**2.1.1 Aflatoxin toxic effects**

Studies by Christensen (1975), over a period of several years, examined 100 different samples of black pepper from all over the world. In dilution cultures of these samples, the number of fungus colonies in whole or ground black pepper averaged 52,000 per gram/black pepper and the upper range was over half a million per gram (Coker, 1998). These colonies were mostly of *A. flavus*, *A. ochraceus* and *A. versicolor*. All three species are known to be aflatoxin producers. Some samples of ground pepper were caked lightly with fungus mycelium when first opened in the laboratory and with time, a number of these became solidly caked with mycelium (Jalili et al., 2011).

How heavily contaminated is 52,000 to 500,000 colonies of fungi, per gram? Let's make a comparison for what is acceptable levels of fungal colonies isolated in other food products at the time Christensen published his results. Wheat, for example, that is intended for milling into flour seldom contains any more than a few thousand colonies of fungi per gram of grain. If barley has as many as 10,000 colonies of the same kind of fungi per gram as in black pepper, it would be rejected for malting in beer making. If breakfast cereals or bread were as contaminated as black peppers, they would have so musty an odour and taste that they would be too revolting to eat. Apparently, the natural spicy odour and flavour of black, as well as white pepper are potent enough to conceal the taste and odour of these fungi.

#### **2.1.2 Mycotoxins of other fungal species of** *Aspergillus***,** *Penicillium* **and** *Fusarium*

#### **2.1.2.1** *Aspergillus ochraceus* **and ochratoxin**

*Aspergillus ochraceus* is also a species complex, and consist of nine species. These species are common in soil, decaying vegetation, and in stored seeds and grains undergoing microbial deterioration. However, this fungus is seldom isolated from more than a small percentage of seeds or grains that are undergoing microbiological deterioration in storage because it is evidently not a good competitor, as is also the case with *A*. *flavus*. This is a general rule, but *A. ochraceus* has been isolated from 40% or more of surface-disinfected kernels of corns from bins in which deterioration was in progress. It has also been the major organism in some lots of whole black pepper (Desjardins and Hohm, 1997; Chang et al., 2011).

Production of ochratoxin, by *A. ochraceus*, was first described in South Africa (Christensen 1975), where it was isolated along with a number of other fungi. In experiments done with this isolate, the LD50 (the single dose that will kill 50 percent of the individual animals tested) of ochratoxin for rats is 22mg/kg (= 22 milligrams of the toxin per kilogram of body weight of the rat), but a lesser amount will result in severe liver damage. A single dose of 12.5 mg/kg (=12.5 milligrams of the toxin per kilogram of body weight of the rat) was administered to pregnant rats on the tenth day of gestation, and of the 88 foetuses involved, 72, or 81.8% died or were resorbed (Coker 1998; He & Zhou 2010). Ducklings seem to be equally sensitive to ochratoxin as they are to aflatoxin (Ates et al., 2011).

Another fungus, *Penicillium viridicatum*, can also produce ochratoxin, and is relatively common in stored corn and is a more common producer of ochratoxin than *A. ochraceus (Blumenthal, 2004)*.

#### **2.1.2.2** *Aspergillus versicolor* **and sterigmatocystin**

122 Health Management – Different Approaches and Solutions

Other seeds of cereal crops, wheat, corn, barley, oats and sorghum are also generally of lowaflatoxin-risk (Nageswararao et al 2002). Weather and climate were also contributing factors. The amount of toxin produced vary with the isolate of *A. flavus*. That is different sources of *A. flavus* will produce different amounts of aflatoxins. Some isolates of *A. flavus* may not even form aflatoxin (Fuchs et al., 1991; Awad et al., 2010). Although the aflatoxins are the major toxins associated with mycotoxicosis, another mycotoxin called cyclopiazonic acid (figure 6), has been associated in the aetiology of Turkey X disease (Bradburn et al., 1994;

Fig. 6. Cyclopiazonic acid associated in the aetiology of Turkey X disease (Bradburn et al., 1994)

Studies by Christensen (1975), over a period of several years, examined 100 different samples of black pepper from all over the world. In dilution cultures of these samples, the number of fungus colonies in whole or ground black pepper averaged 52,000 per gram/black pepper and the upper range was over half a million per gram (Coker, 1998). These colonies were mostly of *A. flavus*, *A. ochraceus* and *A. versicolor*. All three species are known to be aflatoxin producers. Some samples of ground pepper were caked lightly with fungus mycelium when first opened in the laboratory and with time, a number of these

How heavily contaminated is 52,000 to 500,000 colonies of fungi, per gram? Let's make a comparison for what is acceptable levels of fungal colonies isolated in other food products at the time Christensen published his results. Wheat, for example, that is intended for milling into flour seldom contains any more than a few thousand colonies of fungi per gram of grain. If barley has as many as 10,000 colonies of the same kind of fungi per gram as in black pepper, it would be rejected for malting in beer making. If breakfast cereals or bread were as contaminated as black peppers, they would have so musty an odour and taste that they would be too revolting to eat. Apparently, the natural spicy odour and flavour of black, as

well as white pepper are potent enough to conceal the taste and odour of these fungi.

**2.1.2 Mycotoxins of other fungal species of** *Aspergillus***,** *Penicillium* **and** *Fusarium*

*Aspergillus ochraceus* is also a species complex, and consist of nine species. These species are common in soil, decaying vegetation, and in stored seeds and grains undergoing microbial

Kios et al., 2004).

**2.1.1 Aflatoxin toxic effects** 

became solidly caked with mycelium (Jalili et al., 2011).

**2.1.2.1** *Aspergillus ochraceus* **and ochratoxin** 

This species is another storage fungus. However, it is never found as the only fungus or as the predominating fungus in deteriorating cereals. Normally, by the time a grain sample has become very mouldy, *A. versicolor*, along with other *Aspergillus* species and usually other filamentous fungi and yeasts as well. Some of the black pepper mentioned earlier, as being decayed by fungi, was very heavily invaded by *A. versicolor*, but not by this fungus exclusively. This species, under the right conditions, produces sterigmatocystin, a toxic compound given the name because the fungus once was called *Sterigmatocystis*. The toxin is known to cause lung, liver and kidney tumours in laboratory animals and has been implicated as the cause of disease in calves that have consumed feed heavily invaded by *A. versicolor (Ben-Ami et al., 2011).*. Experiments carried out in which the fungus were grown, on feed that was fed to calves, produced symptoms of the disease in the calves. However, tests were not done to detect the toxin in the calves. The toxin has also been detected in mouldy coffee beans in Africa, but no evidence indicates that even if these beans were used to brew coffee that the toxin would be in the drink.

#### **2.1.2.3** *Aspergillus fumigatus* **and fumagillin**

This particular species is known to be an animal pathogen. Infection occurs through inhalation of spores and affects the lungs. Infection may also occur in eggs and the foetuses of cows. However, it also produces a metabolic product that may be considered a toxin or an antibiotic. This species differs from the others that we have discussed in that it is said to be thermophilic, that is, it is found in substrate where there are extremely high temperatures, up to 122ºF (=50ºC). This species is usually found on material that is in the advanced stages of decomposition in which the substrate temperature has been significantly raised by microbial decomposition (Edward, 2009). Under the proper conditions, *A. fumigatus* produces fumagillin. This compound is used as an amoebicide that is, as a means to rid the body of amoebae that are human pathogens and has been used effectively in honey bees as well. However, the correct dosage of this compound is critical. A little bit more than you need to get rid of the amoebae and you will be getting rid of the patient as well (Fokunang et al., 2006).

Mycotoxins: Quality Management, Prevention, Metabolism, Toxicity and Biomonitoring 125

vomiting, after which they sensibly refuse to eat more of the corn. The toxin involved is deoxynivalenol (DON), also known as vomitoxin. The isolation and identification of this

Various methods have been tried to make the vomitoxin contaminated corn more acceptable to pigs. Among some of the means that have been tried are adding molasses to the feed to conceal whatever flavour or odour makes it unacceptable to the pigs, heating the feed, in hopes of destroying or inactivating whatever it is that is making the pig refuse to eat it, and composting it so that the heat will break down the toxin. However, none of these treatments

The detection of infected corn or feed is also a problem. Since we are talking about mycotoxin here, the inability to isolate the causal agent, *F. graminearum*, is not evidence that the mycotoxin is absent. Long after a fungus has died off, mycotoxin secreted into the substrate, will still be present. The refusal of pigs to eat feed or corn is an indication that the refusal factor is present, but not necessarily conclusive. There are a number of reasons as to why pigs will refuse to eat. Pigs may be traumatized by being moved to a new pen, strange surroundings or even being offered different food. The only way that the toxin can be detected is to isolate, purify and identify it by spectrographic or other analysis (Taranu et al.,

During the mid 1970s, when Vietnam was invading Laos, there were stories of "yellow rain" in areas where entire villages were killed. One eye witness account of such an event was told by a Hmong refugee, in Thailand. While tending his poppies, outside of his village, he and his family witnessed the bombing of their village by the Vietnamese, with a yellow powder that came down like yellow rain. Returning to the village, he found all of the animals and most of the people were dead. The bodies were bleeding from the nose and ears and their skin were blistered and yellowed. The few people left alive, when he arrived, were "jerking like fish when you take them out of the water". These people also eventually died. The witness took his family away from the village, but as they left they felt shortness of breath and sick to their stomach. This story is similar to other stories that were heard

It was believed by the United States at that time that the Soviet Union was somehow involved in what occurred in the Hmong village, and medical teams were sent to investigate. However, because of the remoteness of these villages, news of such attacks normally took 4 to 6 weeks to reach someone who could notify the medical teams. By the time investigators reached a village, there was no evidence as to what happened. It would not be until 1980 that a Defense Department chemist recognized the symptoms described by victims of the bombing as similar to trichothecene mycotoxicosis. Samples from victims and from vegetation in the areas were tested and some were found to contain trichothecenes. With this information, President Ronald Reagan accused the Soviet Union of violating the Geneva Convention and Biological Weapons Convention, which of course they denied. However, these accusations would continue for three more years (Sudakin,

While the accusations and denials were aired, the media and scientific community gave a more critical examination of the yellow rain story. The analysis that demonstrated

have made the corn acceptable to pigs and are impractical (Bluhm et al., 2004).

toxin has occurred only within the last 25 years (Bhat 2008).

**2.2.3 Importance of Trichothecenes as a biological weapon** 

concerning yellow rain (Coppock and Jacobsen, 2009).

2011).

2003).

**2.2.3.1 Yellow rain** 

#### **2.2 The genus** *Fusarium*

Species of Fusarium are widespread in nature as saprobes in decaying vegetation and as parasites on all parts of plants (Harris et al., 1999; Walters et al., 2010). Many cause diseases of economically important plants. For this reason, there has been a great deal of research carried out in this genus by both plant pathologist and mycologist. However, there are a number of species that produce mycotoxins, mostly trichothecenes and zearalenone. We will discuss a few common examples.

#### **2.2.1** *Fusarium tricinctum*

The effects of the first trichothecene toxin, T-2, documented was in the 1940s where it was associated with an outbreak of alimentary toxic aleukia (ATA). At its peak, in 1944, the population in the Orenbury District and other districts of the then USSR suffered enormous casualties, more than 10 percent of the population was affected and many fatalities occurred. The term *alimentary toxic* refers to the toxin being consumed in foods and *aleukia* refers to the reduced number of leucocytes or white blood cells in the affected person. Other symptoms included bleeding from nose and throat, multiple, subcutaneous haemorrhages (IARC, 1993; Bily et al., 2004).

The infected food in this case was millet, which made up a great part of the diet of the people in the region, and at times, during WWII, it was not uncommon to allow the millet to be left standing in the fields over winter because bad weather in the fall prevented its harvest at the proper time. During the late winter and early spring the millet would become infected with a variety of fungi, including *F. tricinctum*, and when the people gathered and ate this fungus, many came down with what was diagnosed as ATA. Thousands were affected, and many died. Locally, Joffe, a plant pathologist determined the outbreak of ATA was caused by consumption of a toxin, present in the millet, which had been contaminated by *F. tricinctum* (Biley et al., 2004). This was a remarkable conclusion since this was 20 years before aflatoxin was discovered. However, Joffe did not isolate or identify the toxin involved and as a result his work remained unknown until about 1965 when he presented a summary of his research at a symposium on mycotoxins. The mycotoxin involved was later given the common name T-2, and classified as one of several trichothecenes. Fed orally to rats, it has an LD50 of 3.8mg/kg, which is lower than that of aflatoxin, but still toxic enough.

#### **2.2.2** *Fusarium graminearum* **production**

Corn is a stable in many countries and is used as a major ingredient in preparation of food for pigs and other domestic animals. Like many other grains, the kernels can be infected with fungi before and after harvest, and can affect the nutritional value of corn as food or feed. If the weather is rainy and the ears of corn are maturing in late summer and early fall, *F. graminearum* may infect only a few to a third of the kernels (Bennett et al., 1988; Cheng et al., 2011). Whatever amount of the ear is infected, all the kernels in that portion becomes heavily infected and decayed by the fungus. This fungus-infected corn is unattractive to pigs, as well as other animals, and they refuse to it. For this reason, this phenomenon has been called a *refusal factor*.

Regardless of what the composition of the rest of the feed, if it contains more than 5 percent of kernels with this refusal factor, the pigs will not eat it and weight loss will occur. They will starve rather than consume it. The infected corn contains an emetic compound produced by the fungus, and if this corn is consumed by pigs, they suffer prolonged vomiting, after which they sensibly refuse to eat more of the corn. The toxin involved is deoxynivalenol (DON), also known as vomitoxin. The isolation and identification of this toxin has occurred only within the last 25 years (Bhat 2008).

Various methods have been tried to make the vomitoxin contaminated corn more acceptable to pigs. Among some of the means that have been tried are adding molasses to the feed to conceal whatever flavour or odour makes it unacceptable to the pigs, heating the feed, in hopes of destroying or inactivating whatever it is that is making the pig refuse to eat it, and composting it so that the heat will break down the toxin. However, none of these treatments have made the corn acceptable to pigs and are impractical (Bluhm et al., 2004).

The detection of infected corn or feed is also a problem. Since we are talking about mycotoxin here, the inability to isolate the causal agent, *F. graminearum*, is not evidence that the mycotoxin is absent. Long after a fungus has died off, mycotoxin secreted into the substrate, will still be present. The refusal of pigs to eat feed or corn is an indication that the refusal factor is present, but not necessarily conclusive. There are a number of reasons as to why pigs will refuse to eat. Pigs may be traumatized by being moved to a new pen, strange surroundings or even being offered different food. The only way that the toxin can be detected is to isolate, purify and identify it by spectrographic or other analysis (Taranu et al., 2011).

#### **2.2.3 Importance of Trichothecenes as a biological weapon**

#### **2.2.3.1 Yellow rain**

124 Health Management – Different Approaches and Solutions

Species of Fusarium are widespread in nature as saprobes in decaying vegetation and as parasites on all parts of plants (Harris et al., 1999; Walters et al., 2010). Many cause diseases of economically important plants. For this reason, there has been a great deal of research carried out in this genus by both plant pathologist and mycologist. However, there are a number of species that produce mycotoxins, mostly trichothecenes and zearalenone. We will

The effects of the first trichothecene toxin, T-2, documented was in the 1940s where it was associated with an outbreak of alimentary toxic aleukia (ATA). At its peak, in 1944, the population in the Orenbury District and other districts of the then USSR suffered enormous casualties, more than 10 percent of the population was affected and many fatalities occurred. The term *alimentary toxic* refers to the toxin being consumed in foods and *aleukia* refers to the reduced number of leucocytes or white blood cells in the affected person. Other symptoms included bleeding from nose and throat, multiple, subcutaneous haemorrhages (IARC, 1993;

The infected food in this case was millet, which made up a great part of the diet of the people in the region, and at times, during WWII, it was not uncommon to allow the millet to be left standing in the fields over winter because bad weather in the fall prevented its harvest at the proper time. During the late winter and early spring the millet would become infected with a variety of fungi, including *F. tricinctum*, and when the people gathered and ate this fungus, many came down with what was diagnosed as ATA. Thousands were affected, and many died. Locally, Joffe, a plant pathologist determined the outbreak of ATA was caused by consumption of a toxin, present in the millet, which had been contaminated by *F. tricinctum* (Biley et al., 2004). This was a remarkable conclusion since this was 20 years before aflatoxin was discovered. However, Joffe did not isolate or identify the toxin involved and as a result his work remained unknown until about 1965 when he presented a summary of his research at a symposium on mycotoxins. The mycotoxin involved was later given the common name T-2, and classified as one of several trichothecenes. Fed orally to rats, it has an LD50 of 3.8mg/kg, which is lower than

Corn is a stable in many countries and is used as a major ingredient in preparation of food for pigs and other domestic animals. Like many other grains, the kernels can be infected with fungi before and after harvest, and can affect the nutritional value of corn as food or feed. If the weather is rainy and the ears of corn are maturing in late summer and early fall, *F. graminearum* may infect only a few to a third of the kernels (Bennett et al., 1988; Cheng et al., 2011). Whatever amount of the ear is infected, all the kernels in that portion becomes heavily infected and decayed by the fungus. This fungus-infected corn is unattractive to pigs, as well as other animals, and they refuse to it. For this reason, this phenomenon has

Regardless of what the composition of the rest of the feed, if it contains more than 5 percent of kernels with this refusal factor, the pigs will not eat it and weight loss will occur. They will starve rather than consume it. The infected corn contains an emetic compound produced by the fungus, and if this corn is consumed by pigs, they suffer prolonged

**2.2 The genus** *Fusarium*

discuss a few common examples.

that of aflatoxin, but still toxic enough.

been called a *refusal factor*.

**2.2.2** *Fusarium graminearum* **production** 

**2.2.1** *Fusarium tricinctum*

Bily et al., 2004).

During the mid 1970s, when Vietnam was invading Laos, there were stories of "yellow rain" in areas where entire villages were killed. One eye witness account of such an event was told by a Hmong refugee, in Thailand. While tending his poppies, outside of his village, he and his family witnessed the bombing of their village by the Vietnamese, with a yellow powder that came down like yellow rain. Returning to the village, he found all of the animals and most of the people were dead. The bodies were bleeding from the nose and ears and their skin were blistered and yellowed. The few people left alive, when he arrived, were "jerking like fish when you take them out of the water". These people also eventually died. The witness took his family away from the village, but as they left they felt shortness of breath and sick to their stomach. This story is similar to other stories that were heard concerning yellow rain (Coppock and Jacobsen, 2009).

It was believed by the United States at that time that the Soviet Union was somehow involved in what occurred in the Hmong village, and medical teams were sent to investigate. However, because of the remoteness of these villages, news of such attacks normally took 4 to 6 weeks to reach someone who could notify the medical teams. By the time investigators reached a village, there was no evidence as to what happened. It would not be until 1980 that a Defense Department chemist recognized the symptoms described by victims of the bombing as similar to trichothecene mycotoxicosis. Samples from victims and from vegetation in the areas were tested and some were found to contain trichothecenes. With this information, President Ronald Reagan accused the Soviet Union of violating the Geneva Convention and Biological Weapons Convention, which of course they denied. However, these accusations would continue for three more years (Sudakin, 2003).

While the accusations and denials were aired, the media and scientific community gave a more critical examination of the yellow rain story. The analysis that demonstrated

Mycotoxins: Quality Management, Prevention, Metabolism, Toxicity and Biomonitoring 127

of human oesophageal cancer in the Transkei, southern Africa and China (Rheeder et al., 1992). There is however, sufficient evidence in experimental animals for the carcinogenicity of cultures of *F. moniliforme* that contain significant amounts of the fumonisins, whereas there is limited evidence, in experimental animals, for the

Ochratoxin A (OA) is caused by the fungi *Aspergillus ochraceous*, *A. parasiticus, A. niger* and *Penicillium verrucosum*, (Kuiper-Goodman, 1991; Blumenthal, 2004). This toxin is produced within the temperature range of 15-37°C, with an optimal production at 25-28°C. The exposure to ochratoxin A occur mainly in wheat and barley growing areas in temperate zones of the northern hemisphere (Abarca et al., 2001). The levels of ochratoxin A reported in these products ranges from trace amounts to 600µg/kg, in Canadian wheat. In the United Kingdom, reported levels have included 5000 and 2700µg/kg in barley and wheat respectively (Anderson & Conning, 1993). It also occurs in maize, rice, peas, beans and cowpeas; developing country origins of ochratoxin A include Brazil, Egypt, Chile, Senegal, Tunisia, Nigeria, India and Indonesia (Wild and Hall, 2000). The ability of OA to transfer from animal feeds to animal products has been demonstrated by the occurrence of this toxin in retail pork products, and the blood of pigs in Europe (Fazekas et al., 2001; Friensen et al., 2008). It has been suggested that pork products are a significant human dietary source of OA which has been found in blood (and milk) from individuals in a variety of European countries, such as France, Italy, Germany, Dewnmark, Sweden, Poland the former Yugoslavia, and Bulgaria ( Abarca et al., 2001)). One of the highest reported levels is 100ng/ml OA in blood from the former Yugoslavia (Fuch et al., 1991), while a level of 6.6 ng/ml OA in milk has been reported in Italy (Micco et al., 1991;

The existing or proposed regulations for OA are in place in about eleven countries, the permitted levels ranging from 1 to 50 µg/kg in foods and from 100 to 1000 µg/kg in feeds. In Denmark, for example, the acceptability of pork products from a specific carcass is determined by analysis of the OA content of the kidney. The pork meat and certain organs can be consumed as food if the OA content of the kidney is no more than 25 and 10 µg/kg

The WHO/FAO Joint Expert Committee of Food Additives has recommended a provisional tolerable weekly intake of 112ng/kg body weight of OA (WHO, 1991). The ochratoxin A has been linked with the human disease Balkan endemic nephropathy, which is a fatal chronic renal disease, reported in limited regions of the former Yugoslavia, Romania and Bulgaria (Cocker, 1999). OA causes renal toxicity, nephropathy and immunosuppression in several animal species and it is carcinogenic in experimental animals (Abarca et al., 2001; Yoshinari

Examination of the metabolic fate of aflatoxin B1 can be used to illustrate the importance of the metabolic process in determining toxicity, and as a means of determining exposure to mycotoxins, by measuring; mycotoxin-macromolecular conjugates, the parent mycotoxin and a biochemical change initiated by the mycotoxin, respectively (Coker

carcinogenicity of fumonisin B1 (Naiker and Odhav, 2004).

**2.4 Ochratoxin A** 

Huffman et al., 2010).

et al., 2007).

1999).

respectively (van Egmond, 1989; Wild & Hall 2000).

**3. The metabolism of mycotoxins** 

Trichothecenes were being used was initially based on a single leaf, collected where one of the chemical attacks occurred. Subsequent specimens were collected later that also showed Trichothecenes were present, but the ratio of trichothecenes differed where it was found and was entirely absent in some samples. In addition, little fanfare was given to the over one hundred samples analyzed by the United States Army, which *did not find any indication of trichothecenes*. The eye witness accounts also came into question. Although it was implied that many villages were attacked with yellow rain, all of the witnesses were from a single refugee camp in Thailand, and even these accounts were thought to be unreliable (Kankunen et al., 2009). For example in relating a story of the bombing, one villager had initially said that 213 villagers were killed, but in a later retelling, there were only thirteen people killed and then forty.

Further erosion of the government's yellow rain story came about when a Yale University entomologist, whose expertise was in Southeast Asian bees, examined yellow rain samples and observed that they contained pollen from the native plants in the area. Based on the appearance of these samples, it was concluded that they were faeces of bees. In one species of bees, present in the area, there is a tendency for the bees to swarm when they defecated, as a cleansing ritual, which could give the appearance of yellow rain falling. News of such chemical attacks soon stopped and many civilian scientists were convinced that the entire yellow rain incident was a hoax that was carried out by the military to increase funding for defensive chemical and biological weapons. While a plausible alternative was given as to the cause of the yellow rain, the eye witness accounts while questionable, contradicted this theory. To date, the question as to what caused the yellow rain has still not been satisfactorily resolved and may never be (Hsueh et al., 1999).

#### **2.3 Zearalenone**

Zearalenone is a widely distributed oestrogenic mycotoxin occurring mainly in Maize, in low concentrations, in the developing countries, Europe, Japan, and North America (Hussein and Brasel, 2001). The concentrations in developing countries can be very high, especially when maize is grown in highland regions, under more temperate conditions. Zearalenone is co-produced with deoxynivalenol by *F. graminearum* and has been implicated with DON, in outbreaks of acute human mycotoxicoses (Prelusky et al., 1989). The exposure to zearalenone-contaminated maize has caused hyperoestrogenism in livestock, especially pigs, characterized by vulvar and mammary swelling and infertility (Bennett et al., 1988). There is limited evidence in experimental animals for the carcinogenicity of zearalenone (Kuiper-Goodman, 1991; Ding et al., 2006).

#### **2.3.1 The fumonisins**

The fumonisins are group of recently characterized mycotoxins produced by *F. moniliforme*, a mould that occurs world-wide and is frequently found in maize. Fumonisin B1 has been reported in maize and maize products from a variety of agroclimatic regions including Brazil, Canada, USA, Austria, Italy, France and South Africa (Ding et al., 2006). The toxins especially occur when maize is grown under warm, dry conditions. Exposure to fumonisin B1 (FB1) in maize causes leuko-encephalmalacia (LEM) in horses and pulmonary oedema in pigs (Nair, 1998). LEM has been reported in many countries such as Argentina, Brazil, China, Egypt, South Africa and USA. FB1 is also toxic to the central nervous system, liver, pancreas, kidney and lungs of a number of animal species. The presence of fumonisins in maize has been linked with the occurrence of human oesophageal cancer in the Transkei, southern Africa and China (Rheeder et al., 1992). There is however, sufficient evidence in experimental animals for the carcinogenicity of cultures of *F. moniliforme* that contain significant amounts of the fumonisins, whereas there is limited evidence, in experimental animals, for the carcinogenicity of fumonisin B1 (Naiker and Odhav, 2004).
