Document gEkdX7Gg6b3Q1GLe0ZMXmYraG

industrial Hypfcno BDD en r--. EER cn --rer- JO CCD dtM-C- CV DB HGS CD Z3 CGiiC^ EDS SUPPLEMENTS FOR THOSE SUBSTANCES ADDED OR CHANGED C 453 511904 0283 ANILINE -- Skin CH5NHj TLV -- 2 ppm (8mg/cu m.) Aniline is an oily liquid with a characteristic odor detectable at 1 ppm. It has a boiling point of 184.4 C.. and a melting point of -6.2 C. The vapor pressure at 77C. is 15 mm, and the flash point is 158F (70C). Aniline is used chiefly in the chemical industry, where it is the parent substance for many compounds, including dyes, rubber accelerators and antioxidants, drugs, photographic chemicals, isocyanates, herbicides and fungicides. Occupational aniline poisoning was at one time relatively common. Acute intoxication, due to the formation of methemoglobin, and resulting in cyanosis and possible death from asphyxiation, has been the most frequent consequence of over exposure. The question of whether the effects are due solely to methemoglobin formation has been disputed, however.'-7 In at least one fatal case liver cirrhosis and atrophy were present.' Chronic poisoning with primarily cerebral nervous system symptoms has been reported,' but other authorities deny the existence of chronic aniline poisoning.9 Henderson and Haggard cited data suggesting that 7 to 53 ppm of aniline vapor cause slight symptoms after several hours exposure; concentrations in excess of 100 to 160 ppm cause serious disturbances if inhaled for one hour.9 Oberst and co-workers' exposed several species of animals to 5 ppm of aniline vapor daily for six months and found no effects other than a slight increase in methemoglobin in the blood of rats. Hardy notes that methemoglobinemia from amines, such as aniline, is less insidious and not as prolonged as when caused by nitro compounds.7 Dutkiewicz9 found skin absorption of aniline vapor approximately equal to absorption from inhalation. He proposed 35 mg as the maximal allowable daily dose, corresponding to exposure to about 1 ppm for an eight hour day at mild exertion. The previous TLV of 5 ppm was apparently derived from the data cited by Henderson and Haggard. Accepting these figures (from H & H) at face value. 5 ppm provides practically no margin of safety. This is confirmed to some extent by the study of Oberst. In view of Outkiewicz's more recent work a lower limit is suggested. For the reasons noted above, however, there is reason to set the TLV for aniline somewhat above that for nitrobenzene. A limit of 2 ppm is proposed, provided absorption through the skin by contact with liquid is prevented. References: ' Fairhall, L.T.: Industrial Toxocology. Williams & Wilkins, Baltimore, 1949. 7 Hamilton, A. and Hardy, H.L.: Industrial Toxicology, 3rd ed. Publishing Sciences Group, Action, 1974. 9 Holstein, E.: Arch, Gewerbepath. u. Gewerbehyg. 13, 522 (1955). 4 Von Oettingen, W.F.: The Aromatic Amino and Nitro Compounds: Their Toxicity and Potential Dangers. U. S. Public Health Service Bulletin 271 (1941). 9 A.I.H.A. Hygienic Guide Series (1955). 9 Henderson, Y. and Haggard, H.W.: Noxious Gases, 2d. ed. Reinhold Publishing Corp., New York, 1943. 7 Oberst, F.W., Hackley, E.B., Comstock, C.C.: Arch. Ind. Health: 13, 379 (1956). 9 Dutkiewicz, T.: The Absorption and Metabolism of Aniline in Man, Societies Scientiarum Lodziensis. Lodz, Poland. 1962. ASBESTOS 2 fibers longer than 5 pm per cc. for chrysotile 0.2 fibers longer than 5 pm per cc. for crocidolite 0.5 fibers longer than 5 pm per cc. for amosite According to recent authoritative mineralogical definitions,' asbestos is "(1) A collective mineralogical term encompassing the asbestiform varieties of various minerals: (2) An industrial product obtained by mining and processing primarily asbestiform minerals." For the purpose of considering a recommendation for a threshold value of asbestos dust in the workplace, only the second definition above is applicable. Although there are four types of natural mineral fibers that have been in industrial use, only three have been used in the United States: chrysotile, amosite, and crocidolite. The fourth, anthophyllite, is mined and used in Finland. Of the three types of asbestos that have been used in North America. Canadian chrysotile has formed 95% of all natural mineral fibers used, with amosite and crocidolite (both imported from South Africa) constituting the other 5%. It should be noted that chrysotile is classified as a serpentine mineral whereas the other three types of asbestos are amphiboles. 454 511904 0284 It is now generally recognized that excessive inhalation of asbestos dust causes chronic inflammation of lung tissue and pleural membranes as well as cancer. Whereas identification of asbestos dust as a cause of fibros ing inflammation of lung tissue occurred as early as 1907/ it was not until 1930 that a more definitive study by Merewether and Price5 resulted in the regulations which greatly improved hygenic-conditions in asbestos factories in the United Kingdom. The development of lung cancer in asbestos workers, first reported by Wood and Gloyne5 in the U.K. in 1934 and by Lynch and Smith5 in the U.S. in 1935, was not firmly established until 1955 by the publication of Doll* of a study of workers in an English asbestos textile factory, and in the United States by the paper of Selikoff et al7 in 1964 concerned with cancers in insulation workers. In 1960 the relationship between the inhalation of asbestos dust and mesothelioma was demonstrated by Wagner et al.' Asbestosis is a diffuse but nonuniform fibrosis of the lungs that is generally most severe in the basilar portions. As a result of the fibrosis some of the air spaces (alveoli) are not perfused with blood and alveoli that are perfused with blood may not be adequately ventilated because of stiff, thickened alveolar walls. The fibrosis makes the lungs less compliant, thereby increasing the energy requirement of breathing. There is increasing impairment in diffusion of gases leading to increasing breathlessness. It is not uncommon to find thickening of the visceral pleura, sometimes very severe, by extention of the parenchymal inflammation. This causes an additional increase in the effort of breathing. The parietal pleura may show patches of severe thickening, particularly over a diaphragm and the lower portions of the chest wall -- resulting in the so-called pleural hyaline plaques. These may become visible in xray films of the chest -- particularly, if they become impregnated with calcium salts. Such pleural plaques may develop from asbestos exposure in the absence of asbestosis. They cause no symptoms. A study of the members of an asbestos insulators union revealed that deaths from lung cancer in this population was much greater than expected.7 A later investigation by Hammond and Selikoff of a much larger number of these workers (17,800) showed that nearly all cancers occurred in cigarette smokers.' The conclusion of these authors was: "It seems clear, then, that lung cancer is uncommon among asbestos insulation workers who have no history of cigarette smoking, and that if the risk is increased such an increase is not great." The total lung cancer rate in this cohort of workers was 4.8 times the expected. The asbestos insulators who had a history of cigarette smoking has a lung cancer rate of 5.4 times the expected rate: but compared to the lung cancer rate of the nonsmoking workers, the smoking insulators' lung cancer rate was 14 times greater. All types of asbestos are known to cause the inflammatory changes in the lungs and pleurae described above and lung cancer. However, there is experimental and epidemiologic evidence that there may be differences in the potential of the different asbestos types to produce disease. Thus, it has been suggested that crocidolite has the greatest potential to produce disease: chrysotile, the smallest: with amosite occupying an intermediate position.'0 In a study of 1348 retirees from the asbestos industry by Enterline and Henderson" the respiratory cancer rate of men exposed only to chrysotile was 2.4 times the expected, whereas this rate was 5.3 times the expected for men who had been exposed to a combination of chrysotile and crocidolite. In the asbestos cement industry a similar difference was observed. Workers exposed only to chrysotile and cememt (shingle and sheets) had a respiratory cancer rate of 1.4 times the expected, whereas workers exposed to both, chrysotile and crocidolite and cement (asbestos cement pipes), had a respiratory cancer rate 6.1 times the expected. Mesotheliomas are rare, usually rapidly fatal cancers that originate from the surface lining of the chest or abdominal cavity. From 1960 through 1975, 4539 mesotheliomas have been reported worldwide.'5 The vast majority of these cancers were in people exposed to crocidolite alone or in combination with other types of asbestos. McDonald and McDonald'5 tabulated those reports of mesothelioma where the type of asbestos exposure was known. Although the number of such cases is small, where the exposure was to crocidolite alone or in combination with other types of asbestos, death from mesothelioma constituted 6.1% of the deaths from all causes, with a range of 2.42% to 16.07%. In contrast, deaths from mesothelioma in workers exposed only to chrysotile constituted only 0.3% of the deaths from all causes, with a range of 0.24% to 0.87%. An even greater contrast is found in the Finnish statistics of workers exposed to anthophyllite. Meurman, et al'5 investigated 216 deaths that occurred among approximately 900 miners and millers of anthophyllite during the 32-year period 1936-1967 and found not one case of mesothelioma. Not all mesotheliomas result from asbestos exposure. There is a background of "naturally" occurring mesotheliomas that has been estimated to be about ten for males and four for females per million persons aged 45 years and older.'5 Furthermore, it is not uncommon in the various epidemiologic studies reported that 15% or more ot the mesothelioma cases have no history of ever having been exposed to asbestos. Perhaps the most important indication that mesotheliomas may result from causes other than asbestos exposures: in this instance, also environmental, comes from a report by Baris et al'5 who described a mesothelioma incidence of 2.3% in 1974 in the village of Karain in Turkey (population, 604). This population has been exposed for many generations to dust from the soil that contains kaolin, mica, and vulcanic glass particles, but no asbestos. A small excess of deaths from gastro-intestinal cancers have been noted in several epidemiologic studies of asbestos workers. '5 An association of laryngeal cancer with asbestos exposure has been claimed. Pancreatic cancers and lymphomas have also been mentioned in this connection. However, conversion of the association to a causal relationship rests as yet on an insecure basis. Whether or not there is a dose-effect relationship associated with asbestos dust has been answered affirmatively by a number of epidemiological surveys'5 '9 Whereas this relationship is clear-cut with regard to asbestosis and lung cancer, it is less well-marked with regard to mesothelioma; but it is, nevertheless positive McDonald50 points to a case-control analysis based on seven cases of mesothelioma at Thetford Mines that includes no case with less than 30 mppcf-years exposure and which suggests that the risk increases with 455 511904 0285 exposure. McDonald further points outthat although fiber-equivalents for the dust concentrations in mppcf are difficult to estimate, there is evidence for believing that the conversion factor cannot be less than two. The data of Newhouse and Berry7' demonstrates a doubling of the incidence of mesothelioma for males who had light or moderate exposures. This was equally true for those employed less than two years. In all of the other investigations of mesothelioma incidence, the degree of dust exposure was not indicated, thereby preventing the determination of any dose-effect relationship. The only reliable exposure data from the asbestos industry on which a recommendation for a threshold limit of asbestos exposure can be based, stem from England !Z,a Using the presence of persistent high-pitched rales in the basal portions of the lungs as criterion for the diagnosis of asbestosis, it was determined from a population of asbestos textile workers that less than 100 fiber-years of exposure (2 fibers per cc. over a 50-year working period, or 4 fibers per cc. over a 25-year period) would cause the development of asbestosis in no more than 1% of the workers." This departure from the previous dust standard of 5 mppcf was in recognition of the variability of the asbestos fiber content of factory dust and that the disease was related to the number of asbestos fibers inhaled and not to the amount of nonfibrous dust particles. Also, it was specified that the counted fibers were to be longer than 5 pm. The size limit placed on the counted fibers (longer than 5 pm) was because it was not practical to count shorter fibers with an optical microscope (400 to 450 x magnification under phase-contrast illumination, with a 4MM. objective). It is recognized that for every asbestos fiber longer than 5 pm. there may be as many as 100 or more fibers shorter and thinner that are not visible under the optical microscope. However, there is considerable experimental evidence to indicate that asbestos fibers shorter than 5 pm are not pathogenic." A recent publication by Gillam et al" indicated that the present limit of 2 asbestos fibers per cc. longer than 5 pm set by OSHA is inadequate to protect workers against nonmalignant as well as malignant respiratory disease. This conclusion was based on a study of 440 hard rock gold miners who had been exposed to an asbestiform mineral (cumming-tonite-grunerit'e). These investigators found 10 respiratory cancer deaths (including a carcinoma of the maxillary sinus and a mediastinal carcinoma) when only 2.74 auch deaths had been expected. Five deaths from nonmalignant respiratory diseases other than influenza and pneumonia when 1.85 deaths from these causes had been expected. These deaths included those from silicosis (the respirable dust contained 13% free silica!). It is of interest that although the diagnosis of asbestosis was not mentioned in the paper, Gillam et al" emphasized that finding that the ambient air in the gold mine contained an average of 4.82 fibers per cc., 80 to 90% of which were fibrous amphiboles, "and 60 to 70% of the latter were fibrous grunerite (amosite)." Fibers longer than 5 pm. averaged 0.36 fibers per cc.: and approximately 94% of the airborne fibers were less than 5 pm long, averaging 0.13 in diameter and 1.1 pm in length. McDonald et aI" investigated the records of the same gold mine as Gillam et al but their cohort consisted of 1321 men who had completed 21 years service with the mining company (in contrast to the cohort of 440 men studied by Gillam et al.") The following is a summary of their findings: "All but 10 of the men were traced to the end of 1973 when 651 were still living; cause of death was ascertained for 657 of the 660 who had died. The numbers of deaths observed in various diagnostic categories, with 'expected' figures in parenthesis, were as follows: -- respiratory cancer -- 17 (16.5); abdominal cancer -- 39 (35.1); other malignant diseases -- 37 (39.0); pneumoconioses -- 39 (0); respiratory tuberculosis or silico-tuberculosis -- 39 (3.6); heart disease -- 264 (232.5). Silicosis was given.as the cause in 37 of the 39 pneumoconiotic deaths and mentioned on the certificate in 28 of the 264 coded to heart disease. The occurrence of deaths ascribed to pneumoconiosis, tuberculosis and heart disease was in each case related directly to dust-exposure category whereas deaths coded to respiratory, abdominal and other cancers showed no such relationship. The pattern of mortality of men with long employment in this industry indicates a serious pneumoconiotic hazard characteristic of hard rock miners but not of cancer." (See Table l) It would appear from the McDonald et al study" that there is no basis for the claim made by Gillam et al" that the OSHA standard of two fibers longer than 5 pm per cc. is inadequate to protect the health of workers, or that asbestos fibers shorter than 5 pm produce deleterious health effects. In an 8v& year follow-up of the same population of asbestos workers from which the 100 fiber-years exposure was derived as a reasonably safe level, it was found that mortality was increased for lung cancer.'* There were 31 deaths from this cause whereas only 19.3 had been expected. From non malignant respiratory disease, there were 35 deaths where 25.0 had been expected. In addition, there were five deaths from pleural mesothelioma. It was determined that the mean dust level of the workers had been below five fibers per cc. only in the last decade. In 1951 the mean dust level was 10.8 fibers per cc. and 89% of the men had been exposed to mean levels above 5 fibers per cc. In 1972, the mean dust level was 2.9 fibers per cc. and only 3% of the men were exposed to a mean level greater than 5 fibers per cc., 65% were exposed to a mean level between two and five fibers per cc. and 32% to a mean level below 2 fibers per cc. Because there is a delay of 15 or more years between first exposure and any resulting cancer, the authors consider that the increased mortality demonstrated does not reflect the effects of working conditions over the last 15 or 20 years. They therefore propose to continue the follow-up on workers entering scheduled areas since 1951. In terms of the 100 fiber-year or two fibers per cc. standard suggested by the British Occupational Hygiene Society (B.O.H.S.), it is apparent that the excess mortality reported above can be attributed to asbestos exposures considerably above this level. The workers in the asbestos textile factory from which the B.O.H.S. standard of 2 fibers per cc. was derived have been studied by highly qualified investigators whose reports were published in 1955,* 1965,'* 1968," and 1977.'* These workers represent the only cohort of asbestos workers in the world in which health effects have 456 511904 0286 been correlated with definitive exposure data defined as fibers per cc. It would be premature and ill-advised to change the present OSHA standard of 2 fibers longer than 5 Mm per cc. for chrysotile without indications from this study population of the advisability for such change. The exposure level of crocidolite and amosite. particularly of the former, must be sharply lower than that of chrysotile because of their greater potential for disease production. In view of the lack of accurate information of the dose-effect relationship pertaining to these two types of asbestos, the arbitrary assignment of 0.2 and 0.5 fiber per cc. longer than 5 pm appears reasonable and prudent for both, crocidolite and amosite respectively, since amosite appears to be less pathogenic than crocidolite. Tabulation of Significant Findings In Two Epidemiologic Investigations of Workers In the Same Hard Rock Gold Mine Nonmalignant Respiratory Size of Cohort Number of Deaths Respiratory Cancer Pneumoconiosis Respiratory TBC Silico-TBC Other Nonmalignant Respiratory Disease '37 of the 39 deaths were ascribed to silicosis McDonald et al" 1321 Observed Expected 17 16.5 39' 0 39 3.6 ?? Gillam et al" 440 Observed Expected 10 2.74 5 1.85 References: ' Campbell, W. J., Blake. R. L., Brown, L. L., Cather, E. E.. Sjoberg, J.J.: Selected Minerals and their Asbestiform Varieties: Mineralogical Definitions and Identification-Characterization. Bureau of Mines Information Circular 8751, (1977), p. 14. * Murray, M.: Report, Department, Commission on Compensation of Industrial Disease. Cd. 3496. pp. 127-128, London; H.M.S.O., (1907). 3 Merewether, E.R.A., Price, C.W.: Report on Effects of Asbestos on the Lungs and Dust Suppression in the Asbestos Industry. London: H.M.S.O., (1930). * Wood, W. B., Gloyne, R. S.: Pulmonary Asbestosis. Lancet 2: 1383-1385, (1934). 5 Lynch, K. M., Smith, W. A.: Pulmonary Asbestosis III: Carcinoma of the lung in asbesto-silicosis. Am. J. Cancer 24: 56-64, (1935). ' Doll, R. S.: Mortality from lung cancer in asbestos workers. Brit. J. Indust. Med. 12: 81-86, (1955). ' Selikoff, I. J., Churg, J,, and Hammond, E. C.: Asbestos exposure and neoplasia. J.A.M.A. 188: 22-26, (1964). * Wagner, J. D., Sleggs, C. A., Marchand, P.: Diffuse pleural mesothelioma and asbestos exposure in the North-West Cape Province. Brit. J. Indust. Med. 17: 260-271, (1960). * Hammond, E. C.. Selikoff, I. J.: Relation of cigarette smoking to risk of death of asbestos-associated disease among insulation workers in the United States. I.A.R.C. Sci. Pub. No. 8, pp 312-317, (1973). 10 Wagner, J.D., Gilson, J. C., Berry, G., and Timbrell, VI: Epidemiology of asbestos cancers. Brit. Med. Bull. 27: 71-96, (1971). " Enterline P. E. and Henderson V.: Type of asbestos and respiratory Cancer in the asbestos industry. Arch. Environ. Health 27: 312-317, (1973). '3 McDonald, J. C. and McDonald, A. A.: Epidemiology of mesothelioma from estimated incidence Preventive Med. 6: 426-446, (1977). ,J Meurman, L.D., Kivilioto, R. and Hakama, M.: Mortality and morbidity among the working population of anthophyllite asbestos miners in Finland. Brit. J. Indust. Med. 31: 105-112, (1974). u Baris, Y. I. et al: An outbreak of pleural mesothelioma in the village of Karain, Urgup -- Anatolia. Kanser 5: 1-14, (1975). ,s McDonald, J. C. et al: Mortality in the chrysotile asbestos mines and mills of Quebec. Arch. Environ. Health 22:677-686, (1971). '* Knox, J. F., Doll, R. S., Hill, I. D. Cohort analysis of changes in incidence of bronchial carcinoma in a textile factory. Ann. N.Y. Acad. Sci. 132: 526-535. (1965). " Newhouse, M. L.: A study of the mortality of workers in an asbestos factory. Brit. J. Indus. Med. 26: 294-301, (1969). ' Newhouse. M. L., Berry, G., Wagner, J. D., and Turock, M. E.: A study of the mortality of female asbestos workers. Brit. J. Indus. Med. 29: 134-141, (1972). ' Peto, J., Doll, R., Howard, S. V., Kinlen, L. J., and Lewinsohn, H. C.: A mortality study among workers in an English asbestos factory. Brit. J. Indust. Med. 34:169-173, (1977). 457 511904 0287 70 McDonald J. C.: Exposure relationships and malignant mesothelioma. Opening paper for Session V. Asbestos Symposium. Johannesburg. Oct. 3-7, 1977. 71 Newhouse. M. L. and Berry. G.: Predictions of mortality from mesothelioma tumours in asbestos factory workers Brit. J. Indus. Med. 33: 147-151, (1976). 77 British Occupational Hygiene Society: Committee on Hygiene Standards Ann. Occ. Hyg:7f; 47-69, (1968). 73 Gross, P.: Is short-fibered asbestos dust a biological hazard? Arch. Environ. Health 29: 115-118, (1974). 7` Gillam, J. D., Dement, J. D., Lemen, R.A. et al: Mortality patterns among hard rock gold miners exposed to an asbestos form material. Ann. N.Y. Acad. Sci. 271: 337-344, (1976). 7! McDonald, J. C., Gibbs. G.W., Udell, F.D.K. and McDonald, D.A.: Mortality after long exposure to cummingtonite-grunerite. To be published. (Abstracted in Am. Red. Resp. Dis.) " Knox, J.F., Holmes, S., Doll, R., and Hill, I.D.: Mortality from lung cancer and other causes among workers in an asbestos textile factory. Brit. J. Indus. Med: 25: 293-303, (1968). ASPIRIN COOH O-CC-CHj (CH3COOC 6H4COOH) 5 mg/m3 Molecular Weight: Melting Point: Boiling Point: 180.15 132-136C 140C (dec) Aspirin, or acetylsalicylic acid, occurs as white crystals or as a white crystalline powder which is essentially odorless and has a slightly bitter taste. Stable in dry air, it hydrolyzes slowly in moist air to salicylic and acetic acids. Aspirin is soluble in water, alcohol, chloroform and ether and less soluble in absolute ether. The uses of aspirin are medicinal, as an analgesic, antipryretic and anti-inflammatory in humans, and also as an anticoagulant in other animals. Its reported UD^, in rats is 1.75 g/kg\ although others have found it to be 0.4 to 0.8 g/kg 7 Aspirin is a known respiratory and systemic allergen and can produce anaphylactic phenomena even after small doses.3' In addition, aspirin is an acute irritant to the gastric mucosa/ the skin and eyes/ Direct contact with the eye is painful and may cause a chemical burn/ Very large doses of aspirin have produced teratogenic eftects in experimental animals.' Ingestion of aspirin produces an increased tendency to bleed due to its interference with platelet aggregation's A normal therapeutic dose of aspirin, 600 mg. will produce these abnormalities for five days or longer.<* However, these toxic effects have also been demonstrated by ingestion ot 150 mg., the smallest dose reported to have a pharmacologic effect/ Unpublished data from industrial hygiene surveys' found that aspirin concentrations greater than 100 mg/m3 "were tolerated by employees except for occasional skin irritation." However, no data are available on pulmonary function effects of aspirin inhalation; or on the effects of chronic, long-term aspirin inhalation, either in the respiratory or gastroenteric tracts, or in other organs, tissues, metabolic processes or reproduction. Based on the acute toxic effects of aspirin ingestion on bleeding time and platelet aggregation, a TLV for aspirin of 5 mg/m3 is currently deemed low enough to prevent these effects as well as those of gastric and respiratory irritation. References: 1 Merck Index, 9th ed., p. 114, Merck & Co., Rahway, N.J. (1976). 7 Technical data sheet provided by Dow Chemical Company. 3 Condensed Chemical Dictionary, 8th ed.. p. 82, Van Nostrand Reinhold, New York (1971). 4 Pharmacologic Basis of Therapeutics, 5th ed., Goodman, L.S. and Gilman, A., Eds., pp. 330-337, MacMillan, New York (1975). 5 O'Brien, J.R.: Lancet. 1:779 (1968). 458 517904 0288 o-sec-BUTYLPHENOL -- Skin C2H5(CH3)CHC6H4OH 5 ppm (30 mg/m3) O-sec-Butylphenol is a slightly volatile liquid. (B.R. 224-237C). It is a chemical intermediate in the preparation of resins, plasticizers, surface active agents and other products. The oral and skin absorption LD50's for guinea pigs were found to be between 0.6 and 2.4 g/kg. On prolonged contact with the skin, burns would result. No corneal injury was caused by direct contact with the eye. Rats survived a 7-hour exposure-to an atmosphere saturated with the vapor. Acute occupational exposures have resulted in mild respiratory irritation, as well as skin burns. A TLV of 5 ppm is recommended primarily on analogy to phenol and cresol. Since the toxicological properties of alkyl benzene derivatives are modified by the number and length of alkyl groups. TLV's based on analogy to the parent compound must be considered tentative, until reinforced by additional data. Reference: Dow Chemical Company: Communication to Committee (1977). CARBON DISULFIDE -- Skin CSj TLV, lOppm (Approximately 30 mg/m3) Carbon disulfide is a clear colorless or faintly yellow liquid, almost odorless when pure, but technical grades have a strong disagreeable odor resembling that of hydrogen sulfide with which it is contaminated. It has a boiling point of 46.3C, a flash point of -22F, and an autoignition temperature of 212eF. It is soluble in alcohol, benzene and ether but only slightly soluble (220 mg/100 cc water at 22C) in water. Because of its low flash point and autoignition temperature, it is highly flammable, and a dangerous fire and explosion hazard. The explosive limits in air are 1 to 50%. It can be ignited by friction. Carbon disulfide vapor is absorbed largely through the lungs, although toxic quantities can also be absorbed through the skin.' Its effects are mostly on the nervous system; single exposures are characterized by narcosis and its sequelae. Symptoms of repeated exposure are nervousness, irritability, indigestion, bizarre dreams leading to insomnia, excessive fatigue, loss of appetite and headache.' Many serious cases of intoxication by carbon disulfide have occurred among workers, especially in Europe. Vigliani3 mentioned over 60 cases in Italy prior to 1933, over 160 between 1934 and 1938, and saw some 143 cases between 1940 and 1953. Symptoms included polyneuritis, psychosis, tremors, headache and gastric disturbances. He concluded3 that concentrations above 150 ppm for four hours daily caused chronic intoxication after a few months; 100 to 150 ppm resulted in chronic poisoning, usually after a year or more; concentrations between 50 and 100 ppm caused only sporadic cases of mild intoxication, and levels below 45 ppm never caused intoxication and 30 ppm could be considered safe. Paluch* reported that 148 cases occurred in Poland in 1941-42. He found four cases in one plant where about 300 ppm of CSj were present. Twenty additional cases were mentioned. Mental fatigue, sleepiness and headaches were associated with exposure at concentrations between 60 and 120 ppm. Warow et al.` reported 15 cases, most of them relatively mild, from concentrations between 30 and 45 ppm. Jindrichova and Simko* reported 190 intoxications in one plant over a three-year period, when concentrations of CS2 averaged about 130 ppm; during the next nine years, with concentrations averaging 70 ppm or less, "only" 36 intoxications occurred. Nesswetha and Nesswetha' analyzed 33 cases reported in Germany; in most the MAC of 20 ppm was exceeded. Toyama and Sakurai* found that in Japan exposures at concentrations averaging 40-50 ppm, in 1951-53, were associated with headache, fatigue, emotional disturbances, loss of appetite or other symptoms in 70% of the exposed group. With concentrations reduced to 5-15 ppm (1965) scarcely any symptoms were observed. In this country Gordy and Trumpet* reported six cases in 1938, and noted a report of thirty cases of psychosis in one viscose rayon plant. They suggested that concentrations of CS2 should be kept around 10 ppm. Lewey'0 found psychic signs in 71% of 120 employed viscose workers in 1941. Barthelemy" found that if concentrations were maintained below 30 ppm, no trouble resulted. Rubin and associates'3 reported no significant signs in workers exposed many years at levels below 10 ppm. Kleinfeld and Tabershaw'3 reported two cases where the CS2 concentration was slightly above 20 ppm; they recommended 10 ppm as the TLV. Mihail et al.'3 have recently reported the observation of significant vascular, nervous and biochemical changes in workers exposed to an average concentration of 9 ppm for periods up to two years; according to 459 511904 0289 the authors, the incidence and degree Of these changes were proportional to the exposure. At least half of these workers had been exposed to CS2 for more than 20 years, however, and in the past the concentrations were well above 9 ppm.'* Wiley and co-workers'* exposed animals repeatedly at 37 ppm and found significant toxic effects. They recommended that concentrations be maintained below 32 ppm. It is now recognized that the neural responses to CS2 are greatly influenced by the mineral content of the diet, at least in animals," a highly mineralized diet offering substantial protection from neurologic effects. A series of reports of studies'*22 performed in Finland on viscose rayon workers revealed significant excess mortality (16 deaths vs 3 in cohorts of 343 males) from cardiovascular heart disease in those exposed for at least 5 years between 1942 and 196B when concentrations of carbon disulfide and hydrogen sulfide varied over the years from 20-40 ppm in the `50s to 10-30 ppm in the `60s. Most workers however, had been exposed repeatedly at concentrations far higher than those measured in the general room air because of their having to work with their heads inside the machine coverings during operational difficulties '*" Evidence of neurotoxicity in viscose rayon workers after long-term exposure was reported on a portion (118) of the same cohort examined in the cardiovascular study." About twice as many exposed workers had pathologically reduced conduction velocities (48 vs 24% than the unexposed.) This sub-clinical polyneuropathy (ulnar, deep peroneal and posterior tibial nerves) was believed to be irreversible. Electroencephalograms were abnormal in 21 of 54 exposed, compared with 6 of 50 controls. As part of the cross-sectional study above, microcirculation of the ocular fundus and behavioral symptoms were studied. Delayed peripapillary filling occurred in 68 of 100 exposed workers as against 38 of 97 controls. It was accordingly concluded that in chronic subclinical carbon disulfide poisoning, delayed peripapillary filling is the primary finding, and that the probability of syndrome is caused by carbon disulfide exposure is 100% for either CHD, plus polyneuropathy and the eye disorder, or those 3 components plus behavioral symptoms. On the basis of these investigations, the TLV of 20 ppm was considered to be too high for Finnish rayon workers, and the Finnish authorities in 1972 reduced the Finnish TLV to 10 ppm. Response to exposure to carbon disulfide at or around the TLV of 20 ppm would appear to vary among workers in different countries. One reason already noted -- " nutritional differences; experimental rabbit diets reinforced with a high salt mixture, especially copper and zinc, permitted repeated daily exposures at 1,100 ppm CS, without the observed effects of body weight loss, serum lipiprotein and total cholesterol increase, adrenal hypertrophy and pathologic changes in the brain and spinal cord seen in controls on a normal salt diet. Copper and zinc in the spinal cord in rabbits on the high salt diet were elevated whereas copper was depleted at that site, and no increases in zinc were found in the controls exposed at the same dosage. Thus trace elements in the diet can exert a profound effect on the response from CS* exposure. A different exposure coefficient in the sodium azide-iodine test for responders to CS* overexposure was found in Argentina than in Yugoslavia.25 Whether this difference is due to nutritional differences, or differences in hereditary susceptibility has not been explored. Djuric et al22 by the use of a test involving the administration of Antabuse (tetra ethylthiuram disulfide, TETD) claim to have identified viscose rayon workers who hyperreacted to exposures to CS2 and hence were candidates for polyneuropathy. Those workers with a reduced capacity to metabolize TETD were considered "hyper-susceptibles." The frequency of hypersusceptibles could well vary in different countries. The medical director of a large viscose-rayon plant in the U.S.A. stated that no cases of carbon disulfide intoxication had occurred at his plant since 1942, when exposures were below 25 ppm on the average 25 NIOSH, in its criteria document for carbon disulfide,25 recommended a TWA of 1 ppm, with a 10 ppm ceiling for any 15 minute period. This recommendation is based on cardiovascular and neurologic studies indicating that 10 ppm is the lowest concentration causing demonstrated health effects. A few reports of adverse findings at concentrations below 10 ppm were cited, but their validity was questioned. The 1 ppm TWA is derived from the lowest ill effect concentration of 10 ppm, by applying a safety factor of ten, since death from coronary heart disease is relatively frequent, and cardiovascular disorders are among the effects reported from concentrations slightly above 10 ppm. The following references relate to pertinent cardiovascular studies: Vigliani,2 Hernberg,'* Tolonen,'* and Raitta,2' already cited previously and Hernberg,2* Gavrilescu,2* Tiller,50 Hernberg,5' Cirla,52 and Raitta.52 Significant neurologic studies include Seppalainen,20 aready cited, and,52 and Vasilescu.54 Other relatively recent recent recommendations include; ANSI (1968) 20 ppm; U.S.S.R. (1972) 4 ppm; Czechoslovakia (1969) and Sweden (1974) 10 ppm. The odor threshold has been reported to be 0.1 to 0.2 ppm.2* RECOMMENDATION The 20 ppm limit was selected primarily to prevent neurological disturbances. It has been criticized as too high, even on this basis, by at least two American investigators.* '5 The additional finding of cardiovascular effects in workers exposed at relatively low concentrations indicates that the TLV should be reduced. The sense of the Committee is that a limit of 10 ppm would be appropriate. References; ' Fairhili, L.T.: Industrial Toxocoligy, P. 181, Baltimore, Md. (1957). 2 Vigliani, E.C.; Brit. J. Ind. Med, 11, 235 (1954). 5 Vigliani. E. C.: Ind. Med. & Surg. 19, 240 (1950). 2 Paluch, E.A.: J. Ind. Hyg. & Tox. 30, 37 (1948). 460 511904 0290 5 Warow, P., Colleau, P., Meignie, S.: Arch. d. Mai. Prof. 25, 348 (1964). * Jindrichova, J., Simko, A.: Arch. Gewerbepath, u. Gewerbehyg. 23, 72 (1967). r Nesswetha. L., Nesswetha, W. in: Toxocology of Carbon Disulfide, Brieger, H. and Teisinger, J,, Eds., P. 214, Excerpta Medical Foundation, Amsterdam, Holland (1967). * Toyama, T., Sakurai. H.L. Ibid, p. 197 * Gordi, S. T., Trumper, M.: J. Am. Med. Assn., 110, 1543 (1938). Lewey, F.H.: Ann. Int. Med. T5, 869 (1941). " Barthelemy, H.L.: J. Ind. Hyg. & Tox. 21, 141 (1939). " Rubin, H.H., Arieff, A.J., Tauber, F.W.: Arch. Ind. Hyg. & Occ. Med. 2, 529 (1950). 13 Kleinfeld, M., Tabershaw, I.R.: J. Am. Med. Assn. 159, 667 (1955). " Mihail. J. et al.: Arch. Mai. Prof. 29, 109 (1968). 15 Teisinger, J., Private communication. ' Wiley, F.H., Heuper, W.D., von Oettingen, W.F.: J. Ind. Hyg. & Tox. 16, 733 (1936). " Scheel, L.D.: in "Toxicology of Carbon Disulfide", Brieger & Tiesinger. " Hernberg, S., et al.: Work-Envir. Hlth. 10, 93 (1973). ' Tolonen, M. et at.: Brit. J. Ind. Med. 32, 1 (1975). K Seppalainen, A.M., Tolonen, M.: Work-Envir. Hlth. Scand. J. 11, 145 (1974). ' Raitta, C. el al.: Arch. Klin. Exp. Ophthal. 191, 151 (1974). " Tolonen, M.: Scand. J. Work-Envr. Hlth. 1, 63 (1975). Stokinger. H.E. Mountain, J.T., Scheel. L.D.: Ann. N.Y. Acad. Sci. 151, art 2, 968 (1968). w Djuric, D. et al.: Presented at XVII Int'l Cong. Occup. Hlth, Buenos Aires, Sept. 17-24,1972. " Memorandum dated Apr. 2, 1968 to Dr. L.D. Scheel from Dr. J.A. Calhoun. * Research on Chemical Odors, Part I -- Odor Thresholds for 53 Commercial Chemicals, Manufacturing Chemists Assn., Washington, DC, Oct. 1968. *' NIOSH: Criteria for a recommended standard -- occupational exposure to carbon disulfide, DHEW (NIOSH) Publication No. 77-156, Aug. 1977. Hernberg, S. et al: Brit. J. Ind. Med. 27, 313 (1970) from ref. 27. " Gavrilescu, N., Lilts. R.: In Toxicology of Carbon Disulfide, Brieger. H., and Teisinger, J,, Eds., p. 165, Excerpta Medical Foundation, Amsterdam, 1967. * Tiller, J.R. et al: Brit. Med. J. 4. 407 (1968), from ref. 27. 31 Hernberg, S., et al: Work Environ. Health 2, 27 (1976) from ref. 27. 33 Cirla, A.M.: Med. Lav. 63, 431 (1972), from ref. 27. 33 Raitta, D., Tolonen. M.: Arch. Klin. Exp. Ophthalmol. 195, 149 (1975), from ref. 27. * Seppalainen, A.M. et al: Work Environ. Health 91, 71 (1972) from ref. 27. " Vasilescu, C.: Rev. Roum. Neurol. 9, 63 (1972), from ref. 27. CHLOROACETYL CHLORIDE -- Skin CHjCICOCI TLV 0.05 ppm (0.23 mg/m3) Chloroacetyl chloride is a colorless liquid with a pungent odor. Its boiling point: 105 - 110C: sp. gr. 1.495: vapor pressure at 20C-19mm. It decomposes in water and is nonflammable. Its chief use is as an intermediate in the manufacture of acetophenone and other chemicals. The oral LDm for rats lies between 0.12 and 0.25 gm/kg. It is corrosive to the skin and eyes, and can be absorbed through the skin in lethal amounts. A 5-10 minute inhalation exposure at 4 ppm caused respiratory difficulties in rats, but no effect was observed from inhalation of 2.5 ppm for seven hours.' A 30-day inhalation study with rats, mice and hamsters showed eye and respiratory irritation at 2.5 ppm; the no ill effect level was 0.5 ppm. Medical reports of the effects of acute exposure include: mild to moderate skin burns and erythema: lachrymation and mild eye burns; mild to moderate respiratory effects with cough, dyspnea and cyanosis; and mild gastro-intestinal effects. Industrial hygiene surveys revealed 8-hour TWA exposure of 9 to 17 ppb, with excursions to 140 ppb. At the latter concentration eye irritation and minimal respiratory irritation were noted. The vapors of chloroacetyl chloride are highly irritant; a TLV of 50 ppb (0.05 ppm), or one-tenth the no effect level for animals exposed for 30 days, is recommended. A STEL of 150 ppb, a concentration at which minimal irritation was observed, is suggested. Reference: ' Dow Chemical Company: Communication to Committee (1977). 461 511904 0291 COBALT, METAL DUST AND FUME Co TLV, 0.05 mg/m5 Pulmonary involvement consisting of chronic interstitial pneumonitis has now been reported with sufficient frequency in workers associated with the cemented tungsten-carbide industry to give credence to the belief of Miller, et althat cobalt is the probable etiologic agent, although the carbides of tungsten, tantalum and titanium are commonly present in the exposure atmosphere. An obliterative bronchiolitis adenomatosis has also been produced in guinea pigs intratracheally injected with cobalt metal dust (type and particle size unspecified) albeit at very large doses (50, 25 and 10 mg).5 Fairhall and Keenan5 showed cobalt to be ubiquitously present throughout an entire industrial plant, and serious, and occasionally fatal responses occurred from exposures of the order of 1 to 2 mg or less cobalt/m3. Lung changes frequently were not progressive, which often improved considerably upon removal from exposure. Hypersensitivity appears to be involved, because the pulmonary responses occurred at low incidence, varied in intensity and time of onset. Animal studies tended to confirm the hypersensitivity theory,5 but were not productive of the characteristic lung lesion seen in workers; increases in serum a-globulin and neuraminic acid were found in dogs and rabbits exposed by inhalation to Co metal, metal fume, carbide blend, or by injection of CoCI?. Similar increases in serum A-2 globulin fraction of a welder with a history of insidious onset of exertional dyspnea and abnormal chest x-ray.* Scanning electron microscopy and energy dispersion x-ray microanalysis of the lung revealed Co, Fe, Ni and Cr. Only Co is recognized to be associated with the chest symptoms exhibited. A dermititis of the allergic type has been described by Schwartz* from contact with cobalt and its compounds; a "carboloy-itch" has also been described. Air-borne dust samples of metal dust and fume collected and analyzed in a large industry by the Michigan Department of Health for cobalt in 1946, 1956, 1958, 1960 and 1964 showed a gradual reduction from a high of 14 42 mg/m5 in 1946 to a maximum of 1.5 mg/m5 ten years later. Since 1946, improved control measures have further reduced exposure to concentrations at or below 0.1 mg/m5 determined as cobalt. Concomitant with this reduction, no new cases of systemic cobalt disease or disease or dermatitis have occurred. Another small survey made by the Pennsylvania Department of Health showed breathing zone concentrations could be controlled to about 0.07 mg/m5; without control, the concentrations were about 0.5 mg/m5. Because a limit of 0.1 mg/m5 of Co metal fume and dust can be achieved without undue economic or technical difficulty, and apparently was protective against hypersensitivity reactions, this limit was recommended as a tentative TLV in 1966, with the documentation statement, "Whether 0.1 mg/m5 is sufficiently low to prevent responses in all workers, must await further investigation of this level." Subsequent investigation by Kerfoot, Fredrick and Domeier5 on miniswine exposed by inhalation to Co metal dust resulted in early appearance (3 months) of pulmonary disease at the TLV of 0.1 mg/m5 as evidenced by a marked decrease in lung compliance and an increase in the amount of collagen in the central areas of the pulmonary alveolar septa. The Co dust used was about 50% alpha and 50% beta variety with a size range of from 0.4 pm to 3.6 pm Exposures at both 1 and 0.1 mg/m5 were performed for 3 months daily, 6 hours per day, 5 days per week. Wheezing was taken as evidence of hypersensitivity that occurred during the fourth week of exposure following a one-week sensitizing dose. In view of the serious nature of these findings obtained after a relatively short exposure period at the TLV of 0.1 mg/m5, a recommendation to lower the TLV to 0.05 mg Co/m5 as a time-weighted average value is made. Soviet limit, 0.5 mg/m5 (1970); Czechoslovakia 0.1 mg/m5 (time-weighted average) (1969); Sweden 0.1 mg/m5, as time-weighted average, (1974). References: ' Miller, C. W., Davis. M.W., Goldman, A., Wyatt, J.P.: Arch. Ind. Hyg. & Occup. Med. 8, 453 (1953); Lundgren, K.D., Ohman, H.: Arch path, anat.: 325, 259 (1954); Lundgren K.D., Swensson, A.. Acta Med. Scand.: 145, 20 (1953). 5 Schepers. G.W.H., Arch. Ind. Health, 12, 127 (1955). 5 Fairhall, L.T., Castberg, H.T., Carrozzo, H.J., Brinton, H.P.: Occup. Med. 4, 371 (1947); Fairhall, L.T., Keenan, R.G.. Brinton, H.P., Pub. Health Rep. 64. 485 (1959). 4 Stokinger, H.E., Wagner, W.D.: Arch. Ind. Health 17, 273 (1958). 5 Siegesmund, K.A., et al.: Arch. Envir. Hlth. 28, 345 (1974). * Schwartz, Tulipan, Birmingham: Occupational Diseases of the Skin, 3rd Ed. Lea & Febiger, Philadelphia (1957). ' Kerfoot, E.J., Fredrick, W.G., Domeier, E.: Am. Ind. Hyg. Assn., J. 36, 17 (1975). 462 511904 0292 CYANOGEN CHLORIDE CNCI C. 0.25 ppm (0.6 mg/m1) Cyanogen chloride may exist as a colorless liquid or gas. It possesses a pungent odor detectable at 1 ppm (2.5 mg/m1). Its melting point is -6C., boiling point is 13.8C., vapor pressure of 1000 mm. Hg. at 20 C. It is soluble in water (2500 cc. in 100 ml of H'O at 20 C.) ethyl alcohol: (10,000 cc. in 100 ml. of alcohol at 20 C.) ether: (5000 cc. in 100 ml. of ether at 20 C.) Dissolves readily, soluble in all organic solvents. Tends to form polymers upon storage. Reed found in chronic exposure to cyanogen chloride caused hoarseness, conjunctivitis and edema of the eyelid.' Cyanogen chloride caused marked irritation of the respiratory tract with a hemorragic exudate of the bronchi and trachea and pulmonary edema. F. Flury and F. Zernik in Schadliche Gase* report on exposure tests on 5 different animals. Concentration of approximately 500 ppm (1.0 mg/1) for 3 minutes was fatal to the mouse. A concentration of 120 ppm (0.3 mg/1) for 3.5 minutes was fatal to the cat. A concentration of 46 ppm (0.12 mg/ 1) for six hours was fatal for a dog. A goat exposed to 1000 ppm (2.5 mg/1) for 3 minutes died after 70 hours. A concentration of 1200 ppm (3.0 mg/1) was fatal to the rabbit. Effects of cyanogen chloride on experimental animals have also been studied by Jandorf and Bodanski1 and Aldridge and Evans/ Both papers indicate the action of cyanogen chloride is a combination of pulmonary edema and the interference of the cellular metabolism by the cyanide radical. They found that treatment with oxygen plus amyl nitrate inhalations with artificial respiration seem indicated. Similar information9 for man identifies 1 ppm (0.0025 mg/1) as the lowest irritant concentration for a 10 minute exposure. 2 ppm (0.005 mg/1) was an intolerable concentration for 10 minutes: 46 ppm (0.12 mg/1) was fatal in 30 minutes. Information provided by the Michigan Department of Public Health9 indicates that concentrations of approximately 0.7 ppm (1.78 mg/m3) were unbearable, resulting in severe eye and nose irritation to the individuals involved in the study and resulting in their having to leave the work area. The operation involved the treatment of cyanide plating solutions with liquid sodium hypochlorite. Methods are also available to convert the CN-radical to CNO-using chlorine gas or a 70% calcium hypochlorite solution. As a method for reducing the evolution of cyanogen chloride it is recommended that the solution pH be maintained at 10.0 and that mechanical rather than air agitation be employed. Adequate ventilation of the treatment tank is stressed. It is recommended that in order to prevent undue irritation and the possibility of cellular metabolic interference, that cyanogen chloride not exceed 0.25 ppm as a ceiling limit. Fassett, in Patty/ recommends that the limit value "should certainly be less than 0.5 ppm." No other countries appear to have established a value for cyanogen chloride exposure at this time (1977). References: ' Reed, C.I., J. Industrial Hyg. 2, 140-143, 1920. 1 Flury, F. and Zernik, F., Schadliche Gase, Springer, Berling, (1931). 1 Jandorf, B.J., and Bodansky, O., J. Ind. Hyg. Toxocol 28, 125, (1946). 9 Aldrich, W.N.. and Evans, C.L., Quart. J. Exp. Physiol 33, 241, (1946). 9 Prentiss, A M., Chemicals in War, McGraw-Hill, New York (1937). 9 Communication from the Michigan Department of Health to the TLV Committee (November, 1977). 7 Patty. F A. Edit. Ind. Hyg. & Toxicol. Vol 11, Second Revised Edition, 1967, p. 2006, Interscience, New York. 1,3-DICHLOROPROPENE -- Skin CHCI = CH -- CHjCI TLV 1 ppm (Approx, 4.54 mg/m1) STEL 10 ppm (Approx. 45.4 mg/m1) SYNONYMS: Telone, DD Fumigants Cis and trans isomers of 1.3--dichloropropene occur. Most toxicity studies have been conducted on mixtures of the two isomers or on commercial products containing significant amounts of other three carbon chlorinated compounds. The major usage is as a soil fumigant. The following properties have been published for the compound: "Cis-trans 1,3-dichloropropene (CHCI-CH-CH2CI) is a clear, light straw-colored liquid with a sharp, sweet, penetrating and irritating odor. The physical properties of a cis-trans mixture depend on the ratio of isomers but can be expected to have a specific gravity of around 1.2 at 68/68 F, a boiling point close to 103 C at 760 mg/Hg and a vapor pressure 463 511904 0290 of about 28 mm at 25bC. A flash point of about 83F was determined by the Tag closed cup method; the explosive limits are of the order of 5 to 14.5% by volume. Spontaneous decomposition of the material will not occur under normal conditions if it is placed in a suitable container; however, polymerization can occur. The mixture reacts readily with aluminum, aluminum alloys, other active metals and some metal salts and halogens Epichlorohydrin (1 to 2%) is often added to stabilize the material and to prevent corrosion."' While the material was detected by odor by most people at 1-3 ppm, the odor was very faint and reported to fatigue rapidly. Hence, warning properties appear to be poor particularly to prevent excessive long term exposure.' It apparently reacts with certain materials such as rubber, leather and fur to form a strong smell. The acute toxicity has been studied for the mixture of isomers,' as well as a mixture with chlorinated C3 hydrocarbons.3 A 92% product (a cis-trans mixture) when fed as a 10% solution in corn oil was found to have an acute oral LD^ for male rats of 713 mg/kg and for female rats, 470 mg/kg.' The liver and kidneys of the treated animals were affected as shown by gross examination, and some lung injury may have occurred. The liquid was found to be irritating to the eyes and skin of rabbits and to be absorbed through the skin of rabbits, particularly when diluted with propylene glycol. The LD^ for a 24-hour application under a cuff was 504 mg/kg for the 92% undiluted product but doses of 125 and 250 mg of the compound as a 10% solution in corn oil caused the death of some rabbits treated for 24 hours. This same reference reported: "Limited acute inhalation studies showed that vapor concentrations above 2700 ppm were irritating to the eyes and nose and caused severe lung, nasal, liver and kidney injury to rats. Concentrations of the order of 1000 ppm were also irritating to the eyes and nose and caused lacrymation and unconsciousness if exposure was prolonged. All six of a group of male rats survived a 1-hour exposure to 1000 ppm but all four rats exposed for 2 hours died. A peculiar odor described as skunk or garlic was noted on animals exposed to 700 ppm or greater. A single exposure of 7 hours to 400 ppm was found to be lethal to groups of five male and female guinea pigs, whereas similar groups of male and female rats exposed at the same time survived; however, these rats appeared severely injured and required about eight days to recover the weight they lost as a result of their exposure. There was no evidence of gross liver and kidney injury at that time, but active congestion was obvious in the lungs of all rats."' Based on preliminary chronic studies in which rats and guinea pigs were injured by repeated exposure to either ii or 50 ppm for one month, separate groups of rats, rabbits, guinea pigs and dogs were exposed to either 3 or 1 ppm for 6 months.' Exposures were given 7 hours/day, 5 day/week. When compared to control groups of equal size and age on the basis of demeanor, growth, mortality, appearance, final body and organ weights, hematological examination, and gross and microscopic examination there was no adverse effect in any group exposed to 1 ppm. In the groups of animals exposed to 3 ppm only male rats showed any adverse effect. This group showed some cloudy swelling of the renal tubular epithelium which apparently was reversible, since it was not present in male rats allowed to recover for three months after exposures ceased. No data relative to repeated exposures of humans to 1,3--dichloropropene was found in the literature. The effects of single exposure have been found to be consistent with the effects found in animals.' Skin, eye and respiratory irritation have been reported from excessive exposure. No U.S or foreign industrial standard has been published but based on the above animal data this reference recommends that "when repeated, prolonged exposure to the vapors of 1,3--dichloropropene can occur, seven to eight hour daily time-weighted average exposure of workman not exceed 1 ppm."' Based on evidence of no injury in any of the four species exposed 7 hours/day to 1 ppm for six months and of only slight reversible injury in one sex of the four species exposed to 3 ppm a TLV of 1 ppm is recommended. Based on evidence of penetration through the skin of rabbits a skin notation should be used. A STEL of 10 ppm is also recommended. References: ' Torkelson, T.R. and Oyen, F. AIHA Journal 28:217 (1977). 3 Hine, et al Arch Ind. Hyg. Occup. Med 7:118 (1953). 2,2-DlCHLOROPROPIONIC ACID (DALAPON) CHjCCIjCOOH 1 ppm (6 mg/m3) Dalapon has a boiling range of 185-190C. at atmosphere pressure (90-92C. at 14 mm), is very soluble in water and alcohol, and soluble in ether. It is used, as the sodium salt, as a herbicide. It is corrosive to the skin, and can cause permanent eye injury. The oral LD^ for rats is 0.7 to 1 g/kg. Rats exposured for 7 hours to an atmosphere saturated with dalapon vapor showed no ill effects. A 120-day diet study of rats indicated a no-ill-effect level of 15 mg/kg/day.' Medical reports of the findings following acute exposures show mild to moderate skin, eye, respiratory and gastro-intestinal responses. Occupational vapor exposures up to 2.65 ppm (TWA) have been observed; minimal respiratory irritation was noted at concentrations between 2 and 7 ppm. 464 511904 0294 c Dalapon is presumably a stronger acid than monochloropropionic acid. A TLV cf 1 ppm, to prevent irritation of the eyes and respiratory passages, is recommend. A Soviet paper, however, recommended an MAC of 10 mg/m3, or nearly 2 ppm: higher than for either monochloropropionic acid or propionic acid itself' References: ' Dow Chemical Company: Communication to Committee (1977). * Seravotsnoe, P.C.: Maximum allowable concentrations of harmful substances in the air of working zones. GOST 12.1 005-76. DIETHANOLAMINE HO(CHj)jNH(CHj)^OH 3ppm (13mg/m3) Diethanolamine, with a melting point of 26C., can be either a solid or liquid at room temperature. It has a boiling point of about 270C. It is very soluble in water and alcohol, but insoluble in ether and benzene. It is used as a detergent in paints, cutting oils, shampoos and other cleaners; as an absorbent for acid gases; and as a chemical intermediate in the manufacture of resins and plasticizers. Diethanolamine has been characterized as being of low toxicity.' The oral LD*, for rats and guinea pigs is about 2 g/kg.* Acute toxicity studies show that direct contact may impair vision and denature skin upon repeated application. A 90-day diet study showed a no-effect level of 20 mg/kg/day.J This is quite a little lower than was reported for monoethanolamine (see ethanolamine). Short term occupational exposure levels as high as 38 ppm have been found* The recommended TLV is derived from the above noted feeding study, applying a safety factor of ten, and by analogy with ethanolamine. References: Hawley, G.G.: Condensed Chemical Dictionary, 9th ed. Van Nostrand Reinhold, 1976. Dow Chemical Company: Communication to Committee, 1977. 3 Smyth, J.F. et al: Arch Ind. Hyg. Occ. Med. 4, 119 (1951). DIVINYLBENZENE C6H4(CHCHj)2 TLV 10 ppm (53 mg/m3.) The commercial grade of divinylbenzene, a pale straw colored liquid, contains all three isomeric forms, but the meta isomer predominates. The boiling range is 195-200 C; m.p. -87 C; sp.gr. 0.918; flash point 165 F. It is not miscible with water, but is soluble in methanol and ether. To prevent polymerization, an inhibitor is usually added when the liquid is stored or shipped. Its chief use is as a polymerization monomer for synthetic rubbers, drying oils, casting and ion-exchange resins, and polyesters. The oral LD*, for rats is about 4.1 gm/kg, but skin burns may result from repeated or prolonged contact with the liquid. An acute inhalation study with rats showed no effects from a single 7-hour exposure at 351 ppm.' Mild irritation has been observed in workers acutely exposed by inhalation, as well as from skin and eye contact. Plant surveys have indicated TWA concentrations below 0.4 ppm, with excursions to 4 ppm. No data on the effects of chronic exposure are available. A TLV of 10 ppm is suggested, based in part on similarity to monovinylbenzene (styrene). Below this level irritation of respiratory passages and eyes should be minimal and no other toxic effects are to be expected, so far as is known. Until more data is at hand, however, this limit must be considered tentative. Reference: ' Dow Chemical Company: Communication to Committee (1977). 465 511904 0295 HEXAMETHYL PHOSPHORAMIDE (HMPA) (Synonyms: Hexamethylphosphorlc triamide, frit (dlmethylamlno phosphlneoxlde) Appendix A2 (Skin) Chemical Formula: o ii ICH-jl jN -P - N (CHjIj H C6h, a*3 p Molecular Weight: 179.2 Description: Colorless, mobile liquid with aromatic odor Boiling Point: 233C at 760 mm Vapor Pressure: 0.07 mmHg 25C' 1 mg/m3 = 0.137 ppm 1 ppm = 7.32 mg/m3 There is no basis in human exposure experience for defining a minimal observed effect level for HMPA or a no observed effect level. No effects have been observed under any exposure conditions. Its use in Kevlars aramid fiber production exceeds 10 years in duration. Exposure guidelines are based upon animal experiments and, regarding skin penetration, observations on aminals and humans. The animal studies include investigations that were carried out prior to 1970 as well as more recent work. They have been reviewed by the International Agency for Research on Cancer 1977.' The principal bases for the present classification are the results from long-term inhalation toxicity tests at Du Pont's Haskell Laboratory.3 Dogs exposed six hours a day. five days a week, for five months exhibit rhinitis, squamous metaplasia, and denudation of the nasal turbinate epithelium at the 0.4 and 4 part per million (ppm) levels. The trachea and large bronchi showed no significant tissue reaction, but epithelial denudation was observed in the bronchioles. There were no respiratory tract effects in dogs exposed to 0.P5 ppm. No other histopathologic effects were seen in dogs at any test level. Rats exposed daily for three months to 0.4 and 4 ppm HMPA showed respiratory changes similar to those seen in dogs. However, in contrast to the dogs, rats showed metaplastic or degenerative changes in the epithelium of the trachea and bronchi, as well as in the bronchioles. In addition, rats at the 4 ppm level showed renal tubular degeneration, testicular atrophy, and slight bone marrow hypoplasia. At 0.4 ppm only a renal tubular damage was noted. No pathologic changes attributable to the test compound were found at the 0.05 ppm test level following exposure daily for three months. Between six and nine months of exposure, a dose-related excess of deaths or sacrifices in extremis occurred in rats at the two highest test levels -- 0.4 and 4 ppm HMPA. The majority of these animals had been experiencing difficulty in breathing and had enlarged noses (nasal tumors). Subsequent histopathologic examination revealed squamous cell carcinoma of the nasal cavity originating from the epithelial lining of the nasal turbinate bones. Subsequently it was learned from the rat exposure study at Haskell Laboratory that exposure to 0.05 ppm HMPA was sufficient to induce the typical nasal carcinomas after a latent period of 13 months. Daily exposures of rats to 0.01 ppm were begun in October 1975 and concluded twenty-four months later. At the time of final sacrifice of the rats exposed to 0.01 ppm for 24 months no nasal tumors were observed on gross examination. Histopathologic examination of tissues has not yet been reported. The IARC report' concludes that hexamethylphosphoramide is carcinogenic in rats, having produced squamous cell carcinomas of the nasal cavity. ACGIH concurs in this conclusion. It is classified as an industrial substance suspect of carcinogenic potential for man because of its demonstrated carcinogenesis in rats by inhalation. No TLV is recommended pending the completion of experiments in defining a no-observed-effect level. References: ' Calculated from Mole, M. F., W. S. Holmes, and J. C. McCoubrey, Jour. Chem. Soc., p. 5144 et seq. (1964). ' International Agency for Research on Cancer, 15 211-222, Lyon, France. August 1977. 3 Trochimowicz, H. J., et al., Two-Year Inhalation Toxicity Study of HMPA. Presented at Amer. Indus. Hyg Assoc. Mtg., Atlanta, Georgia. May 1976. 466 511904 0296 2-HYDROXYPROPYL ACRYLATE (HPA) -- Skin CH,CHCOOCH2CHOHCH3 TLV 0.5 ppm (2.9 mg/m3) HPA is a liquid which boils, at 5 mm pressure, at 77 C. It is a monomer used in the manufacture of thermosetting resins for surface coatings. Acute toxicity studies indicate HPA to be more toxic than the corresponding ethyl derivative HEA. The rat oral LDjo was 0.25 - 0.5 g/kg; the skin absorption LD*, in rabbits about 0.25 mg/kg. Direct contact caused severe eye burns and was corrosive to skin. Some sensitization was caused in guinea Pigs. Inhalation at 650 ppm for 7 hours was not fatal to rats, however, industrial exposures have been below f ppm. A medical report of a skin exposure showed no symptoms from a contact described as mild. A 30-day inhalation study in rats, dogs, rabbits and mice (assumed to have been 7 hours a day, 6 days a week) indicated some irritation at the lowest level of 5 ppm. A TLV of 0.5 ppm is recommended, based on irritant effects. As with HEA, the margin of safety is judged not to be unduly large. Reference: Dow Chemical Company: Communication to Committee (1977). n-ISOPROPYLANILINE -- Skin CjHsNHCH (CH,)j TLV 2 ppm (11 mg/m3) STEL 5 ppm (20 mg/m3) N-lsopropylaniline is a liquid with a boiling point of 202C. It is employed in the dyeing of acrylic fibers and as a chemical intermediate. The oral LD*, for rats was 0.25 -- 0.5 g/kg. Acute toxicity data indicated slight skin and eye effects from direct contact. No chronic toxicity, industrial hygiene or medical data are available. Following addition of alkyl groups to benzene derivatives, the toxicological properties are usually modified to some degree, but remain basically similar to those of the parent compound. The oral LDjo of N-isopropylaniline appears to be about the same as that of aniline. With its higher molecular weight, a somewhat lower ppm limit could be considered appropriate for this compound than for aniline. Low concentrations of vapor would result from normal use of a material boiling above 200C. The recommended TLV of 2 ppm, and the skin notation, are based on analogy with aniline and N, Ndimethylaniline. Reference: Dow Chemical Company: Communication to Committee (1977). METHYLENE CHLORIDE (DICHLOROMETHANE) CHjCIj TLV, 100 ppm (Approximately 350 mg/m3) STEL, 500 ppm (Approximately 1750 mg/m3) Methylene chloride is a colorless volatile liquid, soluble in water to only 1% by weight, but completely miscible with most organic solvents. It has a sweetish odor, like most chlorinated hydrocarbons, a specific gravity of 1.335, and a boiling point of 40 C. With its high vapor pressure (315 mm Hg at room temperature, 23.5 C) substantial concentrations of vapor are readily achieved whenever methylene chloride is spilled or spread out over a large surface, even in a space that is not closely confined. It is non-flammable by standard tests but will burn in extreme conditions. Methylene chloride is widely used in paint removers, as a solvent for plastics, as a degreasing agent, in propellant mixtures for aerosol sprays and as a blowing agent in foams. The odor is not a good indication of exposure since concentrations of 100 ppm reportedly are not highly perceptible. Liquid methylene chloride is painful and irritating if splashed in the eyes or if confined on the skin by gloves, clothing or paint remover formulations. A burn can result if it is not promptly removed from the eyes and skin. The acute oral LD^ for rats is about 2000 mg/kg. 467 0297 5119* According to Lehmann and Flory,1 slight narcosis occurs at 4000 to 6100 ppm in several species of animals. The fatal concentration for seven hours' exposure is given by many authorities as about 15,000 ppm.IJ9 Rats exposed 75 days (8 hours a day) at 1300 ppm showed slight liver changes which were not found at 50 days.' Cats exposed four to eight days at 7200 ppm for four weeks were found to have kidney and liver changes. Heppel and associates' found that daily seven-hour exposures at 5000 ppm for six months had no discernible effect on dogs and rabbits, and only reduction in the rate of growth of guinea pigs. At 10,000 ppm, four hours a day for seven and one-half weeks dogs and guinea pigs, but not monkeys, rabbits or rats developed liver injury. Moskowitz and Shapiro9 reported four cases of poisoning with one fatality, apparently due to narcotic action Collier9 reported two cases of poisoning in painters who suffered from headache, giddiness, stupor, irritability, numbness and tingling in the limbs. Kuzelova and Vlasak9 noted complaints of headache, fatigue and irritation of the eyes and respiratory passages by workers exposed at concentrations up to 5000 ppm. Neurasthenic disorders were found in 50%. and digestive disturbances in 30% of the persons exposed. Three acute poisonings, one involving loss of consciousness, were recorded without serious after-effects. Weiss' stated that a chemist after a year's exposure developed toxic encephalosis with acoustical and optical delusions and hallucinations. Concentrations frequently exceeded 500 ppm; values of 660 ppm, 900 ppm, and near the floor, 3600 ppm were noted. Golubovski and Kamchatnova' found liver disease in workers exposed to methylene chloride and methanol which they attributed to the former. Exposure concentrations were not reported. In the early 1940's methylene chloride was considered the least toxic of the chlorinated hydrocarbon solvents when a safe industrial air limit of 500 ppm was proposed by Heppel et al.,' and later adopted by the TLV Committee as protective enough to prevent any significant narcotic effects or liver injury. Subsequently. Stewart et al.,' reported that significant quantities of carbon monoxide and carboxyhemoglobin were produced in humans receiving single exposures at 500-1000 ppm of methylene chloride. The carboxyhemoglobin concentrations reported by Stewart approximated those considered objectionable if due to inhalation of carbon monoxide. More extensive examination of CO production from methylene chloride was later reported by the same investigators." Human volunteers exposed to methylene chloride at 1000 ppm for two hours (2000 ppm-hours, one half of the Ct permitted for an B-hour exposure at 500 ppm) resulted in carboxyhemoglobin levels in excess of those permitted in industry from exposure to CO alone. The finding of the body's capacity to metabolize methylene chloride to CO was confirmed by Ratney, Wegman and Elkins" in a small group of workers exposed to 180 to 200 ppm methylene chloride. Such daily, repeated exposures resulted in equilibrium blood concentrations of carboxyhemoglobin of 9% that decreased to half that value by next day's start of work. The differential Increment in percent carboxyhemoglobin of 4.5% from a day's exposure at 160 to 200 ppm of methylene chloride is approximately the same as that developed from a daily exposure to CO at its TLV of 50 ppm. Di Vincenzo" found that humans exposed to 100 ppm methylene chloride for 8 hours had a carboxyhemoglobin (COHb) value of 3.22% 0.22%, whereas an 8-hour exposure at 150 ppm produced 5.39% 0.06% level and an 8-hour exposure at 200 ppm resulted in COHb level of 6.8% + 0.65%. In an extensive study several healthy adults of both sexes were exposed from 2-10 times "to metyhlene chloride vapor concentrations of 0, 50, 100, 250 or 500 ppm for periods of 1, 3 and 7V4 hours in a controlled environment chamber. These studies were designed to simulate the type of exposures encountered in the industrial setting and consisted of both steady, non-fluctuating vapor concentrations. Exposure resulted in a prompt elevation of carboxyhemoglobin (COHb). The elevation persisted longer than COHb from CO alone since metabloism of the absorbed methylene chloride continued after exposure ceased. This solvent-induced COHb is apparently added to the body burden of carbon monoxide derived from other sources. This study corroborated previous single exposure studies in that no deleterious effects upon the health or performance of healthy adults could be detected when they were repeatedly exposed to 250 ppm or less for 7'h hours per day, five days per week for 2 weeks, or in the case of the male subjects, to 500 ppm on two consecutive days."" Among the parameters studied were complete blood count, clinical chemistry (SMA 12), EKG. serum triglycerides, blood pressure, subjective signs and symptoms, urinalysis (Combistix) urinary urobilinogen, neurological tests, EEG, visual evoked response, pulmonary function and cognative, alertness, time estimation, coordination, arithmetic and inspection tests. The increase in COHb was related to the magnitude of the vapor exposure. Both duration of exposure and vapor concentration were factors. Seven and one-half hour exposures to concentrations as low as 100 ppm for 5 days resulted in COHb elevations about 5% in non-smokers. The odor was not objectionable at 250 ppm and many subjects could not detect it at 50 or 100 ppm. Since the toxic effects of methylene chloride are due in part to its conversion to carbon monoxide, they would presumably be augmented by the presence of carbon monoxide in the air. Poder et a/'9 found the effects of CO and the COHb from methylene chloride to be additive in 3-hour exposure tests with rats. Therefore, whenever there is a combined exposure to the vapors of methylene chloride and carbon monoxide, the appropriate equation for mixtures should be used, in determining whether or not the exposure is acceptable. A time-weighted average TLV of 100 ppm (approximately 350 mg/m9) is recommended for methylene chloride in the absence of occupational exposure to carbon monoxide. This recommendation is based upon experimental data obtained from nonsmoking males at rest, and should keep COHb levels well below 5 percent. A short-term exposure limit (STEL) of 500 ppm (approximately 1750 mg/m9) is recommended since data indicate that neither undesirable CNS responses nor COHb values are likely to occur with such exposures to methylene chloride. Concurrent exposure to other sources of carbon monoxide or physical activity will require assessment of the overall exposure and adjustment for the combined effect. Other recommendations: Cook (1945) and Smyth (1956) 500 ppm; Elkins (1959) 200 ppm; ANSI (1969) 500 ppm; USSR (1970) 15 ppm; Czechoslovakia (1969) 140 ppm. 468 511904 0298 References: ' Lehmann, K.B., Flury, F.: Toxicology and Hygiene of Industrial Solvents, pp. 13-138, Williams & Wilkins, Baltimore (1943). 3 Von Oettingen, W.F.: Halogenated Hydrocarbons. Toxicity and Potential Dangers, pp. 35-41; Pub. Health Service Publ. #414 (1955). 3 Svirbely, J.L., Highman, B., Alford, W.C.. von Oettingen, W.F.: J. Ind. Hyg. & Tox. 29, 382 (1947). Heppel, L.A., Neal, P.A., Perrin, T.L., Orr, N.L., Porterfield, V.T.: J. Ind. Hyg. & Tox. 26, 8 (1944). 5 Moskowitz. S., Shapiro, H.: Arch. Ind. Hyg. & Occ. Med. 6, 116 (1952). Collier. H.: Lancet 1, 594 (1936). 7 Kuzelova, M,, Vlasak, R.: Pracovni lekarstvi 16, 167 (1966); abstr. in Scheitific Reports on Industrial Hygiene and Occupational Diseases in Czechoslovakia, p. 69, Prague (1966). Weiss, G.. Zentralbatt Arbeitsmed. u. Arbeitsschutz 17, 282 (1967). Golubovskii, I.E.: Kamchatnova, V.P.: cited in Hygiene and Sanitation (USSR) 29, 145 (1964). ' Stewart, R. D,, Fisher, T.N., Hosko, J.J., Peterson, J.E., Baretta, E.D., and Dodd, H.C.: Science 176, 295 (1972). " Stewart, R.D., Fisher, T.N., Haska, M.J., Peterson, J.E., Baretta, E.D., Dodd, H.C.; Arch. Environ. Health 25, 342 (1972). '3 Ratney, R. S., Wegman, D.H., Elkins, H.B.: Arch. Environ. Hlth. 26, 223 (1974). 13 Letter Report dated April 3. 1975 from Robert L Raleigh. M.D. Director, Health and Safety Laboratory, Eastman Kodak Company, Rochester, New York. '* Stewart. R.D.. Hake, C.L., Forster, H.V., Lebrun, A.J., Peterson, J.E., Wu, A.: Methylene Chloride: Development of a Biologic Standard for the Industrial Worker by Breath Analysis. ,s Foder, G.G., Prajsnar. D.. Schlipkoter. H.W.: Endogenous CO Formation by Incorporated Halogenated Hydrocarbons of the Methane Series. Staub-Reinhalt Luft 33: 260-61,1973. '* Criteria for a Recommended Standard for Occupational Exposure to Methylene Chloride, U.W. HEW Publication No. (NIOSH) 76-138, March, 1976. 17 Stewart, R.D., Forster, H.V., Hake. C.L., Lebrun, A.J., Peterson. J.E.: Human Responses to Controlled Exposures of Methylene Chloride Vapor, Report No. NIOSH-MCOW-ENVM-MC-73-7 Milwaukee, Wis., The Medical College of Wisconsin, Department of Environmental Medicine, December 1973. 82 pp. " Winneke, G., Behavioral Effects of Methylene Chloride and Carbon Monoxide as Assessed by Sensory and Psychomotor Performance, in Xintaras, C., Johnson, B.L., de Groot, I. (eds): Behavioral Toxicology -- Early Detection of Occupational Hazards, Publication HEW No. (NIOSH) 74-126, U.S. DHEW, Center for Disease Control, NIOSH, 1974, pp. 130-44. ' Hake, C. L., Stewart, R. D., Forster, H.V., Lebrun, A. J.. Peterson, J. E., Wu, A.: Results of the Controlled Exposure of Human Females to the Vapor of Methylene Chloride. Report No. NIOSH-NCOW-ENVM-MC-743. Milwaukee, Wis., The Medical College of Wisconsin, Department of Environmental Medicine, March 1974, 22 pp. 30 Gamborale, F., Annwall, B. A., Hultengren, M.: Exposure to Mythylene Chloride -- II, Psychological Functions. Scand, J. Work Environ. Health 1:95-103, 1975. C 2-NITROPROPANE CH3CH(N02)CH3 TLV, 25 ppm (Approximately 90 mg/m3) A2 This compound has the following synonyms: B-nitropropane, dimethylnitromethane, isonitropropane, nitroisopropane and 2-NP. It has the following trade names: NiPAR 8-20TM (commercial grade 2-nitropropane) and NiPAR S-30TM (a mixture of 1- and 2-nitropropane). It has a molecular weight of 89.09 and a melting point of -91.32C. Its boiling point is 120.25C. The vapor pressure is 12.9 mm Hg at 20C; the vapor density is 3.06 (air=l). Its density is 1.024 0C and the specific gravity is 0.992 20/20C. The open cup flash point is 39C. The lower flammability limit is 2.6%/vol. The upper flammability limit is unknown. It is soluble in water at 1.7 parts and is miscible in most aromatic hydrocarbons, ketones, esters, ethers and the lower carboxylic acids. The odor of 2-nitropropane is very slight, readily masked and provides no warning properties.' 2-nitropropane in concentrations ranging from approximately 5% to 25% is used in a number of solvent systems to improve drying time; to insure more complete solvent release; to provide better flow characteristics and film integrity; to increase wetting ability and electrostatic spraying properties; and to insure greater pigment dispersion. These solvent systems are used in coatings e.g., vinyl, epoxy, nitrocellulose, and chlorinated rubbers, etc., printing inks and adhesives. Occupational exposures may occur in a number of industries including basic construction and maintenance, shipbuilding and marine maintenance (marine coatings) food packaging, furniture and plastic products. NIOSH estimates that approximately 100,000 workers are potentially exposed to 2-nitropropane in these and other industries. Production in the United States exceeds 30 million pounds annually.3 Inhalation studies in several species of laboratory animals were reported by Treon and Dutra.3 Five animal species -- cats, rats, rabbits, guinea pigs and monkeys -- were exposed at dosage levels ranging from 9,000 ppm (32,700 mg/m3) for a period of one hour to 83 ppm (300 mg/m3) for chronic exposure levels for periods as long as 26 weeks. Two animals of each species were exposed at each level and marked difference in response 469 511904 0299 among the species was noted. Cats were the most sensitive and died within 17 days of exposure to 328 ppm (1190 mg/m5) for seven hours per day for several days. There was evidence of severe liver damage and slight to moderate damage to the kidney and heart. At an exposure level of 328 ppm monkeys survived for 100 days and rats, rabbits and guinea pigs survived for 130 days. Treon and Dutra' reported (no histologic changes in the monkeys, rabbits, guinea pigs and rats exposed to 328 ppm (1190 mg/m5) or less regardless of exposure time. However, subsequent examination (March, 1977) of liver sections from two rats which had been exposed to about 300 ppm (1090 mg/m5) for 17 exposures of 7 hours each showed clear cell foci. `These and similar lesions are frequently seen prior to the development of hepatocellular carcinoma in rats exposed to known hepatic carcinogens"' In a recent inhalation study conducted by the Huntington Research Center,5 SpragueOawley male rats and New Zealand male rabbits were exposed to commercial grades of 2-nitropropane for 7 hours a day, 5 days per week. One group of 50 rats and 15 rabbits were exposed to 207 ppm (750 mg/m5), a second group of the same size were exposed to 27 ppm (98 mg/m5), and the third group served as a control. "Liver neoplasms, described as hepatocellular carcinoma or hepatic adenoma, were observed in all ten rats killed after six months of exposure to 207 ppm (750 mg/m5) 2-nitropropane. No tumors were observed in any other animals in this study, including controls.'5 However, hepatocellular cellular hypertrophy, hyperplasia, and necrosis were reported in rats exposed to 207 ppm for three months. Elevated liver weights occurred in rats exposed to 207 ppm 2-nitropropane for one, three and six months. Additional studies are now under evaluation.' Inhalation exposure of cats at 750 ppm of 2-nitropropane for 4.5 hours resulted in the production of 25-35% methemoglobin and 15-25% methemoglobin at an exposure of 280 ppm for a 7 hour exposure.' There are a number of reports concerning acute industrial exposures. Gaultier, et al.,* reported on two cases of acute industrial intoxication one of which was fatal. Illness did not appear until the second day following exposure and liver damage was diagnosed in both cases. In the fatal case, death occurred 16 days post exposure. The exposure occurred during the painting of the inside of a tank and actual air concentrations were not documented. Skinner' reported that prolonged, repeated exposure to concentrations of 20 to 45 ppm (73 to 164 mg/m5) of 2-nitropropane resulted in cases of nausea, vomiting, diarrhea, anorexia and severe headache. Another industrial study revealed that all of a "small group of workers" exposed to concentrations of not more than 165 to 445 ppm (600 to 1620 mg/m5) of combimed 1- and 2-nitropropane for not more than 2 hours a day experienced nausea, dizziness and headache; one worker complained of diarrhea. In another instance, all workers (number not stated) complained of headache and one of nausea and vomiting. Air concentrations were not reported. Williams, et al.,* in 1974, reported an excess of toxic hepatitis among construction workers applying epoxy resins to the walls of a nuclear power plant. Hepatitis was attributed to a known hepatotoxin, p, `-methylene-dianiline, but there was also exposure (via skin absorption possibly) to 2-nitropropane. In view of the recent (April 25, 1977) NIOSH Current Intelligence Bulletin, ``INDUSTRIAL SUBSTANCES SUSPECT OF CARCINOGENIC POTENTIAL FOR MAN", an A2 listing may be indicated pending the evaluation of additional experimental animal studies and the completion of industrial hygiene surveys at 2-nitropropane production facilities. Worker exposure should be reduced to the greatest degree practicable but special regulated areas, special respiratory protection and special protective clothing are not considered essential at this time. However, no change in the TLV is believed to be indicated at this time. A limited number of foreign standards have been published. Many are identical with those of the American Conference of Governmental Industrial Hygienists and were probably derived from that source. The Deutsche Forschungsgemeinschaft, Maximal Arbeitsplazkonzentrationen, 1976' lists a MAK of 25 ppm or 90 mg/m5 for 2nitropropane: Danger from skin absorption is not indicated nor is skin sensitization considered. 2-nitropropane is not included among known or suspect carcinogenic compounds. In 1976 the USSR publication "Maximum Allowable Concentrations of Harmful Substances in the Air of Working Zones" listed a MAC of 30 mg/m5, a Danger Class of 4 and an Aggregate State of v was indicated." (Note; The substance was identified only as nitropropane. Danger Class 1 to 4. Four is the least toxic. Aggregate State: v = vapor; the state of the substance under industrial conditions [emphasis added].) The same value, i.e. 30 mg/m5 appeared in a similar Russian publication in 1966. The Swedish list, Hygienska Gransvarden (1974) issued by the Arbetarkyddsstryrelsen, Stockholm, did not indicate any TLV in air for 2-nitropropane." References: ' Kirk-Othmer Encyclopedia ol Chemical Technology, 2nd Ed., Interscience 1967, Vol. 13: p. 865-888. ' 2-NITROPROPANE. "Current Intelligence Bulletin", National Institute of Occupational Safety and Health. April 25. 1977. 5 Eastman Organic Chemicals, Catalog No. 49. Number 4680, April 1, 1977, p. 126. 4 Treon, J. and Dutra, F.R., Arch. Ind. Hyg. Occupational Med. 5, 52 (1952). 5 Huntington Research Center (HEW/NIOSH Project No. 210-75-0039) 1975 (See Ref. 2). Gaultier, M., Fournier, P.E., Gervais, and Sicok, C., Arch. d. Mai. Prof. 25. 425 (1964). ' Skinner, J.B., Ind. Med. 16, 441 (1947). DOCUMENTATION OF THE THRESHOLD LIMIT VALUES for Substances in Workroom Air. Amer. Conf. Gov't. Ind. Hyg. 2nd Print., 1974, p. 189. Williams, S.V., Bryan, J.A., and Burk, J.R. New Eng. J. of Med. 291: 1256, 1974. "Maximale Arbeitsplatzkonzentrationen," Senatskommission zur Prufung Gesundheitsschadlicher Arbeitsstoffe. Mitteiiung XII, 28, Juni 1976 p. 29. " "Maximum Allowable Concentrations of Harmful Substances in the Air of Working Zones: GOST 12.1.005-76 p. 11 (Russian). " Hygienska Gransvarden. (Anvisningar om hygienska gransvarden for luftfororenin-gar pa arbetsplatsen) Arbetarskyddsstryelsen Stockholm 1974 (Swedish). 470 511904 n-PHENYL-BETA-NAPHTHYLAMINE N-Phenyl-beta-napthylamine (PBNA) is a light gray powder which is insoluble in water and soluble in alcohol, acetone, benzene and chloroform. It is used as a rubber antioxidant, an inhibitor for butadiene, a stabilizer for lubricants and an intermediate in chemical syntheses. The National Institute for Occupational Safety and Health (NIOSH) reported that commercial PBNA contains 20-30 parts per million of beta-napthylamine (BNA), a long-established human bladder carcinogen. Experimental evidence from human volunteers ingesting PBNA and workers inhaling PBNA dust shows that BNA is a metabolite of PBNA. Dogs have also been shown to excrete BNA in their urine when fed PBNA.' The available epidemiologic evidence indicates that PBNA, if a human carcinogen at all, is a weaker one than BNA/ However, the data in this study are limited and not conclusive. Animal studies are similarly not clear cut. Three female dogs fed 540 mg of PBNA daily had no bladder tumors at 4.5 years of observation/ In a like manner, studies conducted by the National Cancer Institute, mice which were fed PBNA for IB months developed a statistically significant increase over controls in the incidence of hepatomas, a common liver tumor in mice having debatable significance to man. Other mice also showed an increased number of tumors from a single subcutaneous injection of PBNA, but the site-specific tumor incidences did not differ from the controls.* No information is available on percutaneous absorption. In summary, the limited experimental and human evidence is not sufficient to clearly establish the carcinogenicity of PBNA but is adequate to place the compound in Category A-2, Industrial Substances Suspect of Carcinogenic Potential for Man because of the evidence that the known human carcinogen, betanapthylamine, is both an impurity in and human metabolite of PBNA. References: ' National Institute for Occupational Safety and Health, Current Intelligence Bulletin, Metabolic Precursors of a Known Human Carcinogen, Beta-Naphtyhlamine. December 17,1976. 5 Fox, A.J., lindars, B.C., Owen, R.A., Survey of Occupational Cancer in the Rubber and Cable-Making industries: Results of a Five-Year Analysis, 1967 to 1971. Brit. J. Ind. Med. 31:140-151, (1974). 5 Proceedings Ninth International Congress on Industrial Medicine, Budapest, 1948. * National Cancer Institute. August, 1968. PROPIONIC ACID CHjCHjCOOH TLV 10 ppm (30 mg/m5) STEL 15 ppm (45 mg/m5) A colorless liquid with a pungent odor, propionic scid boils at 141C; m.p. -20.8C; sp.gr. 0.9942; flash point 130F. It is soluble in water, alcohol, ether and chloroform. Propionic acid and propionates are used as mold inhibitors, fungicides, herbicides, and preservatives for grain and wood chips; as emulsifying agents, flavors and perfumes, drugs, electroplating solutions, and in making cellulose propionate plastics. The oral LD^ for rats is 4.3 gm/kg;' intravenous LDM for mice 625 mg/kg, and skin absorption LD^, for rabbits 500 mg/kg/ An 8-hour inhalation of a saturated atmosphere caused no deaths in rats. Medical reports of acute exposures of workers show mild to moderate skin burns, mild eye redness, and one case of mild cough and asthmatic response. An industrial hygiene survey indicated 8-hour TWA levels below 0.25 ppm, with excursions to 2.1 ppm/ No irritation was noted at these concentrations. A TLV if 10 ppm, with a STEL of 15 ppm, is based largely on analogy with acetic acid, and is designed to prevent significant irritation of eyes or respiratory passages. The Soviet limit (1976) is 2 mg/m5, or about 0.7 ppm. References: ' Smyth, H.F. et al.: Am. Ind.Hyg.Assn. J. 23, 95 (1962). 5 NIOSH: Registry of Toxic Effects of Chemical Substances (1977). 5 Dow Chemical Company: Communication to Committee (1977). 471 511904 0301 SODIUM BISULFITE NaHSOj TLV 5 mg/m3 Sodium bisulfite is a white solid with a slight odor of sulfur dioxide. It is soluble in water, but decomposes on heating. It has a wide variety of uses in the paper, tanning, chemical and food industries, and as a source of sulfur dioxide. Its oral toxicity is not high; rat LD^ about 2 g/kg. It is however, irritating to the eyes, skin and mucous membranes. No data are available on dust concentrations in plant atmospheres. Medical reports of acute exposures have shown mild eye and respiratory responses. The recommended TLV of 5 mg/m3 is considerably lower than that of sulfur dioxide, the active ingredient in sodium bisulfite. However, inhalation of or contact with the dust would result in high local concentrations in contact with small areas of sensitive tissue. A TLV well below that for nuisance dusts seems definitely in order. Reference: Dow Chemical Company; Communication to Committee (1977). SODIUM METABISULFITE Na^SjOg TLV 5 mg/m3 Sodium metabisulfite, or sodium pyrosulfite, may be considered to be the anhydride of sodium bisulfite. It is reportedly the chief constituent of the commercial grade of the latter compound. Its uses, as a preservative in foods, etc., are essentially the same.' The minimum lethal dose, by intravenous injection, is given as 192 mg/kg for the rabbit; the iv LDM for rats is 115 mg/kg for sodium bisulfite.3 A 2-year diet study in rats indicated no adverse effects at 0.215%.3 This would indicate a very low systemic toxicity. Extrapolation to man, allowing a ten fold safety factor, would give an equivalent air concentration of 70 mg/mV While it may react somewhat more slowly than NaHSOj, Na2S205 apparently has the same basic properties. Some irritation of mucous membranes would be expected from inhalation of the dust. A TLV below that of a nuisance dust is therefore recommended. References: ' Hawley, G.G.: Condensed Chemical Dictionary, 9th ed; Van Nostrand Reinhold, New York, 1977. 3 NIOSH. Toxic Substances List, 1973. 3 Til, H P., et al.: Food Cosmet. Toxicol. 10 291 (1972). 4 Dow Chemical Company: Communication to Committee (1977). C TERPHENYLS Terphenyls or diphenyl benzenes are used as heat transfer fluids and reactor coolants. Commercial preparations contain mixtures of three isomers: ortho, meta and para terphenyls. Melting points of these substances are 56.2, 87.4, and 212.7C, respectively. They are insoluble in water, but soluble in benzene and ethanol. The order of solubility in these substances decreases from the ortho to the para form. 472 511904 Haley' et alreported that terphenyl mixtures caused conjunctival irritation in rabbits and were highly damaging to guinea pig skin following intracutaneous injection. Cornish et al./ working with rats established LDyj values of 1900, 2400 and greater than 10,000 mg/kg for ortho, meta and para terphenyl, respectively, para terphenyl appears to be quite innocuous by oral routes, at least partially due to its poor absorption. In 30 day feeding studies, rats fed 250 and 500 mg/kg/day of ortho terphenyl had elevated liver and kidney weight ratios. Animals fed the same amounts of meta terphenyl showed only elevated kidney weight ratios. These effects were not observed in animals fed para terphenyl. Results of nistopathological studies on these animals were similar to controls. Petkau3 et al., and Young et al./ have confirmed the potential nephrotoxicity of unirradiated terphenyl isomers. The latter authors also demonstrated hepatic damage in rats fed 33 mg/kg/day or more of the high boiling fraction of terphenyl mixtures. Adamson et al./ were able to define the extent and duration of transient morphological changes in mitochondria of pulmonary cells in rats exposed to aerosols containing 5 x 10~4 g/l (50 mg/m3) of HB-40 (a mixture of unirradiated terphenyls used as an organic coolant in the Manitoba WR-i reactor) seven hours daily for up to eight days. The number of vacuolated mitochondria increased with days of exposure. Weeks and Lentle55 reported on a clinical survey of 47 persons identified as having constant exposure to HB 40 (treated catalytically with hydrogen to 40% of the maximum hydrogen uptake) in the working areas of the Whiteshell Nuclear Establishment, Manitoba. Canada. The study represented 122 man years of occupational exposure varying from a minimum of six months to a maximum of seven years. It included: occupational and medical histories, smoking habits, blood pressure measurement, pulmonary function tests, tests for serum creatinine, blood counts and urine tests. The concentrations of HB-40 in the air of the WR-1 reactor were found to range between 0.89 mg/m3 in areas containing organic piping equipment and 0.094 mg/m3 in general working areas close by. No skin sensitization or recognizable harm were reported. The terphenyl coolant, however, was -found to act as a primary irritant particularly when workers were wearing protective clothing and the moistness of the skin is increased. There was no evidence that the use of terphenyl coolants is associated with the development of skin tumors. Testa and Masi* reported concentrations in a reactor room under normal operating conditions ranged from 0.1 to 10 mg/m3 when the coolant was heated at 220 to 230C, and 10 to 280 mg/m3 when the coolant was heated 330 to 340 C. Concentrations above 10 mg/m3 were associated with eye and respiratory irritation in exposed workers. In general, because of the low vapor pressures and low order of toxicity of terphenyls, little industrial hygiene hazard should be expected in handling them under ordinary conditions. A TLV of 1 ppm (approximately 9.4 mg/m3) was recommended earlier to protect against irritation of eyes and respiratory tract. However, the transient morphological changes in mitochondria reported by Adamson et al./ in rats exposed to 50 mg/m3 should not be ignored since these levels of terphenyl represent only a few orders of magnitude higher than exposure concentrations reported in reactors. A TLV therefore of 0.5 ppm (approximately 4.7 mg/ m3) is recommended as a safety precaution against possible mitochondrial changes. References: ' Haley, T.J., Detrick, L.E., Kosmeau, N., Williams, P., Upham, H.C., and Burmash, L.: Toxicol. & Applied Pharmacol, 1:515 (1959). 3 Cornish, H.H., Bahor, R.E., Ryan, R.D.: Amer. Ind. Hyg. J., 26:372 (1962). 3 Petkau. A. and Hoogstraaten, J.: Amer. Ind. Hyg. J. 26:380 (1965). 4 Young, G., Petkau, A., Hoogstraaten, J.: Amer. Ind. Hyg. Assoc. J. 30:7 (1969). 3 Adamson, I.Y.R., Bowden, D.H., Wyatt, J.P.: Archives Envir. Health, 19:499 (1969). 6 Weeks, J.L.. Lentle, B.C.: J. Occupa. Med. 12:246 (1970). ' Weeks, J.L.: Archives Environ. Health, 23:123 (1971). * Testa, C.. Masi, G: Analyt. Chem. 36:2284 (1964). TETRASODIUM PYROPHOSPHATE (TSPP) Na4P207 TLV 5 mg/m3 TSPP. a white powder which melts at 880 C, and has a sp.gr. 2.45, also exists as the crystalline decahydrate. It is soluble in water, insoluble in alcohol. It is widely used as a water softener, in soaps and detergents, as a dispersing and emulsifying agent, metal cleaner, in boiler water treatment, in drilling muds, dyeing, wool scouring, as a sequestrant and nutrition supplement. Although basically of low toxicity, it is a somewhat alkaline material and the dust is therefore irritating to the eyes and respiratory passages. For this reason a TLV of 5 mg/m3, half the value for nuisance dusts, is recommended.' Reference: Dow Chemical Company: Communication to Committee (1977). 473 511904 0303 TOLUENE-2.4-DIISOCYANATE (TDI) CH3C6H3(HCO)j TLV 0.002 ppm (Approximately 0.014 mg/m3) STEL 0.005 ppm (0.036 mg/m3) The two commonly used isomers are 2,4 - toluene diisocyanate and 2.6 toluene diisocyanate, commercially available in the following three ratios: 1) 100% 2,4, 2) 80% 2,4; 20% 2,6; 3) 65% 2,4; 35% 2,6. The 80% 2,4, 20% 2,6 mixture represents over 95% of the industrial usage and has the following properties. Molecular Weight 174.16, Flash Point 135C. Specific Gravity of Liquid 1.22 at 25C, Boiling Point 250C, Freezing Point 20 - 22C; vapor pressure at 25C, 0.05 mm. TDI is one of the isocyanates most employed in the manufacture of polyurethane foams, elastomers and coatings. The foams are widely used in furniture, packaging, insulation and boat building, and have many other applications. Polyurethane coatings have many desirable properties, on leather, wire, tank linings and masonry, etc. Elastomers are abrasion and solvent resistant and are used in adhesives, films and linings, and in abrasive wheels and other mechanical items. Studies in animals by Zapp' showed that this isocyanate has a low oral toxicity (approximate lethal dose 5.8 g/kg) but a high toxicity by inhalation. One to two ppm for 30 six-hour exposures resulted in tracheobronchitis. The LDm for three rodent species for a four-hour exposure approximated 12 ppm, according to Duncan et al.3 The animals died of pulmonary edema and hemorrhage. Effects on the liver, kidneys and gastro-intestinal tract were also noted, and dermal effects occurred. Repeated daily six-hour exposures at 0.1 ppm were reported to cause chronic inflammation of the tracheo-bronchial mucosa with fibrosa obliterans as the terminal lesions.3 A fever reaction in animals following intravenous injection of 0.02 mg/kg was reported by Scheel et al.4 Human Data -- TDI is an irritant causing inflammation and occasional sensitization of the skin, lacrimation, smarting, burning and prickling sensation to the eye; abdominal distress, nausea and vomiting, but the major effect is on the respiratory tract.'5 One type of respiratory response is irritation, indicated by a burning nose and throat, and a choking sensation. With high concentrations this may lead to chemical bronchitis with severe bronchospasm.* With sufficient exposure any person will experience these effects even on first exposure.7 Chemical pneumonitis, pulmonary edema, headache, insomnia have also been reported. A second respiratory response to TDI is that of sensitization. Some individuals become sensitized on first exposure while others may develop symptoms after exposure over days, months or years. Other workers have had only minimal or no respiratory symptoms for several months of low level exposure, then suddenly develop acute asthmatic reaction to the same level. The nature of the sensitization process is unknown and many authors have referred to it as allergy, and to the respiratory response in sensitized people as true asthma, comparable to asthma excited by pollens and other exo-allergens. Some TDI sensitized people however, have no history of prior allergic disease. In a 1963 review Brugsch and Elkins* noted reports of 318 cases of TDI intoxication prior to 1961, including two deaths. In most instances data on exposure levels were lacking. Walworth and Virchow,* however, reported 83 cases in a plant where the average TDI concentrations ranged from 0.01 to 0.16 ppm. The maximum incidence of cases occurred when the average concentration of vapor was around 0.1 ppm; very little trouble was noted at 0.01 ppm. Hama'* found TDI vapor levels of 0.03 to 0.07 ppm associated with a high incidence of illness, but no cases were observed from concentrations below 0.03 ppm. Munn" considered the 0.1 ppm limit too high. Elkins et al" reported 42 accepted or established cases of TDI intoxication, and 73 questionable or disputed cases, among workers in 14 plants in Massachusetts between 1957 and 1962. In 14 of the accepted cases the average TDI vapor concentration found in the workroom was about 0.03 ppm, with very few samples showing more than 0.05 ppm; in 11 cases the average concentration was 0.015 ppm; in 9 cases levels below 0.01 ppm were found; in the remainder measurements representative of worker exposure could not be made. The authors recommended a TLV of 0.01 ppm. According to Thompson and Scheel,'3 studies with rats support the probability that lung reactivity to TDI is due to chemical damage and not antibody reactions. Markham and Fishburn'4 reported that workers were affected by concentrations generally below 0.02 ppm. Bruckner et al. described a study of clinical and immunological factors which tends to support the TLV of 0.02 ppm.'* A third type of respiratory response to TDI is that of acute and chronic disease of ventilatory capacity measured as FEV, with or without overt symptoms of respiratory difficulty. Gandevia'* reporting workers exposed to TDI showed an average decrease in mean FEV, of 0.18 liters during the course of a single day with some cumulative deficit from Monday to Friday and possible further cumulative deficit over a period of two working weeks. Williamson* studied 18 workers exposed to less than 0.02 ppm of TDI over 14 months and showed significant difference in ventilatory measurements for 6 sensitized individuals who showed marked decreased in FEV, and FVC. Adams'7 studied 175 workers for five years working in a plant manufacturing TDI where exposures rarely exceeded 0.02 ppm. The group mean annual deterioration of FEV, over the five years had significantly exceeded the predicted rate of decline, but further analysis showed that only 8 employees accounted for the decrease. A later study by Adams'* showed no decrease in FEV, for symptomatic workers but there was a singificant decrease for symptomatic workers. Adams studies are confounded by Selection of Tuesday afternoon for collection of pulmonary function measurements. 474 511904 0304 Peters et al.' studied 38 workers in a polyurethane plant who were exposed to 0.0001 to 0.003 ppm of TDI and showed a decrease of FEV, between Monday am and Monday pm and Friday pm. In a follow-up study 6 months later with TDI exposures of 0 - 0.012 ppm they showed a significant decrease in mean FEV, over the six month interval which was greater than the predicted decline due to aging alone." These workers were followed for two years, when the decline due in FEV, continued at a mean annual rate of 0.11 liters, which exceeds the predicted rate of decline to aging alone.1' Wegman et al." studied 112 workers in a polyurethane manufacturing plant, he divided the workers into 4 exposure groups between 0.002 ppm to 0.013 ppm. All four groups demonstrated significant declines in FEV with the magnitude of decrease correlating with levels of exposure indicating a dose response relationship between exposure and acute respiratory effect. The same group of workers (Wegman)" were restudied two years later, and divided into three exposure groups. Using FEV, as a measure of response, a dose response relationship was observed. Only those in the lowest exposure group (less than 0.0020 ppm) showed normal two year decline. The FEV, of those in the highest exposure group (more than 0.0035 ppm) fell 204 ml in two years which exceeds the expected value by three to fourfold. The decrement in the middle exposure group 0.002 0.003 ppm was borderline (42 ml/yr). A significant association between acute and chronic decrement in FEV, was shown. On the other hand Butcher et al." followed 166 workers over two years in a new TDI manufacturing plant where 8 hour time weighted average exposures varied between 0.001 and 0.012 ppm. They state that exposurerelated excess decline in pulmonary function does not appear to have occurred during the first two years following initial exposure to TDI. Unexplained increments in FEV, and FVC during the study period occur in this population. The previous TLV of 0.02 ppm, which was unchanged for over 15 years, appears to have been a compromise between the findings of Hama,'0 on the one hand, and Elkins et al," on the other. More recent studies, especially those by Peters' group, indicate that even a 0.01 ppm limit is too high."-" NIOSH, in its criteria document for TDI, published in 1973, after a thorough review of the literature available at that time, recommended a workplace environmental standard of 0.005 ppm as a TWA, with a 20-minute ceiling of 0.02 ppm.5 The most recent report by Wegman et al" indicates a threshold of response at about 0.002 ppm. Even this low value may not protect sensitized workers. Other recommendations: West Germany (1974) 0.02 ppm; East Germany (1973) 0.015 ppm; Sweden (1975) and Czechoslovakia 0.01 ppm; U.S.S.R. (1976) 0.007 ppm. References: ' Zapp, J.A., Jr.: Arch, Ind. Health IS, 324 (1957). * Duncan, B., Scheel, L.D.. Fairchild, E. J., Killens, R., Graham, S.: Am. Ind. Hyg. Assn. J,, 23, 447 (1962). 1 Niewenhuis, R., Scheel, L. D., Stemmer, K., Killens. R.: Am. Ind. Hyg. Assn. J. 26, 143 (1965). * Scheel, L.D., Killens, J., Josephson, A.: Am. Ind. Hyg. Assn. J. 25, 179 (1964). 9 NIOSH, Criteria for a Recommended Standard. Occupational exposure to toluene dissocyanate. U. S. Department of Health, Education and Welfare. HSM 73-11022. * Williamson, K.S. Trans. Assoc. Ind. Med. Off. 15:29-35, 1965. 7 Fuchs, S., Valade, P,, Arch, D. Mai. Profess. 12:191-196, 1957. * Brugsch, H. G., Elkins, H.B.: N.E. J. Med. 268, 353 (1963). * Walworth, H.T., Virchow, W.E.: Am. Ind. Hyg. Assn. J. 20, 205 (1959). 7 Hama, G.M.: Arch. Ind. Health 16. 232 (1947). " Munn, A.: Trans. Assn. Ind. Med. Off, 9, 135 (1960). '* Elkins, H.B. et al: Am. Ind. Hyg. Assn. J. 23, 265 (1962). " Thompson, G.E., Scheel, L.D.: Arch. Env. Health 16, 363 (1968). " Markham. T.N. Fishburn. C.W.: J. Occ. Med. 9, 471 (1967). 15 Bruckner, H.C., Avery, S.B., Stetson, D M., Dodson, V.N., Ronayne, J.J.: Arch. Env. Health, 16, 619 (1968). " Gandevia. B.: Br. J. Ind. Med. 20:202-209, 1963. 17 Adams, W.G.F. Proc. R. Soc. Med. 63:378-379, 1970. " Adams, W.G.F, Br. J. Ind. Med. 32:72-78, 1975. " Peters, J.M., Murphy R.L. H., Pagnotto, L.D. Van Ganse, W.F., Arch. Environ. Health. 16:642-647, 1968. " Peters, J.M., Murphy, R.L.H., Ferris, B.G.: Br. J. Ind. Med. 26:115-120, 1969. " Peters, J.M.: Proc. R. Soc. Med. 63:372-375,1970. " Wegman, D.H., Pagnotto, L.D., Fine. L.J., Peters, J.M.: J. Occ. Med. 16:258-260, 1974. " Wegman, D.H., Peters, J.M., Pagnotto, L.D., Fine, L.J., Br. J. Ind. Med. 34:196-200, 1977. " Butcher, B.T., Jones, R.N., O'Neill, C.E., Glindmeyer, H.W., Diem, T.E., Dharmarajan, V, Weill, H., Savaggio, J.E.: Am. Rev. Resp. Dis. 116:411-421, 1977. 475 TRICHLOROACETIC ACID (TCA) cci3cooh TLV 0.75 ppm (5 mg/m5) TCA forms deliquescent crystals which melt at 57.5C: b.p. 197.5C; sp.gr. 1.6298. It is nonflammable, a relatively strong acid, and soluble in water, alcohol and ether. It is used in medicine, pharmacy, as a reagent for albumin detection, in making herbicides. The oral LDW has been reported as 3.3 gm/kg for rats;' for mice 5.64 gm/kg.* By intraperitoneal administration, 500 mg/kg was fatal to mice.5 TCA is corrosive to the skin and eye. but not readily absorbed through the skin. Medical reports of acute exposure effects showed mild to moderate skin and eye burns. A TLV of 0.75 ppm is suggested, based largely on analogy to 2,2 dichloropropionic acid (dalapon, TLV 1 ppm), and the above meager data. The Soviet limit (1976) is also 0.75 ppm (5 mg/m5). References: ' Dow Chemical Company: Communication to Committee (1977). 5 NIOSH: Registry of Toxic Effects of Chemical Substances (1977). ) 3 y 476 511904 0306 ( PLEASE PLACE US ON YOUR STANDING ORDER LIST FOR ANY SUPPLEMENTAL DOCUMENTATIONS THAT MAY BECOME AVAILABLE IN THE FUTURE, OR NOTIFY US AS TO ANY NEW EDITIONS OF THE DOCUMENTATION. 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Box 1937 Cincinnati, Ohio 45201 Rev: 5/79 ( 477 511904 0307 ~> o 478 511904 0308 TLV DOCUMENTATION INDEX A ABATE....................................................................................... 1 ACETALDEHYDE ....................................................... 1 & 288 ACETIC ACID .......................................................................... 2 ACETIC ANHYDRIDE ................................................ 1 & 288 ACETONE ............................................................................... 3 ACETONITRILE ...................................................................... 3 2-ACETYLAMINOFLUORENE .............................................. 4 ACETYLENE DICHLORIDE (See 1.2-Dichloroetyhlene) ACETYLENE TETRABROMIDE (See Tetrabromoethane) ACROLEIN ................................................................................. 5 ACRYLAMIDE ............................................................................5 ACRYLONITRILE ...................................................................... 6 ALDRIN ...................................................................................... ^ ALLYL ALCOHOL .................................................................. 7 ALLYL CHLORIDE ................................................................. 8 ALLYL GLYCIDYL ETHER(AGE)............................................ 9 ALLYL PROPYL DISULFIDE .................................................. 9 ALUMINUM .................................................................. 9 & 435 BORON TRIFLUORIDE..........................................................26 BROMACIL ............................................................................ 443 BROMINE................................................................................. 27 BROMINE PENTAFLUORIDE...............................................27 BROMOFORM ...................................................................... 28 BUTADIENE (1.3 - Butadiene).............................................28 BUTANE ................................................................................. 358 BUTANETHIOL (See Butyl Mercaptan) ............................... 2-BUTANONE (MEK) ........................................................... 29 2-BUTOXY ETHANOL ......................................................... 29 n-BUTYL ACETATE ............................................................. 30 sec-BUTYL ACETATE ......................................................... 30 tert-BUTYL ACETATE .......................................................... 31 n-BUTYL ACrylate ............................................................. 411 N-BUTYL ALCOHOL .............................................. 31 4 350 BUTYL ALCOHOL-SEC..........................................................32 BUTYL ALCOHOL-TERT .................................................... 32 BUTYLAMINE ........................................................................ 32 BUTYL CHROMATE-TERT (As CR03) ....:.....................33 n-BUTYL GLYCIDYL ETHER (8GE) ....................................33 BUTYL LACTATE ...................................................... 33 4 291 4-AMINODIPHENYL-SKIN .................................................. 10 BUTYL MERCAPTAN ............................................................. 34 2-AMI NOETHANOL (See Ethanolamine) O-SEC-BUTYLPHENOL .................................................... 459 2-AMINOPRYIDINE................................................................. 11 p-tert-BUTYLTOLUENE..........................................................34 AMITROLE .......................................................................... 435 AMMONIA ................................................................... 11 1 289 c AMMONIUM CHLORIDE........................................................12 CADMIUM (Dust 4 Salts).................................................... 359 AMMONIUM SULFAMATE .................................................. 12 CAOMIUM (Fume) .................................................... 35 4 292 ( n-AMYL ACETATE ............................................................... 12 sec-AMYL ACETATE ................................................. 13& 454 CALCIUM ARSENATE as As................................................ 36 CALCIUM CYANAMIDE .................................................... 361 ANILINE ................................................................................. 13 CALCIUM HYDROXIDE ......................................... 362 4 411 ANISIDINE ............................................................................... 14 CALCIUM OXIDE ..................................................... 36 4 412 ANTIMONY COMPOUNDS .............................. 14, 354 & 436 CAMPHOR (Synthetic) ........................................................ 37 ANTIMONY TRIOXIDE PROD........................................... 436 CAPROLACTAM (Dust 4 Vapor) ....................................... 293 ANTU (Alpha Naphthyl Thiourea) ..................................... 15 CAPTAFOL (Difolatan) ...................................................... 362 ARSENIC ....................................................... 164354CAPTAN .................................................................... 294 4 363 ARSENIC TRIOXIDE PROD................................................. 439 CARBARYL (Sevm) .................................................................37 ARSINE .....................................................................................16 CARBOFURAN ....................................................... 295 4 364 ASBESTOS (All Forms) (also see Amosite. Chrysotile 4 Crocidolite) ................................... 17 4 454 ASPHALT (Petroleum) FUMES.............................................19 ASPIRIN ................................................................................. 458 ATRAZINE ..............................................................................440 AZINPHOS METHYL ........................................................... 20 CARBON BLACK.....................................................................38 CARBON DIOXIDE .................................................... 39 4 296 CARBON DISULFIDE .............................................. 39 4 459 CARBON MONOXIDE .......................................................... 41 CARBON TETRABROMIDE .................................................298 CARBON TETRACHLORIDE .................................................43 CARBONYL FLUORIDE .................................................... 412 B CATECHOL (Pyrocatechol) ............................................... 298 BARIUM ................................................................................. 21 CESIUM HYROXIDE..............................................................299 BAYGON (Propoxur) ........................................................... 289 CHLORDANE ......................................................................... 44 BENOMYL (Benlate)............................................................. 442 CHLORINATED CAMPHENE.................................................45 BENZENE ................................................................... 22 4 355 CHLORINATED DIPHENYL OXIDE......................................45 BENZIDINE ........................................................................... 23 CHLORINE ............................................................................ 46 p-BENZOQUINONE (See Quinone) CHLORINE DIOXIDE .......................................................... 46 BENZOYL PEROXIDE ......................................................... 23 CHLLORINE TRIFLUORIOE ............................................... 47 BENZYL CHLORIDE...............................................................24 CHLOROACETALDEHYDE ... 48 BERYLLIUM AND COMPOUNDS.........................................24 CHLOROACETOPHENONE ................................................. 48 BIPHENYL (See Diphenyl) ...................................................... CHLOROACETYL CHLORIDE........................................... 461 BISMUTH TELLURIDE ...................................................... 290 CHLOROBENZENE ............................................................. 49 BISPHENOL A (See Diglycidylether) O-CHLOROBENZYLIDENE MALONONITRILE................. 50 BORATES, TETRA, SODIUM SALTS ................................356 CHLOROBROMOMETHANE ............................................... 50 BORON OXIDE .................................................................... 26 CHLORODIFLUOROMETHANE (F22) ............................ 299 BORON TRIBROMIDE........................................................... 26 CHLORODIPHENYL (42% Cl) ........................................... 51 479 511904 0309 TLV DOCUMENTATION INDEX CHLORODIPHENYL (54% Cl) .......................................... 52 CHLOROFORM ................................................. 53. 300 4 413 bis CHLOROMETHYL ETHER ............................................ 301 1- CHLOR-1-NITROPROPANE ...........................................53 CHLOROPICRIN .................................................................. 54 CHLOROPRENE .................................................................. 54 2- CHLORO-6-(Trichloromethyl) PYRIDINE ...................................................................... 304 CHLOROPYRIFOS (Dursban) ............................................ 304 O-CHLOROSTYRENE ....................................................... 302 O-CHLOROTOLUENE......................................................... 302 CHROMATES ........................................................................ 55 CHROMIC ACID 4 CHROMATES ..................................... 55 CHROMIUM, SOL. CHROMATES SALTS.......................... 56 CLOPIDOL (Coyden) ...........................................................305 COAL DUST.......................................................................... 57 COAL TAR PITCH VOLATILES...........................................57 COBALT, METAL. FUME 4 DUST......... 59. 364. 414 4 462 COPPER DUSTS. MISTS 4 FUME.......................... 59 4 305 CORUNDUM (AL203) ....................................................... <35 COTTON DUST......................................................... 60 4 306 CRAG HERBICIDE (Sesone) ................................................ 61 CRESOL (All Isomers) ........................................................... 61 CRISTOBALITE .................................................................... 62 CROTONALDEHYDE ........................................................... 62 CRUFOMATE (Ruelene) ......................................................307 CUMENE ............................................................................... 63 CYANAMIDE ......................................................................... 365 CYANIDES (As CN) ............................................................. 64 CYANOGEN ......................................................................... 64 CYANOGEN CHLORIDE..................................................... 463 CYCLOHEXANE......................................................................65 CYCLOHEXANOL ................................................................ 65 CYCLOHEXANONE ............................................................. 66 CYCLOHEXENE ......................................................................66 CYCLOHEXYLAMINE ....................................................... 308 CYCLOPENTADIENE.............................................................66 D 2.4-D(2.4-DICHLOROPHENOXY ACETIC ACID) ...................................................................67 DDT ........................................................................................ 67 DECABORANE ........................................................................68 DEMETON (Systox) ............................................................. 69 DIACETONE ALCOHOL ........................................................70 DIATOMACEOUS EARTH ................................................ 443 DlAZINON ............................................................................. 70 DIAZOMETHANE ................................................................ 71 DIBORANE ........................................................................... 72 DIBRON (Naled) .................................................................. 73 1.2- DI8ROMOETHANE (Ethylene Dibromide) .......................................... 73 4 309 2-N-DIBUTYLAMINOETHANOL ......................................... 74 DIBUTYL PHOSPHATE......................................................... 75 DIBUTYLPHTHALATE ......................................................... 75 DICHLOROACETYLENE.........................................................75 O-DICHLOROBENZENE...................................................... 76 P-DICHLOROBENZENE ...................................................... 77 3.3- DICHLOROBENZIDINE ............................................. 77 DICHLORODIFLUOROMETHANE (F12) ............................ 78 1.3- DICHLORO-5.5-DIMETHYLHYDANTOIN................. 78 1.1- DICHLOROETHANE ....................................... 79 4 310 1.2- DICHLOROETHANE (Ethylene Dichloride) ...................................................... 79 1.2- DICHLOROETHYLENE........................................ 80 Cl,1-DICHLORO-l-NITROETHANE .................................. 82 DICHLOROMONOFLUOROMETHANE <F21)....... 81 4 415 C-DICHLOROETHYL ETHER ................................. 81 4 311 1.3 DICHLOROPROPENE................................................... 463 2.2- DICHLOROPROPIONIC ACID (Dalapon) ..........................................................................464 DICHLOROTETRAFLUOROETHANE ................................ 82 DICHLORVOX (DDVP) ........................................................ 83 DICROTOPHOS (Bidrin)..................................................... 366 DICYCLOPENTADIENE ..................................................... 367 DICYCLOPENTADIENYL-IRON ........................................ 311 DIELDRIN ............................................................................... 84 DIETHANOLAMINE ............................................................ 465 DIETHYLAMINE ......................................................................84 DIETHYLAMINO ETHANOL..................................................85 DIETHYLENETRAMINE ......................................................... 85 DIETHYL PHTHALATE (DEP).............................................313 DIFLUORODIBROMOETHANE ........................................... 86 DIGLYCIDYL ETHER (DGE) ................................................ 86 OIISOBUTYL KETONE ............................................ 87 4 313 DIISOPROPYLAMINE ........................................................... 87 DIMETHYL ACETAMIDE....................................................... 88 DIMETHYLCARBAMYL CHLORIDE (DMCC).................. 444 DIMETHYLAMINE ...................................................................88 4-DIMETHYLAMINOAZOBENZENE ................................... 89 DIMETHYLANILINE .............................................................. 89 DIMETHYLFORMAMIDE ...................................................... 90 1,1-DIMETHYLHYDRAZINE .................................................. 91 DIMETHYLPHTHALATE (DMP) ........................................ 314 C-DIMETHYL SULFATE .......................................... 92 4 444 DINITROBENZENE (All Isomers) .........................................92 DINITRO-O-CRESOL-SKIN ................................................. 93 3.5-DINITRO-O-TOLUAMIOE (Zoalene) .......................... 316 DINITROTOLUENE-SKIN ......................................................93 DIOXANE .................................................................... 94 4 316 DIOXATHION (Delvar) ......................................................... 369 DIPHENYL ............................................................................... 94 DIPHENYLAMINE .................................................................. 95 DIPROPYLENE GLYCOL METHYL ETHER...................... 96 DIQUAT ................................................................................ 317 DI-SEC. OCTYL PHTHALATE.............................................. 96 DISULFOTON ...................................................................... 318 DISULFURAM........................................................................ 370 DIVINYLBENZENE .............................................................. 465 DYFONATE............................................................................ 370 E ENOOSULFAN (Thiodan)........................................ 97 4 371 ENDRIN ................................................................................... 98 EPICHLORHYDRIN................................................................. 98 EPN .......................................................................................... 99 ETHANOLAMINE ............................................................... 100 ETHION (Nialate) ............................................................... 372 2-ETHOXYETHANOL .............................................. 101 4 319 2-ETHOXYETHYL ACETATE............................................. 101 ETHYL ACETATE ................................................................ 102 ETHYL ACRYLATE................................................................102 480 511904 0310 TLV DOCUMENTATION INDEX ETHYL ALCOHOL.................................................................103 ETHYLAMINE ...................................................................... 103 ETHYL BENZENE................................................................. 104 ETHYL BROMIDE............................................................... 105 ETHYL BUTYL KETONE ......................................................105 ETHYL CHLORIDE............................................................. 106 ETHYL ETHER .................................................................... 106 ETHYL FORMATE............................................................... 107 ETHYL MERCAPTAN ........................................................... 107 ETHYL sec-AMYL KETONE.............................................. 104 ETHYL SILICATE ................................................... 108 4 446 ETHYLENE CHLOROHYDRIN ............................ 108 6 373 ETHYLENE DIAMINE........................................................... 109 ETHYLENE GLYCOL ......................................................... 319 ETHYLENE GLYCOL DINITRATE ................................... 110 ETHYLENE IMINE............................................................... 1H ETHYLENE OXIDE ............................................................. 112 ETHYLIDENE NORBONENE ...............................................320 N-ETHYLMORPHOLINE .................................................... 113 F FENSULFOTHION (Dasanit) ............................................ 373 FERBAM................................................................................. 113 FERRO VANADIUM DUST................................................ 114 FIBROUS GLASS DUST .................................................... 114 FLUORIDE (As F) ............................................................... 116 FLUORINE................................................................. 117 4 321 FLUOROTRICHLOROMETHANE (F 11) ........................ 118 FORMALDEHYDE ...............................................................118 FORMAMIDE ...................................................................... 322 FORMIC ACID .................................................................... 119 FURFURAL .......................................................................... 120 FURFURYL ALCOHOL .......................................... 121 4 323 G GASOLINE .......................................................................... 121 GERMANE....................................................................... 323 GERMANIUM TETRAHYDRIDE ....................................... 323 GLASS. FIBROUS OR DUST............................................. 114 GLUTARALDEHYDE....................................... 374. 416 4 447 GLYCIDOL ........................................................................ 121 H HAFNIUM ............................................................................. 123 HEPTACHLOR .................................................................... 123 HEPTANE ................................................................ 124 4 375 HEXACHLOROBUTADINE .................................................. 448 HEXACHLOROCYCLOPENTADIENE ................................ 324 HEXACHLOROETHANE .................................................... 124 HEXAFLUOROACETONE ..................................................324 HEXAMEHYL PHOSPHORAMIDE ..................................... 466 HEXANE .................................................................... 126 4 276 HEXANONE ............................................................. 126 4 377 HEXONE (MIBK) ................................................................. 126 HEXYL ACETATE-sec ....................................................... 127 HEXYLENE GLYCOL ........................................................... 378 HYDRAZINE ............................................................. 127 4 379 HYDROGEN BROMIDE..................................................... 128 HYDROGEN CHLORIDE.................................................... 129 HYDROGEN CYANIDE ...................................................... 130 HYDROGEN FLUORIDE .................................................... 131 HYDROGEN PEROXIDE. 90%.............................................131 HYDROGEN SELENIDE .................................................... 132 HYDROGEN SULFIDE....................................................... 132 HYDROGENATED TERPHENYLS ..................................... 380 HYDROQUINONE ............................................................... 133 2-HYDROXYPROPYL ACRYLATE ..................................... 467 I INDENE ............................................................................... 134 INDIUM 4 COMPOUNDS (As In) ..................................... 134 INERT DUST (see Nuisance Dusts) IODINE ................................................................................. 135 IODOFORM ..........................................................................381 IRON OXIDE FUME................................................ 136 4 315 IRON PENTACARBONYL..................................................137 IRON SALTS. SOLUBLE. As Fe.........................................138 ISOAMYL ACETATE ..................................... ................. 138 ISOAMYL ALCOHOL......................................................... 139 ISOBUTYL ACETATE ....................................................... 139 ISOBUTYL ALCOHOL............................................ 140 4 382 ISOPHORONE ........................................................ 140 4 327 ISOPHORONE DIISOCYANATE........................................383 ISOPROPYL ACETATE ...................................................... 141 ISOPROPYL ALCOHOL .................................................... 141 ISOPROPYL AMINE ........................................................... 141 n-ISOPROPYLANILINE ........................................................467 ISOPROPYL ETHER................................................ 142 4 327 ISOPROPYL GLYCIDYL ETHER (IGE).............................142 K KETENE ............................................................................... 143 L LEAD .......................................................................... 143 4 328 LEAD ARSENATE ............................................................... 145 LEAD CHROMATE ............................................................... 450 LINDANE .............................................................................. 146 LITHIUM HYDRIDE ........................................................... 147 LPG (liquified Petroleum Gas) ......................................... 146 M MAGNESIUM OXIDE FUME ............................................. 147 MALATHION ........................................................................ 148 MALEIC ANHYDRIDE ........................................................ 148 MANGANESE AND COMPOUNDS.................................. 149 MANGANESE FUME .......................................................... 417 MANGANESE CYCLOPENTADIENYL TRICARBONYL .............................................................. 330 MERCURY (Alkyl Compounds) ......................................... 151 MERCURY (Inorganic) As Hg............................................. 150 MESITYL OXIDE ............................................................... 152 METHACRYLONITRILE ......................................... 333 METHOMYL (Lannate) ...................................................... 384 METHOXYCHLOR................................................................. 152 2-METHOXYETHANOL (See Methyl Cellulose) METHYL ACETATE ............................................................ 153 METHYL ACETYLENE.......................................................... 153 METHYL ACETYLENE-PROPADIENE MIX (MAPP) ................................................................... 154 481 511qOA03^ TLV DOCUMENTATION INDEX METHYL ACRYLATE ......................................................... 154 METHYLAL ......................................................................... 154 METHYL ALCOHOL ............................................................. 155 METHYLAMINE .................................................................. 156 METHYL n-AMYL KETONE ............................................... 157 METHYL BROMIDE ................................................ 157 4 335 METHYL CELLOSOLVE ............................................... ,..158 METHYL CELLOSOLVE ACETATE................................... 159 METHYL CHLORIDE ......................................................... 16 METHYL CHLOROFORM .................................................. 161 METHYL 2-CYANOACRYLATE......................................... 162 METHYL CYCLOHEXANE............................. 162. 386 4 418 METHYL CYCLOHEXANOL.................................... 163 4 335 O-METHYL CYCLOHEXANONE .......................... 163 4 336 METHYL CYCLOPENTADIENYL MANGANESE TRICARBONYL ....................................................... 164 4 331 METHYL OEMETON............................................................. 165 METHYL ETHYL KETONE (MEK) (See 2-Bulanone) METHYL ETHYL KETONE PEROXIDE..............................339 METHYL FORMATE ........................................................... 165 METHYL IODIDE...................................................................166 METHYL ISOAMYL KETONE ........................................... 156 METHYL ISOBUTYL CARBINOL ....................................... 166 METHYL ISOCYANATE .................................................... 167 METHYL MERCAPTAN ..................................................... 167 METHYL METHACRYLATE .............................................. 168 METHYL PARATHION....................................................... 168 N-METHYL-2-PYRROLIDONE............................................ 418 METHYL SILICATE............................................................. 169 C-METHYL STYRENE ........................................................ 170 METHYLDEMETON ............................................................ 165 METHYLENE BIS (4-CYCLOHEXYLISOCYANATE) ....................................... 337 4.4-METHYLENE BIS(2-CHLOROANILINE (MOCA) ......................................................................... 337 METHYLENE BISPHENYL ISOCYANATE (MDI)............. 170 METHYLENE CHLORIDE (dichloromethane)............................. 171. 338, 385 4 467 4.4-METHYLENE DIANILINE.............................................. 450 MICA ................................................................................... 172 MINERAL WOOL FIBER .................................................... 340 MOLYBDENUM. As Mo........................................................173 MONOCROTOPHOS (Azodrin) ....................................... 386 MONOMETHYL ANILINE .................................................. 174 MONOMETHYL HYDRAZINE ........................................... 174 MORPHOLINE .................................................................... 175 N NAPHTHA (Coal Tar) ......................................................... 176 NAPHTHALENE .................................................................... 177 beta-NAPHTHYLAMINE .................................................... 178 NICKEL................................................................................... 178 NICKEL (Soluble Compounds) .......................................... 388 NICKEL CARBONYL.............................................. 180 4 389 NICKEL SULFIDE ROASTING ......................................... 419 NICOTINE ............................................................................ 181 NITRIC ACID ...................................................................... 181 NITRIC OXIDE .................................................................... 182 p-NITROANILINE ............................................................... 182 NITROBENZENE ................................................................. 183 P-NITROCHLOROBENZENE............................................ 184 4-NITRODIPHENYL ......................................................... 184 NITROETHANE .................................................................. 185 NITROGEN DIOXIDE......................................................... 185 NITROGEN TRIFLUORIDE .............................................. 187 NITROMETHANE .............................................................. 187 1- NITROPROPANE ......................................................... 188 2- NITROPROPANE............................................... 188 4 469 n-NITROSODIMETHYLAMINE ......................................... 189 NITROTOLUENE ................................................................. 190 NONANE ............................................................................. 390 NUISANCE AEROSOLS .................................................. 190 0 OCTACHLORO NAPHTHALENE..................................... 191 OCTANE .................................................................. 191 4 391 OIL MIST ............................................................................. 191 OSMIUM TETROXIDE ....................................................... 192 OXALIC ACID............................................................... ... 193 OXYGEN DIFLUORIDE ...................................................... 193 OZONE................................................................................. 194 P PARAFFIN WAX FUME ...................................................... 341 PARAQUAT............................................................... 195 4 422 PARATHION ........................................................................ 195 PENTABORANE ................................................................. 197 PENTACHLORONAPHTHALENE..................................... 198 PENTACHLOROPHENOL.................................................. 198 PENTAERYTHRITOL ......................................................... 199 PENTANE ................................................................ 200 4 391 2-PENTANONE .................................................................. 200 PERCHLOROETHYLENE .................................................. 201 PERCHLOROMETHYL MERCAPTAN ................................202 PERCHLORYL FLUORIDE ................................................ 202 PERLITE ................................................................................. 341 PHENOL ................................................................................. 203 PHENOTHIAZINE ............................................................... 204 PHENYL-BETA-NAPHTHYLAMINE...................... 452 4 471 PHENYL ETHER (Vapor) .................................................. 205 PHENYL ETHER-DIPHENYL MIX (Vapor)...................... 206 P-PHENYLENE DIZMINE .................................................. 205 PHENYLGLYCIDYL ETHER (PGE) ................................. 206 PHENYLHYDRAZINE ......................................................... 207 PHENYLMERCAPTAN..........................................................423 PHENYLPHOSPHINE ......................................................... 342 PHORATE (Thimet) ........................................................... 342 PHOSDRIN (Mevinphos).....................................................208 PHOSGENE ..................................................... 208, 391 4 425 PHOSPHINE ........................................................................ 209 PHOSPHORIC ACID ......................................................... 210 PHOSPHORUS (Yellow) .................................................... 210 PHOSPHORUS PENTACHLORIDE....................................211 PHOSPHORUS PENTASULFIDE ..................................... 211 PHOSPHORUS TRICHLORIDE ..........................................211 PHTHALIC ANHYDRIDE ....................................... 212 4 393 m-PHTHALODINITRILE .................................................... 394 PICLORAM (Tordon) ..........................................................343 PICRIC ACID ...................................................................... 212 PIVAL ................................................................................... 213 PLATINUM (Soluble Salts) ................................... .'.............213 462 511904 0312 TLV DOCUMENTATION INDEX PORTLAND CEMENT..........................................................214 POTASSIUM HYDROXIDE .................................................. 344 PROPANE ............................................................................ 215 PROPARGYL ALCOHOL .................................................. 216 PROPIOLACTONE ............................................................. 216 PROPIONIC ACID.................................................................471 n-PROPYL ACETATE........................................................... 216 PROPYL ALCOHOL ............................................................. 217 n-PROPYL NITRATE ......................................................... 217 PROPYLENE DICHLORIDE .................................................218 1,2-PROPYLENE GLYCOL DINITRATE............................ 426 PROPYLENE GLYCOL MONOMETHYL ETHER............. 286 PROPYLENE IMINE ............................................................. 218 PROPYLENE OXIDE............................................................. 219 PYRETHRUM ...................................................................... 219 PYRIDINE ............................................................................ 220 Q QUARTZ (See Silica-Quartz) QUINONE ............................................................................ 221 R RDX (Cyclotrimethylene Trinitramine) ..............................221 RESORCINOL .................................................................... 395 RHODIUM, METAL FUME 4 DUSTS................................ 222 RONNEL................................................................................. 222 ROSIN CORE SOLDER PYROLYSIS PRODUCTS...................................................................... 223 ROTENONE ........................................................................ 224 RUBBER SOLVENT ........................................................... 396 s SELENIUM COMPOUNDS ................................................ 224 SELENIUM HEXAFLUORIDE.............................................. 226 SILICA (Amorphous) .............................................. 226 & 396 SILICA (Fused) ................................................................... 227 SILICA (Quartz) .................................................................... 227 SILICON ................................................................................. 344 SILICON CARBIDE...............................................................230 SILICON TETRAHYDRIDE (Silane) ................................... 344 SILVER ............................................................................... 231 SOAPSTONE ...................................................................... 232 SODIUM AZIDE .................................................................... 397 SODIUM BISULFITE ......................................................... 472 SODIUM META BISULFITE................................................ 472 SODIUM FLUOROACETATE (1080) ................................ 232 SODIUM HYDROXIDE............................................ 233 & 345 STIBINE ............................................................................... 233 STODDARD SOLVENT .......................................... 233 & 398 STRYCHNINE ........................................................................ 235 STYRENE. MONOMER ...................................................... 235 SUBTILISINS (Proteolytic Enzymes).................. 236 4 345 SULFUR DIOXIDE................................................................. 238 SULFUR HEXAFLUORIDE ................................................ 239 SULFUR MONOCHLORIDE................................................ 240 SULFUR PENTAFLUORIDE................................................ 241 SULFUR TETRAFLUORIDE ................................................ 347 SULFURIC ACID ................................................................. 239 SULFURYL FLUORIDE ...................................................... 241 SYSTOX (See Demeton) T 2.4,5-TRICHLOROPHENOXYACETIC ACID.................... 242 TALC ...................................................................................... 242 TANTALUM ............................................................................243 TEDP..................................................................................... 244 TEFLON DECOMPOSITION PRODUCTS........................245 TELLURIUM ......................................................................... 245 TELLURIUM HEXAFLUORIDE .......................................... 246 TEPP ...................................................................................... 246 TERPHENYLS ......................................................... 247 4 472 TETRABROMOETHANE ..................................................... 248 1.1.2.2- TETRACHLORO-1,2-DIFLUOROETHANE......249 1.1.1.2- TETRACHLORO-2.2 DIFLUOROETHANE...... 249 1.1.2.2- TETRACHLOROETHANE.................................... 249 TETRACHLORONAPHTHALENE....................................... 251 TETRAETHYL LEAD ........................................................... 251 TETRAHYDROFURAN ..........................................................252 TETRA METHYL LEAD (TML)...................... ............... 253 TETRA METHYL SUCCINONITRILE..............................254 TETRANITROMETHANE ................................................... 254 TETRASODIUM PYROPHOSPHATE..................................473 TETRYL ................................................................................. 255 THALLIUM..............................................................................256 THIOGLYCOLIC ACID ....................................................... 427 4.4- THIO-biS (6 Tert Butyl-M-Cresol) .................................................. 400 THIRAM ................................................................................ 257 TIN (Inorganics, except SNH4 4 SN02)............................................................... 257 TIN (Organics) .................................................................... 258 TITANIUM DIOXIDE............................................................. 259 TOLUENE ................................................................. 259 4 348 TOLUENE-2.4-DIISOCYANATE (TDI)................. 260 4 474 O-TOLUIDINE-SKIN ............................................................. 261 TRI BUTYL PHOSPHATE .................................................. 262 TRICHLOROACETIC ACID.................................................476 1.2.4- TRICHLOROBENZENE .............................................400 1.1.2- TRICHLOROETHANE .......................................... 263 TRICHLOROETHYLENE.................................................... 263 TRICHLORONAPHTHALENE ............................................. 265 1.2.3- TRICHLOROPROPANE ......................................... 266 1,1,2-TRI CHLORO, 1.1,2-TRI FLUOROETHANE (Freon 113) ..................................................................... 267 TRICYCLOHEXYLTIN HYDROXIDE (Plictran)................. 349 TRIDYMITE ............................................................................ 268 TRIETHYLAMINE ............................................................... 268 TRIFLUOROMONOBROMOMETHANE .............................268 TRIMETHYLBENZENE ...................................................... 269 TRIMETHYL PHOSPHITE PHOSPHOROUS ACID....... 428 TRINITROTOLUENE (TNT).................................... 270 4 429 TRIORTHOCRESYL PHOSPHATE .................................. 271 TRIPHENYL AMINE ............................................................ 401 TRIPHENYL PHOSPHATE ................................................. 272 TRIPOLI ................................... 350 TUNGSTEN 4 COMPOUNDS' AS W .............................. 272 TURPENTINE ....................................................................... 274 u URANIUM ............................................................................ 274 483 1904 0313 TLV DOCUMENTATION INDEX v n-VALERALDEHYDE ......................................................... 430 VANADIUM ......................................................................... 275 VINYL ACETATE ................................................................ 276 VINYL BROMIDE......................................................... 350&452 VINYL CHLORIDE .................................................. 277 & 402 VINYL CYCLOHEXENE DIOXIDE ................................... 406 VINYL TOLUENE................................................................ 278 VINYLIDENE CHLORIDE .................................................. 351 VM 4 P NAPHTHA .................................................. 407 4 430 w WARFARIN ............................... WELDING FUMES.................. WOOD DUST (Nonallergenic) 279 408 279 X XYLENE ............................................................................... 281 H-XYLENE, ALPHA. ALPHA, DIAMINE............................ 408 XYLIDINE...............................................................................282 Y YTTRIUM ............................................................................. 283 z ZINC CHLORIDE FUME ......................................................283 ZINC OXIDE FUME ........................................................... 284 ZINC STEARATE.................................................................. 352 ZIRCONIUM COMPDS (as ZR) ....................................... 285 484 511904 0314