PUBLICATION 5139
veterinary
Trace Mineral
Deficiency and
joxicity information J
I*
Agriculture
Canada
c 3
Province of British Columbia
Ministry of Agriculture
£ £^ ^culture g
'-SEE"*-*-* r
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A FEDERAL/PROVINCIAL PUBLICATION
CANADA / BRITISH COLUMBIA
VETERINARY TRACE MINERAL DEFICIENCY
AND TOXICITY INFORMATION
This publication was prepared by the author for the
Veterinary Service. Under the provisions of the
Federal-Provincial Regional Cooperative Publishing
Program, the Canada Department of Agriculture has
agreed to print this publication.
R. Puis, Provincial Veterinary Diagnostic Laboratory,
Abbotsford, B.C. V2S 4N8
PUBLICATION 5139, available from
Information Services, Agriculture Canada, Ottawa K1 A 0C7
©Minister of Supply and Services Canada 1981
Cat. No. A63-51 39/1 981 E ISBN: 0-662-11367-5
Printed 1981 3M-3:81
Aussi disponible en francais
FOREWORD
This material is designed to aid practising veterinarians,
veterinary pathologists and other agricultural advisory
personnel in interpreting analytical results received from
veterinary analytical laboratories.
The material is not complete and is being continually
expanded and updated as time and information become available.
The information has been compiled from many thousands of
references, some quite conflicting, others complementary.
I have attempted to restrict the information to one page per
element per species with emphasis on diagnostic tissue levels.
The remainder of the page is devoted to miscellaneous toxicity,
treatment or diagnostic data gleaned from the literature. Few
references have been specifically cited in the text due to
space restrictions, but bibliographies of the references
reviewed during the compilation of each section are available
from the author.
For further in-depth information, particularly on mechanisms of
action, clinical signs, treatment and prevention, the reader is
referred to standard texts, some examples of which are listed
herein under "General Reference Texts".
R. Puis, N.D.A., CD. A., P.Ag.
Veterinary Analytical Toxicologist.
Digitized by the Internet Archive
in 2012 with funding from
Agriculture and Agri-Food Canada - Agriculture et Agroalimentaire Canada
http://www.archive.org/details/veterinarytracemOOpuls
TABLE OF CONTENTS
Page
User Notes •
• • • •
3
Interpretation of Data . •
5
Definition of Terms
7
Abbreviations #, ., •
a
General Reference Texts
9
Factors Affecting Trace Mineral
Uptake by Plants . .
10
Mineral Interrelationships .
11
Arsenic ,
12
Bromine .
19
Cadmium .
20
Chromium .
24
Cobalt
25
Copper #
28
Fluoride #
39
Iodine .
ko
Iron ,
k*
Lead .
52
Magnesium #
58
Manganese .
60
Mercury #
64
Molybdenum .
70
Nickel
73
Selenium .
75
Tungsten ,
69
Uranium ,
90
Vanadium .
92
Zinc
9k
USER NOTES
1. The author considers speed of analysis to be paramount for
diagnostic purposes, with ultimate precision of secondary
importance.
2. In dealing with diagnostic ranges, which are not absolutely
clear cut, wet weight analyses are considered to be
sufficiently accurate,
3. Tissue levels should not generally be used as the sole
diagnostic criteria unless they fall well within a clearly
defined range. (Severe liver damage such as cirrhosis can
lead to mineral levels not reflective of dietary intake).
k* Levels falling at the extremes of ranges or in overlapping
ranges should be supplemented with additional confirmatory
data prior to establishing a firm diagnosis (exposure,
clinical, gross and histopathological signs).
5. More than one diagnosis may be warranted for a case (e.g.
bacterial infection due to reduced immune response resulting
from selenium deficiency).
6. More than one mineral may be involved in a case - in B.C.
copper and selenium deficiency often occur concurrently.
7# Interactions should not be overlooked (e.g. molybdenum
induced copper deficiency or lead and cadmium induced
selenium deficiency.)
b1. Repetition within the notes has been avoided whenever
possible - the notes listed under all species should be read
regardless of the particular species currently under scrutiny,
9. Some of the notes are taken from single unsubstantiated
research reports. They are subject to continual revision and
updating as more data becomes available.
10. Interactions have not been presented in this edition with
any reference to their severity or significance. Some
interactions (copper-molybdenum) are severe, others (copper-
selenium; are less significant.
INTERPRETATION OF DATA
1. Most tissue levels are presented on a wet weight basis in
parts per million (ppm wet wt).
Wet wt x 3.5-4.0 = approximate dry wt for most tissues.
Wet wt x 5.0-6.0 = approximate dry wt for fetal tissues.
2. Dietary levels and some tissue levels (hair, bone) are
presented on a dry weight basis in parts per million (ppm).
3. All kidney levels refer to cortex,
k. Food consumption (dry matter) for cattle varies from 1./+ -
3.0 percent of body weight. Older fleshier beef cattle
consume the lowest amounts. Assuming a dry matter intake of
2.6% of body weight and a body weight of 600 kg (1323 lb)
100 ppm diet =2.6 mg/kg body wt = 1.56 g/day.
5. Overlapping ranges indicate that this particular analysis
is not a reliable indicator of the status of the animal in
the areas of overlap. In general, tissues falling into this
category have been omitted from the tables - some commonly
analyzed tissues such as liver and kidney have been included,
6. Intermediate ranges:
(a) Figures falling between the adequate and high ranges
indicate levels well in excess of requirement but not
approaching a toxic range.
5
Interpretation of Data contd.
b) Figures falling between marginal and adequate indicate
an uncertain area and could fall into either group.
5. Upper ranges for toxicity and lower ranges for deficiency have
in many cases been included. The ranges should be considered
open ended - the values included are the highest or lowest
figures reported in the literature or by personal communication,
and have been included to give analysts some idea of the
maximum or minimum levels likely to be encountered.
DEFINITION OF TERMS
Deficient:
levels at which clinical or pathological
signs of deficiency should be apparent.
Marginal
Adequate
High:
Toxic
levels at which subclinical effects may
prevail, such as reduced immune response,
or reduced growth rate.
levels sufficient for full functioning of
all body mechanisms with a small margin of
reserve to counteract commonly encountered
antagonistic conditions.
levels elevated well above normal but not
necessarily toxic.
levels at which subclinical, clinical or
pathological signs of toxicity would be
expected to occur.
Normal:
used where deficiencies are unknown,
indicates normal background levels.
ABBREVIATIONS
ppm parts per million
>ig/g micrograms per gram (= ppm)
mg/kg milligrams per kilogram (= ppm)
ng/g nanograms per gram (= ppb - parts per billion)
^g/L micrograms per liter
mg/L milligrams per liter
/igj/o micrograms per 100 ml
mg>/0 milligrams per 100 ml
g% grams per 100 ml
mEq/L milliequivalents per liter
n mol/L nano moles per liter
jx mole/ml micro moles per ml
< less than
^ greater than
LD 50 Minimum dose that will kill 50% of exposed animals
IU/L International Units per liter
SF/ml Sigma-Frankel Unit6 per ml
Hb haemoglobin
BUN blood urea nitrogen
CPK Creatine phosphokinase
% GT gamma-glutamyl transferase (transpeptidase)
GSH-Px glutathione peroxidase
SGOT serum glutamic oxalacetic transaminase
o
GENERAL REFERENCE TEXTS
The Merck Veterinary Manual, 5th Edition
Otto H. Siegmund, editor.
Merck & Co. Inc., Rahway, N. J. , U.S.A. 1979.
Trace Elements in Human and Animal Nutrition
4th Edition, E.J. Underwood.
Academic Press, New York. 1977.
Veterinary Toxicology, 1st Edition.
E.G.C. Clarke and M.L. Clarke.
Bailliere Tindall, London. 1975.
Clinical and Diagnostic Veterinary Toxicology
Wm.B. Buck, G.D. Osweiler and G.A.^van Gelder,
Kendall/Hunt Publishing Co., Iowa/ 1973.
Veterinary Medicine, 5th Edition.
D.C. Blood, J. A. Henderson and O.M.Radostits.
Bailliere Tindall, London. 1979.
Trace Element Metabolism in Animals.
C.F. Mills, editor.
E & S Livingstone (Edinburgh & London). 1970.
Trace Element Metabolism in Animals - 2.
W.G. Hoekstra, J.W. Suttie, H.E. Ganther, W.Merts.
University Park Press (Baltimore, London, Tokyo). 1974.
Nutrient Requirements of Domestic Animals series.
National Research Council,
National Academy of Science, Washington, D.C.
FACTORS AFFECTING TRACE MINERAL UPTAKE BY PLANTS
1. Soil pH: lime increases Mb uptake.
lime decreases Fb, Cd, Cu, Zn, Mn uptake.
2. Plant species: some plants have a greater ability to absorb trace
minerals than others. Soil pH has greater effect on some species
than others. Clovers by adding N to soils tend to reduce soil pH.
3. Soil organic matter: availability can be affected by reaction with
organic matter to form unavailable complexes (Cu, Ni, Fe, Al) to
less e.itent Zn and Mn.
Conversely some organic complexes are very soluble and probably
highly available.
4. Soil type: high clay content reduces Cd uptake.
5. Microbial activity: Mn is converted to unavailable form by microbes.
Microbial activity reduced below soil pH 5» 5 which can release
Mn in quantities toxic to plants.
6. Season and climate: trace element absorption varies with stage of
growth of plant.
7. Fertilizers: fertilizers can add impurities which increase trace
elements supply or reduce their availability (Cd). They can
affect the soil pH. They can exert direct effects (P reduces
Zn uptake) (P + S increase Md uptake).
10
MINERAL INTERRELATIONSHIPS
Modification of diagram by
Jacobson et al, J# Dairy Science, V .55, p935,
1972.
Sulphur
S
Phosphorus
P
Fluorine
F
Vanadium
V
Magnesiumj
Mg
Molybdenur
Mo
Sodiunr
Na
Manga ne s*
Mn
Tungsten
X W
Selenium
\ Se
Potassium
K
fCalcium
Ca
Silver
Ag
Cadmium
Cd
Beryllium
Be
Chromium
Cr
Aluminum
Al
11
ARSENIC
Cattle: Tissue Levels
Diet
Liver Kidney
Blood
Urine
Normal
0.03 - 0.40 0.15 - 0.40
0.05
0.5
High
1.0 - 50 1.5 - 5.0
Toxic -
acu
te
2.0 - 15 3.5 - 38
0.17 -
1.0
2-14
chr
onic
7.0 - 70 5.0 - 53
ppm wet wt
Normal forage 0.25 ppm
Normal hair 0.5 - 3.0 ppm
Average soil level 5.0 ppm
Normal milk 0.03 - 0.06 ppm
Deficiency - Arsenic may act as an essential trace element but no
deficiencies have been identified.
Toxicity - depends on the concentration and the form of arsenic.
Trivalent As (arsenite salts; is more toxic than pentavalent As
(arsenate salts;. Elemental As itself is nontoxic.
Arsenic poinoning is no longer common due to the discontinuation of use
of most of the sources of arsenic (insecticides, herbicides, defoliants,
sheep dips, etc.;. Main sources now are discarded cans of arsenlcals
and areas of industrial pollution (smelters;. Ashes from arsenic
treated fence posts that have been burnt contain high level of As.
Toxic dose -
Arsenic trioxide
Sodium arsenite
Monosodium acid )
methanearsonate )
15-45 g
1 - 4 g (7.5 rag/kg body wt)
10 mg/kg body wt/day
Cattle will develop a tolerance to As if fed at sublethal doses over a
period of time. They can subsequently develop a dependence on these
high levels.
Interactions - As is antagonistic to I, Se, Hg and Pb.
Signs of poisoning
Sudden death, colic, ataxia, partial paralysis, salivation polydipsia,
weakness, watery or bloody diarrhea, depression, trembling, chronic
convulsions, hematuria and either hypothermia or fever,
12
ARSENIC
Dogs: Tissue Levels
Liver Kidney Urine
Normal < 0.2 < 0.2 0.1 - 0.3
Toxic > 10.0 y 10.0 ) 10
ppm wet wt
Toxicity - Arsenic poisoning in dogs is no longer common due to the
discontinued use of arsenical rodenticides.
Hog feed containing a therapeutic level of arsanilic acid may cause
chronic arsenic poisoning if fed to dogs.
Toxic dose -
Sodium arsenite - acute single oral dose 50 - 150 mg
Arsenic trioxide - acute single oral dose 100 - 1500 mg
No effect level
Arsenite/ar senate 1.25 mg/kg
Cacodylic acid 30 ppm
Roxarsone (3 nitro) 100 ppm
13
ARSENIC
Horses: Tissue Levels
Liver Kidney
Normal < 0.4 < 0.4
High 1.0 - 5.0
Toxic 7.0 - 15 10.0
ppm wet wt
Toxic dose -
Sodium arsonate 1.0 - 3.0 g/day for 14 weeks.
Arsenic trioxide 10 - 45 g single oral dose.
No effect dose -
Arsenic trioxide 0.24 - 0.72 g/day for 2 years
MAXIMUM RECOMMENDED LEVELS OF ARSENIC
IN DRINKING WATER FOR ALL LIVESTOCK
AND WILDLIFE - 1.0 mg/L
For further details on arsenic see:
"Effects of Arsenic in the Canadian
Environment" f National Research Council
Canada - Associate Committee on Scientific
Criteria for Environmental Quality,
Publication 15391, 1978.
14
ARSENIC
Pigs: Tissue Levels
Liver Kidney Blood
.10 0.01
Normal diet
0.003 - 0,
,20
0.003 -
0.05% cobalt
arsanilate
1.0
1.0
Arsanilic acid
(110-250) ppm
2.0 - If. 5
4.0
Toxic diet
10 - 15
10 - 20
3-Nitro (toxic)
2.3 - 3.8
ppm
wet
wt
Deficiency - arsenic may be an essential trace element - limited
evidence to date.
Toxicity - arsenic tolerance in pigs is about 1/10 that of ruminants.
Single toxic dose - Arsenic trioxide 0.5 - 1.0 g
Sodium arsenite 0.05 - 0.15 g
Arsanilic acid
45 - 100 ppm in diet - growth promotion (90 g/ton = 34 ppm As)
200 - 250 - control of swine dysentry
400 - 2000 - toxic after 4 days to several weeks
8000 - toxic in 2 days.
Toxic condition is reversible if feed withdrawn on appearance of toxic
signs. Arsanilic acid at acutely toxic levels produces a refusal to
eat syndrome.
Signs of Toxicity - inco-ordination, ataxia, apparent blindness,
circling. Therapeutic doses of organoarsenical have occasionally
proved toxic if the animal is severely dehydrated or debilitated.
3-Nitro-Zf-hydroxy phenyl arsanilic acid
Recommended dietary level 37.5 g/ton =6.4 ppm As
Chronic toxic level 190 g/ton or 30 ppm As
Signs of Toxicity - Urination and defecation followed by trembling of
the shoulder, ham and back muscles. Later violent tremors, inco-ordination
and extreme agitation (screaming with nose resting on ground for support)
until animal lies down. At this point trembling ceases, resuming if
forced to stand again immediately. When rested for a few minutes animal
becomes normal. Signs occur only when stressed.
15
ARSEN IC
Poultry: Tissue
Levels
Diet
Liver
i — - ■ •
Kidney
P
Normal
~1
Toxic
Normal
1
Toxic
Non Medicated
0.01 - 0.25
5 - 10
0.01 - 0.20
5 - 10
Nitarsone -200 ppn
1.0 - 3.0
0.3 - 2.5
Roxarsone 45 g/ton
0.7 - 3-5
5 - 10
0.5 - 1.0
3-0
Carbarsone 375 ppn
0.6 - 2.0
0.5 - 1.0
Arsanilic Acid 100
ppm
5-10
ppm
wet
wt
5-10
Nitarsone (4-nitro phenyl a r
sonic acid) '
His
itostat'
Maximum recommended level in feed 0.02% (200 ppm).
300 ppm causes chickens to go off feed - some mortality.
600 ppm causes mortality in turkeys.
LD50 chickens 200 mg/kg body wt.
Roxarsone (3-nitro-Z). hydroxyphenylarsonic acid)
Maximum recommended level in feed 45 g/ton (14*2 ppn As).
90 ppm depresses growth rate and causes leg weakness.
350 ppm for 3-4 wks. is lethal.
LD50 - 200 mg/kg body wt.
Peak level of arsenic occurs in liver 5-H days after commencement of
treatment (up to 3«5 ppn) levels then drop and plateau at 1.0-1. 5 ppn.
Carbarsone (p-ureidobenzenarsonic acid) 'Carbosep'.
Maximum recommend level in feed 375 ppn (0.0375%).
3200 ppn is not toxic to turkeys.
Arsanilic Acid
Maximum recommended level in feed 100 ppn or 90 g/ton (34-3 ppn As).
Turkeys - 400 ppn decrease wt gain, LD50/28 days ^ 800 ppm
Chickens - 1000 ppn decrease wt gain, LD50/72 days = 1500 - 2000 ppn
16
ARSENIC
Rabbits: Tissue Levels
Diet
Normal
Toxic (60 ppm arsanilic acid)
Liver (Total arsenic)
1.0 - 2.5
3.0 - 6.0
ppm wet wt
Toxicity - Arsanilic acid is toxic to rabbits. Younger rabbits are
more susceptible than older rabbits.
Chronic toxic dose -
In water: 16 mg/day - adults
9 mg/day - young
8-10 rag/kg body wt arsanilic acid
In food - > 60 ppm arsanilic acid
Signs of toxicity -
Weight loss or failure to gain weight.
Profuse watery diarrhea, anorexia and depression.
Occasional nystagmus and epileptiform seizures prior to death.
17
ARSENIC
Sheep: Tissue Levels
Diet Liver Kidney Blood Urine
Normal 0.03 - 0.20 0.1 - 0.3
High 4 -8 0.04 - 0.08
Toxic 10-50 10-40 5.0 100-150
ppm wet wt
Sheep and cattle do not find arsenic distasteful and may develop a taste for it.
Sheep are slightly more tolerant of arsenic than cattle.
Toxic single dose
Sodium arsenite 11 mg/kg body wt or 0.2 - 0.5 g
Arsenic trioxide 3-10 g
Arsanilic acid 2000 - 4000 ppm in diet.
Arsenic in the most toxic form is tolerated at 10-20 ppm in diet.
Arsenic in the least toxic form is tolerated at 1000 ppm in diet.
Signs of toxicity
Abdominal pain, depression, groaning, salivation diarrhea.
18
BROMINE
Cattle:
Tissue Levels
Diet
Liver
Kidney
Serum
Normal
5 - 200
10 - 20
30 - 90
0.60 - 2.0
nigh
1000 - 2000
10 - 25
Toxic
3000 - 10,000
300 - 1000
300 - 2000
30 - 50
ppm
dry wt
mEq/L
Normal milk ^43 PPm diet)
0.13 - 0.25 mEq/L
or 5-10 ppm
Toxic signs - lethargy, weakness, ataxia, recumbancy,
Source - hay grown on methyl bromide treated soil.
Horse - as for cattle.
Goat - as for cattle.
Chicks - toxic diet 5,0o0 - 10,000 ppm (high F intake aggravates
Br toxicity.)
Sheep: Tissue Levels
Diet
8.0
30
ppm
Liver
2.0
ppm wet wt
19
CADMIUM
Cattle: Tissue Levels
Normal
High
Toxic (chronic)
(acute)
Diet
0.01 - 0.5
/ 5.0
50 - 500
2000 - 3000
ppm dry wt
Liver
0.02 - 1.0
1.4 - 2.0
50 - 160
50
Kidney
0.05 - 1.5
5.0
100 - 250
>200
ppm wet wt
Blood
0.004 - 0.04
0.04
Normal
High
Toxic
Hair
0.04 - 0.60
0.67 - 16.0
40 - 100
ppm dry wt
Muscle
0.024
ppm wet wt
Milk
ppm wet wt
Bone
0.001 - 0.03 <0.05
0.010 - 0.03
ppm wet wt
Cadmium accumulates in tissues as a function of age (liver and kidney).
Cadmium does not accumulate in bones or muscle tissue. Hair levels
increase in winter, as do levels in grass while it is dormant. Milk
levels reported in literature are unreliable due to contamination by
milking machines and handling equipment. Cd is not excreted in the
milk to any great extent.
Deficiency - There is little evidence to date to indicate Cd acts as
an essential trace element.
Toxicity - Dietary levels: 100 ppm cause abortions
200 ppm cause increased BUN in ruminants
Blooc levels are not diagnosticly elevated in toxicity situations.
Cadmium will cross the placental barrier to feti only at very high dose
levels.
Signs of toxicity - Excess cadmium causes anemia, abortions, still
births, malformed feti, impaired growth rate, hypertension, sodium
retention and reduces immune response.
Interactions - Cadmium is antagonistic to Cu, Fe, Mn, Se, Co and Zn
and vitamin A metabolism. Excess Cd reduces the toxic effect of Pb.
Cadmium is more toxic if the level of Ca in the diet is low. Relatively
low levels of Cd in the diet of pregnant rats (4.3 ,ug Cd/ml drinking
water) will significantly reduce the storage of Cu and Fe in fetal
tissues.
20
CADMIUM
Dog: Tissue Levels
Diet
Normal 5.0
High 30
Toxic
ppm
Liver
0.037
1.0 - 7.0
Kidney
0.12 - 0.18
4.0 - 17.0
> 200
ppm wet wt
Diet
Normal
High
Toxic
Horse: Tissue Levels
Liver
0.01 -
22.0
5.0
Kidney
0.05 - 10.0
4.2 - 23.0
> 200
ppm wet wt
Diet
Normal 0.06 - 0.83
High 5.0-60
Toxic 120
ppm
Pig: Tissue Levels
Liver
0.10 - 0.50
3.0 - 30.0
Kidney
0.15 - 0.99
2.0 - 50
>270
ppm wet wt
Diet
Normal
Toxic
Rabbit: Tissue Levels
Liver
0.30
Kidney
3.6
200 - 300
ppm wet wt
21
CADMIUM
Poultry; Tiasue Levels
Diet Liver Kidney Egg Yolk Muscle
Normal 0.01 - 1.0 0.1 - 0.5 O.k - 1.5 0.02 - 0.10 0.02 - 0.06
High 3-20 5-10 5.0 - 60 0.06 - 0.10 0. Ik - 0.3
Toxic kO - 1000 15 - 100 70 - 1^0 0.16 - 0.3
ppm ppm wet wt
Toxicity - LDr0 wide ranges reported in literature no doubt due to
make up of diet.
200 - 500 ppm diet.
165 - 188 mg/kg body weight.
3 ppm in diet has caused nephritis and enteritis yet enhanced egg
production. 60 ppm in diet has produced no ill effects. 12 - 60
ppm in diet has reduced feed consumption and egg laying. No effects
on fertility of eggs have been identified.
Interactions - Added dietary ascorbic acid protects against Cd
induced anaemia. Low Ca and Fe in diet allows increased Cd absorption.
Liver and kidney Zn levels increased with added levels of Cd in diet
in one trial.
22
CADMIUM
Sheep; Tissue Levels
Normal
High
Toxic
Diet
Liver
Kidney
Wool
Blood
< 0.5
0.0U - 1.U0
0.1U - 0.U8
0.55 - 1.22
0.02 - 0.20
5.0
2.0 - 20
U.o
5o - 5oo
50 - 600
50 - uoo
> 20
0.10 - 0.20
ppra
ppm
wet
wt
ppm dry wt
ppm wet wt
Soil Cadmium -
Normal soil level O.li ppm (range 0.1 - 1.0)
Abnormal soil level 160 ppm (proximity of smelter) .
Soil contamination - superphosphate fertilizer (the main source of soil contamination)
contains an average U2 ppm depending on source of supply.
Municipal sewage sludge may have a high Cd content (range 1 - 3U10 ppm Cd).
Soil and Plant Interrelationships
Phosphate fertilizer reduces uptake of Cd by plant.
Plant uptake of Cadmium increases in acid soils.
High clay content reduces uptake.
Uptake varies with plant species.
Soil Cd Oats Wheat Clover
0.03 ppm 0.03 0.01 0.10
0.21 0.27 1.38
ppm dry wt
Normal grain 0.01 - 0.07 ppm dry wt
Normal grass 0.8 -1.7 ppm
High grass 3.6 - UO.O ppm
23
CHROMIUM
Rabbit: Tissue Levels
Diet
Brain
Kidney
Liver
Serum
Normal
0.66-0.94
0.42-1.58
0.3-1.0
4.3-5.5
High - Toxic
-Trivalent Cr
1.0 -1.96
17.0-30.7
6.0-50
9.0-12.0
-Hexavalent Cr
3.»l-5.66
3.3-11.2
10 -50
13.0-15.0
ppm
wet wt
ppm
Level in blood is not a good indicator of body status:
Hair level may be good indicator.
Bovine Milk 8-13 ng/g (average level)
Eggs 0.05 - 0.15 ppm wet wt
Deficiency
Dietary requirements of livestock are unknown.
Chromium deficiency reduces growth and longevity, disturbs glucose,
protein and lipid metabolism.
Chromium is thought to function as a cofactor with insulin.
Toxicity
Hexavalent Cr is more toxic than trivalent Cr.
Cats tolerate 1000 mg/day, and rats 100 mg/day trivalent Cr. 5 mg/1
Cr III in the drinking water of rats and mice or 20 ppm in the diet
produced no ill effects over their lifetime.
Toxic diet approximately 2 mg/kg/day.
BUN levels increase with chronic chromium toxicity indicating renal
damage.
Interactions
Cr and An are antagonistic.
24
COBALT
Ruminan
t: Tissue Leve
Is
Diet
Liver
Kidney
Milk
Deficient
<0.06
< 0.005
0.014
Marginal
0.07 -
0.10
0.005 - 0.017
Adequate
0.10 -
0.25
0.020 - 0.085
0.071
0.4 - 1.1
High
If
20
0.085 - 5.7
Toxic
> 20
5.0 - 300
30 - 200
■
ppm
ppm we
t wt
yUg/L
Hair Co is an unreliable indicator of the Co status of animals.
Ruminant: Vitamin B,- Levels
Diet
Liver Serum
Cobalt Deficient
0.04 - 0.10 0.04 - 0,
20
Marginal
0.11 - 0.22 0.25 - 0.
35
Adequate
0.25 - 2.24 u.40 - u.
ppm wet wt ng/ml
60
Sheep: Blood Levels
Normal
Cobalt Deficient
Plasma glucose 59 - 72
26 - 36 mg%
Alkaline phosphatase 60 - 90
18 - 44 IU/L
Formiminoglutamic acid 0
0.10 - 0.20/1 mole/ml
SGOT 50 - 70
400 - 600 SF/ml
Blood pyruvate 0.60 - 0.90
1.0 - 2,2 mg%
Ascorbic acid 4-8
1.0 - 3.5 mg/L
Pyruvate kinase 40 - 80
200 - 5000 mU/ml
Sheep: Urine Levels
Cobalt Adequate
Cobalt Deficient
Urinary Methylmalonic Acid <25/ug/ml
30 - 150>ug/ml
Urinary Formiminoglutamic
Acid 0 - 0.01
u mole/ml
0.05 - 0.60
^i mole/ml
25
COBALT
RUMINANTS
Deficiency
Sheep have a higher dietary requirement than cattle - daily requirement
0,08 mg/day for adult sheep.
Signs of Deficiency - ocular discharge, listlessness, anaemia, loss
of apetite, loss of condition and weakness. "Ill thrift". White liver
disease in sheep appears to be the result of Cobalt or Vitamin B12
deficiency coupled with an unknown entity (plant metabolite or
mycotoxin). Cobalt deficiency reduces conception rates in cattle, and
in sheep a reduction in estrus occurs.
At the onset of Co deficiency, Vitamin B12 levels fall first (the most
sensitive indicator), followed by loss of apetite and elevated pyrurate
levels in 10-14 weeks. Other parameter alter after six months on a
deficient diet.
Interactions - Cobalt deficiency eventually leads to:
Thiamine deficiency (reduced erythrocyte transketalase levels) reduced
plasma ascorbic acid, glucose and alkaline phosphatase levels, elevated
pyruvate, pyruvate kinase, SGOT, formimino-glutamic acid serum levels and
increased urine methyl malonic acid.
Cobalt deficiency reduces the storage of copper in bovine and possibly
ovine livers and occasionally elevates ovine serum copper levels.
Possible Mn, Zn and I antagonism.
Treatment and prevention of deficiency - drench with cobalt chloride or
sulphate - effective for about 3 weeks.
Bullet of cobaltic oxide given orally to lodge in reticulo-rumen -
effective for at least 3 years.
Treatment of pasture with 1 to 5 kg CoSO^/hectare - effective at least 1 yr.
Free choice mineral or salt licks containing Co (O.OOi* - 0.01%)
Subcutaneous injection of hydroxocobalamine (2 mg initially then 1 mg/month).
Toxicity - toxicity and deficiency signs are similar - maximum safe daily
dose of cobalt chloride for calves 3-8 mg. Sheep are less susceptible to
toxicity than cattle - toxic diet for sheep is 200 ppm Co.
26
COBALT
Pigs: Tissue Levels
Diet
Liver
Kidney
Serum
Deficient
Marginal
Adequate
1.0
1.0 - 2.0
0.40
0.17 - 0.60
High
100 -
300
6.0 - 8.0
10 - 1?
1.00 - 1.20
Toxic
400
10 - 20
ppm dry wt
25 - 40
1.20 - 1.70
ppm
Urine: Normal 16 - 20 mg/L
High 220 mg/L
Toxic signs - cease eating, gaunt, stiff legged, unco-ordinated, muscle
tremors, hump backed. Cobalt and iron are antagonistic. Added iron
♦ manganese + zinc or methionine reduce toxicity.
Toxic diet - 100 mg/kg body wt for 3 days. Maximum safe daily dose of
cobalt chloride - 1 mg for weaned pigs.
COBALT
Chickens
Maximum diet 4.0 ppm when less than 10 ppm Fe. 50 ppm is toxic.
Additional iron and protein reduces toxicity.
COBALT
Soil - Plant Interrelationships
Liming pasture reduces plant uptake of Co and can induce deficiencies in
sheep even when soil levels of Co are 4.8 ppm.
Deficient soil < 3.0 ppm (<0.25 ppm acetic acid
extractable Co)
Normal soil ^5.0 ppm
High soil Mn (> 1000 ppm) reduces plant uptake of Co.
27
COPPER
Cattl<
s: Tissue Levels
Diet
Liver
Kidney Serum
Hair
Deficient
1.0 - 10.0
0.06 - 0.70
1.0 - 6.7
Marginal
5.0 - 25.0
0.55 - 0.80
6.5 - 8.3
Adequate
25.0 - 150
4.0 - 6.0 0.80 - 1.50
6.7 - 15
High
250
2.50 - 4.0
Toxic
250 - 700
10.0 - 15.0 4.0 - 11.0
ppm wet wt (x
3.5 approx. = dry wt)
ppm dry wt
Milk
Brain
Serum
Ceruloplasmin
Low
0.01 - 0.02
mg/L 4.0 - 9.0
0-80
Normal
0.05 - 0.60
mg/L 9-18
ppm dry wt
130 - 250
OD units
Liver leveli
5
Fetus &
Newborn
1 month 2 month
3 month
Deficient
2.0 - 30
2.0 - 25 2.0 - 20
2.0 - 25
Normal
35 - 200 50 35 40
(av. 100)
ppm wet wt (x 3.5-4.0 for dry wt)
(fetus x 6.0 for dry wt)
Plasma and whole blood copper levels are similar but plasma or serum levels
are better indicators of animals copper status. Not all copper circulating
in the blood is available to the animal. Serum copper levels increase from
third to fifth month of pregnancy. The author has not found serum levels
to be reliable indicators of copper deficiency.
Distribution of copper in the liver is uneven, the caudate lobe having
higher concentrations than those found in the dorsal or ventral lobes.
Availability and interactions -
Minimum recommended dietary level copper 10.0 ppm (B.C. hay average
5.0 ppm)
Recommended Cu/Mo ratio 3.0 minimum, 4.3 adequate, b.O ideal.
28
Cattle: Copper, continued
Soil copper levels > % ppm - normal pasture.
Soil copper levels < 28 ppm - deficient pasture.
Higher than normal sulphur (from soluble protein), molybdenum, cadmium,
zinc or silver content can induce copper deficiency. Molybdenum and
total sulphur are synergistic in inducing Cu deficiency.
Cu in silage appears to be less available than that in hay. High nitrate
levels in feed may depress copper utilization. Phosphate fertilization
of pastures reduces copper uptake by forage plants. Nitrogen and/or
Sulphur fertilization of pasture can decrease soil pH, increasing Cu uptake
and decreasing Mo uptake. Young grass passes through an animal at a faster
rate than old grass; this coupled with higher protein levels reduces
availability of Cu in young grass.
At low Cu soil level clinical hypocupraemia was seen only if Mo pasture
level was />5.0 ppm. In hypocupraemic areas with no clinical signs Mo
pasture levels were 1-4 ppm.
Copper and other minerals in tall fescue are poorly available to cattle.
Estrogens appear to adversely affect copper absorption or utilization.
Signs and Effects of Copper Deficiency in Cattle - Reduced fertility in
cows and semen quality in bulls. Poor hair coat, diarrhea and reduced
growth rate. Sudden death. Inability to suckle, incoordination, stiff
gait, opisthotonus or lateral recumbancy in newborn and young calves.
Cattle can have an extremely high or low copper status without showing any
signs of toxicity or deficiency; the reasons for this are not clearly
understood.
Entities often occuring concurrently with copper deficiency - either
parasitized animals are more susceptible to Cu deficiency or Cu deficient
animals are more susceptible to parasitism (probably the latter). Vitamin
D deficiency tends to occur in Cu deficient animals with concurrent bone
deformities. Magnesium deficiency concurrent with Copper deficiency has
occurred frequently in Scotland in single suckled calves. Calcium plasma
levels tend to be lower in Cu deficient animals. Copper and Selenium
deficiency frequently occur concurrently in B.C. cattle. Copper deficient
animals appear to suffer from reduced immune response mechanisms.
Cattle: Copper, continued
Prevention of copper deficiency: Oral
Free choice trace mineral mix or trace mineralized salt (0.1 - 0.2% Cu)
mixed into ration where possible to give 10 mg/kg in total feed.
Treatment - Calves: 3fl.oz. 1% CuSO^ solution orally. Oral copper
oxide granules (50g) have a longer residual effect (B.D.H).
Parenteral prevention or treatment
Inject 100 mg Cu subcutaneously at 6-7 months pregnancy (.lasts 3 months)
100 mg Cu subcutaneously after calving
50 mg Cu subcutaneously to calf at 2-3 months.
Copper Toxicity -
Young calves are more susceptible than older cattle.
Acute toxic d06e - calves 40-100 mg/kg body wt
cattle 200-6*00 mg/kg body wt.
High dietary levels of protein, Zn, Fe and Mo reduce copper toxicity.
30
COPPER
Dogs: Tissue Levels
Diet Liver Kidney Serum
Deficient
Normal 7-10 20.0 - 70.0 3.0 - 20.0 0.60 - 0.8u
Toxic 400 - 3000
ppm ppm wet wt ppm
Serum levels slightly decreased by stress and castration of males.
Serum levels increased by malignancies, chronic infections and epilepsy.
Females have lower serum copper levels than males.
Decreased serum Cu was associated with decreased T. protein levels.
An inherited defect leading to excessive copper accumulation and copper
toxicity has been identified in some bedlington Terriers. (Twedt, D.C.
et al, JAVMA, 175(3), 269-275).
Clinical Signs of Copper Toxicosis - acute episodes of anorexia,
vomiting, weakness, lethargy and dehydration or indisidious deterioration
of general condition followed by jaundice, ascites, cachexia, hepatic
encephalopathy and death.
31
COPPER
Horses: Tissue Levels
Diet Liver Kidney Serum
Deficient < 3.5 <4.0
Adequate 4.0 - 7.5 7.3 - 9.3 1.0 - 1.70
High 8uO ppm 1000-1500 30 - 40
Toxic
ppm wet weight basis
Serum copper increases from 30 days before parturition until parturition
in mares (up to 2.40 ppm in older - 20 yr mares;.
Copper deficiency can cause bone abnormalities in foals.
MILK: Parturition 1.00 ppm - 4 months 0,2.0 ppm.
Normal fetal liver appears to be in the region of 29 - 110 ppm wet wt.
32
COPPER
Pig
s: Tissue Levels
Diet
Liver
Young-Mature
Kidney
Serum
Deficient
< 5.0
0.60 - 1.02
u.15 - 0.40
Marginal
5.0 - 10.0
4.0 - 7.0
4.0 - 7.0
u.40 - 1.50
Adequate
10 - 20
6.0 - 20.0
7.0 - 10.0
1.70 - 3.0
High
100 - 250
40 - 70
12.0 - 16.0
1.70 - 3.0
Toxic
> 500
150 - 15000
300 - 1200
4.5 - 77
ppm
ppm we
t wt
ppm
Normal copper
Hair
8.0 - 15.
0 ppm
Liver - newborn
50.0
ppm
Blood - newborn
1.0 - 1.2
! ppm
Milk - colostrum
2.95
ppm
23 days
0.92
ppm
Copper adequate
Copper deficient
Plasma Cerul
oplasmin
Activity (A OD 540/min)
0.21 - 0.30
0.01 - 0.
10
Mature pigs accumulate more tissue copper than growing pigs.
Dietary levels - Recommended diet - up to 125 ppm is beneficial.
250 ppm questionable for growing pigs but beneficial
for mature animals as long as Zn and Fe levels are
increased as well. 20 ppm appears minimal for optimum health.
Increased incidence of stillbirths have been recorded in Cu deficient pigs.
Interactions - Molybdenum and Sulphate have no appreciable effect on
copper metabolism in pigs. Sulphide reduces copper uptake and accumulation
in liver. 1800 ppm sulphide in drinking water will prevent Cu accumulation
in the liver when fed a diet containing 500 ppra Cu. Increased calcium levels
in the diet increase copper storage in the liver. Increased copper levels
in the diet increase zinc storage in the liver, but decrease iron storage.
Toxicity - Blood serum is not a good indication of Cu toxicity in pigs.
Chronic copper toxicosis can result in iron deficiency anaemia in growing
Pigs.
33
COPPER
Poultry:
Tissue Levels
Diet
Liver
Blood
Feathers
Chickens:
Growers
9- 200
3.0- 15
o.Ob'-O.lo'
10-15
Layers
10- 130
3.0- 6
0.2O-O.i+5
10-15
Toxic
500-2000
35 -**50
0.22-0. 3a
Ducks:
Normal
10- 50
10 - 60
0.^-0. i+5
High
100- 200
25 -140
Toxic
>200
Turkeys:
Normal
10- 200
5-10
0.18-0.28
Toxic
500-3000
Geese:
Normal
3.0-26.0
Toxic
300- 600
50 -100
ppm
ppm
wet
wt
ppm
Chickens
Average Cu in normal egg = 60 ug
Average Cu liver day old chick = 6-27 ppm wet wt - level decreases over
the first 3 days then increases again to normal. Copper concentration
in the plasma of poultry correlates directly with the functional state
of the ovary.
Dietary Levels - copper requirement 8-10 ppm diet (positive response
to 150 ppm)
copper deficient diet 0.7-4.0 ppm
copper toxic diet > 300 ppm reduces growth rate and
egg production.
1000 ppm lethal.
Copper deficiency causes lameness and misshapen eggs in chickens.
Copper toxicity results in increased feather loss, reduction in weight
or weight gains and reduced feed intake and egg production.
Interactions -additional zinc prevents accumulation of Cu in liver (Mo
does not). Increased Cu supplementation increases the accumulation of
Mo, Fe, Zn and Mn in liver. Added methionine protects against Cu toxicity
in chicks. *,
Copper - Poultry contd.
Turkeys
Less susceptible to toxicity than chickens and probably have a higher
dietary requirement (60 ppm minimum requirement suggested).
500 - 1000 ppm diet may reduce growth rate and feed consumption.
1500 - 2Z+00 ppm diet reduces growth rate.
32ifO ppm lethal in 3 days.
Copper deficiency can result in aortic rupture in turkeys,
if-witro medication increases copper requirement.
Ducks and Geese
Accumulate more copper in the liver than chickens or turkeys fed same
dietary level. Toxic signs have occurred in ducklings fed a diet
containing 2u0 ppm Cu, but only when subjected to stress.
300 ppm in water is lethal to geese.
Swans
Often accumulate high levels of Cu in the liver (150 - 2300 ppm wet wt).
The significance of these levels is not clear. In copper poisoned swans
the kidney levels are also elevated (50 ppm wet wt) and the liver levels
are over 3500 ppm wet wt.
Mute swans seem to accumulate more copper in the liver than whooper swans.
The KeiCu ratio in poultry diets should be 5:1
35
COPPER
Rabbit: Tissue Levels (Adult;
Diet Liver Kidney Serum
Deficient < 4.0 <3.0
Marginal 10-16 4-10 2.5 - 3.8
Adequate 20 - 100 10 - 50
High
Toxic
<4.
,0
10 -
- 18
20 -
. 100
200
ppm
dry n
t
ppm wet wt
Rabbits are born with a reserve store of Cu which is drawn upon during
the suckling period.
Doe diet of 10 ppm gave average newborn liver content of 37.4 ppm dry wt.
Dietary levels - increasing Cu supplementation from 20 to 200 ppm gives
increased rate of gain with 18% protein diet. Only 100 ppm addition
required for same results with 2.2.% protein diet.
Interactions - dietary ascorbic acid is antagonistic to copper assimil-
ation in the rabbit.
36
COPPER
Sheep:
Tissue
Levels
Diet
Liver
Kidney
Serum
Deficient
0.5 - 4.0
0,10 - 0.60
Marginal
5.0 - 20
0.40 - 0.80
Adequate
25 - 100
4.0 - 5.0
0.80 - 2.0
High
100 - 300
1.5 - 5.0
Toxic
250 - 1000
18.0 - 120
3.3 - 20
ppm wet wt
(x 3,
,5 -
dry wt)
Brain
Wool
Milk
Deficient
2.4 - 4. 5
0.5 - 1.0
Marginal
3.5 - 7.0
2.0 - 4.0
Adequate
5.0 - 10.0
ppm dry wt
6.0 - 10.0
0.2 - 0.4
ppm
Fetal and neonate tissue levels are the same as the ewe on a dry wt
basis. Copper does not accumulate in the fetal liver as it does in cattle.
Normal fetal liver 16-20 ppm wet wt basis (x 6.0 = dry wt).
Copper levels in the blood plasma of ewes fall during pregnancy and
rise at parturition.
The author has not found serum or plasma copper levels to be a consistently
reliable indicator of copper deficiency. Serum copper levels increase
with added dietary Mo, this copper is non-ceruloplasmin Cu and is
unavailable to the animal.
Dietary requirements - recommended dietary level of copper 5.0 - 10.0 ppm.
Maximum safe level of dietary molybdenum 8.0 - 10.0 ppm. Maximum safe
level of dietary copper in lamb pellets 20 ppm, or 3.0 mg/kg body wt.
Toxic single dose of copper for sheep with adequate stores, 20-50 rag/kg
body weight.
Copper deficiency effects - reduced immune response, growth rate, wool
pigmentation and length, increased parasitism, bone fractures and wool
breaks with loss of crimp. Reduced fertility - failure of implantation,
embryonic loss and fetal death have been attributed to Cu deficiency
(abortions or still born lambs). Breed differences in susceptability
to Cu deficiency and toxicity have been identified.
37
Copper: Sheep continued
Treatment of Deficiency - Lambs - copper calcium edetate injection,
5-15 mg/month (ewes 90 mg Cu methionate every three months).
Prevention of deficiency - free choice trace mineral salt mix (0.03% Cu).
Higher levels may be used for short periods if deficiency is KNOWN to be
severe (0.15% for 2 months).
Oral (experimental) 3-5 g CuO needles (ewes), 1-2 g (lambs at Z+-5 weeks
of age).
Copper storage decreases dramatically with increased parasitism. Care
should be exercised in basing a diagnosis of Cu deficiency on tissue
levels alone as Cu supplementation coupled with improved parasite control
could lead to a toxicity situation.
Interactions - Higher than normal levels of calcium, cadmium, cobalt,
ferrous sulfide, selenium and molybdenum plus sulphur from protein,
reduce availability and storage of copper in sheep.
Copper retention in the liver is increased by high Mn level in diet. In
molybdenum - sulphate induced Cu deficiency kidney levels rise (7-10 ppm
wet wt>, total plasma Cu remains normal but TCA soluble plasma Cu drops.
Growth rate is reduced by Mo induced Cu deficiency but remains normal
if adequate sulphur is present.
Toxicity - Pastures fertilized with manure from chickens fed high dietary
levels of copper have accumulated sufficiently high copper levels to be
toxic to sheep. Pastures fertilized with manure from copper supplemented
hogs could also be hazardous to sheep. Mineral supplements designed for
cattle generally contain sufficient copper to cause chronic toxicity in
sheep. Confinement housed sheep seem to have a lower copper requirement
and are more susceptible to toxicity.
Toxicity - treatment of copper loaded sheep - Remove source of excess
copper if possible. 5^0 mg ammonium molybdate ♦ 1.0 g sodium sulphate/
ewe/day for 2 weeks in grain or drench. Reduce to 100 mg ammonium
molybdate + 1.0 g 60dium sulphate/ewe/day for further 2 weeks.
38
FLUORIDE
Cattle: Tissue Levels
Normal
High
Toxic
Diet
Bone ^rib)
Urine
Milk
10 - 20
200 - 1800
1.0 - 5.0
<0.l6
50 - 100
2000 - 6000
5.0 - 15
0.50
MOO
6000
20
ppm
ppm dry wt,
fat free
ppm
ppm
Fluoride is transmitted t ran sp lac en tally to the fetus.
Fluorine accumulates in bone as a function of age.
Dietary Levels
Dairy cattle (young heifers) Maximum diet 30 ppm
Slaughter cattle Maximum diet 100 ppm
Sheep (ewes) Maximum diet bO ppm
Maximum water 10 ppm
(finishing lambs) Maximum diet * 100 ppm
Pigs Maximum diet 1^0 ppm
Poultry Maximum diet 300 ppm
Recent field investigations indicate these maximum tolerance levels may be too high.
Interactions - Fluoride interacts with Al, Ca, P and I, and possibly many others.
Signs of Fluorosis
Chalkiness, mottling, staining, hypoplasia, abrasion and excessive wear of
permanent incissor teeth (over 2 years of age).
Lameness, stiffness, treading of the feet, anaemia and hypothyroidism.
Delayed estrus and poor breeoability. Stunted growth.
Source of F
Industrial contamination of environment (fertilizer plants and aluminum smelters).
Mineral supplements (high F in some rock phosphate).
Contaminated water supply (1.0 ppm beneficial and 30 ppm toxic).
Deficiency - little evidence to indicate natural occurrence in livestock. 1.0 ppm
F in forage seems to be nutritionally adequate.
GENERAL REFERENCES
Effects of fluorides in animals: National Academy of Sciences, Washington D.C. 197U
Environmental Fluoride: National Research Council Canada No. Ib08l, 1977
Trace Elements in Human and Animal Nutrition: E.J. Underwood Academic Press irth Ed.
pp 3U7 - 37U.
39
IODINE
Cattle: Tissue Levels
Diet Serum Milk
Dry-Lac tating Protein Bound (PBI) Total (TI)
Deficient < 0.1 3.0 - 4.0 3.0 - 10.0 8-20
Adequate 0.8 - 2.0 4.6 - 12.8 15 - 40 25 - 70
Excessive 10 - 50 30 - 100 90 - 300 510 - 3 070
Toxic - chronic 100 - 300 200 - 1500 4700 - 6400
- acute > 400
ppm >ig/100 ml >ig/L
TI correlates well with dietary intake (better than PBI). Calves are horn
with high total and protein bound I levels in serum which drop to adult
levels in 30 - 40 days, the major decline being in the first 8 days.
Toxicity - toxic dose less if animals under stress, 300 - 500 mg/day.
Ethylene diamine dihydroiodide (EDDI) is toxic to stressed cattle (50%
mortality when stressed with bovine respiratory disease complex).
164 nig I/day nay cause stress in cattle. Lactating cows will tolerate 2-3 g
I as EDDI per day (150 - 200 ppm I in feed or 3-5 mg/kg body wt).
Levels above 2 g I/day as EDDI are toxic to feti.
Acute signs - anorexia, excessive salivation, hyperthermia, coughing, nasal
and occular discharge and inappetance.
Chronic toxicity - enlarged thyroid, reduced growth rate, food consumption
and milk yield, reduced immune response, rough dry hair coat and decreased
fertility, difficulty in swallowing, hacking cough and weepy eye condition,
dead or weak calves.
Sources - sea weed, excessive feed additives, water.
Deficiency - reproductive failure - stillbirth, abortions, hairless or weak
young. Suppressed oestrus with resultant infertility - goitre.
Causes - low dietary intake.
Normal forage I Clover 160 - 180 ppb (dry wt)
Grass 60 - 140 ppb
Range of 60 - 1500 ppb depending on soil levels.
Interactions
Rubidium reduces I uptake, possibly also As and F. There appears to be a
Co - I interaction.
40
Iodine - Cattle contd.
Thiocyanates (metabolised from clover constituents) and perchlorates
are goitrogenic as are most Brassica sp. and many other cruciferous
species. Soybean is mildly goitrogenic.
Prevention of deficiency - free choice salt licks or trace mineral
supplements containing 0.01% I.
Recommended dosage of Iodine for foot rot prevention - 50 mg/kg
kl
IODINE
Deficient
Adequate
Dogs:
Tissue Levels
Diet
1.5 -
ppm
2.0
Total I
5-20
^ug/100 ml
Serum
20 - 100
75 - 200
ng/100 ml
Ik
<0.5 - 3.7
1 - *4
^ug/100 ml
Classical hypothyroidism rarely occurs in dogs - Goiter.
Signs of Deficiency - possible patches of alopecia on legs, moth eaten looking
coats, refractory skin infection, interdigital pyoderma or seborrhea.
Thyrotropin test - T, and T, tests sometimes give false normal results.
Thyrotropin (thyroid - stimulating hormone (TSH)) response test is often
preferred.
Baseline T,/T, levels are determined followed by intravenous administration
of TSH (5 units). Four hours later T, levels are remeasured. In this interval
T, levels in the normal dog will triple, whilst little or no increase will be
seen in the hypothyroid dog.
T^
Leve
1
1
- k
+
0.6
+
2.5
+ 0.6
♦ l.k
ug/dl
T, Level
75 - 200
*_25
1 25
+ 125
■f 95
ng/dl
Normal (euthyroid)
Hypothyroid. Treat with T,
Inactive peripheral conversion
Treat with T,
Problems - plenty of active meta-
bolite. Treatment with T, is often
ineffective. 7
Both T, and T, values are borderline.
Try treatment with T, for 3 months.
Values from Veterinary Reference Laboratory, Inc. Newsletter, Vol.2 No. 9.
See Walsh & Brown. Vet Med/SAC, 1980 Feb. pp 223-225
J+2
IODINE
Horses: Tissue Levels
Diet Serum
Total Protein Bound
Deficient
Adequate 0.1 - 0.2 2.0 - 10.0 1.6 - 2.7
High
Toxic 8.8 30 - 50
ppm ug/100 ml
Fetal thyroid weight - Normal 15 g
Abnormal up to 100 g.
Serum Tri-iodothyronine (T,) Normal Levels
Foals 0.5 - 3.7 n mol/1
Adults 0.3 - «2.0
Serum Thyroxine (T, ) All ages 5-39
T, levels ranging from 0 - 80 n mol/1 have been detected in horses with
normal thyroid function. Consequently T, levels cannot be regarded as a
reliable indicator of thyroid function in the horse.
Dietary requirement - pregnant mares require 1 - 2 mg I/day.
Toxicity - 35 - 50 mg I/day or 8.8 ppm in feed fed to a pregnant mare will
produce goitrous foals with no signs in the mare.
The use of iodized salt blocks, trace mineral supplements and dairy feed
(supplemented with I ) in combination for pregnant mares can induce iodine
toxicity in newborn foals.
43
IODINE
Pigs: Tissue Levels
1200
9.3 - 20
1500
0.30 - 1.60
1000 - 1800
10.0 -
> 2400
;ug/100 ml
ppm dry wt
ppm
Diet Serum Total Thyroid Milk
Deficient < 0.15
Adequate 0.2 - 2.0
High 25 - 800
Toxic 800 - 1600
ppm
Fetal tissues contain 6 times maternal levels.
Toxicity - 400 ppm in diet increases thyroid weight.
800 ppm reduces growth rate, feed intake and liver iron content.
Possible reduced conception at dietary levels in excess of 2.0 ppm.
Deficiency - reduces growth rate and bone maturation, hairless, thickened
skin, reduced reproductive performance and lactation.
Possible induction of deficiency by high nitrate in feed.
44
IODINE
Poultry: Tissue Levels
Diet Plasma T, Plasma T, Egg Iodine
Deficient <0.1 2.0 - k.O
Adequate 0.3 - 1.0 1.7 - 1.8 1.1 8.0 - 12.0
High 10 - ifO Z.k
Toxic 300 - 5000
ppm Mg% ^S%
Plasma Thyroxine (T, ) levels increase in salt deficient chickens.
Dietary requirement - 5-9/Ug/day or 0.3 ppm.
Toxicity - 300 ppm I in diet reduces egg production hatchability and
embryo survival.
5000 ppm I delays sexual maturity in cockerels.
Birds return to normal within 7 days of removing high dietary I.
0,3% KI in water is not toxic to chicks.
Maximum 6afe level dietary I = 40 ppm
5000 ppm I reduces weight gain in broilers.
Organic and inorganic thiocyanate (from rapeseed meal) reduce
I content of eggs.
k3
IODINE
Rabbit: Tissue Levels
Deficient
Marginal
Adequate
Toxic
Diet
0.2
0.2 - 0.3
0.5 - 1.3
200 - 1000
ppm
Serum: Total
Protein Bound
Iodine passes placental barrier in rat, guinea pig and rabbit, resulting in
fetal blood I levels 2 - 2.5 times those of the mother.
Thyroid weight (adults)
Normal 0.23 g
Goitrous 2.0 g
Toxicity - Excessively high mortality occurs in rabbit litters when
doe is fed 250 ppm I in diet.
500 ppm I in diet results in total loss of litter.
46
IODINE
Sheep: Ti ssue Levels
Diet
Serum
Milk
Thyroid
Total
Protein Bound
Deficient
Adequate
High
Toxic
<0.08 2.5
0.1 - 0.4 3.0 - 12.3
1.0 - 800 - 2600
4000 - 30000
ppm jag/100 ml
3.0 - 4.0
10 - 95
1.2 - 8.0 20 - 400
8.0-15 750 - 2500
jig/100 ml ppm wet wt
Serum Thyroxine (T, ) Normal Level
6.0 - 6.6;ug% 80 - 200 n mol/1
Marginal Deficient 4.7 - 515 >ug% 40-60 n mol/1
Severe Deficient level <2.6 n mol/1
Deficient ewes may show normal T, levels. Normal lambs are born with
elevated T, levels declining to levels equal to their dams by 8 weeks of age.
Deficient lambs are born with T, levels similar to or less than those of their
4
dams (the dam levels may be normal).
Toxicity - Chronic signs: hyperthermia and inappetance, goiter.
7 mg I/kg body wt/day or 90 mg/day EDDI or 200 mg/day KI
Acute signs - severe coughing, anorexia, hyperthermia, emaciation,
sluggish movements, nasal discharge, reduced appetite, increased respiratory
and heart rate.
400 mg/day KI
Some evidence to indicate decreased immune response.
Source - high pasture levels, sea weed, use of supplemented dairy feed and
excessive amounts of trace mineralized salt additives designed for cattle.
Deficiency - goiter, reduced fertility and reproductive performance, reduced
birth weight and growth rate of lambs, reduced wool growth.
Causes - goitrogenic plants, deficient pastures.
Prevention - free choice trace mineral or salt blocks or mixes containing
0.07% - 0.10% I.
Treatment - 2 oral doses, 280 mgKI or 360 KIO-j at beginning of 4th and 5th
month of pregnancy, or intramuscular injection 2 months prior to lambing of
1 ml iodised poppyseed oil prep (40% I).
47
IRON
Cattle: Tissue Levels
Diet
Low <40
Adequate 100 - 500
High 1000 - 2000
Toxic 4000
ppm
Liver
Kidney
10-20
Serum
45-300
30-150
0.5 - 3.0
700
300
4.0 - 6.0
ppm
wet
wt
ppm
Deficiency - little data available.
Toxicity - no direct toxic effects have been reported.
10 mg Fe/liter of drinking water has been reported to reduce total water
intake by cattle resulting in reduced milk production.
Interactions - Co, Cu, Zn, Mn and Se deficiency could be induced by high
levels of iron. Iron toxicity is influenced by Cu, P, Mn and Vitamin E.
IRON
Sheep: Tissue Levels
Diet Liver Kidney
Deficient <40 15 - 25 13 - 25
Adequate 100 - 280 30 - 300 30 - 200
High
ppm wet wt
Deficiency - confinement raised lambs have shown positive responses in
growth rate and immune response to 500 mg iron dextran injections administered
at 3 days of age.
48
IRON
Pigs:
Tissue Levels
Liver
Normal Levels
Plasma Iron
Total Iron
Binding Capac
:ity
Hemoglobin
Adequate (Adult) 100-200
100-150
200-500
10 -12+
At Birth 100-200
70-80
215-221
9.0-12+
100 mg Fe intramuscular at day 1-3
Day 10 100-130
100-150
200-600
10 -1/+
Day 20 60-100
100-150
200-600
10 -13
Day 30 25-2+0
100-150
200-600
10 -13
Deficient Levels
Adult 30-50
4.0-8.0
Day 3 to weaning 10-15
15-60
700-900
2+. 0-8.0
ppm wet wt
/ig/100 ml
g%
Pigs are born with the same hemoglobin and liver levels as the adult. These
levels drop to 70% of the initial value by day 3 with resulting anaemia if
no supplementation is given.
Dietary requirement (ppm Fe) Adult Growers
Minimum 80 - 100 100 - 150
Recommended 100 - 300 150 - 300
Maximum 2500
Toxic 2+000
Interactions - dietary ascorbic acid improves Fe absorption.
High levels of Zn, Mn, Cu, Cd, P and I reduce Fe availability.
An iron: copper ratio of 10:1 should be maintained in the diet.
Recommended treatment - Intramuscular injection 100-200 mg Fe as iron
dextran at day 1 or 2.
A second treatment at day 15-20 may be beneficial if late weaning or if pigs
are not consuming creep feed.
Oral administration of iron does not increase body stores of iron therefore
must be fed daily (10-2+0 mg Fe/day as ferrous fumarate).
Ferrous sulphate appears to be the best bioavailable source of Fe for pig
diets.
2+9
Iron - Pigs contd.
Feeding high levels of iron to the sow does not prevent anaemia in
her pigs unless they have access to her feed or feces.
The effect of injecting the sow prior to farrowing with iron preparations
is of doubtful value.
Research conducted at the Wayne Research Center of Allied Mills Inc.
indicates that pigs from sows fed a specific amino acid-iron proteinate
(Wayne Brood N'iron) remain anaemia free.
Feeding program incorporated 250-800 ppm Fe from Wayne Brood N»iron in
the sows diet 30 days prepartum to Ik days lactation.
Milk Fe levels increased from a normal of 1.37 ppm to 2.57 ppm.
Toxicity - toxicities may occur in vitamin E/Se deficient pigs given
intramuscular injections of iron dextran.
50
IRON
Poultry:
Tissue Levels
Diet
Liver
Blood
Haemoglobin
Egg
(Yolk)
Deficient
15
3-5
Marginal
35 - 45
30
5-7
Adequate
60
66 - 200
45-9
134
- 151
High
Toxic
200 - 2000
ppm
ppm wet wt
g/100 ml
ppm
dry wt
Added copper will protect against Fe toxicity up to 1600 ppm Fe in diet.
Iron: Copper ratio in feeds should be 5:1 for maximum growth rate.
Ferrous sulphate is the best bioavailable source of iron.
Lead toxicity increases Fe storage in the liver of waterfowl.
High copper levels cause increased Fe storage in the liver.
51
LEAD
Normal
High
Toxic
Cattle:
Tissue Le
;vels
Diet
Liver
Kidney
Blood
<1.0
0.1-1.0
0.2-2.0
0.02-0.20
5-20
2-10
3-20
0.30-0.40
>100
5-300
10-700
0.35-32.0
ppm
ppm wet
wt
ppm (cortex)
ppm
Milk
Hair
Bone
Normal
High
Toxic
0.002-0.013
0.5-5.0
60-90
1.0-7.0
0.10 - 0.25
10-100
ppm
ppm
ppm dry wt
The proportion of lead in the liver and kidney varies with the acuteness of
the toxicity. It is essential to check both liver and kidney levels as one
or the other may not contain diagnostic levels of lead.
Deficiency - little evidence to indicate lead has any function as an essential
trace element.
Toxicity - Toxic cumulative dose: 5-7 nig Pb/kg body wt/day (300 ppm diet)
Toxic single oral dose: 200-800 mg/kg body wt.
The toxic level of Pb in forage seems to be between 5-300 ppm. Uncertainty
probably due to element interactions.
Interactions - Pb affects copper, iron and selenium metabolism. It is known
to decrease immune response and vitamin E utilization (possibly by inducing
Se deficiency). Increased calcium may reduce Pb toxicity.
Sources of Lead - "Lead freenpaint can contain up to 1% Pb. Other sources:
waste engine oil, putty, roofing tiles, lead batteries, industrial
pollution, automotive exhaust.
Signs of toxicity - anemia, anorexia, fatigue, depression, constipation or
diarrhea, abdominal pain, nephropathy, blindness, head pressing, loss of
weight, abortion.
52
LEAD
Dogs
;: Tissue Levels
Diet
Liver
Kidney
Blood
Hair
Normal
0.1-3.5
0.1-2.5
0.01-0.20
0-88
High
3.6-5.0
5.0-10.0
0.30-0.80
60-87
Toxic
50 -200
10.0-50.0
0.60-7.4
88-
ppm wet wt
ppm
Urine
Lead
Delta-Aminolevulinic
Acid
Normal
0-50
0 -0.0041
Toxic (before
therapy)
>75
0.016-0.020
(24 hrs after
therapy)
chelation
>820
yUg/L
0.015-0.040
mg/mOs
Diagnosis of clinical lead poisoning in the dog should be based on a
combination of clinical signs and laboratory data as blood lead levels are
not always elevated.
Dogs residing in cities or close to heavily travelled highways often have
lead levels close to the upper limit of the normal range.
Lead accumulates in the ends of the long bones and in the hair of chronically
poisoned dogs.
Toxic dose -
Chronic
Acute
3 - 30 mg Pb/kg body wt/day
600 - 1000 mg Pb/kg body wt/day
Young dogs are more susceptible to lead poisoning due to their habit of
chewing during teething and bizarre eating habits.
Signs of toxicity - (similar to canine distemper).
Gastrointestinal - vomiting, colic and occasionally diarrhea.
Nervous - hysteria, clonic-tonic seizures, nervousness, head
pressing, opisthotonos, champing of the jaws, inco-ordination,
apparent blindness, deafness.
The finding of many nucleated erythrocytes in blood without evidence of
severe anemia is considered to be nearly pathognomonic of lead poisoning.
53
LEAD
Horses:
Tissue Levels
Diet
Liver
Kidney
Blood
Normal
1.0
0.5
0.5
0.04-0.25
High
30-50
3.0-5.0
3.0-5.0
0.30-0.60
Toxic -
chronic
100-800
4.0-50
5.0-140
0.33-0.50
acute
1000
ppm
10 -500
ppm wet wt
20 -200
0.60-2.5
ppm
Brain
Urine
Milk
Bone
Normal
0.5
0.04-0.20
0.006-0.
013
3.0-4.0
High
1.0-5.0
8.0-10.0
Toxic
10 -30
0.50-5.0
0.28 -0.
54
40 -200
ppm
ppm (after
chelation
therapy)
ppm
ppm dry wt
Blood levels are not good indicators of toxicity - fatalities have occurred
at 0.30 ppm, conversely levels of 0.60 ppm have been recorded in animals
showing no toxic signs.
Toxic signs - Pharyngeal and laryngeal paralysis (roaring)
Reduced immune response (possibly due to induced selenium
deficiency).
Toxic cumulative dose -
2.4 - 7 mg PbAg body wt/day from natural source.
Inorganic lead appears to be less toxic than lead occurring in naturally
contaminated forage.
Interactions - Cu, Fe and Se metabolism adversely affected by lead.
Pb and Zn appear to be synergistic.
54
LEAD
Poultry; Tissue Levels
Chickens
Normal
High
Toxic
Diet
Liver
0.1-0.5
Kidney
1-10
0.1-1.0
200-1000
5.0-10.0
5.0-12.0
5000
18 -90
20 -150
ppm lead
(acetate)
ppm
wet
wt
Blood
0.04-0.05
2.0 -6.2
4.0 -12.0
ppm
Normal
High
Toxic
Brain
< 1.0
7.0 -10
12.0-15
Bone
<50
150-400
>400
ppm
Chickens are far more resistent to lead poisoning than waterfowl.
Toxic dose - Chronic lethal dose 320 mg/kg body wt/day for 11-20 days.
1000 ppm lead (as acetate) depresses growth rate.
Signs of Toxicity - drowsiness, thirst, weakness, loss of appetite, diarrhea,
anemia, anorexia, peripheral paralysis.
Lead at high levels reduces immune response.
Turkeys - no information.
Ducks - see waterfowl.
Quail and Pheasants - similar to chickens,
55
LEAD
Sheep; Tissue Levels
Normal
High
Toxic
Diet
<1.0
3-60
5-300
ppm
Liver
0.05-0.80
5 -25
10 -100
Kidney
0.10-0.80
5 -100
5 -200
ppm wet wt
Blood
0.02-0.25
0.70-0.90
1.0 -5.0
ppm
Normal
High
Toxic - chronic
Bone (Tibia)
1.0 - 3.0
10 - kO
ppm
Brain
0.1 - 0.5
1.2 - 2.0
ppm wet wt
Wool
*+.0 - 7.0
12.0-18.0
25.0 -
ppm dry wt
Toxic dietary level -
Maximum no effect level
Minimum toxic level
Maximum tolerated dietary level
Minimum single toxic dose
Lead poisoning in sheep is not common.
0.3 mg/kg body wt/day
3.0 mg/kg body wt/day
3.0 - 10.0 ppm
60 - 80 mg/kg body wt
Clinical effects -^-aminolaevulinic acid-dehydratase levels in blood begin to
fall with ingestion of nore than 0.3 mg Pb/kg body wt/day.
Urinary ALA increases after 10 weeks dietary Pb of 3.0 mg/kg body wt/day.
Interactions - Lead reduces copper storage and selenium metabolism.
56
LEAD
Waterfowl: Tissue Levels
Diet Liver Kidney Blood
Normal 0.05-0.50 0.1-1.0 0.02-0.50
Toxic :
Ducks & Swans 10 -6^ 60 -1600 -33
Geese 9 -102 8 -55 3.3 -16
ppm wet wt
Diet
Normal
Toxic
Brain
Bone
Feathers
0.5-1.8 •
2.0-32
<1.0
3.0-2+0
20-300
10-100
ppm wet wt
ppm dry wt
fat free
ppm
Toxic dose - 12 mg/kg/day chronically toxic to ducks.
25 ppm in diet maximum no effect level.
8 pellets #6 shot ingested - lethal to ducks (15 days)
25 pellets #6 shot ingested - lethal to geese (15 days)
5 pellets #k shot ingested - lethal to geese (15 days)
Signs of Poisoning - Flaccid paralysis and prostration, emaciation,
impaction of proventriculus, distension of the gall bladder, green-brownish
staining of the gizzard lining, green discoloration of the liver and
intestinal tract, and a green diarrhea.
Interactions - Lead interferes with Cu, Zn, Fe and Se metabolism.
Elevated iron and zinc levels usually occur in Pb poisoned waterfowl.
Absorption of lead from the digestive tract is increased by a high fibre
diet, presence of Vitamin D2 and starvation.
The accumulation of lead in the organs increases with a low calcium diet.
57
MAGNESIUM
Serum Magnesium
Cattle
Sheep
Goat
Horse
Deficient
0.1-1.8
0.5-1.5
< 2.0
Normal
2.0-3.0
2.0-2.8
mg%
2.8-3.6
2.2-2.8
Pigs
Cats Dogs
Rabbits
Poultry
Deficient
<1.8
Normal
2.7-4.0
1.8-2.7 1.8-2.4
mg%
2.0-2.1
1.8-3.5
Urine Magnesium
Cattle
Deficient
20
Inadequate
20 - 100
Adequate
100- 250
Excessive
300- 400
mg/L
Tissue levels do not represent the magnesium status of the animal.
Deficiency - Hypomagnesemia in dead animals cannot be substantiated chemically
unless urine can be obtained.
Daily urinary excretion of magnesium is a better criterion of magnesium
supply than serum concentration. Serum levels do not fall until the animal
is severely deficient. Urine levels fall immediately the diet becomes
deficient.
Classical grass tetany does not usually occur in cattle until serum levels
drop below 1.1 mg%. Levels below 2.0 mg% are considered hypomagnesemic.
Occurrence - magnesium deficiency generally arises when grass grows rapidly
and is rich in nitrogen and potassium. Susceptibility increases with the
age of the animal.
Signs and effect - irritability, tetany, convulsions. Non-clinical hypo-
magnesemia adversely affects milk yield and heart function.
58
Magnesium contd.
Toxicity - excess dietary magnesium in cattle reduces feed intake,
retards growth and produces diarrhea and emaciation. Dietary
levels greater than 1% magnesium (as oxide) are toxic. Levels
greater than 2% produce bloody diarrhea and at i+% reduce feed
consumption to 25% of normal.
59
MANGANESE
Cattle: Tissue Levels
Deficient
Marginal
Adequate
High
Toxic
Diet
Liver
Kidney
Hair
1.0
1.0
1.0-5.0
10-20
1.5-3.0
0.93-1.2
5.0-15
i+0-200
2.5-6.0
1.2 -2.0
10 -80
1000
120-230
80
2000
ppm dry
wt
ppm
wet
wt
ppm dry wt
Deficient
Marginal
Adequate
High
Toxic
Blood
0.020
0.07-0.09
Serum
0.005
0.006-0.03
Milk
0.020-0.040
ppm wet wt
Bovine fetal and calf levels are generally low (<1,0 ppm wet wt ) seemingly
reaching normal levels by the 5th day of age.
Monitoring feed levels seems to be the best diagnostic aid.
Red and black hair contain more Mn than white - levels increase when cattle
are on pasture irrespective of total dietary intake.
Deficiency signs - Mn deficiency linked to silent heat, reduced conception,
abortions, reduced birth weight, increased percentage of male offspring,
paralysis and skeletal damage.
Toxicity - indicated by reduced growth rate.
Interactions - Iron, cobalt and calcium are antagonistic to Mn in all
species.
High Mn intake may cause calcium retention in feti.
High Mn intake increases I excretion and Fe absorption.
There is a Mn-choline interaction that may be of significance in the "fat
cow syndrome".
60
MANGANESE
Pigs: Tissue Levels
Diet
Liver
Kidney
Blood
Deficient
0.6
0.53-0.97
0.35-0.45
0.006-0.010
Marginal
6.0-20
2.8 -3.1
0.75-1.13
0.010-0.012
Adequate
40 -50
3.0 -4.0
1.5 -2.0
O.Oi+0
High r.
500-1000
4.0 -5.0
2.0 -3.0
Toxic
4000
ppm wet
wt
Rabbits: Tissue Levels
Diet
Liver Kidney
Hair
Deficient
0.63
0.2-0.3 . 0.3-0.8
0.25-0.75
Marginal
Adequate
50
1.0-2.0 2.0-3.0
0.40-1.20
High
Toxic
ppm wet wt
Tissues of all species remain relatively constant over a wide range of
dietary intakes.
Monitoring feed intake seems to be the best means of ascertaining the Mn
status of all species.
Interactions - Low manganese intake reduces the accumulation of Se in pig
tissues.
High manganese may decrease iron storage in the body.
61
MANGANESE
Poultry; Tissue Levels
Diet
Liver
Blood Feathers
Eggs
Yolk
Deficient
1 -10
1.5-4.0
1.2
0.5
2.0
Marginal
10-20
0.030-0.048
4.0
Adequate
4 0-100
2.0-4.0
0.085-0.091 11.0
33
High
1000
Toxic
4000
ppm dry
wt
ppm wet wt
ppm
Egg yolk levels are 4-5 times those in the egg white.
Deficiency - reduces body weight gain and causes hock disorders.
Interactions - there is a significant interaction between dietary
manganese and socium chloride in turkey poults.
Excess dietary copper slightly increases Mn storage in the liver.
62
MANGANESE
Sheep: Tissue Levels
Deficient
Marginal
Adequate
High
Toxic
Diet
6.0
6 -20
i+O -100
400-500
1000
ppm dry wt
Liver
1.0-2.1
2.0-4.4
2.0-3.0
5.0-10.0
Kidney
1.0-1.2
0.5-1.2
0.8-2.5
2.0-2.5
5.0
Wool
1.5-6.0
a. 0-18
ppm wet wt
Blood
0.010-0.020
0.012-0.014
0.020-0.025
0.030-0. 040
ppm
Lambs are born generally with high liver stores.
Interactions - High Mn intake may cause increased copper retention in
sheep and calcium retention in feti.
Plant uptake - Pasture Mn uptake is reduced b*y liming. Corn silages
are generally low in Mn.
63
MERCURY
Cattle: Tissue Levels
Normal
High
Toxic
Diet
<0. 01-0.10
1.0 - 5.0
4.0 - 30
ppm
Liver
<0. 01-0.06
2.0 - 40
2.0 - 40
ppm wet wt
Kidney
<0. 01-0. 09
14 - 146
50 - 200
Blood
<0.10
0.2-3.0
3.0-6.0
ppm
Normal
High
Toxic
Brain
<0.1
0.5-20
ppm wet wt
Milk
3-10
ppb
Hair
0.1
1.0-55
5.0-50
ppm dry wt
Hair levels correlate well with tissue levels.
Methyl mercury is more widely distributed in the body than inorganic mercury.
Toxicity - High tissue residues without toxicity signs have been shown to
occur experimentally. Therefore a diagnosis of mercury toxicity should not
be based solely on tissue residues.
Blood, urine, fecal and milk mercury levels appear to bear little relation-
ship to mercury toxicity until tissues have reached a saturation level and
damage is excessive.
Toxic dose - 0.1 mg Hg/kg body wt of methyl Hg is tolerated by calves for
90 days.
0.2-0.4 is tolerated by calves for 75 days.
Methyl mercury is more toxic than inorganic mercury.
Toxic signs - Ataxia, neuromuscular inco-ordination followed by convulsions
and a moribund state. Renal failure.
Time from ingestion to death averages 20 days.
64
MERCURY
Cats: Tissue Levels
Diet Liver Kidney Blood
Normal ^0.05-0.30 0.01 - 0.10 <0.01 - 0.10 0.01 - 0.30
High 0.5 -0.8 5.0 - 30 5 - 20 0.30 - 5-0
Toxic >1.0 30 - 100 20 - 30 6.0 - 20
ppm methyl Hg ppm wet wt
Brain Fur
Normal 0.01 - 0.10 1 -t 8
High • 8-65
Toxic 10 - 20 45 - 400
ppm wet wt ppm dry wt
Toxic dose (methyl mercury)
I.76 mg Hg/kg body wt for 14 wks.
0.74 mg Hg/kg body wt for 40 wks.
O.46 mg Hg/kg body wt for 60 wks.
A cumulative dose of 20 mg methyl mercury /kg body wt is toxic.
Toxic Signs
Ataxia, inco-ordination, abnormal gait, muscle weakness, tremors and
convulsions.
65
1
Horse:
MERCURY
Tissue Levels
Diet Liver
Normal < 0.1
Toxic (Chronic) 5.0-10.0
ppm
Kidney Blood
< 0.1 <0. 01-0. 10
5.0-300 2.0 -6.0
ppm ppm
Brain
< 0.01
> 3.0
ppm
Toxicity - Normal diet <0.1 ppm
Toxic diet (chronic) 0.40 mg/kg body wt - methyl mercury
Toxic signs - reduced appetite, weight loss, renal disturbance and neuro.
logical dysfunction. Laminitis and bilaterally symmetrical exudative
dermatitis.
66
MERCURY
Pigs; Tissue Levels
Diet Liver Kidney Brain
Normal < 0.1 <0. 01-0. 03 <0. 01-0. 09 <0.10
High 1.0 -6.8 1.0 -tt.O 0.5-5.0
Toxic 5.0 -150 10.0-200 5.0-25
ppm ppm wet wt
Toxicity signs - anorexia, loss of weight, central nervous system depression,
weakness, abnormal gain and inco-ordination. Vomiting and diarrhea.
Signs of toxicity may be delayed up to 3 weeks after a single toxic dose.
Toxic dose - Acute 20 mg/kg body wt methyl mercury
Chronic 0.2 mg/kg body wt methyl mercury
Mercury is cumulative , toxicity occurring after about 20 mg/kg body wt has
been consumed.
Interactions - Selenium counteracts mercury toxicity, resulting in an
increased accumulation of inorganic mercury in the liver and spleen.
67
MERCURY
Poultry:
Tissue Levels
Liver
Kidney
Brain
Blood
0.01-0.10
0.05-0.30
0.1
0.1
1.0 -10
2.0 -10
0.2-10
0.2-0.5
3.0 - 130
5.0 -90
0.5-40
0.1-12
ppm wet
wt
Normal
High
Toxic
Muscle
Feathers
Normal 0.008-0.10 0.07-0.10
High 1.0 -2.0 0.40-1.0
Toxic 5.0 -14.0 6.0 -12.0
White
Eggs
YoTk
0.03 0.03
5 -10 0.5-3.0
10-30 0.9-6.0
ppm wet wt
Total
0.03
0.1-0.9
1.0-2.0
Tissue levels are a good indicator of exposure to mercury, however, in view
of the extremely high levels found in some experimental birds which showed
no signs of toxicity, a diagnosis of mercury toxicity should not be based on
tissue residues alone.
Distribution of mercury in the body depends on the form in which it is
ingested. Organic mercury ingestion leads to higher blood and brain levels
with equal amounts in liver and kidney.
Inorganic mercury leads to high kidney concentrations. The proportion of Hg
in ess yolk v. white and total egg Hg v. methyl Hg varies with the form of
ingested mercury.
Toxicity -
Toxic dose (lethal)
Inorganic Hg
Alkyl (methyl) Hg
Single IV injection Dietary Water
2.6 50-100 500
30 5-ttO
mg Hg/kg body wt ppm
Dietary methyl mercury is more toxic than inorganic Hg. Young birds are
more susceptible.
Mercury has a biological half life of 30 days.
Signs of Toxicity - Inorganic: anorexia, necrosis of gastro intestinal
tract, nephrosis. Organic: abnormal neurological patterns, egg shell
thinning.
66*
MERCURY
Sheep: Tissue Levels
Diet
Normal
High
Toxic
Liver
Kidney
<0.1
<0.1
7-30
18 - 200
10 - 60
20 - 200
ppm
wet
wt
Blood
<0.1
0.2 -
2.0
Vfool
<0.1
0.2 - 10
Sheep appear to accumulate less mercury residues than cattle fed the same
dietary level.
69
MOLYBDENUM
Cattle: Tissue Levels
Normal level
(at normal Cu
level)
Toxic
(Cu deficient)
Liver
0.57-1.14
1.4 -100
Kidney
0.22-0.57
1.15-2.60
ppm wet wt
Milk
Blood
0.018-0.120 0.01-0.05
(0.073 av)
0.10-0.47
Toxicity - levels increase with increased Mo intake but are not toxic
unless Cu levels are low. (Non toxic levels of blood 10.0 ppm and
liver 1000 ppm have been recorded).
Interactions - toxicity is dependent on copper rmolybdenum: sulphur
(protein) in diet. Low Cu and high sulphur aggravate toxicity.
Dietary levels -
Normal pasture Mo 0.5- 3.5 ppm Cu 8-11 ppm
Toxic condition (cattle) 5.0- 6.0 8-11
(sheep) 10.0-12.0 8-11
High levels generally occur only in peat or organic soils.
Mo pasture levels lowest in Winter rising from April to peak in September.
Liming soil increases plant Mo uptake - high levels often occurring in
plants growing in alkaline sloughs.
Cu/Mo ratio diet: ideal 6:1, borderline 2:}-3:i, toxic < 2:1.
Dietary Mo above 10 ppm can cause toxicity regardless of Cu intake.
Prevention of Toxicity - 0.5 - 2.5 g CuSO, daily will protect against
150 ppm Mo.
Deficiency - no essential functions have been identified for molybdenum
in ruminant nutrition.
70
MOLYBDENUM
Chickens: Tissue Levels
Diet Liver Kidney Egg (Yolk)
Deficient < 0.02 0.3
Marginal
Adequate 0.03-1.0 0.4-0.8 1-2 0.03-0.08
High 3 -10 1 -i* 0.30-0.70
Toxic > 200 6.0-10
ppm wet wt ppm wet wt
Deficiency - Mo is an essential trace element for poultry.
Mo deficiency is thought to be partially responsible for a poor hatch-
ability syndrome with weak chicks having clubbed down and long ginger
hairs. It is involved in feather development, and is also thought to be
partially responsible for the scabby hip syndrome and femoral degeneration.
More recent work indicates Mo responsive conditions must be due to an
interaction with at least one other unknown nutritional disorder or
disease syndrome.
Mo is a component of xanthine oxidase and aldehyde dehydrogenase.
Interactions - availability is affected by Cu, Zn, Mn, Sulfate, Cd,
W, F, Fe and methionine.
Deficiency treatment - In some cases UO >ug Mo (as ammonium molybdate)
single oral dose, ha6 alleviated mortality in club down chicks and
improved feather growth (in males only). Addition of 0.2-2.5 ppm Mo
to diet has prevented scabby hip syndrome.
0.2 to 0.5 Jug Mo (as ammonium molybdate) intramuscularly corrected scabby
hip syndrome and restored normal feathering in some experiments.
Toxicity - dietary levels of 3-10 ppm Mo have inconsistently impaired
reproductive performance. Dietary levels greater than 200 ppm Mo reduce
growth rate.
71
MOLYBDENUM
Pigs: Tissue Levels
Diet Liver
Sows Normal 0.6-1.3 ppm
Slaughter Pigs Normal O.tt-1.9 ppm
A toxic diet of molybdenum is 1000 ppm.
72
NICKEL
Cattle: Tissue Levels
Deficient
Marginal
Adequate
High
Toxic
Diet
.002-. 08U
0.1
1.0 -10.0
100 -1000
>1500
ppm
Liver
0.2-0.6
0.2-0.6
ppm wet wt
Kidney
0.02
0.15-0.50
6. a
Milk
0.02-0.10
0.02-0.10
Normal Blood Serum - Nickel
Cat
1. 5-6.it ug/L
Cattle
1.7-4.4
Dog
1.8-4.2
Rabbit
Goat 2.7-4.4 ug/L
Horse 1.3-2.5
Pig 4.2-5.6
6.5-14.0 ug/L
Dietary levels - pastures contain 0.5-3.5 ppm Ni, grains contain
0.3-0.6 ppm Ni.
Deficiency - Nickel deficiency seems unlikely in farm animals, although
little is known about the bioavailability of Ni.
Deficiency signs ( <0.05 ppm Ni in diet)
Lamb 8 - nickel deficient lambs have shown reduced liver copper
stores and elevated liver iron levels. Nickel deficiency reduces
the rumen bacterial urease activity and deficient lambs grow less
rapidly.
Pigs - reduced weight gain, delayed sexual maturity, higier piglet
mortality. Parakeratosis with lowered Zn levels in hair and
liver.
Toxicity - high levels reduce palatability of feed and reduce intake -
chloride more toxic than carbonate.
Interactions - apparent Ni-Zn interaction.
73
NICKEL
Poultry: Tissue Levels
Deficient
Marginal
Adequate
High
Toxic
Diet
< 0.05
100- 300
700-1100
ppm
Liver
Kidney
0.10 0.13
0.36 if. 2
1.0-1.2* 9.7-12.0
ppm wet wt
Muscle
Bone
O.H 0.10
0.25-0.40 0.90-1.0
0.60-2.60 3.b10-6.0
ppm wet wt
Toxicity - excess cobalt enhances Ni toxicity (additive).
No specific signs are noted with a toxicity other than reduced growth
rate.
Reduced growth rate caused by excessive Ni is significantly reduced by
feeding high protein levels.
Studies suggest nickel can be teratogenic in chickens.
Deficiency - Ni interacts with Cu, Zn and Fe.
Signs - decreased yellow pigmentation of shank skin, thickened legs,
swollen hocks, dermatitis of shank skin and anaemia.
74
SELENIUM
Cat: Tissue Levels
Diet Liver Kidney Whole Blood
Deficient
Marginal
Adequate 0.3 0.26-0.54 0.77-1.14 1.7- 2.5
High 4.7 2.0 -4.6 4.2 -9.4 9.1-19.7
ppm ppn wet wt ppm dry wt
The incidence of selenium deficiency in cats is not yet well defined.
75
SELENIUM
Cattle:
Tissue Levels
Diet
Liver
Kidney
Serum
Deficient
<o.io
0.02-0.17
0.18-0.40
0.002-0.
,008
Marginal
0.10-0, 18
0.12-0.25
0.40-1.00
0.020-0.
,040
Adequate
0.25-2.00
0.25-0.50
1.00-1.50
0.070-0,
300
High
3.0 -if.O
0.75-1.25
2.00-2.50
2.5 -3.
5
Toxic (chr
onic)
> 5.0-20
1.25-3.6*
2.5 -5.0
3.5 -4.
,1
(acu
te)
7.0 -10.0
1.0 -3.0
ppm dry wt
ppm wet
wt (dry wt x 3.5
approx. )
Hair
Milk
Muscle
Hooves
Deficient
0.06-0.23
0.004-0.005
0.010-0. 050
Marginal
0.23-0.50
0.011-0.018
0.050-0.070
Adequate
0.50-1.32
0.030-0.050
0.070-0.150
High
1.40-30.0
0.070-1.270
0.250-0.500
Toxic
1.40-45.0
0.080-
0.50 -1.50
10.0
ppm dry wt
ppm wet
wt
ppm
Fetal liver contains double level of maternal liver on dry wt basis (fetal
ppm wet it x 6 2 dry wt). We presently consider 0.30 ppm Se wet wt in the
fetal liver to be an adequate level.
Elevated CPK (> 100 IU/L) is a good indicator of sub-clinical WMD
Elevated LDH and SGOT levels occur in clinical cases.
Serum contains approximately 30% of the whole blood Se in cattle with an
adequate Se intake. Adequate whole blood Se>0.090 ppm.
Dietary requirement - milking cow 4.0-6.0 mg Se/day.
Deficiency signs - acute selenium deficiency can cause white muscle disease
(WMD), diarrhea, muscle stiffness and occasionally recumbancy particularly
in parturient cows (similar to milk fever syndrome). Sudden death due to
cardiac failure with no prior signs of sickness.
Marginal selenium deficiency can result in retained placentas, abortions,
reduced fertility, decreased growth rate, decreased immune response.
?6
Selenium - Cattle contd.
Deficiency prevention - selenized salt or mineral mix containing 25-75
ppm Se free choice or 40 g/day/mature cow. Intraluminal pellets - two
30 g pellets containing 10% Se, last 18 months.
Treatment - injectable (e.g. Dystosel), one injection (0.13 mg Se/kg
body wt) will maintain body reserves of 40-60 days. Treatment 6hould be
followed by a prevention program to prevent recurrence.
Blood Glutathione Peroxidase Activity (GSH-Px u moles/min at 37 c)
Serum Se GSH-Px
Deficient 0.009-0.050 0.2-10.0
Marginal 0.009-0.072 10-19
Adequate 0.104 19-36
0
Reports of a non-selenium dependent glutathione peroxidase have appeared
in the literature. Recent findings indicate that bovine erythrocytes
contain only the selenium dependent form thus substantiating blood
glutathione peroxidase activity as a reliable indicator of selenium
status. Liver and kidney however appear to contain large amounts of non-
selenium glutathione peroxidase.
There appears to be a time lag of about 9 days before supplemented
selenium maximises GSH-Px levels.
Toxicity - LD^q chronic 0.4-0.5 mg/kg body wt or 50 mg/day/cow
subacute 10-20 ppm for 7-8 weeks
acute injectable Se 71-15 times therapeutic dose.
Hair is not a good indicator of toxicity as sulphur (protein) intake
affects deposition in hair.
Signs of toxicity - "blind staggers" or "alkali disease", loss of hair,
lameness, with cracked or deformed hooves.
Interactions - Arsenic, cadmium, copper, lead, mercury, silver, telurium,
zinc and to a lesser extent sulphate reduce the toxicity of selenium.
They can also induce a deficiency of selenium, thus it may be necessary
to increase Se supplementation when As or Cu supplementation is being
used or when animals are exposed to industrial pollution.
77
Selenium - Cattle contd.
Interactions
High linoleic acid intake (e.g. barley) increases incidence of WMD
when Se intake marginal.
Treatment of high moisture corn with proprionic acid to retard spoilage
reduces the vitamin E content with resultant increased WMD.
Plant uptake - Selenium in well-aerated, alkaline soils is more
readily available for plant uptake than similar quantities in poorly
aerated acid soils.
73
SELENIUM
Dogs: Tissue Levels
Diet Liver Kidney Blood
Deficient 0.01-0.20 0.10-0.30
Marginal 0.20-0.50 0.30-0.50 0.22
Adequate 0.51-1.0 1.00- l.Ou-1.50
Borderline
Toxic
ppm dry wt ppm wet wt
Deficiency is implicated in hip dysplacia and reduced immune response
79
SELENIUM
Hor
se:
Tissue Leve
(IS
Diet
Liver
Kidney
Blood(serum)
Deficient
0.01
0.16
0.58
O.OOtf-0.053
Marginal
0.053-0.120
Adequate
0.2-2
.0
0.30-1.0
0.70-2.0
0.140-0.250
High
0.350-
Toxic
30
10.0
ppm
ppm
wet
wt
ppm
Milk
Hair
Deficient
0,
,005-0.009
< 0.50
Marginal
0,
,008-0.015
Adequate
0,
,015-0.040
1.0-3.0
High
5.0-7.0
Toxic
7. 0-30. o
ppm
ppm dry wt
Normal fetal liver Se seems to be in the region of 0.29-0.46 ppm wet wt.
(A liver level of 0.12 ppm has been recorded in foal when mare fed
selenized salt free choice (25 ppm) and injected with dystocel 4 weeks
before foaling.)
Normal serum vitamin E - 4.2-8.7 jug/ml.
Blood level
SGOT
CPK
^GT
Erythrocyte GSH-Px
Se deficient
Elevated
Elevated
50-120
<9.0
Se adequate
200-400
20-100
20-30
9.0 -
IU/L
IU/L
IU/L
u moles/ml
Deficiency -
Si£]
ns - muscu
lar
dystrophy in
foals. Myocar
dial and skeletal
muscle disease often with steatitis. Azoturoa (tying up syndrome).
Reproductive disorders - pyometritis, repeat breedings, early embryonic
death, abortions and sudden death of foals.
Prevention - 1 mg Se + 200 IU vitamin E/day. Daily Se requirement 2.4
yiig/kg/day.
60
Selenium - Horse contd.
Toxicity
Toxic dose = 3.3 ug/kg/day
Chronic toxicity signs - lameness, cracking and sloughing of hooves.
Loss of tail and mane hair, dullness, emaciation, depraved appetite.
81
SELENIUM
Pigs: Tissue Levels
Deficient
Marginal
Adequate
High
Toxic
Diet
0.01-0.08
0.10-0.20
0.20-0.80
3.0 -4.0
7.5 -
ppm dry wt
Liver
0.03-0.10
0.12-0.25
0.30-0.80
3.0 -12.0
12.0-120
Kidney
0.40-0.77
0.77-1.10
1.50-2.90
3.0 -18.0
18 -90
ppm wet wt
(growing pigs lower end of range -
sows higher end of range.)
Serum
0.005-0.060
0.060-0.100
0.120-0.300
0.50 -0.90
Deficient
Marginal
Adequate
High
Toxic
Muscle
0.020-0.050
0.050-0.075
0.100-0.250
0.55
2.00
ppm wet wt
Milk
0.013-0.043
0.120-0.20
4. oth .
ppm at 7 day
Hair
0.18-0.22
0.24
ppm dry wt
Piglets from normal sows are born with a reserve of Se in the liver (1.6-
2.6 ppm wet wt) which depletes during the suckling period (to a minimum
adequate level of 0.30 ppm) i.e. sows milk does not supply sufficient Se
for the needs of the nursing pig. Serum levels may drop from 0.10 to a
critical 0.04 ppm at weaning, but should return to normal when eating solid
food (Se 0.2 ppm). This is a point in favor of early weaning.
Selenium is distributed evenly throughout the liver.
Glutathione Peroxidase Activity GSH-Px
Selenium
Deficient
Marginal
Adequate
Erythrocytes
<50
50 - 100
100 - 200
Plasma
0.25-2.0
2.0 -3.0
3.0 -8.0
>u moles QSH oxidised n moles NADPH oxidized/
/min/g Hb min/mg protein
Deficiency - Stress and exercise seem to hasten development of signs.
82
Selenium - Pigs contd.
Signs of Deficiency - Hepatosis dietetica, mulberry heart disease or
degeneration of skeletal muscles with resultant sudden death mainly in
fast growing animals. Iron injections can cause iron toxicity in Se
deficient piglets. Lowered disease resistance and possible reproduction
problems have been ascribed to Se deficiency.
Minimum recommended diet 0.15 - 0.2 ppm Se ♦ 10 IU vitamin E
or 0.20 - 2.0 ppm Se ♦ 5 IU vitamin E
Treatment of marginal Se deficiency
One injection: 0.25 rag Se/pig before 7 days old
0.06 rag Se/kg body wt at 40 days old.
Minimum dietary level 0.2 ppm Se.
Treatment of severe deficiency
Injection: medium 0.22 mg Se ♦ 15 IU vit. E/kg body wt.
high 1.10 mg Se ♦ 75 IU vit. E/kg body wt.
Diet supplementation to 0.60 ppm Se ♦ 30 IU vit, E/kg.
Se more readily absorbed from drinking water than from feed.
Elevated CPK (^300 IU/ml) is a good indicator of subclinical muscular
myopathy.
Toxicity - toxic dose as NapSeO, 17 >ig/kg body wt (8 pg/lb)
Poor conception caused by 10-20 ppm Se in diet for 7-8 weeks. Animals
showing toxic signs generally have higher liver than kidney levels.
Do not give high level injections to sows during last month of gestation
as this may induce Se toxicity in the feti.
Interactions - Arsenic and sulphur reduce Se retention in tissues.
Silver reduces blood Se levels but increases liver retention.
Proprionic acid treatment of high moisture corn destroys vitamin E.
Se-vitamin E supplementation reduces incidence of swine dysentry in Se
deficient pigs.
Manganese deficiency aggravates Se deficiency.
Riboflavin (vitamin B2) i8 involved in the Glutathione Peroxidase system
a deficiency of which may be implicated in WMD.
83
SELENIUM
Poultry: Tissue Levels
Deficient
Marginal
Adequate
High
Toxic
Diet
0. 01-0. 06
0.06-0.10
0.20-1.0
3.0 -5.0
5.0 -10.0
ppm dry wt
Liver
Kidney
0.10-0.40
O.Z+0-0.50
0.50-0.70
1.5 -2.5
Blood
0.02-0.85
0.85-0.13
0.13-0.20
0.05-0.25
0.25-0.35
0.35-1.00
2.00-4.0
4.0 -
ppm wet wt (x 4 = dry wt approx. )
Deficient
Marginal
Adequate
High
Toxic
Muscle
0.020-0.065
0. 065-0. 075
0.100-0.22
0.400-0.50
ppm wet wt
Whole Eggs
-0.04
0.06-0.10
0.25-1.00
1.50-2.00
2.50
Egg White
0.01-0.05
-0.05
0.05-0.25
0.32-0.80
1.0 -1.4
Egg Yolk
0.05-0.20
0.20-0.40
0.40-1.00
1.00-2.80
3.3 -4.0
(whiteryolk = 2:1)
Recommended minimum dietary level:
Chicks 0.1 ppm Se + 30 IU vit.E/kg or 0.2-2.0 ppm Se
Poults 0.2 ppm Se + 10 IU vit.E/kg or 0.3-2.0 ppm Se
Minimum adequate diet for chicks 0.1 ppm Se + 5 IU vit. E,
Average level vitamin E in poultry feeds 3-5 IU.
Deficiency signs: Exudative diathesis. Chronic Se deficiency results
in reduced growth rate, egg production, hatchability and fertility and
reduced immunity to infectious diseases and coccidiosis.
Toxic levels - Single dose 80 mg/kg
Acute oral LDcq 33 mg/kg body weight
Max tolerated dose 15 mg/kg body wt/day as selenite.
A diet of 5-10 ppm Se did not affect the laying hen
but embryonic development was adversely affected.
80 ppm in feed terminates egg laying with subsequent 30% mortality in hens.
84
Selenium -. Poultry contd.
Availability and interactions -
Se availability reduced by arsenicals, high protein, linseed oil,
unsaturated fats, lead, cobalt, mercury, cadmium, tellurium, silver,
copper and tin.
Dietary ascorbic acid (100 ppm) increases Se absorbtion from diet.
Utilization may be dependant on the antioxidant, Vitamin E or B-6
levels in the diet.
Availability of the Se in various dietary forms is not at all clear due
to literature discrepancies. Ranges reported as a percentage of the
availability of Se as socium selenite (taken as 100%) are as follows:
Substance ' Se Availability
Fish meal 33 - 60%
Soybean meal 15 - 65%
Grains 20 - «5%
Selenomethionine 70 - 80%
In vegetable foods Se seems to be present mainly as selenomethionine.
65
SELENIUM
Rabbit: Tissue Levels
Diet
Deficient 0.10
Marginal
Adequate 0.20
High
Toxic
ppm
Liver
Kidney
Blood
Muscle
1.00
0.35
1.07
1.58
0.35
0.18
7.0k
12.23
5.06
1.35
ppm wet
wt
Toxicity - LD^q/24 hr of Sodium selenite 2.53 mg/kg body weight
Sodium with vit. E 2.73 mg/kg body weight
Selenium metabolism in the rabbit appears to differ from that of other
species. Muscular dystrophy will develop when vitamin E deficient diets
are fed, but selenium has not been found to partially protect against, or
alleviate the condition as is the case in other species. This would
indicate that protection against peroxide damage of tissues in the
rabbit is more dependent on vitamin E than selenium. It seems more
likely, however, that the higher tissue levels of selenium found in
normal rabbits indicates a more efficient use and storage mechanism than
in other species. The possibility then exists that the experimental
rabbits used to evaluate selenium/vitamin E metabolism were not
sufficiently depleted of selenium prior to commencing the investigation.
Rabbits would appear to be less susceptible to selenium d eficiency than
all other domestic species.
All GSH-Px circulating in the blood is of the Se dependent type - however
the liver and kidney contain k3% and 40% respectively of non Se dependent
GSH-Px, this and the total GSH-Px is more than in other species.
86
SELENIUM
Sheep; Tissue Levels
Deficient
Marginal
Adequate
High
Toxic
Diet
0.02-0.10
0.10-0. 16
0.20-0.50
3.00-5.00
5.00-25.0
ppm
Liver
0.005-0.100
0.150-0.250
0.250-1.0
2.00 -10.0
15.0 -30.0
ppm wet wt
Kidney
U.O/*6-0.60O
0.700-1.10
0.90 -3.00
k.O - 6.0
6.0 - 15.0
Serum
0.006-0. 030
O.O3O-O.O5O
0.080-0.500
3.0
Deficient
Marginal
Adequate
High
Toxic
Milk
0.002-0.020
0.025-0.02+0
Wool
0.03-0.30
0.03-0.60
0.70-4.00
Muscle
0.010-0.025
0.025-0.090
0. 090-0. 400
O.k 00-0. 600
0.60 - 2000
ppm wet wt
Glutathione Peroxidase Activity (GSH-Px)
Selenium
Deficient
Marginal
Adequate
Liver
100 - 150
150 - 2i+0
300 - 500
Erythrocytes
2.0 - 6.9
6 - 30
60 - 180
(Erythrocytes - u moles NaDPH reduced/g Hb/min at 37 c)
(Liver EU/g fresh tissue - On. J. An. Sci. l\2 (k) P 9&k)
Erythrocytes GSH-Px seems to correlate best with Se status of sheep.
GSH-Px levels do not correlate with incidence of WMD.
Elevated CPK levels are best indicators of subclinical WMD.
Elevated LDH and SGOT levels indicate muscular damage.
Deficiency - selenium deficiency reduces reproductive performance and
is partially responsible for white muscle disease (WMD).
Se deficiency reduces immune response - supplementation above nutritional
requirements increases number of IgM producing cells and synthesis of
IgM antibody. Se deficient sheep have lowered resistance to bacterial
diseases and parasites.
87
Selenium - Sheep contd.
Selenium supplementation has been found to prevent peridontal disease
affecting the molars of sheep in selenium deficient areas in New Zealand.
Therapeutic oral dose - 1 mg/kg/wk
5 mg/kg/month
Iron/Se bullet.
Deficiency prevention - free choice (or 12.6 g/day/ewe) selenized salt
or mineral mix containing 26-75 ppm Se.
Injectable Se treat once every 3-4 months.
Drench or inject ewes and rams 3-4 weeks before breeding and 3-4 weeks
prior to lambing. Add Se mineral mix to grain ration when fed at lambing
time. Organic or naturally available Se is thought to be more available
than inorganic Se.
Interactions - Se alone will not prevent the occurrence of WMD. Vitamin
E must also be available, 10 ppm vitamin E required to prevent WMD at
0.1 ppm Se level in diet. Vitamin E in legumes appears to be less avail-
able than that in grass. May be amino acid-sulphur interaction affecting
Se absorbtion from the gut.
Cyanide from plant cyanogenic glycosides can induce WMD in Se deficient
lambs.
Super phosphate fertilization of pastures leads to reduced Se levels in
grazing sheep but not in the pasture.
Cobalt deficiency increases susceptability to Se toxicity.
Toxicity - Toxic dose as Na.SeO,, LD5o Intramuscular 0.45 mg/kg
Parentally 5.0 mg/kg
Orally 10-15 mg/kg
Chronic toxic dose O.Otf mg Se/kg/day for 1 year.
88
TUNGSTEN
Poultry:
Tissue Levels
Diet
Liver
Blood
Deficient
Adequate
0.2
0.33
0.1
High
1.0
3.5-li?
Toxic
2k -30
15.4
ppm
dry
wt
ppm wet wt
ppm
Deficiency - the requirement to tungsten by animals is presently unknown.
Interactions - Tungsten inhibits the absorption of Mo from the digestive
tract and may interfere with some enzyme syntheses particularly xanthine
dehydrogenase.
Toxicity
Signs of toxicity - reduced feed intake and weight gain, diarrhea with
death within one day of onset. Distress with labored breathing occurring
only about 1 hour before death.
Emaciation, dehydration and extensive muscle hemorrhaging are apparent
on post mortem examination together with petechial haemorrhages on the
gizzard, proventriculus and in the brain, heart and kidney.
89
URANIUM
Ruminants
Estimated maximum safe dietary intake of natural uranium
Cattle Sheep
Feed 30 ppm dry wt 20 ppm dry wt
Water 10 ppm 20 ppm
Estimated daily intake of natural uranium by sheep and cattle
to produce various effects:
Effect
Slight malaise in sheep, transient
depression of milk yields in cows
Meat unfit for human consumption
Milk unfit for human consumption
Daily
intake of U
Sheep
Cattle
0.05g
O.kg
25g
200g
-
2 kg
Toxicity: Cattl
e
75 ppm U in water as uranyl nitrate resulted in general deterioration of
health for 2 weeks then no further effect.
A minimal deleterious dose is ESTIMATED to be 1/10 this level = O.kg U/
day/mature cow. Ref. Garner. Health Physics 1963 (9) 597-605.
Deficiency - no evidence to suggest uranium acts as an essential trace
element in mammals.
Post Glacial uranium deposits generally occur in alkaline flats or
sloughs and highly organic areas such as peat bogs. They are usually
associated with high Mo and Se deposits.
Normal bovine liver uranium ■ 0.0008 ppm dry wt.
90
URANIUM
Dogs: Tissue Levels
Diet Kidney Bone
High 0.10-0.20 0.2-1.0
Toxic 2.1 - 1.0-2.3
mg/kg body wt/day ppm wet wt
Toxic effects of uranium - chronic
Changes in blood cell morphology.
Disturbance of thyroid function.
Increased basal metabolism, changes in hepatic function.
Hematopoietic deficiency and renal damage.
Most uranium is deposited in the bone (300 day £ life) or kidneys
(15 day i life).
Albumin appears in urine as kidney damage commences.
References
Voegtlin, C. and Hodge, H.C.: Pharmacology and Toxicology of Uranium
Compounds, C. Voegtlin, H.C. Hodge, Editors, McGraw-Hill Company,
New York. National Nuclear Energy Series, 1949,
Yuile, C.L.: Animal Experiments in Uranium, Plutonium, Transplutonic
Elements, H.C. Hodge, J.W. Stannard, J.B. Hursh, Editors, Springer-
Verlag, New York. Handbook of Experimental Pharmacology 36, 165-196, 1973.
Durban, P.W.: Metabolism and Effects of Uranium in Animals, in Health
Experience with Uranium, ERDA Publication 93, US Energy Research and
Development, pg 76, 1975.
91
VANADIUM
Chicken: Tissue Levels
Deficient
Marginal
Adequate
High
Toxic
Diet
0.010-0.035
0.10 -3.0
10 -30
100 -800
ppm dry wt
Liver
Kidney ^JJ±a) Eggs (Yolk)
0.018-0.038 0.180
ppra wet wt
1.3-6.3 0.002-0.003
5.8-8.6
10 -15
ppm dry wt ppm wet wt
Ducks: Tissue Levels
Normal
High
Diet Liver
1-10 0.013-0.080
100 0.540-0.760
Kidney
0.0007-0.002
0.230 -0.320
ppm wet wt
Bone
0.080-0.23
0.230-5.50
Eggs
< 0.0002
0.059-0.068
Toxicity - Increased protein in the diet protects slightly against vanadium
toxicity. Increased lactose enhances toxicity. Toxicity is decreased by
Cr, cottonseed meal, dehydrated grass and ascorbic acid.
Deficiency - Vanadium is an essential trace element for birds. Deficiency
reduces wing and tail feather growth and body growth rate. Vanadium
is involved in body lipid metabolism.
Blood and bone iron levels tend to increase in V deficient chicks. Bone
development is retarded in deficient chicks.
Naturally occurring deficiencies have not been reported bu=t feedstuffs
frequently contain less than the estimated minimum requirement of 0.1 ppm V.
92
VANADIUM
Sheep: Tissue Levels
Deficient
Marginal
Adequate
High
Toxic
Diet
U. 1-10.0
100-200
4 00-800
Liver
0.10-0.22
0.8^-3.0
ppm dry wt
Kidney
0.20-0.^7
3.50-11.6
Cattle: Tissue Levels
Deficient
Normal
Toxic
10-20 mg/kg
day
Liver
0.006-0.007
0.3 -5.1
ppm wet wt
Kidney
4.2-40.0
Milk
0.1-0.2
0.1-0.2
ppb
Deficiency - Vanadium deficiency reduces growth rate and reproductive
performance. V is an essential trace element for animals.
V is poorly absorbed from soils by most plants - spinach, parsley and
mushroom absorb higher amounts.
Soil average 100-200 ppm
Cereal grains 0.0007-0.014 ppm
Pastures 0.03-0.07 ppm
Toxicity - signs - diarrhea, refusal to eat, dehydration, emaciation,
dry hair coat, inability or reluctance to rise and move.
Animals may be able to build up a resistance.
Effects are more pronounced in nutritionally unbalanced diets.
V occurs in certain phosphate supplements (100 ppm) and in fossil fuels,
Excess V accumulates in the liver but i6 excreted fairly rapidly upon
reducing intake.
93
ZINC
Cattle:
Tissue Levels
Diet
Liver
Kidney
Serum
Deficient
2 -10
<Z0
16 -20
0.2-0.4
Low borderline
10 -30
0.5-0.6
Normal (adequate)
50 -100
25-50
18- 0
0.7-1.4
High borderline
1000-5000
Toxic
>5000
>500
130-180
5.2-7.5
ppm
ppm
wet
wt
ppm
Hair
Milk
Feces
Bone (rib)
Deficient
80 -100
12.0-18.0
32-60
Low borderline
Normal (adequate)
100-150
2.3-5.1
160 -220
70-250
High borderline
Toxic
8.4
>8000
ppm dry wt
mg/1
ppm dry wt
ppm dry wt
All blood or serum levels reported in the literature prior to 1977 should
be viewed with a good deal of suspicion due to sample contamination from
•rubber1 stoppers.
Tissue levels are not a good guide to zinc deficiency in the bovine.
Infectious diseases seem to lower liver and serum levels but increase
kidney levels. Bone levels decrease with increasing age of animal.
Muscle zinc: normal levels
Light muscle
Dark muscle
30 ppm wet wt 69 ppm dry wt, fat free
70 ppm wet wt 247 ppm dry wt, fat free
Average zinc level in B.C. forage
Legumes 23 ppm dry wt Corn silage 24 ppm dry wt
Grass hay 21 ppm dry wt Oat forage ZZ ppm dry wt
Grain 33 ppm dry wt
Zinc deficiency - dietary zinc requirement for dairy cattle = 45 ppm
with 0.3% Ca. For each additional 0.1% Ca in diet add 16 ppm Zn.
94
Zinc - Cattle contd.
Deficiency signs - weak hoof horn with increased susceptability to
interdigital dermatitis, foot rot, reduced conception rate, (The effect
of deficiency is more severe in the male than female fertility.
Spermatozoan maturation is severely affected.). Reduced growth rate
and feed intake. Parakeratosis.
Hereditary zinc deficiency can occur in cattle.
Deficiency prevention - free choice or 65 g/day of a salt mineral mix
containing 0.54% Zn.
Interactions - high dietary Cadmium (350 ppm) reduces zinc absorption
in calves.
Zinc, copper and iron are mildly antagonistic.
High zinc levels reduce calcium metabolism.
Toxicity - toxicity of zinc in cattle is uncommon.
2% Zn in dairy feed have killed mature cows.
6 to 6 ppm Zn in water is thought to have adverse effects on cattle.
Young calves are more susceptible to poisoning than adult cattle.
95
ZINC
Dogs: Tissue Levels
Deficient
Normal
Diet
50-100
ppra
Liver
30-50
Kidney
16-30
ppm wet wt
Plasma
0.20
0.60-1.00
Serum levels markedly increased by stress.
Serum levels decreased by hepatic disorders, hysterectomies, hypothyroidism
and infections.
Females have higher serum zinc levels than males.
Alkaline phosphatase levels increased with increased zinc levels.
Decreased serum Zn was associated with reduced T. Protein.
Deficiency & Toxicity
Frequency and incidence in dogs is unknown.
96
ZINC
Horses: Tissue Levels
Diet
Deficient
Lower borderline
Normal 40-100
High borderline
Toxic 3600
ppm
Blood (whole) Liver
2.0-5.0
40-80
Kidney
20-27
6.0-15.0 1300-1900 295-580
ppm wet wt
Bone (rib)
Deficient
Low borderline
Normal 65- 75
High borderline
Toxic 140-340
ppm dry wt fat free
Milk
4.0-2.0
ppm
Toxicity - in lab controlled experiments:
Foal threshold limit 60 mg/kg body wt/day
illness at 90 mg/kg body wt/day = 3600 ppm diet.
Tolerance level under field conditions with unknown interactions is
definitely less.
Toxic signs - swelling at the epiphyseal region of the long bones,
stiffness, lameness, anemia.
Interactions - kidney cortex levels increased with increasing Cd in diet.
97
ZINC
Pigs: Tissue Levels
Diet
Deficient 10-24
Low borderline 30-50
Normal (adequate) 75-500
High borderline 1000-5000
Toxic > 5000
ppm
Liver
20-25
25-35
45-90
Kidney
10-31
ppm wet wt
Serum
0.4-0.6
0.8-1. a
ppm
Low
Normal
High
Hair Bone
Milk
Colostrum-
23 days
60-90
1.0-6.0
22.7-13.9
160-230 95-146
ppm dry wt
ppm
ppm
Young growing pigs have zinc liver levels at the lower end of the range
shown.
Zinc deficiency signs - parakeratosis. Reduced conception rate.
Toxicity - zinc toxicity is dependent on the form in which the zinc is
available, e.g. > 0.1% zinc as lactate or carbonate is toxic.
/>0.5% zinc as oxide is toxic.
Young animals are more susceptible to toxicity than older animals.
Interactions -
Enteric infection decreases zinc retention in pigs - lowering liver and
serum levels.
Increased copper supplementation increases Zn requirement and zinc storage
in the liver. Increased zinc supplementation decreases Cu storage in the
liver.
High calcium, soy-protein and phytate increase zinc deficiency.
High cadmium has no effect on zinc deficiency,
Ni and Co deficiency aggravate Zn deficiency.
9tf
ZINC
Poultry - Tissue Levels
Diet
Deficient 17
Low borderline 50-80
Normal (adequate) 100-200
High borderline 800-2000
Toxic 2230-5000
ppm
Liver
Kidney
Serum
20-40
20-40
40-70 22-32
(chicks-turkeys-quail )
200-700 300-600
ppm wet wt
2.1-2.7
ppm
Feather
Feathers
Bone
Pancreas
Egg Yolk
Deficient
50
13-20 ppm
Low borderline
Normal (adequate)
53-100
110-400
50-125
30-48 ppm
High borderline
1000-3500
0.7-1.0
Toxic
1000-3500
rag/yolk
ppm
dry
wt
ppm wet wt
Tissue levels are not a good indicator of deficiency.
Diet - 100 ppm for 1st 3 weeks protects against feather defects in turkeys.
50 ppm is generally adequate after 3 weeks of age in turkeys.
Chickens require only half these amounts.
Laying hens: 10 ppm will maintain normal zinc content of body tissues.
70 ppm is required to maintain normal zinc content of eggs and
newly hatched chicks.
Toxicity - is affected by the composition of the diet:
800 ppm Zn can be toxic in a sucrose-fish ration.
2000 ppm Zn is not toxic in a corn-fish ration.
Zinc carbonate is more toxic than zinc oxide.
20,000 ppm for 10 days induces moulting.
Dietary levels of zinc above 9000 ppm are unpalatable.
Interactions - high dietary calcium in the presence of phytic acid
(soybean meal) reduces zinc absorption. Zinc is antagonistic to Cut
Fe, Mg and Mn.
99
ZINC
Rabbit:
Tissue Levels
Diet
Liver Kidney
Blood
(whole)
Deficient
0.2
55 20
32
Adequate
70
30-ttO 10-30
32
Toxic
ppm
ppm wet wt
ppm
Liver levels higher in newborn.
Tissue levels appear to be of little use for deficiency diagnosis.
Signs of deficiency - achromotrichia, dermatosis, hair loss, loss of
hair pigment. Reduced fertility, loss of apetite.
100
ZINC
Sheep: Tissue Levels
Diet Liver Kidney Serum Wool
Deficient 1-20 0.22-0.45 <70
Low borderline 30-50 U.40-U.80
Normal (adequate) 50-100 30-75 12-30 0.80-1.50 70-130
High borderline 800-1000 400 1000 4.0 -5.0
Toxic 2000 30.0-50.0
ppm ppm wet wt ppm ppm
Plasma or serum zinc levels are affected by infection, trauma, low
protein intake and pregnancy.
Toxic diet - acute 180 mg Zn/kg body wt.
chronic 20 mg Zn/kg body wt.
Zinc administered by drenching gun (50 mg/kg body wt) is more likely
to cause toxicity than that administered in feed or intraruminal
intubation.
Toxicity signs - diarrhea, loss of weight. High levels of dietary zinc
cause pancreas damage.
Deficient diet - less than 0.05 mg Zn/kg body wt.
Deficiency signs - weak hoof horn with resultant increased susceptability
to foot rot. Deficiency may adversely affect fertility (low conception,
poor implantationand early embryonic death).
Skin lesions, frothy saliva, reduced food consumption and weight loss.
Reduced alkaline phosphatase levels in serum
deficient 1.0 - 3.0 sigma U/ml
adequate 4.0 - 5.0 sigma U/ml
Interactions - high Zn levels may protect against Cu toxicity.
101
LIBRARY / BIBUOTHEQUE
AGRICULTURE CANADA OTTAWA K1A 0C5
3 TD73 D0021S31 S
630.4
C212
P 5139
1981
c.3
OOAg
Puis, R.
Veterinary trace mineral
deficiency and toxicity information
DATE DUE
DATE DE RETOUR
SFP 2 1
SFP U J992
1988
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