EPA 749-F-94-008a CHEMICAL SUMMARY FOR CARBON DISULFIDE 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 These sources include online databases, unpublished EPA information, government pub- lications, review documents, and standard reference materials.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 carbon disulfide are summarized in Table 1. TABLE 1. CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL PROPERTIES OF CARBON DISULFIDE _______________________________________________________________________ Characteristic/Property Data Reference _______________________________________________________________________ CAS No. 75-15-0 Common Synonyms carbon bisulfide, dithio- carbonic anhydride Budavari et al. 1989 Molecular Formula CS2 Chemical Structure S=C=S Physical State liquid Budavari et al. 1989 Molecular Weight 76.14 Budavari et al. 1989 Melting Point -111.6øC Budavari et al. 1989 Boiling Point 46.5øC Budavari et al. 1989 Water Solubility 2300 mg/L @ 22øC Verschueren 1983 Specific gravity 1.263 @ 20/4øC Verschueren 1983 Vapor Density (air = 1) 2.64 Verschueren 1983 KOC 54 U.S. EPA 1986 Log KOW 2.16 U.S. EPA 1986 Vapor Pressure 260 mm Hg @ 20øC; 430 mm Hg @ 30øC Verschueren 1983 Reactivity Flammable; reacts vigorously with oxidizing agents and may generate heat or possibly ignite or explode. Explosive limits in air: 1.3-50%, ignition temperature: 100øC. Keith and Walters 1985 Flash Point -30øC closed cup Budavari 1989 Henry's Law Constant 1.01 X 10-2 atm m3/mol @ 20øC (calculated) U.S. EPA 1986 Fish Bioconcentration Factor ó26 (calculated) U.S. EPA 1986 Odor Threshold 0.05 mg/m3 Verschueren 1983 Conversion Factors 1 ppm = 3.17 mg/m3 1 mg/m3 = 0.32 ppm Verschueren 1983 _______________________________________________________________________ II. PRODUCTION, USE, AND TRENDS A. Production There are 3 producers of carbon disulfide in the United States. Table 2 lists producers, plant locations, and plant capacities. Annual US production capacity is 350 million pounds. In 1992, approximately 207 million pounds were produced in the US. In that same year, 4 million pounds of carbon disulfide were imported into the US and 32 million pounds were exported (Mannsville 1993). B. Use Carbon disulfide is used in a number of industrial applications. The largest use of carbon disulfide is as a reactant in the manufacture of rayon fibers. It is also used in the production of cellulose; in agricultural fumigants; in the production of rubber chemicals; as an agent in metal treatment and plating; as a solvent for cleaning and extraction; in the production of adhesives; and as an extractant for olive oil. Table 3 shows the estimated 1992 US end-use pattern for carbon disulfide. C. Trends One major use of carbon disulfide, as a precursor to carbon tetrachloride, has already been phased out. Demand for carbon disulfide is expected to continue to decline (Mannsville 1993). TABLE 2. United States Producers of Carbon Disulfide _______________________________________________________________________ Company Plant Location Plant Capacity (in millions of pounds) _______________________________________________________________________ Akzo Chemicals (see end note 1) LeMoyne, AL 250 Atochem North America Green Bayou, TX 40 PPG Industries Natrium, WV 60 _______________________________________________________________________ Source: Mannsville 1993 TABLE 3. Estimated 1992 United States End-Use Pattern of Carbon Disulfide __________________________________________________________________________ Use of Carbon Disulfide Percentage of US Carbon (typical Standard Industrial Disulfide Use Classification (SIC) (see end note 2) Code) ___________________________________________________________________________ Rayon (production, SIC 22; use, SIC 23) 40% Agricultural fumigants (production, SIC 2879; use, SIC 01) 18% Rubber chemicals (production, SIC 2869, 2899; use, SIC 30) 16% Cellophane and other regenerated cellulose (production, SIC 2823; use, various industries) 12% Other (no applicable SIC Code(s)) 14% _______________________________________________________________________ Source: Mannsville 1993. III. ENVIRONMENTAL FATE A. Environmental Release Of the total carbon disulfide released to the environment almost all is eventually released to air. Carbon disulfide is a volatile liquid [vapor pressure, 260 mm Hg at 20øC (Verschueren 1983)], and is released into the atmosphere from industrial uses. The largest man made sources of carbon disulfide release are manufacturing and processing facilities, the largest single use of which is the rayon industry. Carbon disulfide also occurs naturally in the environment from biodegradation of organic material, and has been found in the gas over volcanos (ATSDR 1992). It is also widely found in coastal and ocean waters, and studies indicate that it is naturally occurring, possibly originating from anaerobic conditions on the sea floor (U.S. EPA 1986). The oceans are a major global source of carbon disulfide with estimated total emissions of 600,000,000 kg/yr (HSDB 1994) or approximately 270 million pounds per year. In 1992, releases of carbon disulfide to environmental media, as reported to the Toxic Chemical Release Inventory by certain types of U.S. industries totaled about 93 million pounds. Of this amount, a total of 92.9 million pounds (99.9%) were released to the atmosphere, 48 thousand pounds were released to surface water, 3 thousand pounds were released to underground injection sites, and only 21 pounds were released to land (TRI92 1994). The levels of carbon disulfide in environmental media have been tested near hazardous waste sites. It is usually undetectable in air. Concentrations have been measured ranging from 25 to 340 parts per trillion in Philadelphia over a 40 day period (HSDB 1994). Levels detected in the water supply range from a mean of 0.58 ppb in surface water to a mean of 6.29 ppb in ground water near hazardous waste sites. Carbon disulfide was detected in only about 3% of the groundwater sites tested, however. About 2% of the soil samples near hazardous waste sites tested positive for carbon disulfide with a mean concentration of 8.66 ppb (ATSDR 1992). B. Transport Carbon disulfide evaporates to the atmosphere from surface water and soil. It is not expected to be retarded by adsorption to soils rich in organic material (Koc = 54); therefore, transport to ground water is not dependent on the soil conditions. The high vapor pressure and low solubility of carbon disulfide assure rapid partitioning to the atmosphere from surface waters (ATSDR 1992). C. Transformation/Persistence 1. Air - The main degradation pathways for carbon disulfide in the atmosphere are oxidation and hydroxylation. The estimated atmospheric half life for carbon disulfide is estimated at about 12 days. The reaction with hydroxyl radicals occurs primarily in the troposphere. Photolysis does not seem to be a significant degradative pathway for carbon disulfide in the atmosphere (ATSDR 1992; U.S. EPA 1986). 2. Soil - In surface soil, volatilization to air is the most important fate process for carbon disulfide (HSDB 1994). It is also highly mobile and may be leached from the soil by water (ATSDR 1992). Carbon disulfide is toxic to bacteria, and is used as a soil disinfectant. Although there is some evidence of biodegradation, this is not expected to be a significant fate process of carbon disulfide in soil (ATSDR 1992; HSDB 1994). 3. Water - The most important fate process for carbon disulfide is volatilization (ATSDR 1992; HSDB 1994). A half life of 2.6 hours has been measured for volatilization of carbon disulfide using a model river system (HSDB 1994). Under alkaline conditions, it slowly undergoes hydrolysis with an estimated half life of 1.1 year at pH 9. Biodegradation, apparently, does not play a significant role (HSDB 1994). 4. Biota - Bioaccumulation in most organisms is limited by the metabolism and rapid excretion of carbon disulfide. Bioaccumulation in the food chain is predicted to be low (ATSDR 1992; U.S. EPA 1986). IV. HUMAN HEALTH EFFECTS A. Pharmacokinetics 1. Absorption - Studies in humans and animals have demonstrated that carbon disulfide is readily absorbed via the lungs (80% retention in the first 15 min.) and animal studies indicate absorption via the gastrointestinal tract. Absorption through the skin of carbon disulfide in aqueous solution (0.33-1.67 g/L) was demonstrated in animals and humans, and exposure of the skin of rabbits to high concentrations of vapor (ò800 ppm) resulted in measurable absorption (ATSDR 1992). 2. Distribution - In studies with NMRI mice exposed to 35S and 14C- radiolabeled carbon disulfide by inhalation, high levels of carbon disulfide were present in body fat, blood, lungs, liver, and kidneys. Much lower levels were found in the brain. Changes in the distribution of the 35S and 14C radiolabels were noticeable within one hour of exposure indicating rapid metabolism of carbon disulfide (U.S. EPA 1986). Other studies with rats and rabbits reported highest concentrations in lipid-rich tissues, brain and liver, following inhalation exposure (ATSDR 1992). Studies with pregnant mice exposed to 35S and 14C-radiolabeled carbon disulfide by inhalation have demonstrated that carbon disulfide and its metabolites can pass through the placenta at all stages of gestation. Human epidemiological studies have shown carbon disulfide to be present in the milk of occupationally exposed nursing mothers (ATSDR 1992) 3. Metabolism - The metabolites of inhaled or ingested carbon disulfide include thiocarbamide and 2-thio-5-thiazolidinone, resulting from reactions with amino acids; 2-thioazolidine-4- carboxylic acid, resulting from conjugation with glutathione; and thiourea, the probable end product of cytochrome P450 oxidation. These compounds have been found in the urine of workers occupationally exposed to carbon disulfide (U.S. EPA 1986; ATSDR 1992). 4. Excretion - Unmetabolized carbon disulfide is primarily excreted in expired air (10-30% of the absorbed dose) and a small amount (<1%) is excreted unchanged through the kidneys (ATSDR 1992). The amount of carbon disulfide excreted through the lungs falls rapidly after exposure ceases. Half times reported for pulmonary excretion in rats range from 35 to 85 minutes (U.S. EPA 1986). The remaining 70-90% of the absorbed carbon disulfide is metabolized and excreted through the kidneys (ATSDR 1992). The concentration of sulfur compounds in the urine of rats decreased to control levels in 12-14 hours following inhalation exposure to 2 mg/L carbon disulfide for 8 hours (U.S. EPA 1986). B. Acute Toxicity Exposure by inhalation or by mouth to moderate to high levels of carbon disulfide can be fatal to humans. Direct contact with liquid carbon disulfide can burn the skin and the eye. 1. Humans - Carbon disulfide inhalation can result in local irritation and pharyngitis and central nervous system effects (see Section IV.G.1). Slight symptoms have been reported at doses of 320-390 ppm for several hours. Definite symptoms appear at 420-510 ppm for 30 min (total dose ÷ 11.9-14.4 mg/kg) (see end note 3). The symptoms become serious after exposure to 1150 ppm for 30 min.; dangerous to life after 30 min. at 3210-3850 ppm; and fatal in 30 min. at concentrations above 4815 ppm (HSDB 1994). The oral ingestion of 15 mL (÷300 mg/kg) carbon disulfide may be fatal to an adult (HSDB 1994). Skin contact can produce pain and erythema and prolonged contact produces vesiculation and chemical burns. Contact with the eyes causes severe chemical burns of the cornea (HSDB 1994). 2. Animals - LD50 values for oral exposure reported in the literature searched are as follows: rat, 3188 mg/kg; mouse, 2780 mg/kg; rabbit, 2550 mg/kg; guinea pig, 2125 mg/kg (U.S. EPA 1986). LC50 values of 25 g/m3 for 2 hours for rats and 10 g/m3 for 2 hours for mice were also reported (RTECS 1994). C. Subchronic/Chronic Effects Prolonged inhalation exposure to carbon disulfide can adversely affect the human nervous system and cardiovascular system. Prolonged inhalation exposure can damage the nervous system, the cardiovascular sytem, and the kidney of laboratory animals. 1. Humans - Chronic occupational exposure to carbon disulfide has resulted primarily in neurological and cardiovascular effects. Gastrointestinal and immune insufficiency problems have also been recorded. See Section IV.G.1 for information on the neurological effects. Exposure to 144-321 ppm (445-1000 mg/m3) for 5 years or longer resulted in gastrointestinal disturbances in 28 of 100 cases (U.S. EPA 1986). Cardiovascular effects including increased blood pressure, changes in ECG, increased plasma triglycerides and low-density lipoproteins, and increased angina and mortality from coronary heart disease have been reported following exposure to 6-32 ppm (18.7-100 mg/m3) for 5 months to over 5 years. Decreased immunoreactivity was seen after exposure to 3 ppm (duration of the exposure was not given in the secondary reference) (U.S. EPA 1986). 2. Animals - The major target organs for the subchronic/chronic toxicity of carbon disulfide are the nervous system, cardiovascular system, and kidneys. See Section IV.G.2 for information on nervous system effects. Cardiovascular effects seen in rats include increased serum cholesterol with lipid infiltration of coronary arteries, endocardium and aorta; and thickening of the right side of the heart and aorta following exposure to 176-750 ppm carbon disulfide given 6-24 hours/day, 5-7 days/week for 10 weeks to 15 months. Increased serum cholesterol was observed at 176 ppm for 8 months and 313 ppm given only 2.5 hours/day, 6 days/week for 8 months (U.S. EPA 1986). Increased phospholipid content of the cardiac muscle and aorta was also reported following treatment of rabbits with 141 or 256 ppm for 3-6 months. Interstitial nephritis was observed in both rats and rabbits following exposure to 200-750 ppm carbon disulfide 6-24 hours/day for up to 1 year. Decreased urinary output and increased protein content of the urine was observed in rats exposed to 0.42-3.33 ppm, 4 hours/day for 6 months (U.S. EPA 1986). Changes in liver enzymes, but not liver function, were reported in Wistar rats after exposure to 426 ppm, 5 hours/day, 4 days/week for 12 and 26 weeks. Exposure of rabbits to 200 ppm 3 hours/day for 6 months resulted in vacuolation in the cytoplasm of hepatocytes (U.S. EPA 1986). Other effects reported following treatment with carbon disulfide include increased reticulocyte counts in rats and rabbits, increased erythrocyte count in rats, and inhibition of intestinal enzymes with disruption of glucose absorption in rats (U.S. EPA 1986). D. Carcinogenicity There is inadequate evidence for the carcinogenicity of carbon disulfide in humans; no such information is available from animal studies. 1. Humans - Epidemiology studies revealed no definitive increased risk for cancer among workers who were exposed to carbon disulfide for up to 15 years. In one study, 11 male workers who died from lymphocytic leukemia were selected for analysis. It was found that these workers were exposed to 24 organic solvents one of which was carbon disulfide. The best statistical associations with leukemia were seen with carbon tetrachloride and carbon disulfide (7 cases with carbon disulfide). A statistical association involving exposure to a mixture of solvents such as in this study was not considered definitive evidence of carcinogenicity. Other studies reported no association between occupational exposure to carbon disulfide and cancer mortality. In some cases mortality due to cancer was less in the carbon disulfide population than in the control group (U.S. EPA 1986; ATSDR 1992). 2. Animals - No information was located in the secondary references on cancer in animals following exposure to carbon disulfide. E. Genotoxicity No information on the genotoxicity of carbon disulfide was found in the secondary sources searched. F. Developmental/Reproductive Toxicity Prolonged inhalation exposure to low levels of carbon disulfide can cause adverse reproductive system effects in humans. An increased incidence of fetal resorptions has been reported in rabbits exposed to carbon disulfide. Inhalation exposure does not appear to damage the developing offspring of laboratory animals. EPA has derived an oral RfD (reference dose) (see end note 4) of 0.1 mg/kg/day for carbon disulfide, based on the absence of developmental effects in laboratory animals. 1. Humans- A number of epidemiological studies have reported that inhalation exposure to 13-77 ppm carbon disulfide resulted in changes in sperm morphology, decreased hormone levels, and decreased libido in males; and menstrual irregularities in females (ATSDR 1992; U.S. EPA 1986). One report indicated increased menstrual disorders and greater incidence of toxemia in pregnancy after occupational exposure to about 12-18 ppm carbon disulfide. An increase in spontaneous abortions was reported in one study following occupational exposure to about 9 ppm (the length of exposures were not given in the secondary sources) (U.S. EPA 1986). There are no data that indicate an increase in congenital malformations in children born to mothers exposed by any route to carbon disulfide (ATSDR 1992). 2. Animals - Fetal resorption was reported in rabbits exposed orally to 25 mg/kg/day during gestation, but was not seen in rats exposed to 100 mg/kg/day. The 25 mg/kg/day dose was a frank-effect-level (FEL) for fetal resorption in rabbits (U.S. EPA 1994). Inhalation experiments failed to show any effects on fetal development in rats or rabbits exposed to 62.3 or 124.6 mg/m3 (5 and 10 mg/kg/day, rats; 11, 22 mg/kg/day, rabbits) given from 34 weeks before breeding through the entire gestation period. The highest no-observed- adverse effect level (NOAEL) for the study was 22 mg/kg/day; however, this NOAEL was close to the FEL seen in the previous experiment. The NOAEL of 20 ppm (62.3 mg/m3), which was converted to 11 mg/kg/day for oral exposure, was chosen by the U.S. EPA, 1994 to calculate a chronic RfD for carbon disulfide of 0.1 mg/kg/day. The use of this NOAEL was supported by a human NOAEL of 10 mg/kg/day for nervous system effects in an epidemiological experiment (Section IV-G-1). G. Neurotoxicity Inhalation exposure to carbon disulfide casuses adverse nervous system effects in both humans and in animals. 1. Humans - Acute central nervous symptom effects following carbon disulfide inhalation can include dizziness, fatigue, headache, mood changes, lethargy, blurred vision, agitation, delirium, hallucinations, convulsions, and coma. Slight symptoms have been reported at doses of 320-390 ppm for several hours. Definite symptoms appear at 420-510 ppm for 30 min. The symptoms become serious after exposure to 1150 ppm for 30 min.; dangerous to life after 30 min. at 3210-3850 ppm; and fatal in 30 min. at concen- trations above 4815 ppm (HSDB 1994). Exposure to 144-321 ppm (445-1000 mg/m3) for 5 years or longer resulted in polyneuritis in 88 of 100 workers. Encephalopathy was observed in 43 cases. Also seen were tremors, vertigo, psychosis, and myopathy. Polyneuritis has been reported following exposure to 5 ppm (15.6 mg/m3), and reductions in nerve fiber conduction velocity have been reported after exposure to 1.0-7.6 ppm for an average of about 12 years (U.S. EPA 1986). An epidemiological study examined a population exposed to a combined exposure of 7.3 ppm (extrapolated to 10 mg/kg/day) over a period of 12 or more years. Some minimal neurotoxicity was seen, however, the measured parameters, nerve conduction velocities, though reduced, were still within the low normal range of clinical values and there were no specific health consequences. These data were used as confirmatory evidence to support the reference dose calculated by U.S. EPA, 1992 (see Section IV.F.2). 2. Animals - Effects on the nervous system have been observed in rats, rabbits, dogs, cats, and monkeys following subchronic or chronic exposure to carbon disulfide. Degenerative changes in the central nervous system were seen after exposure to 400-750 ppm given 5-8 hours/day for 2-3 months. Degenerative changes in the brain were reported in rhesus monkeys after treatment with 16 ppm, 6 hours/day, 5 days/week for 12-24 months (U.S. EPA 1986). Effects on peripheral nerves including decreased conduction velocity, axonal swelling, degeneration of myelinated fibers and ultrastructural degenerative changes were seen in rats exposed to 288-768 ppm carbon disulfide 5-6 hours/day, 5-7 days/week for 1.5-12 months (U.S.EPA 1986). V. ENVIRONMENTAL EFFECTS A. Toxicity to Aquatic Organisms Carbon disulfide has moderate acute toxicity to aquatic organisms; acute toxicity values range between >1 mg/L and 100 mg/L. LC50 values for fish are: 3.0-5.8 mg/L, 96 hours for Poecilia reticulata (guppy), 45.0-94.0 mg/L, 96 hours for Alburnus; 162 mg/L, 24 hours, 135 mg/L, 48 and 96 hours for Gambusia affinis (mosquitofish) (AQUIRE 1994). The 48 hour LC50 value for Daphnia magna (water flea) is 1.9-2.2 mg/L (AQUIRE 1994). The 96 hour EC50 value for growth in the algae Chlorella pyrenoidosa is 21.0 mg/L (AQUIRE 1994). B. Toxicity to Terrestrial Organisms No information was found in the available literature for terrestrial organism toxicity. The oral LD50 in the rat, 3188 mg/kg, suggests that the chemical would not be acutely toxic to terrestrial animals unless present in very high concentrations. Studies in laboratory animals also suggest that carbon disulfide would not cause developmental/reproductive effects in terrestrial species at expected environmental levels (see section IV.F). C. Abiotic Effects No information on the abiotic effects of carbon disulfide was located in the secondary references searched. According to the definition provided in the Federal Register (1992), carbon disulfide is a volatile organic carbon (VOC) substance. As a VOC, carbon disulfide can contribute to the formation of photochemical smog in the presence of other VOCs. VI. EPA/OTHER FEDERAL/OTHER GROUP ACTIVITY The 1990 Clean Air Act Amendments list carbon disulfide as a hazardous air pollutant and target rayon, cellophane, and carbon disulfide production for EPA review. Occupational exposure to carbon disulfide is regulated by the Occupational Safety and Health Administration. The permissible exposure limit (PEL) is 20 parts per million parts of air (ppm) as an 8-hour time weighted average (TWA) or 30 ppm as a ceiling value (i.e., exposures may not exceed these levels) (29 CFR 1910.1000). NIOSH and ACGIH have recommended a skin notation to their recommended exposure levels, indicating that workplace dermal exposure should be controlled as well. Federal agency and other groups that can provide additional information on carbon disulfide are listed in Tables 4 and 5. TABLE 4. EPA OFFICES AND CONTACT NUMBERS FOR INFORMATION ON CARBON DISULFIDE ________________________________________________________________________ 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 Water Clean Water Act (202) 260-7588 ________________________________________________________________________ TABLE 5. OTHER FEDERAL OFFICE/OTHER GROUP CONTACT NUMBERS FOR INFORMATION ON CARBON DISULFIDE ___________________________________________________________________________ Other Agency/Department/Other Group Contact Number ___________________________________________________________________________ Agency of Toxic Substances & Disease Registry (404) 639-6000 American Conference of Governmental Industrial Hygienists (Recommended Exposure Limit (see end note 5): 10 ppm; [skin] (see end note 6)) (513) 742-2020 National Institute for Occupational Safety & Health (Recommended Exposure Limit (see end note 6): 1 ppm; [skin] (see end note 6)) (800) 356-4674 Occupational Safety & Health Administration (Permissible Exposure Limit (see end note 7): 20 ppm) (Permissible Ceiling Exposure Limit: 30 ppm) (Check local phone book for phone number under Department of Labor) ___________________________________________________________________________ VII. END NOTES 1. Akzo closed a 350 million pound per year plant in Delaware City, DE in late 1991. 2. 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. 3. Calculated using the factor, 3.17 (Verschueren 1983), to convert ppm to mg/m3, which is multiplied by 0.0089 (the calculated occupational 0.5-hour breathing rate, 0.625 m3, divided by the assumed adult body weight, 70 kg) to obtain the dose in mg/kg (U.S. EPA 1988). 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. 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. 6. A [skin] notation indicates that air sampling is not sufficient to accurately quantitate exposure. Measures to prevent significant cutaneous absorption may be required. 7. 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 workweek. VIII. CITED REFERENCES AQUIRE. 1994. EPA ERL-Duluth's Aquatic Ecotoxicology Data Systems. U.S. EPA, Duluth, MN. Retrieved July 1994. ATSDR. 1992. Agency for Toxic Substances and Disease Registry. 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