the same day. Low cotinine concentration among self-reported smokers (Pattern 2) was negatively associated with older age, being African American, number of cigarettes smoked, depth of inhalation, and exposure to passive smoke but positively associated with less recent smoking and depressive symptoms. High cotinine concentrations among self-reported nonsmokers was positively associated with exposure to passive smoke (Pattern 3). The data are consonant with laboratory findings regarding ethnic differences in nicotine metabolism rate. The inverse relationship of cotinine concentration with depressive symptoms has not previously been reported. Depressed adolescent smokers may take in smaller doses of nicotine than nondepressed smokers; alternatively, depressed adolescents may metabolize nicotine more rapidly.     

An association of CYP2A6 genotype and smoking topography.

Nicotine is metabolized into biologically inactive cotinine primarily by the cytochrome P450 enzyme CYP2A6. CYP2A6 genetic variations have been phenotypically grouped as slow, intermediate, and normal metabolizers. Slow metabolizers smoke fewer cigarettes daily and weekly, and have lower carbon monoxide (CO) and plasma nicotine levels, suggesting a reduced smoking rate compared with normal metabolizers. CYP2A6 also is involved in the metabolic activation of tobacco-specific procarcinogenic nitrosamines, such as 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanol (NNAL). NNK is one of the most abundant and potent procarcinogens in cigarette smoke. The present study investigated the association of CYP2A6 genotype with smoking topography, a quantifiable measure of smoking behavior, in a sample of treatment-seeking smokers prior to treatment. Smoking topography measures indicative of quantity of smoke exposure--number of puffs, mean puff volume, and total puff volume--were the outcome variables. Covariates associated with smoking topography were included in the analyses. Results indicated that CYP2A6 genotype group had a significant effect on mean puff volume and total puff volume, but not number of puffs, such that slow metabolizers exhibited reduced puffing compared with others. Smokers having CYP2A6 variants resulting in low activity metabolize nicotine more slowly, and convert procarcinogen nitrosamines to carcinogens more slowly, than do normal metabolizers. The results from this study also suggest a behavioral mechanism that may account for reduced cancer risk in slow metabolizers.     

Gender differences relative to smoking behavior and emissions of toxins from mainstream cigarette smoke.

This study examined whether gender differences exist in the exposure to select mainstream cigarette smoke toxins as a result of differences in smoking behavior or type of cigarettes smoked among 129 female and 128 male smokers. Smoking topography data indicated that, compared with men, women took smaller puffs (37.6 ml/puff vs. 45.8 ml/puff; p = .0001) of shorter duration (1.33 s/puff vs. 1.48 s/puff; p = .002) but drew more puffs per cigarette (13.5 vs. 12.0; p = .001) and left longer butts (36.3 mm or 40.2% of cigarette length vs. 34.3 mm or 39.2% of cigarette length; p = .01). These trends were similar in both African Americans and European Americans. The emissions of select toxins per cigarette, as determined by mimicking human smoking behaviors were greater among the male smokers than the female smokers and correlated significantly with delivered smoke volume per cigarette. The geometric means of emissions of nicotine from cigarettes were 1.92 mg/cigarette (95% CI = 1.80-2.05) for women versus 2.20 (95% CI = 2.04-2.37) for men (p = .005). Cigarettes smoked by women yielded 139.5 ng/cigarette of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK; 95% CI = 128.8-151.0), compared with 170.3 ng/cigarette (95% CI = 156.3-185.6) for men (p = .0007); benzo(a)pyrene (BaP) emissions were 18.0 ng/cigarette (95% CI = 17.0-19.0) for women and 20.5 ng/cigarette (95% CI = 18.8-22.3) for men (p = .01). The gender differences with regard to cigarette smoke yields of toxins were more profound in European Americans than in African Americans. On average, African American men's smoking habits produced the highest emissions of select toxins from cigarettes, and European American female smokers had the lowest exposure to carcinogens and toxins. Several studies have suggested that women may be more susceptible than men to the ill effects of carcinogens in tobacco and tobacco smoke, whereas other studies have not found differences in lung cancer risk between men and women. The present study suggests that gender differences in exposure to tobacco smoke cannot account for a higher rate of lung cancer in female smokers compared with male smokers.     

The reliability and validity of self-reported puffing behavior: evidence from a cross-national study.

Self-reported puffing behavior has considerable potential as an indicator of smoking intensity, particularly in survey research evaluating population-based changes in smoking patterns. However, little is known about the reliability and validity of self-reported puffing behavior. This study compared smokers' perceptions of their puffing behavior with measures of both machine-determined puffing behavior and nicotine uptake to assess the utility of self-report. We assessed self-reported puffing behavior as well as demographic and smoking characteristics of 118 smokers from Australia, Canada, the United Kingdom, and the United States. At two visits, participants were asked to provide a saliva sample and to smoke a cigarette through a portable smoking topography device, the CReSSmicro, to measure puffing behavior. Saliva samples were assayed for cotinine, a measure of nicotine uptake, to provide estimates of smoke exposure. Intraclass coefficients for all measures of self-reported general puffing behavior were above .6, indicating that self-reported measures had fair-to-good test-retest reliability. Self-report, in particular of interpuff interval and number of cigarette puffs, was correlated only moderately with machine-determined puffing measures (.2相似文献   

Effects of low nicotine content cigarettes on smoke intake.

Cigarettes with selective reductions in nicotine delivery have been considered as potential tools to prevent or treat nicotine dependence or to reduce harm by virtue of reduced nicotine and nitrosamine delivery. An important question is whether individuals smoke these products more intensively, as has been shown to occur with ventilated-filter cigarettes. To investigate this issue, we compared conventional highly ventilated filter cigarettes, having very low tar and nicotine yields when smoked by Federal Trade Commission method (1 mg tar, 2 mg carbon monoxide [CO],.2 mg nicotine), with low nicotine content cigarettes, manufactured from a genetically modified strain of tobacco, which had higher tar but lower nicotine yield (14 mg tar, 13 mg CO,.02 mg nicotine). A total of 16 cigarette smokers participated in two 8-hr sessions (order counterbalanced) during which they smoked each type of cigarette ad libitum. Expired-air CO, plasma nicotine, and smoking topography measures were collected. Subjects showed significant increases in smoking when using the highly ventilated filter cigarettes, and puff volume was significantly greater than with the low nicotine content cigarettes. Subjects achieved an expired-air CO level 74% as high as with the low nicotine content cigarettes; the latter produced CO levels similar to those measured at baseline when subjects smoked their habitual brands of cigarettes. Plasma nicotine levels obtained when subjects smoked the highly ventilated filter cigarettes also were significantly higher than when they smoked the low nicotine content cigarettes. These results indicate that the delivery of substantial amounts of smoke, with selective reductions in nicotine yield, appears to prevent compensatory smoking behavior. Further studies should determine whether similar results are obtained in naturalistic environments.     

Smoking behaviour and toxin exposure during six weeks use of a potential reduced exposure product: Omni

Objective: To determine smoking behaviour, acceptability, and toxin exposure when smokers switch to the potential reduced exposure product—Omni cigarette.

Design: 12 week randomised, crossover study of Omni versus own cigarettes.

Participants: 19 light/ultralight and 15 regular smokers.

Outcomes: Cigarettes/day, smoking topography, craving, withdrawal symptoms, urinary cotinine plus its glucuronide (total cotinine), nicotine plus its glucuronide (total nicotine), and carcinogen metabolites (4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol plus its glucuronides and 1-hydroxypyrene).

Results: When switched to Omni, smokers smoked the same number of cigarettes/day, smoked Omni cigarettes less intensely (total puff volume = –11%) and had slightly lower total cotinine (–18%) levels than their own cigarettes, but had a slightly greater carbon monoxide boost/cig (+21%). Craving and withdrawal ratings were similar with Omni and own cigarettes. Carcinogen metabolite levels were somewhat but not significantly lower with Omni. About half of smokers rated Omni as better for their health and about two thirds stated it was weaker and worse tasting than their own cigarettes.

Conclusions: Although Omni may be an adequate behavioural and pharmacological substitute for traditional cigarettes, it may not decrease carcinogen exposure and may increase carbon monoxide. Replications with larger sample sizes and longer follow up are needed. These results indicate the need for regulation of reduced exposure and reduced risk claims.

     

Waterpipe smoking and nicotine exposure: a review of the current evidence.

The waterpipe, also known as shisha, hookah, narghile, goza, and hubble bubble, has long been used for tobacco consumption in the Middle East, India, and parts of Asia, and more recently has been introduced into the smokeless tobacco market in western nations. We reviewed the published literature on waterpipe use to estimate daily nicotine exposure among adult waterpipe smokers. We identified six recent studies that measured the nicotine or cotinine levels associated with waterpipe smoking in four countries (Lebanon, Jordan, Kuwait, and India). Four of these studies directly measured nicotine or cotinine levels in human subjects. The remaining two studies used smoking machines to measure the nicotine yield in smoking condensate produced by the waterpipe. Meta-analysis of the human data indicated that daily use of the waterpipe produced a 24-hr urinary cotinine level of 0.785 microg/ml (95% CI = 0.578-0.991 microg/ml), a nicotine absorption rate equivalent to smoking 10 cigarettes/day (95% CI = 7-13 cigarettes/day). Even among subjects who were not daily waterpipe smokers, a single session of waterpipe use produced a urinary cotinine level that was equivalent to smoking two cigarettes in one day. Estimates of the nicotine produced by waterpipe use can vary because of burn temperature, type of tobacco, waterpipe design, individual smoking pattern, and duration of the waterpipe smoking habit. Our quantitative synthesis of the limited human data from four nations indicates that daily use of waterpipes produces nicotine absorption of a magnitude similar to that produced by daily cigarette use.     

Sex-based and hormonal contraception effects on the metabolism of nicotine among adolescent tobacco-dependent smokers.

Variations in nicotine metabolism influence smoking patterns. Differences between sexes or related to sex hormones may affect nicotine metabolism. Because smoking initiation starts during adolescence, observations gathered from adolescent smokers might broaden our understanding of such sex-based differences. We tested the hypothesis that nicotine metabolism--as indexed primarily by the ratio of trans-3'-hydroxycotinine (3HC) to cotinine--is more rapid among adolescent girl smokers compared with boys and that regular use of hormonal contraceptives influences nicotine and cotinine metabolism. We also hypothesized that more rapid nicotine metabolism is associated with higher nicotine dependence as indexed by smoking frequency and morning urgency. Plasma samples of nicotine, cotinine, and 3HC concentrations were obtained from 120 adolescents (36 boys). Plasma nicotine and cotinine concentrations were similar in boys and girls. Median plasma 3HC concentrations were 44.45 ng/ml for girls versus 35.74 ng/ml for boys (p = .025), and median plasma 3HC-cotinine ratios were significantly higher in girls than in boys (0.317 vs. 0.253, p = .025). After stratifying girls into two groups based on use versus nonuse of hormonal contraception, plasma 3HC-cotinine ratios in girls using hormonal contraception (0.47) were substantially higher (p<.0001) than in boys (0.25) and were significantly higher than in girls not using hormonal contraception (0.28). Controlling for cigarettes smoked per day, ethnicity, and age did not modify these results. Although plasma nicotine, cotinine, or 3HC concentrations were significantly lower in less dependent adolescent smokers, nicotine and cotinine metabolite ratios were similar. This study showed that hormonal contraception in adolescent girls may accelerate cotinine metabolism, an effect likely related to induction of cytochrome P450 2A6 and independent of ethnicity and cigarette consumption. Prospective controlled studies are needed to further evaluate the role of hormonal contraception in patterns of adolescent smoking and nicotine metabolism.     

Cotinine levels in relation to smoking behavior and addiction in young adolescent smokers.

The goal of this study was to identify associations among self-reported nicotine exposure, nicotine addiction, and actual nicotine intake as measured by salivary cotinine levels in adolescent smokers. A total of 170 adolescent smokers with a mean age of 15 years were recruited from seven northern Californian public high schools. Data were collected on smoking behaviors, addiction, craving, and withdrawal. Nicotine dependence was assessed using a modified teen Fagerstr?m Tolerance Questionnaire (mtFTQ), a modified Nicotine Dependence Syndrome Scale (mNDSS), and a simple self-rating. Withdrawal was assessed using the Minnesota Withdrawal Questionnaire, and craving was assessed using a survey created by the authors. Salivary cotinine levels were collected from and analysed in participants who self-identified as smokers; data from the 54 participants who smoked in the past 4 days and whose salivary cotinine levels were greater than 0.1 ng/ml were used in the analysis. Among this group of adolescent smokers, the mean number of cigarettes smoked per day was 3.51 (SD = 3.44) and the mean level of salivary cotinine was 44.1 ng/ml (Mdn = 24.2). Even at this low level of nicotine exposure, cotinine was highly correlated with measures of nicotine dependence such as the mtFTQ (r = 0.497, p = .001), NDSS (r = 0.439, p = .002), timing of craving in the morning (r = -0.601, p = .000), and self-rated addiction (r = 0.562, p = .000). Most interesting, cotinine levels reached a plateau at around 4-5 cigarettes/day.     

Accuracy of parental reporting of secondhand smoke exposure: The National Health and Nutrition Examination Survey III.

The accuracy of parental reports of youth secondhand smoke exposure has received limited attention in the research literature. Such reports were compared to serum cotinine levels among participants of the National Health and Nutrition Examination Survey III who were aged 4-16 years. Likely smokers with serum cotinine values of 14 ng/ml or more and self-reported tobacco users were excluded from the analysis (n = 87), leaving 2,524 youth participants. One adult guardian, typically the parent, was asked to identify household smokers and estimate the number of cigarettes smoked in the home. Using cotinine levels of at least 0.2 ng/ml as the criterion, we found the sensitivity and specificity of any reported smokers in the home to be .65 and .92, respectively. Spearman correlations between cotinine levels and the number of smokers and the number of cigarettes consumed in the household were .67 and .68, respectively, and varied little across subgroups, including age, gender, and ethnicity of the child as well as household poverty status and educational attainment of the parent. Parental reports of household smoking alone fail to capture all youth secondhand smoke exposures, but they correlate well with cotinine levels when expressed as the number of household smokers or the number of cigarettes smoked in the household. Additional research is needed to determine whether reliance on parental reports of secondhand smoke exposure leads to bias in studies examining health outcomes in children and adolescents. Also, additional research is needed to better determine the level of secondhand smoke exposure that is biologically important in children and adolescents.     

The influence of gender, race, and menthol content on tobacco exposure measures.

Research has suggested that race, gender, and menthol cigarette use influence tobacco-smoke exposure measures and smoking-related disease risk. For example, a high proportion of Black smokers prefer menthol cigarettes and, despite smoking fewer cigarettes per day (CPD) than do Whites, tend to have higher cotinine levels. Additionally, Black males are more at risk for smoking-related lung cancer. High cotinine levels and smoking menthol cigarettes may lead to higher toxin intake, which contributes to increased disease risk. We explored the relationship between tobacco exposure variables (i.e., cotinine, CPD, carbon monoxide [CO], nicotine content, and nicotine dependence) with respect to race, gender, and menthol content in a sample of 307 smokers recruited from the greater Boston area to participate in a smoking cessation treatment trial. The pattern of correlations between tobacco exposure measures and cotinine showed a consistently positive correlation between cotinine and CO in all smokers and a correlation between cotinine and CPD in those who smoked nonmenthol cigarettes. Cotinine and CPD correlations varied by gender and race among menthol cigarette smokers. Consistently, we found a significant gender x race x menthol interaction on salivary cotinine level as well as cotinine/CPD ratio. These findings suggest that the relationship between number of cigarettes consumed and salivary cotinine is more complex than previously believed. It is not sufficient to look at race alone; researchers and clinicians need to look at race and gender concurrently, as well as type of cigarette consumed.     

Smoking during the night: prevalence and smoker characteristics.

We report on the smoking patterns and characteristics of individuals who smoke at night. We also explore the relationship between night smoking, nicotine dependence, and cessation outcomes. Participants (N = 691) were heavy smokers enrolled in cessation research clinics. Data were from three studies. Using ecological momentary assessment, participants monitored their smoking (ad libitum, day and night) on electronic diaries (EDs) during a 2-week baseline period and for 4 weeks following a target quit day. A total of 41% of smokers recorded at least one episode of night smoking. Within this group, night smoking occurred on 26% of nights, averaging two episodes per night. ED data correlated with a single self-report item assessing the frequency of night smoking. Night smoking was associated with greater nicotine dependence and daily caffeine consumption. It also predicted risk for lapsing beyond traditional measures of nicotine dependence. Night smoking is common, is associated with nicotine dependence, and it represents additional risk for cessation failure. People who smoke at night may need nicotine replacement therapy overnight. Future research should determine whether treatments that improve sleep quality also improve cessation outcomes in night smokers.     

Effects of smoking cessation and reduction in asthmatics.

The present study examined the effect of smoking reduction and cessation on asthma regulation and biomarkers of exposure to cigarette smoke. In a prospective open design, we allocated 220 asthmatics among three groups: (a) Smoking reduction (reducers), with the aim of smoking fewer than seven cigarettes per day, (b) complete smoking cessation (abstainers), or (c) continuation of usual smoking (continuing smokers). Subjects used nicotine chewing gum or an oral nicotine inhaler to promote reduction and cessation. We monitored changes in the biomarkers carbon monoxide, cotinine, and thiocyanate, and in peak flow, medicine use, bronchial reactivity, and asthma symptoms. The analysis used the three outcome groups, regardless of original allocation to treatment groups. At 4 months, analysis of abstainers (n = 27), reducers (n = 33), and continuing smokers (n = 50) showed marked, statistically significant decreases in expired carbon monoxide of 17 ppm (abstainers) and 15 ppm (reducers); in plasma cotinine of 124 ng/ml (abstainers) and 122 ng/ml (reducers); and in plasma thiocyanate of 5.03 ng/ml (abstainers) and 3.74 ng/m (reducers). For abstainers, we observed improvements in the asthma-specific quality-of-life score, and reductions in self-reported day and night use of rescue beta2-agonists, in doses of inhaled corticosteroids, in daytime asthma symptoms, and in bronchial hyperreactivity. For reducers, smaller improvements occurred for night use of rescue beta2-agonists, doses of inhaled corticosteroids, and bronchial hyperreactivity. Smoking cessation resulted in a marked decrease in three biomarkers of cigarette smoke inhalation and improved asthma regulation, whereas smoking reduction had a less pronounced effect on biomarkers and only a small effect on asthma regulation.     

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

Objective: To investigate whether the Irish smoking ban has had an impact on secondhand smoke (SHS) exposures for hospitality workers. 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. Additionally, a random sample (n = 20) of city centre bars stratified by size (range 400–5000 square feet), were tested for air nicotine concentrations using passive samplers before and after the ban. Main outcome measures: Salivary cotinine concentrations (ng/ml), duration of self reported exposures to secondhand smoke, air nicotine (µg/cubic metre). 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 subjects experienced decreases (range 16–99%), with 60% showing a halving of exposure levels at follow up. Self reported exposure to SHS at work showed a significant reduction from a median 30 hours a week to zero (p < 0.001). There was an 83% reduction in air nicotine concentrations from median 35.5 µg/m³ to 5.95 µg/m³ (p < 0.001). At baseline, three bars (16%) were below the 6.8 µg/m³ air nicotine significant risk level for lung cancer alone; at follow up this increased to 10 (53%). Conclusions: Passive smoking and associated risks were significantly reduced but not totally eliminated. Exposure to SHS is still possible for those working where smoking is still allowed and those working where smoke may migrate from outdoor areas. Further research is required to assess the true extent and magnitude of these exposures.     

Validity of self reports in a cohort of Swedish adolescent smokers and smokeless tobacco (snus) users

Objective: To validate self reports of cigarette and smokeless tobacco (snus) use in a prospective cohort of adolescents. Design: A cross sectional analysis of a cohort sub-sample. Setting: County of Stockholm, Sweden. Subjects: 520 adolescents in the final grade of junior high school (mean age 15.0 years). Main outcome measure: Concordance between self reported tobacco use and saliva cotinine concentration. Results: Using a cut point of 5 ng/ml saliva cotinine to discriminate active tobacco use, there was a 98% concordance between self reported non-use in the past month and cotinine concentration. The sensitivity of the questionnaire compared to the saliva cotinine test, used as the gold standard, was 90% and the specificity 93%. One hundred and fifteen out of 520 subjects (22%) reported monthly tobacco use. Among these, 67% (46/69) of the exclusive cigarette smokers, 82% (23/28) of exclusive snus users, and 94% (15/16) of mixed users (cigarettes + snus) had cotinine concentrations above 5 ng/ml. Among subjects reporting daily use 96% (64/67) had saliva cotinine concentrations above the cut point. Exclusive current cigarette users were more likely to be classified discordantly by questionnaire and cotinine test compared to snus users (odds ratio 3.2, 95% confidence interval 1.2 to 8.6). Conclusion: This study confirms the reliability of adolescents'' self reported tobacco use. In a context of low exposure to environmental tobacco smoke a cut off for saliva cotinine of 5 ng/ml reliably discriminated tobacco users from non-users. Irregular use of tobacco in this age group probably explains the discrepancy between self reported use and cotinine concentrations.     

抽吸参数对卷烟燃烧温度及主流烟气中某些化学成分的影响

用RM1/PLUS单孔道吸烟机结合高分辨的、快速纪录的红外热像仪AGEMA SC3000和GC研究了不同抽吸条件对卷烟燃烧温度及主流烟气中某些化学成分的影响。改变不同的抽吸曲线,发现抽吸时的最高温度随抽吸时流速的增加而升高。抽吸容量的增加能提高卷烟的最高抽吸温度,也使每支卷烟的烟碱、焦油、水分、CO和稠环芳烃的量有明显的增加;抽吸持续时间的增加能降低抽吸最高温度,但是每支烟的烟气输送量变化不明显;抽吸频率的降低能提高卷烟固相的抽吸最高温度,而抽吸最高温度的上升,使得每口主流烟气中的烟碱、焦油、CO等都有所增加,而稠环芳烃的量在所测的温度范围内随着温度的升高大致呈现先上升然后下降的趋势。      

Sex-related differences in serum cotinine concentrations in daily cigarette smokers

Self-reported use of cigarettes generally underestimates the true cigarette exposure of smokers. Serum cotinine is considered the best biomarker to evaluate tobacco exposure. This study determined whether or not there were any significant differences in serum cotinine concentrations between men and women when they reported smoking the same number of cigarettes per day. We analyzed cotinine and tobacco consumption data on 680 women and 840 men, aged 20 years or older, who smoked at least 100 cigarettes during their lifetime and were still actively smoking at the time of the National Health and Nutrition Examination Surveys (1999-2002). Overall, compared with men, women reported smoking fewer cigarettes per day (16.1 vs. 18.7, p<.001) and had lower serum cotinine concentrations (1163.3 nmol/L vs. 1343.9 nmol/L, p<.001). Women were more likely than men to smoke filtered (p = .018) and mentholated (p<.001) cigarettes. After adjustment for the number of cigarettes smoked per day, age, race, body mass index, poverty status, the use of either menthol or regular cigarettes, and the nicotine content in cigarettes, female compared with male smokers had lower serum cotinine concentrations (difference of 117.6 nmol/L; 95% CI = 42.6-192.6, p = .003). The difference was particularly notable in moderate to heavy smokers (i.e., those who smoked more than 15 cigarettes/day). These findings indicate that significant sex-related differences exist in serum cotinine levels among smokers, which suggests that self-reports may overestimate cigarette exposure in women compared with men.     

Smoking reduction fails to improve clinical and biological markers of cardiac disease: a randomized controlled trial.

Cigarette reduction has been proposed as a treatment goal for smokers who are not interested in stopping completely. This randomized controlled trial was designed to determine the effect of a smoking reduction intervention on smoking behavior, symptoms of heart disease, and biomarkers of tobacco exposure. It included 152 patients with heart disease who did not intend to stop smoking in the next 30 days. Participants were randomly assigned to smoking reduction (SR) or usual care (UC). SR subjects received counseling and nicotine replacement therapy to encourage > or =50% reduction in cigarettes per day (CPD). They were followed at 1, 3, 6, 12 and 18 months to assess smoking, heart disease symptoms, quality of life and nicotine, cotinine, carbon monoxide (CO), white blood cell (WBC) count, fibrinogen, hs-C-reactive protein (hs-CRP), F2-isoprostane, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and its glucuronides (total NNAL), and 1-hydroxypyrene (1-HOP). At 6 months SR participants reduced by 10.9 CPD, compared with 7.4 CPD in UC (difference NS). At 18 months, 9/78 SR vs. 9/74 UC participants quit smoking. There were no significant differences between treatment groups in angina, quality of life or adverse events, nicotine, cotinine, CO, WBC count, fibrinogen, hs-CRP, F2-isoprostane, total NNAL or 1-HOP levels at any time point. To determine if smoking reduction, regardless of treatment condition, was associated with improved outcomes, we compared all subjects at 6 months to baseline (mean reduction in CPD from 27.4 to 18.1, p<.01). There were no significant changes in outcome variables except CO, which decreased by 5.5 ppm (p<.01). There were also no significant improvements considering only subjects who reduced by > or =50%, or those who had no history of reduction prior to enrollment in the study. The SR intervention did not significantly reduce CPD or toxin exposure, or improve smoking cessation or clinical outcomes compared to UC. These results emphasize the importance of abstinence for smokers with heart disease to minimize health risks from tobacco.     

Passive smoking in the home: plasma cotinine concentrations in non-smokers with smoking partners

BACKGROUND: Risks of lung cancer and of heart disease attributable to passive smoking have been evaluated mainly in non-smokers married to smokers, but there has been little quantitative assessment of the extent of exposure in marriage partners as indicated by markers of inhaled smoke dose. OBJECTIVE: To relate plasma cotinine concentrations in non-smoking English adults to the smoking behaviour of their partners and to demographic and other factors. DATA: Population survey. Data from two years (1994 and 1996) of the Health Survey for England. MAIN OUTCOME MEASURES: Plasma cotinine concentrations in non-smoking adults married to or cohabiting with a partner. RESULTS: There was a strong dose-response relation between cotinine concentrations in non-smoking adults and the smoking behaviour of their partners, rising from a geometric mean of 0.31 ng/ml in those with non-smoking partners to 1.99 ng/ml in those whose partners smoked 30 or more cigarettes per day. In addition, exposure was greater in men, in the autumn and winter, and in those living in more disadvantaged circumstances, and there was an increasing gradient of exposure from the south to the north of the country. On average, cotinine concentrations in non-smokers with a smoking partner were 0.6-0.7% of those in cigarette smokers. CONCLUSIONS: If cotinine is taken as a measure of risk relevant dose, the implied increase in risk of lung cancer in non-smokers with smoking partners is consistent with the risk observed in epidemiological studies. Smoking by partners in the home is a major source of non-smoking adults' exposure to passive smoking.