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Overview of Coal-Tar Products Poisoning

By Gary D. Osweiler, DVM, MS, PhD, Veterinary Diagnostic and Production Animal Medicine, College of Veterinary Medicine, Iowa State University

A variety of coal-tar derivatives induce acute to chronic disease in animals, with clinical signs that vary based on the constituents. Clinical effects are acute to chronic hepatic damage with signs of icterus, ascites, anemia, and death. Phenolic components may cause renal tubular damage. Coal tar–related poisoning has been reported in farm animals and pets.

Etiology:

The distillation of coal tar yields a variety of compounds, three 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. They have been used for restricted applications as wood preservatives. Cresols, composed mainly of hydroxytoluenes, are used in soaps and 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 (older products), tar paper, creosote-treated wood, and bitumen-based flooring are typical sources.

Phenol is the most important toxicant in coal-tar products and is found in antiseptics, creosote, germicides, cleaners, and disinfectants. The approximate oral acute LD50 of phenol for most species is 0.5 g/kg, except for cats, which are more susceptible because of limited ability to form glucuronides and excrete phenols. Phenols are directly corrosive, and ingestion results in oral and upper gastroenteric necrosis. After oral or dermal absorption, phenols accumulate in the liver and kidneys, commonly resulting in liver damage and renal tubular necrosis.

Cresols are readily absorbed orally and through the skin. The oral lethal dose is 100–200 mg/kg, except in cats, which are more sensitive. Sows in creosote-treated wooden farrowing crates delivered stillborn pigs. Coal tars may 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 no longer used as a binder in clay pigeons, but road asphalt, some insulation, and tar paper and roofing compounds may still contain cresols. Flooring with lignite pitch or asphalt can reduce growth rate and/or cause liver damage in pigs.

Clinical Findings:

The cresols and phenols are locally corrosive, causing necrosis and scarring of skin, mouth, and esophagus; CNS stimulation, tremors, and incoordination; and cardiovascular depression and shock. Capillary damage and hepatic or renal damage can occur. Icterus can result from intravascular hemolysis and hepatic damage. Death can occur from 15 min to several days after exposure. The first sign of pitch poisoning often is several dead animals. Signs may progress to weakness, ataxia, sternal recumbency, icterus, coma, and death. Secondary anemia may develop. Other problems have included stillbirths in pigs and hyperkeratosis in calves.

Lesions:

Phenols, cresols, and creosote produce contact irritation of skin, mouth, and esophagus and nonspecific liver and kidney lesions. The liver is markedly swollen with a diffuse, mottled appearance. 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.

Diagnosis:

Differential diagnoses include toxic plant poisonings (Crotalaria, Senecio, cocklebur), aflatoxicosis, blue-green algae poisoning, fumonisin toxicosis, gossypol toxicosis, yellow phosphorus poisoning, and vitamin E or selenium deficiency. Fragments of 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. Laboratory changes include hypoglycemia, and increases in serum liver enzymes, thymol turbidity, chloride, and phosphorus. Proteinuria, hematuria, and urinary cells and casts reflect kidney damage from phenolic fractions of coal tars.

A rapid presumptive test is to mix 1 mL of urine with 0.1 mL of 20% ferric chloride; purple color indicates phenol, but results should be confirmed by a laboratory.

Treatment:

There is no specific antidote for coal-tar product poisoning. Emetics and gastric lavage are not recommended for recent oral exposure, but activated charcoal and saline cathartics may reduce absorption. Owners may reduce acute exposure by administration of egg whites to dilute and bind the phenols. Dermal exposures are mitigated by bathing with glycerol followed by liquid dish soap. Supportive therapy for shock, liver and kidney damage, respiratory failure, and acidosis are important supportive measures for individual animals. N-acetylcysteine (140 mg/kg, IV, loading dosage, followed by 70 mg/kg, qid for another 3 days) has been recommended. Oral antibiotics, B vitamins, vitamin E, and high-quality–protein diets may aid recovery.