Sn – Tin is found in igneous rocks at 2 ppm; shale at 6 ppm; sandstone and limestone at 0.5 ppm; fresh water at 0.00004 ppm; sea water at 0.003 ppm; soils at 2 to 200 ppm (strongly absorbed by humus); marine plants at 1 ppm; land plants at 0.3 ppm (highest in bryophytes and lichens); marine animals at 0.2 to 20 ppm; land animals at 0. 15 ppm (highest levels are found in the lungs and intestines).
Originally the presence of tin in tissue was attributed to environmental contamination; however, careful and detailed studies by Schwarz demonstrated that tin produced an acceleration of growth in rats and further met the standards for an essential trace element. As a member of the fourth main chemical group of elements, tin has many chemical and physical properties similar to those of carbon, silica, germanium and lead.
Rats fed tin at 17.0 ng/gm show poor growth, reduced feeding efficiency, hearing loss, and bilateral (male pattern) hair loss, while rats fed 1.99 ug/gm were physiologically and anatomically normal; tin was demonstrated to be an essential element by Schwarz in 1970. Tin has been shown to exert a strong induction effect on the enzyme heme oxygenase, enhancing heme breakdown in the kidney. There is also evidence for tin having cancer prevention properties.
A federal study released in November of 1991 showed that men in recent generations have poorer hearing at any given age than in men in earlier generations. Men over age 30 lose their hearing more than twice as fast as woman of the same age.
Tin is a heavy metal. There is some evidence that it is a required nutrient in animals, although it has no known metabolic function at the present time. Rigorous exclusion of tin from diets of laboratory animals impaired reproduction and caused other abnormal growth. If it functions as a nutrient in humans, typical daily ingestion of 1.5 to 5 mg per day more than meets requirements. Tin is still used to line certain cans, and acidic foods like canned pineapple and canned tomatoes can leach out tin from the inside of a can. However, there is little evidence to indicate that tin can be toxic.
Biological interest in tin initially focused on its toxic potential to man through the contact of foods with tin-coated cans and tinfoil. Tin has now been shown to be an essential nutrient for the growth of rats. Schwarz et al. found the growth rate to be enhanced by nearly 60% if 1-2 ppm Sn was added as stannic sulfate to a highly purified diet fed in a plastic isolator environment. Several tin compounds including organic tin derivatives were reported to be effective, indicating that the organism is capable of utilizing tin covalently bound to carbon. Specific biochemical lesions associated with Sn deficiency have not been reported and the biological chemistry of the element remains to be determined. It is also highly desirable that the findings of Schwarz be confirmed and extended in other laboratories and with other species.
Tin Biochemical function
Tin has no known biochemical function. However, Schwarz et al. have described several properties of tin which suggest that it could have a function in the tertiary structure of proteins or other biosubstances. In industry, organic tin compounds are used as catalysts for polymerization, transesterification and olefin condensation reactions.
Claimed deficiency of tin
Early studies of tin deficiency were flawed and thus did not conclusively establish the essentiality of tin. However, a recent study by Yokoi et al. on rats presents reasonable evidence in support of the view that tin is essential. When compared with those fed 2 Mg of tin/g of diet, rats fed 17 ng of tin/g of diet exhibited poor growth, decreased efficiency of food utilization, alopecia, depressed response to sound, and changes in mineral concentrations in various organs.
Tin in the Human Body
A number of studies have been performed in which the trace metal content of human tissue has been determined.
In 1964 Tipton and Shafer examined tin in tissue, emphasizing the lungs, from autopsies of 200 victims of instantaneous accidental death. They note that 137 out of 140 individuals had Cook examined 29 different tissues from 150 adult victims of instantaneous accidental death. They report a 5 to 72-ppm range and 23 average tissue tin (ash weight) content for the human body. Tin was found in 3/4 or more of all tissues examined except the brain and muscle.
Few have examined tin content of the human fetus. Misk finds a trace in the fetal heart and spleen with a higher level in the liver. Schroeder et al. reports no tin in stillborns.
In an early paper, Datta reports that rats excrete 89 to 92% of the tin input in feces and 5.5 to 6.2% in urine.” He concluded that about 2% of the tin input is stored. The general view was that exogenous tin in humans was a contaminant from ingesting canned foods.
The data reviewed in this article clearly support the contention that tin is ubiquitous. Indeed, wherever researched, using methods that avoid the volatility problem and are sufficiently sensitive below 10 ppm levels, tin has been found.
In 1964 the late and highly respected H. A. Schroeder felt that tin was an abnormal trace element with no vital function. This conclusion was based essentially upon a perceived lack of environmental ubiquity, lack of tin in the newborn, and no proven biological effect. The question of ubiquity hopefully has been addressed here. There is as yet no conclusive data regarding lack of tissue tin in infancy, although the theory previously advanced by Cardarelli will simply handle either condition without modification.
At this time there is no proven vital effect of tin in humans. Certainly it can be reasonably asserted that tin is essential to proper dentition in rodents and possibly in humans. The work of Schwarz and colleagues showed that dietary tin was vital to growth in rats. The linkage between tin, the thymus gland, and oncogenesis is discussed elsewhere.
In addition to being ubiquitous, tin possesses a number of properties common to vital trace metals. It is bioaccumulated. Schroeder et al. note that of the 30 common trace metals, tin is 21st in the cosmos, 17th in the geosphere, 12th in the hydrosphere (probably 10th in the plant kingdom author), and 8th in the human body. Carried still further into the microcosm, tin appears to be 5th in the lymphatic system and 3rd in the thymus, superceded only by iron and zinc. Inorganic tin is capable of entering into biological activity at saline pH, and it is far less toxic than other known vital trace elements such as copper and cobalt. Human tissue tin appears not to vary with age. The average concentration of tin in human cells is 106 to 108 atoms -the same range as cobalt, iodine, chromium, and selenium, known vital nutrients.
The biochemical tin compounds, presuming they exist, would almost certainly be low molecular weight, fat-soluble organic tin materials.
Schwarz (1971) produced a Sn deficiency in rats, with growth enhanced by nearly 60% if 1-2 ppm Sn as stannic sulfate was added to the low Sn diet. Tin also has an effect on the pigmentation of teeth (Milne et al., 1972). Tin could well contribute to the tertiary structure of proteins or other biologically important macromolecules, such as nucleic acids. Tin could be an oxidation-reduction catalyst and function as the active site of metalloenzymes (Schwarz, 1974).
The use of riboflavin-deficient rats in Sn essentiality studies is of particular concern, because the oxidation-reduction potential of Sn2+ to Sn4+ is 0.13 V which is near the oxidation-reduction potential of flavin enzymes. Thus, it cannot be stated unequivocally that Sn deprivation reproducibly impairs a function from optimal to suboptimal. Without such evidence, Sn should not be considered an essential element at this time (Nielsen, 1986).
Dr. Nielsen goes on to state that the only evidence that supports essentiality of tin is that a dietary supplement of tin, both in the inorganic or organic form, improved the growth of suboptimally growing, apparently riboflavin-deficient rats but did not result in optimal growth. The use of riboflavin-deficient rats in tin essentiality studies would be of particular concern, because the oxidation-reduction potential of Sn2+ and Sn4+ is 0.13 volts, which is near the oxidation-reduction potential of flavin enzymes. Attempts in another laboratory to show that tin deprivation depressed growth in riboflavin-adequate rats were unsuccessful, even though animals and dietary materials used were from the same sources as those used in the study with apparent riboflavin-deficient rats. Further attempts to obtain findings similar to those of Schwarz et al. probably will be difficult because of apparent dietary and/or metabolic interactions between tin and riboflavin. Probably only certain special conditions will produce tin growth responses in rats. Thus, it cannot be stated unequivocally that tin deprivation reproducibly impairs a function from optimal to suboptimal. Without such evidence, tin should not be considered an essential trace element at this time. Moreover, the description of any possible biological function or nutritional requirement seems inappropriate.
Biol Trace Elem Res 1990 Mar;24(3):223-231
Effect of dietary tin deficiency on growth and mineral status in rats.
Yokoi K, Kimura M, Itokawa Y
Department of Hygiene, Faculty of Medicine, Kyoto University, Japan.
To clarify the influence of dietary tin deficiency on growth and mineral status, the following two different synthetic diets were fed to male Wistar rats: group 1–a diet containing 1.99 micrograms tin/g; group 2–a diet containing 17 ng tin/g. The rats in group 2 showed poor growth, lowered response to sound, and alopecia, with decreased food efficiency compared with rats in group 1. The changes of mineral concentrations in tissues observed in group 2, compared with group 1, are summarized as follows: calcium concentration in lung increased; magnesium concentration in lung decreased; iron concentrations in spleen and kidney increased; iron concentration in femoral muscle decreased; zinc concentration in heart decreased; copper concentrations in heart and tibia decreased; manganese concentrations in femoral muscle and tibia decreased. These results suggest that tin may be essential for rat growth.
Essential and Toxic Trace Elements in Human Health: An Update, pages 355-376, 1993.
Ultratrace Elements of Possible Importance for Human Health: An Update
Forrest H, Nielsen, PhD.
USDA, Agricultural Research Service, Grand Forks Human Nutrition Research Center, Grand Forks, ND 58202
In 1970, Schwarz et al. (1970) reported that low amounts of tin in various forms (0.5 to 2.0 mcg Sn/gm diet) significantly enhanced growth in suboptimally growing rate. Shortly thereafter, in the same laboratory, it was found that 1.0-2.0 mcg Sn/gm diet normalized the pigmentation of rat incisors (Milne et al., 1972). These findings were questioned as being indicators of a tin deficiency because the tin supplements did not result in normal growth, which suggested that tin was acting pharmacologically, or by alleviating an abnormality caused by something other than a tin deficiency (Nielsen, 1984c). Although the early studies were flawed and thus were inconclusive about tin essentiality, a recent study by Yokoi et al. (1990) with rats growing well (over 4 g/day) strongly suggests that tin is essential. When compared to rats fed 2 mcg Sn/gm diet, rats fed 17 ng Sn/gm diet exhibited poor growth, decreased food efficiency, alopecia, depressed response to sound, and changes in mineral concentrations in various organs. Although it seems likely that these findings include true signs of tin deficiency, they need confirmation before conclusively stating that they are.