Carcinogenic effect of tobacco smoking and alcohol drinking on anatomic sites of the oral cavity and oropharynx.

A series of 359 male patients with 424 cancer lesions of the oral cavity and oropharynx identified at a US Department of Veterans Affairs Medical Center were divided according to site of origin of the lesion and compared with 2,280 controls from the same hospital with respect to exposure to tobacco smoking and alcohol drinking. Sites of origin were: floor of the mouth (153), oral tongue (50), anterior tonsillar pillar (49), soft palate (44), lingual aspect of retromolar trigone (11), alveolar ridge (5), buccal mucosa (4), and hard palate (2). Forty-one patients had cancers in multiple sites. Tobacco smoking was more strongly associated with soft-palate lesions than with lesions in more anterior sites. Patients with cancer of floor of the mouth and oral tongue had higher odds ratios for alcohol drinking than subjects with cancers of other sites. This study supports the hypothesis of the carcinogenic effect of tobacco smoke and alcoholic beverages on the oral mucosa through direct contact.     

Tobacco smoking and chewing, alcohol drinking and lung cancer risk among men in southern India

In India, lung cancer is one of the most common and lethal cancers, and tobacco smoking remains its most important etiologic factors. The objective of our study is to examine the effects of different tobacco consumption forms, including smoking and chewing, on lung cancer risk of men in southern India, especially to compare the effects of bidi smoking to cigarette smoking on lung carcinogenesis. We also evaluated the possible role of Indian alcohol beverages and non-Indian alcohol beverages on lung carcinogenesis. We conducted a case-control study in Chennai and Trivandrum. In total, 778 lung cancer cases and 3,430 controls, including 1,503 cancer controls and 1,927 healthy controls, were recruited. The effects of cigarette, bidi smoking, chewing and alcohol drinking on the risk of lung cancer were estimated from unconditional multivariate logistic regression. We also applied the generalized additive model (GAM) with locally-weighted running-line smoothers (loess) to find the most plausible curve for the dose-response relationship. The results from GAM suggest a plateau after 35 years of smoking or 10 cigarette-equivalent pack-years for both cigarette and bidi. The OR is 4.54 (95%CI=2.96-6.95) and 6.45 (95%CI=4.38-9.50) for more than 30 years of cigarette-only and bidi-only smoking, respectively, and 6.87 (95%CI=4.62-10.2) and 10.7 (95%CI=5.82-19.6) for more than 12 weighted cumulative cigarette-only and bidi-only consumption, respectively. The lung cancer risk of former cigarette smokers drops down more quickly after quitting smoking compared to former bidi smokers. There is no evidence for the effect of chewing and lung cancer risk nor clear evidence of an effect of overall alcohol drinking among never-smokers, although Indian alcohol drinking seemed to remain associated with lung cancer risk under limited power (OR=2.67, 95%CI=1.02-7.02). Bidi smoking seems to have a stronger carcinogenic effect than cigarette smoking: this difference holds no matter which aspect of smoking was considered.     

Flavonoids and laryngeal cancer risk in Italy.

BACKGROUND: Flavonoids may play an important role in explaining the protective effect of vegetables and fruit against cancer. PATIENTS AND METHODS: To investigate the relation between flavonoids and laryngeal cancer risk, we have applied data on the composition of foods and beverages in terms of six principal classes of flavonoids to a case-control study of laryngeal cancer conducted from 1992 to 2000 in Italy. Cases were 460 subjects with incident, histologically confirmed laryngeal cancer; controls were 1088 patients admitted for acute, non-neoplastic diseases. Odds ratios (OR) were estimated through multiple logistic regression models, including terms for sociodemographic and lifestyle factors, tobacco smoking, alcohol consumption and energy intake. RESULTS: Significant inverse relations were found for the highest versus the lowest quintile of intake for flavan-3-ols (OR = 0.64), flavanones (OR = 0.60), flavonols (OR = 0.32) and total flavonoids (OR = 0.60), although the overall trends in risk were significant only for flavanones and flavonols. No consistent associations were observed for isoflavones, anthocyanidins and flavones. The estimates did not differ substantially across strata of alcohol drinking, tobacco smoking, body mass index and education, and tended to persist even after controlling for vegetable and fruit intake. CONCLUSION: This study provides support for a beneficial effect of selected flavonoids on laryngeal cancer risk.     

Differential effects of tobacco and alcohol in cancer of the larynx, pharynx, and mouth

Two thousand five hundred forty male patients with cancer of larynx, pharynx, and mouth were examined in the same hospital between 1975 and 1982. Different sites were compared according to alcohol and tobacco consumption: oropharynx, hypopharynx, larynx supraglottis, larynxglottis, epilarynx, lip, tongue-tip, and tongue lateral border, other tongue sites, gum, floor of the mouth, and buccal mucosa. For tobacco, the mean daily consumption of smokers and exsmokers did not differ according to location (except in patients with cancer of the lip, in whom the consumption was lowest). Cancer locations differed significantly according to the daily alcohol consumption. The consumption was the lowest for patients with cancer of the lips and the glottis, the highest for patients with cancer of the epilarynx, hypopharynx, and the floor of the mouth. Significant differences were observed in the percentage of nonsmokers or nondrinkers, even between adjacent locations: supraglottis versus glottis; tongue, tip, and lateral border versus tongue, other sites; floor of the mouth versus buccal mucosa. Some of the results might be particular to elements of the French life-style (e.g., consumption of brown tobacco, high consumption of wine).     

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.     

Tobacco, alcohol and the risk of gastric cancer by sub-site and histologic type.

Few studies have provided information on the role of smoking and alcohol in the carcinogenesis of gastric cancer by sub-site and histologic type. The relationship of snuff dipping with risk of gastric cancer has also been rarely studied. In a population-based case-control study conducted in 5 counties of Sweden from February 1989 to January 1995, a total of 90 cases of gastric cardia cancer, 260 and 164 cases of distal gastric cancer of intestinal and diffuse types, respectively, and 1164 frequency-matched control subjects were personally interviewed about life-time smoking, use of smokeless tobacco and use of alcohol 20 years ago. Current smokers had a higher risk than never-smokers for all 3 kinds of gastric adenocarcinoma [odds ratio (OR) 1.7, 95% confidence interval (CI) 1.0-3.1 for gastric cardia adenocarcinoma; OR 1.8, 95% CI 1.2-2.7 for distal gastric cancer of intestinal type; and OR 2.2, 95% CI 1.4-3.5 for distal gastric cancer of diffuse type], and the risk rose with increasing dose and duration of smoking among current smokers. However, no elevated risk was observed for ex-smokers. Neither intake of alcoholic beverages nor snuff dipping was associated with an increased risk of any type of cardia or gastric cancer. Our study did not support the hypothesis that the role of tobacco differs by sub-site and histologic sub-type of gastric cancer.     

Identification of risk factors for specific subsites within the oral and oropharyngeal region--a study of 647 cancer patients

Studies on site specific risks for oral cancers are few. Present investigation explores the possible role of human sociodemographic factors in causing oral cancer. Majority of patients had poor oral hygiene (85.5%) and belonged to 51-60 years age group (35.7%). Most of the subjects were agriculture workers (30.3%). Tongue and floor of mouth included majority of the affected sites (77.2%). Male to female ratio was highest for tonsil (32.3%) but differed marginally for other subsites. Majority of females used tobacco (81%) while males users of tobacco, alcohol and smoking reported in nearly equal proportions. Tobacco and smoking were found as primary risk factors for several intraoral subsites. However, for tongue, palate and lip no risk factor could be identified from given patients' characteristics. In general, tobacco posed high risk for buccal mucosa and alveolus in comparison to other subsites. Smoking affected tonsil and floor of mouth more than other sites. Alcohol posed more risk for buccal mucosa and floor of mouth than tongue.     

Smoking and colorectal cancer: different effects by type of cigarettes?

Although smoking is suggested to be a risk factor for colorectal cancer, the evidence to date is conflicting and may be confounded. Moreover, the effect of tobacco smoke may vary by time since initiation, type of tobacco product, anatomic subsites, and among ethnic groups. Data were derived from two consecutive population-based case-control studies conducted among Caucasians, Japanese, Native Hawaiians, Filipinos, and Chinese in Hawaii, including 1,959 ethnicity-, sex-, and age-matched case-control pairs. A lifetime history of smoking for different tobacco products and information on other risk factors were obtained by in-person interviews. Odds ratios (OR) and corresponding 95% confidence intervals (95% CI) were estimated using conditional logistic regression models with adjustment for potential confounders. Subjects who ever smoked were at an increased risk of colorectal cancer compared with never smokers (OR, 1.23; 95% CI, 0.99-1.52 for men and OR, 1.27; 95% CI, 1.01-1.59 for women). Increasing quartiles of pack-years over all tobacco products showed a clear dose-dependent association in men [for the highest quartile, Q4 (>40 pack-years) versus never smokers: OR, 1.48; 95% CI, 1.12-1.96; P(trend) = 0.002]. The dose-response trend was also present in women [for the highest quartile, Q4 (>30 pack-years) versus never smokers: OR, 1.38; 95% CI, 0.91-1.95; P(trend) = 0.04] and each ethnic group. There was a suggestion of a difference in risk with type of tobacco product. Non-filtered cigarettes increased risk of both colon and rectal cancer [for Q4 versus never smokers: OR, 1.59; 95% CI, 1.15-2.21; P(trend) = 0.001 and OR, 1.84; 95% CI, 1.18-2.86; P(trend) = 0.02, respectively], whereas filtered cigarettes seemed to increase risk of rectal but not colon cancer (OR, 1.37; 95% CI, 0.88-2.13; P(trend) = 0.06 and OR, 1.05; 95% CI, 0.79-1.39; P(trend) = 0.98, respectively). The effect of smoking was not limited to the distant past, and accumulated pack-years of smoking seemed to be more important than the time in which smoking occurred. The data from this large study corroborate previous reports of a positive association between smoking and colorectal cancer and suggest that the association may vary by type of cigarette.     

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.     

Role of tobacco and alcoholic beverages in the etiology of cancer of the oral cavity/oropharynx in Torino, Italy

A population-based case-control study of cancer of oral cavity-oropharynx was conducted in the city of Torino, Italy, between 1982 and 1984. One hundred twenty-two cases (86 males and 36 females) and 606 controls (385 males and 221 females) were compared with respect to lifelong alcohol and tobacco consumption. A 4- to 6-fold increase in risk among subjects with medium or high tobacco consumption was observed, as well as a trend in increasing risk with duration and with earlier age at the start of smoking. Other findings included a sharp reduction in risk with cessation of smoking, no clear protective effect of usage of filter, no differences in risk according to color of tobacco, and a higher risk for cigar versus pipe/cigarette smokers. An effect of alcoholic beverages was found in subjects with an average daily consumption of 120 or more grams of alcohol, with a higher risk in beer drinkers. Among heavy consumers of alcohol and tobacco, risks of both oral and oropharyngeal cancer were very high. A positive association between oral cancer and low educational level, after adjustment for alcohol and tobacco, was found. Attributable risks for alcohol and tobacco in the population were 23% and 72% in men and 34% and 54% in women.     

Hand-rolled cigarette smoking and risk of cancer of the mouth, pharynx, and larynx.

A case-control study, involving 205 patients with cancer of the mouth, pharynx, and larynx and 273 control subjects with conditions considered not related to tobacco or alcohol consumption, was performed in Montevideo, Uruguay, between January 1988 and December 1990. Smokers of hand-rolled cigarettes showed an increased risk of cancer of the mouth and pharynx (odds ratio [OR] = 2.5; 95% confidence limit = 1.2-5.2) when compared with smokers of manufactured cigarettes. Also, the risk of laryngeal cancer was greater among smokers of hand-rolled cigarettes (OR = 2.7; 95% confidence limit = 1.3-5.7) as compared with smokers of commercial cigarettes.     

Smoking and drinking in relation to cancers of the oral cavity, pharynx, larynx, and esophagus in northern Italy

A hospital-based case-control study of upper aerodigestive tract tumors was conducted between June 1986 and June 1989 in Northern Italy. One hundred fifty-seven male cases of oral cavity cancer, 134 of pharyngeal cancer, 162 of laryngeal cancer, and 288 of esophageal cancer, and 1272 male inpatients with acute conditions unrelated to tobacco and alcohol were interviewed. Odds ratios for current smokers of cigarettes were 11.1 for oral cavity, 12.9 for pharynx, 4.6 for larynx, and 3.8 for esophagus. For all 4 sites, the risk increased with increasing number of cigarettes and duration of smoking habits and, with the exception of esophageal cancer, decreased with increasing age at the start of and years since quitting smoking. Smokers of pipes and cigars showed a more elevated risk of cancer of the oral cavity and esophagus than did cigarette smokers. Significantly increased risks emerged also in heavy drinkers (odds ratio greater than 60 versus greater than or equal to 19 drinks/week = 3.4, 3.6, 2.1, and 6.0 for oral cavity, pharynx, larynx, and esophagus, respectively), deriving predominantly from wine consumption.     

Diet diversity and the risk of laryngeal cancer: a case-control study from Italy and Switzerland

Diet diversity (defined as the number of different foods consumed) has been considered an indicator of a healthy diet, and favorably related to the risk of several digestive tract cancers. We analyzed the relation between diet diversity and the risk of laryngeal cancer using data from a case-control study carried out between 1992 and 2000 in Italy and Switzerland. The subjects of the study were 527 patients with histologically confirmed incident cancers of the larynx and 1297 patients admitted for acute, non-neoplastic diseases, unrelated to tobacco or alcohol consumption. Total diversity was computed as the number of different foods (overall and within four food groups, i.e., vegetables, fruit, meat, and cereals) consumed at least once per week. A significant inverse association was observed for vegetable diversity (OR=0.41, 95% CI: 0.28-0.59, for the highest versus the lowest quartile) and fruit diversity (OR=0.40, 95% CI: 0.27-0.59). Conversely, a direct association was found for meat diversity (OR=1.67, 95% CI: 1.11-2.50), while no meaningful association was found for total diet and cereal diversity. The results were consistent across strata of age, alcohol drinking and tobacco smoking. This study suggests that a diet not only rich but also varied in fruit and vegetables is related to a decreased risk of laryngeal cancer risk.     

Tobacco Smoking and Alcohol Drinking as Risk Factors for Stomach Cancer: a Case-Control Study in Uruguay

Objectives: To estimate the risk of stomach cancer associated with alcohol drinking and tobacco smoking in Uruguayan men.Methods: A case-control including 331 cases and 622 controls was conducted in Montevideo, Uruguay, during the period 1992-96. The study was restricted to men, and both cases and controls were patients admitted to the major four hospitals in Montevideo. Response rates were high and similar for both series (92.8 for cases and 92.6 percent for controls). Controls were frequency-matched to cases on age and residence, and patients with conditions related a priori to tobacco smoking and alcohol drinking were considered ineligible for the study. All patients were interviewed shortly after admission using a structured questionnaire by two trained social workers. Relative risks, approximated by the odds ratios (OR), were estimated by unconditional logistic regression in models including major potential confounders.Results: Smoking duration was associated with an increased risk of 2.2 for smokers of more than 50 years, with a significant dose-response pattern, after controlling for major confounders. Quitters of more than 15 years displayed an OR of 1.1, very close to the risk of never-smokers. A younger age at having started smoking was associated with an increased risk, whereas pack-years of cigarettes showed a significant dose-response. Also, alcohol drinking (particularly hard liquor and beer) was associated with an OR of 2.4 (95 percent confidence interval = 1.5-3.9), after controlling for the effect of tobacco, vegetables, and other types of alcohol beverages.Conclusions: These findings add further support to the role of tobacco and alcohol in gastric carcinogenesis. Cancer Causes and Control 1998, 9, 321-329     

Cigar and pipe smoking,smokeless tobacco use and pancreatic cancer: an analysis from the International Pancreatic Cancer Case-Control Consortium (PanC4)

BackgroundCigarette smoking is the best-characterized risk factor for pancreatic cancer. However, data are limited for other tobacco smoking products and smokeless tobacco.Materials and methodsWe conducted a pooled analysis of cigar and pipe smoking and smokeless tobacco use and risk of pancreatic cancer using data from 11 case–control studies (6056 cases and 11 338 controls) within the International Pancreatic Cancer Case-Control Consortium (PanC4). Pooled odds ratios (OR) and the corresponding 95% confidence intervals (CI) were estimated by unconditional multiple logistic regression models adjusted for study center and selected covariates.ResultsCompared with never tobacco users, the OR for cigar-only smokers was 1.6 (95% CI: 1.2–2.3), i.e. comparable to that of cigarette-only smokers (OR 1.5; 95% CI 1.4–1.6). The OR was 1.1 (95% CI 0.69–1.6) for pipe-only smokers. There was some evidence of increasing risk with increasing amount of cigar smoked per day (OR 1.82 for ≥ 10 grams of tobacco), although not with duration. The OR for ever smokeless tobacco users as compared with never tobacco users was 0.98 (95% CI 0.75–1.3).ConclusionThis collaborative analysis provides evidence that cigar smoking is associated with an excess risk of pancreatic cancer, while no significant association emerged for pipe smoking and smokeless tobacco use.     

Smoking, alcohol drinking and cancer risk for various sites of the larynx and hypopharynx. A case-control study in France.

The aim of this work was to study the effects of alcohol and tobacco consumption on laryngeal and hypopharyngeal cancer and to compare these across subsites (glottis, supraglottis, epilarynx, hypopharynx). Data from a hospital-based case-control study including 504 male cases (105 glottic cancers, 80 supraglottic cancers, 97 epilaryngeal cancers and 201 hypopharyngeal cancers) and 242 male controls with non-respiratory cancers were used for this analysis. Information about sociodemographic characteristics, detailed alcohol and tobacco consumption was collected through face-to-face interviews. Statistical analysis used logistic regression, and subsites were compared with polytomous logistic regressions. The risk of laryngeal and hypopharyngeal cancer increased with tobacco (duration and amount) and alcohol consumption; the effect of both agents was multiplicative. From the lowest to the highest consumption level, odds ratios ranged from 1.4 to 5.9 among regular drinkers and from 3 to 44 among current smokers. Risks among ex-smokers were approximately one-third of those for current smokers. Slightly elevated odds ratios were associated with consumption of black tobacco (OR=1.2) and hand-rolled cigarettes (OR=1.2). The risk of cancer was not clearly associated with the type of alcoholic beverage. Subsites did not differ significantly according to tobacco smoking, but differed according to alcohol consumption, with a significantly higher increased risk for hypopharyngeal than for glottic and supraglottic cancers.     

Independent and combined effects of tobacco smoking,chewing and alcohol drinking on the risk of oral,pharyngeal and esophageal cancers in Indian men

Oral, pharyngeal and esophageal cancers are 3 of the 5 most common cancer sites in Indian men. To assess the effect of different patterns of smoking, chewing and alcohol drinking in the development of the above 3 neoplasms and to determine the interaction among these habits, we conducted a case-control study in Chennai and Trivandrum, South India. The cases included 1,563 oral, 636 pharyngeal and 566 esophageal male cancer patients who were compared with 1,711 male disease controls from the 2 centers as well as 1,927 male healthy hospital visitors from Chennai. We observed a significant dose-response relationship for duration and amount of consumption of the 3 habits with the development of the 3 neoplasms. Tobacco chewing emerged as the strongest risk factor for oral cancer, with the highest odds ratio (OR) for chewing products containing tobacco of 5.05 [95% confidence internal (CI) 4.26-5.97]. The strongest risk factor for pharyngeal and esophageal cancers was tobacco smoking, with ORs of 4.00 (95% CI 3.07-5.22) and 2.83 (95% CI 2.18-3.66) in current smokers, respectively. An independent increase in risk was observed for each habit in the absence of the other 2. For example, the OR of oral cancers for alcohol drinking in never smokers and never chewers was 2.56 (95% CI 1.42-4.64) and that of esophageal cancers was 3.41 (95% CI 1.46-7.99). Furthermore, significant decreases in risks for all 3 cancer sites were observed in subjects who quit smoking even among those who had quit smoking 2-4 years before the interview.     

Polymorphism in the DNA repair gene XPD, polycyclic aromatic hydrocarbon-DNA adducts, cigarette smoking, and breast cancer risk.

DNA repair is essential to an individual's ability to respond to damage caused by environmental carcinogens. Alterations in DNA repair genes may affect cancer risk by influencing individual susceptibility to environmental exposures. XPD, a gene involved in nucleotide excision repair, may influence individual DNA repair capacity particularly of bulky adducts. Using a population-based breast cancer case-control study that was specifically conducted to examine markers of environmental exposures, such as polycyclic aromatic hydrocarbons (PAH), on Long Island, NY, we examined whether XPD genotype modified the associations among PAH-DNA adducts, cigarette smoking, and breast cancer risk. Specifically, we examined the XPD polymorphism at exon 23, position 751 in 1,053 breast cancer cases and 1,102 population-based controls. The presence of at least one variant allele (Lys/Gln or Gln/Gln) was associated with a 20% increase in risk of breast cancer [odds ratio (OR), 1.21; 95% confidence interval (95% CI), 1.01-1.44]. The increase in risk for homozygosity of the variant allele (Gln/Gln) seemed limited to those with PAH-DNA adduct levels above the median(OR, 1.61; 95% CI, 0.99-2.63 for adducts above the median versus OR, 1.05; 95% CI, 0.64-1.74 for adductsbelow the median), although the multiplicative interaction was not statistically significant. The increasein risk for homozygosity of the variant allele (Gln/Gln) was only seen among current smokers (OR, 1.97; 95% CI, 1.02-3.81 for current smokers versus OR, 0.87; 95% CI, 0.57-1.32 for never smokers); the multiplicative interaction was statistically significant. Overall, this study suggests that those individuals with this polymorphism in the XPD gene may face an increased risk of breast cancer from PAH-DNA adducts and 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.