Ochratoxins are worldwide spread secondary metabolites synthesized mainly by some toxigenic species of Aspergillus
] that contaminate various raw agricultural commodities and have dangerous effects on animals and humans. The chemical structure of ochratoxin A (OTA), the most common ochratoxin, consists of a dihydroisocoumarin part coupled, via its 7-carboxy group, with a L-beta-phenylalanine part.
The most relevant toxic effect of OTA in animal cells is the inhibition of protein synthesis, but other important effects are lipid peroxidation, DNA damage and oxidoreductive stress [2
]. Mutagenic effects in mammalian cells, as a consequence of DNA damage induction, have been reported [3
]. Further evidence suggests a genotoxic carcinogen role of OTA, due to the induction of oxidative DNA lesions combined with the creation of covalent bond between OTA reactive metabolites and the damaged DNA [4
]. OTA effects of on animal health are strongly influenced by its kinetic (i.e.
, toxicokinetic and toxicodinamic) parameters, which differ between ruminant and monogastric species. In monogastric (e.g., pigs and poultry species), OTA is absorbed from the gastrointestinal tract without, or with little, prior degradation. On the contrary, in ruminants OTA is subjected to microbial degradation in the rumen before any essential uptake. The most relevant microbial degradation of OTA is carried out by enzymes able of peptide hydrolysis, yielding phenylalanine and the nontoxic dihydroisocoumarin part, currently named as Ochratoxin-alpha [5
]. In the bloodstream, almost all OTA is strongly bound to serum proteins, mainly albumin. Interaction between OTA and serum albumin affects the half-life of the toxin in the bloodstream and differs substantially between species [6
]. Sreemannarayana et al.
] reported an OTA serum half-life of about 77 h in pre-ruminant calves, whereas Galtier et al.
] reported a half-life of 88.8, 8.2 and 4.1 h in pigs, rabbits and chickens, respectively. Actually, differences in OTA serum half-life account for most of the high variability of OTA toxic effect observed among animal species.
Considering the risk of potential transfer from feeds to animal tissues and products, legislative authorities have enacted or proposed regulations for controlling OTA in foods and/or feed commodities. In 2006, the Commission of the European Communities [8
] recommended the member States to ensure the respect of the guidance values indicated for the acceptability of composed feeds, cereal and cereal products for animal feeding. Values vary between feedstuffs and animal species (Table 1
Guidance values for OTA in feedingstuffs with a moisture content of 12%, as set in the Commission Recommendation 2006/576/EC.
Guidance values for OTA in feedingstuffs with a moisture content of 12%, as set in the Commission Recommendation 2006/576/EC.
|Products Intended for Animal Feed||Guidance Valuein mg/kg|
|Feed materials|| |
|Cereals and cereal products||0.25|
|Complementary and complete feedingstuffs|| |
|Complementary and complete feedingstuffs for pigs||0.05|
|Complementary and complete feedingstuffs for poultry||0.1|
Nevertheless, when cereals and cereal products are fed directly, the daily amount of OTA ingested should not be higher than the OTA intake by animal for which only complete feedstuffs are used in the diet. So far the U.S. Food and Drug Administration [9
] has not set advisory limits or action levels for OTA in any commodity, even if this institution has included OTA in the list of Potentially Hazardous Contaminants in Animal Feed and Feed Ingredients. Most information available on the toxic effects of OTA on animals was obtained in experiments carried out on laboratory animals. Nevertheless, in the late 1960s, the scientific community began to study the adverse effects of the ingestion of feed contaminated by Aspergillus ochraceus
on livestock species [10
Several ochratoxigenic mycobiota can grow in grains and forages used for animal feeding and produce OTA and other mycotoxins. Thus, farm animals may be exposed to the toxic effects of OTA together with those of other toxins. Most common mycotoxins occurring together with OTA are: citrinin, zearalenone, penicillic acid and aflatoxin B1 [11
]. In vivo
experiments carried out to evaluate effects of a mycotoxin combination on animals usually yield results that are very difficult to interpret. To overcome these difficulties, Speijers and Speijers [11
] stressed the importance of understanding the way mycotoxins, such as OTA, can interact at the cellular level with other fungal compounds. A special care is needed in the theoretical assumptions, in the planning of experiments and in the statistical analysis of results.
Negative economic implications of OTA on livestock have been reported since the early 1970s [12
]. Because ruminant species are commonly considered to be less susceptible to OTA effects, most research has focused on monogastric species.
Even though the toxic effects of OTA on animals differs markedly between species, studies carried out on monogastrics represent an interesting model for approaching the study of OTA effects on human health. This is a relevant point, considering that OTA is suspected of being the main etiological agent responsible for human Balkan endemic nephropathy and associated urinary tract tumors [4
Hereinafter, most relevant information about the occurrence of OTA contamination in feedstuffs and the effects of OTA on performances and OTA transfer into animal products of the main livestock species is given briefly.
2. Occurrence of OTA in Feeds
Prevention of pre-harvest and post-harvest natural contamination of feedstuffs by OTA is a basic tool in the strategy to minimize the subsequent occurrence of OTA into the feed and food chain.
It is well-known that cereals, mainly in Northern America, Northern and Western Europe and other temperate regions, may be exposed to colonization by fungi of the genus Penicillium
able to produce OTA. These molds do not invade the crop in the field but mainly in the post-harvest phase [1
However, mold species producing OTA differ among ecological conditions and commodities that characterize different geographical regions. In general, Penicillium verrucosum
is responsible of OTA contamination in cool-temperate conditions, whereas Aspergillus ochraceus
is probably the main ochratoxigenic species in hot-tropical regions [13
Because the main abiotic factors which influence mold growth and OTA production are water availability and temperature, Magan and Aldred [1
] suggested that cereals should be quickly dried, reaching a moisture content lower than 14.5% and maintaining this condition during storage, to avoid OTA contamination.
In their review, Scudamore et al.
] reported that OTA is mainly concentrated in the seed coat of cereals, which is often used for animal feeding. Moreover, on-farm production and storage of barley and wheat with a high moisture content increases the risk of mold growth and toxin production. Magan and Aldred [1
] suggested the following moisture content values during storage as a safe threshold: 14–14.5% for wheat, barley and oats; 14% for maize; 13–14% for rice and 7–8% for rape seed.
Cairns-Fuller et al.
] reported that water activity, temperature and CO2
concentration are main factors affecting P. verrucosum
growth and OTA production in wheat grain produced and stored in cooler Northern European climates. Moreover, authors reported that at least 50% of CO2
is required to inhibit P. verrucosum
growth and to reduce by more than 75% its OTA production in wheat grain with a water activity within the interval 0.90–0.995. Therefore, a moisture content of 17–18% (water activity of 0.80–0.83) can be considered as a threshold for avoiding any potential growth of mold and OTA production in wheat grain.
Levels of OTA of 110 to 150 ppb have been found by Shotwell et al.
] in ground corn suspect for the presence of OTA. Moreover, they claimed that until 1969 there has been not any report for the presence of OTA as a natural contaminant even though this mold was widely distributed in nature. Since then, there have been several investigations on the occurrence of mycotoxins, particularly OTA, in feeds and commodities used for animal nutrition.
The fact that the contamination of cereals, or derived products, by OTA is a worldwide problem is confirmed by several studies carried out during the last four decades in several geographic and climatic conditions.
In a survey on over 500 samples of home-grown cereals (barley, wheat and oats) in England and Wales from 1976 to 1979, OTA was found as the most frequent mycotoxin (12.8% of samples being positive) [16
Scudamore et al.
], in an investigation carried out on more than 350 samples of feeds collected in the United Kingdom (limit of quantification of the analysis, LOQ = 0.001 mg/kg), reported that barley and wheat were the feed ingredients with the highest occurrence of OTA (60 and 40% of positive samples, respectively), even if seven out of 15 samples of dried peas/beans also contained OTA.
In samples of several cereals and other feeds, such as soybean and sunflower, collected in Hungary, Rafai et al.
] reported that the average concentration of OTA of soybean, maize and rye was 350, 320 and 250 ppb. Average contamination in other feeds, such as wheat, barley, oat, triticale and sunflower, was lower than 200 ppb. Such contamination levels in Hungary were confirmed by the results of Fazekas et al.
] that reported contamination frequencies of 35.0, 15.6, and 26.7% for barley, wheat and maize, respectively. Moreover, OTA average concentrations were 72 ppb in barley (range: from 0.14 to 212 ppb), 12.2 ppb in wheat (range: from 0.3 to 62.8 ppb) and 4.9 ppb in maize (range: from 1.9 to 8.3 ppb).
Czerwiecki et al.
] reported OTA occurrence in cereal grains from conventional and ecological farms in Poland during 1997 and 1998. In 1997, the frequency and the concentration of OTA were higher in rye, barley and wheat grains from ecological farms (range 0.2–57 ppb) than in conventional cultivation. Differently in 1998, the frequency of OTA contamination of rye and barley was similar for conventional and ecological farms, even if the overall range of OTA concentration in those cereals was higher in ecological (from 1.4 to 35.3 ppb) than in conventional (from 8.8 to 9.7 ppb) farms. Moreover, in that year the frequency of contaminated samples was 48% and 23% in cereals of conventional and ecological farms, respectively. The overall range of OTA concentration in wheat grain varied greatly between conventional (from 0.6 to 1024 ppb) and ecological farm (from 0.8 to 1.6 ppb). Those results suggest that contamination frequency may differ greatly across years and farming systems and that the latter are not a factor able to control the extent of grain contamination by OTA.
Garaleviciene et al.
] showed an OTA content greater than 10 ppb in about 92% of samples of wheat, barley, oats and 52 mixed feeds collected in Lithuanian farms. The magnitude of OTA contamination in cereals produced and stored in Baltic regions was confirmed by Baliukoniene et al.
], who analyzed OTA concentration in wheat and barley produced and stored under different conditions in Lithuania. OTA concentrations were 3.19, 1.78 and 1.13 ppb in wheat grains from small, medium and large granaries, respectively, whereas it varied between 0.92 and 0.37 ppb in barley samples.
In 96 samples of poultry feed collected in Brazil, Rosa et al.
] reported an occurrence of OTA in 100% of the feeds, with concentrations varying from 1.3 to 80 ppb. Moreover, 84 out of 340 Aspergillus
strains isolated were able to produce OTA under in vitro
conditions. Successively, Fraga et al.
] studied the mycological contamination, potential mycotoxin production and occurrence of OTA in 144 samples of poultry feeds and feed ingredients collected from a factory of Rio de Janeiro State in Brazil from April 2003 to March 2004. The study showed that 100% of the poultry feed samples were contaminated with OTA, at levels varying between 0.017 and 0.197 mg/kg, with a mean value of 0.098 mg/kg. Mycological analysis indicated that OTA contamination could be due to the presence of two strains of OTA-producing Aspergillus melleus
In a survey on feeds used for swine nutrition in Brazil, Rosa et al.
] reported that OTA was detected in all 144 feeds analyzed. The concentration of OTA ranged from 42 and 224 ppb in corn samples, from 36 to 120 ppb in brewers grains samples and from 28 to 135 ppb in finished feed samples.
In a recent investigation conducted by Binder et al.
], ingredients and feeds were sampled in animal farms in European, Asian and Pacific regions from October 2003 to December 2005. The occurrence of OTA in Asia and in the Pacific region was detected (limit of detection, LOD = 0.002 mg/kg) in 0.26 of the complete feeds and 0.25 of maize. The incidence of OTA in feeds sampled in Europe and others Mediterranean region was 0.42 in wheat, 0.73 in complete feeds and 0.68 in other feed ingredients.
The risk of intake of relevant amounts of OTA is much lower in cattle than in pigs and poultry species, because cattle feeding is mostly based on forages and only partially on cereals, which are the feeds with the highest risk of contamination.
In a survey on 290 samples of grass silage, whole-crop maize silage and whole-crop wheat or triticale silage collected in randomly selected Dutch dairy farms from 2002 to 2004, Driehuis et al.
] reported that none of the silages contained OTA (LOQ = 8 ppb). In another investigation analyzing the OTA content (LOQ = 8 ppb) in silages and concentrates used in the diet of lactating cows in 24 dairy farms across the Netherlands, Driehuis et al.
]did not detect OTA in any of the feeds samples.
Lund and Frisvad [30
] suggested that an infestation of Penicillium verrucosum
higher than 7% in cereals indicates OTA contamination. Subsequently, Lindblad et al.
] developed a logistic model able to predict the probability of reaching OTA levels exceeding various thresholds in cereal grains on the basis of storage conditions (temperature and water activity) and number of colonies of P. verrucosum
. Because mycological analyses are generally less expensive than chemical analysis to determine mycotoxins, the use of fungal concentrations for estimating the OTA level may be a cheap tool for managing the risk of OTA contamination in cereal grains,
These monitoring techniques, apart from being of great importance for controlling contamination risk in grains used in animal feeding, may be particularly helpful to reduce the exposure to OTA intake in food human consumption.
The Joint FAO/WHO Expert Committee on Food Additives [32
] has further emphasized the relevance of OTA in human food mainly due to consumption of contaminated foodstuffs such as cereal grains. Considering the global importance of cereals in the human/animal diet and their susceptibility to attack by molds producing OTA, Duarte et al.
] showed in their review an updated anthology of data on OTA as a worldwide contaminant in cereal crops and cereal based products destined to human consumption.
4. OTA Presence in Meat, Eggs and Milk
OTA ingested from contaminated diet by livestock species reaches the bloodstream where it persists for long time and may accumulate in organs responsible for its detoxification and excretion. Therefore, it is important to verify the carry-over of this mycotoxin into animal products such as meat, eggs and milk.
Transfer of OTA along the food chain of animal products depends essentially on the following factors: the extent of exposure of animals to an OTA-contaminated diet; the level of transfer of intact OTA into the bloodstream of animals; the degree of OTA persistency in the blood and its accumulation in different tissues; and the magnitude of the transfer of OTA from blood to milk, meat or eggs.
Human exposure to intake of OTA is mainly due to the consumption of contaminated cereals, however an indirect source of OTA exposure may be the consumption of products derived from animals fed contaminated diet. Moreover, the exposure of lactating women to food indirectly contaminated by OTA, such as animal products, may represent a potential way of transferring this toxin to newborn suckling children by milk. This was suggested in a survey carried out on Norway by Skaug et al.
] indicating that women with a high dietary intake of liver paste were more likely to have OTA contaminated milk.
In a review, Jørgensen [96
] reported a historical view (from 1969 until July 2005) of the number of publications regarding the different commodities contaminated by OTA. About 19% of articles focused on OTA in meat and meat products, whereas no publications dealt with OTA in other animal products, such as milk or eggs.
Because OTA has high affinity to blood proteins, in particular to serum albumin, this toxin can likely accumulate in different organs of animals used for food such as muscle and liver.
Since the 1970s, the presence of OTA in muscle, fat, liver and kidneys of pigs fed diets contaminated with OTA has been documented. In fact, Krogh et al.
] showed that OTA concentration differed among pig tissues, with increasing concentrations of OTA being observed from fat, muscle, liver, to kidney. Moreover, authors found that in all tissues (kidney, liver, muscle and fat) the disappearance of OTA after termination of exposure to contaminated diet, showed an exponential trend and values of half-life of residues ranged from three to five days.
In several experiments in which pigs were fed diets with different OTA content for different times, the toxin was detected in different tissues. For example, Jarczyk et al.
] reported that OTA concentrations in kidney, liver and longissimus dorsi muscle (8.74, 5.90 and 4.26 ppb, respectively) of gilts were lower than those of the diet supplied (32.2 ppb of OTA for 14 days). Similar results were reported by Aoudia et al.
] that found OTA concentrations in kidney and liver of 12.49 and 1.02 ppb, respectively in four-week-old piglets fed a contaminated diet with 117.45 ppb of OTA for 28 days. In an experiment carried out on adult pigs, Dall’Asta et al.
] showed that the administration of diets contaminated by OTA at 200 ppb for 40 days led to an average OTA content of 2.21 ppb in samples of raw ham muscle.
In contrast, Malagutti et al.
] reported OTA concentrations in piglet kidney, liver and semimembranous muscle of 69, 52 and 6.1 ng/g, respectively, after four months of administration of a contaminated diet at the dose of 25 ppb. In this case, OTA concentration in the diet was lower than in kidney and liver, but higher than in muscle.
These contrasting results could be mainly explained by differences in the duration of exposure of animals to contaminated diets, which is positively related to OTA in blood. This explanation is supported by the study of Stoev et al.
], in which the concentration of OTA in serum was higher in pigs fed OTA contaminated diet for six months than in those fed the same diet for three months.
The content of OTA in kidney and liver appears to be affected by the time occurring between the last ingestion of contaminated diet and the slaughter of animals. Jarczyk et al.
] showed that the average OTA content of blood, liver and kidney tended to be higher in pigs which had been fed for the last time five hours before slaughter than in those fed 18 hours before slaughter.
The highest OTA concentration is normally found in kidneys, mainly due to the higher blood flow/mass ratio in these organs compared to others such as liver or muscle. In addition, OTA is reabsorbed in all nephron segments and this fact delays its elimination, thus increasing the risk of OTA accumulation in kidney tissue [4
Since the 1970s, several studies have established the quantitative relationships between concentrations of OTA in various tissues of pigs [37
]. Based on this experimental evidence, Denmark established guidelines to control OTA levels in pork products in their slaughter houses. These guidelines determine that in the case of macroscopic changes, pig kidneys have to be analyzed for their OTA content and: (i) if the OTA in kidney is higher than 25 mg/kg, the whole carcass is rejected, because the meat is supposed to be highly contaminated; (ii) if the OTA in kidney is between 10 and 25 ppb, edible offals are eliminated; and (iii) if the OTA in kidney tissue is lower than 10 ppb, only the kidneys are discarded [99
Other European countries have also set guidelines to control the presence of OTA in edible pork tissues, such as Italy (1 ppb for pig meat and derived products, as maximum concentration allowed) and Estonia (10 ppb for pig liver) (FAO, 2004). Other countries, such as France, have done so in the past and are now developing monitoring plans of OTA occurrence in pig kidneys as a tool to evaluate the risk assessment for pork tissue consumers [100
During the last years, several surveys have been carried out in many European countries on OTA in blood and/or in edible tissues of pigs. The results are summarized in Table 4
A wide variation in the incidence of positive samples was observed. These results should be carefully evaluated by considering the limit of detection (LOD) and limit of quantification (LOQ) of the analytical methods used. Moreover, all authors of the surveys cited above suggested that the actual OTA concentration in pork tissues is generally lower than in other food sources and may not represent a health hazard for consumers. Despite that, all authors proposed the extension of the control system based on sampling pork tissues because it is important to keep OTA levels in pork products and, therefore, human OTA consumption as low as possible.
Ferrufino-Guardia et al.
reported the effective transfer of OTA from blood to milk in lactating rabbits, another monogastric livestock species, as a consequence of intake of contaminated diet (10–20 g/kg of body weight per day) [107
]. This study showed that OTA concentration in milk was positively related with its concentration in plasma and its ingested amounts. The high correlation of OTA in milk and in plasma suggests that the passage of this toxin from the bloodstream into the milk is by passive diffusion. In addition, this study showed that OTA accumulates in the kidney, liver, mammary gland and muscle of rabbit, as reported in other animal species.
Incidence of OTA in tissues of slaughtered pigs in different countries.
Incidence of OTA in tissues of slaughtered pigs in different countries.
|Tissue||No. samples||LOD (ppt)||LOQ (ppt)||Incidence of positives (%)||Mean of positives (ppt)||Range (ppt)||Country||Reference|
|muscle for ham||22||0.01||0.03||9||0.05||0.04–0.06||Italy|||
|muscle||54||0.01|| ||77.8||0.024|| ||Italy|
Bozzo et al.
] analyzed the OTA content in the liver, kidney, and muscles of 10 layer hens that received feed contaminated with OTA (ranging between 160 and 332 ppt) for at least two months in two farms. The highest OTA level was found in the kidneys (on average 13.65 ± 3.58 ppt, range: 8.7 to 16.9 ppt), whereas in liver it averaged 4.43 ± 0.64 ppt (range 3.7 to 5.1 ppt). OTA was not detected in muscles (LOD = 0.10 ppt). Similarly, in laying hens fed a diet contaminated by OTA at 2 mg/kg of feed for three weeks, Denli et al.
] found 15.1 μg/kg of OTA in the liver, but did not detect (LOD = 0.15 ppt) OTA residues in eggs.
When hens were fed diet containing OTA at 0.3 and 1 mg /kg of feed, Krogh et al.
] did not detect OTA in eggs. In contrast, Juszkiewicz et al.
] detected OTA in the eggs of laying hens fed OTA at 10 mg/kg of body weight. These results suggest that the passage of OTA from fed into eggs is possible, but only when OTA intake is very high. Therefore, the risk of OTA intake by humans as a consequence of eggs consumption is extremely low.
Also in poultry, Biró et al.
] reported that the residues of OTA accumulated in all organs, with high levels in liver and kidneys and low levels in muscle. In particular, in chickens fed 0.5 mg of OTA per animal weekly for four weeks, after the first two weeks of exposure, OTA was found at 0.28 and 0.20 ng/g in breast and thigh muscle, respectively. Then, OTA residue in muscle increased slightly, reaching its maximum value after four weeks, when the concentration of OTA was 0.84 ng/g in both white and red muscles.
So far, scientists seem not to be really interested in the study of OTA contamination occurrence in poultry. Probably this is mainly because in field conditions it is highly improbable that OTA contamination of poultry diets is high enough to cause residue accumulation of this toxin in meat.
However, since OTA in poultry tends to concentrate mainly in the liver, which is used for producing the Foie Gras in ducks and geese, it would be advisable to implement monitoring programs on OTA occurrence also on poultry edible tissues, as recently adopted in France [100
In several ruminant species, such as cattle, ovine and caprine, OTA transfer in meat and milk as a consequence of contaminated feed ingestion is a rather infrequent event in field conditions, being the toxin processed by rumen microorganisms into less toxic metabolites which are mainly excreted in urine and feces [57
However, under experimental conditions, transfer of OTA administered per os
in cow [84
] and goat [94
] milk has been reported since the 1970s. Ribelin et al.
] showed that a cow given a single dose of OTA at 13.3 mg/kg of body weight, excreted 4.5 mg of OTA in milk during following day, but the toxin was no longer detected in the milk produced afterwards. On the other hand, in cows given OTA 1.66 mg/kg of body weight/d for four days, traces of toxin were detected in milk on days three, four and five; however, for doses of 0.2 or 0.75 mg/kg of body weight, OTA was never detected in milk during the experiment.
Nip and Chu [94
] showed that when two lactating goats were given a single oral dose of 3H-OTA (0.5 mg/kg of body weight), only 0.026% of the toxin was found in milk during the following seven days.
A further confirm of the low transfer of OTA from diet into meat was reported by Shreeve et al.
]. In particular, when two adult cows were administered concentrate diets containing 0.317–1.125 mg of OTA/kg for 11 weeks before slaughter, no residues of OTA were detected in muscle, liver, kidney, serum, milk or urine. Just for one cow, OTA residues (about 5 ppt) were found in kidneys.
During the last decades, other studies have been conducted to confirm the ability of ruminants to degrade OTA, to reduce its passage into the bloodstream and to minimize toxic effects in the food chain.
Xiao et al.
] confirmed an efficient ruminal OTA hydrolysis in sheep in a trial carried out on four female Suffolk sheep given a single dose of OTA (0.5 mg/kg of body weight). Moreover, the amount of OTA reaching the bloodstream was much lower in hay-fed than in grain-fed sheep.
OTA bioavailability in the bloodstream of sheep was confirmed by Höhler et al.
]. Wethers fed 2 mg of OTA/kg feed for four weeks showed a constant blood content of the toxin (about 10 ng/mL) throughout the trial. For a higher level of contamination (5 mg of OTA/kg of feed), the concentration of the toxin in blood increased markedly together with a higher variability (67 to 112 ng/mL of serum).
Even if the transfer of OTA from feed into milk of lactating ruminants has not been clearly demonstrated, few surveys have been carried out to verify the occurrence of OTA in cow milk. Valenta and Goll [112
], analyzing 121 samples of cow milk collected in northern Germany (LOD = 0.01 ng/mL), did not find OTA in all analyzed samples. In contrast, other authors reported the occurrence of OTA in cow milk. For example, Breitholtz-Emanuelsson et al.
] found that five out of 36 cow milk samples collected in Sweden were contaminated by OTA (range of 10–40 ng/L). Similarly, in a survey on Norwegian conventional and organic dairy cow farms, Skaug [114
] detected OTA in six out of 40 conventional (ranging from 11 to 58 ng/L), and in five out of 47 organic (ranging from 15 to 28 ng/L) milk samples, respectively. Moreover, no statistically significant differences were found in OTA content between milk samples produced in organic or conventional farms. More recently, Boudra et al.
] studied OTA occurrence in milk produced in French dairy cow herds during 2003 summer and winter 2003. The toxin was detected in three out of 264 samples, at low levels (5.0, 6.0 and 6.6 ng/L).
Low frequency of OTA occurrence and concentration reported in the above cited studies suggest that, even if milk can be a possible source of this toxin for human diet, it does not represent a particular risk for adult consumers. However, OTA presence in milk may represent a danger for some categories such as children, who consume large amounts of milk.
Ocratoxicosis may occur in farms where feeds are contaminated by OTA. The risk of contamination is high for cereals and other grains, depending on environmental conditions during crop production and storage, whereas it is low in all kind of forages.
OTA contaminated feed affects primarily animal metabolism and health. Under field conditions, less intense effects have been reported for productive and reproductive performances and on product quality and safety. Among livestock, monogastric species are more susceptible to OTA than poligastric ones, due to the combined effect of increased exposure to contaminated feeds and the lack of detoxification by the rumen.
Pigs show a significant and linear reduction of daily gain with increasing doses of ingested OTA. In this species, OTA tends to accumulate in kidneys and, to a lesser extent, in the liver. This may represent a potential danger for human food chain. Indeed, the occurrence of OTA in fat and muscle has been extensively documented as well. However, observed toxin concentrations in pork edible tissues are generally low compared with other food sources and does not represent a health hazard for consumers.
Poultry are less sensitive to OTA than pigs because of their higher efficiency in excreting the toxin. Nevertheless, several experiments show a reduction in performance mainly due to the negative action of the toxin in various organs and metabolic pathways. In broilers, as concentration of toxin in the feed and time of exposure increase, daily growth decreases. Similarly, laying hens reduce eggs weight and production as OTA concentration in feed and time of exposure increase. Poultry accumulate OTA in meat and in eggs in relevant amounts only if exposed to high levels of feed contamination, rather unlikely to find under field conditions. An exception might be represented by food like the French Fois Gras, because OTA tends to accumulate in liver at concentrations even higher than those in feeds given to ducks or geese.
Cattle, sheep and goats are able to degrade OTA in rumen mainly through the action of protozoa thus acute poisoning seems to be an infrequent event under field conditions. Rumen functionality represents the main barrier to the passage of toxin into the bloodstream, so that the correct feeding of animals is the main preventive action against ocratoxicosis. Even if ruminants ingest OTA contaminated feed, the concentration of OTA in their main products remains either below the limits of detection/quantification or under the threshold of risk for consumer health.
In conclusion, feed contamination with OTA is a problem almost exclusively of monogastric livestock, mainly due to the economic losses caused by the reduction of production performances, to the negative impact on animal health and welfare, and to the possibility of toxin transfer into edible tissues of intoxicated animals