Fumonisin B₁ is the most prevalent member of a family of toxins, known as fumonisins, produced by multiple species of Fusarium molds, such as Fusarium verticillioides, which occur mainly in maize (corn), wheat and other cereals. Fumonisin B1 contamination of maize has been reported worldwide at mg/kg levels. Human exposure occurs at levels of micrograms to milligrams per day and is greatest in regions where maize products are the dietary staple.

Fumonisin B₁ is hepatotoxic and nephrotoxic in all animal species tested. The earliest histological change to appear in either the liver or kidney of fumonisin-treated animals is increased apoptosis followed by regenerative cell proliferation. While the acute toxicity of fumonisin is low, it is the known cause of two diseases which occur in domestic animals with rapid onset: equine leukoencephalomalacia and porcine pulmonary oedema syndrome. Both of these diseases involve disturbed sphingolipid metabolism and cardiovascular dysfunction.

In 1970, an outbreak of leukoencephalomalacia in horses in South Africa was associated with the contamination of corn with the fungus Fusarium verticillioides. It is one of the most prevalent seed-borne fungi associated with corn. Another study was done on the possible role of fungal toxins in the etiology of human esophageal cancer in a region in South Africa. The diet of the people living in this area was homegrown corn and F. verticillioides was the most prevalent fungus in the corn consumed by the people with high incidence of esophageal cancer. Further outbreaks of leukoencephalomalacia and people in certain regions with high incidence of esophageal cancer led to more research on F. verticillioides. Soon they found experimentally that F. verticillioides caused leukoencephalomalacia in horses and porcine pulmonary edema in pigs. It was found to be highly hepatotoxic and cardiotoxic in rats. In 1984 it was shown that the fungus was hepatocarcinogenic in rats. The chemical nature of the metabolites causing all this had still not been discovered in 1984. After discovery of the carcinogenicity of the fungus, isolation and chemical characterization of the mycotoxins and carcinogens produced by F. verticillioides was urgent. It was not until 1988 that the chemical nature of the carcinogen was unraveled. Fumonisin B₁ and fumonisin B₂ were isolated from cultures of F. verticillioides at the Programme on Mycotoxins and Experimental Carcinogenesis. The structures were elucidated in collaboration with the Council for Scientific and Industrial Research. Several isomers of fumonisin B1 have been detected in solid rice culture. Now more than 100 different fumonisins are known, the most important ones being fumonisin B₁, B₂ and B₃.

Regarding toxicokinetics there is no human data available, but research on animals has been done.

FB₁ is taken orally via food. Overall, FB₁ is poorly absorbed, less than 6%. Absorption of orally administered fumonisin B₁ (10 mg/kg body weight) to rats is low (3.5% of dose) but rapid (T_max = 1.02 h). FB₁ does not significantly permeate through the human skin and hence has no significant systemic health risk after dermal exposure.

After absorption, some appears to be retained in liver and kidneys. For rats that were fed diets containing fumonisins for several weeks, the concentrations of the fumonisins in the kidneys were approximately 10-fold higher than in the liver.

Plasma distribution of the absorbed dose conformed to a two-compartment open model and the tissue (liver, kidney) concentration time results were consistent with a one-compartment open model.

Elimination half-life in rats is 3.15 h for plasma, 4.07 h for liver, and 7.07 h for kidney. However, FB₁ is rapidly excreted mostly in its original form. Small amounts are excreted in urine; the most are excreted in feces.