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Qidong City, China, has had high liver cancer incidence from endemic hepatitis B virus (HBV) infection and dietary exposure to aflatoxin. Based on etiologic studies, we began interventions in 1980 to reduce dietary aflatoxin and initiate neonatal HBV vaccination. We studied trends in liver cancer incidence rates in the 1.1 million inhabitants of Qidong and examined trends in aflatoxin exposure, staple food consumption, HBV infection markers and annual income. Aflatoxin exposure declined greatly in association with economic reform, increased earnings and educational programs to shift staple food consumption in the total population from moldy corn to fresh rice. A controlled neonatal HBV vaccination trial began in 1983 and ended in November, 1990, when vaccination was expanded to all newborns. Liver cancer incidence fell dramatically in young adults. Compared with 1980–83, the age-specific liver cancer incidence rates in 2005–08 significantly decreased 14-fold at ages 20–24, 9-fold at ages 25–29, 4-fold at ages 30–34, 1.5-fold at ages 35–39, 1.2-fold at ages 40–44 and 1.4-fold at ages 45–49, but increased at older ages. The 14-fold reduction at ages 20–24 might reflect the combined effects of reduced aflatoxin exposure and partial neonatal HBV vaccination. Decrease incidence in age groups >25 years could mainly be attributable to rapid aflatoxin reduction. Compared with 1980–83, liver cancer incidence in 1990–93 significantly decreased 3.4-fold at ages 20–24, and 1.9-fold at ages 25–29 when the first vaccinees were

In an area with high incidence of esophageal cancer, Linxian, staple food is heavily contaminated by fungi of the Fusarium genus. We have found that T-2 toxin produced by Fusarium has both direct cytotoxic and proliferative effects on fetal esophageal epithelium. At higher dosage of T-2 toxin (4 ng/ml for 6 days) the cultured epithelium became necrotic. At a lower dosage range of 0.2-1.2 ng/ml, T-2 toxin caused mitogenic effects including focal basal cell hyperplasia, dysplasia, and increased number of mitoses. Atypical mitoses were also seen. These changes are very similar to the premalignant lesions seen in epithelium adjacent to human esophageal carcinoma. These observations suggest that Fusarium mycotoxin can have a role in human esophageal carcinogenesis and should be further investigated.