EPA 749-F-94-006a

                    CHEMICAL SUMMARY FOR ACRYLIC ACID
                                prepared by
                  OFFICE OF POLLUTON PREVENTION AND TOXICS
                    U.S. ENVIRONMENTAL PROTECTION AGENCY
                              September 1994

     This summary is based on information retrieved from a systematic 
search limited to secondary sources (see Appendix A).  These sources 
include online databases, unpublished EPA information, government 
publications, review documents, and standard reference materials.  No 
attempt has been made to verify information in these databases and 
secondary sources. 

I. CHEMICAL IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES

     The chemical identity and physical/chemical properties of acrylic 
acid are summarized in Table 1.

             TABLE 1.  CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL 
                          PROPERTIES OF ACRYLIC ACID
__________________________________________________________________________

Characteristic/Property      Data                  Reference
__________________________________________________________________________

CAS No.                      79-10-7   
Common Synonyms              2-propenoic acid, 
                             ethylenecarboxylic  
                             acid, vinylformic  
                             acid, acroleic acid   Keith and Walters 1985
Molecular Formula            C3H4O2    
Chemical Structure           CH2 = CH - COOH     
Physical State               colorless liquid       Keith and Walters 1985
Molecular Weight             72.06                  Budavari et al. 1989
Melting Point                14C                   Budavari et al. 1989
Boiling Point                141C                  Budavari et al. 1989
Water Solubility             >10 g/L                Keith and Walters 1985
Density                      d16/4, 1.0621          Budavari et al. 1989
Vapor Density (air = 1)      2.50                   Verschueren 1983
KOC                          not estimated due 
                             to ionization          CHEMFATE 1994
Log KOW                      0.36                   HSDB 1994
Vapor Pressure               3.2 mm Hg at 20C      Verschueren 1983
Reactivity                   
Flash Point                  68C                   Budavari et al. 1989
Henry's Law Constant         3.2 x 10-7 atm m3/mol  HSDB 1994
Fish Bioconcentration        
   Factor                    <1 (estimated)         HSDB 1994
Odor Threshold               1.04 ppm (in air)      HSDB 1994
Conversion Factors           1 ppm = 3.00 mg/m3      
                             1 mg/m3 = 0.33 ppm     Verschueren 1983
_________________________________________________________________________

II. PRODUCTION, USE, AND TRENDS

    A. Production

       There are four acrylic acid producers in the United States. Table 2 
       lists producers, plant locations, and plant capacities. Annual 
       capacity is approximately 1.6 billion pounds.  In 1991, 
       approximately 1.1 billion pounds of acrylic acid were produced. 
       During that same year, 5 million pounds were imported into the 
       US and 75 million pounds were exported (Mannsville 1992).

     B. Use

        Acrylic acid is used in a number of industrial applications. The 
        primary use of acrylic acid, accounting for approximately 
        67 percent of all use, is in the production of acrylic esters 
        and resins, which are used primarily in coatings and adhesives.  
        The fastest growing use of acrylic acid is in the production of 
        superabsorbent polymers.  It is also used in oil treatment 
        chemicals, detergent intermediates, water treatment chemicals, 
        and water absorbent polyacrylic acid polymers (Mannsville 1992).  
        Table 3 shows the estimated 1991 US end-use pattern for acrylic 
        acid.

     C. Trends

        Demand for acrylic acid is expected to increase at a rate of 
        4 to 5 percent per year (Mannsville 1992).

              TABLE 2.  United States Producers of Acrylic Acid
__________________________________________________________________________
     Company               Plant Location           Plant Capacity
                                                (in millions of pounds)
__________________________________________________________________________

     BASF Corporation      Freeport, TX                   300
     Hoechst Celanese      Clear Lake, TX                 450       
     Rohm & Haas           Deer Park, TX                  600
     Union Carbide         Taft, LA                       200
__________________________________________________________________________
Source:  Mannsville 1992.

        
  TABLE 3.  Estimated 1991 United States End-Use Pattern of Acrylic Acid
__________________________________________________________________________

Use of Acrylic Acid                                 Percentage of US
   [typical Standard Industrial                     Acrylic Acid Use
   Classification (SIC)] Code (see end note 1)
__________________________________________________________________________

Acrylate esters (production, SIC 2869)                      67%
Superabsorbent polymers (production, SIC 2821)              21%
Detergents (production, SIC 2841)                            4%
Dispersants (production, SIC 2841)                           3%
Water treatment (production, SIC 2899)                       2%
Miscellaneous (no applicable SIC Code(s))                    3%
__________________________________________________________________________
Source:  Mannsville 1992.

III. ENVIRONMENTAL FATE

     A. Environmental Release

        In 1992, environmental releases of acrylic acid, as reported to 
        the Toxic Chemical Release Inventory by certain types of US 
        industries, include:  4.5 million pounds to underground injection 
        sites, 548 thousand pounds to the atmosphere, 19 thousand 
        pounds to surface water, and 407 pounds to land (TRI92 1994).  
        Acrylic acid is produced naturally by several species of marine 
        algae and has been found in the rumen fluid of sheep (HSDB 1994).

     B. Transport

        Most of the acrylic acid released to the environment is expected 
        to end up in water.  Based on its water solubility and vapor 
        pressure, it is not expected to volatilize from water.  The 
        chemical can be removed from the atmosphere in rain (U.S. EPA 
        1984).  If released to soil the chemical leaches into groundwater 
        or surface waters (U.S. EPA 1984).

     C. Transformation/Persistence

        1. Air - Reaction of acrylic acid with ozone produces glyoxylic 
           acid and formic acid (U.S. EPA 1984).  Polymerization of the 
           acrylic acid monomer occurs in the presence of oxygen 
           (U.S. EPA 1984).  The UV absorption band for the chemical 
           extends to about 320 nm, indicating that direct photolysis 
           may be possible although no information was found (HSDB 1994).
           Acrylic acid reacts with photochemically produced hydroxyl
           radicals and ozone with estimated half-lives of 16.1 hours 
           and 6.5 days, respectively (HSDB 1994).  

        2. Soil - Leaching into ground or surface waters is the major
           route of removal of acrylic acid from soils due to the
           chemical's high water solubility and low vapor pressure 
           (U.S. EPA 1984).  One study indicates that microbial degradation 
           probably occurs as evidenced by the total degradation of 
           acrylic acid within 15 days of being added to soil (HSDB 1994).  
           Direct photolysis may occur at the soil surface (U.S. EPA 1984).

        3. Water - Acrylic acid is removed from water by microbial
           degradation and chemical and photochemical reactions (U.S. EPA 
           1984; HSDB 1994).  In an acclimated sewage inoculum, 81% of 
           the acrylic acid was degraded to carbon dioxide in 22 days 
           (HSDB 1994).  Bacteria capable of degrading the chemical 
           include Rhodococcus sp. and Arthobacter sp. (U.S. EPA 1984).  
           Polymerization in the presence of dissolved oxygen may also 
           occur as well as photoreaction at the water surface 
           (U.S. EPA 1984).

        4. Biota - Based on an estimated fish bioconcentration factor 
           of 0.78, bioaccumulation of acrylic acid is not expected 
           to be significant (HSDB 1994).

IV. HUMAN HEALTH EFFECTS

    A. Pharmacokinetics

       1. Absorption - Acrylic acid is absorbed from dermal contact,
          inhalation, or ingestion (U.S. EPA 1994; ACGIH 1991).  The
          gastrointestinal tract is a major site of absorption even
          after exposure to acrylic acid vapor (ACGIH 1991).  In the
          upper respiratory tract, acrylic acid appears to dissolve 
          in the mucous membranes  of the nasopharynx and nasal 
          turbinates (U.S. EPA 1984); there is very little retention 
          in the lungs (ACGIH 1991).

       2. Distribution - Metabolism and excretion do not appear to be
          so fast as to prevent widespread distribution of unchanged
          acrylic acid in the body (U.S. EPA 1994).  After oral exposure 
          in the rat, the highest concentrations of the chemical were 
          found in the liver, fat, small intestine, brain, and kidneys 
          (U.S. EPA 1984).  One hour after inhalation exposure the 
          highest concentration of acrylic acid was found in urine 
          followed by stomach, intestinal contents, liver, and kidney; 
          mucocilliary clearance may account for stomach and intestinal 
          levels (U.S. EPA 1984).
               
       3. Metabolism - Acrylic acid is metabolized as a short-chained
          fatty acid by the liver (ACGIH 1991).  Carbon dioxide is 
          the major metabolite (U.S. EPA 1984).  Disposition studies, 
          using radiolabelled acrylic acid administered by several 
          routes, show that nearly all of the acrylic acid is absorbed 
          and metabolized to carbon dioxide, with very little radio-
          activity in the urine or the feces (U.S. EPA 1994).

       4. Excretion - Acrylic acid is eliminated primarily in expired
          air.  One hour after either oral or inhalation exposure in 
          the rat, 60% of the administered dose was excreted as CO2 
          in expired air and 6% was excreted in the urine (U.S. EPA 
          1984; ACGIH 1991).  Elimination is biphasic following oral 
          or inhalation exposure with half-times of 39.3 and 30.6 
          minutes, respectively, for the initial phase; values were 
          not reported for the second phase (U.S. EPA 1984).

    B. Acute Toxicity

       Moderate to high levels of acrylic acid in air can cause eye and
       nasal damage and systemic toxicity resulting in damage to the
       kidneys, the liver, and the lungs of laboratory animals.  It is
       unlikely that humans will experience these systemic effects 
       because of the potential of acrylic acid to irritate the skin, 
       eye, and respiratory tract. 

       1. Humans - Liquid acrylic acid is irritating to the eyes and
          skin and vapors are irritating to the respiratory tract 
          (HSDB 1994).

       2. Animals - The oral LD50 for acrylic acid ranges from 250 mg/kg 
          for rabbits to 3200 mg/kg for rats (ACGIH 1991).  In rabbits, 
          the dermal LD50 ranges from 295 to 950 mg/kg (IARC 1979).  One 
          half of the rats in a test group (number of animals not reported) 
          died when exposed to vapor concentrations approaching 
          saturation in air (IARC 1979).  A 1% solution was the lowest 
          that produced "significant injury" to the rabbit eye (IARC 1979). 

          Inhalation exposure of rats to 6000 ppm for 5 hours resulted 
          in nose and eye irritation, respiratory difficulties, and 
          unresponsiveness; death occurred in one animal with lung 
          hemorrhage and degeneration of the liver and kidney tubules 
          (ACGIH 1991). Inhalation exposure of rats to 1500 ppm for 6-hours 
          caused nasal discharge, lethargy, weight loss, and congested 
          kidneys (ACGIH 1991; Guest et al. 1982).

     
   C. Subchronic/Chronic Toxicity

      Degeneration of the nasal olfactory epithelium occurred in rats 
      and mice exposed by inhalation to repeat doses of acrylic acid.  
      EPA has derived an inhalation reference concentration (RfC) 
      (see end note 2) of 0.001 mg/m3 for acrylic acid, based on adverse 
      effects in the nasal epithelium of laboratory animals.  Rats 
      exposed to repeat doses of acrylic acid at high levels in drinking 
      water had decreased body and organ weights.

      1. Humans - No information was found in the secondary sources 
         searched regarding the chronic toxicity of acrylic acid to humans.

      2. Animals - Based on the following study showing degeneration of 
         the nasal olfactory epithelium, the U.S. EPA (1994) calculated 
         a chronic RfC (reference concentration) for acrylic acid of 0.001 
         mg/m3 (or 0.0003 ppm).  Male and female rats and mice were exposed 
         by inhalation to 5, 25, or 75 ppm acrylic acid, 6 hours/day, 
         5 days/week for 13 weeks (U.S. EPA 1994; ACGIH 1991).  Focal 
         degeneration of the olfactory epithelium was observed in rats only 
         at the highest dose but mice were affected in a dose-responsive 
         manner.  No other gross or histopathologies were observed. The 
         lowest-observed-adverse effect level for the study was 14.94 
         mg/m3.

         No adverse effects were observed in rats exposed to 80 ppm, 
         6 hours/day, 5 days/week, for 4 weeks (ACGIH 1991).  Rats exposed 
         to 238 ppm, 4 hours/day, for 5 weeks had irreversible eye and skin 
         changes, reduced body weight, increased reticulocyte counts, and   
         reduced urine concentrating capacity of the kidney; histopathology 
         revealed injury to the gastric mucosa and inflammation of the 
         upper respiratory tract (ACGIH 1991; Guest et al. 1982).  
         Degeneration of the nasal mucosa was also observed in rats exposed 
         to 223 ppm and in mice exposed to 25, 74, or 223 ppm 6 hours/day, 
         5 days/week, for 2 weeks (U.S. EPA 1994).

         Groups of 50 male and female Wistar rats were administered acrylic 
         acid  in drinking water at concentrations of 0, 120, 400, or 1200 
         ppm (estimates to be 0, 8, 27, and 78 mg/kg/day; U.S. EPA 1994).  
         Exposures were for 26 months in males and 28 months in females.  
         No clinical signs of toxicity were observed; there were no clear 
         histopathological indications of organ toxicity.  The NOAEL for 
         this study is 78 mg/kg/day.

         Rats were exposed to acrylic acid in drinking water at 83, 250, or 
         750 mg/kg/day for 90 days (U.S. EPA 1994).  At the high dose 
         (in both males and females) a reduction in body and organ weights 
         and decreased water intake were observed; the NOAEL for changes 
         in body weight and in organ weight was 250 mg/kg/day.  There were 
         no treatment-related histopathologies observed.  In a gavage 
         study, administering 150 or 375 mg/kg/day in water to Wistar rats 
         (10/sex/group), acrylic acid was lethal to one-half and three 
         quarters of the animals in the low and high dose, respectively.  
         Adverse effects were observed in the gastrointestinal tract, the 
         kidneys, and the respiratory tract. 

     D. Carcinogenicity

       There is inadequate evidence of carcinogenicity of acrylic acid 
       in humans and in animals.  Limited information indicates that when 
       applied dermally, acrylic acid appears to be a weak carcinogen and 
       initiator in mice.  IARC classifies acrylic acid as group 3, not 
       classifiable as to its carcinogenicity to humans.

       1. Humans - No information was found in the secondary sources
          searched regarding the carcinogenicity of acrylic acid to humans.
               
       2. Animals - Twenty-five microliters of acrylic acid was applied 
          as a 4% solution to the backs of mice 3 times/week for 1.5 years 
          with or without prior initiation by dimethylbenz[a]nthracene 
          (DMBA) (IARC 1979; ACGIH 1991).  One squamous cell carcinoma and 
          3 papillomas occurred in the acrylic acid plus DMBA treated 
          animals and 2 squamous cell carcinomas occurred in the acrylic 
          acid alone group versus no tumors in the control animals.  
          Acrylic acid is not listed among the chemicals studied or to 
          be studied by the National Toxicology Program (NTP 1994).  IARC 
          (1979 and 1987) classifies acrylic acid as group 3, not 
          classifiable as to its carcinogenicity to humans, based on 
          inadequate human and animal evidence.

     E. Genotoxicity
       
         Acrylic acid was negative for mutagenicity in the Salmonella/
         microsome test with or without activation (U.S. EPA 1984; HSDB 
         1994).  The chemical inhibited the incorporation of thymidine 
         into DNA and of uracil into RNA in Staphylococcus aureus and 
         Escherichia coli (U.S. EPA 1984).

     F. Developmental/Reproductive Toxicity

        Acrylic acid has been tested for developmental and reproductive
        effects under Section 4 of the Toxics Substances Control Act.  
        When given in the drinking water, acrylic acid caused reduced 
        pup weight gain in a two generation study.  EPA has derived an 
        oral reference dose (RfD) (see end note 3) of 0.5 mg/kg/day for 
        acrylic acid, based on this effect.  No other adverse effects on 
        reproductive parameters have been observed following oral 
        administration of acrylic acid to rats.  No adverse developmental 
        effects were observed in laboratory animals exposed to acrylic acid 
        vapor.

        1. Humans - No information was found in the secondary sources 
           searched regarding the developmental or reproductive toxicity of 
           acrylic acid to humans.

        2. Animals - Based on the information described below for reduced 
           weight gain in offspring of treated rats, the U.S. EPA (1994) 
           calculated a chronic RfD (reference dose) for acrylic acid of 
           0.5 mg/kg/day.  In a two-generation reproductive study in rats 
           (25/sex/group), acrylic acid was administered in drinking water 
           at 500, 2500, or 5000 ppm (estimated to be 53, 240, 
           460 mg/kg/day) (U.S. EPA 1994).  No effects were observed for 
           reproductive indices in either generation.  However, there was 
           a significant decrease in pup body weight gain in the F1 and F2 
           generations exposed to 2500 and 5000 ppm that was most 
           pronounced prior to weaning and coincided with decreased 
           maternal water intake; the no-observed-adverse effect level 
           (NOAEL) for reduced pup weight in this study was 500 ppm 
           (53 mg/kg/day).  

           In a single generation study male and female rats were 
           administered acrylic acid in drinking water at doses of 83,
           250, or 750 mg/kg/day for 90 days prior to mating and females 
           continued throughout gestation and lactation (ACGIH 1991; 
           U.S. EPA 1994).  No effects on reproductive indices were 
           observed but treatment related decreases in body weight gain and 
           reduced food and water consumption occurred in the F0 and F1 
           animals.  

           Maternal toxicity from inhalation exposure was observed in 
           the two high dose groups of 30 pregnant Sprague-Dawley rats
           exposed to 40, 120, or 360 ppm on gestation days 6-15 and 
           in the two high dose groups of 16 pregnant New Zealand 
           rabbits exposed to 25, 75, or 225 ppm on gestation days 6-18.  
           No exposure related adverse effects on fetal development 
           occurred.  The NOAELs for developmental effects were 360 ppm 
           in rats and 225 ppm in rabbits (U.S. EPA 1994). U.S. EPA (1994) 
           concluded that developmental effects are not critical to the 
           oral reference dose derivation.

     G. Neurotoxicity

        Based on the available information, acrylic acid does not appear 
        to be a neurotoxicant when administered to rats at very high 
        doses.

        1. Humans - No information was found in the secondary sources
           searched regarding the neurotoxicity of acrylic acid to humans.

        2. Animals - Acrylic acid exposures to rats of 1500 ppm for 
           6-hours caused lethargy (ACGIH 1991; Guest et al. 1982) but 
           this was probably due to other toxic effects such as respira-
           tory distress (see section IV. B) and not direct neurotoxicity.

V. ENVIRONMENTAL EFFECTS

   Acrylic acid has moderate acute toxicity in aquatic organisms; a 
   toxicity value between >1 mg/L and 100 mg/L has been reported.  Due 
   to the breakdown of acrylic acid in the environment and its moderate 
   acute toxicity, the chemical would not be expected to be toxic 
   to aquatic or terrestrial animals at levels normally found in the 
   environment.

   A. Toxicity to Aquatic Organisms

      LC50 values for Leuciscus idus (golden orfe) and Lepomis macrohirus 
      (bluegill) are 315 mg/L (no time given) and 188 mg/L (24-hour), 
      respectively (U.S. EPA 1984).  The 48-hour LC50 for Daphnia magna 
      is 50 mg/L (U.S. EPA 1984).

   B. Toxicity to Terrestrial Organisms

      No information was found in the secondary sources searched regarding 
      the toxicity of acrylic acid to terrestrial animals. Based on the 
      range of LD50 values in laboratory animals (250-3200 mg/kg) and 
      the irritating properties of the chemical, which would discourage 
      continued exposure, it is unlikely that acrylic acid would be toxic 
      to terrestrial animals at levels normally found in the environment.

   C. Abiotic Effects

      According to the definition provided in the Federal Register (1992), 
      acrylic acid is a volatile organic compound (VOC) substance.  
      As a VOC, acrylic acid can contribute to the formation of photo-
      chemical smog in the presence of other VOCs.

VI. EPA/OTHER FEDERAL AND OTHER GROUP ACTIVITY

     The Clean Air Act Amendments of 1990 list acrylic acid as a hazardous 
     air pollutant.  NIOSH and the ACGIH have added a skin notation to 
     their recommended workplace air exposure limits, indicating that 
     workplace dermal exposure should be controlled as well.

     Federal agencies and other groups that can provide additional 
     information on acrylic acid are listed in Tables 4 and 5.

TABLE 4.  EPA OFFICES AND CONTACT NUMBERS FOR INFORMATION ON ACRYLIC ACID.
________________________________________________________________________
EPA OFFICE            LAW                                PHONE NUMBER
________________________________________________________________________
Pollution Prevention  Toxic Substances Control Act
 & Toxics               (Sec. 4/8A/8D/8E)                (202) 554-1404
                      Emergency Planning and Community
                        Right-to-Know Act (EPCRA)
                        Regulations (Sec. 313)           (800) 424-9346
                        Toxics Release Inventory data    (202) 260-1531
Air                   Clean Air Act                      (919) 541-0888
Solid Waste &         Comprehensive Environmental
 Emergency Response    Response, Compensation, and
                       Liability Act (Superfund)/
                      Resource Conservation and Recovery
                       Act / EPCRA (Sec. 304/311/312)    (800) 424-9346
__________________________________________________________________________

        TABLE 5.  OTHER FEDERAL OFFICES/OTHER GROUP CONTACT NUMBERS FOR 
                       INFORMATION ON ACRYLIC ACID
__________________________________________________________________________
Other Agency/Department/Other Group                 Contact Number
__________________________________________________________________________

American Conference of Governmental Industrial 
   Hygienists 
   Recommended TLV-TWA (see end note 4):  2 ppm; 
   [skin] (see end note 5) (ACGIH 1993-1994)        (513) 742-2020
Consumer Product Safety Commission                  (301) 817-0994
Food & Drug Administration                          (301) 443-3170
National Institute for Occupational Safety & Health
   Recommended TWA (see end note 6): 2 ppm; 
   [skin] (NIOSH 1992)                              (800) 356-4674
__________________________________________________________________________

VII.  END NOTES

1.  Standard Industrial Classification code is the statistical 
classification standard for all Federal economic statistics.  The code
provides a convenient way to reference economic data on industries of 
interest to the researcher.  SIC codes presented here are not intended to
be an exhaustive listing; rather, the codes listed should provide an
indication of where a chemical may be most likely to be found in commerce.

2.  The RfC is an estimate (with uncertainty spanning perhaps an order of
magnitude) of the daily exposure level for the human population, including
sensitive subpopulations, that is likely to be without an appreciable risk
of deleterious effects during the time period of concern.

3.  The RfD is an estimate (with uncertainty spanning perhaps an order of
magnitude) of the daily exposure level for the human population, including
sensitive subpopulations, that is likely to be without an appreciable risk
of deleterious effects during the time period of concern.

4.  TLV-TWA, threshold limit value--time-weighted average

5.  A [skin] notation indicates that air sampling is not sufficient to 
accurately quantitate exposure.  Measures to prevent significant cutaneous
absorption may be required.

6.  TWA, time-weighted average.

VIII.  CITED REFERENCES

ACGIH. 1991. American Conference of Governmental Industrial Hygienists, 
Inc. Documentation of the Threshold Limit Values and Biological Exposure 
Indices, 6th ed., pp. 26-29.

ACGIH. 1993-1994. American Conference of Governmental Industrial 
Hygienists, Inc. Threshold Limit Values for Chemical Substances and 
Physical Agents and Biological Exposure Indices. p. 12.

AQUIRE. 1994. EPA ERL-Duluth's Aquatic Ecotoxicology Data Systems. U.S. 
EPA, Duluth, MN. Retrieved August 1994.

Budavari S, O'Neil MJ, Smith A, Heckelman PE (Eds.). 1989. The Merck 
Index, 11th ed. Merck & Co., Rahway, NJ, p. 21.

CHEMFATE. 1994. Syracuse Research Corporation's Environmental Fate Data 
Bases. Syracuse Research Corporation, Syracuse, NY. Retrieved 9/1/94.

Federal Register.  1992.  Part 51 - Requirements for Preparation, 
Adoption, and Submittal of Implementation Plans. Fed. Reg. 57:3945.

Guest D, Katz GV, Astill BD. 1982. Aliphatic Carboxylic Acids. In: Patty's
Industrial Hygiene and Toxicology, 3rd ed., Vol, 2C. GD Clayton and FE 
Clayton, eds. John Wiley & Sons, New York. pp. 4954-4955.

HSDB. 1994. Hazardous Substances Data Bank. MEDLARS Online Information 
Retrieval System, National Library of Medicine. Retrieved August 1994.

IARC. 1987. International Agency for Research on Cancer. IARC Monographs 
on the Evaluation of the Carcinogenic Risk of Chemicals to Humans, Overall 
Evaluations of Carcinogenicity: An Updating of IARC Monographs Volumes 1 
to 42, Supp. 7. IARC, Lyon, France. p. 56.

IARC. 1979. International Agency for Research on Cancer. IARC Monographs 
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Monomers, Plastics, and Synthetic Elastomers, and Acrolein, Vol. 19. IARC, 
Lyon, France. pp. 47-52.

Keith LH and Walters DB (Eds.). 1985. Compendium of Safety Data Sheets for
Research and Industrial Chemicals, Part I. VCH Publishers, Deerfield 
Beach, pp. 58-59.

Mannsville, 1992.  Chemical Products Synopsis, Acrylic Acid.  Mannsville 
Chemical Products Corporation, 1992.

NIOSH. 1992. National Institute for Occupational Safety and Health. NIOSH
Recommendations for Occupational Safety and Health. Compendium of Policy
Documents and Statements. NIOSH, Cincinnati, OH. p. 47.

NTP. 1994. National Toxicology Program. Management Status Report Produced 
from NTP Chemtrack System, 1/11/94. NTP, Research Triangle Park, NC.

TRI92. 1994. 1992 Toxics Release Inventory. Office of Pollution 
Prevention and Toxics, U.S. EPA, Washington, D.C., p. 86.

U.S. EPA. 1984. U.S. Environmental Protection Agency. Health and Envir-
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Research and Development, U.S. EPA, Cincinnati, OH, 25 pp. ECAO-CIN-P048.

U.S. EPA. 1994. U.S. Environmental Protection Agency. Integrated Risk 
Information System (IRIS) Online. Office of Health and Environmental 
Assessment, U.S. EPA, Cincinnati, OH.

Verschueren K (Ed.). 1983. Handbook of Environmental Data on Organic 
Chemicals, 2nd ed. Van Nostrand Reinhold Co., New York, p. 161.

APPENDIX A.  SOURCES SEARCHED FOR FACT SHEET PREPARATION

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Exposure Indices, Sixth edition. American Conference of Governmental 
Industrial Hygienists, Inc., Cincinnati, OH.

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ATSDR.  1989-1994.  Agency for Toxic Substances and Disease Registry. 
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BIODEG.  1994.  Syracuse Research Corporation's Environmental Fate Data 
Bases. Syracuse Research Corporation, Syracuse, NY.

Budavari S, O'Neil MJ, Smith A, Heckelman PE (Eds.).  1989.  The Merck 
Index, 11th ed.  Rahway, N.J.:  Merck & Co., Inc.

CHEMFATE.  1994.  Syracuse Research Corporation's Environmental Fate Data 
Bases.  Syracuse Research Corporation, Syracuse, NY.

Clayton GD, Clayton FE.  1981-1982.  Patty's Industrial Hygiene and 
Toxicology, 3rd ed., Vol. 2C.  New York:  John Wiley & Sons.

GENETOX.  1994.  U.S. EPA GENETOX Program, computerized database. 

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IARC. 1979-1994. International Agency for Research on Cancer.  IARC 
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NIOSH (National Institute for Occupational Safety and Health).  1992.  
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Produced from NTP Chemtrack system.  April 8, 1994.  National Toxicology 
Program, Research Triangle Park, NC.

OSHA.  1994.  Occupational Safety and Health Administration.  Table Z-2.  
Limits for Air Contaminants.

RTECS.  1994.  Registry of Toxic Effects of Chemical Substances.  MEDLARS 
Online Information Retrieval System, National Library of Medicine.

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EPA, Office of Pollution Prevention and Toxics (7408).

U.S. Air Force.  1989.  The Installation Restoration Toxicology Guide, 
Vols. 1-5.  Wright-Patterson Air Force Base, OH.

U.S. EPA (U.S. Environmental Protection Agency).  1991.  Table 302.4 List 
of Hazardous Substances and Reportable Quantities 40 CFR, part 302.4:3-271.

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Advisories.  Office of Drinking Water, U.S. Environmental Protection
Agency, 
Washington, D.C.

U.S. EPA.  Most Current.  Health Effects Assessment Summary Tables.  
Cincinnati, OH:  Environmental Criteria and Assessment Office, U.S.EPA.

U.S. EPA reviews such as Health and Environmental Effects Documents, 
Health and Environmental Effect Profiles, and Health and Environmental 
Assessments.

U.S. EPA.  1994.  Integrated Risk Information System (IRIS) Online.  
Cincinnati, OH:  Office of Health and Environmental Assessment.