EPA 749-F-94-007a CHEMICAL SUMMARY FOR 1-BUTANOL 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 These sources include online databases, unpublished EPA information, government publications, review documents, and standard reference materials.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 1-butanol are summarized in Table 1. TABLE 1. CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL PROPERTIES OF 1-BUTANOL __________________________________________________________________________ Characteristic/Property Data Reference __________________________________________________________________________ CAS No. 71-36-3 Common Synonyms butanol; n-butanol; butyl alcohol Budavari et al. 1989 Molecular Formula C4H10O Chemical Structure CH3CH2CH2CH2OH Physical State refractive liquid Budavari et al. 1989 Molecular Weight 74.12 Budavari et al. 1989 Melting Point -90øC Budavari et al. 1989 Boiling Point 117-118øC Budavari et al. 1989 Water Solubility 9.1 mL/100 mL @ 25øC Budavari et al. 1989 Density d20/4øC, 0.810 Budavari et al. 1989 Vapor Density (air = 1) 2.6 HSDB 1994 KOC 72 (calculated) CHEMFATE 1994 Log KOW 0.88 CHEMFATE 1994 Vapor Pressure 7.00 mm Hg @ 25øC CHEMFATE 1994 Reactivity flammable; contact with strong oxidizers may cause fire and explosion U.S. EPA 1989; HSDB 1994 Flash Point 36-38øC U.S. EPA 1989 Henry's Law Constant 8.81 x 10-6 atm-m3/mole CHEMFATE 1994 Fish Bioconcentration Factor <3 (estimated) U.S. EPA 1989 Odor Threshold 7.1 ppm (in water); 0.83 ppm (in air); winelike odor U.S. EPA 1989; HSDB 1994 Conversion Factors 1 mg/m3 ÷ 0.33 ppm at 20øC 1 ppm ÷ 3.03 mg/m3 at 20øC U.S. EPA 1989 __________________________________________________________________________ II. PRODUCTION, USE, AND TRENDS A. Production 1-Butanol is produced by five companies in the United States. Table 2 lists the producers, along with plant locations and capacities. In 1992, US production of 1-butanol was estimated to be 1,261 million pounds. One million pounds were imported into the U.S., and 149 million pounds were ex- ported (Mannsville 1993). TABLE 2. United States Producers of 1-Butanol _______________________________________________________________________ Company Plant Location Plant Capacity (In Millions of Pounds) _______________________________________________________________________ BASF Corp. Freeport, TX 160 Hoechst Celanese Bay City, TX 300 Shell Chemical Deer Park, TX 150 Texas Eastman Longview, TX 200 Union Carbide Texas City, TX 560 _______________________________________________________________________ Source: Mannsville 1993. B. Use 1-Butanol is used primarily as a chemical intermediate in the production of butyl acrylate and methacrylate. It is also used in the production of glycol ethers and butyl acetate; as a solvent; and as a plasticizer (Mannsville 1993). Small amounts are also used in hydraulic fluids, in detergent formulations, as a medication, and as an extractant in the manufacture of pharmaceuticals (HSDB 1994). Table 3 shows the estimated 1992 end-use pattern for 1-butanol in the United States. C. Trends Demand for 1-butanol in the U.S. is expected to grow at a rate of 2 to 3 percent per year (Mannsville 1993). TABLE 3. Estimated 1992 U.S. End-Use Pattern of 1-Butanol _______________________________________________________________________ Use of 1-Butanol Percentage of US (typical Standard Industrial 1-Butanol Use Classification (SIC) Code) (see end note 1) _______________________________________________________________________ Butyl Acrylate and Methacrylate (production, SIC 2869) 36% Glycol Ethers (production, SIC 2869) 25% Butyl Acetate (production, SIC 2869) 14% Solvents (production, SIC 2869) 12% Plasticizers (production, SIC 2869; use, SICs 282, 308, and others) 7% Miscellaneous [no applicable SIC Code(s)] 6% ________________________________________________________________________ Source: Mannsville 1993. III. ENVIRONMENTAL FATE A. Environmental Release 1-Butanol is released to the environment from natural and human sources (U.S. EPA 1989). 1-Butanol occurs naturally in dried beans (0-7 ppb), split peas (150 ppb), and lentils (120 ppb). It has been reported (levels not quantified) as a volatile component of apple and pear aroma and grape essence; in volatiles from mountain cheese, roasted filberts, and fried bacon; and in human milk collected from volunteers in New Jersey, Pennsylvania, and Louisianna (U.S. EPA 1989). Other natural sources include animal wastes, microbes and insects (U.S. EPA 1989). Human sources of 1-butanol include volatilization from solvents, rendering, sewage treatment, starch manufacture, whiskey manufacture, wood pulping and turbine emissions (U.S. EPA 1989). 1-Butanol was detected in the air of the Black Forest in Germany, in air from Point Barrows, AK (34-445 ppb; 103-1348 micrograms/m3), probably resulting from fermentation of the tundra cover; in ambient air near a solvent reclamation plant in Maryland (1-10 ppm; 3.03-30.3 mg/m3); in indoor air collected in homes in Italy (20 micrograms/m3); and in the breathable air of workers using solvents (3.6 mg/m3) (U.S. EPA 1989). 1-Butanol may be released to water through various wastewater emissions, including those from chemical manufacturing plants, textile plants, pulp mills making kraft paper, sewage treatment plants, oil refineries, and landfill leachates (U.S. EPA 1989). The effluents from a petrochemical facility contained 16.0 mg/L 1-butanol; the daily discharge was ~90 pounds/day (HSDB 1994). In the 1970s, 1-butanol was detected in drinking water concentrates collected from several US cities (concentrations not reported). The chemical was present in surface water samples taken from Lake Ontario, the Hayashida River in Japan (87-318 ppb), and the Lee River in England (<1 ppb) (U.S. EPA 1989). 1-Butanol is released to land from industry and through the deposition of the chemical or of materials containing it into landfills. In one instance, the concentration of 1-butanol in leachate from an artificial sanitary landfill was 0.21 g/L (HSDB 1994). In 1992, environmental releases of the chemical, as reported to the Toxic Chemical Release Inventory by certain types of US industries, totaled about 32.1 million pounds, including 29.7 million pounds to the atmosphere; 2.32 million pounds to underground injection sites; 57,220 pounds to land; and 35,369 pounds to surface water (TRI92 1994). B. Transport 1-Butanol undergoes transport to the atmosphere from soil and water via volatilization (vapor pressure, 7.00 mm Hg; Henry's Law constant, 8.81 x 10-6 atm-m3/mole), a process that is expected to occur at a slow to moderate rate. The chemical, readily soluble in water (9.1 mL/100 mL), is removed from the atmosphere to soil and water by wet deposition (U.S. EPA 1989). Once in the soil, the water solubility and KOC value indicate that the chemical is mobile; however, alcohols such as 1-butanol may adsorb to clay surfaces and leaching may be retarded in some soils (U.S. EPA 1989). C. Transformation/Persistence 1. Air - The main degradation pathway for 1-butanol in the atmosphere is probably reaction with photochemically produced hydroxyl radicals (U.S. EPA 1989). The estimated half-life for this reaction is 2.2 days, based on the rate constant of 7.32 x 10-12 cm3/molecule-sec and the atmospheric hydroxyl radical concentration of 5 x 10+5 molecules/cm3 (U.S. EPA 1989). The physical removal of 1-butanol from the atmosphere by wet deposition is another possible removal mechanism (U.S. EPA 1989). 2. Soil - Because 1-butanol is readily soluble in water, the chemical is expected to be fairly mobile in the soil and may leach into groundwater (HSDB 1994); however, concurrent bio- degradation may reduce the leaching (U.S. EPA 1989). One study demonstrated that 1-butanol biodegraded readily in two different agricultural soils (U.S. EPA 1989). The losses for both soils averaged 67% over 20 days, with the majority of the loss occurring during the first two days. Biodegradation losses were approximately 2-17 times greater than losses by volatilization, which occurred mostly within the first day (U.S. EPA 1989). 3. Water - Experimental studies indicate that biodegradation is the most important fate process for 1-butanol in water (U.S. EPA 1989). Under laboratory conditions (Chemical Oxygen Demand method), 1-butanol was 31% degraded in 2 hours and 82% degraded in 24 hours (CHEMFATE 1994). In a natural river die-away test, using river water as the only inoculum, about 56% of 3 ppm of 1-butanol degraded after 4 days (U.S. EPA 1989). The results of other aerobic screening studies using activated sludge or sewage as inoculum provide additional evidence of the biodegradability of 1-butanol (U.S. EPA 1989). Under anaerobic conditions, 1-butanol (initial concentration of 500 ppm) was degraded 100% after a 4 day lag period, at the rate of about 100 ppm/day (U.S. EPA 1989). Another important fate process for 1-butanol in water, particularly in shallow rivers, is volatilization (U.S. EPA 1989). Under conditions simulating a river 1 meter deep, flowing 1 meter/second with a wind velocity of 3 meters/second, the half-life for 1-butanol was ~4.1 days, whereas the volatilization half-life from a model environmental pond was an estimated 44.5 days. Hydrolysis and photolysis are not expected to be significant pathways of 1-butanol in water (U.S. EPA 1989). 4. Biota - The estimated bioconcentration factor (BCF) for 1-butanol of 2.75 for aquatic organisms (CHEMFATE 1994) suggests that biomagnification of the chemical in the aquatic and terrestrial food chains is not likely (U.S. EPA 1989). IV. HEALTH EFFECTS A. Pharmacokinetics 1. Absorption - Studies in humans and animals have demonstrated that 1-butanol is readily absorbed by the respiratory tract, the gastrointestinal tract, and the skin (U.S. EPA 1989). Twelve humans, exposed to 300 or 600 mg of 1-butanol/m3 for 30 minute periods of rest or exercise, absorbed around 46-48% during rest and 37-41% during exercise. Although the percentage of uptake decreased with exercise, the total uptake increased because ventilation increased during exercise. Absorption through the gastrointestinal tract appears to be complete (U.S. EPA 1989). The total absorption by humans exposed by inhalation and skin is of concern for workers (Rowe and McCollister 1982). One group of investigators calculated that (assuming the rate of absorption through the skin of man was the same as that of dogs) if the hands of a man were immersed in 1-butanol for 1 hour, uptake would total about 390 mg of the chemical; whereas exposure to 50 ppm 1-butanol vapor for 1 hour results in pulmonary uptake of about 91 mg (assuming uptake of 50%). In vivo and in vitro studies have shown that the chemical is also absorbed through the oral mucosa of dogs and the cornea of rabbits' eyes (U.S. EPA 1989). 2. Distribution - In a study in which rats were given oral doses of 450 mg/kg of radiolabeled 1-butanol, the largest amounts of radioactivity were detected 4 or 8 hours after treatment in the liver (3.88% of administered dose), kidney (0.24%) and blood (0.74%). Peak concentrations ranging from 0.009 to 0.12% were detected in the lung, heart, brain, adrenals, and fat (U.S. EPA 1989). In one study, 12.1-16.3% of the administered oral dose remained in the carcass (U.S. EPA 1989). 3. Metabolism - 1-Butanol appears to follow the same metabolic pathway as do other alcohols: oxidation to the aldehyde, then to the acid, and ultimately to carbon dioxide and water (U.S. EPA 1989). In one study in rats, orally administered 1-butanol was metabolized rapidly and nearly completely to carbon dioxide (~80% of the administered dose was eliminated as 14CO2 in expired air; <1% of the dose was eliminated unchanged), mainly by hepatic microsomal alcohol dehydrogenase; smaller amounts of radioactivity (2.6-5.1%) were excreted in the urine as sulfate and glucuronide conjugates and as urea (U.S. EPA 1989). 4. Excretion - Orally administered 1-butanol was excreted within 24 hours by rats, mainly as labeled CO2 in expired breath (78.3 to 83.3%). Of the remainder of the dose, 2.6 to 5.1% was eliminated in the urine, 0.69 to 1.1% was excreted in the feces (U.S. EPA 1989). B. Acute Effects Acute inhalation exposure to low to moderate levels of 1-butanol produces irritation of the eyes, nose and throat in humans. Exposure to high, non-lethal levels cause irritation in animals. Exposure to high, non-lethal levels for several days causes reversible liver and kidney effects in animals. 1. Humans - An average of 10 humans (men and women) exposed to 1-butanol vapor experienced irritation of the eyes, nose and throat at 25 ppm (75 mg/m3), and pronounced throat irritation and later onset of mild headaches at 50 ppm (150 mg/m3) (U.S. EPA 1989). The concentration of 75 mg/m3 converts roughly to an intake of 1.34 mg/kg over a one-hour period (see end note 2). No statement was made as to the reversibility of these effects was made. Skin irritation has resulted from 24-hours of contact with ò7.8% 1-butanol in plant oil (U.S. EPA 1989). 2. Animals - Oral LD50 values for 1-butanol are 0.79 to 4.36 g/kg in rats (U.S. EPA 1989) and 3.5 g/kg in rabbits (Rowe and McCollister 1989); and the skin LD50 is 4.2 g for rabbits (Rowe and McCollister 1982). Animal deaths from overexposure to 1-butanol is believed to be due to respiratory failure (Rowe and McCollister 1982). Oral doses of 1 and 2 mL/kg (0.81 and 1.62 g/kg), administered to rats for 7 days, produced dose-related decreases in the liver content of thiamine, riboflavin, pyridoxine, niacin and pantothenic acid (U.S. EPA 1989). RD50 values (see end note 3) for the acute effects of 1-butanol vapor in mice have been estimated at 1268 ppm (3844 mg/m3) and 4784 ppm (14,503 mg/m3) (U.S. EPA 1989). An inhaled concentration of 24,624 mg/m3 1-butanol, administered for "several days" caused reversible fatty infiltrations of liver and kidneys of mice (U.S. EPA 1989). A single application of 0.005 ml undiluted 1-butanol was severely irritating to the eyes of rabbits; single applications of unspecified amounts of 1-butanol was slightly to moderately irritating to the skin of rabbits (Rowe and McCollister 1982). C. Subchronic/Chronic Effects Humans exposed chronically to high concentrations of 1-butanol have experienced neurological (see section IV.G), ocular, auditory, and dermal effects. Animals exposed chronically to 1-butanol exhibit vascular changes, increased thyroid activity, and pathological lesions of the lungs and intestines at low to moderate concentra- tions, and degenerative changes of the liver and kidneys, and effects on the blood. 1. Humans - In an occupational study that covered about 10 years, exposure to 100 ppm 1-butanol (300 mg/m3) had no effect on hematological parameters, liver function, urine analysis, chest X-rays, eyes, or absenteeism (U.S. EPA 1994). In the same study, exposure to concentrations averaging ò200 ppm resulted in transient corneal inflammation, with associated lacrimation, burning sensation, and photophobia (U.S. EPA 1989). Exposure to 1-butanol has also been associated with a special vacuolar keratitis, characterized by pain and tearing, mainly upon first opening the eyes in the morning (HSDB 1994). Occupational case studies have also shown the following: hearing loss in workers exposed to 80 ppm (240 mg/m3) for 3-11 years, in the presence of industrial noise (controls were exposed to industrial noise without 1-butanol); and eye irritation and corneal lesions at concentrations >50 ppm that were reversible after 5-7 days away from work (U.S. EPA 1989). 2. Animals - Effects observed in long-term oral toxicity studies include decreased enzyme activities and the appearance of mega- mitochondria in the livers of rats exposed to 6.9% 1-butanol in the drinking water (U.S. EPA 1989). Guinea pigs exposed to 100 ppm 1-butanol in air 4 h/day, 6 days/ week for approximately 10 weeks exhibited decreased red blood cell and increased lymphocyte counts, lung hemorrhage, albuminuria, and degenerative changes of the liver and kidneys (Rowe and McCollister 1982). Rats and mice were exposed to 1-butanol vapor concentrations of 0, 0.8, 6.6, or 40 mg/m3 (0.26, 2.2, or 13.2 ppm) continuously for 4 months (U.S. EPA 1989). The rats exposed to 6.6 and 40 mg/m3 had, in addition to neurological symptoms described in section IV.G, pathological lesions that included dilation of blood vessels with diapedesis of erythrocytes, pulmonary edema and atelectasis, and necrotic changes in the parenchyma of the intestines. Rats in all groups had increased thyroid activity. The mice had mainly neurological effects (see section IV.G) (Rowe and McCollister 1982). The study's authors concluded that 0.8 mg/m3 1-butanol would cause no adverse effects under conditions of continuous and prolonged exposure (Rowe and McCollister 1982). The concentration of 40 mg/m3 is roughly equivalent to 25.5 mg/kg/day (see end note 4). D. Carcinogenicity No information was found for the carcinogenicity of 1-butanol in humans or animals. 1. Humans - No information was found in the secondary sources searched to indicate that 1-butanol is carcinogenic to humans. Based on no human and no animal cancer data, the U.S. EPA (1994) classified 1-butanol as class D, not classifiable as to human carcinogenicity. 2. Animals - No information was found in the secondary sources searched on the carcinogenicity of 1-butanol in animals. E. Genotoxicity 1-Butanol was negative for sister chromatid exchanges in Chinese hamster ovary cells in vitro and for gene mutations in Salmonella typhimurium (Ames assay) (GENETOX 1994). F. Developmental/Reproductive Toxicity Information on the developmental toxicity and reproductive system effects of 1-butanol in humans and animals is limited. Evidence from animal studies indicate that exposure to high levels of 1-butanol may adversely affect the developing fetus and the reproductive system. 1. Humans - No information was found in the secondary sources searched on the developmental/reproductive effects of 1-butanol in humans. 2. Animals - No effects on the incidence of malformations or embryolethality were observed in Long-Evans rats treated by gavage with doses of 1-butanol that were 0.02-24% of the oral LD50 on gestation days 6-15 (U.S. EPA 1989). Pregnant Sprague-Dawley rats inhaled 1-butanol concentrations of up to 8000 ppm (24,250 mg/m3), 7 h/day throughout gestation and were killed on day 20 (U.S. EPA 1989). Fetal weights were reduced at 8000 ppm, a dose that produced maternal toxicity in a previous study. Examination of skeletal and soft tissues revealed no teratogenic effects. In another study, levels of circulating testosterone decreased and levels of corticosterone increased in Sprague-Dawley rats exposed to 500 ppm (1516 mg/m3) of 1-butanol for 6 hours (U.S. EPA 1989). Hormone levels returned to normal after one week of exposure. G. Neurotoxicity 1-Butanol affects the human central nervous system, producing adverse effects at moderate concentrations in air. 1-Butanol causes adverse central nervous system effects in animals by both the oral and inhalation routes of exposure. EPA has derived an oral reference dose (RfD) (see end note 5) of 0.1 mg/kg/day for 1-butanol, based on the absence of ataxia and hypertension observed in animals exposed by mouth at a 125 mg/kg/day level. 1. Humans - Eighteen volunteers were exposed to 1-butanol concentrations of 0.3-15 mg/m3 (schedule and duration not specified). At 1.2 mg/m3, the subjects experienced altered sensitivity to light in the dark-adapted eye and altered electrical activity of the brain; there were no effects at 1 mg/m3 (U.S. EPA 1989). On investigator noted severe vertigo in five workers exposed to butyl alcohol during 1929-1944 (ACGIH 1991). Other human subjects, exposed to 50 ppm 1-butanol, experienced headaches (U.S. EPA 1989). 2. Animals - 1-Butanol, administered to male and female rats (30/sex/group) at doses of 0, 30, 125, or 500 mg/kg/day by gavage for 13 weeks, induced ataxia and hypoactivity consistently at 500 mg/kg/day, during the last six weeks of treatment; no other dose-related effects were noted. The no-observed- adverse effect level (NOAEL) for the study was 125 mg/kg/day (U.S. EPA 1994). Based on these data, the U.S. EPA (1994) calculated a chronic oral RfD for 1-butanol of 0.1 mg/kg/day or 9 mg/day for a 70-kg person. 1-Butanol produces CNS depression at oral doses of 2.1 to 2.4 g/kg in rabbits and at atmospheric concentrations of 6600 ppm in mice (HSDB 1994). 1-Butanol, administered orally at doses of 1-2 g/kg, reduced the performance rate of rats (ability to balance on a rising slope) and impaired coordinated muscular activity of mice (U.S. EPA 1989). An inhaled concentration of 24,624 mg/m3 1-butanol, administered for "several days", produced narcosis but no deaths in mice (U.S. EPA 1989). Rats and mice were exposed to 1-butanol vapor concentrations of 0, 0.8, 6.6, or 40 mg/m3 (0.26, 2.2, or 13.2 ppm) con- tinuously for 4 months (U.S. EPA 1989). At 6.6 and 40 mg/m3, the rats exhibited decreases in hexobarbital sleeping time, CNS subliminal impulses, work capacity and oxygen requirements. Rats in all groups had increased reflex activity and a concentra- tion-related increase in blood cholinesterase levels (this effect reversed after termination of exposure). The mice exhibited decreases in hexobarbital sleeping time and CNS subliminal impulses. Mice of all groups had increased reflex activity (U.S. EPA 1989). V. ENVIRONMENTAL EFFECTS 1-Butanol is not expected to be toxic to aquatic or terrestrial organisms at levels normally found in the environment. A. Toxicity to Aquatic Organisms 1-Butanol has low acute toxicity to aquatic organisms; toxicity values are greater than 100 mg/L. Ninety-six hour LC50 values for Pimephales promelas (fathead minnow), tested in static bioassays, are 1,910 mg/L in Lake Superior water and 1,940 mg/L in reconstituted water (Verschueren 1983). Other 96-hour LC50 values were 1510- 1940 mg/L for fathead minnows, 2100 mg/L for copepods, and 2250-2400 mg/L for bleaks (U.S. EPA 1989). Toxicity threshold values for the cell multiplication inhibition test were 650 mg/L for Pseudomonas putida (bacteria), 875 mg/L for Scenedesmus quadricauda (green algae) (Verschueren 1983). B. Toxicity to Terrestrial Organisms Mallard duck eggs immersed for 30 seconds in 100% 1-butanol failed to produce viable chicks by day 18 of incubation (U.S. EPA 1989). No information was found in the available literature for terrestrial mammals. The oral LD50 in the rat, 0.79 to 4.36 g/kg and the results of chronic studies in laboratory animals (section C) (U.S. EPA 1989), suggest that the chemical would not be acutely toxic to terrestrial animals unless present in very high concentrations. C. Abiotic Effects Most 1-butanol in the atmosphere is removed by reaction with hydroxyl radicals (U.S. EPA 1989). According to the definition provided in the Federal Register (1992), 1-butanol is a volatile organic compound (VOC) substance. As a VOC, 1-butanol can contribute to the formation of photochemical smog in the presence of other VOCs. VI. EPA/OTHER FEDERAL/OTHER GROUP ACTIVITY The Clean Air Act Amendments of 1990 list 1-butanol as a hazardous air pollutant. Occupational exposure to 1-butanol is regulated by the Occupational Safety and Health Administration. The permissible exposure limit (PEL) is 100 parts per million parts of air (ppm) as an 8-hour time-weighted average (TWA) (29 CFR 1910.1000). NIOSH and the ACGIH have added a skin notation to their recommended exposure limits, indicating that workplace dermal exposure should be controlled as well. Federal agencies and other groups that can provide additional information on 1-butanol are listed in Tables 4 and 5. TABLE 4. EPA OFFICES AND CONTACT NUMBERS FOR INFORMATION ON 1-BUTANOL ________________________________________________________________________ EPA OFFICE LAW PHONE NUMBER ________________________________________________________________________ Pollution Prevention Toxic Substances Control Act & Toxics (Sec. 4/8E) (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 OFFICE/OTHER GROUP CONTACT NUMBERS FOR INFORMATION ON 1-BUTANOL _______________________________________________________________________ Other Agency/Department/Other Group Contact Number _______________________________________________________________________ American Conference of Governmental Industrial Hygienists (Recommended Exposure Limit (see end note 6): 50 ppm; [skin] (see end note 7)) (513) 742-2020 Consumer Product Safety Commission (301) 504-0994 Food & Drug Administration (301) 443-3170 National Institute for Occupational Safety & Health (Recommended Highest Exposure Limit: (see end note 5) 50 ppm; [skin](see end note 6)) (800) 356-4674 Occupational Safety & Health Administration (Permissible Exposure Limit (see end note 8): 100 ppm) (Check local phone book for phone 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. Calculated by multiplying 75 mg/m3 by 0.018 (the calculated occupational 1-hour breathing rate, 1.25 m3, divided by the assumed adult body weight, 70 kg.) to obtain the dose in mg/kg. 3. The RD50 concentration is that concentration that reduces respiratory rate by 50%. 4. Calculated by multiplying 40 mg/m3 by 0.637 (the standard 24-hour breathing rate, 0.223 m3, divided by the assumed adult rat body weight, 0.350 kg, and assuming 100% absorption) to obtain the dose in mg/kg/day (U.S. EPA 1985). 5. 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. 6. The ACGIH/NIOSH recommended exposure limits are ceiling concentrations that should not be exceeded during any part of the workday exposure. 7. A [skin] notation indicates that air sampling is not sufficient to accurately quantitate exposure. Measures to prevent significant cutaneous absorption may be required. 8. The OSHA permissible exposure limit is a time-weighted average (TWA) concentration that must not be exceeded during any 8-hour work shift of a 40-hour work week. VIII. CITED REFERENCES ACGIH. 1991. American Conference of Governmental Industrial Hygienists, Inc. Cocumentation of the Threshold Limit Values and Biological Exposure Indicies, 6th ed. ACGIH, Cincinnati, OH, pp. 170-171. 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