Effects of type of smoking (pipe, cigars or cigarettes) on biological indices of tobacco exposure and toxicity

Although all forms of smoking are harmful, smoking pipes or cigars is associated with lower exposure to the lethal products of tobacco products and lower levels of morbidity and mortality than smoking cigarettes. Cytochrome P-450-1A (CYP1A) is a major pathway activating carcinogens from tobacco smoke. Our primary aim was to compare CYP1A2 activity in individuals smoking pipes or cigars only, cigarettes only and in non-smokers. We studied 30 smokers of pipes or cigars only, 28 smokers of cigarettes only, and 30 non-smokers male subjects matched for age. CYP1A2 activity was assessed as the caffeine metabolic ratio in plasma. One-day urine collection was used for determining exposure to products of tobacco metabolism. Nitrosamine and benzo[a]pyrene DNA adducts were measured in lymphocytes. CYP1A2 activity was greater (p<0.0001) in cigarette smokers (median: 0.61; interquartile range: 0.52-0.76) than in pipe or cigar smokers (0.27; 0.21-0.37) and non-smokers (0.34; 0.25-0.42) who did not differ significantly. Urinary cotinine and 1-hydroxypyrene levels were higher in cigarette smokers than in pipe or cigar smokers and higher in the later than in non-smokers. DNA adducts levels were significantly lower in pipe or cigar smokers than in cigarette smokers. In multivariate analysis, cigarette smoking was the only independent predictor of CYP1A2 activity (p<0.0001) and of 1-hydroxypyrene excretion in urine (p=0.0012). In this study, pipe or cigar smoking was associated with lower exposure to products of tobacco metabolism than cigarette smoking and to an absence of CYP1A2 induction. Cigarette smoking was the only independent predictor of CYP1A2 activity in smokers. However, inhalation behaviour, rather than the type of tobacco smoked, may be the key factor linked to the extent of tobacco exposure and CYP1A2 induction. Our results provide a reasonable explanation for the results of epidemiological studies showing pipe or cigar smoking to present fewer health hazards than cigarette smoking.     

Self-regulation of smoking intensity. Smoke yields of the low-nicotine, low-'tar'cigarettes

It has been assumed for some time that the ‘tar’and nicotine data for individual cigarette brands, as reportedby the Federal Trade Commission (FTC), do not adequately reflectthe levels of exposure to toxic and carcinogenic agents in thesmoke. The trend of decreasing ‘tar’ and nicotineyields of the sales-weighted average US cigarettes was not followedby a proportionate decline of lung cancer incidence and mortalityrates. Utilizing a ‘tobacco smoke inhalation testing system’,we determined smoking profiles for four men and four women whosmoked low-nicotine cigarettes (     

Tobacco smoking and the risk of upper aero-digestive tract cancers: A reanalysis of case-control studies using spline models

Although tobacco smoking has long been recognized as a major risk factor for cancer of the upper aero-digestive tract (UADT, i.e., oral cavity, pharynx, larynx, and oesophagus), very few studies have provided estimates of the effect of very low tobacco consumption. Step-functions have been the common statistical methods for risk estimates, but the choice of reference category and of interval cutpoints influence the results, especially when data are sparse. In the present analysis, the dose-response relationship between UADT cancers and tobacco smoking was evaluated through logistic regression spline models. We included 1,241 UADT male cases and 2,835 male controls pooled from a large series of case-control studies conducted in northern Italy and in the Swiss Canton of Vaud during the last 2 decades. For cancers of the pharynx, larynx and oesophagus, the risk steadily increased with number of cigarettes/day. The risk of oral, pharyngeal and oesophageal cancers was significantly higher in smokers than in nonsmokers beginning with as low as 2 cigarettes/day. The effect of tobacco smoking at low levels seemed less evident for laryngeal cancer since the raise in risk begun with 6 cigarettes/day. In conclusion, for all the examined UADT sites, a monotonic dose-response relationship between cancer risk and cigarette smoking emerged. The excess of risk among people smoking 2 cigarettes/day highlights the absence of any harmless level for cigarette smoking, and it further supports the need of public health programs against tobacco smoking.     

Carcinogen exposure during short-term switching from regular to "light" cigarettes.

OBJECTIVES: "Light" cigarettes are extremely popular and are perceived by many smokers as less hazardous than higher-yield cigarettes. The objectives of this study were (a) to assess a battery of biomarkers of tobacco smoke exposure that includes tobacco smoke carcinogens, (b) to examine the behavioral nature of compensation, and (c) to examine the consistency of an individual's tobacco smoke exposure when smoking the same cigarette at different times. METHODS: The study was a 3-week crossover study in which smokers smoked their usual cigarettes during weeks 1 and 3, and a light cigarette, with a machine-determined nicotine yield of about 50% of the usual cigarette, during week 2. Blood and urine biomarkers of exposure and subjective questionnaires were collected weekly. RESULTS: Based on cotinine and carboxyhemoglobin levels, compensation averaged 78% and 83%, respectively. Urinary excretion of 4-(methylnitrosamino)-1-(3-pyridyl)-butanol, a metabolite of the tobacco specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-butanone, and a number of polycyclic aromatic hydrocarbon metabolites was similar in all conditions. Compensation was accomplished both by smoking cigarettes more intensively and by smoking more cigarettes per day. Exposures to various tobacco smoke constituents while smoking the usual brand of cigarette in weeks 1 and 3 were highly correlated. CONCLUSION: Our findings support the idea that smokers compensate to a high degree when switched from their usual brand to a light cigarette. Short-term switching resulted in no significant reduction in carcinogen exposure. Our assessment, based on measures of biochemical exposures, supports the idea that switching to light cigarettes is unlikely to reduce the health risks of cigarette smoking.     

Risk of bladder cancer by source and type of tobacco exposure: a case-control study

The association between tobacco use and risk of bladder cancer was investigated in a population-based case-control study conducted in Alberta and south-central Ontario, Canada, between 1979 and 1982. In all, 826 histologically-confirmed cancer cases and 792 randomly selected controls, individually matched to cases for age, sex, and area of residence, were recruited into the study. Compared to those who had never smoked cigarettes, males and females who had ever smoked cigarettes had a statistically highly significant 2-fold increase in risk of bladder cancer; for ex-smokers, the risk was intermediate between that for current smokers and never-smokers. There was a dose-dependent increase in risk of bladder cancer with total lifetime cigarette consumption, of similar magnitude for males and females. In males, risk increased with self-reported degree of inhalation in ex-smokers and in current smokers (statistically significant trend), while in females there was no association in current smokers, and a statistically significant inverse association in ex-smokers. Overall, risks of bladder cancer associated with lifetime consumption of plain and filter cigarettes were similar, and there was little evidence to suggest that switching from plain to filter cigarettes was beneficial. Neither passive smoking nor other forms of tobacco consumption (pipes, cigars, chewing tobacco, or snuff) were associated with altered risk of bladder cancer. The population attributable risk for cigarette smoking was about 47% in males and about 33% in females.     

Nicotine and cotinine in the cervical mucus of smokers, passive smokers, and nonsmokers.

Although epidemiological studies suggest that cigarette smoking is a risk factor for cervical cancer, further evidence is required to document the biological plausibility of this relationship. This study obtained cervical mucus, using a cervical flush technique, from 50 patients in a neoplasia clinic. Nicotine was detected in the cervical mucus of all 25 smokers and cotinine in the mucus of 84% of the smokers; nicotine and cotinine levels were correlated (P < or = 0.10) with both the number of cigarettes usually smoked and the number smoked in the last 24 h. Nicotine and cotinine levels for passive smokers and nonexposed women were much lower than for women who currently smoked, with little difference found between the nonsmoking women who did and did not report passive smoke exposure. In the one woman who reported smokeless tobacco use, both nicotine and cotinine were detected at much higher levels than for other nonsmoking women. These results indicate that tobacco constituents do indeed reach the uterine cervix, suggesting that they could play a causal role in the development of cervical cancer.     

Lung cancer risk associated with cigar and pipe smoking

A case-control study of 1,529 histologically confirmed male lung cancer cases and 2,899 controls matched for sex, age, hospital of admission and interviewer was conducted in France between 1976 and 1980. The results presented concern the effects of smoking habits, especially cigar and pipe use, on the occurrence of lung cancer, in a total of 38 exclusive cigar smokers, 61 exclusive pipe smokers and 586 mixed tobacco smokers. Exclusive cigar or pipe use (RR = 5.6 and 1.6 respectively) has been shown less harmful than exclusive cigarette smoking (RR = 13.3), mixed cigar and cigarette smoking (RR = 8.5) and mixed pipe and cigarette smoking (RR = 8.0). Different inhalation practices were observed according to smoking habits: while among exclusive cigarette smokers 29.8% never inhaled the smoke, among exclusive cigar and exclusive pipe users these percentages were 89.5% and 86.9 respectively. No significant increase with greater exposure to cigar was found among mixed cigar and cigarette smokers after adjustment for exposure to cigarettes, defined by duration and daily consumption of cigarettes (RR = 1.20), and by type of cigarettes smoked--light or dark, filter or nonfilter (RR = 1.13). Similar results were observed among mixed pipe and cigarette smokers after adjustment for cigarette exposure (RR = 0.95 and 1.04).     

Lung cancer and women: results of a French case-control study

Ninety-six women with histologically confirmed lung cancer and 192 matched controls were involved in an international case-control study conducted from 1976 to 1980. The aim of this study was an examination of the effects of different smoking habits, especially the type of cigarettes smoked (light or dark tobacco and filter or nonfilter use) on the occurrence of lung cancer in French females. All these patients were either nonsmokers or lifetime cigarette smokers. Matched relative risk (RR) of smokers compared to nonsmokers was found to be increased for both Kreyberg I (RR = 6.6) and Kreyberg II (RR = 2.1) categories; however, this increase was significant (P less than 0.0001) only for Kreyberg I lung cancer. A significant increase (P less than 0.0001) in matched RR was found with early age at first cigarette smoked, daily consumption, duration of smoking, frequency of inhalation, use of dark tobacco and use of nonfilter cigarettes. Matched RR associated with smokers not always using dark tobacco and those smoking only dark tobacco as compared to nonsmokers were significantly increased (trend test P less than 0.0001). On the contrary, the increase of RR was not significant when either daily consumption, or duration of smoking, or age at first cigarette was taken into account. Lung cancer appeared to be associated with daily consumption and use of nonfilter cigarettes in a matched logistic regression.     

Changes in patterns of cigarette smoking and lung cancer risk: results of a case-control study

Data from a case-control study on lung cancer were used to evaluate how changes in cigarette habits, mainly smoking cessation, switch from non-filter to filter brands, from dark to light tobacco, or from handrolled to manufactured cigarettes, and reduction in daily consumption influence lung cancer risk. The results presented concern all males, exclusive cigarette smokers, involved in the study, i.e. 1,057 histologically confirmed lung cancer and 1,503 matched controls. The general decrease in lung cancer risk with the years since cessation was also found in each subgroup of cigarette exposure defined by duration of smoking, daily consumption and type of cigarettes smoked. Among smokers who had given up smoking from less than 10 years earlier, the lung cancer risks were two-fold higher for those who had stopped smoking for coughing or health reasons than for those who had stopped smoking for reasons other than health problems. A decrease in lung cancer risk, although not significant, was found in people who switched from non-filter brands to filter brands and from dark to light tobacco and in smokers who reduced their daily consumption of cigarettes by more than 25% as compared to smokers who had not changed habits.     

Cigarette smoking and liver cancer among US veterans

The relationship of tobacco use with risk of primary liver cancer was investigated using data from a 26-year mortality follow-up of nearly 250,000 US veterans, mostly from World War I. Significantly increased risks for liver cancer (289 deaths) were associated with most forms of tobacco use, including pipe and cigar smoking. Elevated relative tisks (RRs) were seen for current cigarette smokers (RR=2.4; 95 percent confidence interval [CI] 1.6–3.5) and former cigarette smokers (RR=1.9, 1.2–2.9). A strong dose-response relationship (P<0.001) was found for cigarette smoking, with smokers of 40 or more cigarettes per day having almost a fourfold risk (RR=3.8, 1.9–8.0). Risks were also found to increase significantly with years of cigarette use and with earlier age at the start of cigarette smoking. These results are consistent with those of other cohort and case-control studies, suggesting that cigarette smoking may be related to the risk of liver cancer.All authors are in the Epidemiology and Biostatistics Program, Division of Cancer Etiology, National Cancer Institute. Address correspondence to Dr Hsing at Executive Plaza North, Room 415, Bethesda, MD 20892, USA.     

Lung cancer and use of cigarettes: a French case-control study

A case-control study of 1,625 cases and 3,091 controls was conducted in France from 1976 to 1980 to compare the effects of different smoking habits, especially the use of filter cigarettes, tobacco types (light or dark), and the use of hand-rolled or manufactured cigarettes on the occurrence of lung cancer. All cases had histologically confirmed lung cancer; the controls were matched by sex, age, hospital of admission, and interviewer. The reported results concern only male nonsmokers and males who smoked (or had smoked) cigarettes exclusively, i.e., a total of 1,217 Kreyberg I and Kreyberg II cancer cases and 1,915 controls. Cigarette smoking was associated with both Kreyberg I and Kreyberg II cell categories although with different relative risks (RR) (17.2 and 3.6, resp.). Within the Kreyberg I category, RR were significantly increased (P less than .0001) with certain indices of duration and intensity of cigarette exposure, such as early age at first cigarette smoked, daily consumption, depth of inhalation, and duration of smoking. A significant difference in risk was found within the Kreyberg I category for nonfilter versus filter cigarette smokers (RR = 18.1 and 10.9, resp.) and dark versus light tobacco smokers (RR = 18.1 and 4.9, resp.) but not for hand-rolled versus manufactured cigarette smokers (RR = 19.8 and 16.0, resp.). When all the covariates were taken into account in a matched logistic regression, lung cancer risks for nonfilter versus filter cigarette smokers was RR = 1.23, for hand-rolled versus manufactured cigarette users RR = 1.22, and for dark versus light tobacco users RR = 1.94.     

The sugar content and the pH of the smoke of cigarette, cigar and pipe tobaccos in relation to lung cancer

The risk of lung cancer is greater in cigarette smokers than in cigar or pipe smokers. In Great Britain, which has a very high lung-cancer death rate, cigarette tobacco (flue-cured) has a high sugar content (up to 20%) while cigar tobacco (aircured) has a low sugar content (0.5—2%). Determinations of the sugar content of the tobacco and the pH of the smoke of cigarettes from more than 30 countries, and of a number of cigar and pipe tobaccos, have been carried out. The main differences found between the characteristics of cigarette and cigar and pipe tobaccos are:

• (1) The high sugar content of the popular brands of cigarettes now smoked in many countries, which results in the production of a smoke of acid pH, becoming progressively more acid during the course of smoking, particularly towards the butt-end of the cigarette when the tar content of the smoke is at its highest;
• (2) The low sugar content of cigar tobacco and of the air-dried tobacco used in the cigarettes of certain countries, which gives a smoke of less acid pH becoming progressively more alkaline during the course of smoking;
• (3) The conditions of smoking in a pipe whereby the smoke from all types of tobacco, with both high and low sugar content, is less acid than that of most cigarettes, and becomes progressively more alkaline during the course of smoking.

Since the satisfaction derived from smoking is mainly due to the pharmacological effects of nicotine, it is suggested that the lower lung cancer incidence in cigar and pipe smokers may be related to the fact that nicotine is more readily absorbed in the form of the free base, at alkaline pH, than in the form of a stable salt, at acid pH. To obtain the same degree of “nicotine satisfaction” as in smoking a pipe or cigar, the smoker of cigarettes giving an acid smoke would tend to smoke more, and to encourage more prolonged and extensive contact of the smoke with the mouth and bronchus, and to take the smoke into his lungs, which would thus suffer greater exposure to the “carcinogenic” effects of the smoke than would be the case with cigar or pipe smokers. In preliminary attempts to devise a “safer” cigarette, the addition of substances which give rise to an alkaline vapour at the usual temperature of combustion of cigarettes has been shown to reverse the character of the smoke of high sugar (fluecured) tobacco cigarettes so that it then resembles that of cigars and pipes in becoming progressively more alkaline during the course of smoking.     

Effect of delivered dosage of cigarette smoke toxins on the levels of urinary biomarkers of exposure.

Urinary metabolites of tobacco smoke toxins are often used as biomarkers for the evaluation of active and passive exposure to cigarette smoke toxins. In a study of healthy smokers, we investigated concentrations of urinary biomarkers in relation to concentrations of selected toxins in mainstream cigarette smoke as determined by machine smoking of cigarettes in a manner that mimics an individual's smoking behavior (topography). Concentrations of nicotine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, and benzo(a)pyrene, in mainstream smoke determined under human smoking conditions, and their urinary metabolites cotinine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol, and 1-hydroxypyrene were established for 257 individuals who smoked low-yield (0.1-0.8 mg Federal Trade Commission nicotine/cigarette; mean, 0.66; n = 87), medium-yield (0.9-1.2 mg nicotine/cigarette; mean, 1.1; n = 109), and high-yield cigarettes (nicotine, >1.3 mg nicotine/cigarette; mean, 1.41; n = 61). Levels of urinary metabolites expressed per unit of delivered parent compounds decreased with increased smoke emissions. In smokers of low-, medium-, and high-yield cigarettes, the respective cotinine (ng/mg creatinine)-to-nicotine (mg/d) ratios were 89.4, 77.8, and 57.1 (low versus high; P = 0.06); the 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (pmol/mg creatinine)-to-4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (ng/d) ratios were 0.81, 0.55, and 0.57 (low versus high; P = 0.05); and the 1-hydroxypyrene (pg/mg creatinine)-to-benzo(a)pyrene (ng/d) ratios were 1.55, 1.13, and 0.97 (low versus high; P = 0.008). Similarly, means of cotinine per unit of delivered nicotine in smokers who consumed <20 cigarettes per day was 3.5-fold higher than in those who smoked >20 cigarettes per day. Likewise, a negative correlation was observed between cotinine-to-nicotine ratios and delivered doses of nicotine in subgroups of smokers who used the identical brand of cigarette, namely a filter tip-vented Marlboro (r = -0.59), which is a popular brand among Euro-Americans, and Newport (r = -0.37), a menthol-flavored cigarette without filter tip vents that is preferred by African-Americans. Thus, the intensity of the exposures significantly affects the levels of urinary biomarkers of exposure and should be taken into account in the evaluation of human exposure to cigarette smoke toxins.     

Risk of lung cancer among cigarette and pipe smokers in southern China.

Studies in Shanghai and in north-east China indicate that cigarette smoking is a major contributor to the high rates of lung cancer in those areas, but doubts persist regarding the influence of cigarette use on lung cancer rates in other areas of China. In addition, the risk of lung cancer associated with other methods of tobacco consumption--in particular, the use of bamboo water-pipes and long-stem pipes--is uncertain. A population-based case-control study of 427 male lung cancer patients residing in a mining area of Southern China and 1,011 controls was carried out to address this and other issues. Of these patients, 63% smoked cigarettes and (water and long-stem) pipes; 17% and 14% smoked only cigarettes or pipes, respectively; and 6% did not smoke. Compared to non-smokers, smokers of cigarettes only, smokers of pipes only and mixed smokers were at increased risk; OR = 2.6 (95% CI 1.1-6.2), 1.8 (95% CI 0.8-4.2) and 4.1 (95% CI 2.3-9.2), respectively. Risk increased with duration of tobacco use; however, the rate of increase with years of cigarette use was significantly greater than for years of pipe use (p = 0.03). In addition, risks increased 8-fold in the highest quartile of number of cigarettes per day compared to non-cigarette smokers vs. 2.3-fold for the highest quartile of number of liang (50 g) smoked per month compared to non-pipe-smokers; the trends in the ORs differed significantly (p less than 0.001). Results suggest that, in this area of China, tobacco use is an important cause of lung cancer, and that smoking cigarettes may be more deleterious than smoking pipes (primarily water pipes).     

Smoking and bladder cancer. The modifying effect of cigarettes on other factors

A population-based, incidence case-control study was used to assess the effect of cigarette smoking on other risk factors for the development of bladder cancer. White men (n = 332) between the ages of 21 and 84 with bladder cancer were compared with 686 population-based controls. Cigarette smokers were classified by current smoking status as well as by amount, duration, inhalation patterns, age at first having smoked, and years since having stopped smoking. These variables were associated with a change in the risk for bladder cancer. The population-attributable risk associated with cigarette smoking was 48.5%. Risks from the use of other tobacco products such as cigars, pipes, snuff, and chewing tobacco, and from caffeinated coffee, tea, and alcoholic beverages were evaluated in light of cigarette smoking status. Cigarette smoking was shown to be both a confounder and an effect modifier. Risk estimates for bladder cancer associated with caffeinated coffee and alcoholic beverages were decreased after controlling for the effects of cigarette smoking. However, an increased risk of developing bladder cancer from cigar smoking (Odds ratio [OR] = 2.46) and tea drinking (OR = 3.14) was only seen in men who never smoked cigarettes. An increased but not significant risk was also seen for pipe, snuff, and chewing tobacco use in noncigarette smokers. The population-attributable risk from cigars and tea in the population of white men who had never smoked was 6.3% and 18.9%, respectively. Our results suggest that cigarette smoking may obscure other risk factors unless those who never smoked are separately studied.     

Cigar and pipe smoking and cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC)

The carcinogenicity of cigar and pipe smoking is established but the effect of detailed smoking characteristics is less well defined. We examined the effects on cancer incidence of exclusive cigar and pipe smoking, and in combination with cigarettes, among 102,395 men from Denmark, Germany, Spain, Sweden and the United Kingdom in the EPIC cohort. Hazard ratios (HR) and their 95% confidence intervals (CI) for cancer during a median 9‐year follow‐up from ages 35 to 70 years were estimated using proportional hazards models. Compared to never smokers, HR of cancers of lung, upper aerodigestive tract and bladder combined was 2.2 (95% CI: 1.3, 3.8) for exclusive cigar smokers (16 cases), 3.0 (2.1, 4.5) for exclusive pipe smokers (33 cases) and 5.3 (4.4, 6.4) for exclusive cigarette smokers (1,069 cases). For each smoking type, effects were stronger in current smokers than in ex‐smokers and in inhalers than in non‐inhalers. Ever smokers of both cigarettes and cigars [HR 5.7 (4.4, 7.3), 120 cases] and cigarettes and pipes [5.1 (4.1, 6.4), 247 cases] had as high a raised risk as had exclusive cigarette smokers. In these smokers, the magnitude of the raised risk was smaller if they had switched to cigars or pipes only (i.e., quit cigarettes) and had not compensated with greater smoking intensity. Cigar and pipe smoking is not a safe alternative to cigarette smoking. The lower cancer risk of cigar and pipe smokers as compared to cigarette smokers is explained by lesser degree of inhalation and lower smoking intensity.     

Associations between smoking, passive smoking, GSTM-1, NAT2, and rectal cancer.

Cigarette smoking has been identified as a risk factor for colon cancer, however, much less is known about the association between cigarette smoking and rectal cancer. The purpose of this article is to evaluate the associations between rectal cancer and active and passive cigarette smoking and other forms of tobacco use. We also evaluate how genetic variants of GSTM-1 and NAT2 alter these associations. A population-based case-control study of 952 incident rectal cancer cases and 1205 controls was conducted. Detailed tobacco use information was collected as part of an interviewer-administered questionnaire. DNA was extracted from blood to examine genetic variants of GSTM-1 and NAT2. Cigarette smoking was associated with an increased risk of rectal cancer in men [odds ratio (OR)=1.5, 95% confidence interval (CI), 1.1-2.1 for current smokers; OR=1.7, 95% CI, 1.3-2.3 for smoking >20 pack-years of cigarettes relative to never-smokers]. After adjusting for active smoking, exposure to cigarette smoke of others also was associated with increased risk among men (OR=1.5, 95% CI, 1.1-2.0). Neither GSTM-1 genotype nor NAT2-imputed phenotype was independently associated with rectal cancer. However, the risk associated with smoking cigarettes among those who were GSTM-1 null relative to those who never smoked and had the GSTM-1 present genotype was OR=2.0 (95% CI, 1.2-3.3). This interaction was of borderline significance (P=0.08). Men who had the combined GSTM-1 present genotype and who were rapid acetylators had no increased risk from cigarette smoking. There were no significant associations between cigarette smoking and rectal cancer among women. This study shows that men who smoke cigarettes, especially those who smoke >20 pack-years, are at increased risk of rectal cancer. This association may be influenced by GSTM-1 genotype. Furthermore, exposure to cigarette smoke of others may increase risk of rectal cancer among men who do not smoke.     

Death rates from cancer of the respiratory and oral tracts in different countries,in relation to the types of tobacco smoked

The differences in death rates from respiratory and oral tract cancers among smokers in different countries cannot be attributed entirely to variation in the number of cigarettes smoked, degree of inhalation, or tar and nicotine content of the smoke. The different types of tobacco must also be taken into account. Flue-cured tobacco cigarettes appear to be the most dangerous with regard to respiratory tract cancers. The smoking of air-cured or blended tobacco cigarettes is associated with a lower lung cancer death rate, but a relatively higher death rate from oral tract cancers. The smoking of cigars made from air-cured, fermented tobacco appears to constitute much less of a carcinogenic hazard for both oral and respiratory tract cancers, than does cigarette smoking.     

Tobacco smoking, alcohol consumption, and laryngeal cancer in Madrid.

The associations between cigarette smoking and alcohol consumption and laryngeal cancer were examined in a case-control study carried out between 1982 and 1985 in Madrid. The analysis was based on 50 histologically confirmed male cases and 103 age- and sex-matched controls (45 hospitalized and 58 from the general population). A dose-response effect was observed for cigarette smoking, with an odds ratio (OR) of 4.33 (95% confidence interval of 1.22 to 15.41) for smokers of 30 or more cigarettes per day, when compared with those smoking less than 10 cigarettes per day. The risk clearly rose in line with the length of the smoking habit. In addition, for smokers of black tobacco, the risk was more than double that for smokers of blond tobacco, irrespective of the depth of inhalation. ORs for alcohol consumption rose significantly in accordance with the average grams intake per week and the overall lifetime consumption, but not with years of drinking. The time trends of risks for duration of alcohol consumption suggest the existence of phenomena related to individual susceptibility. A dose response effect was observed in supraglottal and glottal tumors. The effect of the joint exposure to both tobacco and alcohol fit to a multiplicative model.     

Smoking intensity and intent to continue smoking among menthol and non-menthol adolescent smokers in Canada

Purpose

Research suggests that menthol cigarette use is associated with nicotine dependence. However, findings on the relationship between menthol smoking status and quantity of cigarettes smoked are less clear. The objective of this paper was to examine whether menthol cigarette smoking is associated with higher smoking intensity and intention to continue smoking among adolescents.

Methods

A nationally representative sample of 4,736 Canadian students in grades 9–12 was drawn from the 2010–2011 Canadian Youth Smoking Survey. Associations between smoking intensity and menthol smoking were examined using linear regression. A logistic regression was used to examine whether menthol smoking increased the odds that a student reported intention to continue smoking.

Results

Thirty-two percentage of smokers in grades 9–12 smoked menthol cigarettes in the last 30 days. Unadjusted average number of cigarettes reported by menthol smokers was 6.86 compared with 4.59 among non-menthol smokers (p < 0.001). Multivariable results showed that the average number of cigarettes smoked by menthol smokers was greater than non-menthol smokers (β = 1.92; 95 % CI = 1.16–2.68). Similar results were found using the total number of cigarettes smoked in the past week. Additionally, menthol smokers had greater odds of reporting intent to continue smoking compared with non-menthol smokers (OR = 2.95; 95 % CI = 2.24–3.90). These results were similar when separate analyses were conducted for established smokers and experimental smokers.

Conclusions

The findings of this study along with existing evidence suggest the need for banning mentholated tobacco products in Canada, in part because of its significant effect on adolescent smoking.