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Long-Term Administration of Low Doses of Mycotoxins in Poultry
ENVIRONMENT AND HEALTH Long-Term Administration of Low Doses of Mycotoxins in Poultry. 1. Residues of Ochratoxin A in Broilers and Laying Hens C. MICCO,1 M. MIRAGLIA,' R. ONORI,1 A. IOPPOLO,2 and A. MANTOVANI3 Istituto Superiore di Sanitd, Viale Regina Elena 299, 00161 Rome, Italy (Received for publication October 21, 1985)
1987 Poultry Science 6 6 : 4 7 - 5 0 INTRODUCTION
Ochratoxin A (OA), a dehydroisocoumarin derivative, is a nephrotoxic secondary metabolite of Aspergillus ochraceus and of Penicillium viridicatum. It occurs as a natural contaminant, especially in grains [Chu, 1974; Krogh, 1978; World Health Organization (WHO), 1979] used for animal feed. Kidneys have been recognized as the main target organs of OA even in field situations (Krogh et al., 1974; WHO, 1979). It is well-known that OA can be carried over into animal products and, therefore, implications for human health are receiving increasing attention. This toxin is not sufficiently destroyed during the processing and cooking of food (Trenk et al., 1971; Josefsson and Moller, 1980). Madsen et al. (1982) and Mortensen et al. (1983) investigated occurrence of OA residues in pigs after feeding them with OA-contaminated feed, and Krogh et al. (1976) studied the timedependent disappearance of OA residues in tissues of pigs. Prior and Sisodia (1978) and Prior et al. (1980) studied the effect of OA-contaminated feed (down to .5 ppm) on residues in broilers and White Leghorn hens, and Frye and
'Laboratorio Alimenti. Servizio Stabulario. 3 Laboratorio Tossicologia Comparata ed Ecotossicologia. 2
47
Chu (1977) studied the distribution of OA in chicken tissues and eggs. This work was to investigate the occurrence and amount of residues of OA in broiler chickens and laying hens after long-term administration of doses of OA approximating the range of natural contamination in feed (WHO, 1979; Krogh, 1978). These amounts are unlikely to lead either to clinical disease or to gross lesions, causes of rejection by meat inspectors (Elling etal., 1975).
MATERIALS AND METHODS
Feeding Trial. Ninety-seven male and 68 female day-old Hubbard chickens were purchased (Ilari, Ascoli Piceno). They were kept in floor pens and fed with standard nutritional programs for broilers and laying hens, respectively. Broilers and hens were fed standard rations. Total individual feed consumption from the start of contamination to slaughter was 8 kg for broilers and 12.5 kg for hens. At 14 days of age, chickens were subdivided into groups as shown in Table 1. Treated chickens were fed the same diet as the controls except that the treatment diet was uniformly mixed with an ethanolic solution of OA (Fluka AG) to give 50 ppb OA. Groups 1 (broilers) and 4 hens were administered OA in the feed until slaughter, whereas Groups 2 and 5 were withdrawn from contami-
Downloaded from http://ps.oxfordjournals.org/ at New York University on October 19, 2014
ABSTRACT The occurrence and amount of residues of ochratoxin A (OA) in poultry tissues and organs were investigated in a trial aimed at measuring the effects of contamination approaching the patterns more frequently found in natural situations (i.e., small doses of OA in the diet for long periods). Hubbard male broilers and laying hens were treated with an OA-contaminated feed (50 ppb) from the 14th day of age onward. Both groups were further divided into subgroups, some of which underwent continual treatment (64 and 169 days, respectively) and others that were withdrawn from administration (maximum 28 and 82 days, respectively). Determination of residues was performed by high performance liquid chromatography. Residues in liver were higher in broilers (up to 11.0 ppb) than in hens (1.5 ppb), whereas the reverse occurred in kidney (up to .8 and 5.8 ppb, respectively). Residues (.8 ppb) were also in hen thigh muscle but not in breast muscle. Residues of OA in poultry appear to be of possible public health concern. Suggestions for monitoring are given. (Key words: ochratoxin A, poultry, residues of ochratoxin A)
48
MICCO ET AL.
RESULTS
Treated animals did not show clinical signs of OA intoxication or significant gross lesions, although livers and kidneys of Groups 1,4, and 5 appeared slightly discolored (data not shown).
Average body and liver weights are shown in Table 2. Final weights of treated animals were higher than those of controls. Residues of OA in organs and tissues of animals are shown in Table 3. DISCUSSION
A large batch of broilers and laying hens was administered OA-contaminated feed at a low dose (50 ppb) for a long period, thus approximating a possible field situation. This treatment had no adverse effect either on weight gain or on general health except for slight discoloration of the liver and kidneys of Groups 1, 4, and 5; in particular, all treated animals gained more weight than controls. These results are in agreement with those of Prior and Sisodia (1978), who found that no weight depression with 1 ppm OA in feed. However, the significance of these results is still to be assessed. Treated animals would have passed normal meat inspection procedures at the abattoir. As shown in Table 3, residues of OA at 50 ppb in feed were present in liver, kidney, and skin and even in the red muscle (thigh) of the groups not withdrawn from contamination. No OA was detected in any organs and tissues from the control groups. Residues in liver and kidney
TABLE 1. Treatment of animals
Group
Male broilers la lb 2a 2b 3 Control 1 Laying hens 4
Dose ochratoxin A in feed
Total individual consumption of contaminated feed
(ppb)
(kg)
Number of animals
Days of administration
50 50
3.8 8.0
10 23
36 64
50 50
3.8 3.8
7 7
36 36
0 50
Days of withdrawal from treatment
14 28
50 12.5
15
169
5a
50
7.0
10
87
33
5b
50
7.0
13
87
82
6 Control 1
0
30
Both control groups underwent the same feeding program as treated groups.
Downloaded from http://ps.oxfordjournals.org/ at New York University on October 19, 2014
nation at Days 36 and 87, respectively. A corresponding number of control animals was slaughtered at the same time as treated chickens. Animals were sacrificed by jugular excision. Liver, kidney, plucked breast skin, breast muscle, thigh muscle, and abdominal fat were collected. Body and liver weights were recorded and meat inspection procedures were performed. Organs and tissues were pooled and kept frozen at -20 C until analyzed. Determination of Ochratoxin A. Extraction and determination of OA in organs and tissues were performed following the method of Hunt (1979), with slight modifications. Ochratoxin A determination was performed by high performance liquid chromatography using a C, 8 column (RP 18 Lichrosorb, Merck) instead of a C 22 column. The detector was a Waters fluorescence detector 420 with filters 338 and 455 for emission and excitation, respectively. Postcolumn derivatization, as used by Hunt (1979), was omitted.
OCHRATOXIN A IN BROILERS AND LAYERS
49
TABLE 2. Average body weights and weight of livers as a percentage of total body weight of male broilers and laying hens treated with Ochratoxin A contaminated feed (40 ppb) and of corresponding controls
Days of treatment
Group
Days of withdrawal from treatment
Average body weight
(%)
(g)
2.24 2.14 1.59 1.86
852.0 824.2 1,639.1 1.497.3
± 48.7 ± 30.9 ± 145.8* + 108.6
1.73 2.44 1.60 1.86
1.282.4 1,255.9 1.691.4 1,497.3
± 83.6 ± 171.4 ± 120.3* ± 108.6
2.40 2.04
1,841.9 ± 114.3* 1,632.0 ± 91.3
Male broilers la Control lb Control
36 0 64 0
2a Control 2b Control
36 0 36 0
Laying hens 4 Control
169 0
5a Control
87 0
33
1.65 2.14
1,549.0 ± 65.1 1,629.0 ± 105.6
5b Control
87 0
82
2.03 2.04
1.771.5 ± 125.6* 1,632.0 ± 91.3
14 28
•Significantly different from the corresponding control (P<.05).
TABLE 3. OA residues (ppb) in organs and tissues of broilers and laying bens administered with Ochratoxin A (OA) contamined feed (50 ppb) and control
Group
Days of treatment
Days of withdrawal from treatment
Liver
Kidney
Thigh
Breast
Skin
Abdominal fat
(ppv; Male broilers la lb 2a 2b 3 Control 2 Laying hens 4 5a 5b
36 64 36 36
169 87 87
14 28
33 82
6 Control 2 1 2
5.0 11.0
Traces .8
Traces ND 1 Traces ND
ND 2.0
ND ND
Traces ND
ND ND
ND ND
ND ND
1.0 ND
ND ND
ND
ND
ND
ND
ND
ND
1.5
5.8
.8
ND
1.8
ND
.9 ND
3.7 ND
ND ND
ND ND
.7 ND
ND ND
ND
ND
ND
ND
ND
ND
ND = Nondetectable amounts.
As no detectable amounts were found in any control group, all control broilers and laying hens are included in Groups 3 and 6, respectively.
Downloaded from http://ps.oxfordjournals.org/ at New York University on October 19, 2014
Average liver weight/ body weight
50
MICCO ET AL.
eggs and to discover possible interactions between different mycotoxins. ACKNOWLEDGMENTS
The authors are grateful to M. Alessandrini, C. Laconi, V. Masciocchi, A. Romeo, and L. Strangio for their technical support and assistance. REFERENCES Chu, F. S., 1974. Studies on ochratoxins. CRC Crit. Rev. Toxicol. 2:499-524. Elling, F., B. Hald, C. Jacobsen, and P. Krogh, 1975. Spontaneous toxic nephropathy in poultry associated with ochratoxin A. Acta Pathol. Microbiol. Scand. Sect. A Pathol. 83:739-741. Frye C. E., and F. S. Chu, 1977. Distribution of ochratoxin A in chicken tissues and eggs. J. Food Safety 1(2): 147159. Hunt D. C , L. A. Philp, and N. T. Crosby, 1979. Determination of ochratoxin A in pig kidney using enzymic digestion, dialysis and high-performance liquid chromatography with post-column derivetization. Analyst 104:1171-1175. Josefsson B.G.E., andT. E. Moller, 1980. Heat stability of ochratoxin A in pig products. J. Sci. Food Agric. 31:1313-1315. Krogh P., 1978. Causal association of mycotoxic nephropathy. Acta Pathol. Microbiol Scand. Sect A, Suppl. 269:1-28. Krogh P., N. H. Axelsen, F. Elling, N. Gyrd-Hansen, B. Hald, J. Hyldgaard-Jensen, A. E. Larsen, A. Madsen, H. P. Mortesen, T. Moller, O. K. Petersen, V. Ravnskov, M. Rostgaard, and 0 . Aalund, 1974. Experimental porcine nephropathy. Acata Pathol. Microbiol. Scand. Sect. A Suppl. 246:1-21. Krogh P., F. Elling, B. Hald, A. E. Larsen, E. B. Lillehoj, A. Madsen, and H. P. Mortensen, 1976. Time dependent disappearance of ochratoxin A residues in tissues of bacon pigs. Toxicology 6:235-242. Madsen A., H. P. Mortensen, and B. Hald, 1982. Feeding experiments with ochratoxin A contaminated barley for bacon pigs. I Influence on pig performance and residues. Acta Agric. Scand. 32:225-239. Mortensen H. P., B. Hald, A. E. Larsen, and A. Madsen, 1983. Ochratoxin A contaminated barley for sows and piglets. Pig performance and residues in milk and pigs. Acta Agric. Scand. 33:349-352. Prior M. G., J. B. O'Neil, and C. S. Sisodia, 1980. Effects of ochratoxin A on growth response and residues in broilers. Poultry Sci. 59:1254-1257. Prior M. G., and C. S. Sisodia, 1978. Ochratoxicosis in White Leghorn Hens. Poultry Sci. 57:619-623. Trenk H. L., M. E. Butz, and F. S. Chu, 1971. Production of ochratoxins in different cereal products by Aspergillus ochraceus. Appl. Microbiol. 21:1032-1035. World Health Organization Environment Health Criteria Geneva, 1979. Mycotoxins.
Downloaded from http://ps.oxfordjournals.org/ at New York University on October 19, 2014
showed a greater tendency to accumulate in broilers than in layers slaughtered immediately after treatment. However, residues disappeared more quickly in broilers (Groups 2a,b) than in laying hens (Groups 5a,b). Results of the Groups 2 and 5 (those slaughtered after withdrawal of contaminated feed) show that OA residues disappear when the animal is kept on a OA-free diet. This process seems more rapid in broilers than in hens. Considerable differences were found between male broilers and hens: hens showed markedly less residue in liver despite the longer treatment. In contrast, residues in kidney and thigh muscle were higher in hens than in broilers. White muscle (breast) and fat were always free from residues. Further research is required to evaluate whether differences between broilers and hens are due to different metabolic pathways or to dietary factors. Public Health Concerns. Our results may arouse public health concern about OA residues in poultry, and it should be kept in mind that poultry livers and kidneys are frequently used as human food in many countries (e.g. Italy). The following recommendations are made. 1) Poultry feed should be monitored and maximum acceptable levels of OA should be established. In Italy there are still no regulations governing amount of OA either in feed or in human food, but other countries (Belgium, Denmark, USSR) have already set a limit for this mycotoxin. For instance, in Denmark a swine carcass is condemned when OA residues in kidney exceed 25 ppb (Madsen et al., 1982); 2) Levels of residues and their toxicity suggest that it may be worth setting up OA monitoring programs at abattoir plants. In conclusion, our results show that liver and kidney are the organs of choice to monitor for ochratoxin A residues in broilers and hens, respectively. The significance of the high levels of OA in skin deserves further investigation because of the (remote) possibility of external contamination during the feeding trial. Collection and analysis abattoir samples may be useful to reveal the presence of potentially harmful residues in poultry feed and to reject carcasses unfit for human consumption. Further research is underway to determine residues in
1987 Poultry Science 6 6 : 4 7 - 5 0 INTRODUCTION
Ochratoxin A (OA), a dehydroisocoumarin derivative, is a nephrotoxic secondary metabolite of Aspergillus ochraceus and of Penicillium viridicatum. It occurs as a natural contaminant, especially in grains [Chu, 1974; Krogh, 1978; World Health Organization (WHO), 1979] used for animal feed. Kidneys have been recognized as the main target organs of OA even in field situations (Krogh et al., 1974; WHO, 1979). It is well-known that OA can be carried over into animal products and, therefore, implications for human health are receiving increasing attention. This toxin is not sufficiently destroyed during the processing and cooking of food (Trenk et al., 1971; Josefsson and Moller, 1980). Madsen et al. (1982) and Mortensen et al. (1983) investigated occurrence of OA residues in pigs after feeding them with OA-contaminated feed, and Krogh et al. (1976) studied the timedependent disappearance of OA residues in tissues of pigs. Prior and Sisodia (1978) and Prior et al. (1980) studied the effect of OA-contaminated feed (down to .5 ppm) on residues in broilers and White Leghorn hens, and Frye and
'Laboratorio Alimenti. Servizio Stabulario. 3 Laboratorio Tossicologia Comparata ed Ecotossicologia. 2
47
Chu (1977) studied the distribution of OA in chicken tissues and eggs. This work was to investigate the occurrence and amount of residues of OA in broiler chickens and laying hens after long-term administration of doses of OA approximating the range of natural contamination in feed (WHO, 1979; Krogh, 1978). These amounts are unlikely to lead either to clinical disease or to gross lesions, causes of rejection by meat inspectors (Elling etal., 1975).
MATERIALS AND METHODS
Feeding Trial. Ninety-seven male and 68 female day-old Hubbard chickens were purchased (Ilari, Ascoli Piceno). They were kept in floor pens and fed with standard nutritional programs for broilers and laying hens, respectively. Broilers and hens were fed standard rations. Total individual feed consumption from the start of contamination to slaughter was 8 kg for broilers and 12.5 kg for hens. At 14 days of age, chickens were subdivided into groups as shown in Table 1. Treated chickens were fed the same diet as the controls except that the treatment diet was uniformly mixed with an ethanolic solution of OA (Fluka AG) to give 50 ppb OA. Groups 1 (broilers) and 4 hens were administered OA in the feed until slaughter, whereas Groups 2 and 5 were withdrawn from contami-
Downloaded from http://ps.oxfordjournals.org/ at New York University on October 19, 2014
ABSTRACT The occurrence and amount of residues of ochratoxin A (OA) in poultry tissues and organs were investigated in a trial aimed at measuring the effects of contamination approaching the patterns more frequently found in natural situations (i.e., small doses of OA in the diet for long periods). Hubbard male broilers and laying hens were treated with an OA-contaminated feed (50 ppb) from the 14th day of age onward. Both groups were further divided into subgroups, some of which underwent continual treatment (64 and 169 days, respectively) and others that were withdrawn from administration (maximum 28 and 82 days, respectively). Determination of residues was performed by high performance liquid chromatography. Residues in liver were higher in broilers (up to 11.0 ppb) than in hens (1.5 ppb), whereas the reverse occurred in kidney (up to .8 and 5.8 ppb, respectively). Residues (.8 ppb) were also in hen thigh muscle but not in breast muscle. Residues of OA in poultry appear to be of possible public health concern. Suggestions for monitoring are given. (Key words: ochratoxin A, poultry, residues of ochratoxin A)
48
MICCO ET AL.
RESULTS
Treated animals did not show clinical signs of OA intoxication or significant gross lesions, although livers and kidneys of Groups 1,4, and 5 appeared slightly discolored (data not shown).
Average body and liver weights are shown in Table 2. Final weights of treated animals were higher than those of controls. Residues of OA in organs and tissues of animals are shown in Table 3. DISCUSSION
A large batch of broilers and laying hens was administered OA-contaminated feed at a low dose (50 ppb) for a long period, thus approximating a possible field situation. This treatment had no adverse effect either on weight gain or on general health except for slight discoloration of the liver and kidneys of Groups 1, 4, and 5; in particular, all treated animals gained more weight than controls. These results are in agreement with those of Prior and Sisodia (1978), who found that no weight depression with 1 ppm OA in feed. However, the significance of these results is still to be assessed. Treated animals would have passed normal meat inspection procedures at the abattoir. As shown in Table 3, residues of OA at 50 ppb in feed were present in liver, kidney, and skin and even in the red muscle (thigh) of the groups not withdrawn from contamination. No OA was detected in any organs and tissues from the control groups. Residues in liver and kidney
TABLE 1. Treatment of animals
Group
Male broilers la lb 2a 2b 3 Control 1 Laying hens 4
Dose ochratoxin A in feed
Total individual consumption of contaminated feed
(ppb)
(kg)
Number of animals
Days of administration
50 50
3.8 8.0
10 23
36 64
50 50
3.8 3.8
7 7
36 36
0 50
Days of withdrawal from treatment
14 28
50 12.5
15
169
5a
50
7.0
10
87
33
5b
50
7.0
13
87
82
6 Control 1
0
30
Both control groups underwent the same feeding program as treated groups.
Downloaded from http://ps.oxfordjournals.org/ at New York University on October 19, 2014
nation at Days 36 and 87, respectively. A corresponding number of control animals was slaughtered at the same time as treated chickens. Animals were sacrificed by jugular excision. Liver, kidney, plucked breast skin, breast muscle, thigh muscle, and abdominal fat were collected. Body and liver weights were recorded and meat inspection procedures were performed. Organs and tissues were pooled and kept frozen at -20 C until analyzed. Determination of Ochratoxin A. Extraction and determination of OA in organs and tissues were performed following the method of Hunt (1979), with slight modifications. Ochratoxin A determination was performed by high performance liquid chromatography using a C, 8 column (RP 18 Lichrosorb, Merck) instead of a C 22 column. The detector was a Waters fluorescence detector 420 with filters 338 and 455 for emission and excitation, respectively. Postcolumn derivatization, as used by Hunt (1979), was omitted.
OCHRATOXIN A IN BROILERS AND LAYERS
49
TABLE 2. Average body weights and weight of livers as a percentage of total body weight of male broilers and laying hens treated with Ochratoxin A contaminated feed (40 ppb) and of corresponding controls
Days of treatment
Group
Days of withdrawal from treatment
Average body weight
(%)
(g)
2.24 2.14 1.59 1.86
852.0 824.2 1,639.1 1.497.3
± 48.7 ± 30.9 ± 145.8* + 108.6
1.73 2.44 1.60 1.86
1.282.4 1,255.9 1.691.4 1,497.3
± 83.6 ± 171.4 ± 120.3* ± 108.6
2.40 2.04
1,841.9 ± 114.3* 1,632.0 ± 91.3
Male broilers la Control lb Control
36 0 64 0
2a Control 2b Control
36 0 36 0
Laying hens 4 Control
169 0
5a Control
87 0
33
1.65 2.14
1,549.0 ± 65.1 1,629.0 ± 105.6
5b Control
87 0
82
2.03 2.04
1.771.5 ± 125.6* 1,632.0 ± 91.3
14 28
•Significantly different from the corresponding control (P<.05).
TABLE 3. OA residues (ppb) in organs and tissues of broilers and laying bens administered with Ochratoxin A (OA) contamined feed (50 ppb) and control
Group
Days of treatment
Days of withdrawal from treatment
Liver
Kidney
Thigh
Breast
Skin
Abdominal fat
(ppv; Male broilers la lb 2a 2b 3 Control 2 Laying hens 4 5a 5b
36 64 36 36
169 87 87
14 28
33 82
6 Control 2 1 2
5.0 11.0
Traces .8
Traces ND 1 Traces ND
ND 2.0
ND ND
Traces ND
ND ND
ND ND
ND ND
1.0 ND
ND ND
ND
ND
ND
ND
ND
ND
1.5
5.8
.8
ND
1.8
ND
.9 ND
3.7 ND
ND ND
ND ND
.7 ND
ND ND
ND
ND
ND
ND
ND
ND
ND = Nondetectable amounts.
As no detectable amounts were found in any control group, all control broilers and laying hens are included in Groups 3 and 6, respectively.
Downloaded from http://ps.oxfordjournals.org/ at New York University on October 19, 2014
Average liver weight/ body weight
50
MICCO ET AL.
eggs and to discover possible interactions between different mycotoxins. ACKNOWLEDGMENTS
The authors are grateful to M. Alessandrini, C. Laconi, V. Masciocchi, A. Romeo, and L. Strangio for their technical support and assistance. REFERENCES Chu, F. S., 1974. Studies on ochratoxins. CRC Crit. Rev. Toxicol. 2:499-524. Elling, F., B. Hald, C. Jacobsen, and P. Krogh, 1975. Spontaneous toxic nephropathy in poultry associated with ochratoxin A. Acta Pathol. Microbiol. Scand. Sect. A Pathol. 83:739-741. Frye C. E., and F. S. Chu, 1977. Distribution of ochratoxin A in chicken tissues and eggs. J. Food Safety 1(2): 147159. Hunt D. C , L. A. Philp, and N. T. Crosby, 1979. Determination of ochratoxin A in pig kidney using enzymic digestion, dialysis and high-performance liquid chromatography with post-column derivetization. Analyst 104:1171-1175. Josefsson B.G.E., andT. E. Moller, 1980. Heat stability of ochratoxin A in pig products. J. Sci. Food Agric. 31:1313-1315. Krogh P., 1978. Causal association of mycotoxic nephropathy. Acta Pathol. Microbiol Scand. Sect A, Suppl. 269:1-28. Krogh P., N. H. Axelsen, F. Elling, N. Gyrd-Hansen, B. Hald, J. Hyldgaard-Jensen, A. E. Larsen, A. Madsen, H. P. Mortesen, T. Moller, O. K. Petersen, V. Ravnskov, M. Rostgaard, and 0 . Aalund, 1974. Experimental porcine nephropathy. Acata Pathol. Microbiol. Scand. Sect. A Suppl. 246:1-21. Krogh P., F. Elling, B. Hald, A. E. Larsen, E. B. Lillehoj, A. Madsen, and H. P. Mortensen, 1976. Time dependent disappearance of ochratoxin A residues in tissues of bacon pigs. Toxicology 6:235-242. Madsen A., H. P. Mortensen, and B. Hald, 1982. Feeding experiments with ochratoxin A contaminated barley for bacon pigs. I Influence on pig performance and residues. Acta Agric. Scand. 32:225-239. Mortensen H. P., B. Hald, A. E. Larsen, and A. Madsen, 1983. Ochratoxin A contaminated barley for sows and piglets. Pig performance and residues in milk and pigs. Acta Agric. Scand. 33:349-352. Prior M. G., J. B. O'Neil, and C. S. Sisodia, 1980. Effects of ochratoxin A on growth response and residues in broilers. Poultry Sci. 59:1254-1257. Prior M. G., and C. S. Sisodia, 1978. Ochratoxicosis in White Leghorn Hens. Poultry Sci. 57:619-623. Trenk H. L., M. E. Butz, and F. S. Chu, 1971. Production of ochratoxins in different cereal products by Aspergillus ochraceus. Appl. Microbiol. 21:1032-1035. World Health Organization Environment Health Criteria Geneva, 1979. Mycotoxins.
Downloaded from http://ps.oxfordjournals.org/ at New York University on October 19, 2014
showed a greater tendency to accumulate in broilers than in layers slaughtered immediately after treatment. However, residues disappeared more quickly in broilers (Groups 2a,b) than in laying hens (Groups 5a,b). Results of the Groups 2 and 5 (those slaughtered after withdrawal of contaminated feed) show that OA residues disappear when the animal is kept on a OA-free diet. This process seems more rapid in broilers than in hens. Considerable differences were found between male broilers and hens: hens showed markedly less residue in liver despite the longer treatment. In contrast, residues in kidney and thigh muscle were higher in hens than in broilers. White muscle (breast) and fat were always free from residues. Further research is required to evaluate whether differences between broilers and hens are due to different metabolic pathways or to dietary factors. Public Health Concerns. Our results may arouse public health concern about OA residues in poultry, and it should be kept in mind that poultry livers and kidneys are frequently used as human food in many countries (e.g. Italy). The following recommendations are made. 1) Poultry feed should be monitored and maximum acceptable levels of OA should be established. In Italy there are still no regulations governing amount of OA either in feed or in human food, but other countries (Belgium, Denmark, USSR) have already set a limit for this mycotoxin. For instance, in Denmark a swine carcass is condemned when OA residues in kidney exceed 25 ppb (Madsen et al., 1982); 2) Levels of residues and their toxicity suggest that it may be worth setting up OA monitoring programs at abattoir plants. In conclusion, our results show that liver and kidney are the organs of choice to monitor for ochratoxin A residues in broilers and hens, respectively. The significance of the high levels of OA in skin deserves further investigation because of the (remote) possibility of external contamination during the feeding trial. Collection and analysis abattoir samples may be useful to reveal the presence of potentially harmful residues in poultry feed and to reject carcasses unfit for human consumption. Further research is underway to determine residues in