American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) ISSN (Print) 2313-4410, ISSN (Online) 2313-4402 © Global Society of Scientific Research and Researchers http://asrjetsjournal.org/ Mycotoxines and/or Aflatoxines in Milk and Milk Products: Review Melkamu Bezabih Yitbareka, Birhan Tamirb aDepartment of Animal Science, College of Agriculture and Natural Resources, Debre Markos University, Debre Markos, Ethiopia Pobox 269 bCollege of Veterinary Medicine and Agriculture, Addis Ababa University, Addis Ababa, Ethiopia, pobox,34 aemail: melkamu_bezabihy@yahoo.com bemail: berhantamir@yahoo.com Abstract This review was conducted to evaluate micotoxin and or aflatoxines in milk and milk products through critical review. Mycotoxins are secondary metabolites produced by the three major fungus genera Aspergillus, Penicillium and Fusarium. The contamination of food and feeds by Mycotoxin remains a worldwide problem, according to FAO estimation up to 25% of the world’s food crops are significantly contaminated with mycotoxin. Aflatoxin is one of aclasses of mycotoxin. The major aflatoxins are afflation B1, B2, G1 and G2. Aflatoxin M1 (AFM1) is the hepatic hydroxylated metabolites of AFB1. AFM1 is found in milk and milk products obtained from livestock that have ingested AFB1contaminated feed. In lactating animals the conversion rate of AFB1 to AFM1 ranges between 0.5 and 6%. Several research workers reported that there is a linear relationship between the amount of AFM1 in milk and AFB1 in feed which is consumed by dairy cattle. Aflatoxin M1 in milk and milk products is considered to pose certain hygienic risks for human health. These metabolites are not destroyed during the pasteurization and heating process. Many countries standards limits of Aflatoxins M1 ranged between 0 to 0.5 ppb, in milk and dairy products. Key Words: mycotoxin; aflatoxin; milk; milk products. 1. Introduction Mycotoxins are toxic secondary metabolites naturally produced by molds (Aspergillus, Fusarium and Penicillium spp.) [1]. It is well known to cause toxicities to humans and animals [2]. After infesting crops, fungi synthesize the toxins, which will be transmitted to the final food products. The classes of mycotoxins with relevance to health are: aflatoxins, ochratoxins, trichothecenes, zearalenone, fumonisins, tremorgenic toxins and ergot alkaloids [3]. Aflatoxins are a group of structurally-related toxic compounds produced by certain strains of 1 http://asrjetsjournal.org/ American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 the fungi Aspergillusflavus and A parasiticus [4]. Since the toxin-producing mold was identified as Aspergillus flavus in 1960 and the toxin was given the name Aflatoxin by virtue of its origin (A. flavus--> Afla). Aflatoxins have sub-acute and chronic effects such as liver cancer, chronic hepatitis, jaundice, hepatomegaly and cirrhosis in humans [5]. Over 20 naturally occurring aflatoxins are known, the moulds Aspergillus flavus and A. parasiticus produce exclusively aflatoxin B1, B2, G1 and G2, and all the other aflatoxins are derivates of these four. While AFB1 is the most toxic in the group and the toxicity is in the order of B1 > G1 > B2 > G2 [6]. Aflatoxin B1 (AFB1) present in feed of lactating animals gets transformed to 4-hydroxylated metabolite in liver and is excreted in milk as aflatoxin M1 (AFM1). About 1-3% ingested AFB1 is converted into AFM1 [7], but it varies from animal to animal, from day to day and from one milking to the other. The presence of AFM1 in milk poses a major risk for humans, especially children, as it can have immunosuppressive, mutagenic, teratogenic, and carcinogenic effects (Sefidgar et al., 2011). If milk is sold commercially should be checked for aflatoxinM1. When aflatoxinM1 is found at concentrations of 0.5 parts per billion (ppb) or greater, the milk is discarded beca use it cannot be used for products that go in to the human food supply [8]. The AFM1 could be detected in milk 12-24 h after the first AFB1 ingestion, reaching a high level after a few days. When the intake of AFB1 is finished, the AFM1 concentration in the milk decreases to an undetectable level after 72 h [5]. Therefore to know more about the effect of AFM1 in milk and milk products, this review is made from different scientific papers to contribute scientific knowledge for the world. 2. Mycotoxin/Aflatoxine / In Milk and Milk Products 2.1 What is Mycotoxins? In the 1960s more than 100,000 young turkeys on poultry farms in the United Kingdom died in a period of a few months from an unidentified disease, which was named "turkey × disease". Ducklings and other poultry animals were also affected, and high mortalities were observed. A careful survey of the inputs and environment of the affected farms indicated that the disease was associated with feeds and specifically with peanut meal imported from Brazil. A disease with symptoms typical of turkey × disease was reproduced when animals were fed the same peanut meal. Intensive investigations were then carried out on the suspected ingredient to identify the nature of the toxin, which was soon found to be of fungal origin. The toxin-producing fungus was identified as Aspergillus flavus [9] and the toxin was accordingly called aflatoxin/Mycotoxin. While all mycotoxins are of fungal origin, not all toxic compounds produced by fungi are called mycotoxins. The term Mycotoxin is derived from the Greek word ‘mycos’ meaning fungus(mould), and the Latin word ‘toxicum’, which means poison [10]. Mycotoxins are produced by fungi through their secondary metabolism. Mycotoxin concentration can therefore be independent of the growth of the fungi, which is associated with the primary metabolism. The diversity of the compounds formed and the specificity of the fungal strain for mycotoxin production result from the secondary metabolism, which is usually activated by signals from the environment (cold, heat, dryness, fungicide, etc.). Among the numerous mycotoxins, several groups have been identified, produced by the three major fungus genera Aspergillus, Penicillium and Fusarium [10]. According to [10] the same mycotoxin can be produced by several different fungi, and the same fungus can generate several mycotoxins. 2 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 Mycotoxins present in food products and animal feeds are an important problem concerning food and feed safety and significant economic losses are associated with their impact on human and animal health [11]. In addition to being acutely toxic, some mycotoxins are now linked with the incidence of certain types of cancer and it is this aspect which has evoked global concern over feed and food safety, especially for milk and milk products. 2.2 What is Aflatoxin? Aflatoxins belong to the class of mycotoxins and it is a group of approximately 20 related fungal metabolites generally produced by Aspergillus species, namely A. flavus, A. parasiticus, A. ochraceoroseus, A. bombycis, A. nomius, A. fumigitus and A. pseudotamari [12]. These fungi belong to the class Hyphomycetes, subdivision Deuteromycotina and family Aspergillaceae [13]. Aspergillus flavus and A. parasiticus are economically important moulds that produce exclusively aflatoxin B1, B2, G1 and G2, and all the other aflatoxins are derivates of these four [14]. The four major naturally produced aflatoxins are known as B1, B2, G1, and G2. “B” and “G” refer to the blue and green fluorescent colors produced under UV light on thin layer chromatography plates, while the subscript numbers 1 and 2 indicate major and minor compounds, respectively [14]. Aflatoxin B1, the most toxic of the aflatoxins, is the most potent naturally occurring chemical liver carcinogen known. Specific P450 enzymes in the liver metabolize aflatoxin into a reactive oxygen species (aflatoxin-8,9-epoxide), which may then bind to proteins and cause acute toxicity (aflatoxicosis) or to DNA and induce liver cancer [15]. Aspergillus flavus and A. parasiticus colonize a wide variety of food commodities including maize, oilseeds, spices, groundnuts, tree nuts, milk, and dried fruit [16]. Whether these fungi produce aflatoxin depends on drought stress and rainfall, suitability of crop genotype for its climate, insect damage, and agricultural practices [15]. These fungi can also produce aflatoxin in “postharvest” conditions: storage, transportation, and food processing. Aflatoxin contamination is a particular problem in maize, oilseeds, spices, peanuts, tree nuts (almonds, pistachios, hazelnuts, pecans, Brazil nuts, and walnuts), milk (in the form of aflatoxin B1’s metabolite aflatoxin M1), and dried fruit [17]. Maize and peanuts are the main sources of human exposure to aflatoxin because they are so highly consumed worldwide and unfortunately are also the most susceptible crops to aflatoxin contamination [15]. Figure 2 [18] depicts the pathway by which aflatoxin accumulates in food crops and contributes to various adverse human health effects. 3 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 Figure 1 Aflatoxin and disease pathways in humans Source: [18] The darker arrows in Figure 1 denote linkages that have been well-established in agricultural and toxicological research, while the white arrows denote linkages that have been relatively less well-established [18]. The International Agency for Research on Cancer [19] has classified aflatoxin B1 as a group 1 carcinogen (that means carcinogenic to humans) since 1987, and a group 1 carcinogenic agent since 1993 due to the exposure to hepatitis B virus [20]. AFB1 is the most prevalent aflatoxin usually found in cases of aflatoxicosis, and is responsible for acute toxicity, chronic toxicity, carcinogenicity, teratogenicity, genotoxicity and immunotoxicity. AFM1 is a metabolic derivate of AFB1, and AFM2 is a metabolic derivate of AFB2; both come from the metabolism of some animals, and are normally found in milk and urine [16]. FM1 is the most economically important AFB1derivative that found in milk and milk products. Aflatoxin B1 Aflatoxin M1 Figure 2 Chemical Structur of Aflatoxin B 1 and Aflatoxin M1 4 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 2.3 Changing of AFB1 to AFM1 Aflatoxin B1 (AFB1) present in feed of lactating animals gets transformed to 4-hydroxylated metabolite in liver and is excreted in milk as aflatoxin M1 (AFM1). The AFM1 could be detected in milk 12-24 h after the first AFB1 ingestion, reaching a high level after a few days. When the intake of AFB1 is finished, the AFM1 concentration in the milk decreases to an undetectable level after 72 h [5]. According to the report of [21,22], cows can transform AFB1 into AFM1 within 12-24 hours after ingestion of contaminated food. Even at six hours after ingestion, AFM1 residues can appear in milk, and the highest levels are reached after a few days. When the intake of AFB1 is stopped, the AFM1 concentration in the milk decreases to an undetectable level after 72 hours. [21,22], observed that there was a linear relationship between AFB1 dose and excretion of AFM1 into ewes' milk. About 1-3% ingested AFB1 is converted into AFM1 [7] but it varies from animal to animal, from day to day and from one milking to the other. [21] reported that in dairy cows, the relationship between the concentration of AFB1 in the final consumed ration and AFM1 excreted in breast milk could be 300:1; nevertheless this relation is only an approximation because the range is from 34:1 to 1600:1. In Holstein dairy cows consuming final rations with 80, 86, 470, 557, 1493 and 1089 μg of AFB1/Kg (ppb) on dry substance, there were found in milk AFM1 concentrations of 1.5, 0.245, 13.7, 4.7, 12.4 and 20.2 mg/L (ppb) respectively. On the other hand, when diet of Brindle cows was contaminated with 540 ppb of AFB1, 0.92 ppb of AFM1 was produced. In other cows, the values of contamination in the diet ranged between 64 and 1799 ppb of AFB1 giving some residues in milk between 0.35 and 14.2 ppb of AFM1. For high-yielding dairy cows producing up to 40 kg of milk per day, [23] found a carry-over percentage as high as 6.2%. Changes in the plasma-milk barrier and the consumption of large amounts of concentrated feeds in high-merit dairy cows may explain the increase in the carry-over rate of AFM1 in milk. According to [24] AFB1 and AFM1 has a strong correlation, and he proposed the following equation (r2 = 0.915) to estimate the transfer of AFM1 in milk: AFM1 (ng/kg milk) = 10.95 + 0.787 × (µg AFB1 intake per day) This equation indicates that the animals must ingest less than 50 and 25 µg AFB1 per day to comply with the European regulatory levels of contamination in milk set at 0.05 and 0.025 µg/kg of milk for adults and infants, respectively. Thus cows must ingest less than 10 and 5 kg of feed contaminated at the maximum authorised level (5 µg AFB1/kg feed for dairy cattle) to maintain a safe level of AFM1 in milk. 2.4 What is Aflatoxins M1? AFM1 is a metabolite of Aflatoxin B1 (AFB1) and originally discovered in milk of humans and animals fed on moldy grains containing AFB1 [25]. With an intake of AFB1 for 2-60 mg / cow / day, AFM1 residues in milk could range between 1 and 50 ppb. There have been found differences between the amounts of AFM´s produced by different bovine species. 5 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 The AFM1 distribution in some dairy foods made from contaminated milk is approximately: 40-60% in cheese, 10% in butterfat and <2% in buttermilk. AFM1 is highly soluble in water, so it is incomprehensible why this toxin is deposited in the cheese but not in the milk whey [26]. The carcinogenicity of AFM1 is about ten times less than that of AFB1, and for this reason has been included in the class 2B by International Agency for Research on Cancer. The quantity of AFM1 in the milk depends on the concentration of AFB1 in the contaminated feed. It has been reported that milk is one of the main risk factors of human exposure to AFM1. Infants are the foremost milk consumers, which make them more susceptible to the adverse effects of mycotoxins [27]. The lactating animal could be regarded as intermediate host also due to the biological transformation of AFB1 to AFM1 inside the animal body. Consequently, the farm animals may be considered as a reservoir for AFM1. The milk could be established as a major carrier of AFM1 which affects the human health. Generally, presence of Aflatoxins in animal or human bodies cause a disease named Aflatoxicosis, so the presence of AFM1 may be specified as Aflatoxicosis M1. The main target organ in mammals is the liver so Aflatoxicosis is primarily a hepatic disease. Aflatoxins also cause decreased milk production. The occurrence of AFM1 in milk and milk products is a serious problem of food hygiene. Hydroxilation Epoxidation Hydration Interaction with DNA Interaction with enzymes Figure 3 Some metabolic products from AFB1 Afilatoxin B1 (AFB1) AflatoxineM1 (AFM1) Milk Aflatoxin epoxide Dehydroxy Aflatoxine Cancer Acute toxicity 6 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 Aflatoxin contamination in milk and products is produced in two ways. Either toxins pass to milk with ingestion of feeds contaminated with Aflatoxin, or it results as subsequent contamination of milk and milk products with fungi. AFM1 has been reported to cause certain hygiene difficulties in milk and milk products used for food. During the obtaining of cream, AFM1 disperses heterogeneously in milk. AFM1 is not destroyed during the pasteurization process or in yoghurt and cheese making. 2.4.1 AFM1 in Milk Milk is the most important source of calcium and phosphorus of human body and due to having essential amino acids, has an important status in supplying the body’s protein needs. Studies have shown that there is a close relationship between consumption of milk and health status of people in terms of efficiency, Intelligence quotient (IQ), reducing the risk of infectious diseases, regulation of metabolic activities, decreasing blood pressure, increasing beneficial blood lipids (High-density lipoprotein), preventing from colon cancer and osteoporosis [28]. Milk is a key contributor to improve nutrition and food security particularly in developing countries and play a significant role in reducing poverty and malnutrition [29]. However milk, as a liquid, is a highly variable product that rapidly loses its quality and spoils if not to be treated. Since milk may be processed in numerous ways, the effects of storage and processing on stability and distribution of AFM1 are of great concern. [30] reported the effect of cold treatments. They observed that detectable AFM1 decreased by 11 to 25% after 3 days at 5ºC, 40% after 4 days at 0ºC, and 80% after 6 days at 0ºC. Whereas, [31] revealed that freezing at -18ºC for 30 days resulted in an apparent loss of 14%, with 85% lost after 53 days. [32] suggested less degradation of AFM1 at -18ºC with insignificant loss after 53 days. As to the effect of heating contradictory data have been reported. [30] reported that various heat–time treatments caused reductions in the AFM1 concentrations of milks between 12% and 40%. [33] studied the effect of various heat treatments on AFM1 content of cow’s milk and reported that sterilization of milk at 121 °C for 15 min caused 12.21% degradation of AFM1, whereas boiling decreased AFM1 by 14.50%. They concluded that destruction of AFM1 depends on time and temperature combination of the heat treatment applied. In an investigation Conducted by [34] it was observed that pasteurization caused a decrease in the level of AFM1 at the rate of 7.62%. [35] showed that pasteurization can partially reduce the amount of AFM1 in milk. However, some reports showing that aflatoxins are stable during heat-treatments such as pasteurization and sterilization [36]. AFM1 distribution in milk is not homogeneous. Cream separation can affect AFM1 distribution, since 80% is partitioned in the skim milk portion [37] because of AFM1 binding to casein [38]. An amount of 30% of AFM1 is indeed estimated to be associated with the nonfat milk solids and in particular with casein. Contradictory data have been reported on the influence of milk concentration on AFM1. [39] reported no losses of AFM1, whereas some authors observed losses ranging from 60 to 75% following milk concentration [40]. Data from the studies on the occurrence of AFM1 in milk since the 1990s are reported in Table 1. 7 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 Table 1 Occurrence and content of AFM1in Milk Samples Year Region Milk type Samples + samples Range(ng/lit er) Reference 1991 Kazakhstan C * 0 NA [41] 1992 Cuba C 85 22 >500 [42] 1993 Japan C 37 0 NA [43] 1994 USA D 10 4 95 [44] China D 28 21 102.8 Italy D 14 0 NA New Zealand D 3 0 NA Poland D 3 1 85 1995 India R 504 89 100-3.500 [45] 1996 Italy UHT 161 125 <1- 23.5 [46] D 92 49 <1- 79.6 1998 Kuwait C 9 5 * [47] R 7 5 * 1999 Portugal R 31 25 * [48] 1999 Portugal UHT 70 60 * [48] 1999 Argentina R 56 6 Dec-30 [50] PW 5 4 Oct-14 P 16 8 Oct-17 1999-2000 Iran R 186 119 ≤ 10-410 [51] 2001 Turkey R 90 79 12.5-123.6 [52] 2001 Iran R 111 85 15-280 [53] 2002-2003 Brazil R 22 13 * [54] 2002-2003 Brazil P 43 32 * [11] 2002-2003 Brazil UHT 34 34 * [27] 2002 Greece R 54 * * [56] 2003 Iran P 624 624 * 2004 Turkey P 3 2 * [58] UHT 24 14 * 2004 Iran R 319 172 15.4a [59] 2003-2004 Iran R 98 * 53a [60] 2003-2004 Italy R 208 36 5-36.1 [61] * Turkey P 85 75 * [62] 2004-2005 Italy R 344 5 * [63] 2004-2005 Brazil P 12 7 11-161 [64] UHT 12 10 11-161 8 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 2005 Pakistan R 168 168 10-700 [65] 2005 Iran P 128 128 31-113 [66] 2005-2007 Kuwait R 177 176 4.9-67.8 [67] 2006 Iran R * * 43-59 [68] 2006 Iran P 110 110 Aug-89 [69] 2006 Iran PW 42 42 51-914 [70] 2006 Iran P * * 178.8-253.5 [71] 2006-2007 Iran R 240 226 12.56a [72] P 32 31 12.43a 2007 Iran P * * 23.22a [73] 2007 Iran UHT * * 19.53a [74] 2007 Pakistan B 55 19 13a [75] C 40 15 14a G 30 6 2a S 24 4 2a Ca 20 0 0 2008 Iran P 50 50 * [76] UHT 49 49 * 2007-2008 Serbia C 3 * Oct-50 [77] 2007-2008 Iran UHT 210 116 8-249 [78] 2007-2008 Iran C 75 59 60.1a [79] B 75 29 31.9a Ca 40 5 19.0a S 51 19 28.1a G 60 19 30.1a 2008 Spain R 72 68 9.69a [80] 2010 Iran C 88 74 13-394 [81] G 65 28 13-55 S 72 43 15-102 2011 Iran P 91 66 13-250 [82] 2009 Croatia R 61 * 0.6-58.7 [83] 2009 Sudan R 44 42 220-6900 [84] PW 12 8 11-161 P: pasteurized; D: Dry milk; PW: Powdered Milk; R: Raw Milk; C: Cow milk; B: Buffalo milk; S: Sheep milk; G: Goat milk; Ca: Camel milk; NA: Not applicable * Not reported a Average of contaminate 9 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 Many authors showed that seasonal effect influences concentration of aflatoxin M1. They reported higher concentration of AFM1 in cold seasons as compared to hot seasons [85] the reason being in winters mostly milking animals are fed with compound feeds and thus concentration of aflatoxin B1 increases which in turn enhances AFM1 concentration in milk. Moreover, temperature and moisture contents also affect the presence of aflatoxin B1 in feeds. A. flavus and A. parasiticus can easily grow in feeds having moisture between 13% and 18% and environmental moisture between 50% and 60%, furthermore, they can produce toxin [86]. Another reason of low AFM1 level in summer may be attributed to out-pasturing of milking cattle. Aflatoxin M1 (AFM1) in milk is considered to pose certain hygienic risks for human health. These metabolites are not destroyed during the pasteurization and heating process. A total of 85 pasteurized milk samples were analyzed for AFM1 with the ELISA technique, from these samples seventy-five samples (88.23%) were found to be contaminated with AFM1 and 48 samples (64%) exceeded the legal level of AFM1 in milk according to the Turkish Food Codex and Codex Alimentarius limit (50 ng/kg). In Iran, 98 samples were positive for AFM1 with an overall mean level of 0.053 μg/L. Levels of the toxin were also higher in winter and spring than in summer and autumn [87] while in Sarab City of Iran, 77% (total 111 raw milk samples) were contaminated with AFM1 levels (range between 0.015 and 0.280 μg/L) and 40% of the positive samples exceeded the tolerance limit of 0.050 μg/L [88]. In Turkey, 47% of the 129 analyzed samples contained AFM1 levels exceeding the EU accepted limit [89]. In North African countries, randomly selected samples of raw cow milk were contaminated with AFM1 (rang between 30 and 3130 ng/L) [90]. In India, the incidence of contamination of AFM1 ininfant milk, milk based cereal weaning food and liquid milk samples was almost in the magnitude of 87% [91], with 99% of contaminated samples exceeding the EU/Codex recommended limits. [92] reported 42.5% and 52.5% milk samples were found contaminated from buffalo and cow, respectively, with the toxin. AFM1 levels in almost all the contaminated milk samples exceeded 50 ng/kg. From 11,831 processed samples from the territory of the European Union, 280 were from individual small farms, the concentration of aflatoxin M1 in all the samples greater than 0.05 µg/l was detected in only 0.06% of samples, which indicates that the incidence of this mycotoxin are extremely low [93]. 2.4.2 AFM1 in Cheese Occurrence of aflatoxin in cheese can be owing to three possible causes: 1. AFM1 present in raw milk as a consequence of carryover of AFB1 from contaminated animal feed to milk 2. Synthesis of aflatoxin (B1, B2, G1, and G2) by fungi that grow on 3. Cheese (although the low level of carbohydrate does not make it a very suitable substrate) 4. The use of powdered milk contaminated with AFM1 for cheese production Contrasting data have been reported on the influence of cheese preparation on AFM1 recovery. Studies performed in the early years showed variable losses of AFM1 during cheese production: 65%, 47%, <20% and <15% according to Stubblefield and Shannon (1974), respectively. In contrast, later investigations of 10 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 several authors [94] reported increases in AFM1 concentration in cheese as a function of cheese type, technologies, and the amount of water eliminated during processing. For example, [95] investigated some factors, which are involved in the process of making Iranian white brine cheese. They reported that some factors such as renneting temperature, press time, and saturated brine pH affected the amount of water eliminated and in turn the content of AFM1 in the cheese curds. However, many results have been drawn from experiments in which the processed milk contained the toxin at high levels, which seldom appear in the practice. Therefore, additional investigations should verify the influence of cheese making on AFM1 occurrence to avoid uncertainty in actual practice when the concentration of the toxin in the processed milk is at around the maximum permissible level of 0.05 mg/kg that is frequently recorded in monitoring programmes. The increase in AFM1 concentration in cheese has been ascribed to the affinity of AFM1 for casein [96] suggested that since is possible to extract AFM1, it must not be covalently bound but linked by hydrophilic interactions hydrophobic areas of the casein. According to [97] AFM1 is a water-soluble component and due to the hydrophobic sides of the casein molecule, AFM1 has affinity to casein of milk. Therefore, they defined a factor named “Enrichment Factor” (EF) for cheeses. Further surveys should be done to find as for cheese manufacture influences on AFM1 distribution. Some tests have been carried out on several kinds of cheeses as to overall stability of AFM1 during ripening and storage. [98] reported that the concentrations of AFM1 in Camembert cheese were higher at the beginning than at the later time of ripening. These results were in agreement with studies by [99]. Such results however, conflict with reports of earlier studies that indicate different behaviour of AFM1 in various other types of cheeses. Thus, in Camembert , Cheddar and Brick cheeses stored for 3, 14 and 6.5 months, respectively, the concentration of the toxin increased during the early stage of their ripening to decrease thereafter to reach about its initial concentration at the beginning of ripening [100]. On the other hand, the concentration of AFM1 in Parmesan cheese started high at the beginning of the ripening period, decreased until about the fifth month and then slowly increased up to the tenth month of storage [101]. In contrast, the AFM1 content of Mozzarella remained almost constant during storage of 4.5 months [101]. Additionally, studies by [102] showed that the amount of AFM1 in white pickled and Kashar cheeses did not significantly affect over the storage. [103] found that the final ripened cheese was free of aflatoxin M1. These different profiles of AFM1 in various cheese products may be the result of several factors such as heat treatment [104], proteolysis [101,100 , 104], exposure of contaminated milk to light [104], and especially to an inadequate method of analysis [104]. Some results of studies on the behaviour of AFM1 during cheese ripening seem to represent changes in the recovery of toxin by the method during the different phases of the study rather than real changes in the level of AFM1 in cheese [96] Several investigations on the partitioning of AFM1 during cheese production staring with different milk contamination levels reported a wide range of distribution of AFM1 between whey and curd. Some authors observed that half or more of the AFM1 was in the way: 50%, 11 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 50%, 66%, 100%, 60%, and 53-58% according to [115]. [105,106,107,108,109], respectively. In contrast, others reported that most of AFM1 was with curd: ranging from 66% to 72%, from 73% to 77%, 80%, 100%, and 59.1% according to [110,111,112,113,114] respectively. [116] observed that enrichment factor in the production of Feta cheese made from naturally contaminated milk ranged between 4.3 and 5.6. [117] showed that the mean concentration of toxin in curd and cheese was 3.12 and 3.65-fold more than that in whey and 1.68 and 1.80 fold more than that in cheese milk, respectively. It is thought that since AFM1 is a semi-polar component, it has less affinity to serum protein [118]. Regarding the affinity of AFM1 with proteins, Recently, [119] indicated that there is no simple physical method to remove AFM1 from ovine and caprine milk. Neither ultrafiltration, nor acidic or enzymatic treatments were able to influence the toxin’s interaction with casein or whey proteins. Only the combined action of heat and low pH (as used in ricotta cheese production) was able to denature whey proteins to a point where they lost their AFM1- binding capacity. According to [106] these contrasting results can be attributed to different factors such as extraction techniques, methodology, type and degree of milk contamination, differences in milk quality, expression of the results, the presence of a small portion of curd in whey which could influence AFM1 concentration, and the cheese manufacture process. Table 2 Occurrence and content of AFM1in Cheese Samples Year Country Samples + samples Range(ng/kg) Refernce 1990 Syria * 0 NA [120]. 1991 Kazakhestan * * * [121]. 1993 Japan 37 0 NA [122]. 1995 Japan 41 0 NA [123] 1995 Spain 35 16 20-200 [124] 2001-2002 Turkey 600 30 100-800 [125] 2005-2008 Iran 80 66 150-2410 [126] 2004 Italy 41 4 79.5-389 [127] 2005 Turkey 100 99 0-4100 [128] 2005-2007 Kuwait 40 32 23.8-452 [129] 2008 Spain 72 0 - [130] 2010 Iran 75 49 30-313 [130] 2011 Iran 72 59 30-1200 [131] NA: Not Applicable *: Not Reported The incidence of positive cheese samples for AFM1 (Table 2) seem to be widely variable. 12 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 The authors in [123] found no positive samples in imported cheese in Japan. [127] detected few positive samples, whereas [128] observed a high incidence of positive samples. As regards the contamination level, several authors [126,131] found a maximum contamination level over 1000 ng of AFM1 per kg. This latter contamination level could be hazardous. 2.4.3 AFM1 in yogurt Several studies have been conducted regarding the effect of yogurt manufacturing on AFM1 content. Some authors reported no influence on aflatoxin M1 content [84]. In contrast, [52] detected variable increases of AFM1 content in yogurt related to the milk. The effect of fermentation was assessed by [99]. They reported that AFM1 levels in all yoghurt samples showed a significant decrease from those initially present in milk. This decrease in AFM1 was attributed to factors such as low pH, formation of organic acids or other fermentation by- products, or even to the presence of lactic acid bacteria. The low PH during fermentation alters the structure of milk proteins such as the caseins leading to formation of yoghurt coagulum. The change in casein structure during yoghurt production may affect the association of AFM1 with this protein [96] causing adsorption or occlusion of the toxin in the precipitate. As to AFM1 stability over storage of yogurt, [84] observed no reduction of AFM1 in yogurt stored for 7 days at 7 ºC. [55]) observed complete transformation AFB1 in its hydroxy derivative AFB2A caused by the acids present in yogurt. Whereas, [54] revealed a high reduction (up to 97%) of AFM1 in yogurt and acidified milk. [111] observed that enzymatic, microbial, and particularly acid coagulation caused degradation of AFM1 in buffalo milk. [47] reported a high reduction of AFM1 in fermented goat milk. As a result of Study by [99], during refrigerated storage, AFM1 was rather more stable in the yoghurts with pH 4.6 than with pH 4.0. The percentage loss of the initial amount of AFM1 in milk was estimated at about 13 and 22% by the end of the fermentation, and 16 and 34% by the end of storage for yoghurts with pHs 4.6 and 4.0, respectively. Since it is known that exposure of the aflatoxin molecule to strong acid, such as trifluoracetic acid, can cause its acid-catalyzed hydration, leading, for example, from AFB1 to AFB2A [130] , but not its degradation or neutralization, the effect of the weak acidity of yogurt on aflatoxin should be more investigated. Some investigations have been conducted related to the effect of aflatoxin on nutritive properties of yogurt. [111] observed some negative effects of AFM1 on Lactobacillus bulgaricus (cell wall thickening and shortening of cell chain lenghth) and Staphylococcus thermophilus (cell wall thickening and cell shape changing from coccoid to oval). [72] found that S. thermophilus was affected by the presence of in milk during fermentation of yoghurt, exhibiting longer cell chains in the contaminated than in the uncontaminated yoghurt samples. Similarly, [111] observed that the growth rate of S. Thermophilus and curdling time were affected by the higher level and not by the lower level of AFM1. Unlike cheese and milk samples, the presence of AFM1 in yogurt has not frequently been studied. Thus, more investigations are needed because: 1. currently, human consumption of yogurt has greatly increased 2. there are contradictory data on AFM1 stability over manufacture and storage in the literature 3. The presence of aflatoxin in yogurt could reduce the nutritional values of its consumption. 13 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 2.4.4 AFM1 in Other Milk Products Many other milk products such as cream, butter, ice cream may contain AFM1. The presence of AFM1 in these products has rarely been investigated and could be of interesting aspects for study. Some surveys conducted on the occurrence of AFM1 in milk products are reported in (Table. 4). In a study by [52] the levels of AFM1 in the products made from contaminated milk namely butter, butter milk, cream, skim milk was investigated. The mean AFM1 level found in cream samples was 64.4% of AFM1 concentration of bulk-tank milk. Whereas, mean AFM1 level of skim milks was 3% higher than those of bulk-tank milk. These values were close to the results given by [84], and lower than the values given by Wiseman et al. (1983). Levels of AFM1 in butter samples in the study were less, and they were as 33.80% of AFM1 amounts of bulk-tank milk. Mean AFM1 levels obtained from buttermilk samples were similar to those of bulk-tank milk (mean 83% of it). The same results were reported by [115]. During butter processing, protein membrane around fat globules is broken down and serum phase is separated. Due to the chemical structure of AFM1 and its affinity to casein, it adsorbs on this fraction of protein [104], therefore, cream contained less AFM1 than milk, and butter contained less amount of AFM1 than cream. As a result of the associate effects of these factors, AFM1 concentration occurs in lipid phase (like butter and cream) less than serum phase and protein fraction [35]. AFM1 is frequently observed in the aflatoxin exposed individuals and in the breast milk. AFM1 toxicity in this respect is important as it is known that within aflatoxin exposed nursing mothers it can provide a source of aflatoxin exposure to the infant [115].The occurrence of AFM1 in breast milk has been investigated in some regions. There is increased awareness of the link between growth and health of the fetus and infant, and disease risk in later life. Long term pre and postnatal exposure to aflatoxins could be one of the factors contributing to growth faltering and/or the early onset of hepatocellular carcinoma (HCC) in countries with a high incidence of the disease. Additionally, the presence of other aflatoxins, B1, B2, G1, G2 and M2, has also been reported in breast milk [19]. The identification and understanding of factors determining the presence of toxicants in human milk is important and may provide a strong basis for controlling the transfer of chemicals to the infants through breast milk. 2.5 Losses Due To Aflatoxin Infection In addition to financial losses and economic damage to agricultural and animal husbandry industries, losses due to aflatoxin contamination of foods include major pharmaceutical and health costs to treat food poisoning. Based on Food and Agriculture Organization [109] reports, annually, about 20% of the foods produced in the world are contaminated by mycotoxins; in which aflatoxins have a greater share than the others. Prevalence of cancer and livestock disease in farms, weakening of livestock immune system, reduction in milk production and productivity are a few exam ples of dam ages to food and livestock industry. Considering huge economic losses 14 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 and public health protection, prevention and neutralization of the toxins in livestock feed and food products of animal origin such as milk is essential [114] Table 3 Occurrence of AFM1 reported in some regions Count ry type Samples + sample s Range(ng/kg ) Refernce Turkey Butter 92 92 10-7000 [128] Turkey Butter 27 25 0-100 [68] Iran Infant formula 120 116 1-14 [66] Milk-based cereal weaning 80 72 3-35 food Egypt Breast milk 443 248 4.2- 889 [74] Kuwait Breast milk 12 5 8.83-15.2 [67] Iran Kashk 125 53 28-291 [81] Doogh 136 25 13-53 Butter 31 8 13-26 [82] Ice Cream 36 25 15-132 2.6 Permitted Levels of Aflatoxin in Milk and Milk Products Some countries have set permitted levels of aflatoxins in food in order to control and reduce detrimental effects of these toxins. These levels are variable and depend on economic and developing status of the countries (Galvano et al., 1996). In US, Food and Drug Administration (FDA) has permitted a total amount of 20 ng/g in livestock feed and 0 .5 g/kg or 50 ng/l in milk [112]. In European countries, permitted levels of aflatoxin M 1 in milk, milk products and baby food are 0.005 mg/kg [26]. Also, different countries have set different regulations for permitted levels of aflatoxin in livestock feed . For instance, European Union (EU) has set permitted levels of aflatoxin from 0.05 to 0.5 g/kg. Factors such as weather conditions are also effective in determining permitted levels of aflatoxin. However, according to US regulations the level of AFM1 in milk should not be 15 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 higher than 500 ng/kg [132]. There are thus differences in maximum permissible limit of AFM1 in various countries. Currently the limits of AFM1 are highly variable depending upon the degree of development and economic standing of the countries. According to [13] the maximum limits for aflatoxineM1 in milk and milk products in various countries is illustrated in table 4 Table 4 Maximum acceptable level of AFM1 milk and milk products in some regions Country Maximum Acceptabe Level (ng/l) Type European Union 50 Milk Austria 50 Milk Argentina 50 Milk Bulgaria 500 Milk Germany 50 Milk Australia 20 Children's milk Sweden 50 Liquid milk products Netherlands 20 Butter Switzerland 50 Milk and milk products 250 Cheese Belgium 50 Milk USA 50 Milk Czech Republic 100 Children's milk 500 Adult's milk Serbia 500 Milk Iran 50 Raw, Pasteurized, and UHT milk 200 Cheese 20 Butter France 30 Children's milk< 3 years 50 Adult's milk Turkey 50 Milk and milk products 250 Cheese Brazil 500 Milk Source: Hamid, 2011 Mariko (2012) reported the limits of aflatoxin M1 for milk and milk products and in some cases for infant and products for infants, worldwide, as illustrated in Table 5 16 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 Table 5 Aflatoxin M1 limits in different food stuffs Country Foodstuffs Aflatoxin M1 (μg/kg) EU Bosnia and Herzegovina Turkey Raw milk, heat-treated milk and milk for the manufacture of milk- based products 0.050 Infant formulae and follow-on formulae, including infant milk and follow-on milk 0.025 (products ready to use) Dietary foods for special medical purposes intended specifically for infants 0.025 (products ready to use) China Milk and milk products (for milk powder, calculated on a fresh milk basis) 0.5 Formulated foods for infants (milk or milk protein based) 0.5 (calculated on a dry powder basis) Formulated foods for older infants and young children (milk or milk protein based) 0.5 (calculated on a dry powder basis) Formulated foods for special medical purposes intended for infants 0.5 (calculated on a dry powder basis) Codex, GCC, India, Kenya, USA Milk 0.5 Argentina Milk, liquid including milk used in the manufacture of milk and milk products and reconstituted milk 0.5 (1) Milk, powder 5.0 Milk formula ND Mexico Pasteurised, ultrapasteurised, sterilised and dehydrated milk, milk formula and combined milk products 0.5 (1) South Africa Milk 0.05 ND: Not Detectable, (1) Given in µg/l. 17 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 2.7 What to Do if Milk Is Detected With Action Levels of Aflatoxin If aflatoxin is detected in milk, it is critical that records be maintained of all feeds, feeding practices, milk quantities and contamination levels, plus animal health and performance. If the grain or related feed is fed to other animals, these records should be maintained also. After milk has been detected with greater than 0.5 ppb of aflatoxin in one load, all grain products fed to animals should be removed from the ration immediately and new grain and/or related items replaced in the diet. As cottonseed and corn are the most likely sources of aflatoxin contamination, these grains should be tested to determine their level of aflatoxin. The exception to the preceding statement is when an additional milking has occurred on the dairy and the milk then tests below 0.5 ppb aflatoxin. In this case, the feed should be tested before it is removed from the feed supply [59]. It is illegal to sell grain with levels greater than 20 ppb aflatoxin for lactating dairy cows, and the seller of the grain is responsible for damage resulting from the sale of grain. However, in most cases, perhaps 60 percent of the time, the exact source of feed contamination is not determined. In cases of severe contamination and over a prolonged period of time, some data indicate that animals may experience adverse health effects which can affect both present and long-term performance. Calves also are more susceptible to aflatoxin and have died as a result of aflatoxin contamination in feed [59]. Immediately after aflatoxin is detected in milk, the ration should be reformulated with ingredients that contain less than 20 ppb aflatoxin. If the level of milk contamination exceeds 0.5 ppb on a second test, a special dietary chemisorbent should be added to the diet at recommended levels. These compounds include clays (bentonites) at 1 percent of the diet, activated carbon at 1 percent of the diet and glucomannan (Mycosorb®) at 0.05 percent of the diet on a dry matter basis. Some empirical observations indicate that the animal may consume levels of bentonite up to one pound a day. Limited data is available on the numerous compounds that are available to absorb the aflatoxin in the digestive system. However, in one study, about 1/4 pound of hydrated sodium calcium aluminino silicate (HACA – a compound approved for feed as an anti-caking agent) was shown to reduce aflatoxinM1 in milk about 50 percent when cattle consumed feed containing 200ppb aflatoxin. Silky clay loan soil and bentonite have a similar effect but have not been well studied. Many commercially avail- able products also theoretically will bind aflatoxinM1 and should result in lower aflatoxin in milk.Generally,the cost of using the commercially available products is greater than the cost of using bentonite to bind aflatoxin [59] 2.8 Afalatoxin Reduction in Milk and Milk Products 2.8.1 Indirect Methods of Aflatoxin Reduction in Livestock Feed Milk contaminated with aflatoxins is produced mostly from use of infected feed. Therefore, reducing aflatoxin contamination indirectly via control of livestock feed hygiene is possible. To achieve the aim, principles and health considerations during farming and crop production in farms and livestock feed factories, storage of livestock feed in traditional and industrial warehouses is necessary [72]. Livestock feed is mostly include corn, cotton seed and canola, dietary supplements, wheat bran, dried bread, fat powder and alfalfa. Given that a significant percentage of the feed composition is derived from crops, health consideration during planting, 18 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 harvesting and storage of crops are factors affecting grain quality. Drought, rainfall, infection by insects and high moisture during flowering can be referred as major causes of aflatoxin occurrence in farms. Adherence to appropriate irrigation programs, planting varieties resistant to moisture and molds, weed control, insecticides application, harvesting at appropriate time, crop rotation in order to reduce the risk of pathogen transfer from current farming year to the next year and fertilizing oil are useful ways of preventing pre-harvest aflatoxin infection. In addition, appropriate storage of crops which includes placing crops on clean and dry surfaces, protecting crops from moisture, heat, insects and use of fungicides are effective ways of reducing the infection [18]. Adherence to hygienic conditions in factories and livestock feed warehouses both in traditional and industrial levels is another important way of controlling and reducing aflatoxin infection. Controlling mold growth and aflatoxin formation in traditional farms and warehouses is highly important. In this regard, several studies have been carried out on quality of livestock feed and the amount of aflatoxin in produced milk [26]. For example, it has been shown that the amount of aflatoxin in milk produced in autumn and winter is higher compared to spring and summer [61] This is because in cold seasons, feeding livestock on fresh forages is not possible due to unfavorable weather conditions and farmers have to use stored forages. Regarding that warehouse improper temperature and moisture conditions favor mold growth; therefore, it is necessary to improve storage conditions of livestock feed [61]. Results in some countries have shown that meeting safety conditions of livestock feed has led to decrease aflatoxin infection [37] In addition, protecting feed from infection sources, inhibition of microorganisms’ propagation in feed, alleviating infection and inhibition of reinfection are regarded as principles of controlling infection in industrial livestock feed factories. To obtain these ends, continuous and careful monitoring of different procedures of storing raw materials and production, controlling moisture content and temperature by ventilation systems, use of clean and hygienic facilities such as mills and mixers and avoiding from broken or damaged grains when preparing feed are necessary [133]. Moreover, absorbents, chemicals, microorganisms and ionizing rays can be used to prevent mold growth and development of the molds when initial infection has been occurred [34]. Several researches have been conducted on using absorbents in infected livestock feed [83; 56] Use of aflatoxin absorbents in infected feed is a promising way of reducing this infection in livestock feed. Through binding to absorbents, aflatoxins present in feed inhibits from toxic reactions in livestock body as well as from absorption into digestive tract. Properties of the absorbents when choosing them to hinder the aflatoxin infection should include capability of toxicity inhibition in livestock feed, not having detrimental effects on livestock health and being economic [56]. Studies on application of aflatoxin absorbents have been conducted for years. Some aflatoxin absorbents in infected feed include active carbon, alumino (clay, bentonite, montmorillonite, zeolite and phyllosilicates), complex carbohydrates (cellulose and polysaccharides present at cellular wall of yeasts and bacteria such as glucomannans, peptidoglycans), synthetic polymers such as cholestyramine and polyvinyl pyrrolidone and its derivatives. Although this method leads to good results in the laboratory conditions, the use of these substances in livestock body is different and requires time-consuming and various experiments. Livestock species, age and genus influence results of the experiments [83]. 19 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 Furthermore, chemical inhibitors include one or a series of organic acids such as propionic, sorbic, benzoic and acetic acids, organic acid slats such as calcium propionate, potassium sorbate and solid or liquid copper sulfate [134] Also, with respect to FDA standards, use of ammonia for neutralizing aflatoxin in livestock feed has been permitted in US. 95% of aflatoxin in feed has been alleviated with the aid of gaseous or liquid ammonia [49] When applying ammonia, if conditions such as time of use, temperature and concentration are met, reduction of aflatoxin infection is carried out more effectively. Ammonia alleviates toxicity of aflatoxin B1 and converts it to non-toxic compound of aflatoxin D1 through hydrolyzation of aflatoxin B1 and its decarboxylation ([49]. Use of different microorganisms such as lactobacillus pentosus and lactobacillus brevis is another way of reducing aflatoxin in livestock feed. Mechanism of Aflatoxin B1 removal by lactic acid bacteria is not through metabolic degradation, but through binding this toxin to cellular wall of the bacteria. However, some researchers have attributed removal property of aflatoxin by the aforesaid bacteria to their ability in producing acid and lowering pH [57] Application of ionizing rays such as gamma ray in humid environment is also a way of aflatoxin B1 reduction in livestock feed. Aflatoxin B1 decomposes water against gamma ray in moist environment and releases radicals, thus creating conditions required for decomposition of aflatoxins. In dry conditions, aflatoxin B1 shows high resistance to detrimental effects of gamma ray [56]. 2.8.2 Direct Methods of Aflatoxin Reduction in Milk Toxin absorbents, chemical and biological methods are also used directly for reducing aflatoxin in milk [87].Use of toxin absorbents is one of the main methods to reduce aflatoxin amount in milk. Absorbent soils such as bentonite, vermiculite, hydrated sodium calcium aluminosilicate (HSCAS) and active carbon have been known as absorbent compounds for absorbing various toxins in aqueous environments [94]. For instance, bentonite has been known as an effective reducer of aflatoxin M1 in infected milk (Applebaum and Marth, 1982a). Binding capacity and stability of compounds formed between absorbent and toxin are highly variable and influenced by temperature and PH. Information about the effect of absorbents on milk constituents is scarce; however, it has been shown that these substances have slight effect on nutritional quality of milk [112]. In a study, effect of bentonite on milk protein content was not considerable and maximum reduction in protein content was only 5% [82].It should be mentioned that with respect to acceptability of absorbents as healthy additives by international authorities and ability to separate them from milk after absorption of aflatoxin, further investigations are in progress. In addition to absorbents, chemicals such as hydrogen peroxide used for storage of some food products have reduced aflatoxin in milk at different conditions of time and concentration [80].Use of hydrogen peroxide combined with other additives like riboflavin and lactoperoxidase as well as hydrogen peroxide application along with heat treatment have led to more satisfactory results in reducing aflatoxin in milk. In addition, potassium sulfite has been used for neutralizing aflatoxin M1 in milk [80] Biological methods as inexpensive and easy techniques of reducing aflatoxin have also been of interest. Therefore, widespread studies on identifying effective microorganisms are being conducted [87]. For instance, in a study, Flavobacterium aurantiacum which is gram-negative, aerobic, bacilli like and non-sporogenous bacterium has been used for reducing aflatoxin in milk (Line et al., 1994). The bacterium can use aflatoxin 20 American Scientific Research Journal for Engineering, Technology, and Sciences (ASRJETS) (2013) Volume 4, No 1, pp 1-32 present in milk as a substrate and convert it to non-toxic substances. However, formation of proteolytic and lipolytic enzymes by this microorganism leads to undesirable changes in milk flavor [101]. 3. Conclusions Aflatoxins are produced on livestock feed in appropriate moisture and temperature conditions for mold growth. Consumption of feed infected by aflatoxins leads to different problems in reproductive, digestive and respiratory tracts of livestock causing infected milk production. Consumption of infected milk by human incurs major hygienic and pharmaceutical costs to society. Therefore, in order to prevent from introduction of aflatoxin M1 into food industry cycle, its precursor namely aflatoxin B1 should be controlled. To obtain this, meeting hygienic conditions, appropriate storage and control of livestock feed at all stages of planting, growing, harvesting, producing and storing are necessary. For this reason, milk and milk products have to be controlled continuously by accurate and reliable analytical techniques for presence of AFM1 contamination. It is also extremely important to maintain low levels of AFM1 in the feeds of dairy animals. In order to achieve this, dairy cow feds should be kept away from contamination as much as possible. Therefore, animal feeds should be checked regularly for Aflatoxin and, particularly important, storage conditions of feeds must be strictly controlled. The regulatory limits are widely variable and there has been little scientific basis in their setting. Efforts should be made in attempting to provide further and extensive scientific information on human health hazards related to low-level long term Aflatoxins exposure and to standardize the already existing regulatory limits for Aflatoxins. . The occurrence of AFM1 in cow milk and milk products is widespread and the occurrence of Aflatoxin and their metabolites in human breast milk is of great concern. Since serious health hazards to the mother, fetus, and infant could occur. Therefore extensive and periodic surveys should be performed in the incidence and occurrence of AFM1 in milk and milk products. References [1] Reddy KRN, Salleh B, Saad B, Abbas HK, Abel CA, Sheir WT., (2010). An overview of mycotoxin contamination in foods and its implications for human health. Toxin Rev. 29: 3-26 [2] Shetty, P.H., Jespersen, L. ,(2009). Trends Food SciTechnol, 17,48-55. [3] Bunaciu,D.M. 2010. 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Food Additives and Contaminants, No. 8, pp. (213-221) 32 bCollege of Veterinary Medicine and Agriculture, Addis Ababa University, Addis Ababa, Ethiopia, pobox,34 aemail: melkamu_bezabihy@yahoo.com bemail: berhantamir@yahoo.com Abstract 2. Mycotoxin/Aflatoxine / In Milk and Milk Products 2.1 What is Mycotoxins? 2.2 What is Aflatoxin? 2.3 Changing of AFB1 to AFM1 2.4 What is Aflatoxins M1? 2.4.1 AFM1 in Milk 2.4.2 AFM1 in Cheese 2.4.3 AFM1 in yogurt 2.4.4 AFM1 in Other Milk Products 2.5 Losses Due To Aflatoxin Infection 2.6 Permitted Levels of Aflatoxin in Milk and Milk Products 2.7 What to Do if Milk Is Detected With Action Levels of Aflatoxin 2.8 Afalatoxin Reduction in Milk and Milk Products 2.8.1 Indirect Methods of Aflatoxin Reduction in Livestock Feed 2.8.2 Direct Methods of Aflatoxin Reduction in Milk 3. Conclusions References