Lead Poisoning in Cattle

Bovine Neurologic Diseases

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Lead Poisoning in Cattle John C. Baker, D.V.M., M.S., Ph.D.*

Lead poisoning (plumbism) remains one of the most common causes of poisoning in domestic animals and is encountered most frequently in cattle. 9 ,22,25 The yearly, worldwide production of lead is currently estimated at 1.5 X 106 tons, with 40 per cent of this lead being used in the United States. 5 Approximately 150,000 cattle are exposed to toxic levels of lead, with 20,000 cases of acute lead poisoning occurring yearly in the world. 5 ETIOLOGY AND EPIDEMIOLOGY

Lead poisoning in cattle most frequently results from a single accidental ingestion of material containing large quantities of lead. It can also occur if cattle ingest crops or forages contaminated from fumes and dust emitted from industrial lead operations or from ingestion of forages contaminated with lead from motor vehicle exhaust. Inhalation of lead particulates may be an important route of exposure in animals maintained near highways or industrial sources of lead. The frequent occurrence of lead poisoning in cattle relates to several of their behavioral characteristics, which include natural curiosity, frequent licking, and indiscriminate eating habits. Cattle appear to be attracted to materials containing lead and, if given the opportunity, will ingest machinery grease or crankcase oil. Another reason for the frequent occurrence of lead poisoning in cattle is that ingested material containing lead may settle and be retained in the reticulum, thus allowing for the absorption of lead over an extended period of time. There are many possible sources for lead exposure in the farm environment, and some of these are listed in Table 1. In one study, paint and petroleum products accounted for 60 per cent of the cases of lead poisoning occurring in livestock. 23 With the exception of marine paints, there are few lead paints still available. Discarded engine

* Diplomate,

American College of Veterinary Internal Medicine; Assistant Professor, Department of Large Animal Clinical Sciences, Michigan State University College of Veterinary Medicine, East Lansing, Michigan

Veterinary Clinics of North America: Food Animal Practice- Vol. 3, No.1, March 1987

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Table 1.

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Sources of Lead Causing Lead Poisoning in Cattle

Lead-based paints Machinery grease Motor oil Batteries Plumbing lead Caulking compounds Roofing felt Lead-lined tanks Linoleum

Lead arsenate pesticides White lotion (lead acetate) Lead sheeting exposed to weather Oil filters Boiled linseed oil Motor vehicle contamination of forage Pastures near lead mines, smelters, and leadreclaiming operations

oil is a common source of lead poisoning in cattle, but only if leaded gasoline is used. Machinery grease is also a common source and can contain up to 50 per cent lead. Exposure to lead arsenate will result in signs that relate more to arsenic poisoning than lead poisoning, with gastrointestinal signs such as profuse watery diarrhea, severe colic, weakness, and depression predominating. Pastures near heavily traveled highways may carry as much as 390 ppm lead, whereas pastures near lesser used roads only contain 10 ppm. 3 The concentration of lead falls rapidly the greater the distance from traffic. Lead is commonly found in association with cadmium as an en vironmen tal contaminate. 3 Cadmium has similar effects as lead; thus, the overall effects of these two elements are additive. Acute lethal single exposures to lead range from 400 to 600 mg per kg in calves and 600 to 800 mg per kg in adult cattle. 23 The minimum daily dose reported to eventually result in lead toxicity in cattle is approximately 6 to 7 mg per kg.23 However, clinical signs of lead poisoning were experimentally produced in calves dosed with 2.7 mg per kg a day of lead acetate. 29 The type of lead compound, ruminal or intestinal pH, and stage of lactation and/or pregnancy may influence an animal's susceptibility to lead poisoning. 21 Calves fed a diet of milk demonstrated greater, susceptibility when exposed to lead than calves fed a diet of grain and hay.30 Dietary supplementation with sulfate compounds has been shown to decrease lead levels in blood and tissue of sheep. 29 Lead poisoning has been reported to be more common in cattle less than 6 months old, most frequent during spring and summer, and more common in dairy than beef cattle. 2 No breed or gender differences are reported. The fact that dairy cattle are more often affected probably relates to their confinement and restriction to areas of the farm that are likely to contain sources of lead. One theory proposed for the seasonal occurrence is that consumption of spring forages induces a hypophosphatemia causing pica, which leads to the ingestion of lead-containing materials. 24 Another theory proposes that increased sunlight leads to increased vitamin D levels, which

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causes increased absorption of lead from the gastrointestinal tract. 10 However, it seems plausible that the seasonal occurrence of lead poisoning in cattle relates to the increase in farming activity and use of farm machinery in the spring, which provides sources of lead such as crankcase oil, machinery grease, and batteries. In addition, cattle are given greater access to areas of the farm during the spring and summer, thus increasing the chances of exposure to a lead source. PATHOGENESIS

Lead is toxic to protoplasm and affects many organs in the body, but the three most common clinical manifestations in animals are encephalopathy, gastroenteritis, and degeneration of peripheral nerves. Encephalopathy is the most common sign in cattle followed by gastroenteritis. Signs of peripheral nerve involvement are associated with chronic lead poisoning, which is rare in cattle but is a common finding associated with lead poisoning in horses. The nervous tissue lesions are believed to be vascular in origin and arise froln a decrease in blood supply due to capillary dalnage, which results in edelna or collapse of slnall arteries. 14,23 Peripheral nerve lesions appear as seglnental delnyelinization, which interferes with nerve conduction. Gastroenteritis results from the caustic action of lead salts on the gastrointestinallnucosa and is initially manifested by constipation that is followed by diarrhea. When lead is ingested, only a small proportion is absorbed (1 to 2 per cent). The remainder is excreted in the feces in the form of insoluble lead complexes. Even soluble compounds of lead (for example, lead acetate) form insoluble compounds, such as sulfate, in the digestive tract. A large proportion of lead absorbed in acute poisoning is deposited in soft tissue, such as liver and kidney. Lead causes degenerative changes and necrosis in the liver and kidneys. Lead crosses the placental barrier and can produce abortion, sterility, and fetal resorption. 23 Bone deposition occurs in chronic poisoning. In young animals, lead suppresses growth and increases the radiographic density in the active growth centers of long bones. 23 In the untreated animal, lead is slowly excreted through bile and urine. Lead combines with erythrocytes, and unless ingested in large amounts, lead concentrations are low in the plasma. Lead produces anemia by increasing the fragility of red blood cells and inhibiting the utilization of iron and the biosynthesis of heme. It inhibits two enzymes involved in hemoglobin synthesis-delta-aminolevulinic acid dehydratase (d-ALAD) and ferrochelatase. 16 The inhibition of these enzymes leads to increased urinary excretion of porphyrins and delta-aminolevulinic acid (d-ALA), which can be useful in diagnosis. Heme synthetase, an enzyme required for incorporation of iron into the heme molecule, also appears to be inhibited. 23 Inhibition of the enzyme nucleotidase is thought to be responsible for basophilic stippling and increased fragility of red blood cells. 16

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Subclinical doses of lead in mice have been shown to reduce resistance to bacterial infections. 15 Similar findings have been reported in swine, with an increase in the effects of endotoxin seen after challenge with Salmonella choleresuis in pigs that had lead added to their ration. 17 It was concluded that lead induced either an immunosuppression or a hypersensitivity to endotoxin. CLINICAL SIGNS

Nervous signs predominate in cattle and are associated with large doses of lead, whereas gastrointestinal signs are seen with moderate doses of lead. In a survey of lead poisoning in cattle, 90 per cent demonstrated signs of central nervous system involvement and 60 per cent showed signs of gastrointestinal involvement. 23 In cattle, lead poisoning tends to be acute or subacute. The acute form occurs most often in calves, whereas the subacute form is more common in adult cattle. The acute form has a short course (12 to 24 hours), and animals may be found dead without prior observation of clinical signs. In the early stages, increased pulse and respiration and frequent urinations may be observed. Affected animals may stagger and show muscle tremors, especially in the area of the head and neck. The muscle tremors are characterized as cervical, facial, and ear twitching along with bobbing of the head. Champing of the jaws, violent blinking of the eyelids, and frothing of the mouth may be observed. Cortical blindness is common, and cattle may wander aimlessly, circle (circling may be intermittent and not always in the same direction), head press, or walk through objects such as fences or brush. Pupillary dilatation may be present. Periods of excitement may occur and are characterized by bellowing (altered voice), rolling eyes, hyperesthesia, opisthotonus, tetany, and convulsions. These signs represent a poor prognosis, and convulsions generally indicate that death is imminent. Death occurs during a convulsion due to respiratory paralysis. In the subacute form, cattle may live for days, and signs are characterized by dullness and complete anorexia. Body temperature mayor may not be elevated. Blindness, gait abnormalities, muscle tremors, and hyperesthesia may occur. Gastrointestinal signs may be present and include constipation initially, followed by a fetid diarrhea, tucked up abdomen with signs of colic, salivation, bruxism (teeth grinding), and ruminal atony. In both the acute and subacute form of the disease, the palpebral preservation reflex is absent or diminished. 3 Edema of the optic disc may be present but is not common. The chronic form of lead poisoning is uncommon in cattle. Signs associated with this form include weakness, incoordination, joint stiffness, muscle wasting, colic, and convulsive seizures. Pustular eruptions of the skin and oral ulcerations may be observed. 27 Abortion and sterility may occur.

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In subclinical lead poisoning, metabolic changes are reflected in blood parameters and a decrease in growth rates. The "lead line" (also called "blue line" or "Burton's line") is a blue-black discoloration of the gums resulting from the precipitation of lead sulfide. It is of diagnostic importance in man and has been reported in carnivores but not in herbivores.l DIAGNOSIS

In the living animal, there is no single quantitative measurement that adequately defines the body lead burden. 6 When bone, liver, or kidney is available for analysis, lead poisoning is easily diagnosed. Antemortem diagnosis is most commonly achieved by evaluating historical findings and clinical signs together with blood lead concentration. Blood submitted for lead determinations should be collected in heparinized tubes. Whole blood lead concentrations of 0.35 ppm or greater are considered significant in cattle, and concentrations greater than 1 ppm represent a poor prognosis. 23 Values below 0.35 ppm may also be of significance. Background levels of lead for a particular geographic region or farm should be taken into consideration in the interpretation of blood lead concentration. Determining urine lead concentration is of little value because of variability in test results as well as difficulty in collecting 24-hour samples. Urine lead concentration increases greatly following chelation therapy with EDTA. This fact may be helpful diagnostically by comparing urine concentrations of lead on pre- and post-treatment samples (see below). Fecal lead concentrations of 0.35 pplTI or greater are suggestive of lead poisoning. 23 Determining fecal lead concentration gives insight into the time and duration of exposure. A high blood concentration with a low fecal concentration indicates this animal was exposed 1 to 3 weeks before sample collection. Determining lead concentrations in hair is of limited value in cattle because of seasonal growth and shedding. Using blood concentrations alone may be inadequate for diagnosing lead poisoning and does not allow for evaluation of length of exposure, the amount of lead deposition in the body, or the pathophysiologic effects of lead. 6 Because 90 per cent of circulating lead is bound to erythrocytes, the red cell mass can greatly affect the blood lead levels. False-negative results may occur when samples are collected following a long time period after a single exposure. Because of possible problems in the diagnosis of lead poisoning on the basis of blood lead concentrations alone, measurements of metabolic effects of lead can be included as an aid in diagnosis. One measure is the inhibition of the enzyme delta-aminolevulinic acid dehydratase (dALAD), an enzyme important in heme synthesis. Inhibition by lead results in a lower blood concentration of d-ALAD and a marked increase in urinary excretion of delta-aminolevulinic acid (d-ALA). Urinary d-ALA has been demonstrated to correlate with signs of lead poisoning in cattle.1 9 It appears that the test for d-ALAD has more

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diagnostic value than the test for urinary d-ALA.4 Currently, determination of d-ALAD cannot be considered routine in the practice of veterinary medicine. It is recommended that practitioners interested in this test contact their diagnostic laboratory for further information on its availability and instructions on collection and submission of samples. Blood samples for d-ALAD must be collected in plastic tubes using an anticoagulant other than EDTA, and the site of venapuncture should not be swabbed with alcohol. It is necessary to collect samples prior to the start of chelation therapy. Samples should be placed on ice, and if the test cannot be performed in 1 hour, samples must be transferred to liquid nitrogen storage. Values associated with d-ALAD and urinary d-ALA in lead poisoning are presented in Table 2. Zinc protoporphyrin concentration, which increases in lead poisoning, is another metabolic measurement that may aid in the diagnosis of lead poisoning. 6 In chron-ic lead poisoning, a normocytic normochromic anemia may develop. Although basophilic stippling is not considered to be a diagnostic feature in ruminants,3 it has been reported that 0.1 per cent of the red blood cells will show basophilic stippling in chronic lead poisoning in cattle. 23 Cerebrospinal fluid pressure is elevated in acute lead poisoning, but the CSF protein and cell count are usually within normal limits. 18 In subacute cases, the protein and cell count may be elevated. Kidney and liver damage may be present in subacute cases as indicated by proteinuria, increased BUN, and prolonged BSP excretion. Radiography may be helpful by demonstrating the presence of radiopaque material in the reticulum. The evaluation of rumen fluid may reveal absense of protozoa. POSTMORTEM EXAMINATION

In acute cases of lead poisoning, there may be no gross lesions. When lesions are seen they are not distinctive. Cerebral swelling, Table 2.

Tissue Lead Concentrations in Lead Poisoning in Cattle

TISSUE

LEAD CONCENTRATION

Whole blood Feces Kidney Liver Urinary d-ALA Erythrocyte d-ALAD

0.35 ppm or greater6 0.35 ppm or greater (suspect)6 10 ppm or greaterG 10 ppm or greater6 500 J,Lg or greater22 Values are quite variable in young calves. Normal values below 100 nM PBGI ml are rarely observed at any age. Values appear to drop below 100 nM PBGI ml with lead poisoning21

d-ALA = delta-aminolevulinic acid. d-ALAD = delta-aminolevulinic acid dehydratase.

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flattening of the cerebral gyri, and meningeal congestion are reported in acute cases. 18 If the dose of lead was high, moderate abomasitis may be observed along with swelling and degeneration of the kidneys and liver. In subacute cases, gross lesions reported in the brain include cerebral cortical swelling, yellow discoloration, and cavitation. 11 These lesions are most severe in the occipital lobes. Particulate material containing lead may be present in the reticulum. If the contents of the gastrointestinal tract are black and oily, the source was probably crankcase oil. Gastrointestinal contents can be submi tted for lead analysis. Histopathologic brain lesions observed in acute lead poisoning include petechial hemorrhages, severe congestion of cerebrocortical tissue and meninges, cortical neuronal necrosis, edema, prominence of capillaries, and endothelial swelling. 18 Findings in subacute or chronic cases include laminar cortical necrosis, endothelial and astrocytic proliferation, microglial accumulation, and eosinophilic infiltration of the leptomeninges. 11 Extracerebral lesions include cloudy swelling of liver cells and renal tubular degeneration. Acid-fast intranuclear inclusions occur in liver cells and the proximal convoluted tubules of the kidney. These inclusions are frequently absent in acute cases. Samples of tissues for lead analysis should include the liver and kidney. Tissue lead concentrations of 10 ppm or greater are considered diagnostically significant (see Table 2).23 The renal cortex is a more reliable tissue to assay than the liver because it stores more lead. Lead levels between 1 to 10 ppm may possibly represent a significant finding. 23 DIFFERENTIAL DIAGNOSIS Lead poisoning, rabies, polioencephalomalacia, thromboembolic meningoencephalitis (TEME), and listeriosis are the five major diseases to be considered in cattle showing neurologic signs consistent with diffuse brain disease. All too often these diseases appear similar, so clinical evaluation must be thorough and critical, and the appropriate laboratory tests should be performed to establish a diagnosis. Rabies must always be a consideration in cattle showing signs of neurologic disease. It is important to remember that rabies is a progressive disease and does not respond to treatment. In cattle, the disease has a 6- to 7-day course, with death occurring 48 hours after the animal becomes recumbent. It is difficult to distinguish lead poisoning from polioencephalomalacia, but it is helpful to note that there is normal rumen function in polioencephalomalacia, loss or depression of the palpebral eye preservation reflex in lead poisoning, and some animals affected with polioencephalomalacia have dorsomedial strabismus. As in lead poisoning, cattle with polioencephalomalacia may also be blind. Thromboembolic meningoencephalitis is most commonly seen in feedlot cattle in the fall and is often preceded by respiratory disease. Affected animals are usually not blind, but

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retinal hemorrhages may be present. Listeriosis can be differentiated from lead poisoning by signs of unilateral cranial nerve involvement such as circling, head tilt, ear and lip droop, ptosis, and localized areas of anesthesia on the face. Panophthalmitis may also be observed in listeriosis. Analysis of cerebrospinal fluid can be helpful in differentiating these five diseases. Other differentials to be considered are listed in Table 3. These diseases are covered in other articles in this volume. Excellent tables are provided in reference number 3 on differential diagnosis of cattle diseases manifesting signs of brain dysfunction.

TREATMENT

The first step in treatment of lead poisoning in cattle is to locate the source of exposure and remove it to prevent further ingestion by affected animals or other members of the herd. Rumenotomy with removal of lead-containing material from the reticulum or rumen is a consideration but tends to be an unsuccessful procedure because of the difficulty encountered in removal of particulate material from the recesses of the reticulum. Magnesium sulfate administered orally may be of value in removing lead from the gastrointestinal tract by its purgative action as well as reducing absorption by combining with lead to form insoluable sulfates. Chelation therapy is undertaken to facilitate the removal of lead from the body. The chelating agents most commonly used are BAL (2,3-dimercaptol-I-propanol), d-penicillamine (BB-dimethylcystein), and the calcium chelate of ethylenediaminetetracetic acid (EDTA).8 These drugs combine with lead to form poorly metabolized, soluble complexes that are subsequently excreted in the urine. Because of complications with BAL and d-penicillamine, EDTA is tne drug of choice for treatment. The treatment recommended for cattle is a 6.6

Table 3.

Differential Diagnoses of Lead Poisoning

MAJOR DIFFERENTIAL DIAGNOSES

Rabies Polioencephalomalacia Thromboembolic meningoencephalitis Listeriosis MINOR DIFFERENTIAL DIAGNOSES

Hypomagnesemic tetany Nervous ketosis Hypovitaminosis A Nervous coccidiosis Mercury poisoning Brain abscess Meningitis

Encephalitis Cerebral edema Hepatoencephalopathy Sporadic bovine encephalomyelitis (BUSS) Tetanus Post-dehorning sinusitis Organic pesticides

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per cent solution of calcium disodium EDTA *.26 This is administered by slow intravenous injection at a dose of 1 ml per 0.9 kg (1 ml per 2 lb), which provides 73 mg Ca EDTA per kg. Adverse reactions such as increased heart and respiratory rates and the development of muscle tremors are avoided by slow injection of the solution. This treatment is best given in divided doses 2 to :3 times a day for 3 to 5 days. If it is necessary to treat for more than 5 days, a 2-day rest period is recommended, followed by another 5 days of treahnent. This therapy will cause a 20 to 50 times increase in urinary lead excretion through the urine. Ca EDTA removes lead directly from bone and not from parenchymatous organs. Cell membranes are a barrier to the removal of intracellular lead; thus, lead is removed from soft tissue by equilibration with bone. Problems associated with Ca EDTA treatment can include a too rapid mobilization of lead from bone or a rebound in blood lead after termination of therapy, both causing an exacerbation of signs of lead poisoning. 8, 12 Other reported complications of Ca EDTA therapy include hypocalcemia, hypotension, fever, anorexia, anemia, severe pain, thrombophlebitis, and acute renal failure. 8 Ca EDTA may also increase urinary excretion of some essential elements. Oral zinc supplementation (1 mg per kg per day) and provision of trace mineralized salt may be indicated. 28 Recent studies have shown thiamine to be effective in treatment or prevention of lead poisoning in ruminants. 7,8 Thiamine appears to prevent deposition of lead in soft tissue (kidney, liver, and brain) by an unknown mechanism. Therapeutic results were obtained with doses of 250 to 1000 mg given twice a day for 5 days.26 Supportive therapy is an important aspect of treatment of lead poisoning. Affected animals are often dehydrated and anorectic. Force feeding of an alfalfa meal slurry by stomach tube may be indicated, as well as provision of oral or intravenous fluids with balanced electrolytes to correct and maintain hydration. Administration of fluids in the presence of cerebral edema may be contraindicated. Convulsions can be controlled by intravenous administration of barbiturates (phenobarbitol, up to 30 mg per kg to effect) or chloral hydrate (50 to 70 mg per kg as a 5 to 7 per cent solution).28 Dexamethasone (0.1 mg per kg intravenously) and/or mannitol (20 per cent solution, 1 to 2 gm per kg given slowly intravenously) may be indicated for the treatment of cerebral edema. Lead may cause immunosuppression; thus, broad-spectrum antibiotics may be indicated to control secondary bacterial infections. PREVENTION The vast majority of cases of lead poisoning can be prevented by careful handling and disposal of lead-containing materials found and

* Havidote.

Bayvet Division, Miles Laboratory Incorporated, Shawnee, Kansas.

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used on farms. Strict precautions should be taken to prevent animals from gaining access to areas where lead-containing materials are available or disposed of on the farm. Veterinarians should become aware of possible industrial sources of lead in the geographic area of their practices. Grazing pastures or using forage grown near heavily traveled highways should be avoided. A proper balance of salt and minerals in the ration may help to minimize chewing on foreign objects. If pasture contamination with lead occurs, livestock should be removed, forage cut and removed, and the stubble burned. 13

REFERENCES 1. Allcroft R: Lead poisoning in cattle and sheep. Vet Rec 63:583-590, 1951. 2. Blakley BR: A retrospective study of lead poisoning in cattle. Vet Hum Toxicol 26(6):505-507, 1984. 3. Blood DC, Radostits OM, Henderson JA (eds): Veterinary Medicine. Edition 6. London, Bailliere Tindal, 1983, pp 1091-1098. 4. Blumenthal S, Davidow B, Harris D, et al: A comparison between two diagnostic tests for lead poisoning. Am J Public Health 62:1060-1064. 5. Botts RP: The Short-Term Effects of Lead on Domestic and Wild Animals. Washington DC, U.S. Environmental Protection Agency. EPA 600/3-77-009, pp 1-29. 6. Bratton GR, Zmudzki J: Laboratory diagnosis of lead poisoning in cattle: A reassessment and review. Vet Hum ToxicoI26(5):387-392, 1984. 7. Bratton GR, Zmudzki J, Bell MC, et al: Thiamine (vitamin BI ) effects on lead intoxication and deposition of lead in tissues: Therapeutic potential. Toxicol Appl Pharmacol 59:164-172, 1981. 8. Bratton GR, Zmudzki J, Kincaid N, et al: Thiamine as treatment oflead poisoning in ruminants. Mod Vet Pract 62:441-446, 1981. 9. Buck WB, Osweiller GD, Van Gelder GA: Clinical and Diagnostic Veterinary Toxicology. Edition 2. Dubuque, Iowa, Kendal/Hunt Publishing Co, 1980, pp 319-332. 10. Byers RK: Lead poisoning: Review of the literature and report on 45 cases. Pediatrics 23:585, 1959. 11. Christian RG, Tryphonas L: Lead poisoning in cattle: Brain lesions and hematologic changes. Am J Vet Res 32(2):203-216, 1971. 12. Clarke EGC: Lead poisoning in small animals. J Small Anim Pract 14:183-193, 1973. 13. Edwards WC, Day BR: Reclamation of rangeland following a lead poisoning in livestock from industrial airborne contamination of forage. Vet Hum Toxicol 19:247249, 1977. 14. Goyer RA, Rhyne BC: Pathologic effects oflead. Int Rev Exp PathoI12:1-77, 1973. 15. Hemphill FE, Kaeberle ML, Buck WB: Lead suppression of mouse resistance to Salmonella typhimurium. Science 172:1031-1032, 1971. 16. Jones TC, Hunt RD: Veterinary Pathology. Edition 5. Philadelphia, Lea & Febiger, 1983, pp 1000-1006. 17. Lessen ED: Effects of subclinical lead exposure on the resistance of swine challenged with Salmonella choleraesuis var Kunzendorf. Ph. D. thesis, Iowa State University, 1977. 18. Little PB, Sorensen DK: Bovine polioencephalomalacia, infectious embolic meningoencephalitis and acute lead poisoning in feedlot cattle. J Am Vet Med Assoc 155(12):1892-1903, 1969. 19. McSherry BJ, Willoughby RA, Thomson RG: Urinary delta aminolevulinic acid (ALA) in the cow, dog and cat. Can J Comp Med 35:136-140, 1971. 20. Morrison IN, Quarterman J, Humphries WR, et al: The influence of dietary sulphate on toxicity of lead to sheep. Volume 34. Number 2. Proceedings of the Nutrition Society, 1975, pp 74A-78A. 21. Neathery MW, Miller WJ: Metabolism and toxicity of cadmium, mercury and lead in animals: A review. J Dairy Sci 58(12):1767-1781, 1975.

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22. Oehme FW: A survey of poisonings commonly observed by the bovine practitioners. Bovine Pract 9:47 -56, 1974. 23. Osweiler GD, Carson TL, Buck WB, et al: Clinical and Diagnostic Veterinary Toxicology. Edition 3. Dubuque, Iowa, Kendal/Hunt Publishing Co, 1985, pp 107-120. 24. Osweiler GD, Van Gelder GA: Epidemiology oflead poisoning in animals. In Oehme FW (ed): Toxicity of Heavy Metals in the Environment. New York, Marcel Dekker Inc, 1978, pp 143-171. 25. Priester WA, Hayes HM: Lead poisoning in cattle, horses, cats and dogs as reported by 11 colleges of veterinary medicine in the United States and Canada from July 1968 through June 1972. Am J Vet Res 35:567-572, 1974. 26. Sexton JW, Buck WB: Lead. In Howard JL (ed): Current Veterinary Therapy. Philadelphia, WB Saunders Co, 1986, pp 439-440. 27. Sippel WL, Reagor JC: Lead poisoning. In Amstutz HE (ed): Bovine Medicine and Surgery. Edition 2. Santa Barbara, California, American Veterinary Publications, 1980, pp 429-431. 28. Smith JA: Toxic encephalopathies in cattle. In Howard JL (ed): Current Veterinary Therapy. Philadelphia, WB Saunders Co, 1986, pp 855-862. 29. Zmudzki J, Bratton GR, Womac C, et al: Lead poisoning in cattle: Reassessment of the minimum toxic oral dose. Bull Environ Contamin ToxicoI30(4):435-441, 1983. 30. Zmudzki J, Bratton GR, Womac C, et al: The influence of milk diet, grain diet and method of dosing on lead toxicity in young calves. Toxicol Appl Pharmacol 76(3):490-497, 1984. Department of Large Animal Clinical Sciences College of Veterinary Medicine Michigan State University East Lansing, Michigan 48824-1314