EPA 749-F-94-003a CHEMICAL SUMMARY FOR ACETALDEHYDE prepared by OFFICE OF POLLUTION PREVENTION AND TOXICS U.S. ENVIRONMENTAL PROTECTION AGENCY August 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 These sources include online databases, unpublished EPA information, government publica- tions, review documents, and standard reference materials.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 acetaldehyde are summarized in Table 1. TABLE 1. CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL PROPERTIES OF ACETALDEHYDE __________________________________________________________________________ Characteristic/Property Data Reference __________________________________________________________________________ CAS No. 75-07-0 Common Synonyms acetic aldehyde; ethanal; ethyl aldehyde HSDB 1994 Molecular Formula C2H4O Chemical Structure CH3-CHO Physical State colorless liquid Verschueren 1983 Molecular Weight 44.05 Budavari et al. 1989 Melting Point -123.5øC Budavari et al. 1989 Boiling Point 21øC at 760 mm Hg Budavari et al. 1989 Water Solubility miscible Budavari et al. 1989 Density d16/4, 0.788 Budavari et al. 1989 Vapor Density (air = 1) 1.52 ACGIH 1991 KOC not available Log KOW -0.22 (estimated) CHEMFATE 1994 Vapor Pressure 740 mm Hg @ 20øC Verschueren 1983 Reactivity highly reactive; flammable Budavari et al. 1989; Verschueren 1983 Flash Point -36øF (-38øC) (closed cup) Budavari et al. 1989 Henry's Law Constant 7.89 x 10-5 atm-m3/mol at 25øC CHEMFATE 1994 Fish Bioconcentration Factor <1 (estimated) CHEMFATE 1994 Odor Threshold 0.21 ppm (in air) Verschueren 1983 Conversion Factors 1 ppm = 1.83 mg/m3 1 mg/m3= 0.55 ppm Verschueren 1983 _________________________________________________________________________ II. PRODUCTION, USE, AND TRENDS A. Production There are two producers of acetaldehyde in the United States, Eastman and Hoechst Celanese. In 1989, US production of acetaldehyde was estimated to be 740 million pounds. In the same year, 40 million pounds were exported (Mannsville, 1990). B. Use The largest use of acetaldehyde is as a chemical intermediate for the production of acetic acid. The production of esters, principally ethyl acetate and isobutyl acetate, is the second most significant use. It is also used as an intermediate for a number of other chemicals, including pyridine and pyridine bases, pentaerythritol, peracetic acid, 1,3-butylene glycol, and chloral. Acetaldehyde is also used in silvering mirrors; hardening gelatin fibers; denaturing alcohol; and in the manufacture of disinfectants, dyes, drugs, explosives, flavorings, phenolic and urea resins, rubber accelerators and antioxidants, varnishes, and yeast. Table 2 shows the estimated 1986 U.S. end-use pattern for acetaldehyde. C. Trends Both production and demand increased somewhat between 1986-1989. Though demand is expected to remain static at about 700 million pounds, US production may decline due to the addition of production capacity in Mexico. TABLE 2. Estimated 1986 United States End-Use Pattern of Acetaldehyde ___________________________________________________________________________ Use of Acetaldehyde Percentage of U.S. (typical Standard Industrial Acetaldehyde Use Classification (SIC) Code) ___________________________________________________________________________ Acetic acid (production, SIC 2869) 55% Ester production (production, SIC 2861) 15% Pyridine and pyridine bases (production, SIC 2822) 10% Pentaerythritol (production, SIC 2869) 10% Peracetic acid (production, SIC 2869) 5% 1,3-butylene glycol (SIC codes unknown) 2% Miscellaneous and exports (no applicable SIC Code(s)) 3% ___________________________________________________________________________ Source: Mannsville, 1993. III. ENVIRONMENTAL FATE A. Environmental Release Acetaldehyde is released into air or wastewater from facilities producing or using the chemical (HSDB 1994). Acetaldehyde is also released to the environment from the combustion and photo- oxidation of hydrocarbons (HSDB 1994). Acetaldehyde is an intermediate product of respiration in higher plants and occurs naturally in many foods, such as ripe fruits that have tart tastes before ripening, and coffee (HSDB 1994). Acetaldehyde is a component of cigarette smoke (HSDB 1994). In 1992, releases of acetaldehyde to environmental media, as reported to the Toxic Chemical Release Inventory by certain types of U.S. industries, totaled about 8.4 million pounds: 6.42 million pounds to the atmosphere; 1.9 million pounds to underground injection sites; 77,188 pounds to surface water discharges; and 289 pounds to land (TRI92 1994). Concentrations of acetaldehyde measured in air samples taken from different locations vary, depending on several conditions, including weather. The chemical has been detected in ice fog, rain, cloud mist, and fog (CHEMFATE 1994). Urban concentrations measured 5.2 ppb in Baltimore, MD; 35 ppb in Claremont, CA (severe smog); and 170 ppb in another unspecified California city (foggy conditions). Acetaldehyde concentrations reached 590 ppb in clouds over California (site not specified), and levels reached 3.1-13.3 ppb in Grand Canyon, AZ (CHEMFATE 1994). Trace amounts of acetaldehyde have been detected in the drinking water of several U.S. cities (CHEMFATE 1994; HSDB 1994). B. Transport The Henry's Law constant for acetaldehyde, 7.89x10-5 atm.m3/mol at 25øC (CHEMFATE 1994), and its high vapor pressure, 740 mm Hg @ 20øC (Verschueren 1983), indicate that volatilization of the chemical from surface soil or water to the atmosphere will be considerable. C.Transformation/Persistence 1. Air - In air (at 25øC), acetaldehyde reacts with OH radicals, NO3, singlet oxygen, and NO2 at the following rates: 0.15x10-10, 0.12x10-14, 0.31x10-12, and 0.20x10-24 cm3/molecule-sec, respectively. The estimated half-life for the reaction of acetaldehyde with OH produced by UV light is 6.2 hours; the products of this reaction include peroxyacetylnitrate (PAN), methyl nitrate, methyl nitrite, and nitric acid (CHEMFATE 1994). Acetaldehyde absorbs UV light at wavelengths of 290 to 342 nm (CHEMFATE 1994), indicating some potential for photolysis. The photolytic half-lives for acetaldehyde are about 34 hours in the summer and 296 hours in winter at 55ø N latitude. The estimated half-life for the reaction of acetaldehyde with ozone at 25øC, based on the rate constant of 6x10-21 cm3/molecule-sec, is 1910 days (5.2 years) (CHEMFATE 1994). 2. Soil - Acetaldehyde will volatilize rapidly in near surface and surface soils [v.p. 740 mm Hg at 20øC (Verschueren 1983)], or leach into the ground, or undergo microbial degradation (HSDB 1994). Acetaldehyde is not expected to adsorb to soils, other than those containing montmorillonite clay (HSDB 1994). 3. Water - If released to water, acetaldehyde will rapidly biodegrade or volatilize (for a typical river, the half-life is 9.3 hours) (HSDB 1994). Laboratory tests demonstrate that acetaldehyde is easily biodegraded (1) by acclimated sludge and sewage with theoretical biological oxygen damand (BOD) values for several studies ranging from 28% in 24 hours to 100% in 5 hours; (2) by anaerobic treatment; and (3) in seawater (25% degradation in 1 hour, compared with no decline in concentration in sterile controls) (HSDB 1994). 4. Biota - The estimated, low KOW and bioconcentration values for acetaldehyde (CHEMFATE 1994) indicate that there is little potential for the bioaccumulation or bioconcentration of acetaldehyde in biota. IV. HEALTH EFFECTS Acetaldehyde is the major metabolite of ethanol (HSDB 1994). Many of the adverse effects of ethanol are attributed to acetaldehyde (HSDB 1994). Direct administration of acetaldehyde to rats has established alcohol dependency (Brabec 1981). A. Pharmacokinetics 1. Absorption - Acetaldehyde is rapidly absorbed by oral and respiratory routes (ACGIH 1991). Estimated half-lives of acetaldehyde in circulating blood have been reported as <15 minutes (ACGIH 1991) and 3.1 minutes (HSDB 1994). 2. Distribution - Experimental studies indicate that, following inhalation or oral exposure, sufficient first-pass metabolism occurs in the liver and respiratory tract to limit acetaldehyde access to the systemic circulation (ACGIH 1991). However, acetaldehyde was detectable in the liver, blood, kidney, spleen, heart, and bone of rats exposed to the 20 mM vapor for 1 hour and in maternal and embryonic tissues following administration (route unspecified) of >5 g/kg ethanol to pregnant mice (HSDB 1994). 3. Metabolism - Acetaldehyde is metabolized (mainly in mammalian liver) to acetic acid by NAD+-dependent aldehyde dehydrogenase. The rate of metabolism to acetic acid varies, but it is generally considered to be rapid (IARC 1985; ACGIH 1991). Saturation kinetics are not apparent even with large doses (ACGIH 1991). Acetic acid enters the metabolic pool of intermediary metabolism and is used in the production of carbon dioxide and water or in cellular synthesis of cholesterol, fatty acids, and other tissue constituents (HSDB 1994). In vitro, acetaldehyde formed adducts with cytosine- and purine- containing nucleotides (IARC 1985). 4. Excretion - Because the major metabolite of acetaldehyde enters into intermediary metabolism, the excretion of the parent compound or its metabolites may be limited. Acetaldehyde has been detected in expired air (usually no more than 5%) but only its metabolites have been detected in the urine (ACGIH 1991). Intravenous infusion of 0.5% solutions of acetaldehyde into rabbits resulted in the rapid excretion (route not stated) at the rate of 7-10 mg/minute (IARC 1985). N-nitroso-2-methylthiazolidine 4-carboxylic acid was detected in the urine of human subjects during oral and nasal breathing (ACGIH 1991). B. Acute Effects Humans exposed acutely to moderate concentrations of acetaldehyde experience irritation of the eyes and respiratory tract and altered respiratory function. Animals exposed to moderate to high concentrations exhibit skin and eye irritation and notable cellular alterations in the respiratory epithelium and hyper- keratosis of the forestomach. 1. Humans - The acute irritation of acetaldehyde is characterized by the following: eye irritation in sensitive individuals, at 25 ppm for 15 minutes; eye irritation, at 50 ppm for 15 minutes; irritation of respiratory tract, at 134 ppm for 30 minutes (2.15 mg/kg over 30 minutes) (see end note 1); irritation of nose and throat, 200 ppm at 15 minutes (Verschueren 1983). Intravenous infusion of human subjects with 5% acetaldehyde at a rate of 20.6-82.4 mg/min for up to 36 minutes (the lowest dose converts to 10.6 mg/kg over 36 minutes) resulted in an increased heart rate, increased ventilation rates and respiratory dead space, and a decreased alveolar carbon dioxide level (IARC 1985). 2. Animals - The oral LD50 value for the rat is 1.93 g/kg (Brabec 1981). The inhalation LC50 for rats exposed for 30 minutes was 20,000 ppm (ACGIH 1991). Acetaldehyde elicited mild skin irritation (open test) and severe eye irritation in rabbits (ACGIH 1991). Intravenous doses of 1-40 mg/kg had a sympatho- mimetic effect on the heart; doses of <20 mg/kg elevated the blood pressure, and doses >20 mg/kg caused bradycardia and hypotension (ACGIH 1991). C. Subchronic/Chronic Effects Prolonged dermal exposure to acetaldehyde can cause erythema and burns in humans; repeat contact may result in dermatitis. Repeat doses by inhalation, at high concentrations, causes adverse respiratory tract effects in animals. EPA has derived an inhalation reference concentration (RfC) (see end note 2) of 0.009 mg/m3 for acetaldehyde, based on adverse effects, including degeneration of olfactory epithelia, observed in animal studies. 1. Humans - Prolonged contact of acetaldehyde with the skin may result in erythema and burns; repeated contact with the skin may cause dermatitis, resulting from irritation or sensitization (IARC 1985). 2. Animals - Two 4-week animal studies were the basis for the derivation of the inhalation reference concentration (RfC) for acetaldehyde (U.S. EPA 1994). In the first study, Wistar rats were exposed to 0, 150, or 500 ppm acetaldehyde 6 h/day, 5 days/week for 4 weeks. At the end of the study, lavage fluid was collected from the lung and the cells were evaluated; cells from animals exposed to 500 ppm exhibited decreased viability, decreased cell density, and decreased phagocytosis. Microscopic examination revealed degeneration of the olfactory epithelium. No compound-related effects were observed in rats exposed to 150 ppm [identified as a no-observable-adverse-effect level (NOAEL)]. In the second study, Wistar rats were exposed to 0, 400, 1000, 2200, or 5000 ppm acetaldehyde 6 h/day, 5 days/week for 4 weeks. Effects observed included: death (2200 and 5000 ppm); decreased percentage of lymphocytes; increased number of neutrophilic leukocytes; and decreased organ weights (5000 ppm); growth retardation (three highest concen- trations); dose-related degeneration of the nasal olfactory epithelium (all concentrations); and dose-related hyper- and metaplastic changes of the olfactory, laryngeal, and tracheal epithelium (1000, 2200 and 5000 ppm). The 400-ppm concentration, the lowest dose tested, was identified as a lowest-observable- adverse-effect level (LOAEL). The above studies were selected for the determination of the RfC because the same types of lesions appear at longer exposure times and higher exposure levels in chronic studies, and they were concentration (dose)-related. The 150 ppm value from the first study was established as the NOAEL, and the 400 ppm value from the second study was established as the LOAEL. The RfC is 0.009 mg/m3 (U.S. EPA 1994). Wistar rats inhaled acetaldehyde concentrations of 0, 750, 1500 and 3000/1000 ppm for 6 h/day, 5 days/week for up to 28 months (U.S. EPA 1994). Early mortality in the 3000-ppm group prompted the reduction of the concentration to 1000 ppm. All rats in this group were dead by 25 months, and all but a few were dead in the 1500-ppm group; the cause of early death or moribund condition was almost always partial or complete occlusion of the nose by excessive amounts of keratin and inflammatory exudate. The incidence of basal cell hyperplasia of the olfactory epithelium, increased in low and mid-dose rats, was lower in the high-dose group because of the increased incidence of adenocarcinomas (see section IV.D). Hyperplasia and squamous metaplasia, occasionally with keratinization, developed in the larynx of rats exposed to 1500 and 3000/1000 ppm. A LOAEL of 750 ppm was identified for this study (U.S. EPA 1994). In another study, rats exposed to the same concentrations for 52 weeks were allowed to recover for 26 or 52 weeks. The study demonstrated incomplete recovery of the olfactory and respiratory epithelium even after 52 weeks of recovery (U.S. EPA 1994). Hamsters exposed by inhalation to acetaldehyde concentrations of 0, 390, 1340, or 4560 ppm for 6 h/day, 5 days/week for 90 days, exhibited decreased body weights; increased organ weights; and effects on the respiratory epithelium that included necrosis, inflammation, hyperplasia and metaplasia (at 4560 ppm); and statistically significant increase in kidney weight in males and small areas of stratified epithelium in the trachea (at 1340 ppm). The authors identified 390 ppm as the NOAEL for the study (U.S. EPA 1994). Male and female rats received acetaldehyde in the drinking water (25, 125, or 675 mg/kg/day for 4 weeks (HSDB 1994). The only reported adverse effect, hyperkeratosis of the forestomach, was observed at the high dose. D. Carcinogenicity There is inadequate evidence for the carcinogenicity of acetaldehyde for humans. Based on the carcinogenicity of acetaldehyde in animals, EPA has concluded that acetaldehyde is a probable human carcinogen. 1. Humans - Workers in an aldehyde factory in the German Democratic Republic had a higher cancer rate than expected in that section of Germany (IARC 1985). The plant's main process was the dimerization of acetaldehyde. Of nine cases of malignant neoplasm, 5 were bronchial tumors and two were carcinomas of the oral cavity. Statistical analyses were not available. All the cases were smokers and other chemicals (e.g., acetaldol, butyraldehyde, crotonaldehyde, other higher aldehydes, and acrolein) were present in varying proportions. 2. Animals - Wistar rats inhaled acetaldehyde concentrations of 0, 750, 1500 and 3000/1000 ppm (0, 1350, 2700, or 5400/1800 mg/m3) for 6 h/day, 5 days/week for up to 28 months (U.S. EPA 1994). Early mortality in the 3000-ppm group prompted the reduction of the concentration to 1000 ppm. Adenocarcinomas occurred at all exposure levels, and squamous cell carcinoma of the nasal mucosa occurred at the mid and high concentrations (tumor incidence data were not reported) (U.S. EPA 1994). Hamsters (36/sex/group) inhaled decreasing concentrations of acetaldehyde [2500 ppm (4500 mg/m3) to 1650 ppm (2970 mg/m3)] 7 h/day, 5 days/week for 52 weeks (IARC 1985). Six animals, killed at the end of exposure, had no tumors; among the remainder of the animals, killed at 81 weeks, the incidences of laryngeal tumors were increased (p<0.05; 0/30, 8/29, 0/28, 5/29 for control males, exposed males, control females, exposed females, respectively). EPA classifies acetaldehyde as B2, "probable human carcinogen," based on the increased incidences of nasal tumors in male and female rats and laryngeal tumors in male and female hamsters (U.S. EPA 1994). IARC has also concluded that there is sufficient evidence for the carcinogenicity of acetaldehyde to experimental animals and inadequate evidence for its carcinogenicity to humans, resulting in an classification of 2B, "possibly carcinogenic to humans" (IARC 1985). E. Genotoxicity In the EPA GENETOX Program, acetaldehyde is reported as positive for DNA repair in Escherichia coli pol A (Rec-assay) and for sister chromatid exchanges, in vitro, in human lymphocytes and nonhuman cells (GENETOX 1994). Acetaldehyde was not mutagenic in Salmonella or in E. coli, but was positive for chromosome aberrations and sister chromatid exchange both in vitro and in vivo mammalian assays (USEPA 1994). F. Developmental/Reproductive Toxicity No information was found for the developmental/reproductive effects of acetaldehyde in humans. Limited evidence from i.p. studies indicate that acetaldehyde causes adverse developmental effects in animals. 1. Humans - No information was found in the secondary sources searched to indicate that acetaldehyde is a developmental/ reproductive toxicant in humans. 2. Animals - Pregnant CF rats were given intraperitoneal (i.p.) doses of 50 mg acetaldehyde/kg/day on gestation days 8-15; the fetuses, collected on gestation days 16 through 21, had delayed ossification and skeletal malformations (e.g., wavy ribs) (HSDB 1994). In another study, pregnant rats received i.p. doses of 50-100 mg/kg of acetaldehyde on day 10, 11, or 12 of gestation; the fetuses were examined on day 21. Acetaldehyde produced a significant increase in fetal resorptions, growth retardation, delayed skeletogenesis, and an increase in skeletal malformations. When treatment occurred on days 8-15 of gestation, growth retardation and malformations of the face and limbs, and delayed ossification were observed (ACGIH 1991). G. Neurotoxicity The neurotoxicity potential of acetaldehyde in humans cannot be determined from available information. Limited evidence indicates that acetaldehyde cause neurological effects in animals, including central nervous system depression and neural degeneration. 1. Humans - The irritant effects of acetaldehyde vapor, such as coughing and burning of the nose, throat and eyes, usually prevents exposure to a level sufficient to cause depression of the central nervous system (IARC 1985). The results of one study in human volunteers indicated that acetaldehyde penetrates the human blood-cerebrospinal fluid barrier (HSDB 1994). 2. Animals - Rats exposed to LC50 concentrations of acetaldehyde exhibited excitement (ACGIH 1991). Dogs exposed to levels of >134 ppm for 30 minutes experienced inhibition of the central nervous system, and subsequent decrease in the respiratory rate (HSDB 1994). A single i.p. injection (dose not reported) of acetaldehyde produced sustained neural degeneration in the cerebral cortex of rats (HSDB 1994). V. ENVIRONMENTAL EFFECTS A. Toxicity to Aquatic Organisms Acetaldehyde has moderate acute toxicity to aquatic organisms; acute toxicity values are in the range of greater than 1 mg/L to 100 mg/L. LC50 values reported in AQUIRE 1994 for fish include: 37.2 mg/L for 96 hours, Pimephales promelas, the fathead minnow; and 53 mg/L for 96 hours, Lepomis macrochirus, the bluegill. The EC50 value for the immobilization of Daphnia magna (water flea) is 48 mg/L for 48 hours (AQUIRE 1994). B. Toxicity to Terrestrial Organisms No information was found in the secondary sources searched regarding the toxicity of acetaldehyde to terrestrial animals; however, information from laboratory animal studies indicate that adverse effects in animals could occur in the presence of high concentrations of acetaldehyde. C. Abiotic Effects Limited information on the abiotic effects of acetaldehyde was found in the secondary sources searched. According to the definition provided in the Federal Register (1992), acetaldehyde is a volatile organic compound (VOC) substance. As a VOC, acetaldehyde can contribute to the formation of photochemical smog in the presence of other VOCs. Potential environmental degradation products of acetaldehyde such as PAN, methyl nitrate, and methyl nitrite are components of photochemical smog. VI. EPA/OTHER FEDERAL/OTHER GROUP ACTIVITY The Clean Air Act Amendments of 1990 list acetaldehyde as a hazardous air pollutant. The Agency has enacted restrictions for certain waste streams containing the chemical. Occupational exposure to acetaldehyde is regulated by the Occupational Safety and Health Administration. The permissible exposure limit (PEL) is 200 parts per million parts of air (ppm) (29 CFR 1910.1000). Federal agencies and other groups that can provide additional information on acetaldehyde are listed in Tables 3 and 4. TABLE 3. EPA OFFICES AND CONTACT NUMBERS FOR INFORMATION ON ACETALDEHYDE __________________________________________________________________________ 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. 304/311/312) (800) 424-9346 Water Clean Water Act (202) 260-7588 ___________________________________________________________________________ TABLE 4. OTHER FEDERAL OFFICES/OTHER GROUP CONTACT NUMBERS FOR INFORMATION ON ACETALDEHYDE _________________________________________________________________________ Other Agency/Department/Other Group Contact Number _________________________________________________________________________ American Conference of Governmental Industrial Hygienists (Recommended Highest Exposure Limit (see end note 3): 25 ppm) (513) 742-2020 National Institute for Occupational Safety & Health (Recommended Exposure Limit (see end note 4): 18 ppm; Limit of Quantitation) (800) 356-4674 Occupational Safety & Health Administration (Permissible Exposure Limit (see end note 5): 200 ppm) (Check local phone book for phone number under Department of Labor) _________________________________________________________________________ VII. END NOTES 1. Calculated using a factor of 1.8 to convert 134 ppm to 241 mg/m3 which is multiplied by 0.009 (the calculated 30-minute occupational breathing rate of 0.625 m3 divided by the assumed adult body weight, 70 kg) to obtain the dose in mg/kg (U.S. EPA 1988). 2. The RfC is an estimate (with uncertainty spanning perhaps an order of magnitude) of the 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. This is a ceiling exposure limit value that should not be exceeded at any time. 4. Exposure should be reduced to the lowest feasible limit; use of only the most reliable and protective respirators is recommended. 5. The OSHA exposure limit is a time-weighted-average (TWA) concentration that must not be exceeded during any 8-hour workshift of a 40-hour work- week. VIII. CITED REFERENCES ACGIH. 1991. Documentation of the Threshold Limit Values and Biological Exposure Indicies, 6th ed. American Conference of Governmental Industrial Hygienists, Inc., Cincinnati, OH, pp. 1-5. AQUIRE. 1994. EPA ERL-Duluth's Aquatic Ecotoxicology Data Systems. U.S. EPA, Duluth, MN. Retrieved July 1994. Brabec MJ. 1981. Aldehydes and acetals. In: Clayton GD, Clayton FE, Eds. Patty's Industrial Hygiene and Toxicology, 3rd ed., Vol. 2A. New York: John Wiley & Sons, pp. 2629-2639. Budavari S, O'Neil MJ, Smith A, Heckelman PE (Eds.). 1989. The Merck Index, 11th ed. Merck & Co., Inc., Rahway, NJ, p. 38. CHEMFATE. 1994. Syracuse Research Corporation's Environmental Fate Data Bases. Syracuse Research Corporation, Syracuse, NY. Federal Register. 1992. Part 51 - Requirements for Preparation, Adoption, and Submittal of Implementation Plans. Fed. Reg. 57:3945. GENETOX. 1994. U.S. EPA GENETOX Program, computerized database. Retrieved 7/94. HSDB. 1994. Hazardous Substances Data Bank. MEDLARS Online Information Retrieval System, National Library of Medicine. Retrieved June, 1994. IARC. 1985. Acetaldehyde. In: International Agency for Research on Cancer. IARC Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Man, vol. 36. IARC, Lyon, pp.101-132. Mannsville. 1990. Chemical Products Synopsis, Acetaldehyde. Mannsville Chemical Products Corporation. January 1990. Mannsville. 1993. Chemical Products Synopsis, Acetaldehyde. Mannsville Chemical Products Corporation. January 1993. TRI92. 1994. 1992 Toxic Chemical Release Inventory. Office of Pollution Prevention and Toxics, U.S. Environmental Protection Agency, Washington, D.C. U.S. EPA. 1988. U.S. Environmental Protection Agency. Methodology for Evaluating Potential Carcinogenicity in Support of Reportable Quantity Adjustments Pursuant to CERCLA Section 102. Carcinogen Assessment Group, Office of Health and Environmental Assessment, U.S. EPA, Washington, D.C., pp. 21, 22. OHEA-C-073. U.S. EPA. 1994. U.S. Environmental Protection Agency. Integrated Risk Information System (IRIS) Online. Coversheet for Acetaldehyde. Office of Health and Environmental Assessment, U.S. EPA, Cincinnati, OH, Retrieved 7/94. Verschueren K. 1983. Handbook of Environmental Data on Organic Chemicals. Van Nostrand Reinhold Co., New York, pp. 139-141. APPENDIX A. SOURCES SEARCHED FOR FACT SHEET PREPARATION AQUIRE. 1994. Aquatic Information Retrieval online data base. Chemical Information Systems, Inc., a subsidiary of Fein-Marquart Assoc. ATSDR. 1989-1994. Agency for Toxic Substances and Disease Registry. Toxicological Profiles. Chamblee, GA: ATSDR. 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, Eds. 1981-1982. Patty's Industrial Hygiene and Toxicology, 3rd ed. New York: John Wiley & Sons. 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