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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

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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 : 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 and correlated with the source of the toxicant. tissues, 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 toxicant of both , , 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 .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 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; 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 and 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 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 and letting the oil reported in about one-third of the episodes. run into a where cattle were kept. Many , 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 lead that was considerably greater the following lesions were observed: oil than the other values found; this is re­ in the (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 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 production, down and unable to rise, rhythmic head jerking, paddling, emaciation, abortion, nasal and eye discharge, gray gum , stiffness, dehydration, pharyngeal paralysis, rumen atony, aimless walking, constant dribbling of urine, dyspnea, vomi­ tion, blistered , hyperkeratinized 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. Polioen­ No. of PPM Lead on Wet cephalomalacia, infectious thromboembo­ Episodes Weight Basis lic meningoencephalomyelitis, coccidiosis, Tissue Mean Range , organic insecticide poisoning, brain Liver 7 22.4 4.0 -70.0 abscesses, and other diseases which affect Kidney 8 52.3 6.0 -125 the central nervous and gastrointestinal Rumen systems of cattle should be included in contents 7 237.1 10.0 -921 Blood 3 0.51 0.20-1.00 the differential diagnosis. The range of tissue lead levels within Category 3 the same animal may frequently be quite (Junk Piles and Other Unknown Sources) broad. Some tissues may have insignifi­ No. of PPM Lead on Wet cant lead levels while other tissues in the Episodes Weight Basis same animal have levels great enough to Tissue Mean Range warrant a diagnosis of lead poisoning. Liver 16 21.3 1.0 -83.0 Thus, it is possible to have liver lead levels Kidney 16 65.8 12.0 -137 Rumen of 1 part per million with kidney and blood contents 8 171.9 3.0 -650 lead levels in the same animal of 20 and Blood 6 0.66 0.30-1.14 1.0 parts per million, respectively. If the CategonJ 4 history and clinical signs are compatible, (All Sources) a diagnosis of lead toxicosis is then justi­ No. of PPM Lead on Wet fied. For this reason it is imperative that Episodes Weight Basis analyses for lead be conducted on as many Tissue Mean Range different specimens as are available from Liver 52 29.7 1.0 -83.0 a single animal. This also explains the Kidney 57 57.7 6.0 -137 broad range of lead levels in the various Rumen contents 41 442.5 3.0 -11,875 specimens for all animals (Table 5). These Blood 17 0.78 0.20-3.80 data agree in general with those reported ----- .. ---.---- by Hatch and Funnell12 of 175 cases of DISCUSSION lead poisoning in cattle in over a 15-year period. Since lead poisoning in cattle usually It is apparent from these data and other involves several animals in a herd, the reports that the bovinE: animal is more term "episode" is used in this paper for susceptible to lead poisoning than is per­ each instance in which lead poisoning was haps the human, dog, and laboratory ani­ diagnosed in one or more animals within mals such as rats and mice.4,6.7,8.9.10.11.20 the same herd. Lead poisoning has been confirmed by The criteria used in diagnosing lead our laboratory in cattle having blood lead poisoning in our laboratory includes four levels as low as 0.20 parts per million in types of evidence; that is, history or cir­ both experimental and naturally occurring mustantial, clinical signs, postmortem cases. On the other hand, the maximum

Issue, No.3, 1970 115 allowable concentration for lead in human way. This same problem exists with the blood is reported to be O.S partspermilliono postmortem findings; i.e., the same lesion while others report somewhat lower may have been interpreted in two or more values.O.15.18 Dogs are apparently asympto­ ways. A higher percentage of necropsies matic with levels of up to 0.6 part per would have improved the reliability of the million in the blood.20 Hammond and results. Aronson have reported an average of 0.4 The tissue analyses revealed that paint, parts per million lead in the blood of 13 lead battery, and grease sources resulted in horses forages contaminated by a higher tissue lead levels than did oil smelter in Minnesota.ll About half of sources (Table 5), yet the case fatality rate these horses had severe lead poisoning was greater in those episodes where oil and died. They also reported blood lead was the source of lead (Table 2). This may levels of 0.04 parts per million in 16 horses reflect a difference in either absorption hospitalized for minor ailments but not rate from the gastrointestinal tract or inate known to have been exposed to excessive toxicity of the form of lead in question. levels of lead. These data would indicate Approximately 30 percent of lead from that horses are equal to cattle in their sus­ burned gasoline ends up in the crankcase ceptibility to lead pOisoning. oil; the remaining 70 percent goes into the The high spring seasonal incidence of atmosphere.H Used crankcase oil may lead poisoning in Iowa is probably due to contain many thousand parts per million several factors. The months of April and of lead. A grease sample from one episode May are usually when cattle are turned out contained 45 percent (450,000 ppm) ele­ into the pastures where junk piles are lo­ menta] lead by weight. cated. At this time melting snow may Note should be taken of a case which make lead sources more available. Also, occurred in September, 1965, where a the increased sunlight during the spring spray-painted a full corn crib. The and summer months aids in Vitamin D paint did not indicate that lead was production by the skin. Vitamin D is present, but the farmer became concerned thought to aid in the intestinal absorption and had a sample tested. It showed 370 of lead.6 The lower winter incidence could parts per million lead. It was suggested relate to these same factors. that the contaminated corn not be fed to Signs of toxicity appeared within a few livestock. A little known fact that should hours or up to ten days after ingestion of be pointed out is that '1ead-free" paint can lead. Central nervous system depression contain up to 1 percent (10,000 ppm) lead and anorexia were often the first signs and still retain an official "lead-free" desig­ noted. Overt nervous signs usually oc­ nation. curred later, such as muscle twitching, and younger cattle can be killed rhythmic head bobbing, blindness, ataxia, with single oral doses of 200-400 mg. pushing against objects, circling, and lead/kg. body weight given as lead ace­ grinding of teeth. Hyperexcitability and tate.a,7 Older cattle may require 600-S00 convulsions were signs of an unfavorable mg./kg. Adult cattle have died of apparent prognosis, and death usually occurred lead poisoning after consuming as little as shortly thereafter. Since body tempera­ 1 pint (500 ml.) of used crankcase oil, tures were recorded in only 15 of the 63 licking the grease from motors or machin­ cases, these results may be of questionable ery from as small an area as 25 square reliability. Opportunistic secondary in­ inches (150 sq. cm.), or consuming as little fections or hypothalmic damage may be as an estimated 1 cup (250 ml.) of grease involved. The varied clinical signs are containing lead. Chronic toxicity has been probably due partly to the lead poisoning produced with as little as 6 mg./kg./day synrome itself and also partly to the fact over a six-week period given as lead ace­ that many different people observed the tate.5 Hammond and Aronson have re­ affected animals. Hence, one sign may ported that cattle mayor may not exhibit have been interpreted in more than one toxicosis when fed containing 5-6

116 Iowa State University Veterinarian parts per million lead for extended periods 16. Perlstein. M. A. 'and Attale, R. A.: Neurological Sequellae of Plumbism in Children. Clin. Ped. of time.l1 Radeleff reported that herbage 5:292-298. 1966. 17. Badelelf. R. D.: Veterinary Toxicology. 2nd Ed. containing 25-46 parts per million lead Lea & Febiger. Philadelphia. 1970. p. 311. 18. Renert, O. N.; Weiner, P.; and Madden, J.: was sufficient to poison cattle and .17 Asymptomatic Lead Poisoning of Chicago Chilo dren. Ctln. Ped. 9:9-13. 1970. Grass near busy intersections has con­ 19. Van Gelder, G. A. and Buck, W ..B.: Lead Poi •• tained up to 500 parts per million lead,10 oning. Personal Communications. Iowa State Universitv. 1969. undoubtedly increased by the lead expelled 20. Zook. B. C.; Carpenter, J. L.; and Leads. E. B.: iLead Poisoning in Dogs. JAVMA. 155: 1329- in automobile exhaust. 1342. 1969. Poor farm management procedures are the main contributing factors to lead poi­ soning in cattle. This is supported by the occurrence and source data in this report. Allowing animals access to used oil, grease, lead batteries, chipped painted sur­ faces, paint buckets, and other materials in junk piles is responsible for most cases Student Chapter of lead poisoning in cattle. Approves New REFERENCES The Iowa State Student Chapter of the 1. AUcroft. R.: Lead Poisoning in Cattle and Sheep. Vet. Record. 63:585-590. 1951. American Veterinary Medical Association 2. Berman. Eleanor: Atomic Absorption Spectrom· etrv of Trace Metals. Progress in Chern. Tox. 4: approved the design of a new official ·161-166. 1969. 3. Buck, W. ,B.: Laboratory Toxicologic Tests and at the May meeting. The idea for the new Their Interpretation. JAVMA. 155:1928-1941. 1969. emblem was conceived by the student pub­ 4. Buck, W. B.: Lead and Organic Pesticide Poison. lic relations committee last fall and de­ ings in Cattle. JAVMA. 156: 1468-1472. 1970. 5. Buck. W •.B.; James. L. F.; and Binns. W.: signed by William Liska of the sophomore Changes in Serum Transaminase Activities Asso· ciated with Plant and Mineral Toxicity in Sheep class. The seal has the veterinary cadu­ and Cattle. Cornell Vet. 51 :568-585. 1961. 6. Byers, R. K.: Lead Poisoning. Pediatrics. 23: ceus and reads "Iowa State University" and 585-603. 1959. "College of Veterinary Medicine," Cardin­ 7. Chisolm. J. J. and Kaplan. E.: Lead Poisoning In Childhood-Comprehensive Management and al red and gold, Iowa State's official col­ Prevention. J. of Ped. 73:942-950. 1968. 8. Clarke, E. G. C. and Clarke. M. L.: Garner'. Vet· ors, are the colors of emphasis on the new erinary Toxicology Williams and Wilkins. Balti­ more. Md. 1967. Pp. 91-99. emblem. 9. Deichmaan. W. B. and Gerarde, H. W.: Toxicol· The seal was first introduced at the Vei­ ogy of Drugs and Chemicals. Academic Press. New York. New York. 1969. p. 644. shea display last year. It was taken to the 10. Gilfillan. S. C.: Lead Poisoning and the Fall of Rome. J. OccuP. Med. 7:53-60. 1965. national convention in Las Vegas last sum­ 11. Hammond. P. B. and Aronson. A. L.: Lead Pois. oning in Cattle and Horses In the Vicinitv of a mer and was displayed at the National Smelter Ann. New York Acad. Sci. 111:495-611. 1964. Conference of Student Chapters. It is pres­ 12. Hatch. R. C. and Funeell. H. S.: Le.d Levels in ently on display in the Dean's office and Tissues and Contents of Poisoned Cat· tle: A Fifteen-Year Survey. Can. Vet. Jour. 10: has been made into a decal which is on 258-262. 1969. 13. Hessel. D. W.: A Simple and Raoid Quantative sale to faculty and staff from any of the Determination of Le.d l'l Blood. Atomic Absorp­ tion Newsletter. 7: (3 )5!'>-56. 1968. Public Relations Committee members. It 14. Hirschler. D. A. lind Gilbert. L. F.: Nature of is the hope that this emblem can find wid­ Lead in Automobile Exhaust Gas. Archives of Environ. Health. 8:297-313. 1964. er use by the College of Veterinary Medi­ 15. Monrriefl'. A. A.; Koumides. O. P.: Clayton. B. E.; Patrick. A. D.: Renwick. A. G. D.; and Roberts cine into such items as stationary letter­ G. E.: Lead Poi.oning in Children. Arch. Dis. Childh. 39:1. 1964. heads, catalogues and diplomas.

Issue, No.3, 1970 117