The evaluations contained in this document were prepared by the
    Joint FAO/WHO Expert Committee on Food Additives*
    Rome, 21-29 April 1976

    Food and Agriculture Organization of the United Nations

    World Health Organization

    *Twentieth Report of the Joint FAO/WHO Expert Committee on Food
    Additives, Geneva, 1976, WHO Technical Report Series No. 599, FAO Food
    and Nutrition Series No. 1.



         This substance has been evaluated for acceptable daily intake for
    man by the Joint FAO/WHO Expert Committee on Food Additives in 1970
    and 1973 (see Annex I, Ref. 23, p. 39; Ref. 33, p. 417).

         Since the previous evaluation, additional data have become
    available and are summarized and discussed in the following monograph.
    The previously published monographs have been expanded and are
    reproduced in their entirety below.


    General aspects

         There are two possible reasons for the presence of mineral oil in
    food; (1) in trace amounts from its use as a lubricant or separant
    e.g. in tin-greasing before baking, or from traces on the surface of
    knives used to cut dough in breadmaking, or as a coating e.g. of
    fruit; (2) as a substitute for fat either because it is cheaper or in
    slimming foods. The maximum daily intake is calculated to be about
    100 mg of which some 80 mg are contributed from its use on the
    machinery in the baking industry (Fiero, 1961).

         There has been a great deal of work on the effect of mineral oil
    in impeding the absorption of fat soluble vitamins A (and precursors)
    D. E. K. and essential fatty acids. There is no doubt that
    interference with absorption can occur, particularly of carotene if
    amounts in food exceed approximately 6000 ppm (Steigmann et al.,
    1952). Whether the amounts likely to appear in the food of children
    are of clinical importance is much less certain (assuming that it is
    not used as an ingredient as in (2) above). But the diets of many of
    these may contain amounts of these vitamins that are in any case
    marginal or inadequate and there seems no reason for the inclusion of
    mineral oil in foods which are specifically intended for infants with
    the possible exception of rusks (concerning which inquiries are being
    made which will be later reported as they may be subject to the same
    contaminating processes as bread).


    Absorption, distribution and excretion

         Mineral oils are of variable composition depending on the boiling
    point of the fractions used. For food purposes usually liquid
    petrolatum or liquid paraffin are employed which consist essentially
    of n-alkanes and some cyclic paraffins. They are chemically inert

    especially as regards the straight chain alkanes and on ingestion most
    of the mineral oil (98%) remains unabsorbed in the faeces. There is
    evidence now that small amounts of mineral oil (2%) are absorbed as
    such by the intestinal mucosa and are distributed throughout the body.
    A very small fraction may undergo further biochemical transformation.
    Sources of mineral oil are laxatives or oils used in food technology
    as release agents or for lubrication purposes (Boitnott & Margolis,

         Oil droplets, identified as saturated alkane hydrocarbons, have
    been demonstrated in mesenteric lymphnodes and nodes of the porta
    hepatis in man. Similar droplets have been identified in human liver,
    spleen and adipose tissue. The small amounts formed are consistent
    with the calculated intake from food use (47.5 per head per year in
    the United States of America). The quantities of extractable oil and
    types of histological appearance have been reported (Boitnott &
    Margolis, 1970). There is no correlation with age or sex (Kelsall &
    Blackwell, 1969). There is an unusual geographical incidence, being
    about 50% in North America and 10% in Western Europe and in post
    mortem examinations (Cruikshank, 1972). No known harm appears
    associated with these residues (Boitnott & Margolis, 1966).

         Similar deposition of oil and minor absorption was demonstrated
    in rabbits, rats and guinea-pigs fed liquid petrolatum for seven
    months or more. Histochemical evidence showed absorption to be
    proportionate to length of exposure. The mechanism of absorption was
    unknown but the absorbed particles showed evidence of foreign body
    reaction and phagocytic ingestion (Stryker, 1941).

         Mineral oil used as emulsifying medium for s.c. injection was
    transported from the site of injection without causing any systemic
    effects (Brown, 1966).

         Mineral oil passes through the gut wall unchanged and more is
    absorbed in the presence of powerful emulsifiers, provided that the
    particle size of the emulsion is about 0.5 µ (Frazer et al., 1944).
    Prolonged administration of 0.66 ml/kg for 31 days had no effect on
    the amount absorbed when compared with single dosing (Ebert et al.,

         In studies on absorption of aliphatic hydrocarbons in the rat
    (Albro & Fishbein, 1970) simple mixtures of these compounds were
    administered by gastric intubation at dose levels of up to 500 mg/kg.
    The percentage retention of the aliphatic hydrocarbons was inversely
    proportional to the number of carbon atoms and ranged from 60% for
    C14 to 5% for C28 compounds. The major site of absorption was found
    to be the small intestine.


         H3-labelled mineral oil was administered to rats orally and i.p.
    five hours after oral dosing with 0.66 mg/kg bw it could be shown that
    over 80% was not absorbed but excreted in the faeces, 1-5% was
    absorbed unchanged and another 15% appeared in carcass as H3 non-
    mineral oil substance. Some H3 had exchanged with available H and
    possibly some mineral oil had been modified metabolically.
    Radioactivity was found principally in liver, fat, kidney, brain, and
    spleen. Following i.p. administration there was only very slow
    excretion. 11% appeared in the faeces during eight days and only
    traces in the urine (Ebert et al., 1966).

         Administration of 14C-labelled octadecane to cattle indicated
    that while some of the label was incorporated into the lipids of the
    rumen bacteria and the lipid portion of the blood and the body fat,
    most of the octadecane was eliminated in the faeces (Bartley et al.,
    1971). Studies in which straight chain hydrocarbons (C14 to C17) were
    incorporated into the diet of poultry indicated that this species was
    capable of absorbing and utilizing the energy from this material
    (Squibb and Frankenfeld, 1972).


    Special studies on carcinogenicity

         A wide range of fractions of mineral oil contain carcinogenic
    compounds especially higher boiling fractions of the range 300°-350°-
    400°C as shown by skin painting of mice and rabbits (Cook et al.,
    1958) but refined material may be free from these carcinogenic
    constituents (Prigal, 1967). Inoculation of 64 mice with a combination
    of mineral oil and killed staphylococci induced plasma cell tumours in
    seven animals (Potter & Robertson, 1961).


         A group of 36 DBA/2 and 12 CBA female mice were given a total of
    1.5 ml of Primol D mineral oil in three i.p. injections over a 15-week
    period (Rask-Nielsen & Ebbesen, 1965). The survivors were killed at 24
    months of age. Small intraperitoneal granulomatous nodules containing
    oil droplets developed in all mice. 42% of the DBA/2 mice developed
    reticulosarcomatous growths (Dunn type A) in some of the peritoneal
    nodules. Leukemic infiltrations of varying degree of severity were
    found in the livers of several mice and less frequently in other
    organs. However, only one of the CBA mice developed a reticulum cell
    sarcoma. In contrast, BALB/C mice given mineral oil by i.p. injection
    developed plasma cell neoplasms in the intraperitoneal nodules (Potter
    & Boyce, 1962). The purity of the mineral oil samples used in these

    studies is uncertain. Indeed there was some indication that the sample
    used in the later study contained an impurity having physical
    properties similar to those of some carcinogenic polycyclic aromatic

         Some doubts have been raised as to the probable role of virus in
    production of mouse plasma cell tumours (Prigal, 1967). No human
    cancer has been reported following many years of oleothorax use
    (Prigal, 1967).

    Short-term studies


         Ten rats were each fed a total of 17 g liquid paraffin in 18 g
    olive oil over 16 days mixed into their normal diet. Some 65% was
    absorbed as estimated from faecal loss. Another five rats received
    over 28 days a total of 28 g liquid paraffin in their diet. Only 9%
    was absorbed. Lymph collected during absorption from intestinal
    lymphatics showed that absorbed paraffin had been metabolically
    modified (Daniel et al., 1953).


         Fifteen rabbits, weighing between 1.9 and 2.5 kg, were given
    daily 25 ml of a mixture (1:1) of olive oil and paraffin oil (purity
    not stated). The animals were sacrificed at regular intervals, after
    60-406 days of treatment. At this high dosage level, from the first to
    the third week, a relatively important loss of weight is noted, but
    rapidly a state comparable to the controls is regained. Progressively,
    the paraffin oil passes the intestinal epithelium and accumulates in
    the mesenteric lymph glands, then becoming distributed in the rest of
    the body, with preferential deposition in the liver and in the spleen.
    Histologically, diffuse hyperplasia of reticulo endothelial cells,
    somewhat similar to that seen in human Whipple's disease, is observed
    (Borer, 1960).

    Long-term studies


         Two groups of 30 mice had mineral oil applied to their skin three
    times weekly at 15 mg/application for 311 and 478 days respectively.
    No tumours were found (Anonymous, 1960).


         Animals were kept for 15 months on diets supplemented with 10%
    liquid paraffin. The liver contained 0.4% dry weight liquid paraffin.
    Some active metabolism may occur but liver function was not affected

    (Daniel et al., 1953). In another experiment 2% mineral oil was fed in
    the diet to 30 rats for 500 days without adverse effects (Schmähl &
    Reiter, 1953).


         "Mineral oils" have been demonstrated in human tissues. While no
    demonstrable pathological consequences have occurred from the presence
    of such oils in human tissues resulting from ingestion, its storage is
    considered to be undesirable and exposure to mineral oils should be
    kept to a minimum.

         A recent development is the production, by hydrogenation, of oils
    with chemical specifications similar to those of food grade mineral
    oil. Such oils contain more cyclic paraffins since the aromatic
    components are not removed before distillation but are converted to
    saturated cyclic compounds. While these oils have not been shown to
    contain polycyclic cromatic hydrocarbons in concentrations greater
    than occur in food grade oil, there are insufficient toxicological
    data and information on the similarities and differences in the
    composition of the two types of oil to allow a toxicological
    evaluation of the hydrogenated oil.


    Estimate of acceptable daily intake for man

         Not specified.*


    Albro, P. W. & Fishbein, L. (1970) Biochim. Biophys. Acta, 219, 437

    Anonymous (1960) Unpublished data submitted to the World Health
         Organization by Esso Research and Engineering Co.

    Bartley, E. C., Helmer, L. G. & Meyer, R.M. (1971) J. Animal Science,
         33, 1351

    Boitnott, J. K. & Margolis, S. (1966) Bull. Johns Hopk. Hosp., 118,

    Boitnott, J. K. & Margolis, S. (1970) Johns Hopkins Med. J., 127, 65

    Borer, F. (1960) Rev. franē. études clin. et biol., 5, 47

    Brown, E. A. (1966) Review of Allergy, 20, 148 & 235


    *  Applies only to mineral oil not made by hydrogenation process.

    Cook, J. W., Carruthers, W. & Woodhouse, D. L. (1958) Brit. med.
         Bull., 14, 132

    Cruikshank, B. (1972) Personal communication

    Daniel, J. W. et al. (1953) Biochem. J., 54, 37

    Ebert, A. G., Schleifer, C. R. & Hess, S. M. (1966) J. Pharmac. Sci.,
         55, 923

    Fiero, G. W. (1961) Supplement to Food Additive Petition No. 302 to
         the US Food and Drug Administration date 21 February 1961.
         Unpublished report from the Council on White Mineral oil
         submitted to the World Health Organization by the chairman of API
         Sub-committee on White Mineral Oil

    Frazer, A. C., Schulman, J. H. & Stewart, H. C. (1944) J. Physiol,
         103, 306

    Kelsall & Blackwell (1969) Pathology, 1, 211

    Potter, M. & Boyce, C. R. (1962) Nature, 193, 1086

    Potter, M. & Robertson, J. (1961) J. nat. Cancer Inst., 25, 847

    Prigal, S. J. (1967) Annals of Allergy, 25, 449

    Rask-Nielsen, R. & Ebbesen, P. (1965) J. Nat. Cancer Inst., 35, 83

    Schmähl, D. & Reiter, A. (1953) Arzneimittel-Forsch, 3, 403

    Squibb, R. L. & Frankenfeld, J. W. (1972) Poultry Science, 51, 2056

    Steigmann, F. et al. (1952) Gastroent., 20, 587

    Stryker, W. A. (1941) Arch. Pathol., 31, 670

    See Also:
       Toxicological Abbreviations