Smokers Of Blond Tobacco Research Articles

Pancreatic Cancer Risk in Relation to Lifetime Smoking Patterns, Tobacco Type, and Dose-Response Relationships.

Despite smoking being a well-established risk factor for pancreatic cancer, there is a need to further characterize pancreatic cancer risk according to lifespan smoking patterns and other smoking features, such as tobacco type. Our aim was to deeply investigate them within a large European case-control study. Tobacco smoking habits and other relevant information were obtained from 2,009 cases and 1,532 controls recruited in the PanGenEU study using standardized tools. Multivariate logistic regression analysis was performed to evaluate pancreatic cancer risk by smoking characteristics and interactions with other pancreatic cancer risk factors. Fractional polynomials and restricted cubic splines were used to test for nonlinearity of the dose-response relationships and to analyze their shape. Relative to never-smokers, current smokers [OR = 1.72; 95% confidence interval (95% CI), 1.39-2.12], those inhaling into the throat (OR = 1.48; 95% CI, 1.11-1.99) or chest (OR = 1.33; 95% CI, 1.12-1.58), and those using nonfiltered cigarettes (OR = 1.69; 95% CI, 1.10-2.61), were all at an increased pancreatic cancer risk. Pancreatic cancer risk was highest in current black tobacco smokers (OR = 2.09; 95% CI, 1.31-3.41), followed by blond tobacco smokers (OR = 1.43; 95% CI, 1.01-2.04). Childhood exposure to tobacco smoke relative to parental smoking was also associated with increased pancreatic cancer risk (OR = 1.24; 95% CI, 1.03-1.49). Dose-response relationships for smoking duration, intensity, cumulative dose, and smoking cessation were nonlinear and showed different shapes by tobacco type. Effect modification by family history of pancreatic cancer and diabetes was likely. This study reveals differences in pancreatic cancer risk by tobacco type and other habit characteristics, as well as nonlinear risk associations. This characterization of smoking-related pancreatic cancer risk profiles may help in defining pancreatic cancer high-risk populations.

Smoking and Bladder Cancer in Spain: Effects of Tobacco Type, Timing, Environmental Tobacco Smoke, and Gender

We examined the effects of dose, type of tobacco, cessation, inhalation, and environmental tobacco smoke exposure on bladder cancer risk among 1,219 patients with newly diagnosed bladder cancer and 1,271 controls recruited from 18 hospitals in Spain. We used unconditional logistic regression to estimate odds ratios (OR) and 95% confidence intervals (95% CI) for the association between bladder cancer risk and various characteristics of cigarette smoking. Current smokers (men: OR, 7.4; 95% CI, 5.3-10.4; women: OR, 5.1; 95% CI, 1.6-16.4) and former smokers (men: OR, 3.8; 95% CI, 2.8-5.3; women: OR, 1.8; 95% CI, 0.5-7.2) had significantly increased risks of bladder cancer compared with nonsmokers. We observed a significant positive trend in risk with increasing duration and amount smoked. After adjustment for duration, risk was only 40% higher in smokers of black tobacco than that in smokers of blond tobacco (OR, 1.4; 95% CI, 0.98-2.0). Compared with risk in current smokers, a significant inverse trend in risk with increasing time since quitting smoking blond tobacco was observed (> or =20 years cessation: OR, 0.2; 95% CI, 0.1-0.9). No trend in risk with cessation of smoking black tobacco was apparent. Compared with men who inhaled into the mouth, risk increased for men who inhaled into the throat (OR, 1.7; 95% CI, 1.1-2.6) and chest (OR, 1.5; 95% CI, 1.1-2.1). Cumulative occupational exposure to environmental tobacco smoke seemed to confer increased risk among female nonsmokers but not among male nonsmokers. After eliminating the effect of cigarette smoking on bladder cancer risk in our study population, the male-to-female incidence ratio decreased from 8.2 to 1.7, suggesting that nearly the entire male excess of bladder cancer observed in Spain is explained by cigarette smoking rather than occupational/environmental exposures to other bladder carcinogens.

Cigarette smoking and risk of large cell carcinoma of the lung: a case-control study in Uruguay

In the time period 1988–2000, a case-control study on large cell carcinoma of the lung was conducted in Montevideo, Uruguay. The study included 149 cases (139 men and 10 women) and 596 controls (556 men and 40 women) afflicted with diseases not related with tobacco smoking. Cases and controls were frequency matched on age, sex, residence and urban/rural status. According to our results, large cell carcinoma was strongly related with cigarette smoking (OR for heavy smokers 155.2, 95% CI: 30.6–786.1). Furthermore, all cases displayed higher risks for intensity compared with smoking duration. Smokers of black tobacco showed odds ratios (ORs) significantly higher than those presented by smokers of blond tobacco and smoking cessation displayed a reduction in risk of 95%, close to the risk of never smokers. Finally, filter use was not associated with any reduction in risk. It could be concluded that undifferentiated large cell carcinoma of the lung could be included among those lung tumors classified as Kreyberg I cancers.

Association of 1 hydroxypyrene glucuronide in human urine with cigarette smoking and broiled or roasted meat consumption

Humans are exposed to polycyclic aromatic hydrocarbons PAHs from various occupational, dietary, environmental and medicinal sources. We measured 1 hydroxypyrene glucuronide 1 OHP gluc concentration in urines from male non smokers n = 50, smokers of blond tobacco n = 31, smokers of black tobacco n = 16, and pipe smokers n = 3 . Immunoaffinity chromatography was used as a preparative step and synchronous fluorescence spectroscopy as the quantitation method. The concentration of 1 OHP gluc in urine from smokers mean SE: 1.04 0.13 pmol ml-1 urine was significantly higher than in urine from non smokers 0.55 0.05 pmol ml-1 urine by the Wilcoxon rank sum test non smokers versus all smokers, p = 0.001; vs black tobacco smokers, p = 0.001; vs blond tobacco smokers, p = 0.007 . Urinary 1 OHP gluc concentration among subjects who had consumed roasted, grilled or broiled meat within the past 24 h was elevated compared with those who had not p = 0.025 . Multiple linear regression showed significant associations of urinary 1 OHP gluc with number of cigarettes smoked p = 0.002 and consumption of roasted, grilled or broiled meat p = 0.028 . Systemic CYP1A2 activity estimated by caffeine metabolism was significantly correlated with urinary 1 OHP gluc concentration. However, this association was probably due to cigarette smoking, since adjusting for cigarette smoking by multiple linear regression made the association between urinary 1 OHP gluc and CYP1A2 phenotype non significant. These results further support the use of urinary 1 OHP gluc as a biomarker of recent pyrene exposure through inhalation or diet.

Urinary promutagens of smokers: comparison of concentration methods and relation to cigarette consumption

Different extraction techniques can be used to concentrate the promutagens of cigarette smokers' urine before evaluation of their mutagenic potency by Ames test. In this study, three solid adsorbents, C18. XAD2 and CN were compared for their ability to concentrate the promutagens of smokers' urine prior to acetone elution. C18 extracts were observed to have a higher promutagenicity than XAD2 and CN extracts. The mutagenicity of smokers' urine depended on the smoking habits, and a strong correlation was observed between urinary promutagenicity. daily cigarette consumption, and the tobacco type (black or blond). Smokers of black tobacco had a higher urinary genotoxicity than smokers of blond tobacco, after taking into account the level of tobacco consumption. Urinary promutagenicity did not appear to depend on the tar level of cigarettes.

Black (air-cured) and blond (flue-cured) tobacco and cancer risk II: Pharynx and larynx cancer

Two case-control studies have examined the relationship between black or blond tobacco smoking and the occurrence of pharynx or larynx cancer. The first study was carried out in several European countries. Tobacco smoking was found to be associated with higher risks for supraglottic and epilarynx cancer localisations than for pharynx, glottic and subglottic localisation. In all localisations, risk was twice as high again in users of black tobacco after adjusting for alcohol and for lifetime average daily dose of tobacco. The other study was carried out in Uruguay. After taking into account age, age at start of smoking, duration of smoking, years since stopping smoking and filter use, risks were found to be higher in black tobacco smokers than in blond tobacco smokers. All known studies which have been performed in countries where blond tobacco is generally smoked showed lower risks even when adjusted for alcohol. Use of black tobacco appears to be associated with higher risks of cancer of the pharynx and larynx than blond tobacco use.

Tobacco Smoke Inhalation Pattern, Tobacco Type, and Bladder Cancer in Spain

The association between tobacco smoking and bladder cancer was investigated in a multicenter case-control study conducted in five provinces of Spain between 1983 and 1986. A matched analysis was carried out in males, based on 430 histologically confirmed cases, 405 hospital controls, and 386 population controls, matched by age and place of residence. An increased risk was found for smokers as compared with nonsmokers (odds ratio (OR) = 3.79, 95% confidence intervals (CI) 2.41-5.97), and this increase was significantly associated with the intensity of smoking. Smokers of filter-tipped cigarettes had a reduced risk as compared with smokers of non-filter-tipped cigarettes (OR = 0.57, 95% CI 0.32-1.02). A diminution of risk was also observed for smokers of low-tar and low-nicotine ("light") cigarettes. Depth of inhalation was strongly associated with illness. No difference was shown in the logistic regression model between smokers of black tobacco and smokers of blond tobacco after controlling for depth of inhalation. Although the number of persons who smoked blond tobacco exclusively was small, the results suggest that it is important to consider inhalation patterns when studying risk variations between smokers of black tobacco and smokers of blond tobacco. The age at which a person started to smoke did not appear to affect risk. An analysis of the decrease in risk associated with years since quitting smoking suggested that different components of cigarette smoke may play a role at different stages of the carcinogenic process.

Black tobacco, maté, and bladder cancer. A case–control study from uruguay

A case-control study of bladder cancer involving interviews with 111 incident cases and 222 controls was carried out in Montevideo, Uruguay. The analysis was conducted separately for each sex. Point estimates of relative risk associated with smoking variables, ingestion of infusions of the herb Ilex paraguariensis (maté), and selected dietary items were obtained by stratified and logistic regression analysis. Among men, smokers of black tobacco showed a relative risk (RR) 2.7 higher than blond tobacco smokers and maté exposure showed a significant dose-response, after adjustment for age, residence, social class, hospital, type of tobacco, smoking intensity, smoking duration, and vegetable consumption, with a seven-fold increase in risk for heavy consumers. Joint exposure to type of tobacco and maté consumption showed a multiplicative effect. Women showed a similar increase in risk with maté consumption. The results suggest that the high mortality rates of bladder cancer observed in Uruguay could be explained by the combined effect of black tobacco smoking and maté ingestion.

Carcinogen Hemoglobin Adducts, Urinary Mutagenicity, and Metabolic Phenotype in Active and Passive Cigarette Smokers

In 100 healthy volunteers, we have studied the relationship between the type (air- or flue-cured) and number of cigarettes smoked and different biomarkers relevant to the risk of bladder cancer, including the levels of 4-aminobiphenyl (ABP) hemoglobin adduct (a marker of internal dose), urinary mutagenicity in Salmonella typhimurium TA98, and the N-acetylation phenotype (a marker of susceptibility). ABP is a potent bladder carcinogen that is N-acetylated as an overall detoxification step. Levels of the ABP hemoglobin adduct were higher in smokers of black tobacco (air-cured) than in smokers of blond tobacco (flue-cured), confirming our earlier study. In addition, "slow" acetylators had higher levels of the ABP hemoglobin adduct for the same type and quantity of cigarettes smoked. Urinary mutagenicity was also associated with quantity of cigarettes but not with the acetylation phenotype. Convex dose-response relationships were found between the amount smoked and ABP hemoglobin adduct levels or urinary mutagenicity. In 15 nonsmokers who reported exposure to environmental tobacco smoke, ABP hemoglobin adduct levels, unlike urinary mutagenicity, were found to be an aspecific exposure indicator.

Levels of mutagens in the urine of smokers of black and blond tobacco correlate with their risk of bladder cancer.

Levels of urinary mutagens, thioethers, N-nitrosamino acids, nitrate, nicotine, cotinine and creatinine were measured in 21 non-smokers, 26 smokers of blond tobacco, 9 smokers of black tobacco and 5 smokers of both types of tobacco, all eating a similar diet. Results were expressed either per 24 h urine or per mmol creatinine. The sum of urinary nicotine and cotinine levels (N + C) was used as a measure of exposure to the number of cigarettes smoked. Statistically significant positive dose-effect relationships were obtained between the urinary N + C levels and (i) the number of revertants (Salmonella typhimurium TA98, with a metabolic activation system); (ii) the concentration of thioethers; (iii) the levels of N-nitrosoproline or the sum of all nitrosamino acids excreted and (iv) the amount of urinary nitrate. No such correlation was found between N + C levels and induction potency in the SOS chromotest. A linear dose-effect relationship between urinary mutagenicity (i.e. log revertants of S. typhimurium TA98) and N + C levels or number of cigarettes per day was established for smokers of blond tobacco. After adjustment for N + C levels, the urine of smokers of black tobacco contained twice as much mutagenic material as did the urine of blond tobacco smokers (P = 0.02). For other exposure markers, no statistically significant difference was found between the two types of smokers. Epidemiological studies have shown that the risk of urinary bladder cancer is 2.5 times higher in smokers of black tobacco than in blond tobacco. Therefore, our findings on urinary mutagenicity provide experimental evidence that the type of tobacco is the factor responsible for the observed difference in risk and that smoking of black as compared to blond tobacco results in a higher exposure of the urinary bladder to genotoxic hence potentially carcinogenic substances.

Hemoglobin adducts of aromatic amines: associations with smoking status and type of tobacco.

Hemoglobin adducts of 15 aromatic amines were determined in nonsmokers and smokers of blond- or black-tobacco cigarettes living in Turin, Italy. The subjects were all males age 55 or less and were representative of the population previously examined in a case/control study of bladder cancer. 4-Aminobiphenyl adduct levels were found to be significantly different in the three groups, and the differences were approximately proportional to the relative risk of each group. Adjustment for age and cigarette consumption did not materially influence the differences. A significant correlation of adduct levels with cigarette consumption was also observed for all smokers as well as for smokers of blond tobacco. Other amines for which significant differences between smokers and nonsmokers were observed were 3-aminobiphenyl, 2-naphthylamine, o- and p-toluidine, 2,4-dimethylaniline, and 2-ethylaniline. Some of these amines are human bladder carcinogens, and their occurrence in blood as hemoglobin adducts is evidence for their metabolic activation. Thus, by a combination of traditional epidemiological methods and modern chemical analyses, we have provided evidence for a biochemical basis for the often observed association between cigarette smoking and bladder cancer.