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 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. They have been used for restricted applications as wood preservatives. Cresols, composed mainly of hydroxy-toluenes, 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 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 due to their limited ability to conjugate foreign compounds via glucuronides and excrete phenols. After oral or dermal absorption, phenols accumulate in the liver and kidneys, commonly resulting in 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, 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%.

Clinical Findings

The cresols and phenols are locally corrosive; they stimulate the CNS, causing tremors and incoordination, and depress the heart, resulting in vascular collapse. 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 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.

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.

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. Laboratory changes include hypoglycemia and elevations of 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 animals with frank signs. 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, respiratory failure, and acidosis could be useful for valuable individual animals. Oral antibiotics, B vitamins, vitamin E, and high-quality-protein diets may aid recovery.

Last full review/revision March 2012 by Gary D. Osweiler, DVM, MS, PhD, DABVT