EPA 749-F-94-005a CHEMICAL SUMMARY FOR ACRYLAMIDE prepared by OFFICE OF POLLUTION 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 These sources include online databases, unpublished EPA information, government publications, review documents, and standard reference materials.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 acrylamide are summarized in Table 1. TABLE 1. CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL PROPERTIES OF ACRYLAMIDE ________________________________________________________________________ Characteristic/Property Data Reference ________________________________________________________________________ CAS No. 79-06-1 Common Synonyms 2-propenamide Budavari et al. 1989 Molecular Formula C3H5NO Chemical Structure CH2=CH-C-NH2 || O Physical State flake-like crystals Budavari et al. 1989 Molecular Weight 71.08 Budavari et al. 1989 Melting Point 84.5øC Budavari et al. 1989 Boiling Point 125øC Budavari et al. 1989 Water Solubility 2155 g/L at 30øC Budavari et al. 1989 Density d30/4, 1.122 Budavari et al. 1989 Vapor Density (air = 1) 2.46 Verschueren 1983 KOC no significant adsorption HSDB 1994 Log KOW -0.67 (estimated) HSDB 1994 Vapor Pressure 7 x 10-3 torr at 20øC ACGIH 1991 Reactivity Polymerizes violently when heated Keith and Walters 1985 Flash Point 138øC Keith and Walters 1985 Henry's Law Constant 302 x 10-10 atm-m3/mol HSDB 1994 Fish Bioconcentration Factor <2 (measured) HSDB 1994 Odor Threshold odorless Keith and Walters 1985 Conversion Factors 1 ppm = 2.95 mg/m3 1 mg/m3 = 0.34 ppm Verschueren 1983 ________________________________________________________________________ II. PRODUCTION, USE, AND TRENDS A. Production There are three acrylamide producers in the United States. Table 2 lists producers, plant locations, and plant capacities. Annual capacity is approximately 171 million pounds. In 1992, approxi- mately 100 million pounds of acrylamide were produced in the United States. During that same year, 15 million pounds were imported into the United States, and exports were estimated to be less than 2 million pounds (Mannsville 1993). B. Use Acrylamide is used in a number of industrial applications. The primary use of acrylamide, accounting for about 90 percent of all use, is in the production of polyacrylamide polymers. Polyacrylamide polymers have been used as additives in the coagulation process of water treatment. Because the poly- acrylamide was often contaminated with residual acrylamide monomer, EPA now (effective July 30, 1994) requires a treatment technique for acrylamide (see section VI, Table 4). The treatment technique is designed to limit levels of acrylamide in products used in the water treatment, storage, and distribution process. Acrylamide is also used as a chemical intermediate in the production of N-methylol acrylamide and N-butoxyacrylamide and as a superabsorbent in disposable diapers, medical products, and agricultural products. Small amounts of acrylamide are also used in sugar beet juice clarification, adhesives, binders for seed coatings and foundry sand, printing ink emulsion stabilizers, thickening agents for agricultural sprays, latex dispersions, textile printing paste, and water retention aids (Mannsville 1993). Table 3 shows the estimated 1993 US end-use pattern for acrylamide. C. Trends Demand for acrylamide is expected to increase moderately during the next few years (Mannsville 1993). TABLE 2. United States Producers of Acrylamide ________________________________________________________________________ Company Plant Location Plant Capacity (in millions of pounds) ________________________________________________________________________ Cytec Fortier, LA 70 Dow Chemical Midland, MI 66 Nalco Garyville, LA 35 ________________________________________________________________________ Source: Mannsville 1993. TABLE 3. Estimated 1993 United States End-Use Pattern of Acrylamide ________________________________________________________________________ Use of Acrylamide Percentage of US [typical Standard Industrial Acrylamide Use Classification (SIC) Code] (see end note 1) ________________________________________________________________________ Polyacrylamide polymers (production, SIC 2821) 90% Chemical intermediate (production, SIC 2869) 9% Miscellaneous (no applicable SIC Code(s)) 1% ________________________________________________________________________ Source: Mannsville 1993. III. ENVIRONMENTAL FATE A. Environmental Release In 1992, environmental releases of acrylamide, as reported to the Toxic Chemical Release Inventory by certain US industries, included 28 thousand pounds to the atmosphere, 10 thousand pounds to surface water, 4.2 million pounds to underground injection sites, and 963 pounds to land (TRI92 1994). Concentrations of 0.3 ppb to 5 ppm acrylamide have been measured in various rivers near industries that use acrylamide and/or polyacrylamides (HSDB 1994). Cases of human poisoning have been documented from well water contaminated with acrylamide (no amounts given) from sewer grouting (HSDB 1994). Atmospheric levels around six US plants averaged >0.2 microgram/m3 (0.007 ppb) in either vapor or particulate form (HSDB 1994). B. Transport Most of the acrylamide released to the environment is expected to end up in water. Because of its low vapor pressure (7x10-3 torr), the chemical is not likely to volatilize into the atmosphere (HSDB 1994). Should the chemical reach the atmosphere, it most likely exists adsorbed to particulate matter. Its physical and chemical properties indicate that very little of the chemical will exist in the vapor phase. Acrylamide can be removed from the atmosphere in rain water (HSDB 1994). Acrylamide leaches readily into ground water from soils as predicted by its high water solubility (HSDB 1994). C. Transformation/Persistence 1. Air - In the atmosphere, acrylamide reacts with photochemically produced hydroxyl radicals; the estimated half-life is 6.6 hours (HSDB 1994). 2. Soil - Biodegradation is the major route of removal of acrylamide from soils (U.S. EPA 1985). In aerobic soils, the chemical is 74-94% degraded in 14 days while in waterlogged, anaerobic soil 64-89% is degraded in 14 days (U.S. EPA 1985). Depending on the soil type, estimated half-lives range from 21 to 36 hours (U.S. EPA 1985). 3. Water - Biodegradation is also the major route of removal of acrylamide from water. Several microorganisms capable of utilizing acrylamide as a sole carbon and nitrogen source have been isolated, including Arthrobacter sp., Norcardia rhodochrous, Bacillus spaericus, Pseudomonas putrefaciens, and Rhodococcus sp. (U.S. EPA 1985). Acclimation of microorganisms greatly increases the rate of biodegradation (HSDB 1994; U.S. EPA 1985). Complete degradation of 10-20 ppm acrylamide in river water occurred in about 12 days with nonacclimated microorganisms; when the microorganisms were acclimated, degradation was complete in 2 days (U.S. EPA 1985). 4. Biota - Fish bioconcentration factors (BCF) for the carcass and viscera of fingerling trout are 0.86 and 1.12, respectively, indicating that no appreciable bioaccumulation of acrylamide is expected (HSDB 1994). IV. HUMAN HEALTH EFFECTS A. Pharmacokinetics 1. Absorption - Toxic effects of acrylamide have been observed after dermal and oral exposure, indicating absorption by these routes (U.S. EPA 1985). The chemical can also be absorbed through mucous membranes and the lung (HSDB 1994). 2. Distribution - After i.v. administration of radioactive acrylamide to rats, the chemical was found in muscle, skin, fat, blood, testes, liver, kidney, small intestine, lung, brain, spinal chord, and sciatic nerve (U.S. EPA 1985). In mice, the distal half of the sciatic nerve has been shown to accumulate 2.4 times as much acrylamide as the proximal half (U.S. EPA 1985). Acrylamide crossed the placenta with uniform fetal distribution following i.v. administration to rats, rabbits, beagle dogs, and miniature pigs "late in gestation" (U.S. EPA 1985). 3. Metabolism - The major route of acrylamide metabolism is conjugation to glutathione to produce N-acetyl-S-(3-amino- 3-oxypropyl)cysteine (U.S. EPA 1985). Conjugation is catalyzed both enzymatically and nonenzymatically in liver, brain, and skin (IARC 1985). Mercapturic acid and cysteine-S-propionamide have been identified in the urine of rats after oral administration (U.S. EPA 1985). 4. Excretion - The majority of a dose of acrylamide is excreted in the urine as the glutathione conjugate. After a single i.v. dose to a rat, 60% was excreted in the urine within 3 days (U.S. EPA 1985). Glutathione-conjugated acrylamide is also excreted in the bile. Of an administered oral dose, 71% was detected in urine and 6% in feces within 7 days; 15% of the dose appeared in the bile within 6 hours indicating that enterohepatic circulation occurs (U.S. EPA 1985). B. Acute Toxicity Acrylamide is a skin and respiratory tract irritant. Reported oral LD50 values in rats range from 159 mg/kg to 300 mg/kg. 1. Humans - Acrylamide is irritating to the skin and respiratory tract (IARC 1985). 2. Animals - Oral 24-hour LD50 values of acrylamide for rats range from 203 to 300 mg/kg; oral 168-hour LD50 values range from 159 to 191 mg/kg (U.S. EPA 1985). A 10% aqueous solution applied to intact rabbit skin did not cause irritation but when applied to abraded skin produced slight reddening and edema (ACGIH 1991). In the eyes of a rabbit, a 10% solution caused pain and slight conjunctival irritation that completely healed after 24 hours (ACGIH 1991). C. Subchronic/Chronic Toxicity Adverse effects in animals administered small amounts of acrylamide include general systemic toxicity and changes in hematological parameters. 1. Humans - Acrylamide is a human neurotoxicant (effects are described in section IV.G). 2. Animals - Male and female rats were given 0.05, 0.2, 1, 5, or 20 mg/kg/day in drinking water for 92-93 days (U.S. EPA 1985). Gross alterations occurring at the highest dose included perineal soiling, depletion of adipose tissue, decreased liver size, darkened kidneys, mottled lungs, atrophy of skeletal muscle, distention of urinary bladder, and thickening of the stomach; decreases in packed cell volume, total erythrocyte counts and hemoglobin concentrations occurred in both sexes at 20 mg/kg/day and in females at 5 mg/kg/day. Decreased body weight in male rats given 2 mg/kg/day in drinking water (section IV.D) for 738-746 days was the only noncarcino- genic effect observed (U.S. EPA 1985). Acrylamide is a carcinogen and a neurotoxicant to animals. These effects are described in sections IV. D and IV. G, respectively. D. Carcinogenicity Although inadequate evidence is available from human studies, several laboratory animal studies have shown that acrylamide causes a variety of tumors in rats and mice. Acrylamide has been classified by the U.S. EPA as a B2, a probable human carcinogen, and by IARC as a 2B, a possible human carcinogen. 1. Humans - Two epidemiologic studies of occupational exposures to acrylamide were inadequate to evaluate the carcinogenic potential of the chemical to humans (U.S. EPA 1994). Limita- tions included lack of exposure data, inadequate study size, multiple chemical exposures, and incomplete ascertainment of cause of death. 2. Animals - Male and female rats were given 0.01, 0.1, 0.5, or 2.0 mg/kg/day acrylamide in drinking water for 2 years (U.S. EPA 1994). At the two highest doses, a statistically signifi- cantly increased incidence of tumors was seen in the scrotum, adrenal, thyroid, CNS, mammary, oral cavity, and uterus. Acrylamide has been shown to cause lung and skin tumors in mice when administered by gavage, dermally, or intraperitoneally (U.S. EPA 1994; ACGIH 1991). Male and female mice given 6.25, 12.5, or 25 mg/kg, 3 times/week, for 8 weeks by gavage had a dose-responsive increase in lung adenomas (IARC 1985). Based on sufficient evidence of carcinogenicity in animals, acrylamide has been classified by the U.S. EPA as B2, probable carcinogen in humans (U.S. EPA 1994). The oral slope factor (see end note 2) for acrylamide is 4.5 per (mg/kg)/day (U.S. EPA 1994). The drinking water unit risk for acrylamide is 1.3 x 10-4 per (microgram/L) (see end note 3) (U.S. EPA 1994). Acrylamide has been classified by IARC (1987) as 2B, possibly carcinogenic to humans, based on inadequate data in humans but sufficient evidence in animals. E. Genotoxicity Acrylamide causes chromosomal aberrations, dominant lethality, sister chromatid exchanges and unscheduled DNA synthesis in various in vitro and in vivo systems (U.S. EPA 1994). When administered at a level of 500 ppm in the diet for 3 weeks in mice acrylamide caused a high frequency of sister chromatid exchanges and breaks (U.S. EPA 1985). F. Developmental/Reproductive Toxicity No information was found on the developmental/reproductive effects of acrylamide in humans. Acrylamide does not appear to cause structural developmental defects by oral administration to rats. Testicular atrophy and decreased fertility have been reported in male mice given acrylamide by mouth. 1. Humans - No information was found in the secondary sources searched regarding the developmental or reproductive toxicity of acrylamide to humans. 2. Animals - Pregnant rats received 20 mg/kg/day acrylamide by gavage on days 7-17 of gestation (U.S. EPA 1985). One day after birth, pups exposed in utero and unexposed pups were divided and foster-nursed to either treated or untreated dams. At 2 weeks of age, binding of dopamine receptors by radioligand was significantly reduced in male pups exposed to acrylamide in utero regardless of whether they nursed on treated or control dams; reduced dopamine receptor binding occurred in female pups that nursed on treated dams regardless of in utero exposure. These differences of receptor binding were resolved by 3 weeks of age (U.S. EPA 1985). Female rats were treated with 25 or 50 ppm in the diet 2 weeks prior to mating and continued through day 19 of gestation (U.S. EPA 1985). At birth there were no differences in litter size, fetal weight, viability, or gross malformations. At weaning, histopathology showed some degeneration of the sciatic and optic nerves of the treated pups. Normal growth and development occurred in pups from dams given 200 ppm acrylamide in feed from mating to parturition (ACGIH 1991). Slight decreases in fetal weights coincided with maternal toxicity in rats fed 400 ppm for 20 days after mating (ACGIH 1991). Injection of fertilized chicken eggs with 0.03-0.6 mg acrylamide on day 5, 6, or 7 of incubation increased mortality and leg deformities among surviving chicks (IARC 1985). Injection of 0.007, 0.07, or 0.7 mg on day 3 resulted in increased death but no malformations. Male mice treated with 0.5 mmol/kg (0.035 g/kg) by gavage 2 times/week, for 8 weeks had testicular atrophy, reduced numbers of spermatozoa, degenerating spermatids and spermatocytes, and multinucleate giant cells (U.S. EPA 1985). A single i.p. injection to mice of 50, 100, or 150 mg/kg caused decreased mitosis in spermatogonia within 24 hours. Testicular degenera- tion was also seen in male rats given 400 ppm in the diet for 90 days (ACGIH 1991). Testicular and uterine atrophy were observed in male and female rats exposed to 20 mg/kg/day in drinking water for 92-93 days (U.S. EPA 1985). Male rats receiving 0.5, 2, or 5 mg/kg/day for 10 weeks were mated to unexposed females (HSDB 1994). Females mated to high dose males had differences (not defined) in total number of implants/litter, number of viable implants/litter, pre- and post implantation losses, and number of resorptions when compared to females mated to control males. Male and female rats were given 0.5, 2, or 5 mg/kg/day acrylamide in drinking water for 10 weeks prior to mating, and females continued exposure during gestation and lactation (HSDB 1994). The fertilityindex and number of actual pregnancies decreased in the high dose group as compared to unexposed controls. G. Neurotoxicity Acrylamide is a neurotoxin by either oral (in animals) or inhalation exposure (in humans and in animals). Toxic effects are central and peripheral neuropathy causing drowsiness, hallucinations, distal numbness, and ataxia. Recovery is possible after cessation of exposure. EPA has derived an oral reference dose (RfD)(see end note 4) of 0.0002 mg/kg/day for acrylamide, based on adverse nervous system effects in laboratory animals. 1. Humans - Studies of the effects of acrylamide in humans indicate that neurotoxicity, including paresthesias in the fingers, coldness, numbness in lower limbs, and weakness of the hands and feet; no additional detail is provided (U.S. EPA 1985). Acrylamide is a neurotoxin with an affinity for the peripheral ends of the spinal nerves in the extremities (IARC 1985). Exposures in humans have been associated with polyneuropathy with motor and sensory impairment marked by numbness, paresthesias, ataxia, tremor, dysarthria, and mid- brain lesions (HSDB 1994). Ingestion of contaminated drinking water has caused drowsiness, disturbances of balance, confusion, memory loss, and hallucinations (HSDB 1994). A study of factory workers exposed to 0.07 to 2.5 times the NIOSH recommended exposure limit (0.03 mg/m3) showed a dose response relationship for abnormal sensation, decreased motor strength, abnormal gait or rombergism, and skin abnormalities (HSDB 1994). The concentration of 0.03 mg/m3 is rouoghly equivalent to 0.004 mg/kg/day for an 8-hour work day (see end note 5). Among workers exceeding the limit, 67% had symptoms of acrylamide intoxication compared with 14% of workers below theexposure limit. Clinically, acrylamide toxicity is a dying back axonopathy with onset of neuropathy in the distal node of the longest fibers, inhibition of fast axoplasmic transport, and enzyme impairment (HSDB 1994). 2. Animals - The U.S. EPA (1994) has calculated a chronic oral reference dose for acrylamide of 0.0002 mg/kg/day, based on the following information. Axon and myelin degeneration occurred in rats exposed to 5 or 20 mg/kg/day in drinking water for 92-93 days but was no longer apparent by 144 days post treatment. The no-observed-adverse effect level (NOAEL) for this study was 0.2 mg/kg/day (U.S. EPA 1994). Rats given 52, 80, 125, or 200 mg/L (approximately 7, 11, 18, and 28 mg/kg/day) in drinking water for 60-90 days had decreased rotarod performance at the two highest concentrations; histological evaluation of the tibial and sciatic nerves of high-dose rats revealed morphological changes and myelin degeneration (U.S. EPA 1985). Rats were treated with acrylamide at 5, 10, or 20 mg/kg/day by gavage for 13 weeks. High dose rats had decreased hind limb extensor response and spontaneous motor activity. Nerve fiber degeneration was observed in both the mid- and high-dose groups. After a 5 week recovery period, neuropathological changes were still evident in the highdose rats (U.S. EPA 1985). Exposure of rats to 25 mg/kg by gavage for 21 days "markedly" reduced brain dopamine and noradrenaline (HSDB 1994). Severe leg weakness, accompanied by histological evidence of peripheral nerve degeneration occurred in rats treated with 200, 300, or 400 ppm acrylamide in the diet for 48 weeks (U.S. EPA 1985). Gait disorders, observed in cats treated with 3 mg/kg/day in drinking water, progressed to distal muscle weakness and drop- foot in the hind limbs; muscle atrophy occurred subsequent to denervation (U.S. EPA 1985). Dose-related neurotoxicity was observed in cats given 1, 3, or 10 mg/kg/day in a 1-year feeding study (HSDB 1994). EEG abnormalities were seen in cats treated with acrylamide (no dose or duration given) prior to development of ataxia (HSDB 1994). Monkeys were given 3 or 10 mg/kg/day by gavage, 5 days/week for 1 year (U.S. EPA 1985). Severe muscle weakness occurred after 69 days of 10 mg/kg/day and sporadic deficits in reflex reactions were observed at 3 mg/kg/day. Visual acuity and contrast sensitivity were decreased in monkeys for 140 days after treatment (no dose given) (HSDB 1994). Dogs exposed to 7 mg/kg/day for 8 weeks developed sensorimotor peripheral neuropathy and megaesophagus due to vagal axonopathy (HSDB 1994). V. ENVIRONMENTAL EFFECTS Acrylamide has low acute toxicity to aquatic organisms; toxicity values are generally greater than 100 mg/L. Acrylamide is not likely to be acutely toxic to aquatic or terrestrial animals at levels found in the environment. Long-term exposure to terrestrial animals may increase tumor incidence or adversely affect reproductive abilities. A. Toxicity to Aquatic Organisms U.S. EPA (1985) has reported LC50 values for acrylamide for several species of fish, including Carassius auratus (goldfish), Rasbora heteromorpha (harlequin fish), and Poecilia reticulata (guppy). Flowthrough LC50 values of 460 mg/L, 250 mg/L, and 130 mg/L were reported for the harlequin fish in 24-hour, 48-hour, and 96-hour tests, respectively. The static 24-hour and 96-hour LC50 values for the goldfish are 460 mg/L and 160 mg/L, respectively. The 7-day LC50 value for the guppy is approximately 35 mg/L. The 24-hour LC50 for Daphnia magna (water flea, first instar) is 230 mg/L (AQUIRE 1994). B. Toxicity to Terrestrial Organisms No information was found in the secondary sources searched regarding the toxicity of acrylamide to terrestrial organisms. Based on the range of oral LD50's of acrylamide for rats, 159 to 300 mg/kg, the chemical is not expected to be acutely toxic to terrestrial animals at levels normally found in the environment. However, long- term exposure from residues in water, may increase tumor incidence and decrease fertility in males based on chronic drinking water studies in rats. C. Abiotic Effects No information was found on the abiotic effects of acrylamide in the secondary sources searched. VI. EPA/OTHER FEDERAL ACTIVITY The Clean Air Act Amendments of 1990 list acrylamide as a hazardous air pollutant. Occupational exposure to acrylamide is regulated by the Occupational Safety and Health Administration (OSHA). The permissible exposure limit (PEL) is 0.3 milligrams per cubic meter of air (mg/m3) as an 8-hour time-weighted average (TWA). OSHA has added a skin notation to its PEL for acrylamide, indicating that workplace dermal exposure should be controlled as well (29 CFR 1910.1000). Federal agencies and other groups that can provide additional information on acrylamide are listed in Tables 4 and 5. TABLE 4. EPA OFFICES AND CONTACT NUMBERS FOR INFORMATION ON ACRYLAMIDE. ________________________________________________________________________ EPA OFFICE LAW PHONE NUMBER ________________________________________________________________________ Pollution Prevention Toxic Substances Control Act & Toxics (Sec. 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. 302/304/311/312) (800) 424-9346 Water Safe Drinking Water Act (treatment technique requirement; see end note 6) (800) 426-4791 _________________________________________________________________________ TABLE 5. OTHER FEDERAL OFFICES/OTHER GROUP CONTACT NUMBERS FOR INFORMATION ON ACRYLAMIDE. ________________________________________________________________________ Other Agency/Department/Group Contact Number ________________________________________________________________________ American Conference of Governmental Industrial Hygienists (Recommended Exposure Limit (see end note 7): 0.03 mg/m3; [skin] (see end note 8) (513) 742-2020 Consumer Product Safety Commission (301) 817-0994 Food & Drug Administration (301) 443-3170 National Institute for Occupational Safety & Health (Recommended Exposure Limit (see end note 7): 0.03 mg/m3; [skin] (see end note 8) (NIOSH 1990) (800) 356-4674 Occupational Safety & Health Administration Check local phone Permissible TWA (see end note 9), 0.3 mg/m3; book for phone [skin] (see end note 8) (OSHA 1993) number under Department of Labor ________________________________________________________________________ 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 slope factor is a plausible upper-bound estimate of the probability of a response per unit intake of a chemical over a lifetime. The slope factor is used in risk assessments to estimate an upper-bound lifetime probability of an individual developing cancer as a result of exposure to a particular level of a potential carcinogen. 3. The unit risk is a quantitiative estimate in terms of risk per unit intake of a chemical. The unit risk for acrylamide incorporates information on pharmacokinetics and metabolism. 4. 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. 5. Calculated by multiplying 0.03 mg/m3 by 0.143 (the standard 8-hour occupational breathing rate, 10 m3, divided by the assumed adult body weight, 70 kg, and assuming 100% absorption) to obtain the dose in mg/kg/day (U.S. EPA 1988). 6. As defined in 40 CFR 142.2, specifies for a contaminant a specific treatment technique(s) which leads to a reduction in the level of such contaminant sufficient to comply with the requirements of 40 CFR 141. Refer to 40 CFR 141.111 for the treatment technique for acrylamide. 7. The ACGIH/NIOSH exposure limits are time-weighted average (TWA) concentrations for an 8-hour workday (ACGIH) and up to a 10-hour workday (NIOSH) for a 40-hour workweek. 8. A [skin] notation indicates that air sampling is not sufficient to accurately quantitate exposure. Measures to prevent significant cutaneous absorption may be required. 9. PEL-TWA, permissible exposure limit 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. 23-25. 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., Inc., Rahway, NJ, p. 127. HSDB. 1994. Hazardous Substances Data Bank. MEDLARS Online Information Retrieval System, National Library of Medicine. Retrieved August 1994. IARC. 1985. International Agency for Research on Cancer. 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