Different impact from betel quid, alcohol and cigarette: risk factors for pharyngeal and laryngeal cancer

The risks of betel quid chewing with or without tobacco, alcohol drinking and cigarette smoking have been well explored in the oral cavity but not in the pharynx and larynx. We conducted a case-control study to investigate the association of these three risk factors to cancers of the pharynx and larynx in Taiwan. A total cases of 148 pharyngeal cancer, 128 laryngeal cancer and 255 hospital controls, all men, were recruited. Betel quid chewing was a significant independent risk factor (adjusted odds ratio [aOR] = 7.7; 95% confidence interval [CI] = 4.1-15.0) similar to that of alcohol drinking (aOR = 6.6; 95% CI = 3.5-13.0) for pharyngeal cancer, but not for laryngeal cancer (aOR = 1.3; 95% CI = 0.7-2.5) on which cigarette smoking (aOR = 7.1) exerts a stronger significant independent risk than alcohol drinking (aOR = 3.8). For pharyngeal cancers, chewers who consumed >20 quid/day, chewed with inflorescence in the quid or swallowed the betel quid juice were at higher risks; significant dose-response effects were found in daily quantity of drinking and chewing, and cumulative quantity of drinking. Synergistic effects from the 3 risk factors existed both on the pharynx (aOR = 96.9) and the larynx (aOR = 40.3), and attributed for 93.1% and 92.9% respectively. Our study is the first evidence to show that betel quid chewing without tobacco has different impact on the pharynx (digestive tract) and the larynx (airway), and supports the concept that exposure quantity and direct mucosal contact with the betel quid juice may contribute to carcinogenesis. Our results show an important insight into the impact of betel quid chewing on other sites of the digestive tract other than the oral cavity.     

Cigarette and alcohol consumption and the risk of colorectal cancer in Shanghai, China.

The relation of cigarette smoking and alcohol drinking to colorectal cancer risk has been inconsistent in the epidemiological literature. In a population-based case-control study of colorectal cancer in Shanghai, China, where the incidence rates are rising sharply, we examined the association with tobacco and alcohol use. Cases were aged 30-74 years and newly diagnosed with cancers of the colon (N = 931) or rectum (N = 874) between 1990 and 1992. Controls (N = 1552) were randomly selected among Shanghai residents, frequency-matched to cases by gender and age. Information on lifetime consumption of tobacco and alcohol, as well as demographic and other risk factors, was obtained through in-person interviews. Associations with cigarette smoking and alcohol use were estimated by odds ratios (ORs) and 95% confidence intervals (CIs). Among women, the prevalence of smoking and alcohol drinking was low, and no significant association with colon or rectal cancer was observed. Although cigarette smoking among men was not related overall to colon or rectal cancer risk, there was a 50% excess risk of rectal cancer (OR 1.5, 95% CI 0.9-2.5) among those who smoked 55 or more pack-years. Among men, former alcohol drinkers had an increased risk of colon cancer (OR 2.3, 95% CI 1.4-3.7) but not rectal cancer, while current drinkers had a 30-50% excess risk of colon cancer only among those with long-term (30+ years) and heavy (>560 g ethanol/week) consumption. The excess risks were mainly associated with hard liquor consumption, with no material difference in risk between proximal and distal colon cancer. Although cigarette smoking and alcohol drinking in general were not risk factors for colorectal cancers in Shanghai, there were small excess risks for rectal cancer among heavy smokers and colon cancer among heavy drinkers.     

Smokeless tobacco and increased risk of hypopharyngeal and laryngeal cancers: a multicentric case-control study from India

Hypopharyngeal and laryngeal cancers are among the most common cancers in India. In addition to smoking, tobacco chewing may be a major risk factor for some of these cancers in India. Using data from a multicentric case-control study conducted in India that included 513 hypopharyngeal cancer cases, 511 laryngeal cancer cases and 718 controls, we investigated smoking and chewing tobacco products as risk factors for these cancers. Bidi smoking was a stronger risk factor compared to cigarette smoking for cancer of the hypopharynx (OR(bidi) 6.80 vs. OR(cig) 3.82) and supraglottis (OR(bidi) 7.53 vs. OR(cig) 2.14), while the effect of the 2 products was similar for cancer of the glottis (OR(bidi) 5.32 vs. OR(cig) 5.74). Among never-smokers, tobacco chewing was a risk factor for hypopharyngeal cancer, but not for laryngeal cancer. In particular, the risk of hypopharyngeal cancer increased with the use of Khaini (OR 2.02, CI 0.81-5.05), Mawa (OR 3.17, CI 1.06-9.53), Pan (OR 3.34, CI 1.68-6.61), Zarda (OR 3.58, CI 1.20-10.68) and Gutkha (OR 4.59, CI 1.21-17.49). A strong dose-response relationship was observed between chewing frequency and the risk of hypopharyngeal cancer (p(trend) < 0.001). An effect of alcohol on cancer of the hypopharynx and supraglottis was observed only among daily drinkers (OR 2.22, CI 1.11-4.45 and OR 3.76, CI 1.25-11.30, respectively). In summary, this study shows that chewing tobacco products commercially available in India are risk factors for hypopharyngeal cancer, and that the potency of Bidi smoking may be higher than that of cigarette smoking for hypopharyngeal and laryngeal cancers.     

Alcohol and lung cancer risk among never smokers: A pooled analysis from the international lung cancer consortium and the SYNERGY study

It is not clear whether alcohol consumption is associated with lung cancer risk. The relationship is likely confounded by smoking, complicating the interpretation of previous studies. We examined the association of alcohol consumption and lung cancer risk in a large pooled international sample, minimizing potential confounding of tobacco consumption by restricting analyses to never smokers. Our study included 22 case‐control and cohort studies with a total of 2548 never‐smoking lung cancer patients and 9362 never‐smoking controls from North America, Europe and Asia within the International Lung Cancer Consortium (ILCCO) and SYNERGY Consortium. Alcohol consumption was categorized into amounts consumed (grams per day) and also modelled as a continuous variable using restricted cubic splines for potential non‐linearity. Analyses by histologic sub‐type were included. Associations by type of alcohol consumed (wine, beer and liquor) were also investigated. Alcohol consumption was inversely associated with lung cancer risk with evidence most strongly supporting lower risk for light and moderate drinkers relative to non‐drinkers (>0–4.9 g per day: OR = 0.80, 95% CI = 0.70–0.90; 5–9.9 g per day: OR = 0.82, 95% CI = 0.69–0.99; 10–19.9 g per day: OR = 0.79, 95% CI = 0.65–0.96). Inverse associations were found for consumption of wine and liquor, but not beer. The results indicate that alcohol consumption is inversely associated with lung cancer risk, particularly among subjects with low to moderate consumption levels, and among wine and liquor drinkers, but not beer drinkers. Although our results should have no relevant bias from the confounding effect of smoking we cannot preclude that confounding by other factors contributed to the observed associations. Confounding in relation to the non‐drinker reference category may be of particular importance.     

Laryngeal cancer in women: tobacco, alcohol, nutritional, and hormonal factors.

Laryngeal cancer is the neoplasm with the largest male to female sex ratio in most populations. Thus, inadequate data are available on women. We analyzed several risk factors in the combined dataset from two case-control studies conducted between 1986 and 2000 in northern Italy and Switzerland. Cases were 68 women under age 79 years, with incident, histologically confirmed cancer of the larynx. Controls were 340 women, admitted to the same network of hospitals as cases, for acute, nonmalignant conditions, unrelated to tobacco and alcohol consumption. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were estimated by logistic regression models, conditioned by age, study center and year of interview, and including terms for education, body mass index, tobacco, alcohol drinking, and nonalcohol energy intake. Laryngeal cancer was strongly associated with cigarette smoking (OR = 435.7, 95% CI: 38.2-4964.4 for smokers of >/=25 cigarettes/day) and alcohol drinking (OR = 4.3, 95% CI: 0.8-24.1 for >/=5 drinks/day). An inverse relation was found for vegetables (OR = 0.3, 95% CI: 0.1-0.9 for the highest level of consumption), fruit (OR = 0.5, 95% CI: 0.2-1.3), and olive oil (OR = 0.3, 95% CI: 0.1-0.9). Reproductive and hormonal factors were not consistently associated to laryngeal cancer risk. This investigation, based on a uniquely large number of laryngeal cancers in women, provides definite evidence that cigarette smoking is the prominent risk factor for laryngeal cancer in women, accounting for 78% of cases in this population. Alcohol and selected dietary aspects account for approximately 30% of cases, whereas menstrual and hormonal factors do not appear to have a consistent role in laryngeal carcinogenesis.     

Fruits,Vegetables and the Risk of Cancer: a Multisite Case-Control Study in Uruguay

Introduction: Previous studies have suggested that high intake of fruit and vegetables may decrease the riskof a wide range of cancers, but this evidence has been challenged by the results of recent studies. Methods: Tofurther explore the association between fruit and vegetable intake and cancer risk we conducted a case-controlstudy of 11 cancer sites in Uruguay between 1996 and 2004, including 3,539 cancer cases and 2,032 hospitalcontrols. We used unconditional logistic regression to estimate odds ratios and 95% confidence intervals (CIs)of cancer associations. Results: In the multivariable model higher intake of fruits and vegetables combined wasassociated with a decreased risk of cancers of the esophagus (odds ratio, OR=0.63, 95% CI: 0.42-0.97), lung(OR=0.75, 95% CI: 0.57-0.98), breast (OR=0.47, 95% CI: 0.31-0.71), prostate (OR=0.63, 95% CI: 0.44-0.92)and all sites combined (OR=0.73, 95% CI: 0.61-0.87). When evaluated separately, fruit intake was more stronglyassociated with decreased cancer risk than vegetables. These inverse associations were mainly observed in men,among persons with high intake of meat, alcohol drinkers and among smokers. Conclusion: Our results providesome evidence that high intake of fruits and vegetables and particularly fruit may decrease the risk of cancer.However, because of the possibility that these findings could be due to residual confounding from intake ofmeat, alcohol drinking and tobacco smoking, further studies in populations with a large number of participantswith low or no exposure to these potential confounding factors are warranted.     

Body mass index change in adulthood and lung and upper aerodigestive tract cancers

Body mass index (BMI) has been inversely associated with lung and upper aerodigestive tract (UADT) cancers. However, only a few studies have assessed BMI change in adulthood in relation to cancer. To understand the relationship between BMI change and these cancers in both men and women, we analyzed data from a population-based case-control study conducted in Los Angeles County. Adulthood BMI change was measured as the proportional change in BMI between age 21 and 1 year before interview or diagnosis. Five categories of BMI change were included, and individuals with no more than a 5% loss or gain were defined as having a stable BMI (reference group). Adjusted odds ratios (ORs) and their 95% confidence intervals (CIs) were estimated using logistic regression models. Potential confounders included age, gender, ethnicity, education, tobacco smoking and energy intake. For UADT cancers, we also adjusted for alcohol drinking status and frequency. A BMI gain of 25% or higher in adulthood was inversely associated with lung cancer (OR 0.53, 95% CI 0.33-0.84) and UADT cancers (OR 0.44, 95% CI 0.27-0.71). In subgroup analyses, a BMI gain of ≥25% was inversely associated with lung and UADT cancers among current and former smokers, as well as among current and former alcohol drinkers. The inverse association persisted among moderate and heavy smokers (≥20 pack-years). The observed inverse associations between adulthood BMI gain and lung and UADT cancers indicate a potential role for body weight-related biological pathways in the development of lung and UADT cancers.     

High-risk factors in the development of head and neck cancers

It is considered that the great majority of head and neck squamous cell cancers are self-inflicted cancers. The main high-risk factor for squamous cell cancers of the oro-airway region is heavy smoking. Well-known habits of smoking include reverse smoking and betel nut chewing in South Asia. Tobacco smoking has distinct carcinogenecity as both an initiator and promoter. Also the risks associated with smoking and alcohol consumption are synergistic. There are many adjuvant carcinogens which act as promoting factors and which are also causes of cancer in the head and neck area. Distinct promotion factors are poor dental hygiene for mouth cancer, vocal abuse in laryngeal cancer, Plummer-Vinson's syndrome in post-cricoid cancer and chronic sinusitis in maxillary cancer. High-risk factors for carcinogenesis in the larynx are smoking (Brinkman index, over 600), heavy drinking, being over 50 years of age in males and anyone with a husky voice and abnormal sensation in the throat. In the piriform sinus, main risk factors of carcinogenesis are heavy smoking and drinking in males and in the post-cricoid area, those most at risk are female patients with Plummer-Vinson's syndrome. The prevention of head and neck cancers involves discouragement from smoking, and earlier detection of these cancers is very important. If early detection can be achieved, the highest cure rate among human cancers will be achieved.     

Alcohol, smoking, social and occupational factors in the aetiology of cancer of the oral cavity, pharynx and larynx

A case-control study of 374 patients with primary epithelial cancers of the oral cavity, oro- and hypopharynx, and larynx is reported, the controls being patients with selected other cancers, matched for age and sex. Of all eligible patients, 93% were interviewed. Increased risks were seen with alcohol consumption and, less strongly, with smoking, which for all sites could be adequately fitted by either a multiplicative or an additive model. However, the site-specific relationships were different, alcohol consumption being significantly associated only with oral cavity, pharyngeal and extrinsic laryngeal tumours, and smoking only with intrinsic laryngeal tumours. Increased risks were associated with low socio-economic status, the unmarried state, and poor dental care. No significant associations were seen with specific occupational exposures.     

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.     

Family history of cancer and the risk of laryngeal cancer: a case-control study from Italy and Switzerland

Only limited data is available on the relationship between family history of laryngeal and other neoplasms and laryngeal cancer risk. We investigated the issue using data from a multicentre case-control study conducted in Italy and Switzerland between 1992 and 2009 including 852 cases with histologically confirmed laryngeal cancer and 1970 controls admitted to hospital for acute, non neoplastic conditions. Unconditional logistic regression models adjusted for age, sex, study center, education, tobacco smoking, alcohol drinking and number of siblings were used to estimate the odds ratios (ORs) of laryngeal cancer. The multivariate OR was 2.8 (95% confidence interval [CI], 1.5-5.3) in subjects reporting a first-degree relative with laryngeal cancer, as compared to subjects with no family history. The OR was higher when the relative was diagnosed before 60 years of age (OR = 3.5, 95% CI 1.4-8.8). As compared to subjects without family history, non-smokers, and moderate drinkers, the OR was 37.1 (95% CI 9.9-139.4) for current smokers, heavy drinkers, with family history of laryngeal cancer. Family history of colorectal (OR = 1.5, 95% CI 1.0-2.3) and kidney (OR = 3.8, 95% CI 1.2-12.1) cancer were also associated to an increased risk of laryngeal cancer, while no significant increase in risk was found for family history of cancer at all sites, excluding the larynx (OR = 1.1).     

Family history and the risk of oral and pharyngeal cancer

Scanty data are available on familial risk in oral and pharyngeal cancer. The relationship between oral and pharyngeal cancer and family history of cancer in first-degree relatives was investigated using data from a multicentric case-control study conducted in Italy and Switzerland between 1992 and 2005 on 956 cases aged less than 79 years, with histologically confirmed incident oral and pharyngeal cancer, and 2362 controls admitted to hospital for acute, nonneoplastic conditions. Logistic regression models conditioned on sex, age, study centre, and including terms for education, tobacco smoking, alcohol drinking, and number of siblings were used to estimate the odds ratios (OR) of oral and pharyngeal cancer. The multivariate ORs were similar for a family history of oral and pharyngeal cancer (2.6, 95% confidence interval, CI, 1.5-4.5) and laryngeal cancer (3.8, 95% CI, 2.0-7.2). The OR was 3.1 (95% CI, 2.0-4.8) for oral and pharyngeal cancer and laryngeal cancer combined. The OR was 7.1 (95% CI, 1.3-37.2) for subjects with 2 or more first-degree relatives with oral and pharyngeal/laryngeal cancers. Significant increases in risk were also observed for a family history of melanoma (OR = 5.8; 95% CI, 1.3-26.4) and lung cancer (OR = 1.4; 95% CI, 1.0-2.0). Compared to subjects without family history, nonsmokers, and non or moderate drinkers, the OR was 42.6 for current smokers, heavy drinkers with family history. History of oral and pharyngeal cancer and laryngeal cancer is a strong determinant of oral and pharyngeal cancer risk, independent from tobacco and alcohol.     

Alcohol consumption and gastric cancer risk—A pooled analysis within the StoP project consortium

An association between heavy alcohol drinking and gastric cancer risk has been recently reported, but the issue is still open to discussion and quantification. We investigated the role of alcohol drinking on gastric cancer risk in the “Stomach cancer Pooling (StoP) Project,” a consortium of epidemiological studies. A total of 9,669 cases and 25,336 controls from 20 studies from Europe, Asia and North America were included. We estimated summary odds‐ratios (ORs) and the corresponding 95% confidence intervals (CIs) by pooling study‐specific ORs using random‐effects meta‐regression models. Compared with abstainers, drinkers of up to 4 drinks/day of alcohol had no increase in gastric cancer risk, while the ORs were 1.26 (95% CI, 1.08–1.48) for heavy (>4 to 6 drinks/day) and 1.48 (95% CI 1.29–1.70) for very heavy (>6 drinks/day) drinkers. The risk for drinkers of >4 drinks/day was higher in never smokers (OR 1.87, 95% CI 1.35–2.58) as compared with current smokers (OR 1.14, 95% CI 0.93–1.40). Somewhat stronger associations emerged with heavy drinking in cardia (OR 1.61, 95% CI 1.11–2.34) than in non‐cardia (OR 1.28, 95% CI 1.13–1.45) gastric cancers, and in intestinal‐type (OR 1.54, 95% CI 1.20–1.97) than in diffuse‐type (OR 1.29, 95% CI 1.05–1.58) cancers. The association was similar in strata of H. pylori infected (OR = 1.52, 95% CI 1.16–2.00) and noninfected subjects (OR = 1.69, 95% CI 0.95–3.01). Our collaborative pooled‐analysis provides definite, more precise quantitative evidence than previously available of an association between heavy alcohol drinking and gastric cancer risk.     

Polymorphism of Xeroderma Pigmentosum group G and the risk of lung cancer and squamous cell carcinomas of the oropharynx, larynx and esophagus

We investigated the effects of XPG His1104Asp polymorphism (rs17655) on the risk of lung cancer and squamous cell carcinomas of the oropharynx, larynx and esophagus (SCCOLE). This population-based case-control study involves 611 new cases of lung cancer, 601 new cases of oropharyngeal, laryngeal and esophageal cancers, and 1,040 cancer-free controls. The XPG polymorphism was assayed by PCR-RFLP method for 497 lung cancer cases, 443 cases of oropharyngeal, laryngeal and esophageal cancers and 912 controls. Binary and polytomous unconditional logistic regression models were fitted to assess the main effects and the effect modifications between the polymorphism and environmental exposures. With the adjustment for potential confounders, the XPG Asp1104Asp genotype was inversely associated with lung cancer (odds ratio [OR] = 0.62, 95% confidence limits [CL] = 0.38, 1.0) and SCCOLE (OR = 0.47, 95% CL = 0.27, 0.82), with the combined His1104His and His1104Asp genotypes as the referent. With subjects having genotype Asp1104Asp and no tobacco smoking exposure as the common referent, the ORs on lung cancer were 13 (95% CL = 4.4, 37) for heavy tobacco smoking (>20 pack-years), 1.9 (95% CL = 0.78, 4.5) for having at least one copy of 1104His, and 23 (95% CL = 9.5, 56) for the joint effect, respectively. Compared to non-smokers with the Asp1104Asp genotype, the adjusted OR on SCCOLE for heavy smokers (>20 pack-years) having at least one copy of 1104His was 8.0 (95% CL = 2.7, 24). Similarly, compared to non-drinkers with the Asp1104Asp genotype, the adjusted OR on SCCOLE for heavy drinkers (> or =3 drinks/day) with at least one copy of 1104His was 10 (95% CL = 2.7, 38). In conclusion, our study suggests that the XPG Asp1104Asp genotype may be associated with decreased susceptibility to lung cancer and SCCOLE.     

Pipe smoking and cancers of the upper digestive tract

Pipe smoking has been related to the risk of cancers of the upper digestive and respiratory tract, but quantification of the risk for exclusive pipe smokers is still limited. To analyse the association between exclusive pipe smoking and cancers of the upper digestive tract, we used data from a series of case-control studies conducted in Italy and Switzerland between 1984 and 1999. After excluding cigarette and cigar smokers, 41 male oral and pharyngeal cancer cases, 52 male oesophageal cancer cases and 1,032 male controls were included in the present analysis. Odds ratios (OR) of cancers were estimated by the mean of unconditional multivariate logistic regression, including terms for age, study centre, education, body mass index, and alcohol drinking. Compared to never smokers, exclusive pipe smokers had an OR of 8.7 [95% confidence intervals (CI): 4.0-18.9] of all upper digestive tract cancers. The OR was 12.6 for oral and pharyngeal and 7.2 for oesophageal cancer. Pipe smokers who were also heavy alcohol drinkers had an OR of 38.8 (95% CI: 13.6-110.9) as compared to never smokers and light drinkers. Thus, pipe smoking and heavy alcohol drinking appears to interact at least on a multiplicative model.     

Alcohol consumption and risk of laryngeal cancer

Epidemiological studies consistently showed that alcohol drinking increases the risk of laryngeal cancer. This risk increases with the amount of alcohol consumed: in recent studies conducted in North America, Europe, Japan and Korea the multivariate relative risks for the highest levels of consumption ranged between 2 and 10, and were 1.94 for 50 g/day and 3.95 for 100 g/day in a meta-analysis of 20 studies. Further, the risk increases by concomitant tobacco smoking, each agent approximately multiplying the effect of the other. In the absence of smoking the risks are small for moderate alcohol consumption. After stopping drinking, some fall in risk becomes apparent in the long term. The role of age at starting and stopping drinking is still unclear. In various studies, the most commonly used alcoholic beverage appears to be the most associated with laryngeal cancer risk, suggesting that no meaningful difference exists for different types of alcoholic beverages. The supraglottis is more closely related to alcohol consumption, as compared to the glottis/subglottis. Alcohol drinking may influence laryngeal cancer risk particularly through its direct contact or solvent action, perhaps by enhancing the effects of tobacco or other environmental carcinogens.     

Alcohol consumption and site-specific cancer risk: a comprehensive dose–response meta-analysis

Background:

Alcohol is a risk factor for cancer of the oral cavity, pharynx, oesophagus, colorectum, liver, larynx and female breast, whereas its impact on other cancers remains controversial.

Methods:

We investigated the effect of alcohol on 23 cancer types through a meta-analytic approach. We used dose–response meta-regression models and investigated potential sources of heterogeneity.

Results:

A total of 572 studies, including 486 538 cancer cases, were identified. Relative risks (RRs) for heavy drinkers compared with nondrinkers and occasional drinkers were 5.13 for oral and pharyngeal cancer, 4.95 for oesophageal squamous cell carcinoma, 1.44 for colorectal, 2.65 for laryngeal and 1.61 for breast cancer; for those neoplasms there was a clear dose–risk relationship. Heavy drinkers also had a significantly higher risk of cancer of the stomach (RR 1.21), liver (2.07), gallbladder (2.64), pancreas (1.19) and lung (1.15). There was indication of a positive association between alcohol consumption and risk of melanoma and prostate cancer. Alcohol consumption and risk of Hodgkin''s and Non-Hodgkin''s lymphomas were inversely associated.

Conclusions:

Alcohol increases risk of cancer of oral cavity and pharynx, oesophagus, colorectum, liver, larynx and female breast. There is accumulating evidence that alcohol drinking is associated with some other cancers such as pancreas and prostate cancer and melanoma.     

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.     

Multiple primary cancers in patients with initial laryngeal cancer

The risk of a person developing a second primary cancer was evaluated in 1,215 patients with laryngeal cancer at the National Cancer Center Hospital. Overall, 92 (8.2%) of the male patients and 5 (5.7%) of the female patients developed a second cancer, compared with 83.0 and 3.7, respectively, expected on the basis of general population rates, resulting observed: expected values (O/E) to be 1.1 and 1.3. The numbers of second cancers of the lung (O/E = 1.9), oropharynx (O/E = 8.8) and esophagus (O/E = 2.8) were significantly in excess of those expected, while the number of second stomach cancers (O/E = 0.5) was far below expectation. Synchronous second cancers were significantly higher than expected (O/E = 4.6). Smoking, especially heavy smoking, was related to second lung cancers, but alcohol drinking featured less. Histories of benign respiratory tract and digestive organ diseases were related to second oropharyngeal cancers. Alcohol drinking was related to second stomach cancers. Radiation therapy for the initial laryngeal cancer was related to second oropharyngeal cancers, while hazardous occupations related to noxious agents for respiratory systems featured more prevalently in cases of second lung cancer. Further analytical studies should clarify the roles of smoking, drinking, occupation and various forms of therapy on the risk of developing a different second cancer following laryngeal cancer.     

Occupational physical activity,socioeconomic status,and risks of 15 cancer sites in Turkey

A multiple-site case-control study of 15 cancers (stomach; colon; rectum; larynx; lung; melanoma; skin; female breast; male breast; cervix; ovary; uterus; prostate; testis; and bladder) was conducted to evaluate their association with occupational physical activity and socioeconomic status (SES). A hospital-based study population (3,486 male cases and 379 female cases, and 2,127 male and 244 female controls) was established in an oncological treatment center in Istanbul, Turkey, from 1979–84. Assessment of physical activity and SES was based on job titles held by the study subjects. Two measures of physical activity were developed based on energy expenditure and sitting time during working hours. Observed risks were adjusted for age, smoking, and SES. Elevated risks were observed among workers who held sedentary jobs for cancers of the colon (odds ratio [OR=1.6), rectum (OR=1.3), melanoma (OR=1.9), male breast (OR=1.4), prostate (OR=5.0), and ovary (OR=2.0). Cancers of the cervix and uterus showed significantly decreasing risks with decreased activity. Risks of cancers of the colon, rectum, larynx, ovary, and melanoma were enhanced after risks for physical activity indices were adjusted for SES, while the associations between physical activity and cancers of the prostate, cervix, and uterus were weakened after SES adjustment. Risks of melanoma rose significantly with both activity indices after SES adjustment. The results of this study support previously reported associations between physical activity and cancers of the colon and rectum observed in developed countries, and provide additional evidence for cancers of the larynx, prostate, cervix, uterus, and melanoma, and point out the importance of SES in evaluation of physical activity and cancers of the colon, rectum, larynx, prostate, breast, cervix, and melanoma in developing countries.