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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 ISOPROPYL ALCOHOL BACKGROUND INFORMATION PHYSICAL AND CHEMICAL PROPERTIES Chemical formula: C3H8O Molecular weight: 60.09 Chemical names: 2-Propanol, isopropanol, propan-2-o1 Synonyms: Secondary propyl alcohol, alcosolve 2 CAS number: 67–63–0 Freezing point: −89.5°C Boiling point: 82.4°C Specific gravity: 0.786 Vapor pressure: 33 mm Hg (20°C) Flash point: 53°F Auto ignition temperature: 455. 6°C Solubility: Miscible with water, alcohol, ether, and chloroform General characteristics: Colorless liquid with slight odor resembling that of rubbing alcohol Conversion factors: 1 ppm=2.45 mg/m3 1 mg/m3=0.41 ppm OCCURRENCE AND USE Isopropyl alcohol is manufactured in the United States by an indirect hydration technique in which a fraction containing 40–60% propylene that is isolated from refinery exhaust gases reacts with sulfuric acid (Lowenheim and Moran, 1975). In an older (strong-acid) process, 88–93% sulfuric acid reacted with propylene gas at 25–60°C for a long time. In a newer (weak-acid) process, which has replaced the strong¯ acid process, propylene gas is absorbed in 60% sulfuric acid at 85°C for a short reaction time (NIOSH, 1976). Estimated annual production capacity for 1981 was 2.8 million pounds (SRI, International, 1982). Isopropyl alcohol was used primarily in the production of acetone, by dehydrogenating catalytically at 400°C to give acetone and hydrogen (major process) or oxidizing at high pressure to give acetone and hydrogen peroxide. However, the use of isopropyl alcohol in acetone manufacture has been decreasing in recent years. Its second main use is as a solvent: to extract or purify numerous natural products, such as oils, gums, shellacs, waxes, kelp, and pectin; in the manufacture of fish-protein concentrate; as a solvent for synthetic resins, e.g., such coatings as phenolic varnishes and nitrocellulose lacquers; and as a solvent in drug and cosmetic formulations (it is the major component of rubbing compounds used as solvents and rubefacients) (Lowenheim and Moran, 1975; Wickson, 1968; National Formulary Board, 1975), Its use in cosmetics has generally been limited to highly scented or
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 relatively Inexpensive products. The third principal use is in the manufacture of other chemicals, such as isopropyl acetate, isopropylamine, diisopropylamine, herbicidal ester, isopropyl xanthate, isopropyl myristate, isopropyl palmitate, isopropyl oleate, aluminum isopropoxide, and isopropyl ether (Wickson, 1968). Isopropyl alcohol toxicity is of interest to the Navy, because of its presence as an atmospheric contaminant in nuclear submarines. SUMMARY OF TOXICITY INFORMATION Table 6 summarizes some data on toxic doses of isopropyl alcohol in animals and man. The International Agency for Research on Cancer has also reviewed toxicity data (IARC, 1977). EFFECTS ON HUMANS The documented toxicity of isopropyl alcohol in man is confined for the most part to accidental ingestion (not inhalation), with a few cases reported in association with rectal and topical application. Several deaths have reportedly resulted from ingestion of about 1 pint of 70% isopropyl alcohol (Adelson, 1962). Other persons have survived after ingesting similar amounts (Chapin, 1949; Freireich et al., 1967; Juncos and Taguchi, 1968; King et al., 1970). The lethal dose of isopropyl alcohol is estimated as 160–240 ml (Ashkar and Miller, 1971) and 250 ml (McBay, 1973). In 1978, 372 Melanesian men consumed a solution of 82% methyl alcohol and 18% isopropyl alcohol in the mistaken belief that the solution was methylated spirits; 18 of them died. A disparity was noted in the amount of solution consumed and the sequelae; for example, 100 ml produced blindness and death in one case, but 500 ml seemed to cause no disability in two other men who claimed to have drunk this high quantity (Scrimgeour, 1980). The rates of ingestion were not specified. Ballard et al. (1975) reported that 15 of 41 persons working in a drug company became ill and had nausea, vomiting, weakness, and abdominal pain. Their illness was attributed to their exposure to carbon tetrachloride and isopropyl alcohol, inasmuch as 13 of the 15 had been within 25 ft of these chemicals when they were spilled. In two factories manufacturing isopropyl alcohol by the strong-acid process (involving the formation of isopropyl oils as byproducts), an excess risk of cancers of the paranasal sinuses was found (Eckhardt, 1974; Hueper, 1966; Weil et al., 1952). An excess risk of laryngeal cancer may also have been present. However, diisopropyl sulfate, an intermediate substance in the preparation of isopropyl alcohol suspected of being an animal carcinogen, is formed in the strong-acid process. Zakhari et al. (1977) quoted several studies (Garrison, 1953; Vermeulen, 1966; McFadden and Haddow, 1969; Moss, 1970; Wise, 1969) of coma produced in hospital patients by topical application of isopropyl alcohol during sponge baths intended to reduce fever. Blood isopropyl alcohol concentrations ranged from 10 to 220 mg/100 ml; recovery in all cases was complete in 24–36 h.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 Ten volunteers exposed for 3–5 min to isopropyl alcohol vapor at concentrations of 200, 400, and 800 ppm reported mild to moderate irritation of the eyes, nose, and throat at the two higher concentrations (Nelson et al., 1943). Daily oral intake of low doses of isopropyl alcohol (2.6 or 6.4 mg/kg of body weight) by groups of eight men for 6 wk had no effect on blood cells, serum, or urine and produced no subjective symptoms (Wills et al., 1969). Fuller and Hunter (1927) reported that dizziness occurred within a short time of oral exposure of seven human subjects to 20–30 cm3 of 50% solution of isopropyl alcohol. They also experienced moderate to severe headache lasting one to three h. The odor threshold for isopropyl alcohol ranges from 40 ppm (May, 1966) to 200 ppm (Scherberger et al., 1958). Isopropyl alcohol is not a cutaneous irritant (Nixon et al., 1975), although several cases of allergic contact dermatitis have been reported (Fregert et al., 1971; McInnes, 1973; Richardson et al., 1969; Wasilewski, 1968. EFFECTS ON ANIMALS The oral LD50 of isopropyl alcohol in rats, rabbits, and dogs is about 5 g/kg (Lehman and Chase, 1944). The dermal LD50 in rabbits is about 13 g/kg, and inhalation at 16,000 ppm for 8 h was lethal to four of six rats (Smyth and Carpenter, 1948). The intravenous lethal dose in cats is 2.5 ml/kg (Macht, 1922). Isopropyl alcohol vapor at maximal saturation in air (i.e., 5.8% at 25°C) is not lethal to mice exposed for less than 1 h. The LC50 administered for 120 min to mice is 10.39±3.68 mg/L (49,120 ppm). The oral and intraperitoneal LD50s are approximately equal in mice and rats. LC50s measured in rats exposed to isopropyl alcohol for 8 h were 19,000 ppm for females and 22,500 ppm for males. The signs of intoxication after application of isopropyl alcohol are similar to those with ethyl alcohol, although it is 1.5–2 times more toxic than ethyl alcohol (International Agency for Research on Cancer, 1977). Death is usually preceded by dizziness, narcosis, deep coma, and shock (Lehman et al., 1945; Morris and Lightbody, 1938). An orally administered dose of 2 g/kg produced narcotic effects in rabbits for about 8 h (Morris and Lightbody, 1938). Augmented hepatotoxicity of various chlorinated hydrocarbons was noted in mice administered isopropyl alcohol at 2.5 ml/kg 18 h before hydrocarbon exposure (Traiger and Plaa, 1974). Lehman and Chase (1944) demonstrated the doses of isopropyl alcohol that produced anesthesia and death in rabbits and dogs: Anesthetic Dose Lethal Dose Rabbits 3.23 ml/kg 8.23 ml/kg Dogs 3.35 ml/kg 5.12 ml/kg
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 The respiratory system may be paralyzed by isopropyl alcohol; this is usually the cause of death after isopropyl alcohol ingestion (Zakhari et al., 1977). A concentration of isopropyl alcohol in air of 97.5 mg/L caused respiratory minute-volume depression, bronchoconstriction, hypotension, and bradycardia in rats. Single exposure to atmospheric isopropyl alcohol results in an increase in pulmonary resistance and a decrease in pulmonary compliance. These effects are more pronounced if more than six daily exposures are administered (Zakhari et al., 1977). In anesthetized dogs, isopropyl alcohol inhalation caused various effects: depression of myocardial contractility at 1.0% (2.45 mg/L), reduction in cardiac output at 2.5% (6.12 mg/L), and systemic hypotension at 7.5% (18.37 mg/L) (Zakhari et al., 1977). Histopathologic examination of rats exposed at 21,000 ppm for 8 h showed typical lesions of chemical pneumonitis and pulmonary edema accompanied by foamy vacuolization of liver cells and severe focal cytoplasmic degradation (Laham et al., 1980). Baikov et al. (1974) investigated the effects of chronic inhalation of isopropyl alcohol by rats. Groups of 15 animals were exposed to isopropyl alcohol continuously for 24 h/d for 86 d at concentrations of 20, 2.5, and 0.6 mg/m3 (approximately 8.14, 1.02, and 0.24 ppm). The animals inhaling isopropyl alcohol at 20 mg/m3 (8.14 ppm) showed changes in reflex behavior, increases in the retention of BSP, the total leukocyte count, and the number of abnormal fluorescent leukocytes. They also showed a decrease in the blood nucleic acid content, the blood oxidase and catalase activities, and the amount of coproporphyrin in blood. Animals inhaling isopropyl alcohol at 2.5 mg/m3 (1.02 ppm) demonstrated some of the same effects, but none were statistically significant. In animals inhaling isopropyl alcohol at 20 mg/m3 (8.14 ppm), postmortem findings included hyperplasia of the spleen with the development of hemorrhages of the sinuses and erosion of follicular cells, some evidence of liver parenchymal cell dystrophy, hyperplastic ependymal cells, and degenerative changes in the cerebral motor cortex. None of these effects were observed in animals inhaling isopropyl alcohol at 0.6 mg/m3 (0.24 ppm). On the basis of this continuous exposure study, the authors suggested that 0.6 mg/m3 (0.24 ppm) be adopted as the maximal daily average concentration. Some of the physiological responses reported in this study, such as the increase in abnormal fluorescent leukocytes, are obscure and are therefore difficult to interpret. Furthermore, they suffer from a lack of experimental details. Isopropyl alcohol (10%) in the diet of young rats for 30 d had no effect on growth, liver weight, or lipid content (Miyazaki, 1955). Dogs given daily doses of 1.3 g/kg in the drinking water had the appearance of drunkenness 3–5 h after intake, but no consistent pathologic changes over a 6-mo period (Lehman et al., 1945). No evidence of carcinogenicity was found when several strains of mice were exposed to isopropyl alcohol in air at 7,700 mg/m3 3–7 h/d, 5 d/wk, for 5–8 mo. However, the animals were not observed over a normal lifetime and were killed at 8–12 mo of age (Weil et al., 1952). The authors reported no increases in the incidence of lung tumors in mice given subcutaneous injections of 0.025 ml of isopropyl
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 alcohol once a week for 20–40 wk. However, in mice sacrificed at 40 wk, effects of lifetime exposure were not assessed. No skin tumors were detected (NIOSH, 1976) in a group of 30 Rockland mice that received skin applications of isopropyl alcohol twice a week for a year. Because of methodologic limitations in the preceding studies, it is difficult to draw a conclusion regarding the carcinogenicity of isopropyl alcohol (IARC, 1977). Lehman et al. (1945) reported that growth, reproductive function, and embryonic and postnatal development of rats were not affected, except for some retardation of growth early in the life of first-generation offspring when parents and two successive generations of rats were given isopropyl alcohol continuously in the drinking water at 1.5, 1.4, and 1.3 g/kg per day, respectively. Solvent controls of isopropyl alcohol in an assay of the mutagenicity of Fusarium moniliforme were negative when tested in the S. typhimurium reverse-mutation bioassay with strains TA 98 and TA 100 (Bjeldanes and Thomson, 1979). PHARMACOKINETICS After oral intake of 0.1–20 g of isopropyl alcohol, none was excreted in the urine of volunteers during the next 48 h, and no formic acid was detected (Kemal, 1927). Isopropyl alcohol is absorbed from all segments of the gastrointestinal tract, most rapidly in the small intestine and least rapidly in the stomach. Wax et al. (1949) reported that absorption from isolated canine loops of intestine and stomach was 99% complete at the end of 2 h, 82% being absorbed during the first 30 min. Intravenous injections of ethyl alcohol (0.8 cc/kg) significantly reduced the absorption of isopropyl alcohol from the digestive tract. Before 1940, the toxicity of isopropyl alcohol was compared with that of methyl alcohol, in which the long and cumulative action was attributed to low rates of metabolism and excretion. But most data now point to a fairly rapid disposal of isopropyl alcohol, which is eliminated from the bloodstream of dogs within 24 h after administration. The elimination of isopropyl alcohol in rats is decreased by simultaneous ingestion of ethyl alcohol or 1-propanol, but not methyl alcohol or tertiary butyl alcohol. These results suggest that isopropyl alcohol is oxidized by alcohol dehydrogenase (Abshagen and Rietbrock, 1970). Determination of blood isopropyl alcohol and its metabolite, acetone, was carried out during and after a single 4-h exposure (concentration, 500–8,000 ppm) in Sprague-Dawley rats. The amounts of acetone and isopropyl alcohol were directly related to the air concentrations of alcohol inhaled. Increase in exposure time to 8 h considerably increased the amount of blood acetone that could be determined even 20 h after exposure. These findings indicate a slow conversion of this alcohol to acetone, which can be used as a biochemical indicator of exposure, but it is a nonspecific indication and may be produced by other compounds (Laham et al., 1980). Exposure of male Wistar rats to isopropyl alcohol vapor at 12.3 mol/L (300 ppm) for 6 h/d, 5 d/wk, for 5–21 wk with simultaneous ethyl
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 alcohol administration in drinking water (5% v/v) caused a significant increase in isopropyl alcohol removal as assessed by blood isopropyl alcohol and acetone determinations (Savolainen et al., 1979). This study confirmed the production of acetone from isopropyl alcohol. The novel aspect of this study is the more rapid metabolism of acetone induced by ethyl alcohol. This effect might be attributable to synergistic effects of ethyl alcohol and isopropyl alcohol on aldehyde and ketone dehydrogenation. Neurochemical studies revealed decreased superoxide dismutase and azoreductase activities in cerebellar homogenate at the end of the exposure, whereas increased protein degradation was found in glial cells isolated from rats fed ethyl alcohol. Analyses of spinal cord axon lipid composition showed increases in cholesterol content in relation to lipid phosphorus in animals exposed to isopropyl alcohol or to the combination of isopropyl and ethyl alcohol. Spontaneous behavioral tests indicated minor effects on reactivity from the tenth week on with isopropyl alcohol exposure. Coexposure to isopropyl alcohol vapor and ethyl alcohol abolished the increased excitability. Savolainen et al. concluded that isopropyl alcohol vapor causes significant metabolic and functional chages in rats at relatively low doses—300 ppm. Another synergistic effect has been an increase in the toxicity of carbon tetrachloride caused by pretreatment with isopropyl alcohol (Plaa and Traiger, 1973; Traiger and Plaa, 1973; Traiger and Plaa, 1974). The concentration of isopropyl alcohol in rat saliva 15 and 60 min after exposure was proportional to the exposure concentration and the duration of exposure and was closely correlated with the blood concentration (Tomita, 1980). Liver alcohol dehydrogenase is the principal enzyme involved in the oxidation of isopropyl alcohol. The acetone produced by action of the enzyme on isopropyl alcohol is eliminated from the human body in expired air and urine (Zakhari et al., 1977). Rat liver microsomes are capable of oxidizing branched-chain alcohols, and hydroxyl radicals generated from microsomal electron transfer may have a role in isopropyl alcohol oxidation (Cederbaum et al., 1981). INHALATION EXPOSURE LIMITS The OSHA health standards for exposure to air contaminants require that an employee’s exposure to isopropyl alcohol not exceed an 8-h TWA of 400 ppm in the working atmosphere in any 8-h shift of a 40-h workweek (OSHA, 1982); a ceiling of 800 ppm was determined during a sampling time of 15 min (NIOSH, 1976). An estimated 141,000 employees may be exposed occupationally to isopropyl alcohol in the United States (NIOSH, 1976). The American Conference of Governmental Industrial Hygienists established the value of 400 ppm as the TLV for isopropyl alcohol; as described above, this is the TLV currently recommended in the United States (American Conference of Governmental Industrial Hygienists, 1980, 1983). The permissible concentration of isopropyl alcohol was established by the Japan Association of Industrial Health in 1966 at 400 ppm (Japan Association of Industrial Health, 1971). In the
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 U.S.S.R., the maximal permissible concentration of isopropyl alcohol in a single dose or as a daily average is 0.6 mg/m3 (U.S.S.R. Ministry of Public Health Individual Reports, 1971). COMMITTEE RECOMMENDATIONS The National Research Council’s Committee on Toxicology (1960) recommended, as a part of the submarine toxicology program, the EELs and CEL for isopropyl alcohol. The basis for these limits was primarily the ACGIH TLV of 400 ppm, which was recommended by the Committee as the 60-min EEL. The Committee stated: “From the data available it would appear that isopropyl alcohol is not an industrial health hazard. The threshold limit value of 400 ppm set by the ACGIH may cause mild irritation of the eyes, nose and throat, especially in those not regularly exposed.” The 24-h EEL and 90-d CEL were apparently recommended by the Committee on the basis of its judgment concerning tolerable doses for these periods and extrapolations from the 400-ppm 60-min EEL. No new information has become available to suggest changes in previously proposed EELs for 1 and 24 h. However, data from long-term, low-dose, continuous-exposure studies show adverse effects on behavior, liver, and spleen in rats (Baikov et al., 1974). Although these data are not conclusive, prudence dictates that previously recommended long-term exposure limit (CEL) of 50 ppm be lowered to 1 ppm. The present Committee’s recommended EELs and CEL for isopropyl alcohol and the limits proposed in 1960 and 1966 are shown below: 1960/1966 1984 60-min EEL 400 ppm 400 ppm 24-h EEL 200 ppm 200 ppm 90-d CEL 50 ppm 1 ppm
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 TABLE 6 Acute Toxicity of Isopropyl Alcohola Species Route Measure Value Human Eye Irritation 20 ppm Human Oral TDLo 15,710 mg/kg Human Oral LDLo 8,600 mg/kg Human Inhalation TC10 400 ppm Human Subcutaneous LDLo 6 mg/kg Human Unknown LDLo 2,770 mg/kg Rat Oral LD50 5,840 mg/kg Rat Inhalation LC50 16,000 ppm, 8 h Mouse Oral LCLo 192 mg/kg Mouse Intraperitoneal LD50 933 mg/kg Mouse Subcutaneous LDLo 6,000 mg/kg Dog Oral LD50 6,150 mg/kg Dog Intravenous LDLo 5,120 mg/kg Cat Intravenous LDLo 1,963 mg/kg Rabbit Eye Irritation 16 mg Rabbit Oral LDLo 5,000 mg/kg Rabbit Skin LD50 13 g/kg Rabbit Intravenous LDLo 8,230 mg/kg a Data from NIOSH Registry of Toxic Effects of Chemical Substances, 1982.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 REFERENCES Abshagen, U., and Rietbrock, N. 1970. Zum Mechanismus der 2-Propanoloxydation. Interferenzversuche mit niederen aliphatischen Alkoholen in vivo und an der isoliert perfundierten Rattenleber. Naunyn-Schmiedeberg’s Arch. Exp. Pathol. Pharmakol. 265:411–424. Adelson, L. 1962. Fatal intoxication with isopropyl alcohol (rubbing alcohol). Am. J. Clin. Pathol. 38:144–151. American Conference of Governmental Industrial Hygienists. 1980. Isopropyl alcohol. Documentation of the Threshold Limit Values. 4th ed., with Supplemental Documentation through 1983. Cincinnati, Ohio: American Conference of Governmental Industrial Hygienists. p. 239(81). American Conference of Governmental Industiral Hygienists. 1983. TLVs(R): Threshold Limit Values for Chemical Substances and Physical Agents in the Work Environment with Intended Changes for 1983–1984, Ohio: American Conference of Governmental Industrial Hygienists. 93 p, Ashkar, F.S., and Miller, R. 1971. Hospital ketosis in the alcoholic diabetic: a syndrome due to isopropyl alcohol intoxication. South. Med. J. 64:1409–1411. Baikov, B.K., Gorlova, O.E., Gusev, M.I., Novikov, Yu V.,Yudina, T.V. and Sergeev, A.N. 1974. Hygienic standardization of the daily average maximal permissible concentrations of propyl and isopropyl alcohols in the atmosphere. Gig. Sanit. No. 4:6–13. [English summary] Ballard, T.W., Walker, P., Ginn, E., Sanders, R.S., McMurray, D., Horst, E.V., and Hutchenson, R.H., Jr. 1975. Renal failure and hepatitis from inhaled carbon tetrachloride and isopropyl alcohol. Morbidity and Mortality (Center for Disease Control) 24:59–60. Bjeldanes, L.F., and Thomson, S.V. 1979. Mutagenic activity of Fusarium moniliforme isolates in the Salmonella typhimurium assay. Appl. Environ. Microbiol. 37:1118–1121. Cederbaum, A.I., Qureshi, A., and Messenger, P. 1981. Oxidation of isopropanol by rat liver microsomes: Possible role of hydroxyl radicals. Biochem. Pharmacol. 30:825–831. Chapin, M.A. 1949. Isopropyl alcohol poisoning with acute renal insufficiency. J. Maine Med. Assoc.. 40:288–290. [Chem. Abs. 44:10137g, 1950] Eckardt, R.E. 1974. Annals of industry—noncasualties of the work place. J. Occup. Med. 16:472–477.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 Fregert, S., Groth, O., Gruvberger, B., Magnusson, B., Mobacken, H. and Rorsman, H. 1971. Hypersensitivity to secondary alcohols. Acta Derm. Venereol. 51:271–272. Freireich, A.W., Cinque, T.J., Xanthaky, G., and Landau, D. 1967. Hemodialysis for isopropanol poisoning. N. Engl. J. Med. 277:699–700. Fuller, H.C., and Hunter, O.B. 1927. Isopropyl alcohol—An investigation of its physiologic properties. J. Lab. Clinic Med. 12:326–341. Garrison, R.F. 1953. Acute poisoning from use of isopropyl alcohol in tepid sponging. J. Am. Med. Assoc. 152:317–318. Hueper, W.C. 1966. Occupational and Environmental Cancers of the Respiratory System. (Recent Results Cancer Res. 3) New York: Springer-Verlag. p. 105–107, 183. International Agency for Research on Cancer. 1977. IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man: Some Fumigants, the Herbicides 2,4-D and 2,4,5-T, Chlorinated Dibenzodioxins and Miscellaneous Industrial Chemicals, Vol. 15. Lyon: International Agency for Research on Cancer. 354 p. Japanese Association of Industrial Health. 1971. Recommendation for permissible concentrations, etc. Translation of Sangyo Igaku (Jpn. J. Ind. Health) 13:475–484. Juncos, L., and Taguchi, J.T. 1968. Isopropyl alcohol intoxication: Report of a case associated with myopathy, renal failure, and hemolytic anemia. J. Am. Med. Assoc. 204:732–734. Kemal, H. 1927. Beitrag zur Kenntnis der Schicksale des Isopropylalkohols im menschlichen Organismus. Biochem. Z. 187:461–466. King, L.H., Jr., Bradley, K.P., and Shires, D.L., Jr. 1970. Hemodialysis for isopropyl alcohol poisoning. J. Am. Med. Assoc. 211:1855. Laham, S., Potvin, M., Schrader, K., and Marino, I. 1980. Studies on inhalation toxicity of 2-propanol. Drug Chem. Toxicol. 3:343–60. Lehman, A.J., and Chase, H.F. 1944. The acute and chronic toxicity of iso-PrOH. J. Lab. Clin. Med. 29:561–567. [Chem. Abs. 38:59712, 1944] Lehman, A.J., Schwerma, H., and Rickards, E. 1945. Isopropyl alcohol. Acquired tolerance in dogs, rate of disappearance from the blood stream in various species, and effects on successive generation of rats. J. Pharmacol. Exp. Ther. 85:61–69.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 Lowenheim, F.A., and Moran, M.K. 1975. Faith, Keyes, and Clark’s Industrial Chemicals. 4th ed. New York: John Wiley & Sons. p. 496–501. Macht, D.I. 1922. Pharmacological examination of isopropyl alcohol. Arch. Int. Pharmacodyn. Ther. 26:285–286. [Chem. Abs. 16:2923, 1922] May, J. 1966. Geruchsschwellen von Lösemitteln zur Bewertung von Lösemittelgerüchen in der Luft. Staub Reinhalt. Luft 26:385–389. McBay, A.J. 1973. Toxicological findings in fatal poisonings. Clin. Chem. 19:361–365. McFadden, S.W., and Haddow, J.E. 1969. Coma produced by topical applicaton of isopropanol. Pediatrics 43:622–623. McInnes, A. 1973. Skin reaction to isopropyl alcohol. Br. Med. J. 1:357. Miyazaki, M. 1955. Nutritive value of aliphatic alcohols. I. The nutritive value of saturated alcohols with one to five carbon atoms. J. Agric. Chem. Soc. Japan 29:497–501. [Chem. Abs. 49:14942i, 1955] Morris, H.J., and Lightbody, H.D. 1938. The toxicity of isopropanol. J. Ind. Hyg. Toxicol. 20:428–434. Moss, M.H. 1970. Alcohol-induced hypoglycemia and coma caused by alcohol sponging. Pediatrics 46:445–447. National Formulary Board. 1975. National Formulary XIV. Washington, D.C.: American Pharmaceutical Association, p. 367–368. National Institute for Occupational Safety and Health. 1976. Criteria for a Recommended Standard…Occupational Exposure to Isopropyl Alcohol. HEW Publication No. (NIOSH) 76–142. Cincinnati, Ohio: U.S. Department of Health, Education and Welfare, Public Health Service, Center for Disease Control. National Institute for Occupational Safety and Health. 119 p. National Institute for Occupational Safety and Health. 1982. Registry of Toxic Effects of Chemical Substances. 1980 ed. DHHS (NIOSH) Publication No. 81–116. Rockville, Maryland: U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control, National Institute for Occupational Safety and Health. Vol. 1., p. 967. National Research Council. Committee on Toxicology. 1960. Report to U.S. Navy on Isopropyl Alcohol. 3 p. Nelson, K.W., Ege, J.F., Jr., Ross, M., Woodman, L.E., and Silverman, L. 1943. Sensory response to certain industrial solvent vapors. J. Ind. Hyg. Toxicol. 25:282–285.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 Nixon, G.A., Tyson, C.A., and Wertz, W.C. 1975. Interspecies comparisons of skin irritancy. Toxicol. Appl. Pharmacol. 31: 481–490. Occupational Safety and Health Administration. 1983. Toxic and Hazardous Substances. Air contaminants. 29 CFR 1910.1000. Plaa, G.L., and Traiger, G.J. 1973. Mechanism of potentiation of CCl4-induced hepatotoxicity. In Loomis, Ted A., ed. Pharmacology and the Future of Man. Vol. 2. Toxicological Problems. New York: S. Karger. p. 100–113. Richardson, D.R., Caravati, C.M., Jr., and Weary, P.E. 1969. Allergic contact dermatitis to “alcohol” swabs. Cutis 5:1115–1118. Savolainen, H., Pekari, K., and Helojoki, H. 1979. Neurochemical and behavioural effects of extended exposure to isopropanol vapour with simultaneous ethanol intake. Chem. Biol. Interact. 28:237–248. Scherberger, R.F., Happ, G.P., Miller, F.A., and Fassett, D.W. 1958. A dynamic apparatus for preparing air-vapor mixtures of known concentrations. Am. Ind. Hyg. Assoc. J. 19:494–498. Scrimgeour, E.M. 1980. Outbreak of methanol and isopropanol poisoning in New Britain, Papua New Guinea. Med. J. Aust. 2:36–38. Smyth, H.F., Jr., and Carpenter, C.P. 1948. Further experience with the range finding test in the industrial toxicology laboratory. J. Ind. Hyg. Toxicol. 30:63–68. SRI International. 1982. Directory of Chemical Producers, United States of America. Menlo Park, CA: SRI International. 1132 p. Tomita, M. 1980. Investigation of volatile matters in oral cavity. An evaluation of exposure levels by concentration of organic solvents in saliva. II. Shika Gakuho 80:1705–1721. [Chem. Abs. 95:1321d, 1981] Traiger, G.J., and Plaa, G.L. 1973. Effect of aminotriazole on isopropanol- and acetone-induced potentiation of CCl4 hepatotoxicity. Can. J. Physiol. Pharmacol. 51:291–296. Traiger, G.J., and Plaa, G.L. 1974. Chlorinated hydrocarbon toxicity: potentiation by isopropyl alcohol and acetone. Arch. Environ. Health 28:276–278. U.S.S.R. Ministry of Public Health Individual Reports. 1971. Maximum Permissible Concentration of Harmful Substances in the Atmospheric Air of Populated Areas. No. 876–71. Environmental Protection Agency Translation TR 175–74.  p. Vermeulen, R. 1966. Isopropyl alcohol and diabetes. Pa. Med. 69(4):53–54.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 Wasilewski, C., Jr. 1968. Allergic contact dermatitis from isopropyl alcohol. Arch. Dermatol. 98:502–504. Wax, J., Ellis, F.W., and Lehman, A.J. 1949. Absorption and distribution of isopropyl alcohol. J. Pharmacol. Exp. Ther. 97:229–237. Weast, R.C., ed. 1976. CRC Handbook of Chemistry and Physics. 57th ed. Cleveland, Ohio: CRC Press, p. C-459. Weil, C.S., Smyth, H.F., Jr., and Nale, T.W. 1952. Quest for a suspected industrial carcinogen. AMA Arch. Ind. Hyg. Occup. Med. 5:535–547. Wickson, E.J. 1968. Isopropyl alcohol. In Kirk-Othmer Encyclopedia of Chemical Technology. 2nd rev. ed., Vol. 16. New York: Interscience Publishers, p. 564–578. Wills, J.H, Jameson, E.M and Coulston, F. 1969. Effects on man of daily ingestion of small doses of isopropyl alcohol. Toxicol. Appl. Pharmacol. 15:560–565. Wise, J.R., Jr. 1969. Alcohol sponge baths. N. Engl. J. Med. 280: 840. Zakhari, S., Leibowitz, M., Levy, P. and Aviado, D.M. 1977. Isopropanol and Ketones in the Environment. Cleveland, Ohio: CRC Press. 147 p.
Representative terms from entire chapter: