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RESEARCH REPORTINQ SERIES 

Research reports ofthe Office of Research and Development, U.S. Environmental 

Protection Agency, have been grouped into five series. These five broad 

categories were established to facilitate further development and application of 

environmental technology. Elimination of traditional grouping was consciously 

planned to foster technology transfer and a maximum interface in related fields. 

The five series are: 

• •? 

*-•'"" 1. Environmental Health Effects Research 

2. Environmental Protection Technology 

3. Ecological Research 

4. Environmental Monitoring 

5. Socioeconomic Environmental Studies 

This report has been assigned to the ECOLOGICAL RESEARCH series. This series 

describes research on the effects of pollution on humans, plant and animal 

species, and materials. Problems are assessed for their long- and short-term 

influences. Investigations include formation, transport, and pathway studies to 

determine the fate of pollutants and their effects. This work provides the technical 

basis for setting standards to minimize undesirable changes in living organisms 

in the aquatic, terrestrial, and atmospheric environments. 

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This document ie available to tie public through ^NMii^flKtMCfU Information Service. Springfield. Virginia &16f: :• kT#:

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T i TrrTTprnr- T 

EPA-600/3-77-009 

January 1977 

THE SHORT-TERM EFFECTS OF LEAD ON 

DOMESTIC AND WILD ANIMALS 

by 

R. P. Botts 

Corvallis Environmental Research Laboratory 

Corvallis, Oregon 97330 

CORVALLIS ENVIRONMENTAL RESEARCH LABORATORY 

OFFICE OF RESEARCH AND DEVELOPMENT 

U.S. ENVIRONMENTAL PROTECTION AGENCY 

CORVALLIS, OREGON 97330 

ij**m'^^.'.yj&p^^ 
P.5 

T T * T"STffrwv"'" ' 

DISCLAIMER 

This report has been reviewed by the Corvallis Environmental Research 

Laboratory, U.S. Environmental Protection Agency, and approved for publication. 

Mention of trade names or commercial products does not constitute endorsement 

or recommendation for use. 

ii 
P.6 

•T^FT^rrflTf 

FOREWORD 

Effective regulatory and enforcement actions by the Environmental 

Protection Agency would be virtually impossible without sound scientific 

data on pollutants and their impact on environmental stability and human 

health. Responsibility for building this data base has been assigned to 

EPA's Office of Research and Development and its 15 major field installations, one of which is the Corvallis Environmental Research Laboratory 

(CERL). 

The primary mission of the Corvallis Laboratory is research on the 

effects of environmental pollutants on terrestrial, freshwater, and marine 

ecosystems; the behavior, effects and control of pollutants in lake systems; 

and the development of predictive models on the movement of pollutants in 

the biosphere. 

This report presents a discussion on the extent of lead found in wild 

and domestic animals and some of the short term effects of this toxic substance. 

A.F. Bartsch 

Director, CERL 

•rn 
i \WmWtt'Uy/SB!R ' ^ '" ^•^Tmmrmw 

P.7 

ABSTRACT 

Small quantities of lead, a ubiquitous and toxic element, may be found 

in practically all species of plants and animals. The list of animals, both 

domestic and wild, reportedly intoxicated by lead is impressive. 

The sources of lead poisoning vary with species of animals. Lead base 

paints, used motor oils, spent lead shot and pastures contaminated by lead 

smelters seemingly have been most often incriminated. 

The lesions associated with lead intoxication may vary widely both 

within and between species of animals. Lesions and symptoms of the central 

nervous system are the most prominent. 

Toxic levels for various species as reported in the literature vary 

widely and seemingly a single toxic dose for each species, as yet, has not 

been definitely established. 

The diagnosis and treatment of lead intoxication may become laborious 

and time consuming. Most symptoms reported involve central nervous system 

dearrangement. Treatment of most clinical cases is disappointing generally 

because of the acute nature of lead poisoning. 

\v 
CONTENTS 

P.8 

Section Page 

I. Conclusions 1 

II. Introduction 2 

III. Sources of Lead and the Epizootiology of 

Lead Toxicosis 4 

IV. Metabolism of Lead 7 

V. Lesions Associated with Lead Intoxication 11 

VI. Other Functional Effects Associated with Lead 

Poisoning . 14 

VII. Toxic Levels of Lead for Various Species of 

Animals 16 

VIII. Signs, Symptoms and Diagnosis 19 

IX. Clinical Pathology and Chemical Analysis 21 

X. Treatment 22 

XI. References 23 
P.9 

TTnTMTflTrr r • "• • - - n 

Section I 

CONCLUSIONS 

From data reported in the literature crude estimates of the occurrence 

of lead poisoning may be derived. Approximately 150,000 cattle are annually 

exposed to toxic levels of lead and 20,000 acute cases occur per year. Of 

these, 15,000 animals succumb to lead poisoning. In addition, it is estimated that 1,000,000 migratory waterfowl succumb to lead poisoning due to 

consuming spent lead shot. 

The metabolism of lead compounds is very complicated and variable both 

within and between species. For most mammals including man 1-5% of the lead 

taken orally will be absorbed. One may estimate for ruminants that 83.6% is 

excreted through the feces; 14.8% through the urine, and 1.6% through the 

milk. Lead, once taken internally is retained by the body; particularly, 

the bones tenaciously retain lead and may account for as much as 80% of the 

total body burden. 

The exact mechanisms giving rise to the pathological lesions associated 

with lead poisoning have not been clarified. This is particularly true for 

chronic encephalopathy and nephropathy. Several enzymes are known to be 

inhibited by lead and among this group are several enzymes shown or suspected 

of being involved in renal tubular transport. 

Even with the voluminous literature concerning lead, toxic levels for 

various species of animals have not been precisely determined, nor is there 

general agreement on what constitutes a safe level of intake for extended 

periods of time. 

Generally, the treatment of lead poisoning is disappointing because of 

the acute nature of most clinical cases. Thus more emphasis should be 

placed on preventive rather than therapeutic programs to avoid the losses 

due to lead poisoning. 
""T^T TrT"P*1JT|pF '• ^~' 

^ M O 

^ ^ ^ 

Section II 

INTRODUCTION 

Lead is one of the oldest metals used by mankind; Romans and medieval 

Britons constructed lead water pipes (1). Usage has expanded until today 

the total annual U.S. consumption in 1968 was 1,328,970 tons (2). Approximately 184,316 tons annually are emitted to the atmosphere from sources such 

as combustion of gasoline, fuel oil, and coal in addition to several other 

industrial sources. The most abundant lead ore is Galena (PbS) (1). Approximately 32 percent of the U.S. consumption is obtained from primary smelters, 

38 percent from secondary recovery, and 30 percent from imports (2). 

Lead is an ubiquitous and toxic element. Small quantities can be found 

in practically all living tissues of plants and animals. Soils, limestone, 

sandstone, shale and igneous rocks contain quantities varying from 7 to 20 

ppm (3). Much has been written about lead, and thousands of cases of lead 

poisoning have been reported in both the human and veterinary medical literature. The species of animals that have either died or been obviously ill 

from increased lead intake include: 

A. Farm livestock and pets 

1. 

2. 

3. 

4. 

5. 

Wild 

1. 

2. 

3. 

4. 

5. 

6. 

7. 

Horses 

Cattle 

Swine 

Dogs 

Sheep (this review 

naturally occuring 

animals 

Ducks 

Geese 

Andean Condor 

Doves 

Quail 

Pheasants 

Falcon 

failed to 

lead 

find any 

poisoning). 

reports invol ving 
P.1 1 

• r r*';-ff^if'^n*!"rr*"'r 

Zoo animals 

1. 

2. 

3. 

4. 

5. 

6. 

7. 

Non-human 

Leopards 

Australian 

Parrots 

Polar bear 

Lorikeets 

Ferrets 

primates 

fruit bats 

Most of the reported incidents of poisoning involved small numbers of 

animals. However, contamination of vegetation by industrial operations(4-

13) often results in death to several animals at one time. Because lead is 

the most common accidental poison of farm animals (14), it is of considerable 

economic importance to agriculture. 
Section III 

SOURCE OF LEAD AND THE EPIZOOTIOLOGY AND LEAD TOXICOSIS 

The diagnosis of lead poisoning is not precise in all cases. For this 

reason, knowledge of the epizootiology of lead poisoning can help in arriving at a definitive diagnosis, in addition to determining the occurrence of 

the disease and defining the circumstances of exposure. 

EPIZOOTIOLOGY 

Although definite estimates of the incidence, morbidity and mortality 

in domestic and wild animals is lacking, the literature contains some 

information concerning the epizootiology of lead poisoning. Reports often 

state that the morbidity is low and the mortality or case fatality rate is 

high (14, 15). Lead poisoning is diagnosed more frequently in cattle and 

dogs than other species (14). 

For cattle, the incidence of lead poisoning has been estimated as 

approximately 167 cases per year per 1,000,000 animals (2). However, several 

tenuous assumptions were made in order to derive this estimate. The proportional mortality for lead poisoning (e.g., no. of animals dying of lead 

poisoning per all animal deaths) in cattle is estimated to be 1.7 percent 

for calves and 4.5 percent for older cattle (16). The morbidity of animals 

exposured to toxic levels of lead is estimated to be 11-15 percent and the 

case fatality rate is 55-85 percent (17). Two possible explanations are 

offered to explain the above estimates. Either, few animals--only the most 

serious cases—are presented to diagnostic laboratories or few exposed 

animals receive doses of sufficient magnitude to cause illness. If one can 

accept the incidence of lead poisoning to be approximately 0.016 percent (2) 

per year and the morbidity of animals exposed to toxic lead levels to be 11-

15 percent (17), then one may conclude that the ratio of exposed to unexposed 

cattle is 1:600 to 1:900. With a total 1969 cattle population of 123,748,000 

in the U.S., one can estimate that between 137,000 and 190,000 cattle are 

annually exposed to toxic levels of lead and that 20,000 cases of lead 

poisoning occur per year. 

Lead intoxication has a definite seasonal trend for cattle (17), dogs(19) 

and human beings (2). During a five year period (1965-1970), 41 percent of 

the bovine cases of a large diagnostic center occurred during April, May and 

June (17). In contrast, lead poisoning in dogs more often is diagnosed in 

summer and fall (19). The seasonal trend for cattle, at least in Iowa, 

coincides with the time when cattle are released to spring pastures (17). 
P.13 

Very little information is available on the age distribution of lead 

poisoning. For dogs, poisoning apparently occurs more frequently in younger 

animals, possibly because of their indiscriminate chewing habits (2, 19). 

The incidence of lead poisoning is unknown for practically all species 

of wild animals. However, an estimated one million ducks, geese and swans 

die annually in the U.S. of lead poisoning (20). 

The sources of lead poisoning are varied and often depend on such 

factors as the characteristics of the animal and its peculiar husbandry 

considerations. Consumption of spent lead shot for wildlife species such as 

ducks, geese, swans, mourning doves, pheasants, condor and falcons most 

often has been incriminated (21-25) as the source of lead poisoning. The 

consumption of flaking-paint containing lead is a common source for zoo 

animals (26-28). For domestic and pet animals, the sources of lead poisoning 

are more variable. In one study (17) the sources of lead incriminated for 

cattle were paint (29 percent), oil (25 percent), unknown (24 percent) 

junkpiles (11 percent) grease (6 percent) and batteries (5 percent). Table 

1 lists the most often quoted sources of lead by species (4,5,6,7,8,9,10,17, 

29-33). 

Table 1. Sources of Lead Poisoning for Various Species 

of Livestock 

Species Sources 

Cattle 

Horses 

Swine 

Dog 

Lead base paint, used motor oil, grease, 

used batteries, junkpiles containing 

lead, putty, roofing material, linoleum 

contaminated water, contaminated feed 

contaminated pastures from lead smelters 

Contaminated pastures from lead smelters 

Lead base paint 

Paint, linoleum, shot gun slugs, curtain 

weights, plaster 

Some of these diverse sources are more potent 1n terms of their lead 

content. Grease may contain as much as 450,000 ppm (17) and oil as much as 

500 ppm (34). Horses and cattle have died grazing on contaminated pastures 

that contained as much as 2,000 ppm (35) of lead. 
The epizootiology of lead poisoning may be briefly summarized: 

1. For Farm Animals 

a. The disease occurs more often in spring. 

b. The morbidity is low and mortality high. 

c. The sources most often incriminated include paint, used 

oil, grease, and discarded batteries. 

2. For Dogs 

a. The disease occurs more often in summer and fall. 

b. Most often it is a disease of young dogs. 

c. Several sources have been suggested. 

3. For Wildlife 

a. Consumption of spent lead shot is the primary source. 

b. Approximately 1,000,000 migratory birds are lost annually. 

4. For Zoo Animals 

a. Lead base paint consumed after it has flaked from 

cages and enclosures is the primary source. 

Obviously, the salient features of a program to reduce the occurrence 

of lead poisoning would involve: 

1. On the farm, implement clean husbandry practices. In particular 

a. Don't drain the oil from motor vehicles in pastures. 

b. Don't discard batteries, paint buckets, or used grease 

cans in pastures. 

c. Erect fences to keep animals out of old junk piles 

2. With non-lead paint, thoroughly clean and repaint all cages 

for animals. 

3. For wildlife, a preventive program (being implemented)(2) 

involves developing a substitute for lead shot. 
P.15 

Section IV 

METABOLISM OF LEAD 

ABSORPTION 

The absorption of lead compounds is quite complex and involves three 

different routes: inhalation, ingestion, and absorption through the skin. 

Of these inhalation is most efficient, and skin absorption is the least 

efficient. For man, 14-45 percent of inhaled lead is retained, whereas only 

5-15 percent of that ingested is retained (36). Factors that may modify 

retention of lead particulates in the lungs are the particle size, mucous 

flow, ciliary action, and the alveolar clearance rate (36). 

The percent retained by ingestion or the digestive coefficient is 

computed by determining the ratio—the portion retained/portion consumed. The 

digestive coefficient of lead varies widely between species from 5-15 percent 

in man (36) to as little as 1-3 percent in cattle and one percent in rabbits 

(37). For many toxic metals, the rate of absorption depends on such factors 

as the chemical form of the lead, the age of the animal, the pH of the 

gastro-intestinal tract, the gut transient time, the gut microflora, and the 

presence or absence of other metals. For example reducing the calcium level 

in the diet may increase the lead absorption in rats (38). In contrast 

vitamin D has a reverse effect (39). Furthermore lead absorption bv the 

gastro-intestinal tract is greater in young than in old rats (40,41). 

TRANSPORT, DISTRIBUTION AND EXCRETION 

Once lead is absorbed, it enters into a state of exchange between 

tissues and the blood. The various organs retain different amounts of lead. 

Transport, distribution and excretion of lead may be best conceptualized as 

a series of compartments interconnected with one another via the blood 

(Figure 1). 
Fig. 1: Hypothetical Transport of Lead 

Soft 

Tissues 

Bone 

Each compartment receives and will retain lead from the blood. The 

retention time of the lead depends on its biological half-time t*|/2, which 

in turn depends upon the strength of the bond between lead and the binding 

tissue. 

If the transfer from a tissue can be assumed to be a first-order 

decay, the t1/2 is the time required for 1/2 of the present burden of lead 

to be transferred from the tissue to the blood. In many biological systems, 

the transfer of material between compartments can be simulated by assuming a 

first order decay (42,43). Then the transfer rate depends only on the concentration in the originating compartment and the transfer coefficient for that 

compartment. The transfer coefficient, k, is related to ti/2 by the equation: 

k..-M?l 

xl/2 

One can appreciate that the concentrations in the various organs will 

change with time after a single dose of lead is absorbed and that these 

concentrations will depend partly upon the t-j/2-

Since blood is the medium that transports lead, 

role in the metabolism of lead. Based on tracer stud 

wet chemical analysis of tissues and blood from sheep 

that blood contains more than one compartment. Resul 

indicate at least three compartments. Some suggest ( 

red blood eel1s (RBCs), specific metalloproteins, pl 

molecular weight plasma proteins. The transfer rate 

the ti/2 is longer) for "RBCs than for plasmar*or sera; 

part, the concentration would be greater in the RBCs 

Forty and one-half hours after receiving an oral dose 

•plasma ratio was 122 in a calf (46). In contrast, th 

to be 11 in sheep, 40 hours after .an intravenous dose 

it assumes an important 

ies (44) in the dog and 

(45), one may conclude 

ts reported in dogs (44) 

36) four compartments: 

asma proteins and low 

is much slower (that is 

thus, for the most 

than in the plasma. 

of lead, the RBC to 

is ratio was estimated 

(45). This latter 
P.17 

data (45) show that the tj/2 1s longer for RBCs than for serum, and consequently, the fraction bound to serum would be transferred more readily to 

other tissues. Several factors that combine to maintain the level of lead 

in the blood Include the Initial dose of lead, the t|/2 of the compartments 

in the blood, and the tj/2 of the various compartments perfused by the 

blood. From the results reported 1n dogs (44) after 20 days the level in the 

blood fell to an estimated 5.8 percent of the level at the time of Injection 

and, after an additional 260 days, further fell to approximately 2.5 percent. 

This fact demonstrates the persistence of lead once 1t 1s taken Internally. 

The distribution of lead 1n the various tissues at any one time after a 

dose of lead depends on the perfusion of the tissue, the fraction in the 

blood that Is diffusable, and the ti/2 of the perfused tissues. Concentration of lead 1n different tissues demonstrate remarkable variations. Generally, lead 1s concentrated 1n bone, Uver and kidney tissues—concentrations as much as 100 times greater than in plasma or muscle. In a calf 

analyzed 42.5 hours after Injection with lead, 34 percent of the total body 

burden was found in the Uver, 33 percent in the bone, and 21 percent in the 

blood (46). In rabbits 96 hours after Injection, 21 percent of the lead was 

found 1n the Uver, 70 percent in the bone, and one percent in the blood (45). 

The kidney concentrates lead but, because of the relative weight, contains 

appreciably less of the total body burden. A publication reported data for 

a calf that consumed a dally average of 0.1 mg of lead for 169 days (47). If 

one assumes total body ratios of .04 for blood, .04 for bone, and .03 for 

liver, one can estimate that approximately 80% of the total body burden is 

located 1n bone and 5 percent in the Uver. At low Intake levels and after 

a sufficient length of time, an equilibrium 1s reached where excretion equals 

intake. Then the concentrations in the various compartments do not change, 

and that compartments (bone for lead) with the longest t-j/2 will contain an 

appreciable amount of the total body burden. The t-\/o ^or bone in dogs was 

estimated to be 7500 days (48). In contrast a U/o or blood was estimated to 

be 3.5 days(42). 

Lead absorbed by the gastrointestinal tract can be excreted via four 

routes: (1) glandular excretion and epithelial shedding of the gastrointestinal tract, (2) biliar excretion, (3) urinary excretion, and (4) 

mammary glandular excretion (36). 

The relative importance of these routes is unknown for many animals. 

After intravenous injection of lead, the ratio of the fecal (i.e., the sum 

of the glandular excretion and epithelial shedding) to total excretion can 

be computed. In the dog this ratio is approximately 0.65 (44); in sheep over 

a 10 day collection period the ratio was 0.84 (36). The discrepancies between 

this ratio for dogs and sheep may be due to the fact that the dose of lead 

received by the dog (44) was much less on a per weight basis than that received by the sheep (37) or due to differences in the metabolism of lead. 

Toxic doses of lead may change excretory functions and result in changes of 

excretory pathways. For example, when cadmium causes renal damage, cadmium 

excretion increases (36). 
""TTfr'jtr^'' 

Mammary gland excretion is much less than urinary excretion. From data 

collected 6 days in one cow (46), the mammary gland excretion was 10 percent 

of the value for urinary excretion. 

Combining the data from sheep (37) and cow (46), one can compute a crude 

excretion ratio: fecal excretion—83.6 percent; urinary excretion—14.8 

percent; and mammary excretion—1.6 percent. 

10 
P.19 

•r"TY"v"'^jfir'r'-

Section V 

LESIONS ASSOCIATED WITH LEAD INTOXICATION 

The functional and pathological effects quoted in the literature are 

quite irregular and variable for man and various species of animals. 

ANEMIA 

When the synthesis of RBCs and their components is decreased anemia 

occurs. In most cases of lead intoxication, anemia is not a predominating 

clinical.sign; however, the toxic effects of lead have motivated research to 

understand porphyrin metabolism which is controlled by several enzymes (49). 

The list of enzymes that lead inhibits or enhances is impressive. Many of 

these effects are demonstrable in vitro only, and in some instances, at 

concentrations that never have been observed in clinically ill individuals 

(49). 

Heme synthesis may be briefly outlined as (2): 

ALA synthetase (ALAS) 

Succinyl CoA + Glycine ^ 6_amin0 levulinic (]) 

acid (ALA) 

ALA dehydrase . . 

ALA • porphobilinogen (PBG) (2' 

PBG • • uroporphybinogen III (URO III) (3) 

urogenase 

URO III • coproporphybilinogen III (coproIII) (4) 

coprogenase 

Copro III • protoporphyrin IX (proto IX) (5) 

Heme synthetase 

Proto IX — : • Heme (6) 

Steps (1), (2), (3 or 4) , (5) and (6) have been demonstrated to be 

inhibited by lead (2, 49). Overt clinical lead poisoning is accompanied 

by increased ALA and coproporphyrin in the urine and blood (50). In 

vitro studies suggest that steps (2) and (5) are most sensitive toHTead 

inhibition (47). Depressed ALA dehydrase activity in erythrocytes and 

11 

««ua^.yj:UHia^^ 
elevated urine and serum ALA have been observed in cattle chronically 

poisoned (51). In addition to inhibiting heme synthesis lead apparently 

suppresses globulin synthesis (49). 

Other anemia-related abnormalities that have been observed in man and 

animals include: 

1. Shortened survival of RBCs (52) 

2. Reticulocytosis (2,33,53) 

3. Decreased hemoglobin (53, 54, 55) 

4. Basophilic stippling of RBCs (2) 

5. Siderocytosis (54) 

6. Increased osmotic and mechanical fragility (2,49) 

7. Loss of intracellular K+ ions (49) 

8. Immature forms of RBCs in general circulation (33) 

9. Erythroid hyperplasia of the bone marrow (54) 

10. Mitosis of erythrocytes in the peripheral blood in fowl (22,56). 

Basophilic stippling, often mentioned as a symptom of lead poisoning, 

is due to accumulations of cytoplasm and nuclear fragments along with nonheme iron in developing erythrocytes (2). In general, the anemia associated 

with lead poisoning is not severe and is difficult to distinguish from 

anemia due to other causes. 

NEPHROPATHY 

In man, renal insufficiency is a late sequela of lead poisoning (1,2,54). 

The pathogenesis of renal insufficiency is not clearly defined (2) and 

apparently occurs in those individuals who are exposed to lead over long 

periods of time (1,2,54). Lead-induced renal insufficiency is characterized 

by glycosuia and hyper-amino aciduria (2, 54).In addition to amino aciduria 

and glycosuria extreme exposure can cause hypophosphatemia and hyperphosphaturia (Fanconi syndrome) (2). Uric acid excretion sometimes is reduced 

causing saturine gout (2). 

Most clinical findings point to renal tubular dysfunction. Electron 

microscopic and biochemical studies demonstrate alterations in mitochondrial 

structures and cellular oxidation processes (58,59). The enzymes, alkaline 

phosphatase, carbonic anhydrase, ATPases, and cytochrome oxidase all inhibited by lead (49)—are known or suspected of being involved in renal tubular 

transport mechanisms (60). The most consistent lesion associated with lead 

poisoning is intranuclear inclusion bodies of the proximal tubules. These 

inclusions, believed to be lead protein complex (61), are reported in various 

species of mammals and birds dying of lead poisoning (22,56,62,63,64). 

Although cloudy swelling and degenerative changes of the tubules can be 

observed, those conditions are usually mild and inconspicuous (15,65). 

12 
P.21 

In summary, the significance of renal insufficiency in lead poisoning of 

domestic animals is unknown and has not been described, probably because 

domestic animals are not exposed to lead long enough for renal insufficiency 

to be observed. 

NERVOUS SYSTEM 

Symptoms of central nervous system dearrangement predominate in most 

diagnosed cases of lead poisoning. In man acute encephalopathy due to lead 

intoxication is characterized by rapid onset of seizures, often followed by 

coma. In acute encephalopathy (2) vascular injury is the lesion most often 

associated with edema of the brain. In contrast, patients with chronic 

encephalopathy develop progressive mental deterioration with loss of motor 

control (2). The etiology of chronic encephalopathy is not clear and may be 

due to several other factors. 

Encephalopathy dominates in most diagnosed cases of lead poisoning in 

domestic animals. Apparently, as in man, vascular injury is the initiating 

lesion (55). In cattle, brain lesions progress from a prominence of endothelial cells of the capillaries to the development of edema foci and neuronal degenerative changes. These focal lesions develop a laminar pattern 

accompanied by enlargement of astrocytes. Chronically ill animals develop 

lesions in the tips of the gyri, accompanied by capillary endothelial proliferation, astrocytic proliferation, spongy degeneration, neuronal necrosis, 

cavitation due to loss of cells, and capillary proliferation in these areas. 

In dogs, the reported lesions are similar to those in cattle (66). 

Damage to the small vessels include necrotic endothelium, usually associated 

with laminar necrosis in the cerebral cortex. Gliosis and capillary proliferation are observed in the chronically ill. In per acute cases, significant 

lesions may not be observed (67). 

Lesions of the central nervous system are not severe in birds. Chickens 

tolerate relatively high doses of lead (68), and CNS lesions are not well 

defined in the literature. Geese experience cerebral edema with serious 

fluid accumulation in the spaces of Virchow-Rubin (69). However, routine 

staining procedures failed to demonstrate any significant lesions in poisoned 

ducks (22). 

PERIPHERAL NEUROPATHY 

In man, peripheral neuropathy is observed and characterized by motor involvement with no sensory nerve aberrations. Chronically poisoned experimental 

animals develop segmental demyelination of some nerve fibers (2). Electrophysiological studies of poisoned baboons revealed no abnormalities of nerve 

conduction (70). Horses with lead poisoning exhibit signs of severe inspiratory dyspnea (4), possibly having the same histological basis as peripheral 

neuropathy observed in man (15). 

13 
P.22 

Section VI 

OTHER FUNCTIONAL EFFECTS ASSOCIATED WITH LEAD POISIONING 

Numerous organ-systems reportedly (2) impaired by lead intoxication 

include: 

1. Decreased iodine uptake 

2. Decreased gonadotrophic hormones 

3. Abnormal function of the pituitary-adrenal axis 

4. Myopathy of skeletal muscles 

5. Cardiac arrhythmias 

6. Decreased fertility 

7. Abnormal serum albumins and serum globulin levels (54) 

8. Elevated serum cholesterol levels (54) 

As in man, a variety of abnormalities have been reported in domestic 

and experimental animals. Apparently lead is immuno-suppressive evidenced 

by reduced lysozyme in dogs poisoned with lead (54). Lead decreases the 

resistance of mice to Salmonella typhimurium (71), in addition to decreasing 

the number of splenic cells producing both Igm and IgG antibodies (72). Lead 

poisoning in the dog produces acidophilic intranuclear inclusion bodies in 

the liver. Liver function tests reported in dogs (73) and cattle (55) occasionally indicate elevated levels of some enzymes (e.g., serum glutamic 

oxalacetic transaminase, serum pyruvic transaminase, and ornithine and 

carbamyl transferase). 

The gastroenteritis associated with lead intoxication varies from no 

lesions in cattle (15) to severe lesions in sheep (29). One dog experienced a 

perforated gastric ulcer with lead poisoning (74). In another report, 24 

percent of poisoned cattle had some form of gastroenteritis (17). 

Abnormal changes in bony tissue have been reported in horses suffering 

from lead poisoning (63). Their lesions included edematous synovial membranes, erosion of joint surfaces, and exostosis. Radiographs of experimental poisoned dogs demonstrated radio-opaque lines of the distal radii and 

thoracic spines (73). One study of the interactions of lead, zinc, cadmium 

in pigs(75) reported radio-opaque lines in the metaphysis. Other changes 

associated with lead poisoning include chromosome damage (76), abortion 

(76,77), reduced fertility (76), and endocardial and epicardial hemorrhages 

(16). 

The relative frequency of the lesions and reported functional effects 

are unknown and probably vary widely even within species. One report (17) 

14 
- -a—r »'»ff rffifW " 

lists the frequency of gross lesions in cattle as: gastroenteritis (24 

percent), petechiation of the epicardium and myocardium (21 percent), pulmonary congestion (16 percent), and degenerative changes of the kidneys (16 

percent). Other lesions with reported frequencies of less than 10 percent 

are: fatty liver, pale muscles; petechiation of subcutaneous tissue, thymus, 

and trachea; cystitis; opaque cornea; ocular hemorrhage; edema and hyperemia 

of the brain; and swollen mesenteric lymph nodes. 

The lesions reported in ducks and geese poisoned with lead contrast 

sharply with that reported in mammals. In ducks the most notable lesions 

are atrophic pectoral muscles and emaciation with loss of fat deposits (22). 

Other lesions include impaction of the proventriculus, small spleen, and 

vacuolization,of hepatic cord cells. In addition to the lesions reported in 

ducks, geese,'experience marked cephalic edema involving eyelids, submandibular region, and the brain (69). 

i 

15 
P.24 

Tf*"*)'*--*TiMT!Tf * _ —"! 

Section VII 

TOXIC LEVELS OF LEAD FOR VARIOUS SPECIES OF ANIMALS 

The toxic and/or lethal levels of lead, listed in Table 2 by species of 

animals, reported in the literature vary widely. 

Table 2 

TOXIC LEVELS OF LEAD (ORAL DOSE) 

Species Reference Comments 

Cattle 29 

29 

29 

29 

4 

35 

Horses 

81 

35 

Single lethal dose for calves 

200-400 mg/kg B.W. 

Single lethal does for adult cattle 

600-800 mg/kg B.W. 

Adult cattle will tolerate 6 mg/kg 

B.W./day for 2-3 years 

Adult cattle will tolerate 250 ppm 

of lead in ration for 2-3 years 

6mg/kg/day (equivalent to 275 ppm 

in the ration) is minimal chronic 

fatal dose. 

5 out of 8 animals died grazing 

pasture containing a median of 516 ppm 

of lead 

5 out of 15 animals died and an 

additional 5 were symptomatic grazing 

pasture containing 350 ppm. 

1 out of 6 cows died after consuming 5 

mg/kg B.W./day for 69 days. 

2 out of 2 horses died grazing pastures 

with median concentration of 516 ppm. 

16 
Sheep 

Dog 

Poultry 

78 

56 

79 

79 

29 

29 

76 

82 

67 

67 

67 

73 

80 

80 

56 

2.4 mg/kg/day equivalent to 150 ppm in 

ration is the minimum chronic fatal 

dose (for 6 months) 

4 out of 9 animals died and an additional 

2 were symptomatic when grazing pastures 

for 4 months containing 200-840 ppm. 

5 out of 6 young horses and 1 out of 22 

older animals were symptomatic when 

grazing pastures containing 38, 90 

and 246 ppm. 

2 out of 2 sheep apparently normal for' 

45 days consuming 5 mg/kg/day. 

2 out of 2 pregnant animals aborted 

and died on 59th and 106th day 

consuming 9 mg/kg/B.W./day 

1 out of 1 pregnant sheep aborted when 

consuming 1 mg/kg B.W./day for 50 days. 

1 out of 1 died when consuming 8 mg/kg 

B.W./day for 220 days. 

10 out of 10 were asymptomatic for 26 

weeks consuming 4.5 mg/kg B.W./day 

4 out of 4 were symptomatic when 

consuming 100 mg/kg B.W./day for 30 

days. 

3 mg/kg B.W./day for 180 days produces 

symptoms 

10-30 mg/kg B.W./day produces symptoms 

from 13th day 

600 mg/kg/day for 2 days is lethal 

Consuming 100 ppm in the ration produces 

symptoms 

100 ppm of PbAC in ration for 4 weeks 

asymptomatic 

1000 ppm in the ration for 4 weeks 

depressed weight gains 

2000 ppm in the ration for 3 weeks 

asymptomatic 

17 
-IfW 

Ducks 

Fish 

56 

68 

22 

83 

83 

19 

Other aquatic 

life 19 

5000 ppm in ration for 3 weeks produced 

necrosis of renal tubules 

Feeding 160 mg/kg/day for 35 days 

asymptomatic 

10 out of 10 developed symptoms after 

consuming eight #6 lead shot. 

Consuming 6 mg/kg B.W./day for 137 

days was asymptomatic 

Consuming 8-12 mg/kg B.W./day had 

average survival times of 28 and 25 

days. 

Toxic or lethal levels vary widely 

depending on the kind of water and 

length of exposure. Vary from 0.01 

to 63 ppm. 

Toxic levels for daphnia and cyclops 

varied from 0.01 to 128 ppm. 

The fatal or minimal toxic doses reported in the literature are 

difficult to interpret. From Table 2, assuming a safety factor of 2-3, 

older cattle should tolerate 2 mg/kg B.W./day or 80-100 ppm in the 

ration for 2 to 3 years. Sheep should tolerate 10 mg/kg B.W./day or, 

assuming that sheep consume approximately 3 percent of their body weight 

per day, they should tolerate 50 ppm of their ration for approximately 

one-half year. However, pregnant sheep have aborted at these levels (29). 

Assuming a horse consumes 2.1 percent of its body weight per day, 1.0 to 

1.2 mg/kg B.W./day or 40-50 ppm in the ration for time periods of less 

than one-half year should be tolerated. These implied safe levels were 

computed by making several assumptions; consequently, less subtle effects 

could be observed at levels of lead intake lower than these. 

18 
"WIW ' 

Section VIII 

SIGNS, SYMPTOMS AND DIAGNOSIS 

The diagnosis of lead poisoning depends on identifying these factors 

(14): 

1. Opportunity for exposure and the sources. 

2. Symptoms compatible with lead poisoning. 

3. Concentrations of lead in fluids, tissues, and organs of intoxicated animals and concentrations of lead in the source. 

4. Gross and microscopic lesions compatible with lead poisoning. 

In some extreme instances, test animals may have to be exposed to the 

source to determine effects of that particular lead concentration. 

SIGNS AND SYMPTOMS 

The gross symptoms observed in lead poisoning of domestic animals 

result from disturbances of the gastrointestinal tract and central nervous 

system. Most cases of intoxication are acute or subacute; consequently, the 

course of the disease will be short, about 2-3 days (14). 

Cattle 

Experimental evidence collected in young calves indicates that 2-3 days 

after exposure symptoms will be observed; however, this time interval is 

modified by initial dose (24). In fatal cases, the first symptoms observed 

may be impressive; uncontrolled vocalization, extreme ataxia, nystagmus, 

excessive salivation, sudden collapse, and death (29). Generally lack of 

appetite with diarrhea and constipation will be observed. In some instances 

marked anemia 1s observed. 

The frequency of some symptoms for cattle have been reported as (17): 

1. 

2. 

3. 

4. 

5. 

6. 

7. 

8. 

Blindness 

Excessive salivation 

Muscular twitching 

Hyperirritability 

Convulsion 

Depression 

Grinding teeth 

Ataxia 

51% 

45% 

33% 

33% 

32% 

32% 

24% 

18% 

19 
* W1*7 If" • T "^ "MITJWTT: 

9. Circling 16% 

10. Bellowing 13% 

11. Diarrhea 10% 

12. Pushing against objects 10% 

SHEEP 

Generally, the symptoms of sheep contrast with those seen in cattle; 

rather than excitement, depression often 1s reported (30). Progressive 

anorexia, in addition to constipation and diarrhea (29), lethargy and ataxia 

are typical symptoms. 

HORSES 

Inspiratory dyspnea, "roaring" after exercise, is the most often 

reported symptom of horses (4,84). Pharyngeal paralysis with regurgitation 

also occurs, and severe cases evidence ataxia, paralysis, and clonic convulsions (84). 

DOGS 

Symptoms for dogs are similar to those reported for cattle including 

excessive salivation, uncontrolled jaw movements, hyperesthesia of the skin 

and recumbency with pedal movements (67). Onset may be very rapid with 

apparent recovery from an acute episode following by vomiting (67). Pharyngeal paralysis also is reported (30). 

DUCKS AND GEESE 

Severe weight loss, marked weakness, and atrophy of pectoral muscles 

are usually reported in ducks and geese (22,69). Cephalic edema and characteristic high pitched vocalizations in geese, contrast with that reported in 

ducks (69). 

FISH 

Fish residing in fresh water containing lead ions develop a coagulated 

film of mucous over the entire body, particularly noticeable over the 

gills (2). This condition frequently occurs in fish exposed to other heavy 

metals. 

20 
P.29 

"nr-rr^ffTT" 

Section IX 

CLWICAL PATHOLOGY AND CHEMICAL ANALYSIS 

Many of the clinical pathologic observations noted with lead poisoning 

are associated with the development of anemia. Cattle experience hemoglobin 

levels of 5 gm/100 ml and packed cell volumes of 20 percent(55) as well as 

elevated reticulocyte counts (19,55). Serum glutamic oxalacetic transaminase 

and serum glutamic pyruvic transaminase are elevated (73); however, in some 

instances these enzymes are not elevated (55). Increased prophyrins in the 

urine seemingly is an inconsistent finding (53). Delta-amino levulinic acid 

(D.A.L.A.) in the serum and urine of man becomes elevated before the appearance of symptoms (2). In catt1e(49) and sheep(85) elevated D.A.L.A. has been 

reported. Stippling of red blood cells often is reported; however, conditions other than lead intoxication cause stippling of dog RBCs (86). A count 

of 15 or more stippled cells per 10,000 may suggest lead poisoning. Other 

findings reported in Intoxicated animals include: lead lines in the metaphyses and epiphyses of the radii (33,63,73) and epithelial casts in urine 

sediment (19). 

Chemical analysis of fluids, tissues, and sources is the most frequently 

used method to support the clinical diagnosis of lead poisoning. Kidney, 

liver, and blood tissues often are analyzed for lead content. Ten, 20, and 

0.35 ppm in the liver, kidney, and blood respectively are levels indicative 

of lead poisoning (4,30). Others suggest 50 ppm in the kidney cortex and 10 

ppm in the liver as significant (29). Levels considered significant in the 

dog are: blood (35 ug/100 ml); urine (75 yg/liter); hair (88 yg/gram); and 

liver (3.6 yg/gram)(87). 

The antemortem diagnosis of lead poisoning in domestic animals probably 

is not as crucial as for human beings. Primarily because the course of the 

disease is more acute and a few animals will have succumbed before the 

problem becomes evident. The differential diagnosis should include any 

disease of the central nervous and gastrointestinal system (1.7). 

21 
P.30 

"'* P'r"->f*r*" T',flrBff|-|f-"T-''' ,- ,. 

Section X 

TREATMENT 

Because of the acute nature in most domestic animals, the treatment 

generally is disappointing. The treatment regimen may Include (85): 

1 Sedation for convulsive seizures. 

2. Small oral doses of magnesium sulphate. 

3. Parenteral or forced feeding 

4. Ethylenediaminetetracetate (EDTA). 

The recommended dosage of EDTA varies. Some recommend a 12.5 percent 

solution given at the rate of 1.0 g/30 lb (13.6 kg/day) (84). The dose 

should be divided in two doses given intravenously and very slowly. The 

dose can be repeated until symptoms improve. Others suggest a 10 percent 

solution given intravenous at 1.0 gm/30 lb (13.6 kg)/day limiting the total 

dose to 5 gm/30 lb (13.6kg) per week suspended for one week after 7.5 gm/30 

1b(l3.6kg) has been given. Toxic signs Include accelerated heart and respiratory rates with muscular tremors (84). 

22 
P.31 

"-w^'yf^']"rnwiif:'' -~ • — 

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P.37 

"~TM nTr-Ty' p - ir»rrr'" 

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29 
P.38 

TECIHIWtiDAL REIFOBir ©ATA 

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REP°M=600/3~77~009 

3. RECIPIENT'S ACCESSIOK>NO. 

4. TITLE ANO SUBTITLE S. REPORT OATE 

THE SHORT-TERM EFFECTS OF LEAD ON DOMESTIC 

AND WILD ANIMALS 

Januarv 1977 

3. PERFORMING ORGANIZATION COOE 

7. AUTHOR(S) 

R.P. Botts 

3. PERFORMING ORGANIZATION REPORT NO. 

e. PERFORMING ORGANIZATION NAME ANO ADDRESS 10. PROGRAM ELEMENT NO. 

Corvallis Environmental Research Laboratory 

Corvallis, Oregon 97330 

1AA602 

N.edNYtaAeWdhAfoVtob. 

12. SPONSORING AGENCY NAME AND ADDRESS 

Corvallis Environmental Research Laboratory 

200 S.W. 35th St. 

Corvallis, Oregon 97330 

13. TYPE OF REPORT AND PERIOD COVERED 

in-houses literature review 

14. SPONSORING AGENCY CODE 

EPA-0RD 

19. SUPPLEMENTARY NOTES 

16. ABSTRACT 

Small quantities of lead, a ubiquitous and toxic element, may be found in practically 

all species of plants and animals. The list of animals, both domestic and wild, 

reportedly intoxicated by lead is impressive. 

The sources of lead poisoning vary with species of animals. Lead base paints, used 

motor oils, spend lead shot and pastures contaminated by lead smelters seemingly have 

been most often incriminated. The lesions associeated with lead intoxication may vary! 

widely both within and between species of animals. Lesions and symptoms of the centrsfli 

nervous system are the most prominent. Toxic levels for various species as reported 

in the literature vary widely and seemingly a single toxic dose for each species, as 

yet, has not been definitely established. 

The diagnosis and treatment of lead intoxication may become laborious and time consum 

ing. Most sysmptoms, reported involve central nervous system dearrangement. Treatment of most clinical cases is disappointing generally because of the acute nature of 

lead poisoning. 

17. KEY WORDS AND DOCUMENT ANALYSIS 

DESCRIPTORS b.IDENTIFIERS/OPEN ENDED TERMS c. COSATI Field/Group 

animal diseases 

lead poisoning 

animal nutrition 

veterinary medicine 

lead poisoning in wild 

and domestic animals 

sources and effects 

of lead poisoning in 

animals 

02/E 

06/FJ 

18. DISTRIBUTION STATEMENT 

RELEASE TO PUBLIC 

19. M&mw This Report) 2 1 . NO. OF PAGES 

35 

20. SECURITY CLASS (Thispage) 

UNCLASSIFIED 

22. PRICE 

EPA Form 2220-1 (B-73) 30 

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