Conflicting data exist on the changes in the incidence of oesophageal (EAC) and oesophagogastric junction adenocarcinoma (EGJAC). In addition, risk factors of the disease are only partly known. The aim of the study was to evaluate the incidence of EAC and EGJAC in Finland as well as risk factors of these cancers.
The complete number of new EAC and EGJAC cases between January 1980 and December 2007 in Finland was provided by the Finnish Cancer Registry. All treated EAC and EGJAC patients in the Pirkanmaa Hospital District between January 1980 and December 2007 were included in the study.
The incidence of EAC increased significantly in Finland. Barrett's oesophagus (BE) was associated with the risk of EAC and cholecystectomy with the risk of EGJAC.
A significant increase in EAC was found in Finland over the course of nearly 30 years, indicating that the increase in EAC in Finland is existent in the long term. BE was associated with the risk of EAC and cholecystectomy with the risk of EGJAC.
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.
The incidence of cancer was studied in a population-based cohort of 9,353 individuals (8,340 men and 1,013 women) with a discharge diagnosis of alcoholism in 1965-83, followed up for 19 years (mean 7.7). After exclusion of cancers in the first year of follow-up, 491 cancers were observed cf 343.2 expected through 1984 (standardized incidence ratio [SIR] = 1.4, 95 percent confidence interval [CI] = 1.3-1.6). A similar excess risk of cancer was seen among men (SIR = 1.4, CI = 1.3-1.6) and among women (SIR = 1.5, CI = 1.1-2.0). We observed the established associations with cancers of the oral cavity and pharynx (SIR = 4.1, CI = 2.9-5.7), esophagus (SIR = 6.8, CI = 4.5-9.9), larynx (SIR = 3.3, CI = 1.7-6.0), and lung (SIR = 2.1, CI = 1.7-2.6), although confounding by smoking likely increased these risk estimates. While there was evidence of increased risk for pancreatic cancer (SIR = 1.5, CI = 0.9-2.3), alcoholism did not elevate the incidence of cancer of the stomach (SIR = 0.9, CI = 6-1.4), large bowel (SIR = 1.1, CI = 0.8-1.5), prostate (SIR = 1.0, CI = 0.8-1.3), urinary bladder (SIR = 1.0, CI = 0.6-1.5), or of malignant melanoma (SIR = 0.9, CI = 0.3-1.9). Among women, the number of breast cancers observed was close to expected (SIR = 1.2, CI = 0.6-2.2), although a significant excess number of cervical cancers occurred (SIR = 4.2, CI = 1.5-9.1).(ABSTRACT TRUNCATED AT 250 WORDS)
To estimate the incidence, mortality and cancer risk of the congenital malformation esophageal atresia (EA) in a population-based investigation.
A population-based cohort study of EA patients registered in three nationwide registers in Sweden in 1964-2007. The incidence of EA per total number of live births was assessed. Mortality and cancer occurrence were expressed as standardized mortality ratio (SMR) and standardized incidence ratio (SIR) with 95% confidence intervals (CI). Mortality was further analyzed by Cox regression and expressed as hazard ratio with 95% CI.
The EA cohort comprised 1,126 patients. The mean incidence was 3.16 per 10,000 live births, without any temporal changes (p for trend =0.94). Associated anomalies were present in 42% and chromosomal abnormalities in 5%. EA patients had an almost 12 times higher risk of mortality compared to the background population (SMR 11.8, 95% CI 10.3-13.5). The mortality increase was most pronounced during the first 5 years after birth. Survival improved during the study period (p for trend =0.0001). EA did not entail a strongly increased cancer risk (SIR 0.9; 95% CI 0.2-2.6).
EA has a stable incidence, the survival has improved substantially during recent decades, and the cancer risk might not be increased.
We examined cancer incidence in an expanded cohort of Swedish chimney sweeps.
We added male chimney sweep trade union members (1981-2006) to an earlier cohort (employed 1918-1980) and linked them to nationwide registers of cancer, causes of deaths, and total population. The total cohort (n = 6320) was followed from 1958 through 2006. We estimated standardized incidence ratios (SIRs) using the male Swedish population as reference. We estimated exposure as years of employment and analyzed for exposure-response associations by Poisson regression.
A total of 813 primary cancers were observed versus 626 expected (SIR = 1.30; 95% confidence interval = 1.21, 1.39). As in a previous follow-up, SIRs were significantly increased for cancer of the esophagus, liver, lung, bladder, and all hematopoietic cancer. New findings included significantly elevated SIRs for cancer of the colon, pleura, adenocarcinoma of the lung, and at unspecified sites. Total cancer and bladder cancer demonstrated positive exposure-response associations.
Exposure to soot and asbestos are likely causes of the observed cancer excesses, with contributions from adverse lifestyle factors. Preventive actions to control work exposures and promote healthier lifestyles are an important priority.
The increased intake of carbonated soft drinks parallels the incidence of esophageal adenocarcinoma. To determine whether an association exists between carbonated drink intake and esophageal and cardia adenocarcinoma, we analyzed data from a Swedish nationwide, population-based, case-control study. During data collection in 1995-1997, 189 patients with esophageal adenocarcinoma (88% of all eligible), 262 patients with cardia adenocarcinoma (84%), and 820 control subjects (73%) were interviewed in person. All cancers were histologically classified. We calculated odds ratios with 95% confidence intervals using conditional logistic regression and multivariable analyses. Frequency of intake of carbonated soft drinks was not associated with risk of esophageal adenocarcinoma; high consumers (intake more than six times weekly) were at a statistically nonsignificantly decreased risk compared with never users (odds ratio = 0.89, 95% confidence interval = 0.49 to 1.64). Consumption of carbonated low-alcohol beer and combined intake of carbonated drinks were not associated with risk of esophageal adenocarcinoma. No association between intake of carbonated soft drinks or low-alcohol beer and risk of cardia adenocarcinoma was observed.
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 results of two epidemiological studies suggest that high intake of heterocyclic amines, which are formed on the surface of meats cooked at high temperatures, might be associated with increased risk of esophageal or cardia cancers. Our aim was to further investigate heterocyclic amine intake and risk of these cancers. We examined data from a nationwide, population-based, case-control study of risk factors for adenocarcinoma of the esophagus and gastric cardia and squamous cell carcinoma of the esophagus in Sweden, with 185, 258, and 165 cases, respectively, and 815 controls. Heterocyclic amine intake was estimated based on the frequency of consumption and degree of surface browning of commonly fried meats, and the consumption of pan juices. Statistically nonsignificant 50-70% higher risks of esophageal squamous cell carcinoma were observed among individuals in the highest quartile levels of 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline, 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline, and 2-amino-1methyl-6-phenylimidazo[4,5-b]pyridine relative to those in the lowest. Dose-risk trends were evident. Subjects reporting high intake of all three heterocyclic amines had an odds ratio of 2.4 (95% confidence interval, 1.2-4.8) relative to those with low intake of all three substances. In contrast, no association was found with risk of adenocarcinoma of the esophagus or gastric cardia. Heterocyclic amine intake might be associated with an increase in risk of squamous cell carcinoma of the esophagus. Given the dearth of epidemiological data regarding these cancers and the lack of established biological mechanisms, confirmatory data are needed.
High intake of phytoestrogen lignans has been found to be associated with decreased risk of esophageal adenocarcinoma in our previous population-based case-control study in Sweden. To further evaluate this possible association, we tested the hypothesis of an inverse association between dietary lignan intake and risk of esophageal and gastric adenocarcinoma using a prospective design. In a population-based cohort study in Sweden, 81,670 participants who were cancer-free at baseline were followed up during 1998 to 2009. All participants completed a 96-item food frequency questionnaire (FFQ), which was used to assess dietary exposure to lignans (secoisolariciresinol, matairesinol, lariciresinol, pinoresinol, medioresinol, and syringaresinol). All cases of esophageal, gastroesophageal junctional, and gastric adenocarcinoma were identified through linkage to the Swedish Cancer Register. Cox proportional hazard models were used to estimate HRs and 95% confidence intervals (CI), with adjustment for potential confounding factors. During an average follow-up of 9.9 years, a total of 211 cases were identified, including 83 cases of esophageal or junctional adenocarcinoma, and 128 cases of gastric adenocarcinoma. There was no statistically significant association between dietary intake of lignans and any of the studied adenocarcinomas. Compared with participants in the lowest quartile of lignan intake, the adjusted HR of the highest quartile was 0.96 (95% CI, 0.46-2.00; P(trend) = 0.70) for adenocarcinoma of the esophagus or gastroesophageal junction, and 0.89 (95% CI, 0.52-1.55: P(trend) = 0.78) for gastric adenocarcinoma. No clear support for a protective role of dietary intake of lignans in the development of esophageal or gastric adenocarcinoma was found.