Ecological Research Series
THE SHORT-TERM EFFECTS OF LEAD ON
DOMESTIC AND WILD ANIMALS
Environmental Research Laboratory
Office of Research and Development
U.S. Environmental Protection Agency
Corvallis, Oregon 97330
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RESEARCH REPORTING SERIES
Research reports of the 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
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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
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This document is available to the public through the National Technical Informa-
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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
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DISCLAIMER
This report has been reviewed by the Con/all is 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.
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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 installa-
tions, 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 sub-
stance.
A.F. Bartsch
Director, CERL
m
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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.
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CONTENTS
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
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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 estimat-
ed 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.
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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). Approxi-
mately 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). Approxi-
mately 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 litera-
ture. The species of animals that have either died or been obviously ill
from increased lead intake include:
A. Farm livestock and pets
1 . Horses
2. Cattle
3. Swine
4. Dogs
5. Sheep (this review failed to find any reports involving
naturally occuring lead poisoning).
B. Wild animals
1 . Ducks
2. Geese
3. Andean Condor
4. Doves
5. Quail
6. Pheasants
7. Falcon
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C. Zoo animals
1. Non-human primates
2. Leopards
3. Australian fruit bats
4. Parrots
5. Polar bear
6. Lorikeets
7. Ferrets
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.
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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 arriv-
ing 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 propor-
tional 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 cattl* 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).
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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 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
Horses Contaminated pastures from lead smelters
Swine Lead base paint
Dog Paint, linoleum, shot gun slugs, curtain
weights, plaster
Some of these diverse sources are more potent in 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.
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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.
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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 by 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).
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Fig. 1: Hypothetical Transport of Lead
G.I.
Tract
Lungs
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^]/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 concen-
tration in the originating compartment and the transfer coefficient for that
compartment. The transfer coefficient, k, is related to t]/2 by the equa-
tion:
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-|/2-
Since blood is the medium that transports lead, it assumes an important
role in the metabolism of lead. Based on tracer studies (44) in the dog and
wet chemical analysis of tissues and blood from sheep (45), one may conclude
that blood contains more than one compartment. Results reported in dogs (44)
indicate at least three compartments. Some suggest (36) four compartments:
red blood cells (RBCs), specific metalloproteins, plasma proteins and low
molecular weight plasma proteins. The transfer rate is much slower (that is
the ti/2 is longer) for RBCs than for plasma or sera; thus, for the most
part, the concentration would be greater in the RBCs than in the plasma.
Forty and one-half hours after receiving an oral dose of lead, the RBC to
plasma ratio was 122 in a calf (46). In contrast, this ratio was estimated
to be 11 in sheep, 40 hours after an intravenous dose (45). This latter
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data (45) show that the ti/2 is longer for RBCs than for serum, and conse-
quently, 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 tl/2 of the compartments
in the blood, and the ti/2 of the various compartments perfused by the
blood. From the results reported in 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 it is taken internally.
The distribution of lead in 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 t-j/2 of the perfused tissues. Concentra-
tion of lead in -different tissues demonstrate remarkable variations. Gen-
erally, lead is concentrated in bone, liver and kidney tissues—concentra-
tions 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 liver, 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 in the liver, 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 daily 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 in bone and 5 percent in the liver. At low intake levels and after
a sufficient length of time, an equilibrium is 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-|/? for bone in dogs was
estimated to be 7500 days (48). In contrast a t-j/2 of 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 gastro-
intestinal 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 re-
ceiyed 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).
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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--!.6 percent.
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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 y 6_amino Ievu1inic (1)
acid (ALA)
ALA dehydrase
ALA > porphobilinogen (PBG)
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 to lead
inhibition (47). Depressed ALA dehydrase activity in erythrocytes and
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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 non-
heme 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 hyperphospha-
turia (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 inhib-
ited 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).
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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 endo-
thelial cells of the capillaries to the development of edema foci and neuro-
nal 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 prolif-
eration, 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 prolif-
eration 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 involve-
ment with no sensory nerve aberrations. Chronically poisoned experimental
animals develop segmental demyelination of some nerve fibers (2). Electro-
physiological studies of poisoned baboons revealed no abnormalities of nerve
conduction (70). Horses with lead poisoning exhibit signs of severe inspira-
tory dyspnea (4), possibly having the same histological basis as peripheral
neuropathy observed in man (15).
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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) occa-
sionally 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 synovia!, mem-
branes, erosion of joint surfaces, and exostosis. Radiographs of experi-
mental 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 endocardia! 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)
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lists the frequency of gross lesions in cattle as: gastroenteritis (24
percent), petechiation of the epicardium and myocardium (21 percent), pulmo-
nary 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, submandibu-
lar region, and the brain (69).
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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
Cattle
Reference
29
29
29
29
4
Comments
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
Horses
35
81
35
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
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4 2.4 mg/kg/day equivalent to 150 ppm in
ration is the minimum chronic fatal
dose (for 6 months)
78 4 out of 9 animals died and an additional
2 were symptomatic when grazing pastures
for 4 months containing 200-840 ppm.
56 5 out of 6 young horses and 1 out of 22
older animals were symptomatic when
grazing pastures containing 38, 90
and 246 ppm.
Sheep 79 2 out of 2 sheep apparently normal for'
45 days consuming 5 mg/kg/day.
79 2 out of 2 pregnant animals aborted
and died on 59th and 106th day
consuming 9 mg/kg/B.W./day
29 1 out of 1 pregnant sheep aborted when
consuming 1 mg/kg B.W./day for 50 days.
29 1 out of 1 died when consuming 8 mg/kg
B.W./day for 220 days.
76 10 out of 10 were asymptomatic for 26
weeks consuming 4.5 mg/kg B.W./day
82 4 out of 4 were symptomatic when
consuming 100 mg/kg B.W./day for 30
days.
Dog 67 3 mg/kg B.W./day for 180 days produces
symptoms
67 10-30 mg/kg B.W./day produces symptoms
from 13th day
67 600 mg/kg/day for 2 days is lethal
73 Consuming 100 ppm in the ration produces
symptoms
Poultry 80 100 ppm of PbAC in ration for 4 weeks
asymptomatic
80 1000 ppm in the ration for 4 weeks
depressed weight gains
56 2000 ppm in the ration for 3 weeks
asymptomatic
17
-------
56 5000 ppm in ration for 3 weeks produced
necrosis of renal tubules
68 Feeding 160 mg/kg/day for 35 days
asymptomatic
Ducks 22 10 out of 10 developed symptoms after
consuming eight #6 lead shot.
83 Consuming 6 mg/kg B.W./day for 137
days was asymptomatic
83 Consuming 8-12 mg/kg B.W./day had
average survival times of 28 and 25
days.
Fish 19 Toxic or lethal levels vary widely
depending on the kind of water and
length of exposure. Vary from 0.01
to 63 ppm.
Other aquatic
life 19 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
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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 intoxi-
cated 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 is observed.
The frequency of some symptoms for cattle have been reported as (17):
1. Blindness 51%
2. Excessive salivation 45%
3. Muscular twitching 33%
4. Hyperirritability 33%
5. Convulsion 32%
6. Depression 32%
7. Grinding teeth 24%
8. Ataxia 18%
19
-------
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 is 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 convul-
sions (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). Pharyn-
geal 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 charac-
teristic 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
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Section IX
CLINICAL 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 appear-
ance of symptoms (2). In cattle(49) and sheep(85) elevated D.A.L.A. has been
reported. Stippling of red blood cells often is reported; however, condi-
tions 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 meta-
physes 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 yg/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 (17).
21
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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 Ib (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 Ib (13.6 kg)/day limiting the total
dose to 5 gm/30 Ib (13.6kg) per week suspended for one week after 7.5 gm/30
lb(13.6kg) has been given. Toxic signs include accelerated heart and respir-
atory rates with muscular tremors (84).
22
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REFERENCES
1. Browning, E. Toxicity of Industrial Metals (2nd ed.) Apple-Century
-Crofts: N.Y. and London. 1969.
2. Lead:Air Lead in Perspective. National Academy of Sciences:
Washington D.C. 1972. pp. 330.
3. Bowen, H. J. M. Trace Elements in Biochemistry. Academic Press:
N.Y. and London. 1966. 197 pp.
4. Hammond, P. B. and Aronson, S. L. Lead Poisoning in Cattle and
Horses in the Vicinity of a Smelter. N. Y. Acad. Sci. 111:595-
611. 1961.
5. Beijers, J. A. Loodvergiftiging. Tijschr. v. Diergeneesk.
77:587-605. 1953.
6. Harbourne, J. F., C. T. McCrea and J. Watkinson. An Unusual
Outbreak of Lead Poisoning in Calves. Vet. Rec. 83:515-517. 1968.
7. Haring, C. M. and K. F. Meyer. Investigation of Livestock Conditions
and Losses in the Selby Smoke Zone U.S. Bureau Mines Bull. 98:474-
502. 1915.
8. Holm, L. W., J. D. Wheat, E. A. Rode, and G. Firch. The Treatment
of Chronic Lead Poisoning in Horses with Calcium Di-sodium Ethylene
Diamonio Tetracetate. Jour. Am. Vet. Med. Assoc. 123:282-388.
1953.
9. Hughes, W. Lead Poisoning in Horses and Cattle. Vet. J. 79:270-
271. 1923.
10. Hupka, E. Uber Flugstaubvergiftungen im der Umgebund von Metallhutten.
Wein. Terarztl. Monatsschr. 42:763-775. 1955.
11. Knight, H. D. and R. G. Buray. Chronic Lead Poisoning in Horses.
Jour. Am. Vet. Med. Assoc. 162(9):781-786. 1973.
12. Kradel, D. C., W. M. Adams, and B. S. Guss. Poisoning and Eosino-
philic Meningoencephalitis in Cattle-A Case Report. Vet. Med.
60:1045-1059. 1965.
23
-------
13. Miessner, H. Schadigung der Tierweit durch Industrie und Technik.
Deut. Tierarztl. Wchnschr. 39:340-345. 1931.
14. Buck, W. Laboratory Toxicologic Tests and Their Interpretation.
Jour. Am. Vet. Med. Assoc. 155(12):1928-1941. 1969.
15. Jubb, K. V. F. and P. C. Kennedy. Pathology of Domestic Animals,
Vol. 2, Academic Press: N.Y. and London. 1963.
16. Todd, J. R. A Knackery Survey of Lead Poisoning: Incidence in
Cattle in Northern Ireland. Vet. Rec. 74(4):6-118. 1962.
17. Leary, S. L., W. B. Buck, W. E. Lloyd and G. D. Osweiler. Epide-
miology of Lead Poisoning in Cattle. la. St. Vet. 3:112-117.
1970.
18. Agricultural Statistics. U.S.D.A. 1969. U.S. Government Printing
Office: Washington, D.C.
19. Zook, B. C., J. L. Carpenter, and R. M. Roberts. Lead Poisoning in
Dogs: Occurrence, Source, Clinical Pathology and Electroencepah-
lopathy. Am. J. Vet. Res. 33(5):891-902. 1969.
20. Lambou, V. and B. Lim. Hazards of Lead in the Environment with
Particular Reference to the Aquatic Environment. Federal Water
Quality Administration, U.S. Dept. Int. Washington, D.C. August
1970. 28 pp.
21. Bagley, G. E. and L. N. Locke. The Occurrence of Lead in Tissues
of Wild Animals. Bull. Environ. Contamin. Toxicol. 2:297-305.
1967.
22. Baytes, F. Y., D. M. Barnes and J. M. Higbee. Lead Toxicosis in
Mallard Ducks. Bull. Wildlife Dis. Assoc. 4:116-125. 1968.
23. Benson, W. W. B. Pharoah, and P. Millei. Lead Poisoning in a Bird
of Prey. Bull. Environ. Contamin. Toxicol. 11(2):105-108.
24. Locke, L. N., G. E. Bagley, D. N. Frickie, and L. T. Young. Lead
Poisoning and Aspergillosis in an Andean Condor. Jour. Am. Vet.
Med. Assoc. 155(7):1052-1056.
25. Locke, L. N., and G. E. Bagley. Lead Poisoning in a Sample of
Maryland Mourning Doves. J. Wildl. Mgmt. 31:151-518. 1967.
26. Bazell, R. L. Lead Poisoning: Zoo Animals May Be First Victims.
Science 173:130-131. 1971.
27. Zook, B. C., R. M. Sauer, and F. M. Garner. Lead Poisoning in
Captive Wild Animals. J. Wildlife Diseases 3(3):264-272. 1972.
24
-------
28. Zook. B. C., R. M. Sauer, and F. M. Garner. Lead Poisoning in
Australian Fruit Bats. Jour. Vet. Med. Assoc. 157(5):691-694.
1970.
29. All croft, E. and K. L. Baxter. Lead as a Nutritional Hazard to
Farm Livestock. V. The Toxicity of Lead to Cattle and Sheep and
an Evaluation of the Lead Hazard Under Farm Conditions. J. Comp.
Path. 60:209-218.
30. Buck, W. B. Lead and Organic Insecticides Poisonings in Cattle,
Jour. Am. Vet. Med. Assoc. 156(10):1468-1472. 1970.
31. Cristea, J. Acute Lead Poisoning in Pigs. Reel. Med. Vet. 143:749-
754. 1967.
32. Hatch, R. C. and H. S. Funnell. Lead Levels in Tissues and Stomach
Contents of Poisoned Cattle: A Fifteen Year Survey. Can. Vet. J.
10(10):258-263. 1969.
33. Zook, B. C., J. L. Carpenter and E. B. Leeds. Lead Poisoning in
Dogs. Jour. Am. Vet. Med. Assoc. 155:1329-1342. 1969.
34. Slatter, D. H. Sump Oil: A Potent Source of Lead. Australian
vet. J. 49(9):46. 1971.
35. Donovan, P. P., P. T. Feeley, and P. P. Canavan. Lead Contamination
in Mining Areas in Western Ireland. II. Survey of Animals, Pasture,
Foods and Waters. J. Sci. Fd. Agric. 20:43-45. 1969.
36. Accumulation of Toxic Metals with Special Reference to Their
Absorption, Excretion and Biological Half-Times--Addendum, Environ.
Physiol. Biochem. 3:65-107. 1973.
37. Blaxter, K. L. Lead as a Nutritional Hazard in Livestock. II.
The Absorption and Excretion of Lead by Sheep and Rabbits. J.
Comp. Path. 60:141-159. 1950.
38. Fleischman, A. I., H. Yacowits, T. Hayton, and M. L. Bierenbaum.
Effect of Calcium and Vitamin D3 upon Fecal Excretion of Some
Metals in the Mature Male Rate Fed a High Fat Cholesterol Diet. J.
Natur. 95:19-22. 1968.
39. Byers, R. K. Lead Poisoning. Pediatrics 23:585-603. 1959.
40. Kostial, K. , I. Simonovic and M. Pisonic. Lead Absorption from the
Intestine in Newborn Rats. Nature. 233-564. 1971.
41. Six, K. M. and R. A. Goyer. Experimental Enhancement of Lead
Toxicity by Low Dietary Calcium. J. Lab. Clin. Med. 76(6):933-
942. 1970.
25
-------
42. Jacquez, J. A. Tracer Kinetics in Principles of Nuclear Medicine.
(H. N. Wagner, Jr. ed.) W. B. Saunders Co., Philadelphia. 1968.
43. Rescigno, A. and G. Segre. Drug and Tracer Kinetics. Blaisdell
Publ . Co: Waltham, Mass. Toronto and London. 1963.
44. Hursh, J. B. Retention of Pb in Beagle Dogs. Health Physics.
25(l):29-35. 1973.
45. Blaxter, K. L. Lead as a Nutritional Hazard to Farm Livestocks
III. Factors Influencing the Distribtuion of Lead in the Tissues.
J. Comp. Path. 60:177-189. 1950.
46. Potter, G. D., Dn~R. Mclntyre, and G. M. Vattuone. The Fate
Implication of Pb Ingestion in a Dairy Cow and Calf. Health
Physics. 20:650-653. ' 1971.
47. All croft, P- Lead as a Nutritional Hazard in Livestock. IV.
Distribution of Lead in the Tissues of Bovines after Ingestion of
Various Lead Compounds. J. Comp. Path. 60:190-208. 1950.
48. Fisher, H. L., Jr. A Model for Estimating the Inhalation Exposure
to Radon-222 and Daughter Products from Accumulated Lead-210 Body
Burden. Health Physics. 16:597-616. 1969.
49. Valee, B. L. and D. D. Ulmer. Biochemical Effects of Mercury,
Cadmium and Lead. Ann. Rev. Biochem. 41:91-128. 1972.
50. Ulmer, D. D. and B. L. Vallee. Effects of Lead on Biochemical
Systems. In: Trace Substances in Environmental Health, Vol. II,
2nd Ed. (D. D. Hemphill, ed.). Proceedings of Annual Conference at
the University of Missouri, Columbia, pp. 7-27. 1968.
51. Kelliher, D. J., E. P. Hilliard, D. B. R. Poole, and J. D. Collins.
Chronic Lead Intoxication in Cattle. Preliminary Observations on
Its Effects on Erythrocytes and on Prophyrin Metabolism. Irish.
Jour. Ag. Res. 12(l):61-69. 1973.
52. Hernberg. S., Nurminen and J. Hasan. Nonrandom Shortening of Red
Cell Survival Times in Men Exposed to Lead. Environ. Res. 1:247-
261. 1967.
53. Christina, R. G. and L. Tryphonas. Lead Poisoning in Cattle:
Brain Lesions and Hematologic Changes. Am. J. Vet. 32(2] 1:203-216.
1971 .
54. DeBruin, A. Certain Biological Effects of Lead Upon the Animal
Organism. Arch. Environ. Hlth. 23:249-264. 1971.
26
-------
55. Donawick, W. J. Chronic Lead Poisoning in a Cow. Jour. Am. Vet.
Med. Assoc. 148(6):655-661. 1966.
56. Simpson, C.F, and B. L. Damron. Abnormalities of Erythrocytes and
Renal Tubules of Chicks Poisoned with Lead. Am. J. Vet. Res.
31(3):515-523. 1970.
57. Reifenstein, E. C. Osteomalacia and Rickets. In: Principles of
Internal Medicine. 4th Ed. J. R. Harrison, R. D. Adams, I. L.
Bennett, W. H. Renik, G. W. Thorn, and M. M. Wintrobe. McGraw-Hill
Book Co., N.Y., Toronto, and London. 1964.
58. Goyer, R. A. The Renal Tubule in Lead Poisoning. I. Mitochondria!
Swelling and Aminoaciduria. Lab. Invest. 19(1):71-77. 1968.
59. Goyer, R. A. and R. Krall. Ultrastructure Transformation in
Mitochondria Islated from Kidneys of Normal and Lead-Intoxicated
Rats. J. Cell. Bio. 41(2) :393-400. 1969.
60. White, A., W. Handler, and E. L. Smith. Principles of Biochemistry.
McGraw Hill Book Co: N.Y., St. Louis, and San Francisco. 1973.
61. Goyer, R. A., P. May, M. M. Gates, and M. R. Krigman. Lead and
Protein Content of Isolated Intranuclear Inclusion Bodies from
Kidneys of Lead-Poisoned Rats. Lab. Invest. 22:245-271.
62. Campbell, K. I, N. K. T. Weaver, J. A. Taylor, and A. A. Krumm.
Biological Effects in Animals Chronically Exposed to Lead Chloro-
bromide Atmospheres Jour. Am. Vet. Med. Assoc. 159(11):1523-1529.
1971.
63. Nicholas-Schmitt, D. Brown, E. Devlin, A. A. Larsen, E. D. McCausland,
and J. M. Sanville. Lead Poisoning in Horses: An Environmental
Health Hazard. Arch. Environ. Hlth. 23:185-195.
64. Thompson, R. G. Reliability of Acid-Fast Inclusions in the Kidneys
of Cattle as an Indication of Lead Poisoning. Can. Vet. J. 13(4):
88-89. 1972.
65. Little, P. B. and D. K. Sorenson. Bovine Polioencephalomalacia;
Infectious Embolic Meningoencephalitis and Acute Lead Poisoning in
Feedlot Cattle. Jour. Am. Vet. Med. Ass. 155(12):1892-1903.
1969.
66. Zook, B. C. The Pathologic Anatomy of Lead Poisoning in Dogs.
Vet. Path. 9(5):310-327. 1972.
67. Robertson, C. M. A Case of Acute Lead Poisoning in a Dog. Vet.
Rec. 86:195-196. 1970.
27
-------
68. Vengris, V. E. and C. J. Mare. Lead Poisoning in Chickens and the
Effect of Lead on Interferon and Antibody Production. Can. J.
Comp. Med. 38:328-335. 1974.
69. Bagley, L. N. and L. N. Locke. Lead Poisoning in Canada Geese in
Delaware Avian Dis. 11:601-608. 1967.
70. Hopkins, A. Experimental Lead Poisoning in the Baboon. Br. J.
Ind. Med. 27:130-140. 1970.
71. Hemphill, F. E., M. L. Kaeberle and W. B. Buck. Lead Suppression
of Mouse Resistance to Salmonella typhimurium. Science. 172:1031-
1032.
72. Keller, L. D. and S. Kovacic. Decreased Antibody Formation in Mice
Exposed to Lead. Nature 250:149. 1974.
73. Stowe, H. D., R. A. Groyer, M. M. Krigman, M. Wilson and M. Gates.
Experimental Oral Lead Toxicity in Young Dogs. Arch. Path. 95(2):
106-116. 1973.
74. Sass, B. Perforating Gastric Ulcer Associated with Lead Poisoning
in the Dog. Jour. Am. Vet. Med. Assoc. 157(1):76-78. 1970.
75. Hsu, Frank Shin-Yun. Lead, Zinc, and Calcium Interation in Growing
Pigs, Diss. Abst. Int. B. 35(2):917-918. 1974.
76. Carson, T. L., G. A. Van Gelder, W. B. Buck, and L. J. Hoffman.
Effects of Low Level Lead Ingestion in Sheep. Clinical Toxicology.
6(3):389-403. 1973.
77. Egan, D. A. and T. O'Cuill. Opencast Lead Mining Areas. A Toxic
Hazard to Grazing Stock. Vet. Rec. 84:230. 1969.
78. Egan, D. A. and T. O'Cuill. Cumulative Lead Poisoning in Horses in
a Mining Area Contaminated with Galena. Vet. Rec. 86:736-738.
1970.
79. James, L. F-, V. A. Lazard, and W. Binns. Effects of Sublethal
Doses of Certain Minerals on Pregnant Ewes and Fetal Development.
Am. J. Vet. Res. 27(116):132-135. 1966.
80. Damron, B. L., C. L. Simpson, and R. H. Harms. The Effect of
Feeding Various Levels of Lead on the Performance of Broilers,
Poultry Sci. 48(4) :1507-1508. 1969.
81. Shupe, J. L., W. Binns, L. F. James, and R. F. Keeler. Lupine: A
Cause of Crooked Calf Disease. Jour. Am. Vet. Med. Assoc. 15(2)-
198-203. 1967.
28
-------
82. Van Gelder, G. A., T. Carson, R. M. Smith, and W. B. Buck. Behavioral
Toxicologic Assessment of the Neurologic Effect of Lead in Sheep.
Clinical Toxicology 6(3):405-418. 1973.
83. Coburn, D. R., D. W. Metzler, and R. Treichler. A Study of Absorption
and Retention of Lead in Wild Waterfowl in Relation to Clinical
Evidence of lead Poisoning. J. Wild. Manag. 15:186-192. 1951.
84. Blood, D. C. and J. A. Henderson. Veterinary Medicine, 2nd Ed. The
Williams and Wilkins Co., Baltimore. 1963. 1013 pp.
85. Prigge, E., and J. H. Hapke. Die Festellunger Einer Experimentellen
Sub-Klinischen Blievergiftung Bei Schafen. Deutsche Tier. Wochen-
shrift 79(19):475-476, 481-482. 1972.
86. Zook, B. C., M. C. Connell, and G. E. Gilmore. Basophilic Stippling
of Erythrocytes in Dogs with Special Reference to Lead Poisoning.
Jour. Am. Vet. Med. Assoc. 157:2092-2099. 1970.
87. Zook, B. C., L. Kapito, J. L. Carpenter, D. V. Cramer, and H.
Schwachmann. Lead Poisoning in Dogs: Analysis of Blood, Urine,
Hair and Liver for Lead. Am. J. Vet. Res. 33(5):903-909. 1972.
29
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TECHNICAL REPORT DATA
(Please read Instructions on the reverse before completing)
1. REPO
M-600/3-77-009
2.
3. RECIPIENT'S ACCESSION>NO.
4. TITLE AND SUBTITLE
THE SHORT-TERM EFFECTS OF LEAD ON DOMESTIC
AND WILD ANIMALS
5. REPORT DATE
January 1977
6. PERFORMING ORGANIZATION CODE
7. AUTHOR(S)
R.P. Botts
8. PERFORMING ORGANIZATION REPORT NO
9. PERFORMING ORGANIZATION NAME AND ADDRESS
Corvallis Environmental Research Laboratory
Corvallis, Oregon 97330
10. PROGRAM ELEMENT NO.
1AA602
11. CONTRACT/GRANT NO.
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-house, literature review
14. SPONSORING AGENCY CODE
EPA-ORD
15. SUPPLEMENTARY NOTES
16. ABSTRACT
Small quantities of lead,
all species of plants and
reportedly intoxicated by
a ubiquitous and toxic element, may be found
animals. The list of animals, both domestic
lead is impressive.
in practically
and wild,
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 centra
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. Treat-
ment of most clinical cases is disappointing generally because of the acute nature of
lead poisoning.
7.
KEY WORDS AND DOCUMENT ANALYSIS
DESCRIPTORS
b.lDENTIFIERS/OPEN ENDED TERMS
c. cos AT I 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/F,T
B. DISTRIBUTION STATEMENT
RELEASE TO PUBLIC
19.
This Report)'
21. NO. OF PAGES
35
20. SECURITY CLASS (This page)
UNCLASSIFIED
22. PRICE
EPA Form 2220-1 (9-73)
30
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