The relations between tobacco, alcohol and risk of gastric cancer need to be established, and any gain from preventive measures should be estimated. We conducted a population-based, prospective cohort study in Nord-Trondelag county in Norway. During 1984During -1986, adult residents were invited to a health survey and they answered questionnaires that assessed exposure to tobacco and alcohol, together with potential confounding factors. The exposure assessment regarding alcohol was limited to a 14-day period. New gastric cancers that occurred during follow-up (1984-2002) were identified by linkage to the Norwegian Cancer Registry. Cox proportion hazards regression models were used to calculate hazard ratios (HRs) with 95% confidence intervals (CI), adjusted for sex, education and body mass index. Follow-up of 1,117,648 person-years at risk among 69,962 cohort members revealed 251 gastric cancers, including 224 noncardia cancers. The risk was almost twice as high in daily smokers (HR 5 1.88 [CI 95% 5 1.33-2.67]) as in never smokers. Independent doseresponse relations were found with earlier age at initiation (p 5 0.02), frequency (p 5 0.00) and duration of smoking (p 5 0.00). Attributable risk (AR) of gastric cancer among current smokers was 8.7/100,000 person-years and the corresponding population AR was 18.4%. No statistically significant associations between various degrees of exposure to alcohol and risk of gastric cancer was revealed, but combined high use of cigarettes (>20/day) and alcohol (>5 occasions/14 days) increased the risk of noncardia gastric cancer nearly 5-fold (HR 5 4.90 [95% CI 5 1.90-12.62]), compared to nonusers. It is concluded that smoking is a dosedependent risk factor for gastric cancer. Combined high exposure to smoking and alcohol further increases the risk. Successful preventive measures could considerably reduce the incidence of gastric cancer. ' 2006 Wiley-Liss, Inc.
There is a relation between excess body mass index and overall cancer incidence and mortality, but the relation to noncardia gastric cancer is inconsistent. A high physical activity level decreases the risk of several cancers, but few studies have focused on gastric cancer. We conducted a population-based, prospective cohort study in Nord-Trondelag county in Norway. During 1984 to 1986, all adult residents were invited to participate in a health survey, where body height and weight were measured, and frequency, duration, and intensity of recreational physical activity, together with potential confounding factors, were assessed by questionnaires. New gastric cancers occurring during followup in 1984 to 2002 were identified by linkage to the Cancer Registry of Norway. Cox proportional hazards regression models were used to calculate hazard ratios with 95% confidence intervals, adjusted for age, sex, occupation, salt intake, smoking, and alcohol drinking. Follow-up of 73,133 cohort members (88% of all inhabitants) revealed 313 gastric cancers, including 264 noncardia cancers. No statistically significant associations were revealed between different levels of body mass index and risk of noncardia gastric cancer. A statistically significant 50% risk reduction among persons reporting at least a moderate level of recreational physical activity, based on a summary score of physical activity (hazard ratio, 0.5; 95% confidence interval, 0.3-0.9), and a dose-response relation was indicated (P for trend = 0.01). It is concluded that recreational physical activity might have a protective effect against gastric cancer. The sedentary lifestyle gaining ground in western societies might counteract the ongoing decrease in incidence of gastric cancer. (Cancer Epidemiol Biomarkers Prev 2008;17(1):135-40)
A novel histologic phenotype of chronic esophagitis, ie, lymphocytic esophagitis, is reported in 20 patients. Lymphocytic esophagitis is characterized by high numbers of intraepithelial lymphocytes (IELs) gathered mainly around peripapillary fields and by none (n = 12) to occasional (n = 8) CD15+ intraepithelial granulocytes. IELs expressed CD3, CD4 (42%), CD8 (36%), and granzyme B (0.2%), whereas T-cell intracytoplasmic antigen (TIA) 1 was not expressed. Of the 20 patients, 11 (55%) were 17 years or younger. Of 20 patients, 5 had no symptoms in the upper gastrointestinal tract. Only 4 (20%) of 20 patients had symptoms of gastroesophageal reflux disease and 6 (30%) of gastroduodenitis; 2 (10%) had celiac disease; 4 (20%) had carcinoma of the esophagus (1) or elsewhere (3); 1 (5%) each had hiatus hernia, gastric ulcer/asthma/blood hypertension, Hashimoto thyroiditis, and cirrhosis/diabetes; and 8 (40%) had Crohn disease. Hence, a novel histologic phenotype of chronic esophagitis called lymphocytic esophagitis is reported. Because phenotype is defined as the visible features resulting from the interaction between the genetic makeup and the environment, it is suggested that those factors might have a decisive role in the development of lymphocytic esophagitis.
There is an unexplained male predominance among patients with gastric cancer, and many carcinogens are found in maledominated dusty occupations. However, the relation between occupational exposures and risk of gastric cancer remains unclear. To investigate whether airborne occupational exposures might influence the risk of noncardia gastric cancer, we used a large, prospective cohort study of male Swedish construction workers. These workers were, during the period 1971-1993, regularly invited to health examinations by a nationwide occupational health service organization. Data on job titles and other variables were collected through self-administered questionnaires and forms completed by the health organization's staff. Industrial hygienists assessed 12 specific airborne occupational exposures for 200 job titles. Gastric cancer, death or emigration occurring during follow-up in 1971-2002 were identified by linkage to the Swedish registers of Cancer, Causes of Death and Total Population, respectively. Incidence rate ratios (IRR) and 95% confidence intervals (CI), adjusted for attained age, tobacco smoking, calendar period and body mass, were derived from Cox regression. Among 256,357 cohort members, contributing 5,378,012 person-years at risk, 948 noncardia gastric cancers were identified. Increased risk of this tumor was found among workers exposed to cement dust (IRR 1.5 [95% CI 1.1-2.1]), quartz dust (IRR 1.3 [95% CI 1.0-1.7]) and diesel exhaust (IRR 1.4 [95% CI 1.1-1.9]). Doseresponse relations were observed for these exposures. No consistent positive associations were found regarding exposure to asbestos, asphalt fumes, concrete dust, epoxy resins, isocyanates, metal fumes, mineral fibers, organic solvents or wood dust. In conclusion, this study provides some support to the hypothesis that specific airborne exposures increase the risk of noncardia gastric cancer. ' 2007 Wiley-Liss, Inc.
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