Tar and Nicotine Yields of U.K. Cigarettes 1972–1983: Sales-weighted Estimates from Non-industry Sources

We have estimated sales-weighted tar and nicotine yields of cigarettes in the United Kingdom from 1972 to 1983 using sources outside the tobacco industry. Our estimates are shown to be valid and accurate, and can be quickly updated. The data show a substantial decline of 27 per cent in overall sales-weighted tar yields from an average of 20.5mg per cigarette in 1972 to 15.0mg in 1983, whereas the sales-weighted nicotine yields over this period have remained static at about 1.3mg per cigarette. Likewise, the proportion of smokers who smoke a low-tar brand (<11mg) has stuck at about 15 per cent since 1977. This suggests a barrier to consumer acceptability which appears to be linked mare closely to nicotine than to tar. Finally, there has been an overall 26 per cent reduction in the ratio of tar yield to nicotine yield, from a sales-weighted average of 15.5 in 1972 to 11.5 in 1983. Thus it appears that, without having to reduce their nicotine intake, British smokers may now be exposed to about a quarter less tar than in 1972, and this includes the majority who have not switched to a low tar brand.     

Some short-term effects of changing to lower yield cigarettes

The rate of clearance from the lung of the hydrophilic tracer molecule 99mTc DTPA was used to investigate the short-term effects on lung epithelial function when smokers switched to cigarettes with lower yields of tobacco smoke constituents. Two separate studies were performed. In the first study, subjects smoked conventional mid- and low-tar cigarettes. The second study used two specially manufactured cigarettes with similar tar and nicotine yields, but differing carbon monoxide yields. Neither study demonstrated any significant improvement in 99mTc DTPA clearance. The yields of carbon monoxide determined under standard machine smoking conditions implied that there would be a 44 percent reduction in exposure to carbon monoxide when subjects switched from smoking conventional mid-tar to low-tar cigarettes. However, measurements of carboxyhemoglobin showed that the smokers compensated for the lower yields and their exposure was reduced by only 11 percent. Similarly, in the second study, the subjects reduced their exposure by 7 percent instead of the expected 44 percent. Urine nicotine/cotinine excretion measurements in this study indicated that there was no complimentary increase in nicotine absorption suggesting the possibility that subjects may be able to regulate their intake of individual components of the cigarette smoke. Thus, the unexpected result from this study was the finding that cigarette smokers could, in some way, regulate their intake of smoke from cigarettes of different composition so as to maintain a constant exposure of smoke constituents.     

Studies on the nicotine exposure of individual smokers. I. Changes in mouth-level exposure to nicotine on switching to lower nicotine cigarettes.

Twenty-four subjects smoked two brands of filter-tipped cigarettes delivering different amounts of nicotine, on the following 4-week schedule: 1. Smoking their usual brand for 1 week. 2. Smoking another brand similar in size, but delivering less nicotine, for 2 weeks. 3. Reverting to their usual brand for 1 week. The amount of nicotine entering the mouth, defined as the mouth-level exposure, was estimated from a determination of the amount of nicotine trapped in the filter of each cigarette smoked. The results indicate a substantial variation in mouth-level exposure for the subjects studied, even among smokers of cigarettes that deliver similar amounts of nicotine when smoked on a machine under standard conditions. For the majority of subjects, however, changing to a lower nicotine cigarette reduced the total daily mouth-level exposure to nicotine and, therefore, presumably the total tar intake.     

Long-Term Switching to Low-Tar Low-Nicotine Cigarettes

Puffing patterns and blood measures of smoke intake were studied in 12 subjects before and after switching to low-tar (10.9 mg) low-nicotine (0.7 mg) cigarettes for 12 weeks. Puff rate, puff volume, total volume puffed per cigarette and the number of cigarettes smoked were not changed significantly after switching lo the lower yield cigarettes. The reduction in mouth-level nicotine intake (calculated from butt content) was identical to the 47 per cent reduction in the machine-smoked nicotine yields. This is in keeping with the measures of puffing in showing the absence of any tendency to compensate for the reduced yields by increasing the intensity of puffing. In contrast, plasma nicotine and cotinine levels were reduced proportionally less than the nominal yields indicating that the subjects compensated to some extent by increasing inhalation. The average reductions in plasma nicotine and cotinine were identical (30per cent). Plasma thiocyanate and COHb levels were not significantly different after switching to the lower yield cigarettes but the estimated tar intake to the lungs was reduced by about 15per cent. Although the low-yield cigarettes were rated as slightly too weak, there was no significant loss of satisfaction. The fact that subjects tolerated a 30 per cent reduction in plasma nicotine without loss of satisfaction and without puffing more intensively suggests that the increase in inhalation was not determined by a need to maintain nicotine intake. This and the, discrepancies between natural and experimental switching studies are discussed.     

Money and Health Messages as Incentives for Smoking Low Tar/Nicotine Cigarettes: Changes in Consumption and Exhaled Carbon Monoxide

Cigarette brands advertised as ‘low’ tar are increasing sales yearly; undoubtedly because smokers hope they are less hazardous than ‘high’ tar/nicotine cigarettes. However, it is questionable how much switchers to ‘low’ tar/nicotine brands actually reduce their exposure to toxic components in smoke. A switching project examined the cigarette purchases over fifteen weeks of 121 paid volunteers in four experimental and one control group (separately within sex). Experimental groups received differing combinations of money and/or health message incentives to encourage switching to brands with lower tar/nicotine delivery. Subjects in all but one experimental group significantly decreased tar/nicotine exposure; controls did not. Money incentives produced the greatest decrease. The effect of health messages was unclear. Switchers' exhaled carbon monoxide (CO) remained higher than would be expected from the theoretically lower CO delivery of their brands. Small increases in number of cigarettes smoked per day did not account adequately for the persistently high exhaled CO.     

A Comparative Study of the Amount of Smoke Absorbed From Low Yield ('Less Hazardous') Cigarettes Part 2: Invasive Measures

A group of 22 volunteers who smoked daily more than 20‘high’nicotine (0.8 to 1.1 mg) Canadian cigarettes were switched to lower yield brands in two stages aver an eight-week period. The control group (six subjects) switched brands with nicotine yields within ± 0.1 mg of their usual brand while the treatment group smoked reduced yield brands (first stage, 33% reduction; second stage 61% reduction). all averages for levels of blood carboxyhemoglobin, plasma thiocyanate and serum cotinine were found to change significantly from week to week but there was no discernible difference between the treatment and the control group in week to week pattern. Although the majority of smokers in this study did not increase their exposure to cigarette smoke by smoking low yield cigarettes, it can not be said that the switch resulted in ‘safer’ smoking.     

Smoking mentholated cigarettes impairs coronary microvascular function as severely as does smoking regular cigarettes

OBJECTIVE: Smoking mentholated cigarettes inhibits the metabolism of nicotine and increases systemic exposure to cigarette smoke toxins. However, the possible effects of smoking mentholated cigarettes on coronary microvascular functions are unknown. We sought to investigate whether smoking mentholated cigarettes impairs coronary flow reserve (CFR) more so than smoking regular cigarettes. METHODS: Twenty otherwise healthy smokers of regular cigarettes (6 women, 14 men; mean age, 25.6 +/- 6.4 years) and 22 non-smoking control subjects were included in the study. To compare the acute effects of mentholated (0.9 mg nicotine, 11 mg tar, 12 mg carbon monoxide) and regular (0.9 mg nicotine, 12 mg tar, 12 mg carbon monoxide) cigarettes on CFR, all subjects underwent an echocardiographic examination that included CFR measurements at baseline. Twenty to 30 minutes after subjects had smoked 2 regular cigarettes and 2 mentholated cigarettes, CFR was again measured in subjects in the smoking group. RESULTS: In response to smoking 2 regular and 2 mentholated cigarettes, CFR values declined from 2.56 +/- 0.60 to 2.06 +/- 0.38 (P < 0.004) and from 2.56 +/- 0.60 to 2.14 +/- 0.30 (P < 0.005), respectively. Smoking mentholated and regular cigarettes impaired CFR to the same degree (P = 0.547). CONCLUSIONS: When compared with smoking regular cigarettes, smoking mentholated cigarettes has similar acute detrimental effects on coronary microvascular functions.     

Relationship of respiratory symptoms and pulmonary function to tar, nicotine, and carbon monoxide yield of cigarettes

The data from consecutive surveys of the Tucson Epidemiologic Study (1981-1988) were used to evaluate the relationship in cigarette smokers of respiratory symptoms and pulmonary function to tar, nicotine, and carbon monoxide (CO) yields of the cigarette. There were 690 subjects who reported smoking regularly in at least one survey, over age 15. After adjustment for intensity and duration of smoking and for depth of inhalation, the risk of chronic phlegm, cough, and dyspnea were not related to the tar and nicotine yields. In 414 subjects with pulmonary function tested in at least one of the three surveys the spirometric indices used were significantly related to the daily dose of tar, nicotine, and CO (product of the cigarette yield and daily number of cigarettes smoked). The effects were more pronounced for past than for current doses. However, the differentiation of pulmonary function due to various yields of cigarettes was small in comparison to the difference in pulmonary function between smokers and nonsmokers.     

Self-titration of nicotine: evidence from the Scottish Heart Health Study

Data from 2754 cigarette smokers who smoke no other forms of tobacco are extracted from the baseline cross-sectional survey of the Scottish Heart Health Study. Carbon monoxide in expired-air (CO-E), serum thiocynate and serum cotinine measurements from these smokers are compared with the carbon monoxide (CO), nicotine and tar yields of the cigarettes which they smoke, controlling for daily cigarette consumption, the sex of the smoker and the other cigarette yields. CO-E is found to increase positively with CO and tar yield, but inversely with nicotine yield. Thiocyanate increases positively with CO, is not significantly affected by tar, but increases inversely with nicotine. Cotinine is affected only by tar, in a positive direction for women. We conclude that smokers appear to self-titrate their consumption of nicotine by more aggressive smoking of lower-strength cigarettes.     

A Comparative Study of the Amount of Smoke Absorbed From Low Yield ('Less Hazardous') Cigarettes.

Twenty-two smokers (≥20 cigarettes per day with an average nominal nicotine delivery of .96 mg) were split randomly into treatment (16 subjects) and control (6 subjects) groups. During the first two-week period (P₁), all subjects smoked their usual brand. For the next three weeks (P₂) the treatment group switched to a cigarette averaging .64 mg, while the control group switched to another brand within ± .1 mg of their usual brand. During the last three weeks (P3) the treatment group switched to a still lower vented cigarette (.38 mg nicotine) while the control group switched to another brand again having a nominal delivery within ± .1 mg of their usual brand. Both treatment and control groups were dissatisfied with their substitute brands suggesting that the dissatisfaction may be to the act of switching cigarettes rather than to any decrease in cigarette yield. The non-invasive exposure measures employed (average number of cigarettes per day, daily mouth level nicotine intake, butt length, expired air carbon monoxide and saliva thiocyanate) demonstrated that the almost complete compensation of the treatment group was achieved with a combination of increased cigarette consumption, smoking intensity and depth of inhalation. Thus, the assumed health advantage for relatively heavy smokers switching to lower delivery cigarettes is largely offset by the tendency of smokers to compensate.     

Cigarette smoking: Carboxyhemoglobin,plasma nicotine,cotinine and thiocyanate vs self-reported smoking data and cardiovascular disease

Measurement of the absorption of cigarette smoke constituents were compared with self-reported daily consumption from 450 smokers to determine the most reliable dose dependent indicator of smoke inhalation and risk for coronary heart disease. A plateau of plasma nicotine and cotinine concentration at levels above 20 cigarettes per day with a continued increase of carboxyhemoglobin and thiocyanate with increasing consumption of cigarettes occurred. Classification of smokers into groups smoking cigarettes yielding more or less than 1 mg nicotine showed that smokers of low yield brands had lower plasma levels of nicotine and cotinine, but comparable levels of carboxyhemoglobin and thiocyanate. Plasma nicotine bore no relationship to smoke inhalation, while the number of cigarettes consumed per day showed a weak correlation to smoke inhalation. Despite the lower nicotine yield of cigarettes, modification in smoking behaviour enabled the smoker to derive as much carbon monoxide and thiocyanate constituents from low and high yield cigarettes; thus counteracting the advantage of low nicotine yield brands. The relationship of these parameters to the risk of coronary heart disease is discussed.     

Cigarette yield and the risk of myocardial infarction in smokers

BACKGROUND: Although cigarette smoking is a major risk factor for acute myocardial infarction (MI), cigarette tar yield has not been clearly demonstrated to affect MI risk. METHODS: A case-control study of first MI in smokers aged 30 through 65 years was conducted among 68 hospitals in an 8-county area during a 28-month period. Case subjects were smokers hospitalized at any of the area hospitals with a first MI. Approximately 4 community control smokers per case subject were randomly selected from the same geographic area using random digit dialing. Detailed data on smoking history and cigarette brand were collected. RESULTS: We identified 587 case subjects and 2685 controls who smoked cigarettes with known tar yields. After adjustment using multivariable logistic regression, the odds ratios (ORs) for subjects smoking medium- and high compared with low-tar-yield cigarettes were 1.86 (95% confidence interval [CI], 1.21-2.87) and 2.21 (95% CI, 1.47-3.34), respectively. The adjusted OR increased as tar per day intake increased (P<.001 for the trend); compared with the lowest category of tar per day, the ORs (95% CIs) for increasing tar per day were 1.16 (0.83-1.62), 1.85 (1.35-2.52), 2.42 (1.54-3.78), and 2.50 (1.78-3.52). There was a similar trend of increasing ORs as tar per day increased in smokers of lower-yield cigarettes (P<.001 for the trend) and when low-yield cigarette smokers were excluded (P<.001 for the trend). CONCLUSIONS: Smoking higher-yield cigarettes is associated with an increased risk of MI, and there is a dose-response relationship between total tar consumption per day and MI.     

Human smoking patterns and smoke deliveries

This study, based on a sample (N = 517) of adult medical patients at a southeastern medical center who were current users of cigarettes, reports the interrelationships among the puff characteristics of cigarette smoking behavior and smoke deliveries of tar and nicotine. Average puff duration, average puff volume, and the number of puffs were found to be significantly positively correlated with daily tar and nicotine intake. Intervals between puffs and total time smoking were not correlated with nicotine and tar intake. It was concluded that "how" a person smokes affects "how much" this person is exposed to tar and nicotine.     

Cardiovascular effects of long-term cigarette smoking and nicotine administration.

The nature of the cardiovascular risk in cigarette smokers has not been characterized. To compare the relative effects of long-term smoking and nicotine administration on the cardiovascular system, 18 month old beagle littermates were prepared with a permanent tracheostomy. They were classified into three groups: I, seven control dogs; II, nine dogs that smoked seven cigarettes/day; and III, eight dogs that received an equivalent amount of nicotine. After a period of up to 22 months, the animals were catheterized under anesthesia for assessment of left ventricular function and volumes by indicator-dilution technique. Heart rate, stroke volume, left ventricular end-diastolic pressure and volume and intraventricular conduction times did not differ significantly in the three groups. Left ventricular ejection fraction was 44 +/- 3 percent (mean +/- standard error of the mean) in the control group, 35 +/- 3 percent in the dogs that smoked cigarettes (P less than 0.05) and 27 +/- 3 percent in those given nicotine (P less than 0.01) despite similar values for end-diastolic variables in the three groups. The first derivative of left ventricular pressure (dP/dt) normalized for pre- and afterload was 2.4 +/- 0.2 cm/sec -1 in the control group, 1.41 +/- 0.12 in the cigarette-smoking group (P less than 0.005) and 1.34 +/-0.08 in the nicotine group (P less than 0.01). Although mean aortic pressure was significantly elevated in both the smoking (127 +/- mm Hg) and nicotine (127 +/- 10 mm Hg) groups, there was no significant correlation with the contractility indexes. Reduction of afterload to normal levels did not affect the abnormal ventricular performance. Hypertrophy, inflammation and abnormalities of cell ultrastructures were not present, and myocardial lipid and cation composition were normal. Since interstitial fibrosis was evident in both experimental groups, an alteration of elastic elements may be operative. These cardiovascular abnormalities appear to be predominantly dependent on the nicotine of cigarettes.     

Can weight gain during weaning from smoking be limited using nicotine gum?

One hundred subjects smoking more than 20 cigarettes per day were divided into two groups allocated at random to either nicotine gum or a placebo gum. Forty-eight subjects stopped smoking, irrespective of the treatment received. The magnitude of weight gain after given up smoking and the benefits of nicotine gum were evaluated. Weight gain was found to increase in ex-smokers compared with persistent smokers, but the increase was less pronounced in subjects who chewed nicotine than in those who chewed the placebo, although the difference was not statistically significant. However, enough gum must be chewed for the appetite and feeling of hunger to be reduced.     

Comparative analysis of the effects of hubble-bubble (Sheesha) and cigarette smoking on respiratory and metabolic parameters in hubble-bubble and cigarette smokers

OBJECTIVES AND BACKGROUND: Hazard of smoking tobacco is believed to be minimized by smoking hubble-bubble (HB) instead of cigarettes. Our aims were to (i) develop an assay for estimating nicotine and cotinine; and (ii) evaluate the effect of smoking on respiratory and metabolic parameters in cigarette and HB smokers. METHODS: Urine samples were collected from 152 volunteer smokers (75 cigarette and 77 HB) as well as from 16 healthy controls. We optimized an HPLC method for the determination of nicotine and cotinine. Subjects were asked to complete a chronic respiratory symptoms questionnaire and to undergo spirometry. Fasting blood samples were collected for the determination of their lipid profile. RESULTS: The intra-assay coefficients of variation for nicotine and cotinine were 16.6% and 6.6%, respectively. The mean of cotinine in cigarette smokers (1321.4 ng/mL) was significantly (P = 0.008) higher than the mean cotinine (677.6 ng/mL) in HB smokers. The mean nicotine level in cigarette smokers (1487.3 ng/mL) was significantly (P < 0.0001) higher than the mean nicotine (440.5 ng/mL) in HB smoker. The urinary cotinine and nicotine levels of the control subjects were lower than the detection levels of the assay. The mean high-density lipoprotein cholesterol was lower in cigarette smokers (0.99 mmol/L) compared with HB smoker smokers (1.02 mmol/L) but this was not significant (P = 0.28). Spirometric values were comparable among the three groups but the chronic respiratory symptoms in the smoking groups appeared at an earlier age in the HB smokers compared with the cigarettes smokers (P < 0.05). CONCLUSION: Smoking HB does not reduce the risk of tobacco exposure and it's potentially harmful metabolites on health.     

Smoking reduction promotes smoking cessation: results from a double blind, randomized, placebo-controlled trial of nicotine gum with 2-year follow-up

Aim To test the effect of nicotine gum and placebo in smokers not motivated or not able to quit smoking with regard to smoking reduction and smoking cessation. Design This randomized study evaluated nicotine gum versus placebo for up to 1 year in 411 healthy smokers highly motivated to reduce cigarette use. Smoking reduction was defined as self‐reported daily smoking less than 50% of baseline and any decrease (1 p.p.m. or more) in carbon monoxide. Setting Pulmonary department, Copenhagen, Denmark. Findings The overall success rate for sustained smoking reduction was significantly higher at all time‐points for active versus placebo gum (6.3% versus 0.5% after 24 months). Nicotine gum achieved significantly higher point prevalence cessation rates than placebo at 12 and 24 months [11.2% versus 3.9% (odds ratio = 3.1; 95% CI, 1.4–7.2 and 9.3% versus 3.4% (odds ratio = 2.9; 95% CI, 1.2–7.1), respectively]. There was a linear relationship between decrease in number of daily cigarettes and decrease in plasma cotinine, exhaled carbon monoxide and plasma thiocyanate, with significantly greater reduction in the nicotine gum group after 4 and 12 months (maximum treatment duration) but not after 24 months. The decrease in toxin intake was smaller than the decline in daily cigarette consumption, suggesting that compensatory smoking occurred. Conclusions Nicotine gum promoted cessation in this population of smokers unwilling to quit. Among reducers, the toxin intake correlated with reduced cigarette consumption although some compensatory smoking occurred.     

The effect of nicotine on aortic endothelium. A quantitative ultrastructural study

This study used quantitative electron microscopy to assess ultrastructural features of endothelial injury occurring with exposure to nicotine. Fourteen mice were given nicotine in their drinking water for 5 weeks. The dose (5 mg/kg body wt/day) was equivalent to a human smoking 50-100 cigarettes/day. A control group of mice was unexposed to nicotine over the same period. Stereological analysis of electron micrographs of endothelium from both groups revealed that the nicotine-exposed endothelium showed greater cytoplasmic vacuolation, mitochondrial swelling and subendothelial oedema than the control endothelium. In addition the intercellular cleft morphology was significantly (P less than 0.005) less complex than in the control endothelium. This difference in cleft morphology suggests the nicotine-exposed endothelium is more permeable than the control endothelium. The ultrastructural differences noted in this study are indicative of endothelial damage, and provide structural evidence to support the hypothesis that nicotine contributes to the pathogenesis of arterial disease in smokers.     

The effects of nicotine gum and counseling among African American light smokers: a 2 x 2 factorial design

AIM: Approximately 50% of African American smokers are light smokers (smoke < or = 10 cigarettes a day). The prevalence of light smoking in the United States is increasing, yet there has not been a single smoking cessation clinical trial targeting light smokers. The purpose of this 2 x 2 factorial, randomized clinical trial was to evaluate the efficacy of nicotine gum (2 mg versus placebo) and counseling (motivational interviewing versus health education) for African American light smokers. DESIGN: Participants were assigned randomly to one of four study arms: 2 mg nicotine gum plus health education (HE); 2 mg nicotine gum plus motivational interviewing (MI); placebo gum plus HE; and placebo gum plus MI. PARTICIPANTS AND SETTING: A total of 755 African American light smokers (66% female, mean age = 45) were enrolled at a community health center over a 16-month period. INTERVENTION AND MEASUREMENTS: Participants received an 8-week supply of nicotine gum and six counseling sessions during the course of the 26-week study. Biochemical measures included expired carbon monoxide (CO) and serum and salivary cotinine. FINDINGS: Seven-day quit rates for nicotine gum were no better than for the placebo group (14.2% versus 11.1%, P = 0.232) at 6 months. However, a counseling effect emerged, with HE performing significantly better than MI (16.7% versus 8.5%, P < 0.001). These results were consistent across outcome time-points (weeks 1, 8, and 26). CONCLUSIONS: Results highlight the potential positive impact of directive information and advice-oriented counseling on smoking cessation. Studies are needed to assess other interventions that may further improve quit rates among African American light smokers who are motivated to quit.