FAO Meeting Report No. PL/1965/10/2
    WHO/Food Add/28.65


    The content of this document is the result of the deliberations of the
    Joint Meeting of the FAO Committee on Pesticides in Agriculture and
    the WHO Expert Committee on Pesticide Residues, which met 15-22 March

    Food and Agriculture Organization of the United Nations
    World Health Organization

    1 Report of the second joint meeting of the FAO Committee on
    Pesticides in Agriculture and the WHO Expert Committee on Pesticide
    Residues, FAO Meeting Report No. PL/1965/10; WHO/Food Add./26.65.




    Chemical name



         Propene nitrile; vynyl cyanide; cyanoethylene

    Empirical formula


    Structural formula


    Relevant physical and chemical properties

    Physical state (atmospheric pressure 20°C): colourless, volatile
    liquid (some technical grades slightly yellow)

    Boiling-point: 77°C

    Odour: like mustard

    Flash Point: 0°C (open cup)

    Flammability limits in air: 3 to 17% by volume


         Water: 7.5 g/100 ml

         Organic solvents: soluble in all common organic solvents

    Specific gravity (liquid): 0.800

    Specific gravity (gas): 1.83


         Acrylonitrile is a potent, highly effective fumigant; however its
    high flammability and cost deter its use. Although it is not widely
    employed at present for the fumigation of foodstuffs, acrylonitrile is
    occasionally used to treat grain, dried fruit, walnuts and tobacco. It
    is also sometimes used as a "spot fumigant" in flour mills and


         Residues are similar to those resulting from the use of hydrogen

    Effect of fumigant on treated crop

         The effects of acrylonitrile are similar to those of hydrogen
    cyanide. Commodities having a high moisture content absorb more
    fumigant than commodities with a low moisture content. Acrylonitrile,
    used alone or mixed with carbon tetrachloride, does not affect the
    germination of a wide range of vegetable, cereal and flower seeds
    (Glass and Crosier, 1949; Lindgren et al., 1954). It is, however,
    highly toxic to nursery stock and growing plants and seriously damages
    fresh fruit.


         Acrylonitrile is highly toxic and the intoxication can be induced
    by the oral, percutaneous or inhalation routes (in the form of

    Biochemical aspects

         On the basis of results with acrylonitrile in different species
    of animals, its toxicity is considered to be equivalent to that of
    hydrogen cyanide which is evolved from acrylonitrile in the organism
    (Dudley and Neal, 1942; Dudley et al., 1942; Levina, 1951). Hydrogen
    cyanide was demonstrated in the blood of rats after seven hours'
    exposure (100 ppm in air) but only in small amounts (1 micromole/100
    ml). In dogs the blood concentration of cyanide was ten times greater
    after the same exposure. No hydrogen cyanide was found in the blood of
    rats after exposure to lower concentrations in the air (Brieger et
    al., 1952). From experiments in dogs, it was recommended that
    thiocyanate determinations in serum and urine be used to discover
    cases of dangerous absorption in workers exposed to acrylonitrile
    (Lawton et al., 1943).

         On the other hand, a number of authors have not confirmed that
    the effects of acrylonitrile are due to hydrogen cyanide (Benes and
    Cerna, 1959; Désgrez, 1911; Ghiringhelli, 1954; Lindgren et al., 1954;
    Paulet and Desnos, 1961; Sexton, 1950). After the administration of
    acrylonitrile to guinea-pigs, rats and rabbits very little cyanide was
    recovered from the urine, as thiocyanate, compared with the amounts

    excreted in cyanide poisoning (Benes and Cerna, 1959; Ghiringhelli,
    1956; Paulet and Desnos, 1961). After subcutaneous injection of
    acrylonitrile (130 mg/kg) to guinea-pigs, the hydrogen cyanide
    concentration in blood was 0.128 mg % (average). This concentration is
    too low to be able to cause death in animals; for comparison the
    average HCN concentration in the blood of dogs after intoxication with
    inhaled HCN was 1.1 mg % and 0.85 mg % after oral HCN poisoning
    (Ghiringhelli, 1954; Gettler and Baine, 1938).

         The use of thiosulfate, nitrite and glucose as antidotes to the
    acute poisoning of animals with acrylonitrile has not been successful
    or convincing (Benes and Cerna, 1959; Ghiringhelli, 1954; Dudley and
    Neal, 1942). The combination of thiosulfate and nitrite had a certain
    anti-acrylonitrile effect in mice (Benes and Cerna, 1959).

         Furthermore, the rate of cyano-methaemoglobin formation in rats
    killed by acrylonitrile is lower than that in animals surviving
    potassium cyanide and much lower than in animals killed by it (Magos,

         Thiosulfate with phenobarbitol and commonly used stimulating
    preparations protected 70-90% of animals (rats, rabbits, mice) against
    doses of acrylonitrile exceeding the LD100 (Paulet and Desnos, 1961).
    In guinea-pigs, unmetabolized acrylonitrile was proved by a
    chromatographic method 24 and 30 hours after oral and subcutaneous
    detected administration (Benes and Cerna, 1959).

    Acute toxicity

    Animal      Route           LD50 mg/kg      References

    Mouse       oral              40-46       American Cyanamid, 1951
                                   27         Benes & Cerna, 1959
                subcutaneous       35         Benes & Cerna, 1959

    Rat         oral               78         Benes & Cerna, 1959
                                   93         Smyth & Carpenter, 1948

    Guinea-pig  subcutaneous      130         Ghiringhelli, 1954
                oral               50         Negherbon, 1959

    Rabbit      intravenous        69         Paulet & Desnos, 1961

    Detailed investigation of acute poisoning with acrylonitrile after
    intravenous injection in dog and rabbit indicates considerable
    differences from cyanide intoxication. In the symptomatology nervous
    disorders dominate the picture. Electroencephalographic records show
    that the higher nervous centres are affected. Important physiological
    differences from cyanide poisoning are absence of polypnoea, increased

    oxygen consumption during the first phases of intoxication, and
    lowering of the HbO2 level in the mixed venous blood. Hyperglycaemia
    and a decrease in the plasma inorganic phosphate concentration were
    also found (Paulet and Desnos, 1961).

         Man.    There are only few reports on the toxic effect of
    acrylonitrile on man. Accidental deadly poisonings are described in
    two children. In the first case it was an inhalation poisoning, in the
    second a percutaneous one (Grunske, 1949, Lorz, 1950).

         In industrial workers exposed to acrylonitrile vapours, in
    different cases light jaundice, anaemia, leucocytosis, headache or
    gastro-intestinal symptoms were observed (Wilson, 1944). In a small
    group of men working with a mixture of nitrites for a number of years,
    symptoms of liver and kidney irritations were reported; they
    disappeared, however, when the exposure was interrupted (Wilson and
    McCormick, 1949).

         The threshold limit value for acrylonitrile in air is 20 ppm
    (about 45 mg/m3) (Anon, 1964).

    Comment on experimental studies reported

         The acute toxicity and the mechanism of the toxic effect of
    acrylonitrile have been studied. Its mode of action is not known but
    it can be said that it is not similar to that of hydrogen cyanide.


         On the basis of the toxicological investigations done hitherto,
    the acceptable daily intake of acrylonitrile for man cannot be

    Further work required

         Biochemical studies on the effect of the fumigant on food.
    Additional toxicological studies are required before an acceptable
    daily intake level for man can be considered.


    Anon, (1964) Threshold limit values for 1964. Arch. environm.
    Hlth., 9, 545

    American Cyanamid Co., New York (1951) The chemistry of acrylonitrile,
    Cyanamid's Nitrogen Chemicals Digest

    Benes, V. & Cerna, V. (1959) J. Hyg. Epidem. (Praha), 3, 106

    Brieger, H., Rieders, F. & Hodes, W. A. (1952) Arch. industr. Hyg.,
    6, 128

    Désgrez, A. (1911) C.R. Acad. Sci. (Paris), 153, 895

    Dudley, H. C. & Neal, P. A. (1942) J. industr. Hyg., 24, 27

    Dudley, H. C., Sweeney, T. R. & Miller, J. W. (1942) J. industr.
    Hyg., 24, 255

    Gettler, A. O. & Baine, J. O. (1938) Amer. J. med. Sci., 195, 182

    Ghiringhelli, L. (1954) Med. d. Lavoro, 45, 305

    Ghiringhelli, L. (1956) Med. d. Lavoro, 47, 192

    Glass, E. H. & Crosier, W. F. (1949) J. econ. Ent., 42, 646

    Grunske, F. (1949) Dtsch. med. Wschr., 74, 1081

    Lawton, A. H., Sweeney, T. R. & Dudley, H. C. (1943) J. industr.
    Hyg., 25, 13

    Levina, E. N. (1951) Gig. i Sanit., 2, 34

    Lindgren, D. L., Vincent, L. E. & Krohne, H. E. (1954) J. econ.
    Ent., 47, 923

    Lorz, H. (1950) Dtsch. med. Wschr., 75, 1087

    Magos, L. (1962) Brit. J. industr. Med., 19, 283

    Negherbon, W. O. (1959) Handbook of Toxicology, vol. 3, Saunders,

    Paulet, G. & Desnos, J. (1961) Arch. int. Pharmacodyn., 131, 54

    Sexton, W. A. (1950) Chemical constitution and biological activity,
    Von Nostrand Co. Inc., New York

    Smyth, H. F. & Carpenter, C. P. (1948) J. industr. Hyg., 30, 63

    Wilson, R. H. (1944) J. Amer. med. Ass., 124, 701

    Wilson, R. H. & McCormick, W. E. (1949) Industr. Med. Surg., 18,

    See Also:
       Toxicological Abbreviations
       Acrylonitrile (EHC 28, 1983)
       Acrylonitrile (HSG 1, 1986)
       Acrylonitrile (ICSC)
       Acrylonitrile (WHO Food Additives Series 19)
       ACRYLONITRILE (JECFA Evaluation)
       Acrylonitrile (CICADS 39, 2002)
       Acrylonitrile (IARC Summary & Evaluation, Volume 71, 1999)