FAO Nutrition Meetings
    Report Series No. 40A,B,C
    WHO/Food Add./67.29


    The content of this document is the result of the deliberations of the
    Joint FAO/WHO Expert Committee on Food Additives which met at Rome,
    13-20 December, 19651 Geneva, 11-18 October, 19662


    1 Ninth Report of the Joint FAO/WHO Expert Committee on Food
    Additives, FAO Nutrition Meetings Report Series, 1966 No. 40; 
    Wld Hlth Org. techn. Rep. Ser., 1966, 339

    2 Tenth Report of the Joint FAO/WHO Expert Committee on Food
    Additives, FAO Nutrition Meetings Report Series, 1967, in press; 

    Food and Agriculture Organization of the United Nations
    World Health Organization


    Chemical name                 DL-2-hydroxy propionic acid;
                                  DL-1-hydroxyethane carboxylic acid

    Empirical formula             C3H6O3

    Structural formula
                                  CH3 - C - COOH

    Molecular weight              90.08

    Definition                    Commercial products contain lactic acid
                                  and water and may contain lactic
                                  anhydride in the more concentrated
                                  solutions. The total acid content,
                                  calculated as C3H6O3 is not less
                                  than 95 per cent. and not more than 105
                                  per cent. of the amount specified.

    Description                   A colourless or yellowish, nearly
                                  odourless liquid with an acid taste.

    Use                           As on acidulant.

    Biological Data

    Biochemical aspects

         L(+)-lactate is a normal intermediary of mammalian metabolism. It
    arises from glycogen breakdown, from amino acids and from dicarboxylic
    acids, e.g. succinate. Other sources of production are muscular
    contractile activity, and liver and blood metabolism. Some
    micro-organisms specifically produce lactic acid as main product of
    the metabolism; L. delbrueckii produces L(+)-lactic acid, the
    physiological isomer, and L.lelchmanii, the D(-)-isomer.

         Various groups of rats were killed 3 hours after the
    administration of L(+), D(-) or DL-lactic acid (1700 mg/kg) orally or
    by s.c. injection. The L(+)-isomer produced the largest rise in liver
    glycogen; 40-95 per cent. of the L(+)-lactate absorbed in 3 hours
    being converted; practically none were formed from the D(-)-isomer.
    D(-)-lactate produced the highest blood lactate level and 30 per cent.
    of the amount absorbed was excreted in the urine; no L(+)-lactate was
    found. D(-)-lactate was utilized four times more slowly but both D(-)
    and L(+)-isomers were absorbed at the same rate from the intestine
    (Cori & Cori, 1929). The absorption of sodium DL-lactate from the
    intestine of groups of 6 male and female rats was determined at 1, 2,

    3 and 4 hours after oral feeding of 215 mg/kg body-weight of material.
    The rate of absorption decreased with time and was roughly
    proportional to the amount of lactate present in the gut. Slow
    evacuation of the stomach limited the rate of absorption in some
    animals (Cori, 1930). At blood levels over 200-250 mg per cent.
    lactate, rabbits showed excitation, dyspnoea and tachycardia (Collazo
    et al., 1933).

         After oral administration to a human subject of 1-3000 mg
    lactate, 20-30 per cent. was excreted in the urine during 14 hours
    (Fürth & Engel, 1930).

         When sodium DL-lactate was given i.v. to starving dogs, 7-40 per
    cent. was recovered in the urine, none was found in the faeces
    (Abramson & Eggleton, 1927). Rabbits ware given orally 600-1600 mg/kg
    body-weight of racemic lactic acid. Most animals died within 3 days.
    Urinary excretion varied between 0.26 per cent. and 31 per cent.
    Alkalosis did not affect the excretion (Fürth & Engel, 1930),

         In vitro studies have shown that mammalian tissue produces only
    L(+)-lactate although some tissues can oxidize both isomers. Rat liver
    tissue used almost entirely L(+) and practically no D(-)-isomer, as
    measured by oxygen consumption and carbohydrate synthesis. Rat kidney
    tissue used a definitely measurable amount of D(-)-isomer. Grey matter
    of rat brain was unable to utilize the D(-)-isomer. L(+)-lactate
    stimulated oxygen consumption and CO2 production of all rat tissues;
    similarly D(-)-lactate slightly stimulated respiration of liver and
    heart but not brain tissue. Similar effects occurred in duck tissue.
    Heart tissue is able to utilize both isomers almost equally well.
    14C-L(+)-lactate produces 14O2 more rapidly than D(-)-lactate in the
    intact rat although the D(-) form is fairly well metabolized. After 2
    hours, both isomers are oxidized at equal rates (Brin, 1964). More
    recent studies have defined the cell sites for metabolizing the
    isomers in microorganisms and higher animals and identified the
    pathways in normal animals, cattle with D(-) lactacidosis and mentally
    ill patients (Brin, 1964). L(+)-lactate was oxidized 3-5 times as
    rapidly as D(-)-lactate by duck and rat heart and liver slices and
    10-20 times as rapidly by brain slices, using 14C labelled substrate,
    as shown by oxygen consumption and 14CO2 production. The D(-)-isomer
    was used equally as well as the L(+)-isomer by duck and rat heart
    slices, two-thirds as well by brain and one-third as well by duck and
    rat liver and duck brain. High utilization of D(-)-isomer requires
    special metabolic pathways (Brin et al., 1952).

    Acute toxicity


    Animal       Route                 LD50         References

    Rat          i.p. (Sod. lactate)   2 000          Rhône-Poulenc, 

                 oral (lactic acid)    3 730          Smyth et al., 1941

    Guinea-pig   oral                  1 810          Smyth et al., 1941

    Mouse        oral                  4 875          Fitzhugh, 1945

         Rats have been stated to survive 2000-4000 mg/kg body-weight
    administered s.c. Mice were killed by doses of 2000-4000 mg/kg
    body-weight whether or not alkalosis was present Fürth & Engel, 1930),
    In man, accidental intraduodenal administration of 100 ml 33 per cent.
    lactic acid was fatal within 12 hours (Leschke, 1932). Other workers
    quote an adult human maximum tolerated dose of 1530 mg/kg body-weight
    (Nazario, 1952).

    Short-term studies

         Bird. Feeding of 10 per cent. lactic acid has been blamed for
    the development of polyneuritic crises resembling B1 deficiency on
    diets rich in carbohydrates, proteins or fats (Lecoq, 1936).

         Rat. Groups of 2 animals received daily doses of 1000 and 2000
    mg/kg body-weight of sodium lactate (as lactic acid) over 14-16 days.
    Body analyses showed no cumulation (Fürth & Engel, 1930).

         Dog. Two dogs received 600-1600 mg/kg body-weight of lactic
    acid orally 42 times during 2.5 months without ill effects (Faust,

         Infants. Forty full-term newborn infants were given a
    commercial feeding formula containing 0.4 per cent. DL-lactic acid. No
    effect was observed on the rate of weight gain, from the second to the
    fourth week of life (Jacobs & Christian, 1957).

         Healthy babies were fed milk formulae acidified with 0.4-0.5 per
    cent. DL-lactic acid for periods of 10 days, during the first 3 months
    of their life. An increase in the titrable acidity of the urine, and
    lowering of urinary pH was observed. Babies on "milk rich" formula
    (4/5 milk mixture) excreted twice as much acid in the urine as babies
    on diets containing less milk and approximately 33 per cent. developed
    acidosis. Clinical manifestations were: decrease in the rate of

    body-weight gain and decrease in food consumption. On replacing the
    acidified diet with "sweet milk" diet these effects were reversed very
    rapidly (Droese & Stolley, 1962).

         When 0.35 per cent. DL-lactic acid was administered to healthy
    babies from the tenth to the twentieth day of life, a three-fold
    increase in the urinary excretion of the physiological L(+)-lactic
    acid and a twelve-fold increase in the D(-)-lactic acid was observed.
    On withdrawing lactic acid from the diet the level of lactic acid
    excreted in the urine returned to normal. Since the racemic mixture
    used consisted of 80 per cent. of the L(+) and 20 per cent. of the
    D(-) forms it seems that the metabolism of the D(-) form by the young
    full-term baby is more difficult than the L(+) form. The increase in
    the urinary excretion of either form of lactic acid indicated that the
    young infant cannot utilize lactic acid at a rate which can keep up
    with 0.35 per cent. in the diet. A number of babies could not tolerate
    lactic acid. In such cases there was rapid loss of weight, frequent
    diarrhoea, reduction of plasma bicarbonate and increased excretion of
    organic acids in the urine. All these effects were reversed on
    withdrawing lactic acid from the diet (Droese & Stolley, 1965).

    Long-term studies

         No animal studies are available.

         Man has consumed meat and other items of food containing lactates
    for centuries, apparently without any adverse effects.


         In evaluating lactic acid, emphasis is placed on its
    well-established metabolic pathways after normal consumption in man.
    It is an important intermediate in carbohydrate metabolism, However,
    human studies determining the maximum load of lactate are not
    available. There is some evidence that babies in their first three
    months of life have difficulties in utilizing small amounts of DL and
    D(-)-lactic acids.


         Lactic acid has a sufficiently acid taste to limit the amount
    used in food.

    Estimate of acceptable daily intake of L(+)-isomer

         No limit need be set for the acceptable daily intake for man of
    the L(+)-isomer of lactic acid.

    Estimate of acceptable daily intakes for man of D(-)-isomer

                                  mg/kg body-weight

       Conditional acceptance          0-100

    Limitations of use

         Neither the D(-) nor DL-Lactic acid should be added to food for
    very young infants, except for therapeutic purposes.

         For adults the acceptable daily intake of DL-lactic acid is
    calculated from the D(-)-lactic acid content.

    Further work required

         Metabolic studies on the utilization of D(-) and DL-lactate acids
    in infants and adults.


    Abramson, H. A. & Eggleton, P. (1927) J. Biol. Chem., 75, 745,
    753, 763

    Brin, M. (1964) J. Ass. Food and Drug. Off., 178

    Brin, M., Olson, R. E. & Stare, F. J. (1952) J. Biol. Chem., 199,

    Collazo, J. A., Puyal, J. & Torres, I. (1933) Anales Soc. Esp. Fis.
    Quim., 31, 672

    Cori, G. T. (1930) J. Biol. Chem., 87, 13

    Cori, C. F. & Cori, G. T. (1929) J. Biol. Chem., 51, 389

    Droese, W. & Stolley, H. (1962) Dtsch. med. J., 13, 107

    Droese, W. & Stolley, H. (1964) Symp. über die Ernährung der
    Frühgeborenen, Bad Schachen, May 1964, 63-72

    Faust, E S. (1910) Cöthener Chem. Z., 34, 57

    Fitzhugh, O. G. (1945) Unpublished data, submitted to WHO

    Fürth, O. & Engel, F. (1330) Biochem. Z., 228 381

    Jacobs, H. M. & Christian, J. R. (1957) Lancet, 77, 157

    Lecoq, M. R. (1936) C.R. Acad. Sci., 202, 1304

    Leschke, E. (1932) Munch. Med. Wschr., 79, 1481

    Nazario, G. (1951) Rev. Inst. Adolfo Lutz, 11, 141

    Rhône-Poulenc (1965) Unpublished report

    Smyth, H. F. jr, Seaton, J. & Fischer, L. (1941) J. Ind. Hyg.
    Toxicol., 23, 59

    See Also:
       Toxicological Abbreviations