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Toxicity to birds

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Three publications are available on the toxicity to birds.

Landers 2013:

An experiment was conducted with Pekin ducks to determine the toxicity of melamine (MEL) and cyanuric acid (CYA) in ducks fed treatments from day 3 to day 21 of age. Two hundred and twenty three threeday-old male ducks were assigned to one of 10 treatment groups. Treatments included: (1) a basal diet (BD) containing no MEL or CYA; (2) BD+0.5% MEL; (3) BD+1.0% MEL; (4) BD+1.5% MEL; (5) BD+0.5% CYA; (6) BD+1.0% CYA; (7) BD+1.5% CYA; (8) BD+0.5% MEL +0.5% CYA; (9) BD+1.0% MEL +1.0% CYA and (1 OJ BD+1.5% MEL +1.5% CYA Control and treatments fed MEL alone or MEL +CYA were fed to 5 pens of 5 ducks each. Treatments fed CYA alone were fed to 4 pens of 4 ducks each. Compared to controls, birds fed1.0% MEL had lower (P<0.05) feed intake (Fl) and body weight gain (BWG), heavier (P<0.05) relative kidney weights and higher (P<0.05) mortality. No mortality was observed in birds fed CYA alone or MEL +CYA combinations. No differences in Fl, BWG, relative kidney weights or mortality were noted among controls and ducks fed CYA alone or MEL+CYA combinations. Melamine crystals were only observed in the bile of ducks fed1.0% MEL alone. Renal histopathology included mild dilation of the embryonal nephrons and collecting tubules. Eosinophilic to basophilic casts, some containing spherical eosinophilic crystals were also present in the embryonal nephrons and collecting tubules. Histopathology results suggested that1.00 % MEL in the diet of ducks could cause severe renal pathology and mortality due to renal failure. The renal pathology observed in ducks was similar to that seen in other poultry species fed toxic concentrations of MEL. CYA alone up to 1.5% of the diet was not toxic to ducks and CYA reduced the toxicity of MEL when the two compounds were fed in combination.


Wang 2011:

Thepurposeof thisstudywas toevaluatethetoxicity potential ofcyanuricacid (CYA)and a combinationof melamine(MEL) andCYA in broilers.Atotalof 1200maleCOBB500broilerswere randomly allocatedinto1of10treatment groupsbya5x2 factorialdesignin a 42-d experiment.The dietary treatmentswere as follows:T1toT5:basal dietswith 0,10,20,33.3,and50 mg CYA per kg diet; T6to T10:basaldiet withCYAregimenssimilar toT1to T5butwith100 mgMEL perkgdiet. There were6replication pens with20chicksperpen.No differenceswere observed in alanine transaminase (ALT) and aspartate aminotransferase (AST) activities.But on d 22, uric acid (UA) and creatinine (Crea) concentrations were significantly greater whenbirds were fed CYA ac33.3mg/kgwithMEL 100mg/kg, and Crea concentration was alsohigherwhen birds werefedCYA at50mg/kg. Nocrystalswere found in kidneysbut dilatedrenaltubulesand smallbloodvessel expansion were foundinkidneys ofbirdsfed CYAat50mg/kgandCYAat33.3mg/kg withMEL100mg/kg.Theapoptosis rate (AR)ofkidneysofallbirds fed CYAand MELcontaminated diets werehigher than thecontrolgroup. Theseresults indicated that thedietaryaddition ofCYAandMELcould induce kidney damage, andtheeffects wereharmfulwhen the ratio ofCYA/MELwas1:3.


Ding 2011:

The purpose of this study was to characterize the toxicity potential of melamine (MEL), cyanuric acid (CYA), and a combination of MEL and CYA in broilers. A total of 720 commercial 1-day-old COBB 500 male broilers were randomly allotted into 6 groups with 6 replicates each and 20 broilers in each replicate. The dietary treatments were as follows: group I was the control group, group II included 10 mg/kg MEL and 3.3 mg/kg CYA, group III included 30 mg/kg MEL and 10 mg/kg CYA, group IV included 100 mg/kg MEL and 33.3 mg/kg CYA, group V included 100 mg/kg MEL, and group VI included 33.3 mg/kg CYA. The trial lasted for 42 days. CYA alone and the combination of MEL and CYA had adverse effects on the performance, but MEL alone had no effects on the performance. On day 21, the uric acid (UA) content of group IV was increased in serum (p < 0.05); on day 42, the serum aspartate aminotransferase (AST) activity and the level of tumor necrosis factor (TNF)-αand interleukin (IL)-8 increased in group IV (p < 0.05); 100 mg/kg MEL alone increased the level of TNF-αand the rate of renal apoptosis (p < 0.05); and 33.3 mg/kg CYA alone increased the level of IL-8 and the rate of renal apoptosis (p < 0.05). The livers contained MEL concentrations of 17–125 mg/kg wet weight and CYA concentrations of 28–73 mg/kg, and the muscle contained MEL concentrations of 14–105 mg/kg wet weight. It was indicated that MEL alone, CYA alone, and a combination of MEL and CYA inhibit the growth and damage the kidney and liver. 

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