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    Acrylic Acid

    This report contains the collective views of an international group of
    experts and does not necessarily represent the decisions or the stated
    policy of the United Nations Environment Programme, the International
    Labour Organisation, or the World Health Organization.

    First draft prepared at the National Institute of Health Sciences,
    Tokyo, Japan, and the Institute of Terrestrial Ecology, Monk's Wood,
    United Kingdom

    Published under the joint sponsorship of the United Nations
    Environment Programme, the International Labour Organisation, and the
    World Health Organization, and produced within the framework of the
    Inter-Organization Programme for the Sound Management of Chemicals.

    World Health Organization
    Geneva, 1997

         The International Programme on Chemical Safety (IPCS) is a joint
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    WHO Library Cataloguing in Publication Data

    Acrylic Acid

    (Environmental health criteria ; 191)

    1.Acrylates - adverse affects      2.Acrylates - toxicity
    3.Environmental exposure           4.Occupational exposure

    ISBN 92 4 157191 8                 (NLM Classification: QV 50)
    ISSN 0250-863X

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         2.1. Identity
               2.1.1. Primary constituent
               2.1.2. Technical product
         2.2. Physical and chemical properties
               2.2.1. Physical properties
               2.2.2. Chemical properties
         2.3. Conversion factors
         2.4. Analytical methods
               2.4.1. In air
               2.4.2. In industrial effluents
               2.4.3. In polyacrylate materials
               2.4.4. In biological samples


         3.1. Natural occurrence
         3.2. Anthropogenic sources
               3.2.1. Production levels and processes
                Manufacturing process
                Other sources
                Production data
               3.2.2. Experimental production of acrylic
                       acid by bacterial isolates
               3.2.3. Uses


         4.1. Transport and distribution between media
         4.2. Transformation
               4.2.1. Abiotic degradation
               4.2.2. Biodegradation
                Aerobic biodegradation
                Anaerobic biodegradation
               4.2.3. Bioaccumulation and biomagnification


         5.1. Environmental levels
         5.2. General population exposure
         5.3. Occupational exposure during manufacture,
               formulation or use


         6.1. Human studies
         6.2. Studies on experimental animals
               6.2.1. Absorption, distribution and excretion
                Oral exposure
                Inhalation exposure
                Dermal exposure
                          Intravenous administration
               6.2.2. Metabolism
                 In vitro investigations
                 In vivo investigations
                Metabolic pathways


         7.1. Single exposure
         7.2. Irritation and sensitization
               7.2.1. Eye irritation
               7.2.2. Skin irritation and sensitization
                Skin irritation
                Skin sensitization
               7.2.3. Upper respiratory tract irritation
         7.3. Short-term exposure
               7.3.1. Oral
               7.3.2. Inhalation
         7.4. Long-term exposure
         7.5. Reproduction, embryotoxicity and teratogenicity
               7.5.1. Reproduction
               7.5.2. Embryotoxicity and teratogenicity
         7.6. Mutagenicity and related end-points
               7.6.1.  In vitro and insect studies
               7.6.2.  In vivo mammalian studies
         7.7. Carcinogenicity
         7.8. Other  studies
         7.9. Factors modifying toxicity


         8.1. General population exposure
               8.1.1. Acute toxicity
                Poisoning accidents

         8.2. Occupational exposure
               8.2.1. Poisoning accidents
               8.2.2. Effects of short- and long-term exposure


         9.1. Microorganisms
         9.2. Aquatic organisms
         9.3. Terrestrial organisms


         10.1. Evaluation of human health risks
               10.1.1. Exposure of the general population
               10.1.2. Occupational exposure
               10.1.3. Toxic effects
               Carcinogenic and mutagenic effects
               Non-cancer effects
               10.1.4. Risk evaluation
               Inhalation exposure
               Oral exposure
         10.2. Evaluation of effects on the environment
               10.2.1. Exposure
               10.2.2. Effects
               10.2.3. Risk evaluation


         11.1. Conclusions
         11.2. Recommendations for protection of human health







         Every effort has been made to present information in thecriteria
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                                 *     *     *

         A detailed data profile and a legal file can be obtained from the
    International Register of Potentially Toxic Chemicals, Case postale
    356, 1219 Chtelaine, Geneva, Switzerland (telephone no. + 41 22 -
    9799111, fax no. + 41 22 - 7973460, E-mail

                                 *     *     *

         This publication was made possible by grant number 5 U01
    ES02617-15 from the National Institute of Environmental Health
    Sciences, National Institutes of Health, USA, and by financial support
    from the European Commission.

                                 *     *     *

         The Federal Ministry for the Environment, Nature Conservation and
    Nuclear Safety, Germany, provided financial support for this

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    Dr B.I. Ghanayem, National Institute of Environmental Health
         Sciences, Research Triangle Park, North Carolina, USA

    Dr D. Guth, Office of Research and Development, National Centre
         for Environmental Assessment, Research Triangle Park North
         Carolina, USA

    Mr L. Heiskanen, Environmental Health and Safety Unit,
         Department of Health and Family Services, Canberra, Australia

    Mr P.D. Howe, Institute of Terrestrial Ecology, Monks Wood,
         Abbots Ripton, Huntingdon, United Kingdom ( Co-rapporteur)

    Dr P. Lundberg, Department of Toxicology and Chemistry,
         National Institute for Working Life, Sweden ( Chairman)

    Dr K. Rydzynski, The Nofer Institute of Occupational Medicine,
         Lodz, Poland ( Co-rapporteur)

    Dr R.O. Shillaker, Pesticides Safety Directorate, Ministry of
         Agriculture, Fisheries & Food, United Kingdom

    Dr S.A. Soliman, Department of Pesticide Chemistry, Faculty of
         Agriculture, Alexandria University, Alexandria, Egypt


    Dr M. Wooder, Rohm and Haas Uk, Ltd., Croydon, Surrey, United
         Kingdom (representing the American Industrial Health Council)

    Dr A. Lombard, Service Hygine Industrielle Toxicologique, ELF-
         ATOCHEM, Paris, France (representing the Centre for Ecotoxicology
         and Toxicology of Chemicals)


    Dr B.H. Chen, International Programme on Chemical Safety, World
         Health Organization, Geneva, Switzerland ( Secretary)


         A WHO Task Group on Environmental Health Criteria for Acrylic
    Acid met at the Institute of Terrestrial Ecology, Monks Wood,
    Huntington, United Kingdom, from 16 to 19 April 1996.  Dr S. Dobson
    opened the meeting and welcomed the participants on behalf of the
    Institute.  Dr B.H. Chen, IPCS, welcomed the participants on behalf of
    the Director, IPCS, and the three IPCS cooperating organizations
    (UNEP/ILO/WHO).  The Task Group reviewed and revised the draft 
    monograph and made an evaluation of the risks for human health and the
    environment from exposure to acrylic acid.

         Dr K. Rydzynski, the Nofer Institute of Occupational Medicine,
    Poland, prepared the first draft of this monograph.  Dr R.O.
    Shillaker, Pesticides Safety Directorate, Ministry of Agriculture,
    Fisheries and Food, United Kingdom, contributed to the preparation of
    the first draft.  The second draft was prepared by Dr K. Rydzynski
    incorporating comments received following the circulation of the first
    draft to the IPCS Contact Points for Environmental Health Criteria. 
    Dr D. Guth, National Centre for Environmental Protection, USA,
    contributed to the preparation of the final text of the evaluation. 
    The meeting was chaired by Dr P. Lundberg, National Institute for
    Working Life, Sweden.

         Dr B.H. Chen and Dr P.G. Jenkins, IPCS Central Unit, were
    responsible for the overall scientific content and technical editing,

         The efforts of all who helped in the preparation and finalization
    of the document are gratefully acknowledged.


    ACGIH          American Conference of Governmental Industrial
    CHO            Chinese hamster ovary
    EC50           median effective concentration
    FID            flame ionization detector
    GC             gas chromatography
    GSH            reduced glutathione
    GV             guidance value
    HPLC           high performance liquid chromatography
    LC50           median lethal concentration
    LD50           median lethal dose
    LOAEL          lowest-observed-adverse-effect level
    LOEL           lowest-observed-effect concentration
    NMR            nuclear magnetic resonance
    NOAEL          no-observed-adverse-effect level
    NOEC           no-observed-effect concentration
    NOEL           no-observed-effect level
    OSHA           Occupational Safety and Health Administration (USA)
    TCA            tricarboxylic acid cycle
    TI             tolerable intake
    TT             toxicity threshold
    UDS            unscheduled DNA synthesis

         Acrylic acid is a colourless liquid, with an irritating acrid
    odour, at room temperature and pressure. The odour threshold of
    acrylic acid is low (0.20-3.14 mg/m3). It is miscible with water and
    most organic solvents.

         Acrylic acid is commercially available in two grades; technical
    grade and glacial grade. Acrylic acid polymerizes easily when exposed
    to heat, light or metals, and a polymerization inhibitor is therefore
    added to commercial products.

         The worldwide production of acrylic acid in 1994 was estimated to
    be approximately 2 million tonnes. It is used primarily as a starting
    material in the production of acrylic esters as a monomer for
    polyacrylic acid and salts and as a co-monomer with acrylamide for
    polymers used as flocculants, with ethylene for ion-exchange resin
    polymers, with methyl ester for polymers, and with itatonic acid for
    other co-polymers.

         Acrylic acid residues in air and other media can be quantified by
    means of gas chromatographic, high performance liquid chromatographic
    and polarographic techniques. The detection limits of these methods
    are 14 ppm in air and 1 ppm in other media.

         Acrylic acid has been reported to occur naturally in marine algae
    and has been found in the rumen fluid of sheep.

         Being miscible with water, acrylic acid would not be expected to
    adsorb significantly to soil or sediment. Under soil conditions,
    chemicals with low Henry's Law constants are essentially non-volatile.
    However, the vapour pressure of acrylic acid suggests that it
    volatilizes from surface and dry soil.

         Acrylic acid emitted into the atmosphere will react with
    photochemically produced hydroxyl radicals and ozone, resulting in
    rapid degradation. There is no potential for long-range atmospheric
    transport of acrylic acid because it has an atmospheric lifetime of
    less than one month.

         Acrylic acid may be formed by hydrolysis of acrylamide monomer
    from industrial waste in soil, especially under aerobic conditions.

         When released into water, acrylic acid readily biodegrades. The
    fate of acrylic acid in water depends on chemical and microbial
    degradation. Acrylic acid is rapidly oxidized in water and can
    therefore potentially deplete oxygen if discharged in large quantities
    into a body of water. Acrylic acid has been shown to be degraded under
    both aerobic and anaerobic conditions.

         No quantitative data on levels of acrylic acid in ambient air,
    drinking-water or soil are available. However, acrylic acid occurs in
    wastewater effluent from its production via the oxidation of

         No data on general population exposure are available. However,
    consumers may be exposed to unreacted acrylic acid in household goods
    such as water-based paints. People living in the vicinity of plants
    producing acrylic acid or its esters or polymers may be exposed to
    acrylic acid in the ambient air. A potential source of internal
    exposure to acrylic acid may result from metabolism of absorbed
    acrylic acid esters.

         Inhalation and contact with skin are important routes of
    occupational exposure.

         Regardless of the route of exposure, acrylic acid is rapidly
    absorbed and metabolized. It is extensively metabolized, mainly to
    3-hydroxy propionic acid, CO2 and mercapturic acid, which are
    eliminated in the expired air and urine. Owing to its rapid metabolism
    and elimination, the half-life of acrylic acid is short (minutes) and
    therefore it has no potential for bioaccumulation.

         Although a wide range of LD50 values has been reported, most
    data indicate that acrylic acid is of low to moderate acute toxicity
    by the oral route and moderate acute toxicity by the inhalation or
    dermal route.

         Acrylic acid is corrosive or irritant to skin and eyes. It is
    unclear what concentration is non-irritant. It is also a strong
    irritant to the respiratory tract.

         Positive and negative skin sensitization results have been
    reported with acrylic acid, but it appears that the positive results
    may be due to an impurity.

         In drinking-water studies on rats, the no-observed-adverse-effect
    level (NOAEL) was 140 mg/kg body weight per day for decreased body
    weight gain in a 12-month study and 240 mg/kg body weight per day for
    histopathological changes in the stomach. A chronic drinking-water
    study on rats showed no effect at the highest dose tested (78 mg/kg
    body weight per day). A lowest-observed-adverse-effect level (LOAEL)
    of 15 mg/m3 (5 ppm) by the inhalation route was observed in mice
    exposed to acrylic acid for 90 days, based on very mild nasal lesions
    in females at this level. Nasal effects in rats were observed at
    225 mg/m3 (75 ppm), but not at 15 or 75 mg/m3 (5 or 25 ppm).

         Available reproduction studies indicate that acrylic acid is not
    teratogenic and has no effect on reproduction.

         Both positive and negative results have been obtained in
     in vitro genotoxicity tests. An  in vivo bone marrow chromosome
    aberration assay gave negative results. No firm conclusions can be
    drawn from an  in vivo DNA binding study or from a dominant lethal

         Available data do not provide evidence for an indication of
    carcinogenicity of acrylic acid, but the data are inadequate to
    conclude that no carcinogenic hazard exist.

         There have been no reports of poisoning incidents in the general
    population. No occupational epidemiological studies have been

         Because acrylic acid toxicity occurs at the site of contact,
    separate guidance values are recommended for oral and inhalation
    exposure. Guidance values of 9.9 mg/litre for drinking-water and
    54 g/m3 for ambient air for the general population are proposed.

         The toxicity of acrylic acid to bacteria and soil microorganisms
    is low.

         Algae are the most sensitive group of aquatic organisms studied,
    with EC50 values, based on growth, ranging from 0.04 to 63 mg/litre
    and a no-observed-effect concentration (NOEC) for the most sensitive
    species of 0.008 mg/litre. EC50 values (based on immobilization) for
     Daphnia magna are 54 mg/litre (24 h) and 95 mg/litre (48 h). Acrylic
    acid is more toxic to daphnids than is the alkaline salt. Acute
    toxicity studies with fish have yielded results ranging from
    27 mg/litre (96-h LC50) for the rainbow trout to 315 mg/litre (72-h
    LC50) for the golden orfe. The 96-h NOEC for acrylic acid toxicity to
    rainbow trout was found to be 6.3 mg/litre, based on a lack of
    sublethal/behavioural responses.

         Because of its low octanol-water partition coefficient, acrylic
    acid is unlikely to bioconcentrate in aquatic organisms. There have
    been no reports of biomagnification in food chains.

         No data are available concerning the effects of acrylic acid on
    terrestrial organisms.


    2.1  Identity

    2.1.1  Primary constituent

    Common name:             acrylic acid

    CAS name:                2-propenoic acid

    CAS registry number:     79-10-7

    EEC No:                  607-061-00-8

    DOT UN:                  22-18-29

    RTECS Number:            AS 4375000

    Synonyms:                acroleic acid (Sax & Lewis, 1989)
                             2-propenoic acid (Sax, 1984)
                             vinylformic acid (Sittig, 1985)
                             propene acid (Sax, 1984)

                             ethylenecarboxylic acid
                             (Verschueren, 1983)
                             UN 2218
                             propenoic acid (Weast et al., 1989)
                             ethene carboxylic acid (IUPAC name)

    Chemical formula:        C3H4O2

    Chemical structure:


    Relative molecular mass: 72.06

    2.1.2  Technical product

         Acrylic acid is commercially available in two grades: technical
    grade (94%) for esterification and glacial grade (98-99.5% by weight
    and a maximum of 0.3% water by weight) for production of water-soluble
    resins (IARC, 1979; CHRIS, 1989). Acrylic acid polymerizes easily when
    exposed to heat, light or metals, and so a polymerization inhibitor is
    added to commercial acrylic acid to prevent the strong exothermic
    polymerization (NLM, 1989). The inhibitors that are usually used in
    acrylic acid preparations are the monomethyl ether of hydroquinone
    (methoxyphenol) at 200  20 ppm, phenothiazine at 0.1% and
    hydroquinone at 0.1%. Methylene blue at 0.5 to 1.0% and  N,N'-
    diphenyl- p-phenylenediamine at 0.05% can also be used (IARC, 1979;
    CHRIS, 1989; OHM/TADS, 1989; BASF, 1993).

    2.2  Physical and chemical properties

    2.2.1  Physical properties

         Acrylic acid is a colourless liquid at room temperature and
    pressure (IARC, 1979; Windholz, 1983; CHRIS, 1985). It has an
    irritating acrid odour and it is totally miscible with water and most
    organic solvents. Some of the most important physical properties of
    acrylic acid are summarized in Table 1.

        Table 1.  Physical and chemical properties of acrylic acid


    Property                                      Value              References

    Odour threshold concentration (mg/m3)         0.20-3.14          Fazzalari, 1978; Amoore & Hautala, 1983;
                                                                     Ruth, 1986; Grudzinski, 1988; HSDB, 1989

    Melting point (C at 1 atm)                   12.3-14.0          CHRIS, 1989; Weast et al., 1989
    Boiling point (C at 1 atm)                   141.3-141.6        CHRIS, 1989; Weast et al., 1989
    Flash point (C)
         open cup
         closed cup                               54.0-68.3          IARC, 1979; Kirk-Othmer, 1984; Sax & Lewis 1989;
                                                  46-48.5            Elf Atochem, 1992; BASF, 1994a

    Autoignition temperature (C)                 390-446            IARC, 1979; HSDB, 1989; BASF, 1992; Elf Atochem, 1992

    Flammable limits (%)
         lower                                    28                 HSDB, 1989

    Burning rate (mm/min)                         1.6                CHRIS, 1989

    Specific gravity (g/ml at 20C)               1.0497-1.0511      IARC, 1979; CHRIS, 1989; Weast et al., 1989

    Relative vapour density (air =1 at 20C)      2.5                HSDB, 1989

    Viscosity (mPa.s at  20C)                    1.22-1.30          BASF, 1992; Elf Atochem, 1992

    Saturated concentration in air
     (g/m3 at 20C)                               22.8               Verschueren, 1983

    Volatility (mmHg at 20C)                     3.1; 7.76          Riddick et al., 1986

    Vapour pressure (mmHg)
         at 39C                                  10                 OHM/TADS, 1989
         at 75C                                  60

    Table 1.  (contd)


    Property                                      Value              References

    Henry's law constant (atm.m3/mol)             3.2  10-7         Singh et al., 1984

    Surface tension (dyne/cm)                     28.1 at 30C       Dean, 1987

    Heat of fusion (cal/g)                        30.03-37.03        CHRIS, 1989; Weast et al., 1989

    Heat of polymerization (cal/g)                -257               CHRIS, 1989

    Heat of combustion (cal/g)                    -327 at 25C       Weast et al., 1989

    Heat of vaporization (cal/g)                  10.955             Weast et al., 1989

    Activated carbon absorbability (g/g)          0.129              Verschueren, 1983

    Partition coefficient (log Kow at 20-25C)    0.161-0.46         Korenman & Lunicheva, 1972; GEMS, 1983; Hansch & Leo, 1987;
    BASF, 1988

    Dissociation constant (pKa at 25C)           4.25               Weast et al., 1989

    Critical temperature (C)                     342                CHRIS, 1985

    Critical pressure (atm)                       57                 CHRIS, 1985

    Solubility: in water and most organic         completely         Dean, 1987; Sax & Lewis, 1989; Weast et al., 1989
     solvents (alcohol, chloroform, benzene)      miscible

    Refractive index (nD20-25)                    1.4224-1.4185      Kirk-Othmer, 1984

    Maximum absorption (nm, in methanol)          252                Weast et al., 1989

    2.2.2  Chemical properties

         Acrylic acid preparations containing polymerization inhibitors
    are reasonably stable when stored at 15-25C and handled according to
    supplier's recommendations. Heating can cause vigorous polymerization
    in some circumstances. Acrylic acid reacts readily with free radicals
    and electrophilic or nucleophilic agents (Kirk-Othmer, 1984). It may
    polymerize in the presence of acids (sulfuric acid, chlorosulfonic
    acid), alkalis (ammonium hydroxide), amines (ethylenediamine,
    ethyleneimine, 2-aminoethanol), iron salts, elevated temperature,
    light, peroxides, and other compounds that form peroxides or free
    radicals. In the absence of an inhibitor, peroxides are formed when
    oxygen is sparged into acrylic acid. This mixture can undergo violent
    polymerization if heated to 60C (CHRIS, 1989). The mechanism of auto-
    accelerating polymerization of acrylic acid in hexane-methanol
    solution, which can become explosive, has been studied by Bretherick

         Acrylic acid rapidly decomposes in the atmosphere by
    photochemical attack on the double bond (NLM, 1989; OHM/TADS, 1989).

         Acrylic acid is corrosive to many metals but not to stainless
    steel or aluminium (Kirk-Othmer, 1984; AAR, 1987).

    2.3  Conversion factors
         In air:
         1 ppm   = 3.0 mg/m3 (NLM, 1989)
         1 mg/m3 = 0.33 ppm (NLM, 1989)

    2.4  Analytical methods

    2.4.1  In air

         A summary of methods for the detection of acrylic acid in air is
    given in Table 2.

        Table 2.  Methods for the analysis of acrylic acid in air


    Sampling                 Analytical methods      Detectiona     Detection limit          Comment               Reference

    Air samples absorbed     GC on a glass column    FID            33 mg/ml acetone         The method is         Vincent &
    on silica gel treated    packed with 1% FFAP                    (lower) to               significantly         Guient, 1982
    with  p-methoxyphenol     on Chromosorb T                        2084 mg/ml acetone       affected by high
    followed by desorption                                          (upper); this is         humidity. Samples
    with acetone (94%                                               equivalent to            can be stored for
    recovery)                                                       concentrations ranging   up to 11 days at
                                                                    from 0.5 ppm to 30 ppm   room temperature or
                                                                    (1.5-90 mg/m3) of        under refrigeration
                                                                    acrylic acid in a        without affecting
                                                                    48-litre sample volume   recovery. Recommended
                                                                                             as useful for
                                                                                             determining acrylic
                                                                                             acid in the

    Table 2.  (contd)


    Sampling                 Analytical methods      Detectiona     Detection limit          Comment               Reference

    Air samples              Reverse phase           UV detector    1 g per sample;          The sensitivity of    OSHA, 1981
    collected by             HPLC                    210 nm         assuming 24 litre        the analytical
    drawing a known                                                 sample volume, this      method permits
    volume of air             column: 25 cm                         is equivalent to         sampling times
    through two              4.6 mm i.d.                            0.042 mg/m3              as short as
    XAD-8 sampling           stainless steel                        (0.014 ppm)              15 min. Under
    tubes connected          column packed                                                   conditions of
    in series,               with Zorbax 8 m                                                 this procedure,
    followed by              ODS-bound, spherical                                            the possibility
    desorption with          silica particles                                                of interference
    methanol/water                                                                           from acetaldehyde,
    (1:1)                     mobile phase:                                                   acetic acid,
                             96:4 (V/V)                                                      acrylamide,
                             water/acetonitrile                                              acrolein,
                             containing 0.1% by                                              acrylonitrile,
                             volume phosphoric                                               methacrylic
                             acid; flow rate:                                                acid is excluded.
                             1 ml/min; injection                                             Method recommended
                             volume: 25 litre                                                and fully validated
                             retention                                                       by OSHA for acrylic
                             time:6 min                                                      acid determinations
                                                                                             in workplace air

    Table 2.  (contd)


    Sampling                 Analytical methods      Detectiona     Detection limit          Comment               Reference

    Air is pumped            HPLC equipped           Conductivity   1 mg/m3 air              The method is         Simon et
    through a florisil       with Aminex HPX         detector       (10 litre                rapid, easy and       al., 1989
    tube at a rate of        OFH organic acid                       sample volume)           appears suitable for
    1 litre/min. The         analysis column                                                 the determination
    sorbent is mixed         (300 mm  7.8 mm).                                              of acrylic acid
    with water (5 ml)        Eluent, 2.5  10-4                                              when present in
    and 1N H2SO4 (10 l)     M benzoic acid                                                  industrial emissions
    prior to injection       is pumped at                                                    containing other
    to the chromatographic   0.8 ml/min                                                      aliphatic acids

    a  FID = Flame ionisation detector
         Air samples are collected on silica gel treated with
     p-methoxyhydroquinone used as an inhibitor of polymerization
    (Vincent & Guient 1982) or on XAD-8 sampling tubes (OSHA, 1981). XAD-8
    sampling tubes contain solid sorbent, i.e. acrylic ester polymer, of
    16-50 mesh (OSHA, 1981).

         After separation with gas chromatographic (GC) technique or
    reverse phase high performance liquid chromatography (HPLC), flame
    ionization detection (Vincent & Guient 1982) or UV detection at 210 nm
    (OSHA, 1981) are utilized, respectively. The latter method was
    modified and recommended by OSHA as a fully validated method for the
    determination of acrylic acid in workplace air (OSHA, 1981). This
    method, when coupled with an ion suppression technique, proved
    successful for the retention and separation of acrylic acid.

         A retention time of approximately 6 min is obtained with a Dupont
    Zorbax ODS 8-m silica packed column and a water/acetonitrile (96:4)
    mobile phase containing 0.1% (by volume) phosphoric acid. The
    phosphoric acid serves to suppress the ionization of acrylic acid
    resulting in the retention of the undissociated form of the molecule.
    Under these conditions acrylic acid is separated from potential
    interfering substances: methacrylic acid, acrylamide, acrolein,
    acrylonitrile and acetic acid. Propanoic acid, a saturated precursor
    of acrylic acid, can be resolved from acrylic acid in a 13-min
    analysis at 1 ml/min flow rate using a 0.1% aqueous phosphoric acid
    mobile phase. Detection of acrylic acid at 210 nm is approximately 100
    times more sensitive than that of propanoic acid, owing to the
    unsaturated nature of acrylic acid. This method permits the detection
    of acrylic acid in the presence of very high levels of propanoic acid.

         A third method utilizes high-performance ion-exclusion
    chromatography with conductimetric detection (Simon et al., 1989). The
    use of 2.5  10-4 M benzoic acid as the mobile phase in this method
    allows the separation of acrylic acid from propionic acid and other
    aliphatic acids.

    2.4.2  In industrial effluents

         A gas chromatographic method has been developed for the analysis
    of acrylic acid and some other related pollutants present in small
    quantities in the effluent from a methyl acrylate plant in India
    (Singh & Thomas, 1985). In this method, effluent samples were injected
    directly to the GC system without prior extraction or concentration. A
    Porapak Q (4 feet  1/8 inch I.D.) column and a FID were utilized in
    this method. The experimental parameters for the analysis are: column
    temperature, 165C; injector and detector temperature, 250C; carrier
    gas, N2 at 50 ml/min; hydrogen pressure, 1.3 kg/cm2; air pressure,
    2.2 kg/cm2 and injection volume, 1-10 l. The method was found to be
    sensitive for detecting acrylic acid at concentrations as low as
    1 ppm.

    2.4.3  In polyacrylate materials

         A differential pulse polarographic method was used for the
    determination of residual acrylic acid in sodium polyacrylate
    polymeric systems (Husain et al., 1991). The method has the advantage
    of analysing acrylic acid in trace quantities directly without
    resorting to separation techniques. Sample solutions of the tested
    polymers were extracted with  N,N-dimethylformamide several times and
    the extraction mixture was made up to 25 ml, with the solvent
     tert-butyl ammonium iodide (0.02 M) in  N,N-dimethylformamide
    serving as the supporting electrolyte. The polarographic measurements
    were performed with a Metrohm E-506 Polarecord equipped with a three-
    electrode system (a dropping mercury electrode (DME), Ag/AgCl
    (saturated KCl) reference electrode, and an auxiliary platinum
    electrode). Using this method, free acrylic acid in polymers at levels
    of 10-100 ppm can be measured with a precision of  3%.

    2.4.4  In biological samples

         Methods for the analysis of acrylic acid in aqueous samples and
    tissues extracts in metabolic studies have been reported (Mao et al.,
    1994; Mitchell & Petersen, 1988; Black et al., 1995). In these
    methods, high-performance ion-exclusion chromatography and/or reverse
    phase HPLC with radiometric, refractive index, photo diode-array and
    UV detectors were used for the separation and quantification of
    acrylic acid.

         In another study, residues of acrylic acid in an anaerobic
    degradation mixture were quantified using a gas chromatographic
    technique with a flame ionization detector (FID) (Stewart et al.,
    1995). The column was an 80/120 Carbopak B-DA/4% Carbowax 20 M. The
    column and FID temperatures were 175 and 200C, respectively. The
    carrier gas was helium at a flow rate of 24 ml/min. The detection
    limit was 1 mg/litre.


    3.1  Natural occurrence

         Acrylic acid has been reported to occur naturally in the
    following species of marine algae: 9 species of Chlorophyceae, 10
    species of Rhodophyceae and 11 species of Phaeophyceae (Sieburth,
    1960, Glombitza, 1970a,b, 1979). It is also produced in
     Phaeodactylum  tricornutum,  Phaeocystis spp. and  Polysiphonia
    lanosa (Brown et al., 1977), as a result of hydrolysis of dimethyl--
    propiothetin (Verschueren, 1983).

         Acrylic acid has been identified as an antibacterial substance in
    oysters (Brown et al., 1977), scallops, ( Patinopecten yessoensis)
    (Kodama & Ogata, 1983), and the digestive tract of penguins (Sieburth,
    1960; Herwig 1978). It is thought to originate from the phytoplankton
     Protogonyaulax (Kodama & Ogata, 1983),  Phaeocystis spp (Sieburth,
    1960) and  Phaeodactylum tricornutum (Brown et al., 1977) on which
    the molluscs and penguins fed. It has also been shown that under
    natural conditions acrylic acid is generated by certain species of
    algae and acts as a microbiocide (Glombitza, 1970a,b, 1979; Heyser &
    Glombitza, 1972). It has also been identified as the agent responsible
    for the antimicrobial activity of the marine algae  Gracilaria
     corticata and  Ulva lactuca (Bandara et al., 1988).

         Acrylic acid has been found in the rumen fluid of sheep as a
    result of bacterial fermentation of carbohydrates (Noble & Czerkawski,
    1973), where it is converted by rumen microorganisms to propionic acid
    (Whanger & Matrone, 1967). It can also be produced from lactic acid by
    the anaerobic rumen bacterium  Megasphaera elsdenii in the presence
    of 3-butynoic acid (Sanseverino et al., 1989).

         Acrylic acid has been found in agricultural rum obtained by
    fermentation of sugarcane juice by the action of  Micrococci spp
    (Ganou-Parfait et al., 1988).

    3.2  Anthropogenic sources

    3.2.1  Production levels and processes  Manufacturing process

         The first commercial process for the manufacture of acrylic acid
    and its esters involved hydrolysis of ethylene cyanohydrin in sulfuric
    acid. This route is no longer commercially significant (Kirk-Othmer

         Most commercial acrylic acid is now produced via a process in
    which propylene is vapour-oxidized to acrolein, which is in turn
    oxidized at 300C with molybdenum-vanadium catalyst to acrylic acid
    (NLM, 1989). Other methods of production are as follows:

    *    a modification of the Reppe process by the reaction of acetylene,
         carbon monoxide and alcohol with a nickel catalyst;

    *    by hydrolysis of acrylonitrile;

    *    condensation of ethylene oxide with hydrocyanic acid followed by
         reaction with sulfuric acid at 160C;

    *    a process in which formaldehyde undergoes a type of aldol
         reaction with a large molar excess of acetic acid in the vapour
         phase in a catalyst tube containing calcium Decalso (Kirk-
         Othmer, 1984);

    *    a heterolytic dehydration pathway of lactic acid in supercritical
         water (Mok et al., 1989).  Impurities

         Commercial acrylic acid is available in two grades: technical and
    glacial. Glacial grade is 98-99.5% acrylic acid (NLM, 1989). This may
    contain, as impurities, water up to 0.3% w/w and acrylic acid dimer up
    to 0.1% w/w (BASF, 1992; Elf Atochem, 1992).  Other sources

         Acrylic acid has also been detected in trace amounts in
    commercial propionic acid (Kostanyan et al., 1969).  Production data

         Available data on the production of acrylic acid are shown in
    Table 3.

    Table 3.  Production data


    Country                  Year     Production of     Reference
                                      acrylic acid
                                      (in kilotonnes)

    China                    1994         105           CEFICA (1995)a

    European Community       1975         155           IARC (1979)
                             1994         665           CEFIC (1995)a

    Japan                    1976          70           IARC (1979)
                             1994         420           CEFIC (1995)a

    Korea                    1994          60           CEFIC (1995)a

    Taiwan                   1994          50           CEFIC (1995)a

    USA                      1993         332           US ITC (1983)
                             1985         361           US ITC (1985)
                             1986         348           US ITC (1986)
                             1987         499           US ITC (1987)
                             1988         480           US ITC (1988)
                             1991         554           NLM (1991)
                             1994         685           CEFIC (1995)a

    a    Submission of the European Council of Chemical Industry
         Federations (CEFIC) to the European Union Chemicals risk
         assessment document.

         The worldwide production of acrylic acid was approximately
    1.13 million tonnes in 1991 (Chemical Marketing Reporter, 1992).
    Worldwide capacity for acrylic acid production was reported to be
    2 million tonnes in 1994 (CEFIC, 1995).

    3.2.2  Experimental production of acrylic acid by bacterial isolates

         The following bacterial species have been utilized in
    experimental systems to produce acrylic acid:

    *    from acrylonitrile: (1) by the action of epsilon-caprolactum-
         induced  Rhodococcus rhodochrous J1 (Nagasawa et al., 1990);
         with a periodic substrate feeding system the highest accumulation
         (390 g/litre) was obtained; (2) by  Arthrobacter sp. isolated
         from petrochemical industry waste (Narayanasamy et al., 1990).

    *    from acrylamide by the action of  Pseudomonas sp. and
          Xanthomonas maltophilia isolated from herbicide-contaminated
         soils (Nawaz et al., 1993, 1994); batch culture of these bacteria
         completely degraded 62.8 mM acrylamide to acrylic acid and
         ammonia in 24 and 48 h, respectively.

    3.2.3  Uses

         Acrylic acid is used primarily: as a starting chemical for ethyl
    acrylate,  n-butyl acrylate, methyl acrylate, 2-ethylhexyl acrylate;
    as a monomer for polyacrylic acid and salts, cross-linked high (and
    low) molecular weight polymers; as a co-monomer with acrylamide for
    polymers used as flocculants; with ethylene for ion-exchange resin
    polymers; with methyl ester for polymers; and with methylene succinic
    acid (itaconic acid) for other co-polymers (SRI, 1981; NLM, 1989).

         In 1987, 25% of the acrylic acid produced in the USA was used for
    surface coatings; 20% for polyacrylic acid and salts, including super-
    absorbent polymers, detergents, water treatment and dispersants; 13%
    for textiles and non-wovens; and 9% for adhesives and sealants
    (Kavaler, 1987).

         Until 1979, in the European Union countries more than 80% of
    acrylic acid was used for the production of polyacrylates and in Japan
    90% was used in the production of acrylic esters (IARC, 1979). In
    1988, European use of acrylic acid was 69% for esters, 10% for
    detergents, 8.5% for flocculants and dispersants and 6.5% for super-
    absorbers (CEFIC, 1995).a


    a    Submission of the European Council of Chemical Industry
         Federations (CEFIC) to the European Union chemicals risk
         assessment document.

         Other uses are in the production of copolymers for dental
    adhesives (Bowen, 1979), in the production of hydrogels used for
    contact lenses (Kirk-Othmer, 1984), in surface coating formulations
    (Kirk-Othmer, 1984), and in latex applications to increase stability
    in order to prevent premature coagulation (Kirk-Othmer, 1984).


    4.1  Transport and distribution between media

         Acrylic acid is miscible with water (Riddick et al., 1986) and
    therefore would not be expected to adsorb significantly to soil or
    sediment (Lyman et al., 1982). The Henry's Law constant for acrylic
    acid is reported to be 3.2  10-7 atm m3/mol (Singh et al., 1984).
    Under soil conditions, chemicals with such low Henry's Law constants
    are essentially non-volatile (Lyman et al., 1982). However, the vapour
    pressure of acrylic acid suggests that it volatilizes from surface and
    dry soil (Howard, 1991).

         The adsorption and desorption of acrylic acid were examined in
    five different soils: an aquatic sandy loam sediment, a loamy sand, a
    clay loam and two loams. The average Koc for the adsorption of
    acrylic acid to soil was 43, and ranged from 23 to 63. The Koc values
    for the desorption data were widely scattered with values ranging from
    18 to 837. This indicates that the degree of adsorption is not
    correlated to the organic carbon content (OC), which ranged from 0.46%
    for the loamy sand to 4.58% for one of the loams. The results of this
    study indicate a high mobility of acrylic acid through soil (Archer &
    Horvath, 1991).

         Using the fugacity model of Mackay & Peterson (1981) the
    theoretical distribution of acrylic acid has been estimated. About 97%
    of acrylic acid released to the environment should be associated with
    the aquatic environment (the water phase), approximately 1.6% in air,
    1% in sediment and < 1% in soils, suspended solids and biota
    (Staples, 1993).

         Since the atmospheric lifetime of acrylic acid is less than one
    month (Atkinson, 1987), there is no potential for long-range transport
    of this compound.

    4.2  Transformation

    4.2.1  Abiotic degradation

         The UV absorption band of acrylic acid extends to about 320 nm
    (Weast & Astle, 1985). Vapour phase acrylic acid reacts with
    photochemically produced hydroxyl radicals primarily by addition to
    the double bond and with atmospheric ozone, resulting in an estimated
    overall half-life of 6.6 h to 6.5 days (Atkinson & Carter, 1984).
    Based upon the estimated rate constant for vapour phase reactions and
    assuming hydroxyl radical concentrations of 5  105 radicals per cm3
    and an ozone concentrations of 7  1011 molecules per cm3 (Atkinson
    and Carter, 1984; Atkinson, 1987), a half-life of 2.5-23.8 h was
    estimated by Howard et al. (1991).

         Acrylic acid was found to be stable to hydrolysis at pH values
    between 3.7 and 11 (Shah, 1990).

    4.2.2  Biodegradation  Aerobic biodegradation

         When added to water, acrylic acid is rapidly oxidized, and
    wastewater containing the compound can deplete reservoirs of oxygen
    (Ekhina & Ampleeva, 1977).

         Several biodegradability studies show that acrylic acid will
    readily biodegrade (Lyman et al., 1982; Keystone Environmental
    Resources, 1989a; Douglas & Bell, 1992). The BOD5 (biological
    oxygen demand, 5 days) for glacial acrylic acid, using acclimated,
    fresh dilution water and raw sewage from a local treatment plant as
    the inoculum, was determined to be 0.315 g of oxygen consumed per gram
    of product. The COD (chemical oxygen demand) under the same conditions
    was 1.48 g/g (Keystone Environmental Resources, 1989)a; therefore,
    the BOD5/COD ratio was 0.21. A BOD5/COD ratio of 0.26 was also
    reported by Lyman et al. (1982). Biodegradation of acrylic acid in a
    14-day BOD test was up to 68% (CITI, 1992). Acrylic acid at a
    concentration of 3 mg/litre attained 81% biodegradation within 28 days
    in a closed-bottle test based on the consumption of oxygen (Douglas &
    Bell, 1992). The pass level of 60% was reached within 10 days of
    exceeding the 10% level, and so acrylic acid is considered to be
    "readily biodegradable" according to EC classification criteria (EEC,

         The metabolism of 14C-acrylic acid in sandy loam soil has been
    studied under aerobic conditions for up to 28 days after treatment at
    a rate of 100 mg/kg. Acrylic acid was rapidly metabolized; after 3
    days no acrylic acid was detected in soil extracts. Carbon dioxide
    evolution accounted for 72.9% of applied radioactivity by day 3 and a
    total of 81.1% over the 28-day study period. The half-life for acrylic
    acid under these conditions was estimated to be less than 1 day
    (Hawkins et al., 1992).

         Acrylic acid formed from hydrolysis of acrylamide added to soil
    was totally degraded within 15 days of its formation (Nishikawa et
    al., 1979). In a 42-day screening study using a sewage seed inoculum,
    71% of acrylic acid was mineralized under aerobic conditions. After
    previous acclimatization, 81% of acrylic acid degraded to carbon
    dioxide in 22 days (Pahren & Bloodgood 1961; Chou et al., 1978).


    a    Report sent by J.M. Flaherty to J. McLanghlin, Rohm and Haas
         Spring House (work order numbers M8903002 and M8902005).

         A collection of strains utilizing acrylonitrile, acrylamide and
    acrylic acid as sole carbon and/or nitrogen source was isolated from
    environmental samples. Strains with maximum decomposing activity were
    identified as  Pseudomonas pseudoalcaligenes 6p;  P.alkaligenes 5g
    and  Brevibacterium spp. 13 PA (Moiseeva et al., 1991).

         An aerobic gram-negative bacterium ( Pseudomonas sp.) isolated
    from tropical garden soil was found to be able to degrade a high
    concentration of acrylamide (4 mg/litre) to acrylic acid and ammonia,
    which were utilized as sole carbon and nitrogen sources, respectively,
    for growth (Shanker et al., 1990).

         A strain of  Byssochlamys sp. produced -hydroxypropionic acid
    (-HPA) when grown on media containing high concentrations of acrylic
    acid. The maximal production of -HPA was 4.8% when the initial
    culture medium contained 7% acrylic acid and 2% glucose and the
    initial culture pH was adjusted to 7.0 (Takamizawa et al., 1993).

         Acrylic acid has been reported to be significantly degraded
    (> 30%) in the MITI test, a biodegradability screening test of the
    Japanese Ministry of International Trade and Industry (Sasaki, 1978).
    Acrylic acid was completely degraded in a standard Zahn-Wellens test
    and the authors concluded that it is biodegradable (BASF, 1993).

         Acrylic acid has been found to be degraded by a strain of
     Alcaligenes denitrificans isolated from a landfill soil. The
    bacterium degraded acrylic acid through the intermediate formation of
    L-(+)-lactic and acetic acids, which were further metabolized
    (Andreoni et al., 1990).  Anaerobic biodegradation

         Speece (1983) reported that acrylic acid can undergo ultimate
    anaerobic biodegradation. In an anaerobic screening study utilizing
    10% sludge from a secondary digester as an inoculum, acrylic acid was
    judged to be degradable, with over 75% of theoretical methane being
    produced within 8 weeks of incubation (Shelton & Tiedje, 1984).

         In another study, acrylic acid was toxic to unacclimated
    anaerobic acetate-enriched cultures and was poorly utilized (21%) in a
    completely mixed anaerobic reactor with a 20-day hydraulic retention
    time after a 90-day acclimatization period (Chou et al., 1978). A
    possible explanation for the conflicting results of anaerobic
    degradation is the observation that acetate cultures have to exhaust
    the acetic acid as carbon and energy source before they can utilize a
    cross-fed compound (Chou et al., 1978).

         The biodegradability of acrylic acid using methanogenic acetate
    enrichment culture was studied by Stewart et al. (1995). Acrylic acid
    was degraded with almost no effect on methanogens with spikes up to
    100 mg/litre. However, concentrations of 500, 1000 and 1500 mg/litre
    were found to inhibit the methanogens for several days before

    recovery. Acrylic acid was eventually degraded to less than 1 mg/litre
    (> 99% of initial concentration) in all cases by the end of the
    study (55 days).

    4.2.3  Bioaccumulation and biomagnification

         From the low value for log Kow, ranging from 0.161 to 0.46
    (Hansch & Leo, 1987; BASF, 1988), one would expect the
    bioconcentration of acrylic acid in organisms to be negligible Bysshe
    (1990) using a regression equation calculated theoretical
    bioconcentration factors ranging from 0.78 to 1.3. Veith et al. (1979)
    estimated the bioconcentration factor to be in the range of 1.6 to

         There have been no reports of biomagnification of acrylic acid in
    the food chain.


    5.1  Environmental levels

         No quantitative data are available for environmental levels of
    acrylic acid in ambient air, water or soil. Acrylic acid has been
    found to occur naturally in some marine algae (Sieburth, 1960; Brown
    et al., 1977) and some molluscs (Kodama & Ogata, 1983). The acrylic
    acid content of  Phaeocystis spp. can be 7.4% of dry weight
    (Sieburth, 1960). Other marine algae have been found to contain
    acrylic acid:  Chlorophyceae, 0.124-16.5 mg/g dry weight;
     Rhodophyceae, 0-0.131 mg/kg dry weight; and  Phaeophyceae 0-0.02 mg/g
    dry weight (Glombitza, 1970a, 1979).

    5.2  General population exposure

         No data are available for general population exposure. However,
    consumers may be exposed to unreacted acrylic acid in the following
    household goods: polishes, paints and coatings, adhesives, rug
    backing, plastics, textiles and paper finishes (USEPA, 1981).
    Information on the typical content of unreacted acrylic acid in these
    kinds of products is unavailable.

         Populations living in the vicinity of plants producing acrylic
    acid or manufacturing its esters or polymers may be exposed to acrylic
    acid in the ambient air. The concentrations of emitted vapours of
    acrylic acid in the plume from such plants were found to vary from 22
    to 183 mg/m3 (Grudzinski, 1988). However, there are no data on
    concentrations of acrylic acid in the ambient air of populated areas.

         Acrylic acid occurs in wastewater effluents from its production
    by the oxidation of propylene at concentrations not exceeding
    0.5 mg/litre (Wise & Fahrentholdt, 1981). After treatment of
    wastewater from a production facility in Europe, acrylic acid levels
    were below the limit of detection (0.1 mg/litre) (CEFIC, 1995)a.
    However, effluent from a methyl acrylate plant in India was found to
    contain 2500 mg/litre as acrylic acid (Singh & Thomas, 1985).


    a    Submission of the European Council of Chemical Industry
         Federations (CEFIC) to the European Union chemicals risk
         assessment document.

         Since there is evidence that acrylic acid esters are hydrolysed
    to acrylic acid in laboratory animals (Ghanayen et al., 1987) and in
    human tissues  in vitro (Wiegand, 1990), a potential source of
    internal exposure to acrylic acid may result from metabolism of
    absorbed acrylic acid esters (Frederick et al., 1994; Sanders et al.,

    5.3  Occupational exposure during manufacture, formulation or use

         Occupational exposure is the most important means of human
    exposure to acrylic acid. Inhalation and contact with skin are
    important routes of exposure.

         The National Institute of Occupational Safety and Health (NIOSH)
    conducted two observational nationwide surveys, a decade apart, to
    determine the extent of exposure of workers to a variety of substances
    in their work environment. The National Occupational Hazard Survey
    (NOHS) was conducted during 1972-1974 using a stratified probability
    sample of 4636 businesses in 67 metropolitan areas throughout the USA
    employing nearly 900 000 workers (NIOSH 1974, 1977). According to the
    NOHS, an estimated 28 600 workers were potentially exposed to acrylic
    acid, approximately 10% of whom were exposed to acrylic acid and 90%
    to trade-name products. However, this estimation excluded the exposure
    of the general population to trade-name chemicals possibly containing
    acrylic acid. Acrylic acid was seen in 16 major industry groups and in
    41 occupational groups in the NOHS.

         During 1981-1983 NIOSH conducted the National Occupational
    Exposure Survey (NOES), using a stratified probability sample of 4490
    businesses in 98 different geographic locations of the USA employing
    nearly 1.8 million workers (NIOSH, 1990). According to the NOES, an
    estimated 96 500 workers were potentially exposed to acrylic acid,
    approximately 10% of whom were exposed to acrylic acid and 90% to
    trade-name products. Acrylic acid was seen in 25 major industry groups
    and in 67 occupational groups (NIOSH, 1990).

         One study conducted at a large manufacturing facility of the Rohm
    and Haas Company in the USA, where several chemicals including acrylic
    acid and a variety of acrylates and methacrylates were used, indicated
    that ethyl acrylate and acrylic acid levels varied from 0.01 to
    56 ppm. Most areas of the plant had levels (as 8-h time-weighted
    averages) well below the hygiene standards recommended at that time by
    the OSHA and the ACGIH of 10 ppm for acrylic acid and 5 ppm for ethyl
    acrylate (ACGIH, 1988, OSHA, 1989). Many of the available industrial
    hygiene data were specific for high, short-term exposure tasks
    (5-40 min samples) when chemicals were pumped into containers for
    shipping or when lines were open for new connections, or to obtain
    samples. They revealed levels at the high end of the above-mentioned
    range (Schwartz et al., 1989).

         Exposures of workers to acrylic acid for short periods of time of
    less than 15 min and for full shift expressed as time-weighted average
    (TWA) concentration have been compiled from four producing companies.
    Operators had a mean short-term exposure limit (STEL) value of
    8.4 mg/m3 (range < 0.3 to 189 mg/m3); loading/unloading operations
    a mean of 3.9 mg/m3 (range 1.2 to 12 mg/m3); and those engaged in
    quality assurance a mean of 0.3 mg/m3 (range of less than 0.3 to
    0.6 mg/m3). Concerning the 8-h TWA, the operators showed levels of
    0.48 mg/m3 (range of 0.03 to 3 mg/m3) and loading/unloading
    operations a mean of 0.39 mg/m3 (range of 0.27 to 1.98 mg/m3)
    (Casciery & Clary, 1993).

         No such data are available from other countries.


    6.1  Human studies

         Apart from  in vitro skin absorption studies, no data are
    available on kinetics, metabolism or elimination or acrylic acid in

         The absorption of 14C-acrylic acid (site of label unspecified)
    dissolved in acetone, water or phosphate buffer (pH 6.5) was tested
    using samples of excised (postmortem) human and mouse skin  in vitro
    (Corrigan & Scott, 1988). Acrylic acid concentrations of 0.01, 0.1,
    1.0 and 4.0% were applied at 100 l/cm2 under occlusive conditions.
    Samples were taken from the receptor fluid up to 32 h. Rates of
    absorption decreased in the order of magnitude as follows: acetone >
    water > phosphate buffer. Independent of the vehicle, the absorption
    rate increased as a function of acrylic acid concentration.
    Permeability coefficients, which ideally are concentration-independent
    expressions of absorption rate, for human skin ranged from 0.37 to
    0.72  10-3 cm/h for water and from 0.47 to 1.81  10-4 cm/h for
    phosphate buffer. Permeability coefficients were not calculated for
    acetone because of evaporation of this volatile vehicle during the
    course of the experiments (Corrigan & Scott, 1988).

         A briefly reported  in vitro percutaneous penetration study
    using excised human cadaver skin indicated that 14C-acrylic acid
    absorption can vary significantly as a function of pH and delivery
    vehicle.  In vitro flux, estimated after a 1 mg dose was applied,
    varied by 600 times within the treatments studied and decreased in the
    order: acetone (600 g/cm2 per h) > phosphate buffer pH 6.0 
    (23 g/cm2 per h) > ethylene glycol (15 g/cm2 per h) > phosphate
    buffer pH 7.4 (1 g/cm2 per h) (D'Souza and Francis, 1988).

    6.2  Studies on experimental animals

    6.2.1.  Absorption, distribution and excretion  Oral exposure

         After oral gavage administration of an aqueous solution of
    (1-11C)-acrylic acid (26 g/kg body weight) to female Sprague-Dawley
    rats, it was rapidly absorbed and expired mainly as 11CO2 within 1 h
    post-administration. The uptake appeared biphasic. The short alpha-
    phase had an apparent first-order absorption constant (Ka) of 19% of
    the available dose per minute (biological half-time = 3.6 min) and the
    Ka of the -phase was 30% (biological half-time = 23 min). Relative
    retention of radiolabel (dpm per g tissue versus dpm per g body
    weight) after 65 min was above unity in liver (2.6), adipose tissue
    (1.9), small intestine (1.5), kidneys (1.2) and spleen (1.0).
    Approximately 6% of the radiolabel was excreted in the urine within 
    65 min (Kutzman et al., 1982).

         In another study, single gavage doses of 4, 40 or 400 mg/kg body
    weight of (2,3-14C)-acrylic acid in 0.5% aqueous methylcellulose
    solution were administered to male Sprague-Dawley rats. Approximately
    35, 55 and 60%, respectively, of the administrated dose were
    eliminated, mostly as 14CO2, within 8 h. By 24 h 50-65% of the dosed
    radioactivity was eliminated and the excretion of radioactivity had
    virtually ceased. After 72 h, 44-65% of the administrated
    radioactivity had been eliminated as 14CO2; 2.9-4.3% in urine, 2.4-
    3.6% in the faeces and 18.9-24.6% remained in the tissues examined
    (liver, stomach, muscle, blood, plasma, adipose tissue). The residual
    radioactivity was highest in the adipose tissue (9-15%), followed by
    muscle (6.5-7.5%) and liver (1.7-2.2%) (De Bethizy et al., 1987).

         The disposition of (1-14C)-acrylic acid was also determined in
    male Sprague-Dawley rats following oral administration by gavage in
    water at 400 mg/kg body weight. Excretion of acrylic acid-derived
    radioactivity was determined by collection of urine, faeces and
    expired air for 72 h following administration. The predominant route
    of excretion was in the expired air with approximately 80% of the
    radioactivity exhaled as 14CO2 within 24 h and 83.2% after 72 h.
    Elimination of radioactivity as exhaled volatile organic compounds was
    negligible (less than 0.5% of the radiolabel). Within 24 h of dose
    administration, excretion of radioactivity accounted for 5.0% in the
    urine and 8.8% of the radiolabel in faeces. Tissue concentrations of
    radioactivity after 72 h were generally low: 0.4% of the total dose in
    the liver, 0.39% in muscle and 0.18% in skin (Winter & Sipes, 1993).

         A comparative bioavailability and disposition study in male
    Fischer-344 rats and male C3H mice after a single administration of
    (1-14C)-acrylic acid (40 or 150 mg/kg body weight in water) by gavage
    has been conducted. This study confirmed that acrylic acid is rapidly
    absorbed and metabolized. In rats and mice about 80-90% of the dose
    was exhaled as 14CO2 within 24 h (Black et al., 1995). In rats,
    excretion of radiolabel in urine and faeces within 72 h accounted for
    < 5% and < 1% of the dose, respectively. Elimination of
    radioactivity in rats as exhaled organic volatile compounds was less
    than 0.5% of the radiolabel. Similar patterns were observed in male
    mice (Black et al., 1995).  Inhalation exposure

         A tissue distribution study has been conducted in 39 female
    Sprague-Dawley rats nose-exposed to (1-11C)-acrylic acid vapour for 
    1 min (concentration not indicated). Radioactivity was widely
    distributed; 90 seconds after exposure 18.3% of the delivered dose
    remained in the rats. Approximately 28.0% of this radioactivity was
    associated with the snout and 42.9% of the radioactivity was found in
    the head; this was considered to be solubilized in the mucous of the
    turbinates and the nasopharynx. After 65 min, the activity in the
    snout was reduced to 8.1% and approximately 60% of the label was
    expired as 11CO2. The elimination of labelled CO2 appeared to be

    biphasic, with a half-time of approximately 30.6 min during the
    alpha-phase. The amount of radioactivity retained in liver and fat
    increased markedly between 1.5 and 65 min post-exposure (Kutzman et
    al., 1982).  Dermal exposure

         In one  in vitro experiment, the dermal penetration capacity of
    (1-14C)-acrylic acid was tested using excised mouse skin. Skin slices
    were treated in a diffusion chamber with 0.01, 0.1, 1 and 4% (w/v)
    100 l/cm2 of acrylic acid dissolved in acetone, water or phosphate
    buffer pH 6.5. The results were comparable with the study performed on
    excised human skin (section 6.1). Permeability coefficients for mouse
    skin were 0.96-1.73  10-3 cm/h for water and 1.91-3.1  10-4 cm/h
    for phosphate buffer. The permeability coefficients and steady-state
    absorption rate data indicate that mouse skin is approximately three
    times more permeable than human skin to acrylic acid (Corrigan &
    Scott, 1988). This difference may not be biologically significant.

         In a briefly reported study, male Sprague-Dawley rats were
    administered dermally 5 mg 14C-acrylic acid per kg body weight
    (D'Souza & Francis, 1988). Phosphate buffer of pH 6 or 7.4 or acetone
    was used as a formulating agent. In each case the formulation was
    applied to the shaved back of the rats and covered with a glass
    chamber. The rate of appearance of 14CO2 measured at 0.5, 1, 2, 4,
    8, 16 and 24 h after application was used as a measure of the
    absorption rate of acrylic acid. The absorption rate was dependent on
    the vehicle and decreased in the following order, acetone > phosphate
    buffer of pH 6 > phosphate buffer of pH 7.4. Cumulative absorption
    after 24 h was 22% from acetone, approximately 19% from phosphate
    buffer of pH 6, and 9% from phosphate buffer of pH 7.4. The results of
    the  in vivo investigations were comparable to those of the  in
    vitro studies obtained by the same authors (D'Souza & Francis, 1988).

         The disposition of (1-14C)-acrylic acid was determined in male
    Sprague-Dawley rats after topical application of 100 l of a 4% (v/v)
    solution of acrylic acid in acetone to an area of 8.4 cm2 of the skin
    (501 g/cm2) using a skin-mounted, charcoal-containing trap covered
    with fixed aluminium discs to ensure complete recovery of the label.
    Excretion of acrylic-acid-derived radioactivity was determined by
    collection of urine, faeces and expired air for 72 h following
    administration of acrylic acid. Approximately 73% of the radioactivity
    volatilized from the skin and was trapped in the charcoal sorbent.
    After 72 h, 6% of radioactivity was detected at the site of
    application in the skin or on the skin surface. Approximately 75% of
    the absorbed dose, representing about 16% of the applied dose, was
    exhaled as 14CO2 within 12 h. Excretion of radioactivity in the
    urine accounted for approximately 9% of the applied radioactivity
    (approximately 4% of the absorbed dose), the faeces containing only
    negligible amounts of radioactivity. After 72 h, less than 0.4% of the
    applied dose was retained in tissues other than skin (Winter & Sipes,

         In another study, 1% (v/v) acetone solutions of 14C-acrylic acid
    at doses of 10 or 40 mg/kg were applied to the clipped skin of the
    shoulder region of male F-344 rats or male C3H/HeN Crl BR mice. A non-
    occlusive "frame" device was cemented to the skin surface of animals
    to allow for free evaporation of acrylic acid, which was trapped using
    on-line volatile organic traps. Since this technique was inefficient,
    activated-charcoal-impregnated filter paper sheets were placed
    occlusively on the treated skin surface of a second high dose group of
    animals to provide for absorption of evaporating acrylic acid (Black
    et al., 1995). In rats, the reported 72-h recovery was low and ranged
    from 50 to 60% of the applied dose. Evaporation accounted for most of
    the applied acrylic acid, but approximately 26 and 19% of the applied
    high and low doses were absorbed in rats within 72 h, respectively.
    The major route of elimination of absorbed acrylic acid was via
    exhalation of 14CO2 and accounted for 69.5 and 77% of the absorbed
    low and high doses, respectively. Minimal faecal elimination of
    absorbed acrylic-acid-derived radioactivity was reported (< 1%), and
    tissues and carcasses contained approximately 2-3% of the absorbed
    chemical at 72 h.

         In mice, the 72-h recovery ranged from 61.5 to 84.0% of the
    applied acrylic acid dose. As in the rat experiments, while most of
    the applied acrylic acid was lost to evaporation, absorption accounted
    for 11-12% of the applied dose. Exhalation of 14CO2 accounted for
    83.5 and 77.7% of the absorbed high and low doses, respectively.
    Elimination via other routes was negligible, and less than 1% of the
    absorbed dose remained in the tissues and carcasses at 72 h (Black et
    al., 1995).  Intravenous administration

         Single i.v. doses of (1-14C)-labelled acrylic acid (10 mg/kg
    body weight in phosphate-buffered saline) were given to male F-344
    rats and male C3H/HeNCrlBR mice into the tail veins. In rats 63% of
    the 14C-dose was eliminated as 14CO2 after 4 h and 68% after 72 h,
    while almost no 14C was recovered as exhaled organic volatiles.
    Tissue samples (liver, kidney and fat) and plasma contained 1.9% at 1
    h, 0.4% at 8 h, and 0.2% at 72 h of the recovered dose. Overall the
    recovery was 72.8  10.8%. In mice, 51% of the radioactivity was
    exhaled as 14CO2 over the 72-h collection period, the majority
    exhaled in the first 4 h. The volatile radioactive fractions were
    about 0.6% of the total dose. Overall, 55.7  6.6% of this intravenous
    10 mg/kg dose was recovered in mice (Frantz & Beskitt, 1993).

    6.2.2  Metabolism   In vitro investigations

         Oxidation of (2,3-14C)-acrylic acid was studied by incubating
    acrylic acid with hepatic microsomal preparations obtained from male
    Sprague-Dawley rats. No metabolites were detected by HPLC and acrylic
    acid was recovered unchanged from the incubation mixture (De Bethizy
    et al., 1987).

         Results of the  in vitro metabolism of (1-14C)-acrylic acid
    incubated with freshly isolated hepatocytes and liver homogenates of
    male F-344 rats or mitochondria isolated from liver homogenates of
    male F-344 rats indicate that acrylic acid is rapidly metabolized to
    14CO2. Addition of equimolar amounts of propionic acid, 3-hydroxy-
    propionic acid or 3-mercaptopropionic acid caused a significant
    inhibition of the oxidation of acrylic acid by isolated mitochondria.
    A single major metabolite co-eluting with 3-hydroxypropionic acid was
    found by HPLC analysis in the mitochondrial incubation mixtures. The
    authors suggested that acrylic acid is metabolized  in vitro by
    mammalian enzymes to CO2 via 3-hydroxypropionate by the non-vitamin-
    B12 - dependent pathway for propionate metabolism (Finch & Frederick,

         The oxidation rate of acrylic acid in 13 different tissues
    (liver, kidney, forestomach, glandular stomach, small and large
    intestine, spleen, brain, heart, lung, skeletal muscle, fat and skin)
    of male and female C3H/HeNCrlBR mice was measured by incubating tissue
    slices with (1-14C)-acrylic acid and collecting 14CO2. All the
    tissues studied oxidized acrylic acid to a certain extent, but
    activity in kidney, followed by liver, was much higher than in other
    tissues. Oxidation of acrylic acid followed pseudo-Michaelis-Menten
    kinetics in the liver, kidney and skin, with a Km for all these
    tissues of approximately 0.67 mM. Marked differences were observed in
    the Vmax values, 2890  436 nmol/h per g for kidney, 616  62 nmol/h
    per g for liver and 47.9  5.8 nmol/h per g for skin. Half-lives in
    these tissues were 0.13, 0.867 and 10.2 h, respectively. Lung,
    glandular stomach, heart, spleen, fat and large intestine preparations
    oxidized acrylic acid at rates from 10 to 40% of the rate determined
    in the liver; in the remaining tissues reaction rates were less than
    10% of those in the liver. Rates of metabolism in tissues from male
    and female mice were similar.3-Hydroxypropionic acid was the only
    metabolite detected by HPLC analysis following incubation of tissues
    with (1-14C)-acrylic acid. To determine if CO2 was formed from the
    C1 carbon, and if acetyl-CoA was derived from carbons 2 and 3 of
    acrylic acid, the authors incubated (2,3-14C)-acrylic acid and
    (1-14C)-acetate with liver and kidney slices and measured the rate of
    14CO2 formation. It was concluded that CO2 originated from C1, but
    that acetyl-CoA was derived from carbons 2 and 3 of acrylic acid. Both
    substrates were oxidized well by the tissues, thus providing for the
    complete metabolism of acrylic acid to CO2. The results demonstrate
    that the rate of acrylic acid metabolism varies significantly among
    mouse tissues and suggested that the kidneys and liver are major sites
    of acrylic acid metabolism (Black et al., 1993).  In vivo investigations

         After oral administration of (2,3-14C)-acrylic acid (4, 40 or
    400 mg/kg body weight in 0.5% methylcellulose) to male Sprague-Dawley
    rats, the major portion of the radioactivity (up to 65%) was exhaled
    as 14CO2 within 24 h. In urine four metabolites were identified by
    HPLC analysis. One of the two major metabolites eluted very near to

    the solvent front and did not co-elute with acetic acid pyruvic acid
    or lactic acid. The second metabolite co-eluted with 3-hydroxypro-
    pionic acid. Traces of two other unidentified residues were also
    detected. Radioactivity could not be detected at the retention times
    corresponding to that of 2,3-epoxypropionic acid, glyceric acid or
     N-acetyl- S-(2-carboxy-2-hydroxyethyl)-cysteine, suggesting that
    acrylic acid is not epoxidized to 2,3-epoxypropionic acid  in vivo.
    It was suggested that acrylic acid was metabolized by the non-vitamin-
    B12-dependent pathway for propionic acid metabolism, with degradation
    to CO2 being the main route of elimination. Residual radioactivity in
    tissues may be due to incorporation of 14C from acrylic acid into
    acetyl-CoA (De Bethizy et al., 1987).

         Using HPLC and NMR analysis, 3-hydroxypropionic acid,  N-acetyl-
     S-2-(2-carboxyethyl)-cysteine and  N-acetyl- S-(2-carboxyethyl)-
    cysteine-S-oxide were identified as urinary metabolites after oral
    administration of (2,3-14C)-acrylic acid (400 mg/kg body weight in
    water by gavage) to male Sprague-Dawley rats. According to the
    authors, the detection of mercapturates may be a consequence of the
    high dose used in this study (Winter et al., 1992).

         HPLC analysis for acrylic acid and its metabolites in rats
    revealed that a metabolite that coeluted with 3-hydroxypropionic acid
    was found in the urine, plasma and liver of rats that had received
    acrylic acid by gavage. Furthermore, a material that co-eluted with
    authentic acrylic acid was detected in the urine and liver, but not in
    the plasma, of these rats. Acrylic acid, but not 3-hydroxypropionic
    acid, was also detected in the urine of rats after cutaneous
    application (Black et al., 1995). In mice, 3-hydroxypropionic acid was
    identified in the liver after gavage administration of acrylic acid.
    No acrylic acid was detected in the liver of these animals (Black et
    al., 1995).  Metabolic pathways

         Acrylic acid is rapidly metabolized to CO2, a major metabolite
    formed via acrylyl-CoA by the non-vitamin-B12-dependent pathway of
    mammalian propionate catabolism (Finch & Frederick, 1992; Winter et
    al., 1992; Black et al., 1993; Winter & Sipes, 1993). This pathway
    occurs in the mitochondrion (Finch & Frederick, 1992) and consist of
    reactions analogous to fatty acid -oxidation (Schultz, 1991).
    -oxidation is the major route of propionate catabolism in many
    invertebrates and plants (Wegner et al., 1968; Halarnkar & Blomquist,
    1989); however the primary pathway of propionate catabolism in mammals
    is that involving the vitamin-B12-dependent enzyme, methyl-malonyl-
    CoA mutase (Black et al., 1993). A small amount of 3-hydroxypropionic
    acid was identified as the major urinary metabolite of acrylic acid
    (De Bethizy et al., 1987; Winter et al., 1992). There is no evidence
    to suggest that epoxide intermediates are formed during the metabolism
    of acrylic acid (De Bethizy et al., 1987).  N-acetyl- S-(2-
    carboxyethyl) cysteine and  N-acetyl- S-(2-carboxyethyl) cysteine-
     S-oxide were identified in the urine of rats that had received

    400 mg/kg (2,3,-14C)-acrylic acid by gavage (Winter et al., 1992),
    suggesting a direct reaction between acrylic acid and reduced

         The major route of metabolism for acrylic acid esters has been
    shown to involve the rapid cleavage of the ester bond by carboxyl
    esterases (see Fig. 1) (Ghanayem et al., 1987; Sanders et al., 1988;
    Frederik et al., 1994). Thus exposure to acrylic acid esters may
    constitute a significant internal exposure to acrylic acid. A
    secondary metabolic pathway involves conjugation of the acrylic acid
    ester with glutathione to yield acetyl- S-(2-carboxyethyl) cysteine
    alkylesters. (Ghanayem et al., 1987; Sanders et al., 1988). This
    intermediate may be further metabolized to  N-acetyl- S-(2-
    carboxyethyl) cysteine and  N-acetyl- S-(2-carboxyethyl)-cysteine-
     S-oxide. However, it is currently uncertain what proportion of  N-
    acetyl- S-(2-carboxyethyl) cysteine, or its oxide, formed from the
    metabolism of the acrylic acid esters originates from the reaction of
    the intact ester with glutathione and what proportion originates from
    the conjugation of the released acrylic acid with glutathione (see Fig

         On the basis of available information, proposed metabolic
    pathways for acrylic acid are summarized in Fig. 1. The proposed
    scheme also includes relationships between metabolism of acrylic acid
    and its esters (e.g., ethyl acrylate) and metabolism of propionate via
    the major vitamin-B12-dependent pathway.

    FIGURE 2


    7.1  Single exposure

         The acute toxicity of acrylic acid is difficult to ascertain,
    owing to the wide range of LD50 values reported (Table 4). However
    most data indicate that the substance is of low to moderate toxicity
    by the oral and inhalation routes and of moderate toxicity by the
    dermal route. It has been proposed that the wide variation in oral
    LD50 values may be due to the different forms in which acrylic acid
    has been applied, i.e. undiluted, in aqueous solution at various
    concentrations or in neutralized solution (BG Chemie, 1991).

         Stomach lesions, necrosis and haemorrhage have been reported
    following oral dosing of rats with acrylic acid (Ghanayem et al.,
    1985; DeBethizy et al., 1987). The lowest dose at which lesions were
    seen was 144 mg/kg.

         CrL:CDBR rats were exposed (whole body) to aerosol (mean mass
    median diameter of 2.3 m  2.3) concentrations of acrylic acid
    ranging from 8775 to 14 145 mg/m3 (2925 to 4715 ppm) for 30 min, 8139
    to 12 624 mg/m3 (2713 to 4208 ppm) for 60 min, and 3669 to 
    10 239 mg/m3 (1223 to 3413 ppm) for 120 min. Additionally, rats were
    exposed (whole body) to acrylic acid vapour concentrations ranging from
    2784 to 6426 mg/m3 (928 to 2142 ppm) for 60 min. Exposure to acrylic
    acid produced treatment-related signs of nasal mucosa, upper airway and
    lower airway irritation, ocular irritation, corneal opacities and
    dermal toxicity in all experimental groups. Deaths, as a function of
    both aerosol concentration and exposure duration, were seen in the
    30-, 60- and 120-min aerosol exposures. No deaths resulted from the
    vapour exposures. Following the 14-day observation period, necropsies
    revealed treatment-related alterations of the lungs, eyes and skin
    consistent with that of an irritant. However, comparison of LC values
    suggested no difference in toxicity between the aerosol and vapour
    (Hagan & Emmons, 1991).

        Table 4.  The acute toxicity (LD50 and LC50) of acrylic acid for experimental animals


    Species     Route               Parameter         Dose                Reference

    Mouse       oral                LD50              830 mg/kg           Klimkina et al., 1969

    Mouse       oral                LD50              1200 mg/kg          Zeller, 1958

    Rat         oral                LD50              193 mg/kg           IARC, 1979

    Rat         oral                LD50              340 mg/kg           Carpenter et al., 1974

    Rat         oral                LD50              1350 mg/kg          Majka et al., 1974

    Rat         oral                LD50              1500 mg/kg          Zeller, 1958

    Rat         oral                LD50              2520 mg/kg          Fassett, 1963

    Rat         oral                LD50              2100-3200 mg/kg     Miller, 1964

    Rat         oral                LD50              2500 mg/kg          Verschueren, 1983

    Mouse       subcutaneous        LD50              1590 mg/kg          Sittig, 1985

    Rabbit      percutaneous        LD50              295 mg/kg           Carpenter et al., 1974

    Rabbit      percutaneous        LD50              640 mg/kg           Gelbke & Hofman, 1979

    Rabbit      percutaneous        LD50              750 mg/kg           IARC, 1979

    Rabbit      percutaneous        LD50              950 mg/kg           Fassett, 1963

    Mouse       inhalation          LC50 (2 h)        5300 mg/m3          RTECS, 1989

    Rat         inhalation          LC50 (30 min)     26 000 mg/m3        Hagan & Emmons, 1991

                                    LC50 (60 min)     11 100 mg/m3

                                    LC50 (120 min)    7500 mg/m3

    Table 4. (contd.)


    Species     Route               Parameter         Dose                Reference

    Rat         inhalation          LC50 (4 h)        3600 mg/m3          Majka et al., 1974

    Rat         inhalation          LC50 (4 h)        > 5100 mg/m3        Klimisch & Zeller, 1980

    Mouse       intraperitoneal     LD50              17 mg/kg            Lawrence et al., 1972

    Mouse       intraperitoneal     LD50              128 mg/kg           RTECS, 1989

    Mouse       intraperitoneal     LD50              140 mg/kg           Zeller, 1958

    Rat         intraperitoneal     LD50              24 mg/kg            Majka et al., 1974

    Rat         intraperitoneal     LD50              24 mg/kg            Singh et al., 1972

         In a single inhalation study in rats, no deaths occurred when
    six animals were exposed to acrylic acid at a concentration of
    12 000 mg/m3 (4000 ppm) for 4 h and observed over 14 days (Union
    Carbide Corp., 1977).

         A single 4-h exposure of six rats to 6000 mg/m3 (2000 ppm) of
    acrylic acid caused no death (Carpenter et al., 1974).

         One 5-h exposure to an atmosphere saturated with acrylic acid
    (6000 ppm or 17 700 mg/m3) given to four rats (2 male, 2 female)
    produced nose and eye irritation, respiratory difficulty and
    unresponsiveness in all rats. One rat died. Histopathological
    examination showed lung haemorrhage and degenerative changes in the
    liver and kidney tubules of all rats (Gage, 1970), but these were
    possibly secondary changes in dying animals.

         Rats exposed for 1 h to acrylic acid concentrations of 300, 900
    or 1500 mg/m3 (100, 300 or 500 ppm) exhibited exposure-dependent
    decreases in both respiratory frequency and minute volume (Silver et
    al., 1981).

         In a sensory irritation study, the single exposure to acrylic
    acid vapour estimated for a 50% reduction of the respiratory rate
    (RD50) was 1539 mg/m3 (513 ppm) in F344/N rats and 2055 mg/m3
    (685 ppm) in B6C3F1 mice. During exposure to 225 mg/m3 (75 ppm) of
    acrylic acid vapour for 6 h, a 20-30% decrease in minute volume was
    observed in both species (Buckley et al., 1984).

    7.2  Irritation and sensitization

    7.2.1  Eye irritation

         Application of acrylic acid in different concentrations (glacial,
    10%, 3% and 1%) to rabbit eyes revealed that it is corrosive in high
    concentrations, i.e. glacial and 10%; 1% and 3% solution caused eye
    irritancy (Majka et al., 1974). There are also other reports of
    undiluted acrylic acid causing eye irritation and corneal damage
    (Carpenter et al. 1974; BG Chemie, 1991).

    7.2.2  Skin irritation and sensitization  Skin irritation

         Undiluted acrylic acid is corrosive to rabbit skin (Carpenter et
    al., 1974; Majka et al., 1974; BG Chemie, 1991). A study with rabbits
    reported that a one-minute exposure to a 50% or 20% aqueous solution
    caused, respectively, erythema and oedema or slight erythema (BG
    Chemie, 1991). Another study reported a 10% solution to be corrosive
    when applied to rabbit skin and that a 0.6-5% solution caused
    irritation of various severity (Majka et al., 1974).

         The irritant effects of repeated dermal exposure have also been
    investigated. A 5% acrylic acid solution in acetone caused skin
    irritation in the mouse after daily non-occlusive application for 14
    days (DePass et al., 1984). No irritation was seen with a 1% solution.
    In another study, groups of three strains of mice received dermal
    applications of 0.1 ml acrylic acid in acetone 3 times a week for 13
    weeks at concentrations of 0, 1 or 4% (Tegeris et al., 1987, 1988). At
    4%, there were signs of significant skin irritation (desquamation,
    fissures and eschar), with proliferative, degenerative and
    inflammatory changes being detected histologically in the epidermis
    and dermis, from weeks 1 to 2. At 1%, minimal proliferative changes,
    detected histologically, were the only effects seen. No differences
    were found between the response of the three strains of mice.  Skin sensitization

         Acrylic acid has been tested for contact sensitivity in guinea-
    pigs. In one study, a 20% aqueous solution of pure unstabilized
    acrylic acid was applied to the skin once a day until definite skin
    irritation was seen. When challenged topically 11 days later with a 2%
    solution, there was no evidence of skin sensitization up to 24 h post-
    challenge (BG Chemie, 1991).

         In another study, the highest non-irritating concentration of
    acrylic acid (not specified) was applied topically four times in 10
    days. At the time of the third application, Freund's adjuvant was
    injected intradermally. When challenged two weeks later, none of the
    10 guinea-pigs showed evidence of skin sensitization (Rao et al.,

         Three out of six guinea-pigs exposed to acrylic acid, said to be
    99% pure, showed a skin sensitization response in a Polak test (Parker
    & Turk, 1983). Induction was by dermal injections of a total of 1 mg
    acrylic acid, together with adjuvant, followed by topical challenge
    with 5% acrylic acid. However, the impurities and inhibitors of the
    acrylic acid used were not mentioned in the report.

         Acrylic acid was found to be an extreme sensitizer by the guinea
    pig maximization test and a weak sensitizer by the Landsteiner Draize
    test. The compound used for testing was considered pure, but no
    analytical data were provided (Magnusson & Kligman, 1969).

         Acrylic acid gave a clearly positive result in the Freunds
    Complete Adjuvant test in guinea-pigs (Waegemaekers & van der Walle,
    1984). Induction was by three intradermal injections of 1.2% followed
    by topical application of 2.2 or 7.2%. The positive response was
    believed to be due to the historical impurity, alpha,-
    diacryloxypropionic acid. This impurity was identified in acrylic acid
    from just one of three suppliers. Limited testing of acrylic acid from
    the other two suppliers gave negative skin sensitization results. It
    should be noted that the impurity is not present in acrylic acid
    resulting from current production methods involving distillation.

         Commercial acrylic acid also contains a small amount of
    polymerization inhibitors, usually hydroquinone monomethyl ether
    (methoxyphenol). This is a known skin sensitizer in guinea-pigs (van
    der Walle et al., 1982). Other inhibitors used with acrylic acid have
    also been reported to have skin-sensitizing properties, namely pheno-
    thiazine (Costellati et al., 1990) and diphenyl- p-phenylenediamine
    (Magnusson et al., 1968; Kalimo et al., 1989). However, it is unclear
    whether the small amount of one of these inhibitors present
    (0.02-0.1%) could contribute to the skin-sensitizing properties of
    commercial acrylic acid.

    7.2.3  Upper respiratory tract irritation

         Olfactory cell proliferation, as measured by tritiated thymidine
    incorporation, was investigated in male F-344 rats and B6C3F1 mice
    exposed to 224 mg/m3 (75 ppm) acrylic acid 6 h daily for 5 days. A
    17-fold increase in cell proliferation occurred in mice and a 4-fold
    increase in rats (Swenberg et al, 1986). Further information on upper
    respiratory tract irritation is given in sections 7.1 and 7.3.2.

    7.3  Short-term exposure

         Results of key studies on the short-term repeated exposure
    effects of acrylic acid are presented in Table 5.

        Table 5.  Key studies on the noncarcinogenic effects of repeated exposures to acrylic acid


    Species, route and dosage       LOELa               NOELa              Observed effects                Reference

    Rat, Fisher-344 oral,           250 mg/kg bw/day    83 mg/kg bw/day    Decreased body weight,          De Pass et al.,
    drinking-water, 0, 83,                                                 reduced water and food          1983
    250, 750 mg/kg body                                                    consumption, changes in
    weight/day for 3 months                                                organ weights

    Rat, Wistar, gavage, 0,         150 mg/kg bw/day                       50% mortality in both           Hellwig et al.,
    150, 375 mg/kg bw/day,                                                 treatment  groups, dose-        1993
    5 times/week for 3                                                     dependent irritation in the
    months                                                                 forestomach and
                                                                           glandular stomach,
                                                                           purulent rhinitis, tubular

    Rat, Wistar, oral,
     drinking-water, 0, 9, 61,
     140, 331 mg/kg body
     weight/day for 3 months        331 mg/kg bw/day    140 mg/kg bw/day   Reduced water and food          Hellwig et al.,
                                                                           consumption in males            1993

    Rat, Wistar, oral,              140 mg/kg bw/day    61 mg/kg bw/day    Reduced water and food          Hellwig et al.,
     drinking-water, 0, 9, 61,                                             consumption in males            1993
     140, 331 mg/kg body
     weight/day for 12 months


    Table 5. (contd.)


    Species, route and dosage       LOELa               NOELa              Observed effects                Reference

    Rat, Wistar, oral,                                  78 mg/kg bw/day    No treatment-related            Hellwig et al.,
     drinking-water, 0, 8, 27,                                             toxic effects including         1993
      78 mg/kg body                                                        tumorogenicity
     weight/day for 26
     (males) or 28 (females)

    Rat, inhalation, 80, 300        300 ppm             80 ppm             Nose irritation, lethargy       Gage, 1970
     ppm, 6 h/day 5                 (900 mg/m3)         (240 mg/m3)        reduced body weight gain
     20 exposures

    Rat, Fisher-344                 225 ppm (675        75 ppm             Decrease of adipose             Miller et al.,
    inhalation, 0, 25, 75,          mg/m3)              (225 mg/m3)        tissue in females, lesions      1979
     225 ppm, 6 h/day,                                                     of nasal mucosa
     5 days/week for 2 weeks

    Rat, Fisher 344                 75 ppm              25 ppm             Lesions of nasal olfactory      Miller et al.,
     inhalation, 0, 5, 25,          (225 mg/m3)         (75 mg/m3)         epithelium                      1981
     75 ppm, 6 h/day,
     5 days/week for
     13 weeks

    Rat, F-344, and mouse           75 ppm                                 Olfactory cell proliferation    Swenberg et al.,
     B6C3F1 inhalation,             (225 mg/m3)                            17-fold in mice, 4-fold in      1986
     75 ppm, 6 h/day, 5 days                                               rats

    Table 5. (contd.)


    Species, route and dosage       LOELa               NOELa              Observed effects                Reference

    Mouse, B6C3F1                   25 ppm                                 Decrease in body weight         Miller et al.,
     inhalation, 0, 25, 74,         (75 mg/m3)                             gain, lesions in nasal          1979
     223 ppm, 6 h/day                                                      mucosa
    5 days/week for 2 weeks

    Mouse, B6C3F inhalation         5 ppm               5 ppm              Atrophy, disorganization,       Lomax et al.,
     0, 5, 25 ppm for 6 or 22       22 h/day            6 h/day            necrosis of  the olfactory      1994
     h/day and 25 ppm for                                                  epithelium of nasal
     4.4 h/day for 2 weeks,                                                cavity.  Recovery after 6
     6 weeks recovery period                                               weeks except for mice
                                                                           exposed to 25 ppm for
                                                                           22 h/day where
                                                                           metaplasia was seen

    Mouse, B6C3F1                   5 ppm                                  Slight focal lesions of         Miller et al.,
     inhalation, 0, 5, 25,          (15 mg/m3)                             nasal olfactory                 1981
     75 ppm, 6 h/day 5                                                     epithelium
     days/week for 13 weeks

    a  LOEL = lowest-observed-effect level; NOEL = no-observed-effect level

    7.3.1  Oral

         Acrylic acid was administered via oral gavage to ten rats for 20
    days with doses increasing by 50% every fourth day (range:
    135 mg/kg to 684 mg/kg). Reduction in body weight gain and minor
    histopathological changes in the stomach were found at higher doses
    (Majka et al., 1974).

         In a 3-month study (Hellwig et al., 1993), groups of 10 male and
    10 female Wistar rats were gavaged, 5 times per week, with acrylic
    acid at doses of 150 or 375 mg/kg body weight. A control group of 10
    males and 10 females was gavaged with water. A high mortality rate was
    observed in experimental groups; 50% of both males and females in the
    low-dose group and 60% (males) and 90% (females) in the high-dose
    group died. Cyanosis, dyspnoea and irritation ulceration of
    forestomach and glandular stomach, purulent rhinitis and lung
    emphysema and alveolar hyperaemia were the main findings reported.
    Necrotizing tubular nephroses were seen in the animals that died
    during the study. The symptoms and histopathological findings were
    substantially the same in both groups, but they were less pronounced
    and observed in a smaller number of animals given acrylic acid at
    150 mg/kg body weight.

         Acrylic acid was given to Wistar rats in drinking-water for
    3 months as part of a 12-month study (Hellwig et al., 1993). Further
    details are given in section 7.4.

         In a subchronic study acrylic acid was incorporated into the
    drinking-water of rats (15/sex/group) for 3 months, resulting in doses
    of 0,83, 250 and 750 mg/kg per day. At the high and intermediate dose
    levels, reduction in body weight gain and changes in organ weights
    were observed. These effects coincided with a dose-related reduction
    in food and water consumption. At the 83 mg/kg dose, the only effect
    was a slight reduction in water consumption. No significant treatment-
    related histological effects were seen at any dose level (DePass et
    al., 1983).

    7.3.2  Inhalation

         In a short-term inhalation study (Gage, 1970) no adverse effects
    were observed in eight rats (four males and four females) exposed to
    240 mg/m3 (80 ppm) acrylic acid vapour, 6 h/day, 5 days/week for 20
    exposures. Eight rats (four males and four females) exposed at
    900 mg/m3 (300 ppm) showed signs of nasal irritation, lethargy and
    reduced body weight gain. Histological and haematological examinations