Nonassociation of aflatoxin with primary liver cancer in a cross-sectional ecological survey in the People's Republic of China.


Three ways to measure aflatoxin, in 65 communities. (17 communities in all other aflatoxin studies, combined) Big range of cancer mortality rates. Chemist at JHU School of Medicine. Urine samples measured metabolite. and found no relationship. By this time, agencies had already advised that there WAS an association. But highly significant relationship with diet/cholesterol. Higher cholesterol, higher cancer Predisposed to hepatitis B, higher cancer. Cancer was largely a nutritional and viral disease.

JHU chemist wouldn't co-author the paper, because it impacted regulations international trade. He and his colleagues had an association with industry to produce an analytical methodology to analyze for presence of aflatoxin. Moreover, they had an interest in aflatoxin being regarded as an important carcinogen. They also had a chemical which they thought could be used as a drug in order to reduce aflatoxin-exposed people. The proposed drug was toxic to the liver.

Running high risk of causing more deaths. "Unforeseen health problems" resulted from the study. Project abandoned after many millions spent. That particular episode illustrated the way we think about science. Specific chemical approach, rather than nutrition.

TitleNonassociation of aflatoxin with primary liver cancer in a cross-sectional ecological survey in the People's Republic of China.
Publication TypeJournal Article
Year of Publication1990
AuthorsCampbell TC, Chen JS, Liu CB, Li JY, Parpia B
JournalCancer research
Date Published1990 Nov 1
KeywordsAflatoxins, Age Factors, Alcoholic Beverages, Arachis hypogaea, Cadmium, China, Cholesterol, Cross-Sectional Studies, diet, Environmental Exposure, Environmental Monitoring, Hepatitis B Surface Antigens, Humans, Liver Neoplasms, Regression Analysis, Risk Factors, Zea mays

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 less than 0.001), plasma cholesterol (P less than 0.01), frequency of liquor consumption (P less than 0.01), and mean daily intake of cadmium from foods of plant origin (P less than 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.

Alternate JournalCancer Res.
PubMed ID2208157
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