Alcohol consumption and the risks of adenocarcinoma and squamous cell carcinoma of the esophagus

Pandeya, N., Williams, G., Green, A. C., Webb, P. M. and Whiteman, D. C. (2009) Alcohol consumption and the risks of adenocarcinoma and squamous cell carcinoma of the esophagus. Gastroenterology, 136 4: 1215-1224. doi:10.1053/j.gastro.2008.12.052

Author Pandeya, N.
Williams, G.
Green, A. C.
Webb, P. M.
Whiteman, D. C.
Title Alcohol consumption and the risks of adenocarcinoma and squamous cell carcinoma of the esophagus
Journal name Gastroenterology   Check publisher's open access policy
ISSN 0016-5085
Publication date 2009-04
Year available 2008
Sub-type Article (original research)
DOI 10.1053/j.gastro.2008.12.052
Volume 136
Issue 4
Start page 1215
End page 1224
Total pages 10
Place of publication Maryland Heights, MO, United States
Publisher W.B. Saunders
Collection year 2010
Language eng
Subject C1
9204 Public Health (excl. Specific Population Health)
1117 Public Health and Health Services
Formatted abstract
Background and Aims: Alcohol has been declared a carcinogen for cancers of the esophagus, although the evidence relates largely to the squamous subtype. Evidence for an effect on adenocarcinomas is scant and inconsistent.

Methods: We compared nationwide samples of patients with esophageal adenocarcinoma (EAC) (n 365) or esophagogastric junction adenocarcinoma (EGJAC) (n 426) or esophageal squamous cell carcinoma (ESCC) (n 303) with controls sampled from a population register (n 1580). We used generalized additive models to assess nonlinear effects of self-reported alcohol intake on cancer risk, and calculated odds ratios (ORs) and 95% confidence intervals (CIs) using multivariate logistic and piecewise regression.

Results: We observed no association between average weekly alcohol intake and EAC or EGJAC risk. For ESCC, the relationship with alcohol was nonlinear. At intakes  of less than 170 g/wk there was no significant association; at greater than this level, there was a significant linear effect (OR, 1.03; 95% CI, 1.02–1.05 per 10 g alcohol/wk). For ESCC, but not EAC or EGJAC, a statistically significant multiplicative interaction between smoking and alcohol was observed (P .02). In analyses by beverage type, ESCC risks, but not EAC or EGJAC, increased linearly with beer intake (OR, 1.05; 95% CI, 1.04 –1.07). Those who drank modest levels of wine (<50 –90 g/wk) or port or spirits (<10 –20 g/wk) had significantly lower risks of all 3 cancers than nondrinkers; higher intakes were associated with increased risks of ESCC only.

Conclusions: Alcohol intake above the recommended US dietary guidelines significantly increases the risk of ESCC, but not EAC or EGJAC. Smoking modifies the effect of alcohol intake on ESCC risk. 
Keyword Gastric Cardia
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: ERA 2012 Admin Only
School of Public Health Publications
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Created: Fri, 04 Sep 2009, 10:29:45 EST