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Epidemiology of Lead Poisoning in Cattle S Volume 32 | Issue 3 Article 1 1970 Epidemiology of Lead Poisoning in Cattle S. L. Leary Iowa State University W. B. Buck Iowa State University W. E. Lloyd Iowa State University G. D. Osweiler Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/iowastate_veterinarian Part of the Large or Food Animal and Equine Medicine Commons, and the Veterinary Toxicology and Pharmacology Commons Recommended Citation Leary, S. L.; Buck, W. B.; Lloyd, W. E.; and Osweiler, G. D. (1970) "Epidemiology of Lead Poisoning in Cattle," Iowa State University Veterinarian: Vol. 32 : Iss. 3 , Article 1. Available at: https://lib.dr.iastate.edu/iowastate_veterinarian/vol32/iss3/1 This Article is brought to you for free and open access by the Journals at Iowa State University Digital Repository. It has been accepted for inclusion in Iowa State University Veterinarian by an authorized editor of Iowa State University Digital Repository. For more information, please contact [email protected]. Epidemiology of Lead Poisoning in Cattle by S. L. Leary. W. B. Buck. W. E. Lloyd. and G. D. Osweilert The case histories of lead poisoning This report contains the findings of 63 diagnosed in 63 herds of cattle over the episodes of lead poisoning in cattle that past five years were studied. The toxicosis were compiled from the records of the was founCl to be most prominent during Iowa Veterinary Diagnostic Laboratory. the spring months and resulted in a 61 The episodes span a five-year period from percent case fatality rate. The clinical April of 1965 through May of 1970. signs observed involved mainly the central nervous and gastrointestinal systems, as METHODS did the postmortem findings. The mean tissue lead levels were determined and Lead determination in liver and kidney correlated with the source of the toxicant. tissues, rumen contents, and environ­ mental specimens such as paint, oil, and grease employed the method reported by INTRODUCTION Berman using a spectrophotometer.2 * Lead poisoning has been a part of man's TABLE I-Seasonal Occurrence of Episodes of history since probably 4200 B.C. It has Clinical Lead Toxicoses in Cattle'" been incriminated as a part of the cause Seasonal of the fall of the Roman Empire. 1O Even No_ of Percent Total with the increased awareness of lead tox­ Month Cases of Total Percent icity today. it still continues to be a com­ January 7 mon toxicant of both livestock, pets, and February 3 1; } 29 man. Buck reported lead as one of the March 7 12 most common causes of livestock poison­ April 5 May 16 } 41 ing in the United States.3 Zook stated it June 4 2~ was the most common cause of poisoning July 9 20 August 2 1~ } 21 in dogs. Perlstein and Attale reported in September 2 1966 that lead accounted for 80 percent October 0 of all deaths in children due to accidental November 1 9 December 4 poisoning. IS ~} Totals 60 100 100 • The information presented in this report was ob­ tained under partial support of a grant by the * This covers 'a four-year period (June 1, 1966, American Petroleum Institute and Contract No. to May 30, 1970) instead of the five-year pe- CPA-22-107 by the National Air Pollution Control riod that the rest of the data represents. Administration. t From the Toxicology Section, Veterinary Diagnostic Laboratory, College of Veterinary Medicine. Iowa • Model 303 Spectrophotometer, Perkin-Elmer Corp.. State University. Ames, Iowa. Norwalk, Connecticut. 112 Iowa State University Veterinarian Blood lead determinations were done using pulmonary congestion (16%); kidney de­ the procedure described by Hesse1. 13 generation (16%). Others mentioned (in < 10% of the epi­ RESULTS sodes) were: fatty liver; pale and watery muscle; petechiation of subcutaneous tis­ Season Occurrence of Episodes sues, thymus, and trachea; cystitis; cloudy cornea; hemorrhage in eyeballs; brain A definite seasonal trend was noted with edema and hyperemia; metal or paint 91 percent of the episodes occurring in the materials in rumen and reticulum; swollen first nine months of the year. Also, three mesenteric lymph nodes. months (April, May, and June) accounted for 41 percent of the total for the year Sources of Lead (Table 1). One month (May) alone ac­ counted for 26 percent of the total epi­ The source of lead in each episode, sodes (Fig. 1). where it was known, is tabulated in Table 4. Morbidity and Fatality Rates TABLE 4-Sources of Clinical Lead Toxicoses In cases where sufficient information in Cattle was known, the statistics, shown in Table No. of Percent 2, were determined. Used oil (Category 2) Source Episodes of Total as a source of clinical lead poisoning pro­ Paint 18 29 duced a lower morbidity rate than did Oil 16 25 Category 1 (lead batteries, paint, grease); Unknown 15 24 Junk piles 7 11 but a higher percentage of those affected Grease 4 6 from oil sources died than those exposed Batteries 3 5 to other sources. Totals 63 100 Clinical Signs Paint proved to be the most common source of poisoning. This included old Ninety percent of the affected cattle ex­ board fences and farm buildings painted hibited some sign(s) of central nervous with lead-containing paints thinned with system involvement, and 60 percent ex­ boiled linseed oil (probably containing hibited signs of gastrointestinal involve­ litharge, a lead product),!! and old paint ment. This information is summarized buckets left in or near pastures and feed­ in Table 3. Body temperatures were re­ lots. Used crankcase oil was the next most corded in only 15 cases and were normal common source. This included old oil in eight but increased (up to 111 0 F.) in buckets and cans left in lots and pastures, the other seven. Acute death (less than and even one case of draining a tractor 24 hours after onset of clinical signs) was crankcase near a fence and letting the oil reported in about one-third of the episodes. run into a feedlot where cattle were kept. Many animals, however, survived for a longer period of time ranging from a few Chemical Analysis hours to about ten days. Tissue lead levels were determined in Necropsy Findings most cases. The results (in ppm lead on a wet weight basis) are seen in Table 5. Necropsies were done in 37 of the 63 In Category 1, rumen content mean in­ episodes. Of these, no gross lesions were cludes one value of 11,875 parts per mil­ observed in ten. In the remaining cases lion lead that was considerably greater the following lesions were observed: oil than the other values found; this is re­ in the gastrointestinal tract (30%); gastri­ flected in that parameter. Note that the tis and/or enteritis (24%); petechiation of Category 1 mean levels were higher than epicardium, and/or myocardium (21 %); those for oil (Category 2). Issue, No.3, 1970 113 TABLE 2-Morbidity and Fatality Rates in Relation to Source of Clinical Lead Toxi­ coses in Cattle Category Category Category All 1* 2t 3:1: Sources No. of episodes 15 9 12 37 Total no. animals 864 374 1,030 2,268 Total no. animals clinically affected 130 46 110 286 Total no. animals died 73 38 62 173 Morbidity No. affected X 100 15% 12% 11% 13% Total no. inherd Cause specific death rate No. died X 100 9% 10% 6% 8% Total no. in herd Case fatality rate No. died X 100 56% 83% 56% 61% No. affected in herd (Grease, Lead Batteries, and paint sources) t Used crankcase oil. :I: Junk piles' and other unknown sources. TABLE 3-Clinical Signs Noted in Lead-Poisoned Cattle No. of Percent of System Clinical Sign Episodes Total Episodes CNS Blindness 32 51 Muscle twitching 25 40 Hyperirritability 21 33 Depression 20 32 Convulsions 20 32 Grinding teeth 15 24 Ataxia 11 18 Circling 10 16 Pushing against objects 7 11 (One or more of these signs were reported in 90% of the episodes) Gastro­ Excessive salivation 26 45 intestinal Anorexia 16 21 Tucked abdomen 6 10 Diarrhea 6 10 (One or more of these signs were reported in 60% of the episodes) Other* Acute death 22 35 Bellowing 8 13 .. Other signs reported (in <8% of the cases) were: Abnormal posture, decreased milk production, down and unable to rise, rhythmic head jerking, paddling, emaciation, abortion, nasal and eye discharge, gray gum line, stiffness, dehydration, pharyngeal paralysis, rumen atony, aimless walking, constant dribbling of urine, dyspnea, vomi­ tion, blistered teats, hyperkeratinized skin areas, protruding tongue, pica, opisthoton­ us, nystagmus, coma. In 2 episodes clinical signs were not observed. 114 Iowa State University Veterinarian TABLE 5-Levels of Lead in Tissues and Ru­ findings, and chemical analyses. We con­ men Contents Associated with Clin­ sider it essential to find at least 10 parts ical Lead Toxicosis in Cattle per million lead on a wet weight basis in Category 1 (Grease, Batteries, and Paint Sources) the liver or kidney tissues and/or at least 0.35 part per million lead in the whole No. of PPM Lead on Wet Episodes Weight Basis blood to justify a definitive diagnosis of Tissue Mean Range lead poisoning in cattle. It is also impera­ tive that clinical signs and history or cir­ Liver 40 33.7 5.0 -50.0 Kidney 44 60.7 14.0 -110 cumstantial evidence be compatible with Rumen that of lead poisoning. It is important to contents 32 507.8 3.0 -11,875 employ microbiological as well as gross Blood 8 0.96 0.57-3.80 and histopathologic examination of the tissues as a means of differentiating lead Category 2 (Used Crankcase Oil Sources) poisoning from other diseases.
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