Human exposure occurs at levels of micrograms to milligrams per day and is greatest in regions where maize products are the dietary staple.

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.

In 1970, an outbreak of leukoencephalomalacia in horses in South Africa was associated with the contamination of corn with the fungus Fusarium verticillioides.

[2] Another study was done on the possible role of fungal toxins in the etiology of human esophageal cancer in a region in South Africa.

[2] 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.

[8] Absorption of orally administered fumonisin B1 (10 mg/kg body weight) to rats is low (3.5% of dose) but rapid (Tmax = 1.02 h).

[8] Because of their similarity, fumonisins are able to inhibit sphingosine-sphinganin-transferases and ceramide synthases and are therefore competitive inhibitors of sphingolipid biosynthesis and metabolism.

Fumonisin B1 inhibits the enzyme ceramide synthase (sphingosine N-acyltransferase), which acylates sphingoid bases.

Increased apoptosis seems to play an important role in the toxic effects including tumor induction.

[14] Also, the decreased concentrations of complex sphingolipids appear to play a role in the abnormal behavior and altered morphology of the affected cells.

Fumonisin B1 occupies the space and electrostatic interactions of both sphinganine (or sphingosine) and fatty acyl-CoA in ceramide synthase.

The part of FB1 that has structural similarity with sphingoid bases (the aminopentol part) may interact with the sphinganine binding site, whereas the negatively charged tricarbyllic acid groups may interact with the fatty acyl-CoA binding site.

[13] The risks of fumonisin B1 have been evaluated by The World Health Organization's International Programme on Chemical Safety and the Scientific Committee on Food of the European Commission.

[16] Epidemiological studies and clinical trials have pointed out folate deficiency as a major risk factor for neural tube defects.

[17] FB1 disrupts sphingolipid metabolism and therefore this could affect folate uptake and cause neural tube defects.

It is believed that this outbreak might have been due to high levels of FB1 that were observed in corn during previous years.

A low socioeconomic status and a less varied diet, that mainly consists of corn and wheat, is associated with the appearance of esophageal cancer.

Other studies show that higher concentrations of FB1, FB2 and F. verticillioides are present in corn growing in regions with a high percentage of esophageal cancer.

This is observed by people in regions in Italy, Iran, Kenia, Zimbabwe, United States and Brazil with high incidence of esophageal cancer.

The corn and sorghum were contaminated by Fusarium and Aspergillus and contained high levels of FB1 compared with samples of unaffected households.

[22] In pigs and rats there is a wide distribution of FB1 and small amounts have been found to accumulate only in liver and kidneys.

Important mechanisms for cancer development due to fumonisin B1 could be oxidative damage (production of reactive oxygen species) and lipid peroxidation.

[6] Based on all these animal studies FB1 is classified by The International Agency for Research on Cancer (IARC) as possibly carcinogenic to humans (Group 2B).

Lethal pulmonary edema was developed within 4–7 days after exposure to feed with concentrations of FB1 >16 mg/kg body weight (>92 parts per million).

[6] The risks of fumonisin B1 have been evaluated by The World Health Organization's International Programme on Chemical Safety and the Scientific Committee on Food of the European Commission.

[8] Bioavailability of FB1 can be reduced by treating fumonisin-contaminated corn with glucomannans extracted from the cell wall of the yeast Saccharomyces cerevisiae.