**3.2 Food**

OTA has a widespread diffusion, and it has in fact been detected in agricultural commodities, livestock products and processed food (Abrunhosa et al., 2010).

The main OTA contamination concerns cereals and their products, listed in Table 4, which include food and beverages for human consumption, but also by-products that are usually utilized as animal feeds. Ochratoxin contamination can occur from temperate to tropical climates, from hot and wet climatic conditions to low temperature environments, and affects numerous countries: Northern America, Northern and Western Europe, African countries, South Asia and South America (Battaccone et al., 2010; Cabanes et al., 2010; El Khoury & Atoui, 2010; Moss, 2002b). Vega et al. (2009) suggests that cereals should be considered a major source of OTA contamination, as 50% of human daily intake of this mycotoxin is due to the consumption of different cereal derived products.


Table 4. Cereals contaminated by OTA (Abrunhosa et al., 2010; Scudamore et al., 2003).

Cereals may be colonized by both *Aspergillus* and *Penicillium*. The two fungal species do not invade the crop in the field, but mainly do in the post-harvest phase. Considering that the main abiotic factors that influence mould growth and OTA production are water availability and temperature, cereals should be dried quickly after harvesting and maintained at a lower moisture content than 14.5% during storage to avoid OTA contamination (Magan & Aldred, 2005). OTA is mainly concentrated in the seed coat, which is often used for animal feeding. Moreover, on-farm production and the storage of barley and wheat with a high moisture content increases the risk of mould growth and toxin production (Scudamore et al., 2003). Some cereal processing, like malting, malt fermentation, bread production and feed extrusion, can contribute significantly to reduce OTA concentration in the final food products (Baxter et al., 2001; Scott et al., 1995; Scudamore et al., 2003). Other practices can increase OTA values; for example, cracked grains and cereal cleanings are often the most contaminated fractions and are usually directed for feed proposes (Scudamore et al., 2003).

Wine is considered the second source of the human consumption of OTA. Many works have highlighted the presence of considerable levels of this toxin in wines, musts and grape juices. This occurrence has been explained by the fact that grapes are contaminated in the vineyard by various ochratoxigenic species, belonging above all to the *Aspergillus* section *Nigri* genus (*A. carbonarius* and *A. niger* aggregates) and that OTA production increases rapidly with the maturation stage. Thus, the date of the grape harvest would have an important effect on the OTA content in grapes and their derived products (Cabanes et al., 2002; El Khoury et al., 2006).

OTA contamination of many other raw agricultural products has been well documented; such a contamination occurs in a variety of food and feeds, such as coffee beans, pulses, spices, meat and cheese products (Wolff et al., 2000).

#### **3.3 Toxicity**

178 Food Industrial Processes – Methods and Equipment

OTA has a widespread diffusion, and it has in fact been detected in agricultural

The main OTA contamination concerns cereals and their products, listed in Table 4, which include food and beverages for human consumption, but also by-products that are usually utilized as animal feeds. Ochratoxin contamination can occur from temperate to tropical climates, from hot and wet climatic conditions to low temperature environments, and affects numerous countries: Northern America, Northern and Western Europe, African countries, South Asia and South America (Battaccone et al., 2010; Cabanes et al., 2010; El Khoury & Atoui, 2010; Moss, 2002b). Vega et al. (2009) suggests that cereals should be considered a major source of OTA contamination, as 50% of human daily intake of this mycotoxin is due

> **cereals**  Corn (grains, gluten); Rice; Wheat; Barley; Oats; Rye; Sorghum; Millet **cereal products for human consumption**  Beer; Baby food; Breakfast cereals; Bread **cereal feed products**  Cracked grains; Cereal cleanings; Wheat bran; Corn bran; Rice bran

Table 4. Cereals contaminated by OTA (Abrunhosa et al., 2010; Scudamore et al., 2003).

Cereals may be colonized by both *Aspergillus* and *Penicillium*. The two fungal species do not invade the crop in the field, but mainly do in the post-harvest phase. Considering that the main abiotic factors that influence mould growth and OTA production are water availability and temperature, cereals should be dried quickly after harvesting and maintained at a lower moisture content than 14.5% during storage to avoid OTA contamination (Magan & Aldred, 2005). OTA is mainly concentrated in the seed coat, which is often used for animal feeding. Moreover, on-farm production and the storage of barley and wheat with a high moisture content increases the risk of mould growth and toxin production (Scudamore et al., 2003). Some cereal processing, like malting, malt fermentation, bread production and feed extrusion, can contribute significantly to reduce OTA concentration in the final food products (Baxter et al., 2001; Scott et al., 1995; Scudamore et al., 2003). Other practices can increase OTA values; for example, cracked grains and cereal cleanings are often the most contaminated fractions and are usually directed for feed proposes (Scudamore et al., 2003). Wine is considered the second source of the human consumption of OTA. Many works have highlighted the presence of considerable levels of this toxin in wines, musts and grape juices. This occurrence has been explained by the fact that grapes are contaminated in the vineyard by various ochratoxigenic species, belonging above all to the *Aspergillus* section *Nigri* genus (*A. carbonarius* and *A. niger* aggregates) and that OTA production increases rapidly with the maturation stage. Thus, the date of the grape harvest would have an important effect on the OTA content in grapes and their derived products (Cabanes et al.,

OTA contamination of many other raw agricultural products has been well documented; such a contamination occurs in a variety of food and feeds, such as coffee beans, pulses,

commodities, livestock products and processed food (Abrunhosa et al., 2010).

to the consumption of different cereal derived products.

2002; El Khoury et al., 2006).

spices, meat and cheese products (Wolff et al., 2000).

**3.2 Food** 

OTA can have several effects, such as nephrotoxic, hepatotoxic, neurotoxic, teratogenic and immunotoxic effects on several species of animals, and can cause kidney and liver tumours in mice and rats; OTA toxicity varies depending on the sex, the species and the cellular type of the tested animal (El Khoury & Atoui, 2010).

Nephropathy is the main toxic effect of OTA; it is potentially nephrotoxic in all nonruminant mammals (Ribelin et al., 1978). OTA plays an important role in the etiology of porcine nephropathy (Elling et al., 1985). This mycotoxin was also associated with human nephropathy and it is suspected to be the cause of the human Balkan Endemic Nephropathy (BEN) and the Tunisian Nephropathy (TCIN) (Hassen et al., 2004; Pfohl-Leszkowicz, 2009).

The administration of OTA at gestation period in rats induced many malformations in the central nervous system. OTA can be regarded as a possible cause of certain lesions as well as damage at the cerebral level. OTA seems to be highly toxic for the nervous cells and able to reach the neural tissue (Soleas et al., 2001).

OTA is a potent teratogen for laboratory animals. It can cross the placenta and accumulate in fetal tissue, causing various morphological anomalies. It has been reported to elicit prenatal dysmorphogenesis in rats, mice, hamsters and chick embryos (El Khoury & Atoui, 2010).

OTA also has an immunosuppressor effect. Necroses of lymphoid tissues has been reported, and humoral and cellular immunity affections have also been described (Creppy et al., 1991; Holmberg et al., 1988). OTA seems to play a role in the inhibition of proliferation of the peripheral T and B lymphocytes and stops the production of interleukin 2 (IL2) and its receptors (Lea et al., 1989). Moreover, it blocks the activity of killer cells as well as the production of interferon (Pfohl-Leszkowicz & Castegnaro, 1999). OTA is taken as an important immunosupressor agent, in fact it is considered to be the cause of lymphopenia, regression of the thymus, and suppression of the immunity response (Petzinger & Weidenbach, 2002).

OTA is anticipated to be a human carcinogen based on sufficient evidence of carcinogenicity in experimental animals. Hepatocellular tumors, renal cell tumors, hepatomas, and hyperplastic hepatic nodules have been observed in male mice (Huff et al., 1992). OTA has been correlated with hepatocellular and renal-cell carcinomas and adenomas in mice and rats (El Khoury & Atoui, 2010). On the other hand there are no adequate studies of the relationship between exposure to OTA and human cancer; incidence and mortality from urothelial urinary tract tumours have been correlated with the geographical distribution of Balkan endemic nephropathy in Bulgaria and Yugoslavia (Feier & Tofana, 2009).
