Symposium on Equine Medicine
Waste Oil: Toxic for Horses Arthur A. Case, M.S., D.V.M.,* and James R. Coffman, D.V.M., M.S.**
A toxicosis developed in many horses and other species following exposure to an irritating, volatile, and apparently very toxic substance which was included in waste motor oil applied to settle dust in the arenas adjoining riding horse stables. Three of 16 arenas in Missouri that were treated by the same applicator during the June, 1971 to August, 1972 period have been affected while 13 arenas have not been affected. The fumes proved to be toxic and soon affected any kind of life around the stable and arena. Birds in the rafters died within a few days, cats succumbed in a week to 10 days, and dogs suffered a more prolonged illness. Two children, seven and eleven years old, were severely affected in the first arena where they played with their ponies and pets and collected and buried dead sparrows and other birds which fell out of the rafters. Both little girls are now recovering. Two small boys exposed in the ·second arena in central Missouri were less severly affected, suffering an acne-like dermatitis similar to "cable rash" in those working with pentachloro compounds in certain industrial plants. The deadly sequence of events at the first arena stable to be affected has been described elsewhere. 1 • 2 The first person to realize the danger was the local veterinarian who was affected by the fumes in the arena as he was attending a sick horse. The owners were warned to remove the horses and other pets from the stables and to stay out of the arena until the fumes disappeared. His warning came too late as events of the following months were to prove (personal communication with Dr. ]. H. bans, Jr.t). *Professor of Veterinary Medicine and Surgery, Extension Veterinarian, School of Veterinary Medicine, University of Missouri, Columbia **Associate Professor of Veterinary Medicine and Surgery, School of Veterinary Medicine, University of Missouri, Columbia tCounty Veterinary Hospital, 1416 Harvester Road, St. Charles, Missouri, 63301. Veterinary Clinic:; of North America- Vol. 3, No. 2, May 1973
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The first arena stable to be affected was treated but once in mid June, 1971. More than half of those quarter horse mares and stallions have died after long and progressive illness. A gelding 2 months old when exposed lingered almost a year before he died. Some of the less affected mares aborted and a few have made apparent recoveries. Several had one or two remissions and then died. The latest report indicates 34 of 54 horses have died and five or six of those remaining may not make full recoveries. The second enclosed arena with the stable under the same roof was not affected as much, although at least seven horses have died from exposures in that stable or arena. This arena was treated three times by the same person who treated the first: about August 30, 1971, in December, and again in February, 1972. Fumes were noticed immediately in August; the person operating the equipment had to be given emergency aid and was removed from the arena to the open air. Most owners took their horses out of the stable as soon as possible but even then several suffered chronic, progressive deterioration and eventually died. The third arena (unenclosed) to report toxic reactions in horses shown or exercised there was treated near the first of August, 1972 and to date one death has occurred in those horses. The chief signs of toxic reactions have been contact dermatitis and loss of weight. Only several have been affected, but it is too early to predict the outcome. The syndrome as seen in the latest instance does not seem to be as serious an illness as the one shown by the horses from the first two arenas which were under a roof and had stables under the same roof.
CLINICAL COURSE The horses exhibited a progressive deterioration in health extending over a period of 3 to 4 weeks to many months. Anorexia, listlessness, and loss of body weight were characteristic, followed by emaciation, weakness, and an unsteady gait. Many horses were affected by a chronic cough, lacrimation, and serous nasal discharge suggestive of chronic respiratory infection. One stallion weighing about ll 00 pounds lost over 400 pounds within a period of 4 weeks; an owner likened the appearance of the horses to "a walking rack of hide and bones with loss of hair and sores all over them." Dermatitis
One of the earliest signs shown by the affected horses was a skin irritation resembling a contact dermatitis. It was first noticed on the nose and face, and along the limbs and ventral surface of the body. Mild at first, the dermatitis progressed into an almost generalized ulcerative dermatitis with extensive loss of hair, especially of the mane and tail. Mice, cats and dogs also showed the same skin conditions before death.
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The dermatitis extended to inflammation of the mucous membranes of the lips, mouth, and nasal passages and varied from mild lesions similar to mild photosensitization to a severe ulcerative inflammation reminiscent of glanders. In one of the terminal cases submitted at our veterinary clinic, one of us thought the horse did have glanders, so measures were taken to rule out Malleomyces mallei infection even though this infectious disease was eradicated from the United States many years ago. The loss of hair may range from a few patches to a generalized loss of the hair coat including the mane and tail, reminding one to rule out thallium poisoning. Loss of Weight All animal species affected, as well as the children, showed loss of appetite and a subsequent loss of body weight, often to a remarkable 50 per cent. Only by tempting the horses with sugary substances could the animals be persuaded to eat. This has also been reported by owners of affected dogs and cats at the first arena. Mothers of the four children also observed the craving for sweets. Glucose with other parenteral medicants proved useful for treatment of horses and may have reversed an otherwise fatal sickness in several instances. Some horses showed remissions of signs, started to improve in condition, and then suffered relapse and eventual death. One young horse was ill nearly a year before finally dying. Clinical Chemistry This history and obvious clinical signs proved to be more useful than laboratory aids in attempting to make a diagnosis. Hemoglobin and hematocrit, blood urea nitrogen (BUN), serum glutamic oxalacetic transaminase (SCOT), serum arginase, total protein, direct and indirect bilirubin, alkaline phosphatase, and bromsulphalein clearance time were determined and serum protein electrophoresis was done on horses submitted for examination. The animals which we did have as patients seemed to strike an average that was within normal ranges for most values. The exceptions were in lowered values for gamma globulin and prolonged bromsulphalein clearance time. Early in the outbreak at the first stable and arena, decreased cholinesterase activities were found in red blood cells when sick horses were compared to normal horses (reported by Dr. Evans). This information indicated that a search for the identity of the toxic agent should include the organophosphate and carbamate compounds as well as the chlorinated compounds. All such efforts have failed to date. Only hightemperature polychlorinated biphenyls (PCB's) have been found in the treated soil but not in the animals or their secretions (milk). The search for volatile toxic substances continues, but this has been an exceedingly difficult problem to solve.
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Postmortem Studies
Horses submitted for necropsy, histopathologic, microbiologic, and virologic procedures showed the same general picture as the sick horses, indicating exposure to a very toxic volatile agent with hepatoxic properties. Mucous membranes, like the skin, showed inflammations ranging from mild to deep ulcerative lesions. The most remarkable lesions were in the fat storage (adipose) tissues and bile ducts (personal communications with Drs. L. D. Kintner* and S. L. Nelson**). Generalized Serous Atrophy. In all horses examined the almost complete lack of any demonstrable fat in the normal body adipose tissues was prominent. Edema up to 1 em. thick was in the fascia of various parts of the body. Edema was most generalized in the fascia and subcutaneous tissue of the hind legs, especially with animals that were recumbent before death. Fat deposits in the coronary grooves of the heart, the perirenal area, and in the mesenteric adipose tissues were undergoing serous atrophy. Histopathologically, there was edema of the cerebral cortex in some animals, and necrotic areas in the adrenal cortex (Dr. Kintner). Biliary Cirrhosis. In all of the horses examined at postmortem, the chief lesions involved the bile ducts. The entire biliary tree was dilated and filled with bile-stained mucus. The bile duct entering the duodenum was greatly enlarged (3 em. in diameter). Histopathologically, there was a diffuse portal cirrhosis with most portal areas containing more than two bile ducts. Some liver lobules were completely encircled by numerous bile ducts. Connective tissue and mononuclear cells had infiltrated the portal areas. The larger collecting ducts were very large. Epithelial cells had formed papillae which projected into the lumen. Many of the hepatic cords contained bile pigment due to bile stasis. Spleen and Lymph Nodes. The spleen was only about one third normal size and most lymph nodes were small and inactive. This was of particular interest in light of the hypogammaglobulinemia observed in four affected horses. Urinary System. Apparently, the toxic substance was irritating to the liver and mucous membranes of the mouth but not the urinary system (Dr. Kintner). Effects on Other Species
The cats and dogs were affected by almost complete loss of fat in normal body reservoirs and other signs of emaciation as well as chronic respiratory, mouth and nasal lesions (Dr. Nelson). Loss of hair was also observed in the dogs and cats as well as mice which were around the arenas. Insects and spiders disappeared from both the enclosed arena and adjoining stables. *Professor of Veterinary Pathology, University of Missouri, Columbia. **Associate Professor of Veterinary Pathology, University of Missouri, Columbia.
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CONCLUSIONS The exact identity of the toxic substance(s) is unknown although tests have been performed by several laboratories. The search for the deadly material and its source continues in every way considered practical. Whatever the poisonous substance proves to be, it is known to be lethal for all species of living things exposed to it and the effective amount is apparently in the super-toxic range. The acute irritating effects are followed by chronic hepatoxicosis characterized by marked biliary cirrhosis in those animals living long enough to develop such disease changes. Until the exact identity of the toxic agents (or combination of such) is known and their source determined, the only recommendation possible is "do not use discarded motor oil on enclosed areas where man or his animals work or live."
REFERENCES l. Case, A. A.: Disaster. Sheep Breeder and Sheepman, 91 (No. II): 24-26, 1971. 2. Case, A. A.: Toxicosis of public health interest-children and animals poisoned by a volatile agent in discarded motor oil. Clinical Toxicology, 5:267-270, 1972.
Department of Veterinary Medicine and Surgery School of Veterinary Medicine University of Missouri Columbia, Missouri 65201