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[Cancer Research 50, 6882-6893, November 1, 1990]
© 1990 American Association for Cancer Research

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Nonassociation of Aflatoxin with Primary Liver Cancer in a Cross-Sectional Ecological Survey in the People's Republic of China1

T. Colin Campbell2, Junshi Chen, Chongbo Liu, Junyao Li and Banoo Parpia

Division of Nutritional Sciences, Cornell University, Ithaca, New York 14853 [T. C. C., B. P.], Institute of Food Hygiene [J. C.] and Institute of Virology [C. L.], Chinese Academy of Preventive Medicine, and Department of Cancer Epidemiology, China Cancer Institute [J. L.], Chinese Academy of Medical Sciences, Beijing, China

A comprehensive cross-sectional survey was undertaken in The People's Republic of China of possible risk factors for primary liver cancer (PLC) to include 48 survey sites, an approximately 600-fold aflatoxin exposure range, a 39-fold range of PLC mortality rates, a 28-fold range of hepatitis B virus surface antigen (HBsAg+) carrier prevalence, and estimation of exposures for a large number of other nutritional, dietary, and life-style features.

PLC mortality was unrelated to aflatoxin intake (r = -0.17) but was positively correlated with HBsAg+ prevalence (P < 0.001), plasma cholesterol (P < 0.01), frequency of liquor consumption (P < 0.01), and mean daily intake of cadmium from foods of plant origin (P < 0.01). Multiple regression analyses for various combinations of risk factors showed that aflatoxin exposure consistently remained unassociated with PLC mortality regardless of variable adjustment. In contrast, associations of PLC mortality with HBsAg+, plasma cholesterol, and cadmium intake remained, regardless of model specification, while the association with liquor consumption was markedly attenuated (was nonsignificant) with adjustment for plasma cholesterol.

The sharp contrast between the findings of no aflatoxin effect upon PLC prevalence in this survey and the positive correlation reported for previous but more restricted surveys is discussed. Based on the results of this survey and the data of laboratory animal and in vitro studies, an explanatory model for the etiology of PLC is proposed, taking into consideration the role of nutrition in the etiology of this disease.

1 Supported in part by NIH Grant 5RO1CA33638, Chinese Academy of Preventive Medicine, United Kingdom Imperial Cancer Research Fund, United States Food and Drug Administration, American Institute for Cancer Research, and CPC International, Inc.

2 To whom requests for reprints should be addressed, at Division of Nutritional Sciences, Cornell University, Martha V. Rensselaer Hall, Ithaca, NY 14853-4401.

Received 2/27/90. Accepted 8/ 2/90.




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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 © 1990 by the American Association for Cancer Research.