**3. Presence of mycotoxins and their toxicity in fish**

If the risk to humans by consuming fish products is to be calculated, the first step would be to estimate the uptake and retention of mycotoxins in different fish

**Figure 1.** *Exposure routes and factors influencing mycotoxin retention in fish.*

species and in different parts of the fish (**Figure 1**). Therefore, the following sections will summarize what is known about chemical characteristics in fish bodies and the toxicity in the animals resulting from the most important mycotoxins.

DON has a mean lowest-observable effect level (LOEL) in fish of 3541 ± 776 μg/ kg (±SEM; **Figure 2**), whereas the contamination levels in commercial fish feeds range from 0 to 825 μg/kg [27, 28, 41]. Similar to findings in chickens, DON appears to be excreted rapidly by carp (*Cyprinus carpio*), leaving no relevant residues in the edible parts [42, 43]. FB1 metabolization also occurs quickly in chicken and the remaining values in tissues stay low. However, exact information on the kinetics or biotransformation of fumonisins in fish is not available [44, 45]. Due to this and the large differences in the toxicity of fumonisins in fish (**Figure 2**), no exact risk can be calculated for farmed fish [1]. Typical disorders in higher vertebrates resulting from FB1 exposure have often been linked to the disruption of the sphingolipid metabolism [46], and similar effects have also been observed in fish [47]. Nevertheless, a low potential risk has been assumed for most vertebrates, with the exception of pigs [45]. Despite the fact that the guidance values for fumonisins in complete fish feeds have been set by the European Commission and the US to 10 mg/kg based, some countries have chosen to set different guidance levels [48, 49]. Although FB1 can affect fish at low concentrations, for example in carp (exposed to 500 μg/kg [50, 51]), the concentration range of the lowest-observable effects in fish is relatively broad, with a mean range of 26,480 ± 7124 μg/kg (±SEM; **Figure 2**), a level that is not achieved for either actual or estimated natural contamination of fish feeds [1, 52].

Previous studies have reported lethal concentrations of OTA that lead to 50% mortality (LC50) ranging from 2 to 58 mg/kg body weight in various higher vertebrate species [53, 54]. Fish species appear to be particularly sensitive to OTA, and since disposition appears to mainly take place in the kidneys of fish and not in muscles [55], this not only affects its toxicity, but is also relevant for food safety. High sensitivity to OTA in fish has been demonstrated in several studies. The LC50 value for OTA in adult seabass (*Dicentrarchus labrax* L.) was found to be 280 μg/kg body weight [56], 360 μg/l for zebrafish (*Danio rerio*) embryos [57], and 5.53 mg/kg

**21**

these assumptions.

**Figure 2.**

*species exposed to MON.*

*Food Safety: The Risk of Mycotoxin Contamination in Fish*

body weight in rainbow trout (*Oncorhynchus mykiss*) [58]. However, the route of exposure may play a role when comparing these different studies. Furthermore, the absorption efficiency in the gut also determines the bioavailability of the mycotoxins in fish, as has been demonstrated for oral exposure to OTA in common carp [59]. If the LOEL for exposure of fish to OTA are summarized (**Figure 2**), the mean range is 1077 ± 566 μg/kg (±SEM), which indicates that the currently recommended guidance value for OTA in cereals and cereal products intended for animal feed of 250 μg/kg does not protect fish from potential damage [48]. This is in stark contrast

*Variability in mycotoxin toxicity for fish, as shown by the differences in the lowest-observable effect levels (LOEL) in different fish species. References: 92 studies for AFB1 [63, 64, 70–149] comprising 21 different fish species, 7 studies for OTA [56–58, 94, 150–152] comprising 5 fish species, 15 studies for FB1 [47, 50, 51, 153–165] reporting levels for 7 fish species, 12 studies for DON [42, 144, 166–175] yielding information for 5 different fish species, 10 studies for ZEN [144, 176–184] reporting LOEL for 5 different species, 10 studies [185–193] reporting effects of different levels of T-2 toxins on 4 different fish species, and 3 studies [162, 194, 195] for 3 different* 

to the guidance level of 20 μg/kg that exists in some non-EU countries [49].

ZEN has a mean toxicity value of 2389 ± 1285 μg/kg (±SEM), based on the LOEL calculations for five different fish species shown in **Figure 2**. Although the number of studies reporting effects of ZEN in fish is very limited, they may indicate that fish are more sensitive to water-borne ZEN than to dietary ZEN, which is why the mean LOEL level, including both, dietary and water-borne exposure for fish, shows quite a high standard error of the mean. ZEN concentrations above the LOEL levels in water samples have not been reported for aquatic environments [36–38]. Although the actual ZEN contamination of commercial fish feeds appears not to exceed the current guidance level for this mycotoxin in cereals and cereal products in the EU of 2000 μg/kg [27, 48], dietary exposure to this mycotoxin may still do harm to farmed fish. The guidance values in other countries that recommend maximum ZEN levels of 20–1000 μg/kg have a higher probability of protecting fish from damage [49], since the ZEN levels in fish feeds often do not exceed concentrations of 200 μg/kg [27, 60]. Nevertheless, more exact reports on ZEN toxicity in fish and the actual contamination levels in commercial fish feeds are needed to support

T-2 toxin has a mean toxicity of 3201 ± 1236 μg/kg (±SEM) in fish, based on the currently available LOEL for different fish species (**Figure 2**). This level is considerably higher than the actual contamination level found in salmonid fish feed

*DOI: http://dx.doi.org/10.5772/intechopen.89002*

#### *Food Safety: The Risk of Mycotoxin Contamination in Fish DOI: http://dx.doi.org/10.5772/intechopen.89002*

#### **Figure 2.**

*Mycotoxins and Food Safety*

**Figure 1.**

species and in different parts of the fish (**Figure 1**). Therefore, the following sections will summarize what is known about chemical characteristics in fish bodies and the

DON has a mean lowest-observable effect level (LOEL) in fish of 3541 ± 776 μg/ kg (±SEM; **Figure 2**), whereas the contamination levels in commercial fish feeds range from 0 to 825 μg/kg [27, 28, 41]. Similar to findings in chickens, DON appears to be excreted rapidly by carp (*Cyprinus carpio*), leaving no relevant residues in the edible parts [42, 43]. FB1 metabolization also occurs quickly in chicken and the remaining values in tissues stay low. However, exact information on the kinetics or biotransformation of fumonisins in fish is not available [44, 45]. Due to this and the large differences in the toxicity of fumonisins in fish (**Figure 2**), no exact risk can be calculated for farmed fish [1]. Typical disorders in higher vertebrates resulting from FB1 exposure have often been linked to the disruption of the sphingolipid metabolism [46], and similar effects have also been observed in fish [47]. Nevertheless, a low potential risk has been assumed for most vertebrates, with the exception of pigs [45]. Despite the fact that the guidance values for fumonisins in complete fish feeds have been set by the European Commission and the US to 10 mg/kg based, some countries have chosen to set different guidance levels [48, 49]. Although FB1 can affect fish at low concentrations, for example in carp (exposed to 500 μg/kg [50, 51]), the concentration range of the lowest-observable effects in fish is relatively broad, with a mean range of 26,480 ± 7124 μg/kg (±SEM; **Figure 2**), a level that is not achieved for either actual or estimated natural contamination of fish feeds [1, 52]. Previous studies have reported lethal concentrations of OTA that lead to 50% mortality (LC50) ranging from 2 to 58 mg/kg body weight in various higher vertebrate species [53, 54]. Fish species appear to be particularly sensitive to OTA, and since disposition appears to mainly take place in the kidneys of fish and not in muscles [55], this not only affects its toxicity, but is also relevant for food safety. High sensitivity to OTA in fish has been demonstrated in several studies. The LC50 value for OTA in adult seabass (*Dicentrarchus labrax* L.) was found to be 280 μg/kg body weight [56], 360 μg/l for zebrafish (*Danio rerio*) embryos [57], and 5.53 mg/kg

toxicity in the animals resulting from the most important mycotoxins.

*Exposure routes and factors influencing mycotoxin retention in fish.*

**20**

*Variability in mycotoxin toxicity for fish, as shown by the differences in the lowest-observable effect levels (LOEL) in different fish species. References: 92 studies for AFB1 [63, 64, 70–149] comprising 21 different fish species, 7 studies for OTA [56–58, 94, 150–152] comprising 5 fish species, 15 studies for FB1 [47, 50, 51, 153–165] reporting levels for 7 fish species, 12 studies for DON [42, 144, 166–175] yielding information for 5 different fish species, 10 studies for ZEN [144, 176–184] reporting LOEL for 5 different species, 10 studies [185–193] reporting effects of different levels of T-2 toxins on 4 different fish species, and 3 studies [162, 194, 195] for 3 different species exposed to MON.*

body weight in rainbow trout (*Oncorhynchus mykiss*) [58]. However, the route of exposure may play a role when comparing these different studies. Furthermore, the absorption efficiency in the gut also determines the bioavailability of the mycotoxins in fish, as has been demonstrated for oral exposure to OTA in common carp [59]. If the LOEL for exposure of fish to OTA are summarized (**Figure 2**), the mean range is 1077 ± 566 μg/kg (±SEM), which indicates that the currently recommended guidance value for OTA in cereals and cereal products intended for animal feed of 250 μg/kg does not protect fish from potential damage [48]. This is in stark contrast to the guidance level of 20 μg/kg that exists in some non-EU countries [49].

ZEN has a mean toxicity value of 2389 ± 1285 μg/kg (±SEM), based on the LOEL calculations for five different fish species shown in **Figure 2**. Although the number of studies reporting effects of ZEN in fish is very limited, they may indicate that fish are more sensitive to water-borne ZEN than to dietary ZEN, which is why the mean LOEL level, including both, dietary and water-borne exposure for fish, shows quite a high standard error of the mean. ZEN concentrations above the LOEL levels in water samples have not been reported for aquatic environments [36–38]. Although the actual ZEN contamination of commercial fish feeds appears not to exceed the current guidance level for this mycotoxin in cereals and cereal products in the EU of 2000 μg/kg [27, 48], dietary exposure to this mycotoxin may still do harm to farmed fish. The guidance values in other countries that recommend maximum ZEN levels of 20–1000 μg/kg have a higher probability of protecting fish from damage [49], since the ZEN levels in fish feeds often do not exceed concentrations of 200 μg/kg [27, 60]. Nevertheless, more exact reports on ZEN toxicity in fish and the actual contamination levels in commercial fish feeds are needed to support these assumptions.

T-2 toxin has a mean toxicity of 3201 ± 1236 μg/kg (±SEM) in fish, based on the currently available LOEL for different fish species (**Figure 2**). This level is considerably higher than the actual contamination level found in salmonid fish feed in South America [28], and much lower than the guidance levels of 250 mg/kg for T-2 toxin set by the European Commission for cereal products in compound feeds [61] and individual recommendations in other countries (max. 80–100 mg/kg) for T-2 toxin in complete feed and all grains [49]. From these data, it can be assumed that fish do not regularly suffer from T-2 toxicity, and there have been no reports of accumulation of this mycotoxin in edible parts of the fish.

The situation for AFB1 is, however, quite different. The mean LOEL for fish has been calculated to be 1248 ± 275 μg/kg (±SEM) (**Figure 2**). However, AFB1 appears to be readily absorbed by the intestine [62] and a LOEL of less than 1 μg/kg has been observed in Nile tilapia (*Oreochromis niloticus*) and rainbow trout [63, 64], which shows that this mycotoxin can be a problem for farmed fish. In commercial fish feeds, AFB1 levels are commonly less than 10 μg/kg [65, 66], but may be considerably higher in some cases [67–69]. Critical levels for fish have been estimated to be a mean of 4.30 μg/kg in commercial feeds [1], which indicates that farmed fish are exposed to a risk from AFB1 intoxication.

Less information is available on the toxicity of ENNs and BEA in fish, but from initial experiments it can be assumed that at least some ENN toxins have toxic effects on zebrafish embryos (unpublished results, C. Pietsch). However, how relevant this toxicity is in comparison to the actual ENN contamination in commercial feeds remains unclear. Similar to other emerging mycotoxins, these substances have already been detected in the plasma of pigs after exposure to ENNs [196], indicating that the uptake of these substances occurs in vertebrates. In addition, it has been shown that food processing affects the presence on ENNs and BEA in bread [197, 198], and thermal processes, in particular, also appear to influence the ENN content in fish tissue [199]. Finally, the presence of high ENN and BEA levels in feed ingredients appears to overestimate the actual risk of fish feed contamination and the potential effects on farmed fish [1]. Thus, more research is needed on the toxicology and the biotransformation of ENNs and BEA in vertebrates.

An issue that also makes mycotoxin research difficult is the fact that we do not know enough about mycotoxin mixtures and their effects. Natural contamination of feed ingredients leads to the occurrence of several mycotoxins at the same time and their interactions remain mostly unknown.
