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OCR for page 491
T.
In
Tin (Sn) is a soft, white, lustrous, crystalline, malleable metal that has
been of great economic importance since the Bronze Age, when early
metallurgists found ti~copper alloys very useful in the fabrication of
weapons and utensils. Tin is not ubiquitous. The world's largest de-
posits of tinstone (SnO2), high in the Bolivian Alps, together with the
tin from the Federation of Malaya, furnish about 60 percent of the
world's annual tin needs of 170,000 tons or 60 g per capita (Mantel!,
1949~. More than 50 percent of this tin by weight is used in the manu-
facture of tin plate. The major use of this tin plate, of course, has been
in the manufacture of the 6'tin can." Significant amounts of tin are also
used in tinning copper and steel wire and in the manufacture of various
alloys including solder, bronze, and Babbitt. More recently, tin has
been found useful in plasticizers and stabilizers in plastics, as fungi-
cides (especially wood preservatives), disinfectants, and miticides, in
the manufacture of cast iron and paints, and in radiopharmaceuticals
for nuclear medicine (LaSpada, 19681.
Concern for the biological aspects of tin has historically pertained to
its potential of contaminating the contents of the tin cans. Lacquering
or resin coating the tin plate has reduced this potential. Substitution
materials such as aluminum, tin-free steel, and plastic and cardboard
containers for canned, frozen, and dehydrated foods have also lessened
the exposure of food to tin. It will be recognized, however, that due to
some of the newer uses for tin, concern will continue for tin con-
tamination at various points in the food chain.
491
OCR for page 492
492 MINERAL TOLERANCE OF DOMESTIC ANIMALS
ESSENTIALITY
Schwarzet al. (1970) demonstrated tin to be essential for growth in rats.
These experiments, conducted in plastic isolators to prevent environ-
mental contamination of the rats with tin, indicated that 1 ppm tin added
to meticulously prepared, tin-free, purified control diets enhanced the
growth rate of the rats 53 percent. Both inorganic and organic forms of
tin were effective, with stannic sulfate giving the best results. Ad-
ditional studies on the essentiality of tin need to be conducted with
other species and in other laboratories.
METABOLISM
Little is known about the metabolism of tin. The efforts of Perry and
Perry (1959), Kehoe et a/. (1940), and Tipton and Cook (1963) indicate
inorganic tin is poorly absorbed, at least in man. Benoy et al. (1971)
reported tin, obtained from the contamination of canned foods, is only
4 percent absorbed by the oral route and only 2.7 percent absorbed 18
hours after subcutaneous administration. At the cellular level, as a
potent inducer of heme oxygenate (Kappas and Maines, 1976), tin
enhances heme breakdown in the kidney and impairs heme-dependent
cellular functions. Cremer (1962) stated that tetraethyl tin compounds
are rapidly converted to triethyl tin compounds in the liver. The tri-
ethyl tin compounds are uncouplers of oxidative phosphorylation.
Organic forms of tin may also form condensation complexes with
several ligands and may therefore contribute to protein structure
(Schwarz et al., 19701. Some organic forms of tin may cross the
bloo~brain barrier.
SOURCES
There is agreement that the contents of '`tin cans," especially acidic
foods, may indeed become contaminated with tin from the tin plating,
especially when not resin-coated. Levels of 1,370 ppm tin have been
recorded in canned fruit juices (Benoy et al., 19711. Canned pet foods
are subject to similar contamination potential, but these foods seldom
are as strongly acidic as, for instance, tomato juice. deGoeji and Kroon
(1973) demonstrated that resin-coating tin plate reduced the amount of
tin contamination by a factor of 50, providing the resin remains intact.
The newer uses for tin mentioned above involve both inorganic and
organic tin. Inorganic forms, such as stannous chloride, stannic oxide,
OCR for page 493
T.
In
493
stannous sulfate, stannous tartrate, and stannous acetate may be pres-
ent in industrial paints in amounts up to 3 percent. Organic forms,
especially the alkyl tin compounds, for example triethyl tin chloride,
tributyl tin oxide, dibutyl tin oxide, trioctyl tin dilaurate, dim-octyl tin
acetate, tri-n-butyl tin, tnethyl tin sulfate, and dimethyl tin dichloride,
may be present in plastics in concentrations of about 1 percent.
Little information is available on the natural tin content of livestock
feedstuffs. Pasture herbage growing in Scotland has been reported to
contain 0.~0.4 ppm tin on a dry basis (Mitchell, 19481. That investi-
gator also reported lichen growing on selicic rocks may contain in
excess of 72 ppm tin. Schroeder et al. (1964) analyzed a wide variety of
substances for their tin contents. Some representative values (parts per
million wet tissue) include lean ground beef, 2.76; gelatin, 3.5; beaver
meat, 7.28;- milk in tinned bulk containers, 0.68; dog chow, 1.0; com-
mercial rat diet, 0.8; and agricultural superphosphate, 3.34.
TOXICOSIS
LOW LEVELS
Tin toxicity studies with large animals have been rare. Organotin com-
pounds such as triethyl tin chloride and trimethyl tin chloride, which
have shown potential as insecticides for the sheep blowfly, have been
found well tolerated by sheep at levels 2 to 3 times the expected volume
usage and 2 or more times the necessary concentrations (Hall and
Ludwig, 1972~.
In chronic studies with orally administered triethy! tin hydroxide
(Stoner et al., 1955), domestic fowl were found more tolerant of the
drug than other species. Hens tolerated 160 ppm for 15 weeks, whereas,
20 ppm was the approximate tolerance level for rats and rabbits.
Barnes and Stoner (1958) have also studied the toxicity of a wide
variety of alkyl tin compounds administered by different routes to
rabbits, rats, and mice. The effects of the dialkyl compounds tended to
be generalized and involve the biliary tract, while the trialkyl com-
pounds tended to cause edema of the central nervous system. The
trialkyl salts were less toxic than the dialkyls, and, of the latter group,
butyl was the most toxic. The dioctyl tin salts, which are suitable and
effective substitutes for industrial uses of dibutyl salts, were found
completely nontoxic per os or per cutaneous.
Animal studies with tin-contaminated canned fruit juices and solid
foods have been conducted (Benoy et al., 1971~. Consumption of tin
from the canned fruit juice source in a single feeding equivalent to
OCR for page 494
494 MINERAL TOLERANCE OF DOMESTIC ANIMALS
approximately 2, 3, 7, and 14 me tin per kilogram of body weight had
no effect on rats, pigeons, cats, and dogs, respectively. An effect of the
tin~ontaminated food was induced only in cats consuming in excess of
7 mg tin per kilogram of body weight from fruit juice containing 1,370
ppm tin. This caused gastrointestinal disturbances with vomition in 20
to 40 percent of the cats. It was suggested that-this was due to gastro-
intestinal irritation rather than central nervous system toxicosis. Cats
acquired a tolerance to dietary tin after continued exposure.
The effects of 0.03, 0.1, 0.3, and 1.0 percent dietary inorganic tin
from several sources ranging from 44 to 63 percent tin have been
studied in normally fed rats for ~ and 13-week periods (deGroot et al.,
19731. Stannic oxide and stannous oxide, sulphide, and oleate had no
effect at any level or duration. Stannous chloride, orthophosphate,
sulfate, oxalate, and tartrate at 0.3 percent of the diet (equal to more
than 1,320 ppm tin) caused growth retardation, decreased feed eff~-
ciency, and mild anemia within 4 weeks. Stannous chloride at 1 percent
(6,300 ppm tin) for 13 weeks caused pancreatic atrophy, testicular
degeneration, renal calcification, and status spongiosis of the brain. In
other studies (deGroot, 1973), SO ppm dietary tin as stannous chloride
had no effect for up to 13 weeks in weanling rats; lSO ppm also had no
effect provided the dietary copper level was greater than 6 ppm. Levels
of tin from SOD to 5,300 ppm caused severe growth depression and
anemia. The severity of these effects was diminished by 200 ppm
supplemental iron.
The toxicity of oral sodium pentafluorostannite (NaSn2 F5), an active
prenatal anticariogenic agent containing 67 percent tin, has been in-
vestigated by Conine et al. (1976~. In rats fed 20, 100, and 175 mg
NaSn2Fs per kilogram of body weight equal to 13.4, 67, arid 117 mg tin
per kilogram for 30-day periods, there was dose-related growth inhibi-
tion and decreased serum glucose. The highest two levels caused proxi-
mal renal tubular degeneration and death.
Gaunt et al. (1968) have studied the effects of ~80 ppm dim -butyl tin
dichloride, a common stabilizer in polyvinylchloride plastic, in the diets
of rats for 90 days. The no-effect level was estimated at 40 ppm or less
for a 90-day period. The highest level fed caused a slight reduction in
growth rate and a mild anemia.
Another tin compound used as a plasticizer and polyvinylchloride
stabilizer, dioctyl tin S,S-bis (iso-octylmercapto) acetate, has been fed
to rats at the level of 200 ppm for periods up to 3 months. The tin-fed
rats experienced significant decreases in body weight and developed
increased liver and kidney weights in comparison to controls. This
same compound administered by daily gavage to reproducing female
rats at rates of 20 to 40 mg per kilogram of body weight caused 17
OCR for page 495
T.
1~
495
percent fetal deaths, increased fetal resorption, and diminished birth
weights. In 12-month studies, this rate of tin administration caused 20
percent mortality in rats (Nikonorow et al., 1973~.
Schroeder e' al. (1968) provided rats and mice with drinking water
containing 5 ppm tin ions for the natural life span of these rodents. This
level of tin did not affect the growth rates of either sex of rodent, but
it did reduce the life span (Iongevity) of the female rats. The associated
lesions in these rats included severe fatty degeneration of the liver,
hepatic necrosis, and vacuolar changes in the renal epithelium. Similar
renal changes were also noted in males.
HIGH LEVELS
In rabbits, stannous chloride, stannous tartrate, or stannous acetate
administered orally at the~rate of 1 g (equal to 440 630 mg tin) every
~10 days caused gastritis, posterior paresis, hepatic degeneration, and
death in 1 to 2 months (Eckardt, 19091.
The effects of trim-busy! tin oxide, administered conjunctivally to
rabbits, have been evaluated because of its commercial bactericidal,
fungicidal, insecticidal, and algicidal uses (Pelikan, 19691. Single doses
ranged from 0.46 to 4.6 mg per kilogram of body weight placed onto the
left conjunctival sac in a single 0.03 ml dose. The dose-related elects
included edema of eye lids, decreased corneal transparency, altered
aqueous humor, corneas necrosis in 24 hours, corneal ulcers In 2-5
days, generalized body weakness, and hyperreflexia. The highest doses
caused death of the rabbits.
The acute effects of tetra-, trim, di-, and mono-alkyl tin compounds
have been reported for several species (Stoner et al., 1955; Scheinberg
et al., 1966; and Robinson, 1969~. The tr~ethy} tin compounds were
fount! to be the most toxic. In rats, tr~ethy} tin sulfate was found
equally lethal by intravenous, intraperitoneal, or oral routes with an
arm of 5.7 mg per kilogram of body weight. This compound caused
secretion of "red tears," and its toxicity was exaggerated by increased
ambient temperatures (Stoner et al., 1955~. Rabbits were more sensitive
to triethy! tin sulfate than rats; however, the reactions were similar
including muscular weakness, tremors, and convulsions. These investi-
gators concluded the central nervous system to be the main site of
action for the alkyl tin compounds.
Fischer and Zimmerman (1969) have studied the effects of repeated
intravenous administrations of insoluble stannic oxide in several spe-
cies. Rats administered 1-4 injections of 200, 400, 600, or 800 mg tin per
kilogram of body weight survived a maximum of 26 months. New
Zealand White male and female rabbits administered 1-5 injections of
OCR for page 496
496 MINERAL TOLERANCE OF DOMESTIC ANIMALS
200 mg tin per kilogram of body weight, via the ear vein, survived ~26
months. In mongrel dogs intravenously administered, tin stimulated
puagocytosis but did not induce fibrosis or neoplasia. Bischoff and
Bryson (1976) reported a similar inert character of 4-mg quantities of
tin crystals (like asbestos fibers) injected into the thoracic cavity of
3-month-old mice observed for 19 months. The needles initiated a
foreign body reaction but no neoplasia or other changes.
Yamaguchi et at. (1976) reported that the major effect in rats of 30 mg
tin as SnCl2 per kilogram of body weight administered intraperitoneally
was a significant inhibition of urinary calcium excretion. In other
parenteral experiments, Benoy et al. (1971) found that subcutaneously
administered tin as tin citrate caused no remarkable changes in rats or
mice.
The clinical manifestations and ^0 of tin pyrophosphate and poly-
phosphate compounds in rats have been explored because of the
increasing use of 99technetium metaphosphate compounds as radio-
pharmaceuticals for bone scanning (Stevenson et a]., 1974~. Sublethal
doses of pyrophosphate (12-20 mg per kilogram of body weight) admin-
istered intravenously caused decreased serum ionized and total calcium
levels and prolonged QT intervals in electrocardiograms consistent with
hypocalcemia. The arm (5 minutes) for the pyrophosphate and poly-
phosphate compounds were calculated to be 41 and 29.4 mg/kg of body
weight, respectively. In acute studies, dim-butyl tin dichloride at the
rate of 50 mg/kg of body weight in single oral doses caused edema and
inflammation of the bile duct in rats, and the ~D50 was 20~400 mg/kg of
body weight (Gaunt et al., 1968~.
The rD50 of NaSn2 Fs administered by several routes to rats and mice
has also been determined (Conine et al., 1975~. The values were 19, 81,
and 573 mg/kg for the ~v, UP, and orally administered drug, respectively,
in mice and 12.9, 70, and 593 mg/kg, respectively, in weanling rats.
Fasting increased the toxicity and the deaths were preceded in both
species by ataxia, muscular weakness, and central nervous system
depression.
Gaines and Kimbrough (1968) have found the ~0 of triphenyl tin
(fentin) hydroxide administered by gavage in peanut oil to Sherman
strain rats was 36 mg/kg of body weight in females and 240 mg/kg of
body weight in males. Signs of toxicosis included sluggishness, un-
steady gait, mild diarrhea, anorexia, bloody nose, and death.
The ~D50 of several organotin compounds of potential value as sheep
insecticides have been established for mice immersed for 15 seconds in
the solutions of the tin compounds. The ~D50 for triethyl and trimethyl
tin chloride were found to be 35 and 50 mg/kg of body weight, respec-
tively (Hall and Ludwig, 1972~.
OCR for page 497
T.
In
FACTORS AFFECTING TOXICITY
497
The major factors influencing the toxicity of tin relate to its solubility,
the acid-base balance of the host, degree of acquired tolerance, and
type of diet. The alkyl derivatives are quite soluble, as well as volatile,
especially around pH 7. In the case of inorganic forms, as may con-
taminate canned foods, exposure to air, organic acids, fats, and salt
favor the removal of stannous (Sew) ions from tin plate. Based upon
the quantities of tin found in urine, Perry and Perry (1959) have sug-
gested that metabolic alkalosis enhances tin absorption and increases
urinary tin, while metabolic acidosis tends to reduce the absorption of
tin from the gastrointestinal tract. deGroot et al. (1973) found that tin
in natural-ingredient diets appeared to be less toxic than in semipurified
diets. This is probably associated with the sparing action of certain
minerals on the toxicity of tin. Copper and iron were found by deGroot
(1973) to decrease the toxicity of tin. The species and sex of tin-exposed
animals also are important. For example, female rats are several times
more susceptible to parenteral triphenyl tin hydroxide than male rats,
and guinea pigs are quite refractory to the toxic alkyl for compounds.
MAXIMUM TOLERABLE LEVELS
The maximum tolerable levels for tin are dependent upon several fac-
tors, including source and route of administration. For inorganic Sn++
administered daily to rodents over their life span, no eject level ap-
pears to be less than 5 ppm (Schroeder et al., 19681. However, provided
adequate dietary iron and copper are present, the safe upper levels for
oral inorganic tin (Sn++) may approximate 150 ppm (deGroot, 19731.
For parenterally administered inorganic tin (Sn++), the no-effect
level (intravenous) is less than 12 mg/kg of body weight in rodents
(Stevenson et al., 1974~. For one of the most toxic organic tin com-
pounds, triethy! tin dichloride, the no-effect level is less than 20 ppm for
periods of up to 4 weeks (Stoner et al., 1955~. The safe upper level
for intravenously administered triethyl tin sulphate is approximately
5 mg~kg body weight under normal environmental temperatures (Stoner
et al., 1955~.
TISSUE LEVELS
Because tin is poorly absorbed, the levels of tire in tin-exposed animals
remain remarkably low. Kehoe et al. (1940) reported the highest level
OCR for page 498
498 MINERAL TOLERANCE OF DOMESTIC ANIMALS
of tin in long bones (0.8 ppm, wet weight), 14 ,ug/dl in blood, and a
virtual absence of tin in brain tissue of normal humans. Schroeder et al.
(1968) found the spleens of the rodents on long-term tin toxicity studies
to contain the highest levels of tin (1.88 ppm wet weight). In human
tissue, Schroeder et al. (1964) found the highest levels of tin in the wall
of the ileum (range of 53 to 172 ppm in ash), while the range of tin levels
in liver, kidney, and lungs approximated 20 to 64 ppm in ash. No tin was
found in tissue of the newborn.
SUMMARY
Despite a variety of commercial uses for tin compounds (tin plate,
plasticizers and stabilizers for polyvinylchIoride products, fungicides,
pesticides, radiomedicine pharmaceuticals) and their frequent direct
contact with foods, the potential for tin toxicosis is negligible because
the element is poorly absorbed. Of the inorganic tin forms, stannous
chloride is among the most toxic, while the triethyl tin compounds
appear to be the most toxic organic forms. Inorganic tin induces an-
orexia with accompanying growth depression, impairs hematopoiesis,
and alters calcium metabolism. Pancreatic, hepatic, and renal lesions
have also been observed in inorganic tin toxicosis. The organic alkyl tin
compounds have a special capacity for inducing inflammation of the
biliary tract and edema of the central nervous system, regardless of the
route of administration.
OCR for page 499
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507
OCR for page 508
508 MINERAL TOLERANCE OF DOMESTIC ANIMALS
REFERENCES
Barnes, J. M., and H. B. Stoner. 1958. Toxic properties of some dialkyl and trialkyl tin
salts. Br. J. Indust. Med. 15:15.
Benoy, C. J., P. A. Hooper, and R. Schneider. 1971. The toxicity of tin in canned fruit
juices and solid foods. Food Cosmet. Toxicol. 9:645.
Bischoff, F., and G. Bryson. 1976. Toxicologic studies of tin needles at the intrathoracic
site of mice. Res. Commun. Chem. Pathol. Pharmacol. 15:331.
Conine, D. L., M. Yum, R. C. Martz, G. K. Stookey, J. C. Muhler, and R. B. Forney.
1975. Toxicity of sodium pentafluorostannite, a new anticariogenic agent. I. Com-
parison of the acute toxicity of sodium pentafluorostannite, sodium fluoride and stan-
nous chloride in mice and/or rats. Toxicol. Appl. Pharmacol. 33:21.
Conine, D. L.' M. Yum, R. C. Martz, G. K. Stookey, and R. B. Forney. 1976. Toxicity
of sodium pentafluorostanrute. A new anticariogenic agent. III. Today toxicity study
in rats. Toxicol. Appl. Pharmacol. 35:21.
Cremer, J. E. 1962. Tetraethyl lead toxicity in rats. Nature (London) 195:607.
deGoeji, J. J. M., and J. J. Kroon. 1973. lAEA/FAO/WHO Symposium on Nuclear Tech-
niques in Comparative Studies of Food and Environmental Contamination, Otaniemi,
Finland. IAEA, Vienna.
deGroot, A. P. 1973. Subacute toxicity of inorganic tin as influenced by dietary levels of
iron and cooper. Food Cosmet. Toxicol. 11:955.
deGroot, A. P., V. J. Feron, and H. P. Till 1973. Shon term toxicity studies in some salts
and oxides of tin in rats. Food Cosmet. Toxicol. 11:19.
Eckardt, A. 1909. Beitrag zur Frage der Zinnvergiftunger. Z. Unters Nahr.-u Genus-
smittel 18:193.
Fischer, H. W., and G. R. Zimmerman. 1969. Long retention of stannic oxide. Lack of
tissue reaction in laboratory animals. Arch. Pathol. 88:259.
Gaines, T. B., and R. D. Kimbrough. 1968. Toxicity of fentin hydroxide to rats. Toxicol.
Appl. Pharmacol. 12:397.
Gaunt, I. F., J. Colley, P. Grasso, M. Creasey, and S. D. Gangolli. 1968. Acute and
short-term toxicity studies on dim-butyltin dichloride in rats. Food Cosmet. Toxicol.
6:599.
Hall, C. A., and P. 1~. Ludwig. 1972. Evaluation of the potential use for several organotin
compounds against the sheep blowfly (Lucilia spp.). Vet. Rec. 90:29.
Kappas, A., and M. D. Maines. 1976. Tin: A potent inducer of heme oxygenase in kidney.
Science 192:60.
Kehoe, R. A., J. Cholak, and R. V. Storey. 1940. A spectrochemical study of the normal
ranges of concentration of certain trace metals in biological materials. J. Nutr. 19:579.
LaSpada, A. 1968. Patterns of World Tin Consumption 1957-1968. The International Tin
Council, London.
Mantell, C. L. 1949. Tin: Its Mining, Production, Technology and Applications.
Reinhold, New York.
Mitchell, R. L. 1948. The Spectrographic Analysis of Soils, Plants and Related Material.
Tech. Commun. Burl Soil Sci. No. 44.
Nikonorow, M., H. Mazur, and H. Piekacz. 1973. Effect of orally administered plasti-
cizers and polyvinylchloride stabilizers in the rat. Toxicol. Appl. Pharmacol. 26:253.
Pelikan, Z. 1969. E~ects of bis (tri-n-butyltin) oxide an the eyes of rabbits. Br. J. Ind.
Med. 26:165.
Perry, H. M., Jr., and E. F. Perry. 1959. Normal concentrations by some trace metals in
human urine: Changes produced by ethylenediaminetetraacetate. J. Clin. Invest.
38:1452.
OCR for page 509
T.
In
S09
Robinson, I. M. 1969. Effects of some organotin compounds on tissue amine levels in
rats. Food Cosmet. Toxicoh 7:47.
Scheinberg, L. C., J. M. Taylor, I. Herzog, and S. Mandell. 1966. Optic and peripheral
nerve response to triethyltin intoxication in the rabbit; Biochemical and ultrastructural
studies. J. Neuropathol. Exp. Neural. 25:202.
Schroeder, H. A., J. J. Balassa, and I. H. Tipton. 1964. Abnormal trace metals in man:
Tin. J. Chron. Dis. 17:483.
Schroeder, H. A., M. Kanisawa, D. V. Frost, and M. Mitchener. 1968. Germanium, tin,
and arsenic in rats: Effects on growth, survival, pathologic lesions and life span. J.
Nutr. 96:37.
Schwarz, K., D. B. Milne, and E. Vinyard. 1970. Growth effects of tin compounds in rats
maintained in a trace element-controlled environment. Biochem. Biophys. Res. Com-
mun. 40:22.
Stevenson, J. J., W. C. Eckelman, P. Z. Sobocinski, R. C. Reba, E. L. Barron, and
S. G. Levin. 1974. The toxicity of Sn-pyrophosphate: Clinical manifestations prior
to acute mso. J. Nucl. Med. 15:252.
Stoner, H. B., J. M. Barnes, and J. I. Duff. 1955. Studies on the toxicity of alkyltin
compounds. Br. J. Pharmacol. Chemother. 10:16.
Tipton, I. H., and M. J. Cook. 1963. Trace elements in human tissue. Part II. Adult
subjects from the United States. Health Phys. 9:103.
Yamaguchi, M., H. Sato, and T. Yamamoto. 1976. Decrease of calcium concentration in
urine of rats treated with stannous chloride. Chem. Pharm. Bull. (Tokyo) 24:3199.
Representative terms from entire chapter:
tin compounds
