For definition of Groups, see Preamble Evaluation.
VOL.: 56 (1993) (p. 445)
Chem. Abstr. Name: 1,2,3-Propanetricarboxylic acid, 1,1'-[1-(12-amino-4,9,11-trihydroxy-2-methyltridecyl)-2-(1-methylpentyl)-1,2-ethanediyl] ester
Chem. Abstr. Name: 1,2,3-Propanetricarboxylic acid, 1,1'-[1-(12-amino-9,11-dihydroxy-2-methyltridecyl)-2-(1-methylpentyl)-1,2-ethanediyl] ester
Chem. Abstr. Name: 3,5,7,9-Undecatetraenoic acid, 2-ethylidene-11-[4-hydroxy-4-(2-hydroxyethyl)-2-oxo-6-oxa-3-azabicyclo-[3.1.0]hex-1-yl]-4,6,10-trimethyl-11-oxo, methyl ester, [1R-[1a(2E,3E,5E,7E,9E),4a,5a]]-
Fumonisin B1, fumonisin B2 and fusarin C are produced by Fusarium species that occur primarily on maize. These toxins may occur particularly when maize is grown under warm, dry conditions. Exposure occurs through dietary consumption of contaminated maize. Populations that eat milled or ground maize as a dietary staple can therefore be exposed to significant amounts of fumonisins and to lesser amounts of fusarin C.
The only studies available were correlation studies, most of which indicated some relationship between oesophageal cancer rates and the occurrence of F. moniliforme or its toxins in maize.
Cultures of F. moniliforme were tested by oral administration in two experiments in male rats of one strain. A culture of F. moniliforme known to produce significant amounts of fumonisins B1 and B2 induced neoplastic nodules, hepatocellular carcinomas and cholangiocellular carcinomas; in addition, forestomach papillomas and carcinomas were observed. A culture of F. moniliforme, known to contain mainly fusarin C, did not induce such tumours.
Two studies in which male rats were fed maize naturally contaminated with F. moniliforme were inadequate for evaluation.
Fumonisin B1 was tested for carcinogenicity by oral administration in the diet in one experiment in male rats, producing hepatocellular carcinomas. It induced the formation of foci of altered (g-glumatyltranspeptidase-positive) hepatocytes.
No data were available to the Working Group on the carcinogenicity of fumonisin B2.
Fusarin was tested in one study in female mice and female rats by oral gavage. It induced papillomas and carcinomas of the oesophagus and forestomach in mice and rats.
Fumonisin B1 causes outbreaks of leukoencephalomalacia in horses and pulmonary oedema in pigs. It is toxic to the central nervous system, liver, pancreas, kidney and lung in a number of animal species. Fumonisin B2 is hepatotoxic in rats.
Fumonisins B1 and B2 do not induce unscheduled DNA synthesis in rat hepatocytes in vivo or in vitro or mutation in bacteria.
In single studies, fusarin C induces chromosomal anomalies, gene mutation and DNA damage in cultured rodent cells. It induces mutations in bacteria.
There is inadequate evidence in humans for the carcinogenicity of toxins derived from F. moniliforme.
There is sufficient evidence in experimental animals for the carcinogenicity of cultures of F. moniliforme that contain significant amounts of fumonisins.
There is limited evidence in experimental animals for the carcinogenicity of fumonisin B1.
There is inadequate evidence in experimental animals for the carcinogenicity of fumonisin B2.
There is limited evidence in experimental animals for the carcinogenicity of fusarin C.
Toxins derived from Fusarium moniliforme are possibly carcinogenic to humans (Group 2B).
For definition of the italicized terms, see Preamble Evaluation.
See Also: Toxicological Abbreviations