1.1 Substance
   1.2 Group
   1.3 Synonyms
   1.4 Identification numbers
      1.4.1 CAS number
      1.4.2 Other numbers
   1.5 Main brand names, main trade names
   1.6 Main manufacturers, main importers
   2.1 Main risks and target organs
   2.2 Summary of clinical effects
   2.3 Diagnosis
   2.4 First-aid measures and management principles
   3.1 Origin of the substance
   3.2 Chemical structure
   3.3 Physical properties
      3.3.1 Colour
      3.3.2 State/Form
      3.3.3 Description
   3.4 Other characteristics
   4.1 Uses
      4.1.1 Uses
      4.1.2 Description
   4.2 High risk circumstance of poisoning
   4.3 Occupationally exposed populations
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eye
   5.5 Parenteral
   5.6 Others
   6.1 Absorption by route of exposure
   6.2 Distribution by route of exposure
   6.3 Biological half-life by route of exposure
   6.4 Metabolism
   6.5 Elimination by route of exposure
   7.1 Mode of Action
   7.2 Toxicity
      7.2.1 Human data Adults Children
      7.2.2 Relevant animal data
      7.2.3 Relevant in vitro data
      7.2.4 Workplace standards
      7.2.5 Acceptable daily intake (ADI) and other guideline levels
   7.3 Carcinogenicity
   7.4 Teratogenicity
   7.5 Mutagenicity
   7.6 Interactions
   8.1 Material sampling plan
      8.1.1 Sampling and specimen collection Toxicological analyses Biomedical analyses Arterial blood gas analysis Haematological analyses Other (unspecified) analyses
      8.1.2 Storage of laboratory samples and specimens Toxicological analyses Biomedical analyses Arterial blood gas analysis Haematological analyses Other (unspecified) analyses
      8.1.3 Transport of laboratory samples and specimens Toxicological analyses Biomedical analyses Arterial blood gas analysis Haematological analyses Other (unspecified) analyses
   8.2 Toxicological Analyses and Their Interpretation
      8.2.1 Tests on toxic ingredient(s) of material Simple qualitative test(s) Advanced qualitative confirmation test(s) Simple quantitative method(s) Advanced quantitative method(s)
      8.2.2 Tests for biological specimens Simple qualitative test(s) Advanced qualitative confirmation test(s) Simple quantitative method(s) Advanced quantitative method(s) Other dedicated method(s)
      8.2.3 Interpretation of toxicological analyses
   8.3 Biomedical investigations and their interpretation
      8.3.1 Biochemical analysis Blood, plasma or serum Urine Other fluids
      8.3.2 Arterial blood gas analyses
      8.3.3 Haematological analyses
      8.3.4 Interpretation of biomedical investigations
   8.4 Other biomedical (diagnostic) investigations and their interpretation
   8.5 Overall interpretation of all toxicological analyses and toxicological investigations
   9.1 Acute poisoning
      9.1.1 Ingestion
      9.1.2 Inhalation
      9.1.3 Skin exposure
      9.1.4 Eye contact
      9.1.5 Parenteral exposure
      9.1.6 Other
   9.2 Chronic poisoning
      9.2.1 Ingestion
      9.2.2 Inhalation
      9.2.3 Skin exposure
      9.2.4 Eye contact
      9.2.5 Parenteral exposure
      9.2.6 Other
   9.3 Course, prognosis, cause of death
   9.4 Systematic description of clinical effects
      9.4.1 Cardiovascular
      9.4.2 Respiratory
      9.4.3 Neurological Central Nervous System (CNS) Peripheral nervous system Autonomic nervous system Skeletal and smooth muscle
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary Renal Others
      9.4.7 Endocrine & reproductive systems
      9.4.8 Dermatological
      9.4.9 Eye, ears, nose, throat: local effects
      9.4.10 Haematological
      9.4.11 Immunological
      9.4.12 Metabolic Acid-base disturbances Fluid & electrolyte disturbances Others
      9.4.13 Allergic reactions
      9.4.14 Other clinical effects
      9.4.15 Special risks
   9.5 Others
   9.6 Summary
   10.1 General principles
   10.2 Life supportive procedures
   10.3 Decontamination
   10.4 Elimination
   10.6 Antidote treatment
      10.6.1 Adults
      10.6.2 Children
   10.6 Management discussion
   11.1 Case reports from literature
   12.1 Specific preventive measures
   12.2 Other

    International Programme on Chemical Safety
    Poisons Information Monograph 652

    1.  NAME

        1.1  Substance


        1.2  Group


        1.3  Synonyms

             Acrylic acid amide;
             Acrylic amide;
             Acrylamide monomer;
             Ethylene carboxamide;
             Propenoic acid amide.

        1.4  Identification numbers

             1.4.1  CAS number


             1.4.2  Other numbers

                    DOT:                    UN 2074
                    RCRA Waste number:      U007
                    RTECS registry number:  AS 33250000

        1.5  Main brand names, main trade names

             USA: AAM; Optimum; Amresco Acryl-40; Optimum; Acrylage 1

        1.6  Main manufacturers, main importers

             American Cyanamid Company
             Headquarters:                  1 Cyanamid Plaza, Wayne, NJ
             Production facilities:         Avondale, LA 70094.
                                            Linden, NJ 07037.

                                            Botlek, The Netherlands.
             Dow Chemical USA
             Headquarters:                  2020 Dow Center, Midland, MI
             Production facility:           Main Street, Midland, MI
             Nalco Chemical Co.
             Headquarters:                  One Nalco Center, 
                                            Naperville, IL  60566-1024.
             Production facility:           Garyville, LA 70051.
             BF Goodrich Co.                6100 Oak Tree Blvd, 
                                            Cleveland, OH
                                            Tel: (216) 447-7802,
             Cosan Chemical Corp.           400 14th St, Carlstadt, NJ
                                            Tel (201) 460-9300.

    2.  SUMMARY

        2.1  Main risks and target organs

             Acrylamide is a potent neurotoxin affecting both the
             central and peripheral nervous systems.  The magnitude of the
             toxic effect depends on the duration of exposure and the
             total dose.
             Only the acrylamide monomer is toxic.  Acrylamide polymers
             are non-toxic.

        2.2  Summary of clinical effects

             Acute ingestion
             Behavioural disturbance.
             Auditory and visual hallucinations.
             Depressed level of consciousness.
             Adult respiratory distress syndrome.
             Delayed peripheral neuropathy.
             Chronic Occupational exposure
             Contact dermatitis.
             Excessive sweating, especially of extremities.
             Weight loss with normal appetite.
             Neurobehavioural changes.

             Truncal ataxia.
             Signs and symptoms of motor and sensory peripheral

        2.3  Diagnosis

             The initial diagnosis is based on a history of ingestion of
             even a few grams of acrylamide crystal.  The patient who
             presents asymptomatic may develop severe symptoms with a
             delay of many hours.  The diagnosis should be considered in
             an individual with access to acrylamide (for example a
             laboratory worker) who develops a central nervous system,
             cardiovascular and respiratory disturbance over a period of
             Acrylamide intoxication is a clinical diagnosis and should be
             strongly suspected whenever truncal ataxia with peripheral
             neuropathy is detected in an acrylamide-exposed worker. The
             presence of excessive sweating and redness and peeling of the
             skin of the hands and feet makes the diagnosis even more
             Laboratory studies are unhelpful.
             Evidence of peripheral neuropathy on nerve conduction studies
             supports the diagnosis of acrylamide neurotoxicity.  Normal
             studies do not exclude the diagnosis.

        2.4  First-aid measures and management principles

             Acute oral, dermal or inhalational exposures are
             initially managed by appropriate decontamination.  Victims of
             acute exposure should be followed for signs or symptoms of
             Established toxicity following occupational exposure is
             managed by prevention of further exposure.  No specific
             therapy exists.
             Prevention of toxicity from repeated occupational exposure is
             most important.  This is achieved by minimising exposure
             amongst workers handling the chemical.


        3.1  Origin of the substance

             All acrylamide in the environment is synthetic.
             Commercial production commenced in 1954.
             Acrylamide, a vinyl monomer, is formed from the hydration of
             acrylonitrile by sulfuric acid monohydrate at 90 to 100C. 
             From the resulting sulfate solution, acrylamide is extracted
             by neutralization with ammonia and subsequent cooling to
             isolate the crystalline monomer.
             Copper salts are added to the solution to suppress formation
             of by-products of polyacrylamide and acrylic acid. 
             Alternatively, acrylamide can be produced by direct catalytic
             conversion in which an aqueous solution of acrylonitrile is
             passed over a fixed bed of copper or copper-metal admixtures
             at 25 to 200C (Macwilliam, 1978).

        3.2  Chemical structure

             Structural names:              2-Propenamide
             Molecular formula:             C3H5NO
             Molecular weight:              71.08

        3.3  Physical properties

             3.3.1  Colour


             3.3.2  State/Form

                    Crystalline solid at room temperature.
                    Liquid form is 40% (weight/volume) solution in
                    specially deionized water.

             3.3.3  Description

                    Melting point:   84.5C
                    Vapour pressure:        0.009 kPa at 25C
                                            0.004 kPa at 40C
                                            0.09 kPa at 50C
                    Boiling point:          87C at 0.267 kPa
                                            103C at 0.667 kPa
                                            125C at 3.33 kPa

                    Heat of polymerization: 19.8 kcal/mole
                    Density: 1.122 g/cm3 at 30C
                    Solubility in g/L solvent at 30C:
                    Acetone               631
                    Benzene               3.46
                    Chloroform            26.6
                    Ethanol               862
                    Ethyl acetate         126
                    n-heptane             0.068
                    Methanol              1550
                    Water                 2155
                    Conversion factor:    1 ppm acrylamide in air = 5
                    (Budavari et al., 1989)

        3.4  Other characteristics

             Readily polymerizes if heated to melting point or if exposed
             to ultraviolet radiation  (Budavari et al., 1989).


        4.1  Uses

             4.1.1  Uses

             4.1.2  Description

                    Acrylamide is used for the production of high
                    molecular weight polyacrylamides which are modified to
                    produce different physical and chemical properties
                    suited to a wide variety of industrial
                    Large quantities of polyacrylamide gel are produced on
                    site for use as a grouting agent, particularly for the
                    sealing of mineshafts in the mining industry.
                    Polyacrylamides are used in large quantities as
                    flocculators (substances that aid the separation of
                    suspended solids from aqueous systems) in the
                    following industries:

                    Water treatment.
                    Pulp and paper processing.
                    Crude oil production processes.
                    Mineral ore processing.
                    Concrete processing.
                    Soil and sand treatment.
                    Smaller quantities of polyacrylamides are used in the
                    following applications:
                    Cosmetic additives.
                    Permanent press fabrics.
                    Electrophoresis, molecular biology 
                    Photographic emulsions.
                    Adhesive manufacture.
                    Food processing.

        4.2  High risk circumstance of poisoning

             Only the acrylamide monomer is neurotoxic.  Those
             workers involved in the synthesis of acrylamide monomer or
             polymerization processes are at risk of exposure.

        4.3  Occupationally exposed populations

             Any workers required to handle acrylamide monomer
             especially in industries where large quantities are used.
             Virtually all reported cases have occurred in the following
             groups of workers:
             Acrylamide monomer production facility workers.
             Flocculator production workers.
             Mineworkers involved in grouting operations.


        5.1  Oral

             Well absorbed. Unusual route in human exposure.

        5.2  Inhalation

             Well absorbed. Important route in occupational

        5.3  Dermal

             Well absorbed. Important route in occupational

        5.4  Eye

             No data available.

        5.5  Parenteral

             Not reported in humans.  Acrylamide is well absorbed
             following intravenous, intramuscular, intraperitoneal and
             subcutaneous administration in animals.

        5.6  Others

             Not reported in humans.  Well absorbed following mucosal
             application in animal experiments.

    6.  KINETICS

        6.1  Absorption by route of exposure

             Acrylamide is rapidly and well absorbed by intravenous,
             intraperitoneal, subcutaneous, intramuscular, oral,
             transmucosal and dermal routes (Kuperman, 1958).  In rats,
             absorption of acrylamide following oral administration is
             virtually complete.  However, only about 25% of a dose
             applied to the skin is absorbed over the subsequent 24 hours
             (Dearfield et al., 1988).  [Note: all data derived from
             animal studies].

        6.2  Distribution by route of exposure

             Following absorption, acrylamide is rapidly distributed
             throughout the total body water.  Tissue distribution is not
             significantly affected by dose or route of administration.
             Highest concentrations are found in red blood cells.  Despite
             the prominence of neurological effects, acrylamide is not
             concentrated in nervous system tissues (Miller et al.,
             Acrylamide readily crosses the placenta (Edwards, 1976). 
             [Note: all data derived from animal studies].

        6.3  Biological half-life by route of exposure

             In blood, acrylamide has a half-life of approximately 2
             hours. In tissues, total acrylamide (parent compound and
             metabolites) exhibits biphasic elimination with an initial
             half-life of approximately 5 hours and a terminal half life
             of 8 days (Edwards, 1975; Miller et al., 1982).

             Acrylamide does not accumulate in the body.  [Note: all data
             derived from animal studies].

        6.4  Metabolism

             Acrylamide undergoes biotransformation by conjugation
             with glutathione (Edwards, 1975; Miller et al., 1982) or
             reduction by microsomal cytochrome P-450 (Kaplan et al.,
             1973) with glutathione conjugation probably being the major
             route of detoxification.  The metabolites are non-toxic
             (Edwards, 1975).  [Note: all data derived from animal

        6.5  Elimination by route of exposure

             Greater than 90% of absorbed acrylamide is excreted in
             the urine as metabolites.  Less than 2% is excreted as
             unchanged acrylamide.  Smaller amounts are excreted in the
             bile and faeces (Miller et al., 1982).
             Approximately 60% of an administered dose appears in the
             urine within 24 hours (Miller et al., 1982).  [Note: all data
             derived from animal studies].


        7.1  Mode of Action

             Exposure to acrylamide produces a distal axonopathy
             (also known as "dying-back" neuropathy) in both humans and
             experimental animals.  Both central nervous system (CNS) and
             peripheral nervous system (PNS) neurons are affected although
             CNS damage appears to require exposure to much higher
             concentrations.  There is some potential for regeneration of
             PNS neurons but damage to CNS neurons is permanent.

             The mechanism by which this distal axonopathy is produced
             remains unknown although several theories have been advanced,
             all supported by some experimental evidence.  It appears that
             acrylamide interferes with axonal retrograde transport
             mechanisms essential for the survival of the axon.

             Acrylamide has been shown to bind to DNA (Carlson & Weaver,
             1985) which may result in the production of unsound
             structural proteins essential for axonal function.  It has
             also been postulated that acrylamide enters the neuron at the
             neuromuscular junction by pinocytosis and then binds to
             tubulin sulfhydryl goups in the axon resulting in disassembly
             of microtubules and consequent disruption of retrograde
             transport (Smith & Oehme, 1991).  Other mechanistic theories
             include deregulation of axonal and/or Schwann cell elements

             and water (LoPachin et al., 1992a, b) and altered neuronal
             calcium homeostasis interfering with calmodulin-dependent
             enzymes and phosphorylation of cytoskeletal proteins (Xiwen
             et al., 1992; Reagan et al., 1994).

             Acrylamide may mediate some of its CNS effects by altering
             neurotransmitter concentration and function.  Acrylamide has
             been shown to decrease CNS concentrations of noradrenalin,
             dopamine and 5-hydroxytryptamine and also appears to alter
             responsiveness to dopamine by affecting postsynaptic dopamine
             receptor affinity and density (Tilson, 1981).

        7.2  Toxicity

             7.2.1  Human data


                             No relevant data.


                             No relevant data.

             7.2.2  Relevant animal data

                    Numerous investigators have looked at
                    dose-response and dose-effect relationships in a
                    variety of animal models.  There do not appear to be
                    significant differences between mammalian species
                    The LD50 for a single dose of oral acrylamide in rats,
                    guinea pigs and rabbits is 150-180 mg/kg (McCollister
                    et al., 1964).
                    Evidence of neurological effect has been observed
                    following single oral doses of 126 mg/kg in rats and
                    rabbits (McCollister et al., 1964) and 100 mg/kg in
                    dogs (Kuperman, 1958).
                    Using chronic dosing schedules, it has been observed
                    that cumulative oral doses of 500-600 mg/kg using
                    daily doses of 25-50 mg/kg/day are required to produce
                    ataxia in rats, dogs and baboons (McCollister et al.,
                    1964; Thomann et al., 1974; Hopkins, 1970).  Smaller
                    daily doses do not produce a clinical effect until a
                    larger cumulative dose is attained;  Fullerton &

                    Barnes (1966) observed that administration of
                    acrylamide at daily doses of 6 to 9 mg/kg did not
                    produce evidence of neurotoxicity in rats until a
                    cumulative dose of 1200 to 1800 mg/kg was
                    McCollister et al. (1964) observed that doses of up
                    to 3 mg/kg/day for 90 days administered to rats did
                    not result in adverse effects.  Spencer et al. (1979)
                    reported that Rhesus monkeys fed up to 2 mg/kg/day did
                    not show any adverse clinical effects at 325

             7.2.3  Relevant in vitro data

                    No relevant data.

             7.2.4  Workplace standards

                    Occupational Safety and Health Act (OSHA) (USA)
                    air contaminant standard, time-weighted average: 0.03
                    mg/m3 (skin)
                    American Conference of Government Industrial
                    Hygienists (ACGIH), threshold limit value (TLV): 0.03
                    mg/m3 (skin)
                    National Institute for Occupational Safety and Health 
                    (NIOSH) (USA), time-weighted average: 0.3 mg/m3
                    Designation "(skin)" following air concentration
                    values indicates that the compound may be absorbed
                    through the skin and that, even though the air
                    concentration may be below standard, significant
                    additional exposure through the skin is possible
                    (Lewis, 1993).

             7.2.5  Acceptable daily intake (ADI) and other guideline

                    Not relevant.

        7.3  Carcinogenicity

             Chronic acrylamide exposure has been associated with
             increased incidence of mesothelioma and cancers of the
             central nervous system, thyroid gland, other endocrine
             glands, mammary glands and reproductive tracts in rats 
             (Johnson et al., 1986) and with lung adenomas in mice (Bull
             et al., 1984).

             Epidemiologic studies of workers exposed to acrylamide have
             failed to demonstrate any relation between exposure to
             acrylamide and either overall incidence of malignancy or
             incidence of specific cancers (Sobel et al., 1986; Collins et
             al., 1989).

        7.4  Teratogenicity

             Administration of acrylamide to pregnant rats has been
             shown to produce neurotoxic effects (tibial and optic nerve
             degeneration) in neonates at levels that are non-toxic to the
             dams (Dearfield et al., 1988).  The lowest observed effect
             occurred at doses of 20 mg/kg/day.
             Edwards (1976) dosed pregnant rats with cumulative doses up
             to 400 mg/kg between days 0 and 20 of gestation and found no
             evidence of developmental or neurological abnormality in
             weanling rats despite evidence of neuropathy in the dams.
             No human data are available.

        7.5  Mutagenicity

             Acrylamide is regarded as a potential mutagen based on
             experimental evidence that it can bind to DNA.  The weight of
             evidence however suggests that acrylamide does not produce
             detectable gene mutations (Dearfield et al., 1988).

        7.6  Interactions

             Concurrent administration of methionine reduces the
             neurotoxic potency of acrylamide (Hashimoto & Ando,
             Supplementation of the diet with pyridoxine delays the onset
             and severity of acrylamide toxicity in rats (Loeb & Anderson,


        8.1  Material sampling plan

             8.1.1  Sampling and specimen collection

            Toxicological analyses

            Biomedical analyses

            Arterial blood gas analysis

            Haematological analyses

            Other (unspecified) analyses

             8.1.2  Storage of laboratory samples and specimens

            Toxicological analyses

            Biomedical analyses

            Arterial blood gas analysis

            Haematological analyses

            Other (unspecified) analyses

             8.1.3  Transport of laboratory samples and specimens

            Toxicological analyses

            Biomedical analyses

            Arterial blood gas analysis

            Haematological analyses

            Other (unspecified) analyses

        8.2  Toxicological Analyses and Their Interpretation

             8.2.1  Tests on toxic ingredient(s) of material

            Simple qualitative test(s)

            Advanced qualitative confirmation test(s)

            Simple quantitative method(s)

            Advanced quantitative method(s)

             8.2.2  Tests for biological specimens

            Simple qualitative test(s)

            Advanced qualitative confirmation test(s)

            Simple quantitative method(s)

            Advanced quantitative method(s)

            Other dedicated method(s)

             8.2.3  Interpretation of toxicological analyses

        8.3  Biomedical investigations and their interpretation

             8.3.1  Biochemical analysis

            Blood, plasma or serum


            Other fluids

             8.3.2  Arterial blood gas analyses

             8.3.3  Haematological analyses

             8.3.4  Interpretation of biomedical investigations

        8.4  Other biomedical (diagnostic) investigations and their

        8.5  Overall interpretation of all toxicological analyses and
             toxicological investigations

             Following significant acute exposure, it is appropriate
             to monitor serum electrolyte concentrations, blood glucose
             concentration, hepatic and renal function, and blood
             There are no methods routinely available for determining
             acrylamide or its metabolites in blood, urine or faeces.
             Chest X-ray
             Other investigations as dictated by clinical condition.
             * Nerve conduction studies.
             Nerve conduction studies may reveal evidence of reduction in
             maximal conduction velocity of peripheral nerves in severe
             cases of peripheral neuropathy.  More commonly, the maximal
             conduction velocities recorded in acrylamide-poisoned
             patients are within two standard deviations of control

             values.  The most consistent finding is a reduction in nerve
             action potential amplitude in distal sensory nerves
             (Fullerton, 1969).  This test is likely to be more sensitive
             if a pre-exposure baseline study is available for
             * Sural nerve biopsy
             Characterstic histopathologic findings have been described in
             sural nerve biopsy specimens from acrylamide-poisoned
             individuals with clinical evidence of peripheral neuropathy
             (Davenport et al., 1976). These findings include diffuse
             fibrosis, loss of nerve fibres, enlarged axons,
             neurofibrillary tangles, Wallerian degeneration and focal
             dilation of myelin sheaths.  On electron microscopy, axons
             are seen to be packed with haphazardly-arranged fine
             Sural nerve biopsy is not recommended in the routine
             evaluation of patients suspected of suffering from
             acrylamide-induced peripheral neuropathy.
             * Haemoglobin adducts
             Measurement of haemoglobin adducts has been proposed as a
             method of biomonitoring in acrylamide-exposed workers
             (Calleman et al., 1994).


        9.1  Acute poisoning

             9.1.1  Ingestion

                    There are only two reported cases of acute
                    acrylamide ingestion (Donovan & Pearson, 1987; Shelly,
                    1996; see section 11.1 for full details of these
                    cases).  In both cases a symptom-free period of hours
                    was followed by progressive onset of  severe
                    multi-system toxicity which included decreased level
                    of consciousness, seizures, hypotension and acute
                    adult respiratory distress syndrome.  Delayed onset of
                    peripheral neuropathy was observed in both

             9.1.2  Inhalation

                    No immediate clinical effects have been linked
                    to acute inhalational exposure.

             9.1.3  Skin exposure

                    No immediate clinical effects have been linked
                    to acute dermal exposure.

             9.1.4  Eye contact

                    No human data available.
                    Instillation of 10% aqueous solution into the
                    conjunctival sac of cats results in immediate minor
                    conjunctival irritation that resolves completely
                    within 24 hours.  Instillation of 40% aqueous solution
                    results in minor conjunctival irritation and
                    significant corneal injury.  Corneal injury is avoided
                    if the 40% solution is immediately rinsed following
                    instillation (McCollister et al., 1964)

             9.1.5  Parenteral exposure

                    Not described in humans.
                    Parental administration of acrylamide to experimental
                    animals results in a state of generalised central
                    excitation including seizures following a latency
                    period that is inversely related to dose (Kuperman,

             9.1.6  Other

                    Not relevant.

        9.2  Chronic poisoning

             9.2.1  Ingestion

                    Central and peripheral neurotoxicity is
                    described in a Japanese family when the well water
                    they used for drinking and cooking was contaminated
                    with 400 ppm of acrylamide.  Members of the family
                    developed varying degrees of truncal ataxia and mental
                    confusion after an exposure of four weeks followed by
                    signs and symptoms of peripheral neuropathy somewhat
                    later as the central signs were improving.  Complete
                    recovery occurred in all individuals over a period of
                    weeks to months following termination of the exposure
                    (Igusu et al., 1975).

             9.2.2  Inhalation

                    Acrylamide is well absorbed following
                    inhalational exposure, and absorption via this route
                    is likely to be second only to skin absorption in
                    contributing to the development of neurotoxicity.
                    Neither immediate nor delayed local effects are
                    associated with inhalation.
                    Almost all reported cases of human acrylamide toxicity
                    have occurred in the context of chronic occupational
                    exposure with predominant routes believed to be
                    combined inhalational and dermal (see 11.1 for
                    detailed description of individual reported
                    The clinical course is characterized by the
                    development of symptoms and signs of a motor and
                    sensory peripheral neuropathy (see that
                    slowly progress in severity if exposure continues.
                    Other prominent initial symptoms and signs are
                    excessive sweating of the hands and feet and
                    inflammation of the skin of the hands and feet with
                    blistering and desquamation.  Muscle pain and weakness
                    are less common.  If exposure is prolonged, evidence
                    of central nervous dysfunction develops, especially
                    truncal ataxia and behavioural change.  Malaise and
                    weight loss are almost always reported.
                    There is considerable interindividual variation in the
                    severity, rapidity of progression and delay in onset
                    of symptoms following initial exposure. This is most
                    likely to reflect differences in the cumulative dose
                    of acrylamide that is absorbed.

             9.2.3  Skin exposure

                    Acrylamide is well absorbed via the skin and
                    the majority of cases of poisoning have been ascribed
                    to repetitive dermal and inhalational exposure in
                    workers handling the monomer.  The clinical syndrome
                    that develops in these workers is described above in

             9.2.4  Eye contact

                    Not relevant.

             9.2.5  Parenteral exposure

                    Not relevant.

             9.2.6  Other

                    Not relevant.

        9.3  Course, prognosis, cause of death

             Following acute ingestion, the patient remains symptom-free
             for a period of hours depending on the dose ingested.  The
             initial sign of toxicity is usually behavioural change or
             hallucinations.  This may rapidly progress to a markedly
             decreased level of consciousness and tonic-clonic seizures.
             Hypotension and decreased cardiac output may develop soon
             after the central nervous system manifestations.  These
             central nervous and cardiovascular manifestions may last many
             days and be accompanied by toxicity of other systems
             including the respiratory, gastroenterological and
             haemotological systems.  Peripheral neuropathy occurs as a
             delayed effect and may not be evident until the patient is
             recovering from the central nervous system and cardiovascular
             effects.  There are only two reported cases of severe
             toxicity following acute ingestion and in both instances,
             complete recovery occurred with aggressive supportive care.
             The peripheral neuropathy may take from weeks to months to
             completely resolve.
             The signs and symptoms of chronic occupational acrylamide
             toxicity are progressive in nature for as long as exposure
             above a certain critical dose continues.
             Following removal from further exposure, the dermatitis
             resolves relatively quickly and the peripheral neuropathy
             resolves over a period of weeks to months.  Central effects
             such as truncal ataxia may take much longer to resolve and,
             in severe cases, complete recovery may never occur (Murray &
             Seger, 1994).
             Death has not been reported from either acute or chronic
             acrylamide exposure in humans.

        9.4  Systematic description of clinical effects

             9.4.1  Cardiovascular

                    Acute exposure
                    Hypotension requiring aggressive supportive care with
                    vasopressor agents occurred in both reported cases of
                    acute ingestion of acrylamide (Donovan & Pearson,
                    1987; Shelly, 1996).
                    Chronic exposure
                    Cardiovascular complications have not been described
                    in association with chronic exposure.

             9.4.2  Respiratory

                    Acute exposure
                    Adult respiratory distress syndrome (ARDS) developed
                    some days following acute ingestion of acrylamide in
                    both reported cases (Donovan & Pearson, 1987; Shelly,
                    Chronic exposure
                    Respiratory complications have not been described in
                    association with chronic exposure.

             9.4.3  Neurological

            Central Nervous System (CNS)

                             Acute exposure
                             Hallucinations followed by seizures occurred
                             within a period of hours following acute
                             ingestion of acrylamide (Donovan & Pearson,
                             1987; Shelly, 1996).
                             Chronic exposure
                             Truncal ataxia is almost universally reported
                             in workers with moderate to severe acrylamide
                             toxicity.  Other features suggesting CNS

                             toxicity include tremor and slurred speech.
                             The adult members of the Japanese family
                             poisoned by contaminated well water presented
                             with features of an acute organic brain
                             syndrome including vivid visual
                             hallucinations together with truncal ataxia
                             (Igisu et al., 1975).  Mental confusion is
                             not a prominent feature in
                             occupationally-exposed individuals although
                             more subtle behavioural changes have been

            Peripheral nervous system

                             Acute exposure
                             Delayed onset of peripheral neuropathy is
                             reported following acute ingestion of
                             acrylamide.  Complete recovery occurred in
                             both cases (Donovan & Pearson, 1987; Shelly,
                             Chronic exposure
                             Peripheral neuropathy is the cardinal
                             manifestation of occupational acrylamide
                             toxicity and its symptoms are the most
                             frequent presentation of this condition.  The
                             peripheral neuropathy has both motor and
                             sensory components and progresses in severity
                             if exposure continues.  Symptoms initially
                             involve the hands and feet and may progress
                             to involve the entire upper and lower
                             extremities. Symptoms include paraesthesiae
                             and numbness, coldness, and difficulty with
                             fine movements such as writing.  Signs
                             include impaired touch or vibration sense in
                             a glove and stocking distribution, impaired
                             joint position sense, absent tendon reflexes
                             and atrophy of the small muscles of the hand. 
                             Complete recovery usually occurs over a
                             period of weeks to months following removal
                             of the worker from further

            Autonomic nervous system

                             Excessive sweating of the
                             extremities is an early and almost universal
                             symptom of chronic acrylamide toxicity. It
                             has not been reported following acute

            Skeletal and smooth muscle

                             Muscle pain is sometimes reported as
                             an early symptom of occupational exposure. 
                             Frank loss of power may occur in advanced
                             cases of toxicity. Muscle wasting has been
                             reported only in the intrinsic muscles of the

             9.4.4  Gastrointestinal

                    Gastrointestinal bleeding occurred following acute
                    ingestion of acrylamide (Donovan & Pearson, 1987). A
                    moderate elevation in serum amylase is reported
                    following acute exposure (Shelly, 1996).
                    Weight loss despite a normal appetite is frequently
                    reported in association with chronic occupational
                    exposure to acrylamide.

             9.4.5  Hepatic


                    Hepatoxicity is reported following acute ingestion of
                    acrylamide (Donovan & Pearson, 1987; Shelly,
                    Hepatoxicity has not been reported in association with
                    subacute or chronic exposure.

             9.4.6  Urinary


                             Transient impairment in renal
                             function has been reported following acute
                             ingestion (Shelly, 1996).  It was considered
                             a complication of decreased cardiac


                             Urinary retention and incontinence
                             have been reported in association with
                             occupational exposure.

             9.4.7  Endocrine & reproductive systems

                    Not reported.

             9.4.8  Dermatological

                    Dermatological manifestations of toxicity have not
                    been reported following acute exposure.
                    Local dermatitis, usually involving the hands, with
                    mild erythema and peeling of the skin is an early
                    effect of exposure and usually precedes the
                    development of peripheral neuropathy.
                    Eczema, with a patch-test positive for acrylamide,
                    developed in a worker handling acrylamide despite the
                    use of polyvinylchloride gloves (Dooms-Gossens et al.,

             9.4.9  Eye, ears, nose, throat: local effects

                    Two adults exposed to contaminated well water
                    reported rhinorrhoea as their initial symptom (Igusu
                    et al., 1975).  This has not been reported in cases of
                    occupational exposure.

             9.4.10 Haematological

                    Thrombocytopenia has been reported following acute
                    exposure (Shelly, 1996).
                    Haematological complications have not been

             9.4.11 Immunological

                    Not reported.

             9.4.12 Metabolic

           Acid-base disturbances

                             Severe metabolic acidosis occured

                             within hours of acute ingestion of acrylamide 
                             (Shelley, 1996).

           Fluid & electrolyte disturbances

                             No data available.


                             No data available.

             9.4.13 Allergic reactions

                    Eczema has been reported (See 9.4.8).

             9.4.14 Other clinical effects

                    Fatigue and somnolence are frequently reported
                    in association with occupational exposure.

             9.4.15 Special risks

                    No data available on risks associated with
                    pregnancy or lactation.

        9.5 Others

             Toxicity following acute ingestion of acrylamide is
             characterized by an initial symptomatic period lasting
             several hours followed by progressive onset of a central
             nervous system disturbance, including seizures, and then
             subsequent multisystem dysfunction.  Delayed peripheral
             neuropathy occurs as the other features of toxicity are
             resolving.  Eventual complete recovery is possible if
             aggressive supportive care is instituted.
             Chronic acrylamide toxicity is characterized by local
             dermatitis, excessive sweating, fatigue, weight loss and
             features of progressive CNS disturbance (especially truncal
             ataxia) and peripheral neuropathy.  The severity of symptoms
             and the rapidity of onset appears to relate to the duration
             of exposure to, and the daily dose of, acrylamide.  Recovery
             over a period of weeks to months following removal from
             exposure is the usual course.

        9.6  Summary


        10.1 General principles

             Patients with a history of acute acrylamide ingestion should
             be admitted for 24 hours of careful observation of
             cardiorespiratory function and neurological status. Gastric
             decontamination may be appropriate following early
             presentation.  The management of established toxicity is
             careful supportive care including maintenance of airway,
             breathing and circulation and control of seizures.
             There is no specific therapy for acrylamide dermatitis,
             encephalopathy or peripheral neuropathy other than removal
             from further exposure. Prevention of exposure by rigorous
             enforcement of safety standards in the workplace and worker
             education is most important (see section 12.2). Exposed
             workers who develop neurological symptoms should be removed
             from any employment where further acrylamide exposure may

        10.2  Life supportive procedures

             Emergency institution of measures designed to maintain
             airway, breathing and circulation may be necessary in the
             rare event of a massive acute exposure to acrylamide.  Such
             measures might include endotracheal intubation, assisted
             ventilation, administration of supplemental oxygen,
             pharmacologic control of seizures and administration of
             intravenous fluids and vasopressors.  Even following a
             massive acute exposure, there is likely to be a significant
             delay (usually several hours) prior to the onset of seizures
             and/or cardiorespiratory failure.

        10.3  Decontamination

             Because acrylamide is well absorbed via the skin, the
             skin should be thoroughly washed following acute dermal
             exposure.  Exposed workers should wash after each shift and
             their clothing should be removed and washed after each
             Following inhalational exposure, the victim should be removed
             to fresh air as soon as possible.
             Following acute eye exposure, the eyes should be thoroughly
             rinsed with water for several minutes.

             Following acute ingestion, induction of emesis is not
             indicated because of the risk of subsequent seizures. Gastric
             emptying by lavage may be of value if performed as soon as
             practicable in the awake patient or following endotracheal
             intubation in the obtunded patient. It is not known whether
             activated charcoal effectively binds acrylamide but its
             administration soon after a significant acute ingestion is
             reasonable.  The oral cavity should be rinsed after ingestion
             of acrylamide.

        10.4 Elimination

             There are no effective methods available to enhance the
             elimination of absorbed acrylamide.

        10.6 Antidote treatment

             10.6.1 Adults

                    There is no antidote available for which
                    efficacy has been established (see 10.6 for further

             10.6.2 Children

                    There is no antidote available for which
                    efficacy has been established (see 10.7 for further

        10.6 Management discussion

             It has been suggested that pyridoxine may reduce
             neurotoxicity if administered soon after a massive acute
             exposure (Loeb & Anderson, 1981).
             This suggestion is based on observations in laboratory
             animals and the efficacy of pyridoxine in human poisoning is
             unsubstantiated. Although an appropriate dose of pyridoxine
             in this circumstance is unknown, an intravenous dose of 5 g
             of 10% solution over 30 minutes is reasonable (such high
             doses are administered without toxic complication to patients
             following isoniazid overdose).
             Because acrylamide undergoes biotransformation by conjugation
             with glutathione, the administration of N-acetyl cysteine or
             other agents that replenish hepatic glutathione stores is of
             theoretical benefit immediately following massive acute
             exposure.  The therapeutic benefit of this therapy has not
             been evaluated although methionine reduced the neurotoxicity
             of acrylamide in rats (see section 7.6).

             At present there is no adequate monitoring test available for
             use in exposed workers.  Arezzo et al. (1983) have proposed
             the use of a quantitative measure of the threshold of
             vibration sensation in the fingers and toes.  Calleman et al.
             (1994) have proposed biomonitoring of acrylamide-exposed
             workers by the measurement of haemoglobin adducts. The
             usefulness of these tests requires further evaluation.
             In established cases of acrylamide toxicity, the only
             treatment is removal from further exposure.  This should take
             place at least until complete resolution of all symptoms and
             signs of toxicity occurs.  This may take from weeks to months
             or, in severe cases, may never occur.  It is controversial as
             to whether poisoned workers should return to handling
             acrylamide even if complete recovery is documented.  There is
             some evidence from animal experiments that such individuals
             may be more sensitive to toxicity upon reexposure.
             In terms of environmental contamination, the chief danger to
             humans appears to be from ground water contamination.
             Particular care must be taken to prevent ground water
             contamination during grouting operations.  Where such
             contamination occurs it is essential to prevent consumption
             by humans of the contaminated water.


        11.1 Case reports from literature

             Auld & Bedwell (1967) reported a 21-year-old male
             admitted to hospital with a seven-week history of progressive
             rash, fatigue, weakness of the upper and lower extremities
             and profuse sweating of the extremities.  He had spent 35
             hours/week for each of the preceding 14 weeks working in a
             mine, loading a 10% aqueous solution of acrylamide into a
             hopper, adding a catalyst (B-dimethyl-amino-propionitrile)
             and then pumping the mixture into the soil.  Extensive dermal
             contact with acrylamide was reported. Physical examination
             was notable for bluish-red discoloration and profuse sweating
             of all extremities and evidence of a peripheral neuropathy
             (decreased temperature sensation, light touch, joint position
             sense and vibration and absent tendon reflexes of the lower
             limb).  Gradual and complete resolution of symptoms and signs
             occurred over the next 14 weeks following removal from
             further exposure to acrylamide.
             Garland & Patterson (1967) reported a series of  six workers
             from 3 factories making flocculators from acrylamide.  All
             workers had extensive dermal contact with acrylamide.  All
             six developed ataxia and clinical evidence of peripheral
             neuropathy following an exposure ranging from 4 to 60 weeks.

             Other prominent symptoms included profuse sweating of the
             extremities, erythema and peeling of the skin of the hands,
             and fatigue. The less severely affected cases made complete
             recovery over a period of weeks.  The two most severely
             affected cases remained symptomatic some months later.
             Igusu et al. (1975) reported a family of five who developed
             central nervous system disturbances including hallucinations,
             mental confusion, behavioural disturbance and severe truncal
             ataxia over a period of one month following contamination of
             their well water with acrylamide from road grouting carried
             out within 2.5 meters of the well.  Acrylamide concentrations
             in the well water were measured at 400 ppm and the family
             used the water for drinking, cooking and bathing.  The
             central nervous symptoms resolved within two weeks of
             cessation of exposure at about which time the development of
             a sensory peripheral neuropathy was noted in the three more
             severely affected cases.  Complete recovery occurred in all
             cases by four months.
             Davenport et al. (1976) reported a 25-year-old admitted to
             hospital with loss of sensation and unsteady gait after
             working with acrylamide for six months.  His job involved
             mixing acrylamide powder with other reagents in a sealed
             reactor vessel.  The initial reported symptom was irritation
             and erythema of the palms and soles beginning several weeks
             after exposure began, followed by several months of fatigue,
             anorexia and weight loss with ataxia developing two weeks
             before presentation.  Examination revealed excessive sweating
             and blistering of the hands and feet, evidence of a
             peripheral sensory neuropathy, mild weaknes of the muscles of
             the ankles and wrists and an ataxic gait. Electrophysiologic
             studies confirmed a peripheral neuropathy with prolonged
             distal motor latencies and poor or absent sensory conduction.
             Sural nerve biopsy revealed diffuse fibrosis and loss of
             nerve fibres, focal dilation of the myelin sheath and, on
             electron-microscopy, axons packed with bundles of fine
             filaments.  There was no progression or regression of
             clinical findings over the ensuing two months without
             reexposure to acrylamide.
             Kesson et al. (1977) reported a 57-year-old male whose
             employment involved the polymerization of acrylamide monomer
             in the confines of a small concrete tunnel.  He complained of
             increased sweating, peeling of the skin of the hands and
             tingling and weakness of the hands. Examination revealed
             evidence of peripheral neuropathy.  Evaluation of the
             worksite identified five other less severely affected workers
             and all reported onset of skin irritation within two weeks of
             starting to handle acrylamide.  The index case and one other
             showed little clinical improvement at one year after
             cessation of further exposure to acrylamide.

             Donovan & Pearson (1987) described the only reported case of
             toxicity following single oral ingestion of acrylamide. A
             23-year-old female intentionally ingested 18 g of acrylamide
             crystal as a suicide gesture.  Asymptomatic on presentation,
             she developed hallucinations and hypotension five hours later
             followed by seizures at nine hours post-ingestion. The
             subsequent clinical course was stormy and characterized by
             gastointestinal bleeding, adult respiratory distress
             syndrome, hepatotoxicity and peripheral neuropathy beginning
             on day 3. She survived with intensive supportive care to be
             discharged at three weeks post-ingestion but still had
             evidence of peripheral neuropathy at follow-up two months
             Murray & Seger (1994) reported a mineworker with evidence of
             acrylamide neurotoxicity who remained disabled ten years
             after cessation of prolonged inhalational exposure to
             acrylamide monomer.


        12.1 Specific preventive measures

             Management centres on prevention of toxicity in workers
             at risk. Fundamental to this process are education and
             hygiene.  Workers need to be aware that acrylamide is a
             potent neurotoxin and that is is easily absorbed via the
             skin, respiratory tract or gastrointestinal tract.  The need
             to be aware that the effects of exposure, although not
             immediately noticeable, are cumulative.  Workers should be
             familiar with the initial symptoms of acrylamide exposure,
             especially skin peeling, excessive fatigue, abnormal
             sweating, problems with balance, and "pins and needles" or
             loss of feeling in the feet or hands.  They should be
             encouraged to report any such symptoms.
             Dermal and inhalational contact with acrylamide monomer
             should be rigourously avoided.  Ideally this involves the
             development of closed systems for handling acrylamide
             monomer.  If at all possible, handling of the monomer in a
             confined space should be avoided.  Workers handling the agent
             should wear long polyvinyl gloves, washable overalls and head
             covers and facemasks that will prevent inhalation of dust.
             Eating at the workplace should be prohibited.  Workers should
             wash thoroughly at the end of each shift and after any
             unintentional exposure.  Work  clothing should be washed
             Clear warnings of the danger of exposure should be on all
             packaging for acrylamide.

        12.2 Other

             Not relevant.


        Arezzo JC, Schaumburg HH & Petesen CA (1983)  Rapid screening
        for peripheral neuropathy with the Optacon.  Neurology, 33:
        Auld RB & Bedwell SF (1967)  Peripheral neuropathy with
        sympathetic overactivity from industrial contact with acrylamide.
        Can Med Assoc J, 96: 652-654.
        Budavari S, O'Neil MJ, Smith A & Heckelman PE (1989) The Merck
        Index, 11th ed. Rahway, New Jersey, Merck & Co., Inc.
        Bull RJ, Robinson M, Laurie RD, Stoner E, Greisiger JR, Meier JR &
        Stober J (1984)  Carcinogenic effect of acrylamide in Sencar and
        A/J mice. Cancer Res, 44: 107-11.
        Calleman CJ, Wu Y, He F, Tian G, Bergmark E, Zhang S, Deng H, Wang
        Y, Crofton KM, Fennel T & Costa LG (1994)  relationships between
        biomarkers of exposure and neurological effects in a group of
        workers exposed to acrylamide.  Toxicol App Pharmacol 126:
        Carlson GP & Weaver PM (1985)  Distribution and binding of
        [14C]acrylamide to macromolecules in SENCAR and BALB/c mice
        following oral and topical administation.  Toxicol Appl Pharmacol,
        79: 307-13.
        Collins JJ, Swaen GMH, Marsh GM, Utidjian MD, Caporossi JC & Lucas
        LJ (1989) Mortality patterns among workers exposed to acrylamide.
        J Occup Med 31: 614-617.
        Davenport JG, Farrel DF & Sumi SM (1976) 'Giant axonal neuropathy'
        caused by industrial chemicals: neurofilamentous axonal masses in
        man. Neurology, 26: 919-923.
        Dearfield KL, Abernathy CO, Ottley MS, Brantner JH & Hayes PF
        (1988) Acrylamide: its metabolism, developmental and reproductive
        effects, genotoxicity, and carcinogenicity.  Mutation Research,
        195: 45-77.
        Dooms-Gossens A, Garmyn M & Degreef H (1991) Contact allergy to
        acrylamide.  Contact Dermatitis, 2: 71-72.
        Donovan JW & Pearson T (1987)  Ingestion of acrylamide with severe
        encephalopathy, neurotoxicity and hepatotoxcity.  Vet Hum Toxicol,
        29: 462 [abstract].

        Edwards PM (1975)  The distribution and metabolism of acrylamide
        and its neurotoxic analogues in rats.  Biochem Pharmacol, 24:
        Edwards PM (1976)  The insensitivity of the developing rat fetus
        to the toxic effects of acrylamide.  Chem Biol Interact, 12:
        Fullerton PM (1969) Electrophysiological and histological
        observations on peripheral nerves in acrylamide poisoning in man.
        J Neurol Neurosurg Psychiat, 32: 186-192.
        Fullerton PM & Barnes JM (1966) Peripheral neuropathy in rats
        produced by acrylamide.  Brit J Industr Med, 23: 210-221.
        Garland TO & Patterson MWH (1967)  Six cases of acrylamide
        poisoning. Brit Med J, 4: 134-138.
        Hashimoto K & Ando K (1971) [Studies on acrylamide neuropathy.
        Effects of the permeability of amino acids into nervous tissue;
        distribution and metabolism.]  In: Proceedings of the Osaka
        Prefectorial Institution, Public Health Education and Industrial
        Health, 9: 1-4 (In Japanese).
        Hopkins AP (1970)  The effect of acrylamide on the peripheral
        nervous system of the baboon.  J Neurol Neurosurg Psychiatr,
        Igisu H, Goto I, Kawamura Y, Kato M, Izumi K & Kuroiwa Y (1975)
        Acrylamide encephaloneuropathy due to well water pollution.  J
        Neurol Neurosurg Psych, 38: 581-584.
        Johnson KA, Gorzinski SJ, Bodner KM, Campbell R, Wolf C, Friedman
        M & Mast R (1986)  Chronic toxicity and oncogenicity study on
        acrylamide incorporated in the drinking water of Fischer 344 rats.
        Toxicol Appl Pharmcol, 85: 154-168.
        Kaplan Ml, Murphy SD & Gilles FH (1973)  Modification of
        acrylamide neuropathy in rats by selected factors.  Toxicol Appl
        Pharmacol, 24: 564-579.
        Kesson CM, Baird AW & Lawson DH (1977)  Acrylamide poisoning. 
        Postgrad Med J, 53: 16-17.
        Kuperman AS (1958)  Effects of acrylamide on the central nervous
        system of the cat.  J Pharmacol Exp Ther, 123: 180-192.
        Lewis RJ (1993)  Hazardous chemicals desk reference, 3rd ed. New
        York, New York, Van Nostrand Reinhold, p 25.
        Loeb AL & Anderson RJ (1981)  Antagonism of acrylamide
        neurotoxicity by supplementation with vitamin B6. Neurotoxicology,
        2: 625-633.

        LoPachin RM, Castiglia CM & Saubermann AJ (1992a)  Acrylamide
        disrupts elemental composition and water content of rat tibial
        nerve.  I. Myelinated axons.  Toxicol Appl Pharmacol, 115:
        LoPachin RM, Castiglia CM & Saubermann AJ (1992b)  Acrylamide
        disrupts elemental composition and water content of rat tibial
        nerve.  II. Schwann cells and myelin.  Toxicol App Pharmacol, 115:
        MacWilliam DC (1978)  Acrylamide.  In: Mark HF, Othmer DF,
        Overberger CG, Seaborg GT, eds.  Kick-Othmer Encyclopedia of
        Chemical Technology, 3rd ed, Vol I.  New York, John Wiley & Son,
        pp 298-311.
        McCollister DD, Oyen F & Rowe VK (1964)  Toxicology of acrylamide.
        Toxicol App Pharmacol, 6:172-181.
        Miller MJ, Carter DE & Sipes IG (1982)  Pharmacokinetics of
        acrylamide in Fisher 334 rats.  Toxicol Appl Pharmacol, 63: 
        Murray LM, Seger DL (1994)  Acrylamide neurotoxicity following
        occupation inhalation exposure (Abstract).  XVI International
        Congress of the European Association of Poison Centres and
        Clinical Toxicologists, Vienna, Austria.
        Reagan KE, Wilmarth KR, Friedman M & Abou-Donia MB (1994)
        Acrylamide increases in vitro calcium and calmodulin-dependent
        kinase-mediated phosphorylation of rat brain and spinal cord
        neurofilament proteins. Neurochemistry International, 25:
        Shelly (1996)  Regina vs. Calder.  In: Transcript records of New
        Zealand High Court, Christchurch, New Zealand,  March 1996.
        Smith EA & Oehme FW (1991)  Acrylamide and Polyacrylamide:  A
        review of production, use, environmental fate and neurotoxicity.
        Reviews on environmental health, 9: 215-228.
        Sobel W, Bond CG, Parsons TW & Brenner FE (1986)  Acrylamide
        cohort mortality study.  Brit J Indust Med, 43: 785-788.
        Spencer PS, Sabri MI, Schaumburg HH & Moore CL (1979)  Does a
        defect in energy metabolism in the nerve fiber underlie axonal
        degeneration in polyneuropathies?  Ann Neurol, 5: 501-507.
        Thomann P, Koella WP, Krinke G, Peterman H, Zak G & Hess R (1974)
        The assessment of peripheral neurotoxicity in dogs: Comparative
        studies with acrylamide and clioquinol.  Agent Actions, 4:

        Tilson HA (1981)  The neurotoxicity of acrylamide: An overview.
        Neurobehav Toxicol Teratol, 3: 445-461.
        Xiwen H, Jing L, Tao C & Ke Y (1992)  Studies on biochemical
        mechanism of neurotoxicity induced by acrylamide in rats.  Biomed
        Environ Sci, 5: 276-281.


        Author:     Lindsay Murray
                    Center for Clinical Toxicology
                    501 Oxford House
                    Vanderbilt University Medical Center
                    Nashville, TN 37232
                    Tel:     +1-615-9360760
                    Fax:     +1-615-9360756
        Date:       July 1996
        Reviewer:   Wayne Temple
                    National Toxicology Group
                    University of Otago
                    New Zealand
        Date:       August 1996
        review:     Cardiff, United Kingdom, September 1996
                    (Review group members: A. Borges, A. Brown, R. Ferner,
                    M. Hanafy, L. Murrray, M.O. Rambourg, W. Temple)

        Editor:     Mrs J. Dumnil
                    International Programme on Chemical Safety
        Date:       June 1999

    See Also:
       Toxicological Abbreviations
       Acrylamide (EHC 49, 1985)
       Acrylamide (HSG 45, 1991)
       Acrylamide (ICSC)
       Acrylamide (WHO Food Additives Series 55)
       ACRYLAMIDE (JECFA Evaluation)
       Acrylamide (IARC Summary & Evaluation, Volume 60, 1994)