Medium Tar Cigarettes Research Articles

Smoking high tar cigarettes increases risk of death from lung cancer, but no differences in risk for smokers of very low, low and medium tar cigarettes

Question What is the relationship between lung cancer mortality and tar rating of smoker's cigarette brand? Study Design Multivariate analysis of data from prospective cohort study. Main results Risk of death due to lung cancer was significantly higher in smokers of high-tar cigarettes compared with people smoking low, very low and medium tar cigarettes (see Table 1). There were no significant differences in the risk of lung cancer mortality for people smoking very low or low tar cigarettes compared with smokers of medium tar cigarettes. Stopping smoking considerably reduced risk of lung cancer. People quitting before age 35 years had a very similar risk to those who had never smoked. Table 1 Risk of mortality from lung cancer by tar level of cigarette smoked in the whole cohort Tar level Males Females Hazard ratio (95% CI) Hazard ratio (95% CI) 0–7 mg 1.17 (0.95 to 1.45) 0.98 (0.80 to 1.21) 8–14 mg 1.02 (0.90 to 1.16) 0.95 (0.82 to 1.11) 15–21 mg 1.0 1.0 ⩾22 mg 1.44 (1.20 to 1.73) 1.64 (1.26 to 2.15) Unclassifiable 1.10 (0.97 to 1.25) 0.72 (0.56 to 0.93) Authors’ conclusions There was no detectable difference in risk of lung cancer among people who smoked very low, low or medium tar cigarettes. An increased risk was identified in people who smoked high tar cigarettes. These findings persisted after adjustment for demographics, diet and medical history and for cigarettes/day.

Cigarette tar yields in relation to mortality from lung cancer in the cancer prevention study II prospective cohort, 1982-8.

To assess the risk of lung cancer in smokers of medium tar filter cigarettes compared with smokers of low tar and very low tar filter cigarettes. Analysis of the association between the tar rating of the brand of cigarette smoked in 1982 and mortality from lung cancer over the next six years. Multivariate proportional hazards analyses used to assess hazard ratios, with adjustment for age at enrollment, race, educational level, marital status, blue collar employment, occupational exposure to asbestos, intake of vegetables, citrus fruits, and vitamins, and, in analyses of current and former smokers, for age when they started to smoke and number of cigarettes smoked per day. Cancer prevention study II (CPS-II). 364 239 men and 576 535 women, aged > or = 30 years, who had either never smoked, were former smokers, or were currently smoking a specific brand of cigarette when they were enrolled in the cancer prevention study. Death from primary cancer of the lung among participants who had never smoked, former smokers, smokers of very low tar (< or = 7 mg tar/cigarette) filter, low tar (8-14 mg) filter, high tar (> or = 22 mg) non-filter brands and medium tar conventional filter brands (15-21 mg). Irrespective of the tar level of their current brand, all current smokers had a far greater risk of lung cancer than people who had stopped smoking or had never smoked. Compared with smokers of medium tar (15-21 mg) filter cigarettes, risk was higher among men and women who smoked high tar (> or = 22 mg) non-filter brands (hazard ratio 1.44, 95% confidence interval 1.20 to 1.73, and 1.64, 1.26 to 2.15, respectively). There was no difference in risk among men who smoked brands rated as very low tar (1.17, 0.95 to 1.45) or low tar (1.02, 0.90 to 1.16) compared with those who smoked medium tar brands. The same was seen for women (0.98, 0.80 to 1.21, and 0.95, 0.82 to 1.11, respectively). The increase in lung cancer risk is similar in people who smoke medium tar cigarettes (15-21 mg), low tar cigarettes (8-14 mg), or very low tar cigarettes (< or = 7 mg). Men and women who smoke non-filtered cigarettes with tar ratings > or = 22 mg have an even higher risk of lung cancer.

Cigarette tar yields in relation to mortality from lung cancer in the cancer prevention study II prospective cohort, 1982-8

Objective To assess the risk of lung cancer in smokers of medium tar filter cigarettes compared with smokers of low tar and very low tar filter cigarettes.Design Analysis of the...

Cigarette smoking, tar yields, and non-fatal myocardial infarction: 14,000 cases and 32,000 controls in the United Kingdom. The International Studies of Infarct Survival (ISIS) Collaborators.

To assess the effects of cigarette smoking on the incidence of non-fatal myocardial infarction, and to compare tar in different types of manufactured cigarettes. In the early 1990s responses to a postal questionnaire were obtained from 13,926 survivors of myocardial infarction (cases) recently discharged from hospitals in the United Kingdom and 32,389 of their relatives (controls). Blood had been obtained from cases soon after admission for the index myocardial infarction and was also sought from the controls. 4923 cases and 6880 controls were current smokers of manufactured cigarettes with known tar yields. Almost all tar yields were 7-9 or 12-15 mg/cigarette (mean 7.5 mg for low tar (< 10 mg) and 13.3 for medium tar (> or = 10 mg). The cited risk ratios were standardised for age and sex and compared myocardial infarction rates in current cigarette smokers with those in non-smokers who had not smoked cigarettes regularly in the past 10 years. At ages 30-49 the rates of myocardial infarction in smokers were about five times those in non-smokers (as defined); at ages 50-59 they were three times those in non-smokers, and even at ages 60-79 they were twice as great as in non-smokers (risk ratio 6.3, 4.7, 3.1, 2.5, and 1.9 at 30-39, 40-49, 50-59, 60-69, 70-79 respectively; each 2P < 0.00001). After standardisation for age, sex, and amount smoked, the rate of non-fatal myocardial infarction was 10.4% (SD 5.4) higher in medium tar than in low tar cigarette smokers (2P = 0.06). This percentage was not significantly greater at ages 30-59 (16.6% (7.1)) than at 60-79 (1.0% (8.5)). In both age ranges the difference in risk between cigarette smokers and non-smokers was much larger than the difference between one type of cigarette and another (risk ratio 3.39 and 3.95 at ages 30-59 for smokers of similar numbers of low and of medium tar cigarettes, and risk ratio 2.35 and 2.37 at ages 60-79). Most possible confounding factors that could be tested for were similar in low and medium tar users, with no significant differences in blood lipid or albumin concentrations. The present study indicates that the imminent change of tar yields in the European Union to comply with an upper limit of 12 mg/cigarette will not increase (and may somewhat decrease) the incidence of myocardial infarction, unless they indirectly help perpetuate tobacco use. Even low tar cigarettes still greatly increase rates of myocardial infarction, however, especially among people in their 30s, 40s, and 50s, and far more risk is avoided by not smoking than by changing from one type of cigarette to another.

Adverse Influence of Cigarette Smoking on the Endothelium

The effect of smoking on the blood vessel intima was examined by comparing indices of endothelial activity in serum from smokers with that from non-smokers. Serum from smokers contained higher levels of von Willebrand factor (p < 0.01), the smoking markers cotinine (p < 0.02) and thiocyanate (p < 0.01), and was more cytotoxic to endothelial cells in vitro (p < 0.02) than serum from non-smokers. The acute effects of smoking two unfiltered medium tar cigarettes was to briefly increase von Willebrand factor (p < 0.001) and cytotoxicity of serum to endothelial cells in vitro (p < 0.005), but lipid peroxides or thiocyanate were not increased by this short exposure to tobacco smoke. Although there were correlations between von Willebrand factor and smokers consumption of cigarettes (r = 0.28, p < 0.02), number of years smoking (r = 0.41, p < 0.001) and cotinine (r = 0.45, p < 0.01), the tissue culture of endothelial cells with physiological levels of thiocyanate or nicotine suggested that these two smoking markers were not cytotoxic. They are therefore unlikely to be directly responsible for increased von Willebrand factor in the serum of smokers. We suggest that smoking exerts a deleterious influence on the endothelium and that the mechanism is complex.

Effects of low-yield cigarettes on electroencephalographic dynamics.

Previous research had indicated that the smoking of medium tar and nicotine (T/N) yield cigarettes produced a psychostimulant action on electroencephalographic (EEG) activity which was apparent after a single cigarette and was evident as early as the fourth puff. The present study adopted the identical smoking and recording procedure to examine whether low-T/N yield cigarettes produced qualitatively similar EEG profiles as previously observed with medium-yield cigarettes. Although the results indicated similarities in post-smoking EEG profiles of low- and medium-yield cigarettes, discrepancies with several EEG components and temporal (puff-by-puff) EEG features suggested that low-yield cigarettes may exert less impact on brain electric activity. The results are discussed in relation to motivational theories of smoking behavior.

Microcomputer-aided measurement of puff parameters during smoking of low- and medium-tar cigarettes.

A portable microcomputer-assisted flow transducer was developed for analysing puff parameters during smoking of low- and medium-tar cigarettes. Smoke flow was determined by measuring pressure difference between two sites within an orifice flowmeter. According to the Bernoulli equation, the pressure difference is proportional to the square of flow. For calibration of the method, various sizes of air volumes were puffed through the flowmeter by a piston syringe. The calibration curve, which consisted of the flow as a function of the square root of pressure difference, was linear (r = 0.98). The automatic microcomputer analysis consists of the following variables: mean flow and mean volume of inhaled smoke gas, puff duration, time interval between two puffs, number of puffs and total volume inhaled. Eight volunteers smoked 10 low- and 10 medium-tar cigarettes during the cross-over experiments. The investigation indicated that the total inhalation volume of smokers in the case of low-tar cigarettes is twice as large as in the case of medium-tar cigarettes.

Microcomputer-aided measurement of puff parameters during smoking of low- and medium-tar cigarettes

Microcomputer-aided measurement of puff parameters during smoking of low- and medium-tar cigarettes

Urinary excretion of mutagens in smokers of cigarettes with various tar and nicotine yields, black tobacco, and cigars

Frameshift mutagens were isolated and concentrated from smokers' urine employing a method recently described. Urine concentrates of the habitual smokers and non-smokers who smoked cigarettes with low-, medium-, and high tar/nicotine yields, RCN (Reduced Condensate and Nicotine; artificial cigarettes containing cotobacco materials), black tobacco, and cigars were tested for mutagenicity in the Salmonella/mammalian microsome assay using Salmonella typhimurium TA98. Non-smokers who smoked 5 and habitual smokers who smoked 10 cigarettes of various tar and nicotine yields excreted more mutagens in urine with low-tar cigarettes than with medium- or high-tar cigarettes. Consuming more than 10 cigarettes a day resulted in a higher urinary excretion of mutagens with medium-tar cigarettes than with high-tar cigarettes. Smoking 5 RCN cigarettes a day by habitual smokers resulted in a higher urinary excretion of mutagens than smoking 5 commercial brand of cigarettes. In contrast, smoking 10 RCN cigarettes resulted in a lower urinary excretion of mutagens than smoking 10 commercial brand of cigarettes. The highest mutagenic activity was found with the urine of a habitual black tobacco smoker. Smoking cigars by non-smokers resulted in a very weak mutagenic activity of urine.

Increased risk of respiratory symptoms in young smokers of low tar cigarettes.

The effect of cigarettes yielding less than 10 mg tar was investigated in a representative sample (n = 4729) of 16 and 18 year old Finns. The rate of response was 80%. Cough and phlegm were significantly increased in young people smoking low tar cigarettes. When more than nine cigarettes were smoked daily respiratory symptoms were 2.4-6.2 times more prevalent among those who smoked low tar cigarettes than among those who never smoked. No differences were found between the smokers of low tar and medium tar cigarettes (yielding tar 10-18 mg). These data disagree with the hypothesis that the new low tar brands of cigarettes are less likely to cause respiratory symptoms than the old medium tar brands.

Cigarette smoking and platelet adhesion.

Non-abraded rabbit endothelium has been exposed to human blood taken from male non-smoking volunteers before and after the smoking of two medium tar cigarettes, in an in vitro system using a Baumgartner chamber. In each case the blood was allowed to circulate for 10 min at a constant flow rate. Blood from 10 volunteers has been tested in this way. Scanning electron microscopy of the endothelial surfaces demonstrates large numbers of adherent platelets when 'post-smoking blood' is used, but very few and in some cases none with the 'pre-smoking' blood. As a further control to ensure that this phenomenon did not occur as a result from changes in the vessel related to the time during which it had been removed from its normal physiological environment, blood from further non-smoking volunteers was passed over seven of the remaining pieces of vessel at the completion of these runs. Platelets were either absent or very few in number, as with the pre-smoking samples.

Sister-chromatid exchanges in lymphocytes of smokers in an experimental study

The frequency of sister-chromatid exchanges (SCEs) was studied in peripheral blood lymphocytes of 26 young male smokers and 10 non-smokers who had recently entered military service. The levels of SCEs were examined in 4 consecutive blood samples taken after short experimental periods of smoking only low-tar (LT) or medium-tar (MT) cigarettes. The incidence of SCEs was significantly higher in the the group of smokers than in the group of non-smokers. The SCE levels of the smokers were found to be associated with the personal smoking history; the observed increase in the SCE frequency correlated with the years of smoking measured as cumulative pack years. The difference in type of cigarette did not influence the SCE frequencies.

Urinary excretion of thioethers among low-tar and medium-tar cigarette smokers.

The urinary excretion of thioethers was studied among smokers of medium-tar cigarettes (16.3 mg/cig.) and low-tar cigarettes (5.4 mg/cig.). The test persons (26 smokers and 11 nonsmokers) were healthy young men in the military service. The smokers had an increased excretion of thioethers into the urine (P = 0.002 with Mann-Whitney U-test) when compared with the nonsmokers. No differences in the amount of urinary thioethers were detected between the low-tar and medium-tar cigarette smokers. The smokers (varying from 2.0 to 8.5 mmol/mol creatinine) had more individual variation than the nonsmokers (varying from 1.5 to 4.5 mmol/mol creatinine). Furthermore, the individual variation in the group of low-tar cigarette smokers did not markedly differ from the individual variation of medium-tar cigarette smokers.

The metabolism of prostaglandin E2 is decreased by high- and medium-tar but not by low-tar cigarette smoke in isolated rat lungs.

The effects of smoke from low-, medium- and high-tar cigarette brands on the metabolism of prostaglandin E2(PGE2) were investigated in isolated rat lungs. When isolated lungs were ventilated with smoke of high- or medium-tar cigarettes during an infusion of PGE2 into the pulmonary circulation, the amount of unmetabolized PGE2 was increased and that of 15-ketometabolites (15-keto-PGE2 and 13,14-dihydro-15-keto-PGE2 together) was decreased in the perfusion effluent compared to air ventilated control lungs. This decrease in the pulmonary metabolism of PGE2 was seen by both filter and non-filter high/medium-tar cigarettes. When isolated rat lungs were ventilated with smoke of low-tar cigarettes no change in the metabolism of PGE2 was detected. The pressor response of the vascular bed to the infusion of PGE2 was inhibited with smoke of both low- and high-tar cigarettes.