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[Cancer Research 49, 4024-4029, July 15, 1989]
© 1989 American Association for Cancer Research

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Effect of Smoking and Alcohol Consumption on Laryngeal Cancer Risk in Coastal Texas1

Roni T. Falk2, Linda W. Pickle3, Linda Morris Brown, Thomas J. Mason4, Patricia A. Buffler and Joseph F. Fraumeni, Jr.

Epidemiology and Biostatistics Program, Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland [R. T. F., L. W. P., L. M. B., T. J. M., J. F. F.]; and the Epidemiology Research Unit, School of Public Health, University of Texas Health Science Center at Houston, Houston, Texas [P. A. B.]

Data from case-control studies of respiratory cancer conducted in the Texas Gulf Coast region between 1975 and 1980 were used to examine the effects of smoking and alcohol on laryngeal cancer risk. Analyses were limited to living white males, aged 30–79, which included 151 histologically confirmed incident laryngeal cancer cases and 235 population-based controls. A dose-dependent effect for cigarette smoking was observed, with odds ratios ranging from 4.4 for ever smoking up to one-half pack daily, to 10.4 for smoking more than two packs per day. Risks were strongest for current smokers and declined markedly following smoking cessation. Higher risks were associated with smoking nonfiltered than filtered cigarettes. No significantly elevated risks were associated with the use of other tobacco products. Odds ratios for alcoholic beverages did not increase linearly with increasing use; instead risks were twofold for consumption of four or more drinks weekly. Patterns of risk associated with beer and hard liquor were not consistent and few participants drank wine. Although the data were sparse, a dose-response effect for alcohol intake was suggested for tumors of the supraglottis (n = 23), while for nonsupraglottic cases, alcohol risks were elevated but did not increase beyond those observed for four drinks per week. Predicted risks for the combined effects of cigarette and alcohol use were intermediate between an additive and multiplicative form of interaction.

1 This study was supported in part by NCI Contract N01-CP-92015.

2 To whom requests for reprints should be addressed, at Epidemiology and Biostatistics Program, Division of Cancer Etiology, National Cancer Institute, Executive Plaza North—Room 430, Bethesda, MD 20892.

3 Present address: Vincent T. Lombardi Cancer Research Center, Georgetown University, Washington, DC.

4 Present address: Fox Chase Cancer Center, Philadelphia, PA.

Received 9/29/88. Revised 4/ 3/89. Accepted 4/11/89.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1989 by the American Association for Cancer Research.