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OCR for page 256
Lead
The symbol for lead, Pb, is derived from the Latin plumbum. This
heavy, pliable metal is a bright bluish color, although easily tarnished
to dull gray with an oxide film. Lead rarely occurs in the native form,
but is usually found in the sulfide form in its chief ore, galena. The other
common inorganic salts, lead carbonate (cerussite), lead sulfate (angle-
site), and lead chlorophosphate (pyromorphite), are highly insoluble.
The industrial use of lead in the United States has doubled in the last
30 years to a stable annual consumption around 1,300,000 tons
(National Research Council, 1972) with the storage battery industry as
the leading consumer. Substantial amounts are also used in gasoline
additives, pigments, ceramics, pesticides' and plumbing (Paone, 1970~.
Lead is considered to be one of the major environmental pollutants
and has been incriminated as a cause of accidental poisoning in domes-
tic animals more than any other substance (National Research Council,
1972~. One of the primary sources of lead contamination in the air, soil,
and water is combustion of fuel containing lead additives. Underwood
(1977) and the National Research Council (1972) have excellent
reviews.
ESSENTIALITY
Lead is generally not considered to be an essential mineral for animals.
However, in a recent study by Schwarz (1974), the addition of 1 ppm
256
OCR for page 257
Lead
257
lead as lead subacetate increased the growth of rats by 16 percent (1.79
vs. 2.08 g/day) over controls receiving no supplemental lead. Increasing
the lead level from 1.0 to 2.5 ppm decreased this growth response by 33
percent from 0.29 to 0.19 g/day over controls. Lead oxide and lead
nitrate produced similar responses.
r
METABOLISM
Many reviews are available concerning the metabolism of lead
(National Research Council, i972; Vallee and UlImer, 1972; Ham-
mond, 1973; Neathery and Miller, 1975~. The bioavailability of lead
may be altered by diet, growth rate, and physiological stresses, such as
malnutrition, pregnancy, and lactation (White et al., 1943; Allcroft,
1950; Blaxter, 1950a,b; Jones, 1965~.
Lead tends to accumulate in the bones, consequently, the majority of
body lead (about 90 percent) can be accounted for in the skeleton
(Schroeder and Tipton, 1968) and appears to be relatively immobile.
Nonruminant animals absorb approximately 10 percent of dietary lead,
and ruminants absorb less than 3 percent (National Research Council,
1972~. Balance studies on humans ingesting environmental quantities of
lead have shown that only 5 to 10 percent of ingested lead is absorbed
(Kehoe, 1964; Thompson, 1971~. During chronic exposure a steady
state appears to be reached in which metabolic excretion, by way of
urinary and fecal excretion, approximately equals absorption. This
occurs after an initial tissue saturation level is reached; therefore, levels
of lead in many tissues and body fluids have been shown to increase
with increasing exposure to lead. Lead absorption in the human infant
and rat pup occurs at considerably higher rates than in the adult. In the
rat pup, high lead absorption was associated with lactation period
(Kostial et al., 1971, 1974; Forbes and Reina, 1972~. A decrease in
absorption of oral 2~2Pb in rats from nearly 90 percent to 15 percent
occurred within 20 to 30 days of age (Forbes and Reina, 19721.
Oral administration of 25 flu daily of cholecalciferol to weanling rats
increased absorption of lead acetate 33 percent (Smith et al., 1978~.
Vitamin D3 injected intraperitoneally to young rats (20,000 fug 48 hours
before oral administration of radioactive lead increased lead absorption
from the intestine and its deposition into both kidney and bone (Hart
and Smith, 1979~. Experiments with various vitamin D metabolites
(Mahaffey, 1979) showed that 1,25-dihydroxyvitamin D3 caused the
greatest increase in gastrointestinal lead absorption in rats.
In dogs studies with 203Pb, following acute administration of lead, a
OCR for page 258
258 MINERAL TOLERANCE OF DOMESTIC ANIMALS
significant fraction of plasma lead was ultrafi~lterable, and a large frac-
tion of the filtered lead underwent tubular reabsorption in the kidney.
The results provide no direct evidence for kidney tubular secretion of
lead (Vandere' al., 19771. When 30 mg lead as lead acetate was injected
intravenously in rabbits, the total quantities recovered from tissues
were bone marrow 14.1, liver 10.1, bone~.2, and muscle 1.1 me
after 4 days (Blaxter, 1950b).
The absorption of metallic lead in rats was inversely related to parti-
cle size, which ranged from 6 to 200,u (Barltrop and Meek, 1979~.
SOURCES
Environmental lead is largely airborne but returns to soil, water, and
plants as dust and can become a hazard, especially to grazing livestock.
Recent studies (Bolter et al., 1975) indicated that lead deposits from
smelters, as PbS, PbSO4, PbO PbSO4, or elemental lead, were from 2
to 7 times more soluble in organic acids of decaying foliage than in
water. Lead from automobile exhaust was primarily lead bromochlo-
ride (PbBrCl) (Olson and Skogerboe, 1975), but the lead halides were
converted to other compounds, primarily lead sulfate (PbSO4), and
deposited in soil.
Alkylated lead compounds are extremely unstable upon exposure to
air and light. Acute toxicity of the alkyl lead compounds is greater and
clinically different from that of inorganic lead compounds, but quantita-
tive toxic dosages are similar for the different compounds with long-
term subacute exposure (Hammond, 19731.
Most of the investigations on effects of lead in animals have been
conducted with inorganic salts or with the more soluble compounds
such as lead acetate. This limits the direct comparison of these results
to actual environmental situations where lead occurs in other forms.
Lead sulfate (PbSO4), the inorganic lead compound that appears to be
the major form contributing to the environmental burden and that may
be more soluble in an organic medium than an aqueous solution, has not
been studied in animals.
The main source of excess lead intake for cattle was that in paint
(Garner and Papworth, 1967) until the restrictions on the use of lead-
base pigments in paints. Other sources of ingestible lead include storage
battery plates, putty, linoleum, asphalt roofing, engine oil, insecticide
baits, and contaminated feeds (Garner and Papworth, 1967; Blood and
Henderson, 1968; Buck, 1970; Christian and Tryphonas, 1971; Aron-
son, 1972~. A major source of poisoning in wild water fowl is spent lead
OCR for page 259
Lead
259
shot (Rae and Crisp, 1954; Trainer and Hunt, 1965; Cook and Trainer,
1966; Grandy e' al., 19681.
TOXICOSIS
Clinical toxicosis in animals exposed chronically to lead is indirect and
probably results through interference in normal metal-dependent en-
zyme functions at specific cellular sites characterized by apparent
clinical abnormalities in hematological, neural, renal, or skeletal sys-
tems. Alleviation and diagnosis of toxicosis will depend on clarification
of the mechanisms involved. Lead poisoning in livestock is well docu-
mented and reviews have been published by Lidie (1970), the National
Research Council (1972), Ammerman et al. (1973), Clarke (1973),
Bremmer (1974), MacLeavey (1977), and Forbes and Sanderson (1978~.
Lead toxicosis is characterized by one or more of several clinical
signs and underlying pathophysiological effects (Ammennan et al.,
1977~. The main clinical signs in various species are:
microcytic hypochromic anemia
anorexia, fatigue, depression;
intestinal colic (constipation, diarrhea, abdominal pain);
4. vomiting, increased salivation, esophageal paralysis in dogs;
5. nephropathy;
6. irritability, peripheral neuropathy, encephalopathy, blindness in
cattle, laryngeal paralysis in horses;
7. weight loss;
8. abortion; and
9. maniacal excitement in young calves.
The main pathological ejects are:
1. derangement of porphyrin and heme synthesis;
2. interference in protein and Robin synthesis;
3. increased mechanical fragility of cell membranes resulting in
shortened life of RBC'S;
4. enzyme changes where small concentrations of lead (lO=6M) may
inhibit or enhance activities;
renal tubular intranuclear inclusion bodies, containing protein-
bound lead, calcium, and phosphorus;
6. basophilic stippling of erythrocytes and inhibitors of hemoglobin
synthesis; and
altered endocrine function.
7.
OCR for page 260
260 MINERAL TOLERANCE OF DOMESTIC ANIMALS
LOW LEVELS
Relatively large amounts of absorbed lead can be sequestered prefer-
entially in the skeleton with subsequent gradual release to the blood for
excretion during long-term, low-level consumption. Chronic lead toxi-
cosis is rarely seen in ruminants, but is more common in the non-
ruminant. It is usually recognized, however, only when distinct signs of
poisoning are apparent.
Lead poisoning was produced in cattle within 6 to 8 weeks when fed
lead acetate at 6 to 7 mg lead per kilogram of body weight daily (Buck
et al., 1961; Hammond and Aronson, 1964~. No adverse effects were
observed (Allcroft, 1950) when cattle were fed 1 to 2 g lead daily as lead
acetate, carbonate, or sulfide over a 2-year period. Dinius et al. (1973)
fed calves a concentrate diet containing O. 10, and 100 ppm added lead
as lead chromate for 100 days and saw no effect on feed consumption
or weight gain. There was increased accumulation of lead in the liver
and kidney with 100 ppm lead. Kelliher et al. (1973) observed reduced
growth and feed utilization when calves were fed 15 mg lead (lead
acetate) per kilogram of body weight for 283 days. There was no ad-
verse effect on performance when lead acetate [Pb(C2H3O2~2 3H2O]
was fed to lambs at added levels of 10, 100, 500, or 1,000 ppm lead (rick
et al., 1976~.
Coburn et al. ~ 1951 ~ fed lead nitrate at 6 mg lead per kilogram of body
weight daily for 137 days to ducks and did not observe any adverse
effects, but when the dose was increased to 8 to 12 mg/kg, the survival
periods averaged 28 and 25 days, respectively. Damron et al. (1969)
studied the effects of feeding 0, lO, 100, l,O00, and 2,000 ppm added
lead as lead acetate on feed intake and weight gain of broilers during a
4-week period. Decreased weight gain, feed efficiency, and feed intake
were noted at 1,000 and 2,000 ppm.
There is evidence indicating that horses may be more susceptible to
chronic lead toxicosis than cattle. Horses were poisoned on pastures
adjacent to a smelter and succumbed to the toxicity following a lead
intake during the winter period of 2.4 mg lead per kilogram of body
weight daily (Hammond and Aronson, 1964~. Horses exposed to a daily
intake as low as 1.7 mg/kg body weight (approximately 80 ppm Pb in
forage dry matter) were poisoned (Aronson, 1972~.
Due to the interference of lead in the biosynthesis of heme
(Hammond, 1973), assays on urine for 8-aminolevulinic acid (ALA) or its
dehydrase (ALAN) in red blood cells (McSherry e! al., 1971; McIntire et
al., 1973; Lauweryset al., 1974), and assays for erythrocyte zinc proto-
porphyrin (APP) (Lamola and Yamane, 1974; Lamola et al., 1975),
OCR for page 261
Lead
261
which may be present in amounts other than normal, have reflected
subclinical effects of lead ingestion. Blood lead level, ALA in urine and
plasma, and urine porphyrin concentrations were indicative of chronic
accidental lead exposure to paint by cattle that were being monitored
prior to lead administration Billiard et al., 19731. The level of red blood
cell Ale iS also a sensitive test for lead exposure in Japanese quail
(Stone et al., 19771. For most mammalian species, blood lead levels in
excess of 40 to 50 ,ug/dl are associated with recognizable effects of
toxicosis of lead (Hsu et al., 19751. Elevated blood lead may persist for
long periods of time after withdrawal of the lead source, as the body
burden is slowly depleted through lead excretion.
Lead-induced anemia in rats, a microcytic hypochromic type, has
been shown to result from an interference with copper and iron metab-
olism (Klauder and Petering, 1977~. Copper may be the target upon
which ingested lead has its antagonistic eject on hematopoiesis.
HIGH LEVELS
Acute lead toxicosis represents the greatest incidence of accidental
poisoning in domestic animals. Horses appear to be more susceptible to
lead poisoning than cattle, although cattle and dogs are the animals
most frequently diagnosed with lead intoxication. The problem has
been observed rarely in swine and sheep and it is uncommon in cats,
goats, and zoo animals (Priester and Hayes, 1974; Staples, 19751.
Chickens are very resistant to lead poisoning (Damron et al., 1969;
Vengris and Mare, 1974~. In the foal (Willoughby et al., 1972a), calf
(Aronson, 1972; Buck, 197S), canine pup (Zook, 1972), and child under
3 years (King, 1971; Green et al., 1973; Kolbye et al., 1974; Bryce-
Smith and Waldron, 1974), `'pica," or consumption of nonfood items,
has been implicated in the majority of accidental lead poisonings. Lead
pica can be habitual in some cases and requires removal of the source.
Allcroft (1951) stated that 200 to 400 mg of lead as acetate, basic
carbonate, or oxide per kilogram of body weight ingested in 1 day were
sufficient to cause death in calves up to 4 months old. Single oral doses
of 600 to 800 mg/kg may be a lethal dose to older cattle (Buck, 1970~.
Blood and Henderson (1968) reported that 30 g of lead acetate as a
single dose are lethal to sheep, which agrees with results of Blaxter
(1950a). Death was reported in sheep (Bennett and Schwartz, 1971)
with an accumulative dose of 417 mg/kg lead (lead arsenate, PbHAs04)
after 7 months.
Lead intoxications in swine are usually accidental and acute (Cristea,
19671. Link and Pensinger (1966) reported that pigs were relatively
OCR for page 262
262 MINERAL TOLERANCE OF DOMESTIC ANIMALS
resistant to the toxic action of lead acetate administered orally. Neither
11 nor 66 me of elemental lead per kilogram of body weight produced
acute toxicosis in 7-week-old pigs. Three pigs weighing 20 kg were
dosed weekly with 12 g of lead acetate for 3 weeks. No clinical signs
other than slight hypersensitivity were observed; however, liver levels
of 10 to 20 ppm lead (dry basis) were found (Nelson, 1971~. Damron et
al. (1969) also found chickens to be relatively resistant to lead poisoning
at levels up to 2,000 ppm.
Blood and Henderson (1968) reported that a single oral dose of
500 g of lead acetate was lethal to horses. Most common sources of lead
for sheep and cattle are usually not a problem for horses, because they
are less likely to lick old paint cans, storage batteries, peeling paint, or
motor oil (Aronson, 19721. Knight and Burau (1973) also observed lead
poisoning in horses grazing pastures near a smelter that contained 325
ppm lead (dry basis).
FACTORS INFLUENCING TOXICITY
Dietary calcium has been used for decades to decrease lead toxicity.
Voluntary ingestion of lead by weanling rats was increased during
periods of calcium deficiency, suggesting that this deficiency con-
tributes to lead pica (Snowdon and Sanderson, 1974~. Adult rats con-
suming 3 or 200 ppm lead (as acetate) in drinking water for 10 weeks
showed less toxicosis when 0.7 percent than when 0.1 percent calcium
was in the diet (Mahaffey et al., 19731. Excessive dietary calcium and
phosphorus decreased lead absorption in rats or lambs, and dietary
calcium decreased retention of lead in bone and tissues. (Morrison et
al., 1974; Quarterman and Morrison, 1975; Quarterman et al., 1978~.
Foals consuming 0.25 or 0.6 percent calcium and 0.3, 0.4, or 0.6
percent phosphorus, and challenged with 30 ppm dietary lead for 14
weeks, showed increased liver lead only with the lower calcium and
phosphorus levels (Willoughby et al., 1972b). Increased dietary cal-
cium (1.1 versus 0.7 percent) for 13 weeks also protected weanling
swine against toxicity from 1,000 ppm dietary lead as acetate (Hsu et
al., 1975~. Tissue and blood lead levels were decreased, and bone ash
and specific gravity were increased by higher calcium.
Lead toxicosis in animals may be complicated by simultaneous expo-
sure to excessive mercury, cadmium, zinc, molybdenum, copper, or
other microelements. Addition of dietary copper at 1, 5, and 20 ppm
increased accumulation of lead in liver and kidney tissue of rats when
lead was ingested at 200 ppm (Cerklewski and Forbes, 1977~. The
beneficial effect of high zinc on lead toxicity has been described in
OCR for page 263
Lead
263
horses (Schmitt et al., 1971; Willoughby et al., 1972b), in rats
(Cerklewski and Forbes, 1976a; Cerklewski, 1979), and in swine (Hsu
et al., 1975~. Iron supplementation also decreased lead deposition in
tissues of rats (Six and Goyer, 19721. Rats deficient in vitamin E and
challenged with high levels of lead had toxic signs more severe than
vitamin E-supplemented rats. These signs included decreased hemato-
crit, increased reticulocyte count, and splenic enlargement (Levander
eta)., 1975, 1977b). Further studies (Levanderet al., 1977a) revealed
that spherocytes develop more rapidly in vitamin E-def~cient, lead-
poisoned rats than in vitamin E-supplemented, nonpoisoned rats and
may help explain the splenomegaly, increased erythrocyte mechanical
fragility, and decreased red cell filterability observed.
Dietary selenium at 1 ppm did not reduce toxic effects in Japanese
quail fed 500 or 1,000 ppm lead (Stone and Soares, 1976~. In rats 1 ppm
selenium increased the toxic effects of 200 ppm lead (Cerklewski and
Forbes, 1976b).
When 300 ppm fluorine as NaF and 200 ppm lead as Pb(C2H302)2
were fed in combination to rats, there was severe weight loss and a 30
percent death rate, which were not observed when either element was
fed alone (Mahaffey and Stone, 1976~.
There are conflicting reports concerning the effect of protein on lead
toxicity. Early studies by Baernstein and Grand (1942) indicated that
low dietary protein enhanced susceptibility to lead toxicity in rats.
Conversely, Milev et al. (1970) reported that increasing dietary protein
from 20 to 60 percent increased the retention of a single oral dose of
Pub from 7 to 49 percent. The protein may influence the retention of
lead by decreasing absorption. Isocaloric protein-free diets also en-
hanced the retention of lead in comparison to the 20 percent protein
diet, but only by a factor of 2. Gontzea e' al. (1964) observed that
pair-fed rats on a 9 percent protein diet had higher lead concentrations
in blood, liver, and kidney than rats fed 18 percent protein. Gontzea et
al. (1964) suggested that the aminoaciduria caused by lead may increase
protein deficiency in low-protein diets, but an adequate level of dietary
protein might enhance elimination of lead by the kidneys.
Acute lead poisoning in animals is usually fatal if the animals are not
treated promptly. Attempts should be made to remove the lead from the
gastrointestinal tract, and sedatives can be used to relieve convulsions
(Garner and Papworth, 1967; Blood and Henderson, 1968~. Repeated
infusions of calciu~EDTA have been used for diagnosis and treatment
of lead toxicosis in cattle (Holm et al., 1953a,b; Lewis and Meikle,
1956; Hammond and Sorensen, 1957; Aronson et al., 1968~. Renal
intranuclear inclusion bodies have been proposed as detoxification
OCR for page 264
264 MINERAL TOLERANCE OF DOMESTIC ANIMALS
sequestrations of lead. They contain protein-bound lead, calcium, and
phosphorus. In rat studies (Goyer and Wilson, 1975), EDTA administra-
tion dislodged the bodies increasing urinary lead excretion. These
"inclusion bodies" have been observed in kidney, liver, brain, and
osteoblasts of bone marrow in lead poisoned animals and in nuclei of
plant leaf cells grown on soil high in lead.
TISSUE LEVELS
No significant changes in the tissue level of lead were found in liver,
kidney, heart, spleen, brain, bone, or muscle of sheep when dietary
lead as lead acetate was 100 ppm (rick et al., 1976~. Tissue levels
increased when dietary levels were 500 or 1,000 ppm (Figures 2 and 3~.
Similar results were obtained for calves fed 100 ppm lead for 100 days
(Dinius et al., 1973~. Liver and kidney contained 2.3 and 4.7 ppm lead
(wet weight), and none was detected in muscle. From slaughter animals
in Canada, 256 samples of beef and pork liver and kidney and poultry
240-
220-
200
180
CL
~ [40
IS
J
120-
100-
3 80-
~n
60-
40-
20-
BONE, ASH BASIS
KIDNEY, DRY BASIS
LIVER, Do BASIS
.'
~-
_
.~-'
-
o- - r-1 1 1 1 1 1 1 1 1 ~
O 100 500
SUPPLEMENTAL DIETARY LEAD, ppm
1000
FIGURE 2 Influence of dietary lead on lead deposition in bone, kidney, and liver in
sheep after 84 days.
OCR for page 265
Lead
TO -
..o-
~D
3.0-
2.0
J
~ 1.0
BRAIN
SPLEEN
HEART
MUSCLE
/
~ _--
-
-
-
-
-
_.
_
-
-
-
-
O- ~ ~ ~ ~ ~ ~ ~ ~ I ~ I
O tOO 500 1000
SUPPLEMENTAL DIETARY LEAD, ppm
265
FIGURE 3 Influence of dietary lead on lead deposition in brain, spleen, heart, and
muscle in sheep after 84 days.
liver ranged from 0.4~1.77 ppm lead (wet weight) (Prior, 1976~.
Fenstermacher e' al. (1946) concluded that 10 ppm (dry weight) or more
lead in liver should be considered suspicious of lead poisoning and ~3
ppm normal. Kidney cortex lead levels above 25 ppm (dry weight) are
considered as being of diagnostic significance (Todd, 1962; Garner and
Papworth, 1967. Lead levels in milk and urine are variable and
usually low.
MAXIMUM TOLERABLE LEVELS
Cattle, sheep, and chickens have been fed 10 ppm supplemental lead in
a soluble form for extended periods without adverse effects. Significant
increases in tissue lead levels occurred when 100 ppm lead was fed to
the same species. Dietary lead at 1,000 ppm has been tolerated by
ruminants and poultry for several months with no visible signs of toxi-
cosis. Approximately 300 ppm dietary lead resulted in observable signs
of toxicosis in horses of various ages. Young growing pigs fed 11 mg
lead per kilogram of body weight suffered from diarrhea, and 33 mg
OCR for page 266
266 MINERAL TOLERANCE OF DOMESTIC ANIMALS
resulted in decreased growth and muscle tremors. Death occurred with
a dietary intake of 66 mg lead per kilogram of body weight. With regard
to acute toxicosis, the ingestion of 200 to 400 mg lead (as acetate) per
kilogram of body weight caused acute death in calves and lambs up to
4 months old. In older cattle and sheep, the lethal single oral dose was
600 to 800 mg/kg of body weight. A single oral dose of 500 g lead acetate
(700 mg lead per kilogram of body weight) was lethal to horses.
The maximum tolerable dietary level for lead is considered to be 30
ppm for most species, although detectable increases in lead concentra-
tion may occur in certain tissues.
SUMMARY
Lead is considered to be one of the major environmental pollutants and
has been incriminated as a cause of accidental poisoning in domestic
animals more than any other substance. One of the primary sources of
lead contamination in air, soil, and water is combustion of fuels con-
ta~n~ng lead additives. Young animals are more susceptible to lead
toxicosis because they are more prone to lead pica and have a higher
rate (90 percent) of absorption from the intestinad tract. Adult non-
runiinants, however, absorb only 10 percent of ingested lead and rumi-
nants may absorb less than 3 percent. Clinical toxicosis appears to be
exerted through interference in normal metal-dependent enzyme func-
tions and is characterized by abnormalities in hematolog~cal, neural,
renal, or skeletal systems.
OCR for page 267
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OCR for page 272
272 MINERAL TOT ERANCE OF DOMESTIC ANIMALS
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Representative terms from entire chapter:
lead acetate
