BACKGROUND: The reasons for the increasing incidence of and strong male predominance in patients with oesophageal and cardia adenocarcinoma remain unclear. The authors hypothesised that airborne occupational exposures in male dominated industries might contribute. METHODS: In a nationwide Swedish population based case control study, 189 and 262 cases of oesophageal and cardia adenocarcinoma respectively, 167 cases of oesophageal squamous cell carcinoma, and 820 frequency matched controls underwent personal interviews. Based on each study participant's lifetime occupational history the authors assessed cumulative airborne occupational exposure for 10 agents, analysed individually and combined, by a deterministic additive model including probability, frequency, and intensity. Furthermore, occupations and industries of longest duration were analysed. Relative risks were estimated by odds ratios (OR), with 95% confidence intervals (CI), using conditional logistic regression, adjusted for potential confounders. RESULTS: Tendencies of positive associations were found between high exposure to pesticides and risk of oesophageal (OR 2.3 (95% CI 0.9 to 5.7)) and cardia adenocarcinoma (OR 2.1 (95% CI 1.0 to 4.6)). Among workers highly exposed to particular agents, a tendency of an increased risk of oesophageal squamous cell carcinoma was found. There was a twofold increased risk of oesophageal squamous cell carcinoma among concrete and construction workers (OR 2.2 (95% CI 1.1 to 4.2)) and a nearly fourfold increased risk of cardia adenocarcinoma among workers within the motor vehicle industry (OR 3.9 (95% CI 1.5 to 10.4)). An increased risk of oesophageal squamous cell carcinoma (OR 3.9 (95% CI 1.2 to 12.5)), and a tendency of an increased risk of cardia adenocarcinoma (OR 2.8 (95% CI 0.9 to 8.5)), were identified among hotel and restaurant workers. CONCLUSIONS: Specific airborne occupational exposures do not seem to be of major importance in the aetiology of oesophageal or cardia adenocarcinoma and are unlikely to contribute to the increasing incidence or the male predominance.
BACKGROUND: Although most epidemiological studies do not support a role for alcohol in the aetiology of pancreatic cancer, an increased risk among heavy drinkers cannot be excluded. METHODS: In a retrospective cohort based on the Swedish Inpatient Register, we analysed the risk of pancreatic cancer among patients admitted to hospital for alcoholism (n=178 688), alcoholic chronic pancreatitis (n=3500), non-alcoholic chronic pancreatitis (n=4952), alcoholic liver cirrhosis (n=13 553), or non-alcoholic liver cirrhosis (n=7057) from 1965 to 1994. Follow up through to 1995 was accomplished by linkage to nationwide registers. Standardised incidence ratios (SIRs) express the relative risks by taking the general Swedish population as reference. To minimise the possible influence of selection bias, we excluded the first year observations. RESULTS: Alcoholics had only a modest 40% excess risk of pancreatic cancer (SIR 1.4, 95% confidence interval (CI) 1.2-1.5). Overrepresented smokers among alcoholics might confound a true SIR of unity among alcoholics to approximately 1.4. SIR among alcoholic chronic pancreatitis patients (2.2, 95% CI 0.9-4.5) was considerably lower than that among non-alcoholic chronic pancreatitis patients (8.7, 95% CI 6.8-10.9), and decreased with increasing duration of follow up in both groups, indicating that most of the excess might be explained by reversed causation from undiagnosed cancers. Among patients with alcoholic liver cirrhosis, the increased risk of pancreatic cancer was also moderate (SIR 1.9, 95% CI 1.3-2.8) while no significant excess risk was found among non-alcoholic liver cirrhosis patients (SIR 1.2, 95% CI 0.6-2.2). CONCLUSIONS: The excess risk for pancreatic cancer among alcoholics is small and could conceivably be attributed to confounding by smoking.
BACKGROUND: Gastro-oesophageal reflux is a strong risk factor for oesophageal adenocarcinoma. Bile and pancreatic enzymes may be particularly carcinogenic. Cholecystectomy causes an increased gastric level of these constituents. A decreased risk of oesophageal adenocarcinoma has been observed in persons infected with cagA-positive Helicobacter pylori. There is a strong correlation between ulcer disease and Helicobacter pylori infection. The aim of this study was to determine whether previous cholecystectomy or peptic ulcer disease affects the risk of oesophageal carcinoma. METHODS: Data were collected as a nationwide population-based case-control study in Sweden between 1995 and 1997. Multivariate adjusted odds ratios (ORs) were calculated with logistic regression. RESULTS: There was no statistically significant association between cholecystectomy and the risk of oesophageal carcinoma. Among persons with previous peptic ulcer, the adjusted OR for oesophageal adenocarcinoma was below unity (OR = 0.6, 95 per cent confidence interval 0.3-1.1). The relative risk estimates for cardia adenocarcinoma and oesophageal squamous cell carcinoma were close to unity. CONCLUSION: Cholecystectomy, despite its effect on the composition of gastric juice, does not appear to increase the risk of adenocarcinoma of the oesophagus or gastric cardia. While the data do not contradict a protective effect of H. pylori, the results are also consistent with absence of such an effect.
The striking male predominance in patients with adenocarcinoma of the esophagus (male:female ratio = 6:1) is not explained by known risk factors. We hypothesized that sex hormones could be responsible for this sex imbalance. If the hypothesis is correct, treatment that increases the estrogen level and/or decreases the testosterone level in males might reduce the risk of developing esophageal adenocarcinoma. To test our hypothesis, we performed a population-based, retrospective cohort study among all patients given a diagnosis of prostate cancer in Sweden between 1958 and 1992. The vast majority had received prolonged antiandrogenic treatment, typically with estrogens. A total of 100,215 patients were followed up for an average of 4 years. The standardized incidence ratio, the ratio of the observed to the expected number of incident cancers, was used as a measure of relative risk, with the expected number derived from the entire Swedish population. We observed 14 adenocarcinomas of the esophagus during follow-up in the cohort, compared to the 16 expected, yielding a relative risk close to unity (standardized incidence ratio = 0.9; 95% confidence interval = 0.5-1.5). Analysis by latency intervals after prostate cancer diagnosis revealed no clear trend toward increasing or decreasing risk over time. In conclusion, our Swedish data did not provide any support for our hypothesis of a role of sex hormones in the etiology of esophageal adenocarcinoma.
We performed a nationwide population-based case-control study of hot beverage consumption and oesophageal cancer in Sweden. Drinking beverages very hot did not increase the risk for oesophageal squamous cell carcinoma, oesophageal adenocarcinoma, or gastric cardia adenocarcinoma.
The incidence of adenocarcinoma of the oesophagus has increased rapidly in recent decades. In order to appreciate the potential for prevention by means of dietary modification, we estimated the aetiological fractions and the increments in absolute risk attributable to low intake of fruit and vegetables for adenocarcinoma and squamous cell carcinoma of the oesophagus and for adenocarcinoma of the gastroesophageal junction. We conducted a nationwide population-based case-control study in Sweden, with participation of 608 cases and 815 controls. We used unconditional logistic regression to estimate relative risks, from which we calculated aetiological fractions. Individuals in the highest exposure quartile (median 4.8 servings/day) versus the lowest (median 1.5 servings/day) showed approximately 50% lower risk of oesophageal adenocarcinoma and 40% lower risk of oesophageal squamous cell carcinoma, but no risk reduction for gastric cardia adenocarcinoma. Approximately 20% of oesophageal adenocarcinoma, and likewise squamous cell carcinoma, in Sweden was attributed to consuming less than three servings of fruit and vegetables per day. A very large number of individuals (over 25,000) would need to increase their fruit and vegetable consumption moderately in order to prevent one oesophageal cancer per year. Moderate relative risk reductions translate into weak absolute risk reductions for oesophageal cancers in Sweden.
In a Swedish nationwide case-control study, gastroesophageal reflux and obesity were identified as strong and independent risk factors for esophageal adenocarcinoma. A moderately strong association was found with adenocarcinoma of the gastric cardia. No significant association was found with squamous cell carcinoma of the esophagus. With increasing duration and severity of reflux symptoms and with increasing body mass index (BMI) the risk increased in a dose-dependent manner. When combined, reflux symptoms and obesity entailed greatly increased risk estimates, with relative risks exceeding 100 compared with persons with neither reflux symptoms nor obesity. However, because adenocarcinoma of the esophagus and gastric cardia are rarities, the absolute risk of developing these tumors was still not high. Our calculations revealed that even in the group with the highest risk, endoscopic surveillance is not readily recommended. Possible reasons for the increasing incidence of adenocarcinoma of the esophagus include 1) a suspected increase in the prevalence of reflux disease; 2) the increasing prevalence of obesity reported in western populations; and 3) the widespread use of medications that relax the lower esophageal sphincter and might cause reflux. All of these hypotheses suffer from inconsistencies that need to be solved before any firm conclusions can be drawn concerning the reasons for the increasing incidence of esophageal adenocarcinoma.
The association between gall bladder removal (cholecystectomy) and hepatocellular carcinoma warrants investigation. An increased intrahepatic bile duct pressure following cholecystectomy might cause chronic inflammation in the surrounding liver tissue, which might induce cancer development.
A nationwide Swedish population-based cohort study in 1965-2008 included 345,251 patients undergoing cholecystectomy because of gallstone. The number of observed hepatocellular carcinoma cases was divided by the expected number, calculated from the corresponding background Swedish population, thus providing standardised incidence ratios (SIRs) with 95% confidence intervals (CIs).
During follow-up of 4,854,969 person-years, 333 new cases of hepatocellular carcinoma were identified, rendering an overall increased risk (SIR 1.24, 95% CI: 1.11-1.38). The risk increased with longer follow-up (P for trend=0.003). Among patients who underwent cholecystectomy 30-43 years earlier, SIR was 2.00 (95% CI: 1.32-2.87). The results were similar after exclusion of 15,634 patients with any recorded risk factor, that is, diabetes, obesity, hepatitis, liver cirrhosis, alcoholism, or blood transfusion.
Cholecystectomy might be associated with a long-term increased risk of hepatocellular carcinoma.
The role of sex hormonal influence in explaining the strong male predominance in oesophageal adenocarcinoma (EA) needs attention.
A nation-wide nested case-control study was initiated from the Swedish Multi-Generation Register with subjects born since 1932. The study exposures were the number of children and age at having the first child. Cases of EA, gastroesophageal junctional adenocarcinoma (EJA), and oesophageal squamous cell carcinoma (SCC) were identified. Ten age- and sex-matched controls were randomly selected for each case. Conditional logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs).
In women, 115 EA, 246 EJA, and 363 SCC were identified. Comparing parous with non-parous women, a decreased risk of EA was indicated (OR=0.66, 95% CI 0.38-1.14), which became statistically significant when EA and EJA were combined (OR=0.73, 95% CI 0.53-0.99). All these associations were, however, at least as strong in men. Age at first birth did not show significant risk in women, but showed risk in men. In addition, the results were similar for SCC in both sexes.
These findings indicate that associations between the reproductive factors parity and age at first birth, and risk of EA might not be explained by sex hormonal influence.
Cites: Br J Cancer. 2000 Jul;83(1):127-3210883680
Cites: Cancer. 2010 Mar 15;116(6):1572-8120186831
Cites: Am J Epidemiol. 2001 May 1;153(9):865-7411323317
In the first cohort study of the question we followed 92 986 (42 663 men and 50 323 women) adult patients hospitalized for asthma in Sweden from 1965 to 1994 for an average of 8.5 years to evaluate their risk of oesophageal and gastric cardia adenocarcinoma. Standardized incidence ratio (SIR) adjusted for gender, age and calendar year was used to estimate relative risk, using the Swedish nationwide cancer incidence rates as reference. Asthmatic patients overall had a moderately elevated risk for oesophageal adenocarcinoma (SIR = 1.5, 95% confidence interval CI, 0.9-2.5) and gastric cardia cancer (SIR = 1.4, 95% CI, 1.0-1.9). However, the excess risks were largely confined to asthmatic patients who also had a discharge record of gastro-oesophageal reflux (SIR = 7.5, 95% CI, 1.6-22.0 and SIR = 7.1, 95% CI, 3.1-14.0, respectively). No significant excess risk for oesophageal squamous-cell carcinoma or distal stomach cancer was observed. In conclusion, asthma is associated with a moderately elevated risk of developing oesophageal or gastric cardia adenocarcinoma. Special clinical vigilance vis-à-vis gastro-esophageal cancers seems unwarranted in asthmatic patients, but may be appropriate in those with clinically manifest gastro-oesophageal reflux.