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Coal-tar Poisoning : Introduction |  |
| A variety of coal-tar derivatives induce acute to chronic disease in animals. Clinical effects are acute to chronic hepatic damage with signs of icterus, ascites, anemia, and death. Coal-tar pitch poisoning has been reported from Canada, Germany, Ireland, Poland, and the USA. Toxicosis in domestic food animals and pets has been reported. |
| Etiology: |
| The distillation of coal tar yields a variety of compounds, 3 of which are notably toxic:
cresols (phenolic compounds),
crude creosote (composed of cresols, heavy oils, and anthracene), and
pitch. Tars are also produced from crude petroleum or wood. Creosote contains less volatile liquid and solid aromatic hydrocarbons of coal tar and some phenols. Cresols, composed mainly of hydroxytoluenes, are used as disinfectants. Coal-tar and pine-tar pitch are the brown to black, amorphous, polynuclear hydrocarbon residues left after coal tar is redistilled. Access of animals to coal tars is often by direct chewing on or
consumption of product, rather than inclusion in feed or water. Clay pigeons, tar paper, creosote-treated wood, and bitumen-based flooring are typical sources. |
| Phenol is the most important toxicant in coal-tar products. The approximate oral acute LD50 of phenol for most species is 0.5 g/kg, except for cats, which are more susceptible due to their limited ability to conjugate and excrete phenols. |
| Cresols, which are mixtures of methylphenols, are used as disinfectants and are readily absorbed through the skin. The lethal dose is 100-200 mg/kg, except in cats, which are especially sensitive. Because creosote derived from coal tar is toxic to wood-destroying fungi and insects, it is used as a wood preserver. Sows confined to wooden farrowing crates treated with 3 brush applications of creosote were reported to have stillborn pigs, and the surviving pigs grew slowly. Some
sources suggest that coal tars reduce absorption of vitamin A by sows. Other species are less susceptible (eg, the lethal dose of creosote in calves is 4 g/kg). Pitch is used as a binder in clay pigeons, road asphalt, insulation, and tar paper and roofing compounds, and to cover iron pipes and line wooden water tanks. Pigs that consume 15 g of clay pigeons over a 5-day period will die. Floor slabs with one-third lignite pitch reduced growth rate in pigs ~25%. |
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| Clinical Findings: |
| The cresols are locally corrosive; they stimulate the CNS and depress the heart, which results in vascular collapse. Capillary damage and hepatic or renal damage can occur. Death can occur from 15 min to several days after exposure. The first sign of pitch poisoning often is several dead pigs. Other pigs are depressed, and signs may progress to weakness, ataxia, sternal recumbency, icterus, coma, and death. Secondary anemia may develop. Associated problems have included
stillbirths in pigs and hyperkeratosis in calves. Blood glucose is reduced terminally, while thymol turbidity and serum chloride and phosphorus are increased. |
Lesions:
| Cresols and creosote produce contact irritation and nonspecific liver and kidney lesions. In pitch poisoning, the liver is markedly swollen with a diffuse, mottled appearance. The lobules are clearly outlined by a light-colored zone, and their centers contain deep-red dots the size of a pinhead. There is centrilobular liver necrosis, with blood replacing the lost cells and filling the center of the lobule. Renal tubular degeneration and necrosis also can be present. The
blood clots slowly or not at all. The carcass is icteric. Excessive fluid is found in the peritoneal cavity. |
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| Diagnosis: |
| Differential diagnoses include toxic plant poisonings (
Crotalaria
,
Senecio
, cocklebur), aflatoxicosis, fumonisin toxicosis, gossypol toxicosis, yellow phosphorus poisoning, and vitamin E or selenium deficiency. Fragments of clay pigeons, tar paper, or other sources of coal tars found in the GI tract, or chemical detection of coal-tar products in liver, kidney, serum, or urine, aid in confirming the diagnosis. A rapid presumptive test is to mix 1 mL of urine with 0.1 mL of 20% ferric chloride; purple color is indicative of phenol, but results
should be confirmed by a laboratory. |
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| Treatment: |
| There is no specific antidote for animals with frank signs. For recent oral exposure, activated charcoal and saline cathartics may reduce absorption. Supportive therapy to combat shock, respiratory failure, and acidosis could be useful for valuable individual animals. Demulcents or egg whites orally may help to reduce local corrosive effects in the stomach and intestines. Oral antibiotics and high-quality-protein diets may aid recovery. |
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