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    TIN

    EXPLANATION

         Tin was previously evaluated for tolerable intake for humans
    by JECFA in 1966, 1970, 1971, 1975, 1978, and 1982 (Annex 1,
    references 11, 22, 26, 38, 47, and 59). A provisional maximum
    tolerable daily intake of 2 mg of tin per kg bw was established by
    the committee. The committee also noted that 200 ppm or more of tin
    in foods and beverages can be expected to produce acute toxic
    effects, including abdominal cramps, nausea, and/or diarrhea.

    INTRODUCTION

         The Codex Committee on Food Additives (1986) indicated that
    there is a need to clarify the information presented in the 26th
    report, as well as to provide more information about the chemical
    forms of tin which cause gastric disturbances. The following is a
    reexamination of available human data. Although no very recent
    studies are available, several pertinent reports published in 1975
    or earlier are summarized. Because of the nature of this problem,
    the information presented is limited to data on humans.

    DIETARY EXPOSURE

         Approximately 50% of the world production of tin is used for
    plating. Tin coatings are generally corrosive resistant and easy to
    solder and hence have been used extensively for food containers and
    food processing equipment. Tin has also been used in the production
    of tin alloys, such as solders, bronzes and pewters which may be
    used in the manufacture of food containers. Inorganic tin compounds
    are used as pigments in the ceramic and textile industry. Organo-
    tin compounds are used as heat stabilizers in the production of PVC
    plastics, curing agents for silicon rubber, and catalysts in the
    production of polyurethane. Triorganotins are used as fungicides,
    miticides, insecticides and bactericides (Friberg et al., 1986;
    Reilly, 1980; WHO, 1980).

         The combustion of fossil fuels contributes to the amount of
    tin in air. Excluding point source industrial emissions, tin levels
    in air have been found to be generally less than 0.3 g/m3 and the
    intake of this metal from air would therefore be less than
    6 g/person/day (Friberg et al., 1986; WHO, 1980; Ministry of
    Agriculture, Fisheries and Food, 1985).

         For the general population, drinking water is not a
    significant source of tin. When found, tin levels averaged 6 g/l
    and consumption of 1.5 to 2.0 l/day would result in a daily intake
    of 9 to 12 g tin/person (Friberg et al., 1986; WHO, 1980;
    Ministry of Agriculture, Fisheries and Food, 1985).

         In most unprocessed foods, tin levels are generally less than
    1 g/g. Higher concentrations are found in canned foods as a result
    of dissolution of the tin coating or tin plate. The concentration
    of tin in canned foods depends on a number of factors, including
    the type and acidity of the food, time and temperature of storage,
    and the presence of air in the can headspace. Oxidizing agents such
    as nitrates and iron and copper salts, certain pigments, and
    sulphur compounds all accelerate dissolution of tin. Other
    substances, such as tin salts, sugars, and colloid like gelatin,
    retard detinning. Lacquering of cans also reduce corrosion and
    prevent detinning. Tin concentrations in foodstuffs in unlacquered
    cans frequently exceed 100 g/g, while in lacquered cans, tin
    levels are generally below 25 g/g. Storing foods in opened
    unlacquered cans results in substantial increases in the tin
    concentration of the food. Given all of these factors, it becomes
    apparent why tin levels found in canned foods are quite variable
    (Reilly, 1980; Ministry of Agriculture, Fisheries and Food, 1985;
    Tipton et al., 1966; Schroeder et al., 1964; Dick et al., 1978).

         The intake of tin by different segments of the population is
    dependant on the type(s) and amount of canned food ingested and its
    tin level. For example, a 60 kg adult consuming 1 (one) litre of
    juice containing 100 g/g tin, would ingest 1.7 mg/kg bw of tin
    whereas a 20 kg child consuming 1/2 litre of the same juice would
    ingest 2.5 mg/kg bw.

         In summary, food and in particular canned food, represents the
    major route of human exposure to tin, Intake levels from this
    source can vary widely and for some segments of the population can
    reach several mg/kg bw.

    BIOLOGICAL DATA

    Observations in man

         Warburton et al. (1962) reported that 31 persons suffered
    from nausea, abdominal cramps and/or vomiting within 1-2 hours
    after drinking a fruit punch containing 2,000 ppm tin. The
    reconstituted pineapple-grape-fruit juice used to make the punch
    had been delivered in a 5-gallon retinned milk container. No
    information was available as to when the juice was processed or how
    long and in what kind of container it was stored before delivery.
    However the lining of the container in which the juice was
    delivered showed obvious signs of corrosion, probably due to the
    unusually high acidity (pH=3) of the juice. The illness reportedly
    lasted from 2 to 48 hours after onset. Omori (1966) reported that
    a canned orange-based drink containing 425 ppm tin produced a
    similar outbreak of intoxications, manifested by nausea, vomiting,
    diarrhea, fever and headache. Most of the 1,838 affected persons
    recovered within a day or two. The inside surface of the can in
    which the juice was stored was covered by a thin black rusty layer
    indicative of corrosion (Omori et al., 1973).

         Nausea, vomiting and diarrhea were observed in a large,
    unspecified number of persons in Kuwait who consumed formulated
    orange juice and apple juice containing 250-385 ppm tin (Metal Box
    Co., Ltd., unpublished report, 1967, cited in Benoy et al.,
    1971). Kojima (1969) reported 8 cases of poisoning from tomato
    juice containing 247 ppm tin. Similarly, vomiting, diarrhea and
    other signs of distress were observed in 15 students who had
    consumed a canned orange beverage containing 100-494 ppm tin, and
    in 8 other persons that had consumed tomato juice containing
    156-221 ppm tin (Horio et al., 1967).

         In 97 well documented cases, severe abdominal bloating,
    vomiting and diarrhea were noted after the consumption of canned
    tomato juice with tin levels ranging from 141 to 405 ppm (Barker &
    Runte, 1972). The mean tin concentrations ranged from 245 to 363
    ppm in the various lots implicated as the cause of these
    intoxications. The cans were visibly detinned, an effect which was
    attributed to unusually high nitrate levels on the tomatos used to
    make the juice. Excessive nitrate fertilization of tomato plants
    was related to complete corrosion of the can lining within 6 months
    of storage, yielding tin levels of 381-477 ppm (mean = 418 ppm),
    compared to 29-81 ppm (mean = 50 ppm) in juice from non-corroded
    cans.

         Similar cases have been reported after consumption of canned
    cherries, asparagus, herrings, and apricots (Schryver, 1909). For
    example, Luff & Metcalfe (1890) found that canned cherries
    containing tin at 3,430 ppm or more produced gastrointestinal
    distress in 4 persons within 0.5-2 hours after consumption. The
    juice of the canned cherries was strongly acid due primarily to the
    presence of malic acid. Pickled herrings preserved in vinegar and
    implicated in another outbreak were found to contain 1030 ppm tin

    in the solids and 316 ppm tin in the liquid (Gunther, 1899, cited
    in Schryver, 1909). Savage (1939) cited a report of nausea, vomiting
    and abdominal pain in four members of one family occurring 0.5-3
    hours after the consumption of canned apricots containing 800 ppm tin.

         Nausea and vomiting were noted after consumption of peach
    preserves containing 563 ppm tin (Nehring, 1972, cited in WHO,
    1980). The food sample also contained 93 ppm nitrate, as well as
    1.7 ppm nitrite, 1.5 ppm zinc, 0.1 ppm cadmium, 0.16 ppm lead, 1
    ppm copper, and 115 ppm chloride. Also, about half of the 85
    persons answering a questionnaire reported nausea, vomiting and
    diarrhea occurring within 1 hour after consuming canned peaches in
    which the fruit contained 413-597 ppm tin (mean = 533 ppm) and the
    juice contained 298-405 ppm tin (mean = 369 ppm) (Svensson, 1975,
    cited in WHO, 1980). Ungar & Bodlander (1887, cited in Schryver,
    1909) found that canned asparagus containing 300-4000 ppm tin was
    associated with gastrointestinal symptoms. Furthermore, Kwantes
    (1966, cited in Benoy et al. 1971) reported a few small outbreaks
    of poisoning related to the consumption of solid foods (salmon,
    fruit salad and rhubarb) in which tin levels ranged from 250 to 650
    ppm. Canned fruit containing as much as 250 ppm (212-250 ppm) tin
    reportedly produced no ill effects in 4 subjects (Momontova, 1940,
    cited in WHO, 1980).

         In contrast to the findings described above, Dack (1955)
    reported that no ill effects were produced in 4 subjects consuming
    canned pumpkin containing 383-476 ppm tin and canned asparagus
    containing 361 ppm tin. The average daily ingestion of tin in this
    study ranged from 426 to 490 mg.

         No toxic effects were observed in several studies in which 
    the juice or food was processed specifically to raise tin
    concentrations up to 703 ppm. For example, Benoy et al. (1971)
    pooled orange juice samples implicated in the Kuwait incident,
    reportedly containing 250-385 ppm tin, and then concentrated the
    juice under vacuum to yield a tin level of 498 ppm. Five volunteers
    showed no toxic effects after drinking a volume of the concentrated
    juice which provided 1.59-2.44 mg of tin per kg bw. Likewise, no
    toxic effects were produced after these volunteers consumed tin at
    1.73-3.58 mg/kg bw in orange juice in which the tin levels were
    increased to 540 ppm or 730 ppm by repeatedly aerating the juice,
    adding it cold to cans with a large headspace and then pasteurizing
    the cans in a rotating retort. Adding 50 ppm nitrate to the juice
    containing 730 ppm tin did not enhance its toxicity. However,
    orange juice in which the tin level was increased to 1370 ppm by
    the pasteurization method and consumed in a volume which provided
    4.38-6.71 mg tin per kg bw, produced nausea and/or diarrhea. Only
    one case of nausea recurred when the trial was repeated 1 month
    later. The apparent development of tolerance observed in this study
    remains to be explained.

         No adverse effects were noted in 9 volunteers fed a C-ration
    diet consisting of canned fruits and meats which had been stored
    for 20 months at 37C (Calloway & McMullen, 1966). The tin content
    in the food ranged from 254 to 538 ppm, expressed on the basis of
    dry solids. It was estimated that these subjects consumed an
    average of 163 mg of tin per day (ranging from 116 to 203 mg/day)
    and that virtually all of the ingested tin was recovered in the
    feces. Nitrogen absorption from the gastrointestinal tract was
    decreased, suggesting that the tin in the food was associated with
    protein as an indigestible complex, as previously proposed by Goss
    (1917). C-rations stored at 1C for 20 months contained less than
    50 ppm tin, and also produced no adverse effects in the volunteers.

    COMMENTS AND EVALUATION

         It is clear that different types of canned foods are consumed
    in varying amounts and that levels of tin are higher in unlacquered
    cans than in lacquered cans. Infants and small children, on a body
    weight basis, are more likely than adults to consume higher levels
    of tin from a single source, i.e. canned juice. Furthermore, it is
    acknowledged that factors other than tin levels may play a role in
    potentiating adverse effects and yet others may serve to moderate
    potential toxic effects. In the absence of more specific details
    pertaining to these factors as well as information on the chemical
    forms of tin which cause acute gastric irritation, it was not
    possible to incorporate such considerations into the evaluation of
    this matter. It was concluded from the limited human data available
    that tin concentrations as low as 150 g/g in one incident
    involving canned beverages and 250 g/g in other canned foods may
    produce acute manifestations of gastric irritation in certain
    individuals; however, it was also noted that some canned products
    containing levels up to 700 g/g of tin produced no detectable
    toxic effects.

         Therefore, the Committee recommended that efforts be made to
    keep tin levels in canned foods as low as practicable. In this
    regard, tin concentrations in canned foods should be limited to
    those consistent with the application of good manufacturing
    practices (FAO, 1986). The Committee converted the previously
    established tolerable daily intake of 14 mg of inorganic tin per kg
    of body weight into a PTWI and emphasized that this value was
    applicable to chronic tin exposure.

    REFERENCES

    Barker, W.H. & Runte, V. (1972). Tomato juice-associated
    gastroenteritis, Washington and Oregon, 1969.  Am. J. Epidemiol.,
    96, 219-226.

    Benoy, C.J., Hooper, P.A. & Schneider, R. (1971). The toxicity of
    tin in canned fruit juices and solid foods.  Fd. Cosmet. Toxicol.,
    9, 645-656.

    Calloway, D.H. & McMullen, J.J. (1966). Fecal excretion of iron and
    tin by men fed stored canned foods.  Am. J. Clin. Nutr., 18, 1-6.

    Codex Committee on Food Additives (1986). Report of the Eighteenth
    Session of the Codex Committee on Food Additives. The Hague, 5-11
    November 1985, Food and Agriculture Organization of the United
    Nations, Rome, (Unpublished FAO document, ALINORM 87/12).

    Dack, G.M. (1955). Chemical poisons in food. In:  food poisoning,
    University of Chicago Press, Chicago, pp. 24-25.

    Dick, G.C., Hughes, J.T., Mitchell, J.W. & Davidson, F. (1978).
    Survey of trace elements and pesticide residues in the New Zealand
    diet. I. Trace element content.  New Zealand J. Sci., 21, 57.

    FAO (1986). Guidelines for Can Manufacturers and Food Canners, Food
    and Agriculture Organization of the United Nations, Rome (Food and
    Nutrition Paper No. 36).

    Friberg, L., Nordberg, G.E. & Vouk, V.B. (1986). Handbook on the
    toxicology of metals, 2nd Edition, Elsevier Science Publisher,
    Amsterdam, New York, Vol. II, pp. 565-574.

    Goss, B.C. (1917). Absorption of tin by proteins and its relation
    to the solution of tin by canned foods.  J. ind. Eng. Chem., 9,
    144-148.

    Horio, T., Iwamoto, Y. & Shiga, I. (1967). Comm. 5th Int. Congr.
    Canning, Vienna.

    Kojima, K. (1969). Unpublished reports submitted to WHO.

    Luff, A.P. & Metcalfe, G.H. (1890). Four cases of tin poisoning
    caused by tinned cherries.  Br. med. J., 1, 833-834.

    Ministry of Agriculture, Fisheries and Food (1985). A survey of
    aluminium, antimony, chromium, cobalt, indium, nickel, thallium and
    tin in food, 15th Report of the Steering Group on Food
    Surveillance, Food Surveillance Paper No. 15, HMSO, London, pp.
    63-72.

    Omori, Y. (1966). Tin as a potential cause of intoxication by
    canned orange juices: Proceedings of the 11th Pacific Scientific
    Congress, Tokyo, 1965.  Folia. Pharmac. Jap., 61, 77.

    Omori, Y., Takanaka, A., Tanaka, S. & Ikeda, Y. (1973).
    Experimental studies on toxicity of tin in canned orange juice.  J.
     Food Hyg.  Soc., 14, 69-74.

    Reilly, C. (1980).   Metal contamination in food, Applied Science
    Publisher Ltd., London, p. 142.

    Savage, W. (1939). Canned foods in relation to health.  Lancet,
    237, 991-995.

    Schroeder, H.A., Bulasa, J.J. & Tipton, I.H. (1964). Abnormal trace
    metals in man: Tin.  J. Chron. Dis., 17, 483.

    Schryver, S.B. (1909). Some investigations on the toxicology of
    tin, with special reference to the metallic contamination of canned
    foods.  J. Hyg., 9, 253-263.

    Tipton, I.H., Stewart, P.L. & Martin, P.G. (1966). Trace elements
    in diets and excreta.  Health Phys., 12, 683.

    Warburton, S., Udler, W., Ewert, R.M. & Haynes, W.S. (1962).
    Outbreak of foodborne illness attributed to tin.  Pub. Health Rep.,
    77, 789-800.

    WHO (1980). Environmental Health Criteria 15. Tin and organotin
    compounds: A preliminary review, International Programme on
    Chemical Safety, World Health Organization, Geneva.
    


    See Also:
       Toxicological Abbreviations
       Tin (ICSC)
       Tin (WHO Food Additives Series 46)
       TIN (JECFA Evaluation)