Page 768 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition
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Avian Toxicology Chapter | 53  727




  VetBooks.ir  physiologically regulated increased iron uptake in sensitive  several ways. First, loss of insulating properties of the
                                                                  Crude oil and other petroleum products affect birds in
             species are all contributing factors to this condition (Cork,
             2000; Sheppard, 2002). A diet containing 50 100 mg/kg
                                                                feathers results in rapid hypothermia. Oiled birds lose
             iron on a dry matter basis has been recommended for sensi-  their ability to fly, and they frequently die from starva-
             tive avian species.                                tion, exhaustion, or drowning (Friend and Franson, 1999).
                Increasing cellular iron concentrations leads to lyso-  Second, crude oil and other petroleum products are irritat-
             somal injury and release of ionic iron, causing oxidative  ing to skin, mucous membranes, and the respiratory tract.
             damage to membranes and proteins. Liver, heart, and  Aspiration of oil into the respiratory tract and lungs can
             spleen are most commonly affected. Clinically, dyspnea,  cause aspiration pneumonia. Third, systemic absorption of
             abdominal distension, weight loss, and depression are  chemicals found in crude oil or petroleum products causes
             major signs. Fibrotic changes in the liver affect its func-  adverse effects on several organ systems, including repro-
             tion, commonly leading to ascites, hypoalbuminemia, and  ductive, hematopoietic, nervous, immune, and hepatobili-
             icteric symptoms. The accumulation of hemosiderin in the  ary systems. Lastly, petroleum is extremely toxic to bird
             lysosome of ISD-susceptible species is a common finding  embryos. Exposed birds are often emaciated. On postmor-
             in birds (Cork, 2000; Klasing et al., 2012).       tem, presence of oil in the respiratory or GI tracts, intesti-
                Diagnosis is by radiography (enlargement of liver,  nal congestion, and swelling of salt glands are noted
             heart, and spleen), elevation in liver enzymes and trans-  sometimes (Friend and Franson, 1999).
             ferrin concentrations. A liver biopsy might help in ante-  Diagnosing petroleum intoxication as a cause of death
             mortem diagnosis. To treat the condition, chelation with  can be challenging. There are no characteristic gross or
             deferiprone (75 mg/kg, PO, once daily for 90 days)  histopathologic lesions specific to petroleum intoxication.
             (Sandmeier et al., 2012), CaEDTA and BAL have been  A diagnosis is based on a history or evidence of exposure
             utilized. Prophylactically, testing the iron content of the  and  compatible  clinical  and  postmortem  findings.
             ingredients, choosing ingredients with low bioavailability  Exposed birds, especially those with white or light-
             of iron and feeding a low-iron diet with natural chelators  colored feathers, are easily identified because of the per-
             such as tannins, phytates and fiber might be useful.  sistence of oil on feathers and skin. Feathers, skin, or
                                                                organs of birds that do not have external evidence of
                                                                exposure can be analyzed for the presence of chemicals
             ENVIRONMENTAL TOXICANTS                            typically found in crude oil or petroleum products (Jessup
                                                                and Leighton, 1996).
             Petroleum
             Exposure of avian wildlife to crude oil is a significant cause
             of morbidity and mortality. Although oil spills involving  Cyanide
             large tanker accidents such as the grounding of the Exxon
             Valdez in Alaska or Deepwater Horizon received public  Cyanide (hydrocyanic acid) poisoning often occurs
             attention, other scenarios related to oil drilling and produc-  following ingestion of a cyanide salt or inhalation of
             tion, off-loading of oil from tankers, production, processing,  hydrogen cyanide gas. Avian wildlife intoxications have
             and refining of oil, road transport, and improper disposal of  occurred following exposure to cyanide from gold or
             waste oil and petroleum products result in considerable  silver mining processes (Friend and Leighton, 1999).
             wildlife exposure (Jessup and Leighton, 1996). Because oil  Birds are most often intoxicated by ingesting cyanide-
             floats on the surface of water, birds that live on water or  contaminated water from tailings ponds. Most mortality
             dive through water for food are more likely to be exposed  events occur in the spring and fall as migratory birds pass
             during spills. Marine birds and bird species that utilize  through mining areas. Large-scale cyanide spills have
             environments near to shore are also likely to be exposed to  caused widespread contamination of rivers in Europe and
             oil if spills reach shorelines. Raptors such as peregrine fal-  South America.
             cons that feed on other birds can be exposed to oil from  Cyanide is a rapidly acting cellular poison and it binds
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             contaminated prey (Zuberogoitia et al., 2006).     to ferric (Fe ) iron of mitochondrial cytochrome oxidase.
                Crude oil and petroleum products are complex mixtures  This enzyme mediates the transfer of electrons to molecu-
             of chemicals, including a variety of aromatic and aliphatic  lar oxygen, which is the last step in oxidative phosphory-
             compounds. The toxicity of crude oils and petroleum pro-  lation (Delaney, 2001). Cells are unable to use oxygen,
             ducts varies depending on their chemical compositions.  resulting in tissue anoxia, increased anaerobic metabo-
             Another complicating factor in assessing the toxicity of  lism, and rapid development of lactic acidosis. The acute
             crude oil is the fact that soon after environmental release,  oral toxicity of sodium cyanide has been studied in sev-
             the process of “weathering” occurs, which changes its  eral bird species. LD 50 s ranged from 4.0 to 21 mg/kg BW
             chemical and physical properties.                  (Wiemeyer et al., 1986).
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