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 These sources include online databases, unpublished EPA information, government publications, review documents, and standard reference materials.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 14øC Budavari et al. 1989 Boiling Point 141øC 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 20øC Verschueren 1983 Reactivity Flash Point 68øC 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. 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