**2.4 Ochratoxin A**

126 Health Management – Different Approaches and Solutions

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

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

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

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

satisfactorily resolved and may never be (Hsueh et al., 1999).

(Kuiper-Goodman, 1991; Ding et al., 2006).

people killed and then forty.

**2.3 Zearalenone** 

**2.3.1 The fumonisins** 

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; Huffman et al., 2010).

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

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 et al., 2007).
