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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 CARBON DISULFIDE BACKGROUND INFORMATION PHYSICAL AND CHEMICAL PROPERTIES (Hildenskoild, 1959; Windholz et al., 1976; NIOSH, 1977; Seppalainen and Haltia, 1980) Structural formula: CS2 Molecular weight: 76.14 Chemical names: Carbon disulfide, CS2; carbon bisulfide; dithiocarbonic anhydride CAS number: CAS No. 75–15–0 Freezing point: −116°C Boiling point: 46.5°C (at 1 atm) Odor: Odorless or sweet, ethereal (when pure), pungent (when impure) Odor detection threshold: 0.02–0.08 ppm Flash point, closed cup: −30°C Ignition temperature: 100°C Explosive range: 1–50% in air Vapor density: 2.67 Vapor pressure: 100 mm Hg at −0.5°C; 300 mm Hg at 17.8°C Solubility in water: 0.294% at 20°C Miscibility: Miscible in methanol, ethanol, ether, benzene, chloroform, and oils Reactions: Reacts with mercapto, amino, and hydroxy groups. Solubility coefficient: Air to blood, 2.5; blood to tissues, 5.6. Conversion factors: ppm=0.32 (mg/m3) mg/m3=3.13 (ppm) OCCURRENCE AND USE CS2 is not a natural constituent of the environment and was discovered in the laboratory in 1796. Its narcotic effects were tested in 1848 and industrial use began in 1851. First used as a solvent for phosphorus in the manufacture of matches, CS2 was later used as a solvent for fats, lacquers, and camphor; for refining paraffins and petroleum; for the extraction of natural oils, and, most extensively, for the vulcanization of rubber. Today, its most important use, occupational exposure, and injury potential occur in the production of viscose rayon fibers for textile applications and cellophane films for packaging. It is also used in pesticide production, in extraction of oils, and as a laboratory reagent (Seppalainen and Haltia, 1980). Approximately 782 million pounds were produced in the United States in 1974 (U.S. Dept. of Commerce, 1976). NIOSH (1977) estimated that 30,000 full-time U.S. employees were potentially exposed to CS2. In 1965, the U.S. Coast Guard expressed interest to the Committee on Toxicology in short-term exposure limits in connection with transportation of molten sulfur and bulk transfer of CS2.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 SUMMARY OF TOXICITY INFORMATION EFFECTS ON HUMANS Data on the effects of exposure to CS2 are summarized in Table 11. Uncontrolled Exposure According to Bittersohl et al. (1972), exposure to CS2 at 300 ppm produces slight symptoms of poisoning after several hours; at 400 ppm, it gives rise to prenarcotic symptoms; at 1,150 ppm for 30 min, it leads to severe forms of poisoning; and at 3,200–3,800 ppm, it is life-threatening. According to Paluch (1954), exposure at 2,000–3,300 ppm leads to narcosis in 30 min, and death occurs after 30–60 min of exposure at 5,000 ppm. Acute psychosis was a common manifestation of CS2 poisoning in rubber vulcanization plants until this process was discontinued at the end of the nineteenth century. During World War II, many cases of chronic poisoning, in which peripheral neuropathy was the leading complaint, occurred in the viscose rayon industry (Vigliani, 1954). There are several epidemiological reports of occupational disease after low-concentration, long-term exposure to CS2 or a combination of CS2 and hydrogen-sulfide (H2S) (NIOSH, 1977). Peripheral neuropathy, as revealed by lowering of maximal motor nerve conduction velocities (MCVs), was found in 118 workers (110 controls) exposed at 20–60 ppm for 1–27 yr; exposure was at less than 30 ppm during the last 12 yr (Seppalainen et al., 1972). Similarly, MCVs of peroneal nerves were lowered and abnormal electromyograms were prevalent in a study of 254 subjects (54 controls) exposed at 20–80 ppm for 2–31 yr, with exposure at less than 20 ppm during the last 3 yr (Gilioli et al., 1978). Another study (Knave et. al., 1974) reported lowered MCVs in a group of 51 subjects (52 controls) exposed at less than 20 ppm for 1–30 yr. CNS effects reported by Styblova (1977) consisted of abnormal electroencephalograms (EEGs) in 33.2% of 250 workers (compared with 6.6% of 61 controls) employed in the production of rayon staple. EEGs were abnormal in 39% of 54 subjects (compared with 12% in controls) exposed at 10–15 ppm for 10–15 yr (Seppalainen and Linoila, 1976). Psychic effects of CS2 have also been measured epidemiologically. Mancuso and Locke (1972) found an increased risk of suicide among 4,899 viscose rayon workers, and another study (Hanninen et al., 1978) of 206 workers (and 152 controls) found psychomotor disturbances and personality changes indicative of depression. Psychologic testing of 102 workers showed an impairment of intelligence functions and performance tests compared with those in controls (Cassitto et al., 1978). The exact CS2 concentration necessary to produce neurologic disease in humans is unknown, but Seppalainen and Haltia (1980) stated recently that no new cases had occurred among workers who started their work in the Finnish viscose rayon industry in the late 1960s or thereafter, when airborne CS2 concentrations were mostly below 10 ppm and at times 10–20 ppm. However, mild cases of polyneuropathy appeared in a viscose film factory in Finland, where the mean exposure had remained about the same for 17 yr, and where the Finnish TLV of 10 ppm had frequently been
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 exceeded, although concentrations usually stayed below 20 ppm (Seppalainen and Haltia, 1980). Tiller et al. (1968) found a 2.5-fold excess mortality from coronary heart disease among viscose rayon workers exposed to CS2 for 10 yr or more. A prospective Finnish study (Hernberg et al., 1973) of 343 male viscose rayon workers exposed at 10–30 ppm found the 5-yr mortality from coronary heart disease was almost 5 times that in a comparison cohort (other causes of death were evenly distributed). Another study (Gavrilescu and Lilis, 1967) reported atherosclerosis and hypertension in workers exposed to CS2 at concentrations as low as 7 ppm. Teleky (1955) claimed on the basis of first-hand experience that reduction of corneal reflex was the first sign of toxic action in workers chronically exposed to CS2 vapor. Controlled Exposure Mack et al. (1974) exposed men 21–40 yr old to CS2 at 10, 20, 40, or 80 ppm for 6 h and at 20 ppm 6 h/d for 5 d, in a study of inhibition of drug metabolism. They noted that exposure at 10–20 ppm for 6 h could retard the normal metabolism of such common drugs as analgesics, hypnotics, antidiabetics, and anticonvulsants. Clinical and Pathologic Effects Cardiovascular effects similar to those seen in atherosclerosis have been ascribed to CS2 exposure. Long-term exposure can produce vascular changes in the heart, eyes, brain and kidneys (NIOSH 1977). Hypertension, angina, abnormal plasma glucose and creatinine concentrations, and electrocardiographic changes have all been found. Neurologic effects vary with the degree of exposure. Heavy (but not specified) occupational exposure, now a thing of the past, used to cause dramatic behavioral changes after weeks or months of exposure. Patients often were manic or depressed and could become so frenzied that they attacked their workmates and relatives, or committed suicide (Seppalainen and Haltia, 1980). Long-term, lower-level (20–170 ppm) exposure has been causally associated with toxic encephalopathy (pseudobulbar paralysis, mental deterioration, extrapyramidal signs), although signs and symptoms of peripheral neuropathy usually predominate. This begins within 4–6 mo of occupational exposure at 170 ppm or after several years at 65–100 ppm. Neuropathy predominantly affects the legs, causing difficulty in walking and absence of reflexes in severe cases, but not complete paralysis. Neuropathy also develops at lower concentrations (20–40 ppm) with symptoms of paresthesia, muscle pain, diminished muscle strength, and distal sensory loss. Both encephalopathy and neuropathy may worsen for 1–2 yr after occupational exposure stops, but partial recovery may then take place, or almost complete recovery if the damage has not been too severe (Seppalainen and Haltia, 1980). Renal effects, such as nephrosclerosis, were seen in some autopsies of patients with CS2 poisoning. Chronic renal dysfunction was also found among workers with 10 yr or more of exposure to CS2 (Toyama and Sakurai, 1967). CS2 exposure affects the eye by inducing vascular rigidity, slowed circulation, increased ophthalmic pressure, and retinal
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 microaneurysms (Goto and Hotta, 1967; Goto et al., 1971, 1972; Hotta et al., 1972; Maugeri et al., 1966; Raitta and Tolonen, 1975; Raitta et al., 1974; Savic, 1967; Szymankowa, 1968). Retinal degeneration and conjunctival inflammation were reported at concentrations below 3 ppm (Szymankowa, 1968), although methods used to determine the concentrations were not reported (NIOSH, 1977). Reproductive effects, resulting in impaired sexual function (impotence and loss of libido), are frequent complaints in chronic poisoning. Androsterone and testosterone excretion are reduced (Delic et al., 1966; Delpech, 1856). Female viscose rayon workers reportedly may develop menstrual and ovarian dysfunction at concentrations of less than 3 ppm (Vasilyeva, 1973). Infertility, threatened pregnancy terminations, and spontaneous abortions have been reported, the latter at concentrations down to 9 ppm and below (Petrov, 1969). Other results of CS2 exposure include respiratory effects (Ranelletti, 1933) and hepatic effects including liver enlargement in the presence of normal liver function. Gastrointestinal effects among heavily exposed workers, possibly due to changes in autonomic nervous system function, include epigastric pain, nausea, and dyspepsia (Seppalainen and Tolenen, 1974). Skin and mucous membranes are severely irritated by CS2. EFFECTS ON ANIMALS The neurotoxic effects of prolonged exposure to CS2 recently have been summarized by Seppalaienen and Haltia (1980). Dogs exposed at 400 ppm 8h/d, 5 d/wk develop hindlimb weakness (from peripheral neuropathy) after 5–8 wk and forelimb weakness after 9 wk. Other signs of intoxication include ataxia, jerking, choreiform movements, loss of position sense, and behavioral chances (apprehension, excitation, and aggressiveness). Rabbits exposed at 750 ppm 6 h/d, 5 d/wk slowly lost weight after 4 wk and developed hindlimb difficulties after 7 wk. Rats exposed at 750 ppm 6 h/d, 5 d/wk exhibited motor impairment after 18 wk, and animals exposed at 770 ppm displayed similar signs after only 8 wk. During exposure, MCVs decrease in rats and rabbits before paresis is evident. When weakness is apparent in rabbits, paretic muscles display fibrillation potentials indicative of denervation. Pathologic studies using contemporary techniques show that a central-peripheral distal axonopathy underlies the polyneuropathy. The dominant feature in exposed animals is the appearance of giant axonal swellings filled with 10-nm neurofilaments multifocally in the distal parts of long spinal cord tracts and distally in long peripheral nerves. Distal nerve fiber breakdown follows the development of these swellings and results in motor and sensory denervation. Other effects reported include vascular damage, reproductive changes, and fetal effects. Several experimental studies (Guarino and Arciello, 1954; Lewey, 1941; Petrov, 1969) have shown that CS2 causes vascular changes in various organs. Testicular damage (few spermatogonia and degenerated Leydig cells) was found by Gondzik (1971) in rats given CS2 at 12.5–25 mg/kg intraperitoneally in peanut oil. Embryotoxicity in rats exposed to CS2 and H2S at 3.2 ppm was reported by Bariliak and co-workers (1975). Bronchitis was found in rats exposed to as low as 0.3 ppm plus H2S at 0.7 ppm (Misiakiewicz et al., 1972). Effects on animals of exposure to CS2 are summarized in Table 12.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 PHARMACOKINETICS Absorption, Distribution, Metabolism, and Excretion Respiratory absorption seems to be proportional to the concentration of CS2 in the air (Demus, 1967). Previously nonexposed subjects breathing CS2 at 17–30 ppm absorbed 80% in the first 15 min. After equilibrium is reached in about 1–2 h, 40–50% of the vapor is retained (Vigliani, 1961). CS2 is also absorbed via the skin. Once absorbed, CS2 is taken up twice as much in red blood cells as in plasma. About 70% is metabolized (Demus, 1967). CO2 and CO have been identified as metabolites (Dalvi and Neal, 1978; DeMatteis and Seawright, 1973). In man, CS2 disappears rapidly from the bloodstream and accumulates in lipid-rich tissues and organs. Experimental studies have revealed initial distribution to the liver, with a more uniform distribution occurring later. Human studies have shown that 10–30% of CS2 is exhaled and 1% eliminated in urine, leaving about 70–90% available for biotransformation. Three metabolites have been isolated from human urine, including the principal urinary CS2 metabolite thiocarbamide (thiourea) and mercaptothioaxolinone (Pergal et al., 1972a, b). Sites and Mechanisms of Toxicity Several hypotheses have been developed to explain the toxic action of CS2 (World Health Organization, 1979): Chelation by metabolites of various trace metals essential for enzyme function; Enzyme inhibition; Disturbance of vitamin metabolism, especially of B6 and nicotinic acid; Disturbance of catecholamine metabolism; and Disturbance of lipid metabolism. INHALATION EXPOSURE LIMITS Exposure limits established for CS2 in various countries (Japan Assoc. Ind. Health, 1971; Soc. Ital. Med. Lav., 1975; Winnell, 1975) are given below: United States 1974 20 ppm (60 mg/m3) (TWA) W. Germany 1974 60 mg/m3 (TWA) E. Germany 1973 50 mg/m3 (TWA) Sweden 1975 30 mg/m3 (TWA) Czechoslovakia 1969 30 mg/m3 (TWA) USSR 1972 10 mg/m3 (ceiling) Italy 1975 30 mg/m3 (TWA) Japan 1961 60 mg/m3 (TWA)
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 COMMITTEE RECOMMENDATIONS EXPOSURE LIMITS In 1965, the Committee recommended the follwing EELs for CS2: 10-min EEL: 200 ppm 30-min EEL: 100 ppm 60-min EEL: 50 ppm The most thoroughly documented effects—neurologic and cardiovascular disease—develop after prolonged exposure to CS2 at a minimum concentration of 10 ppm (and an unknown concentration of H2S, which commmonly coexists with CS2). Exposure at similar concentrations over a period of years has given rise to reproductive disorders, embryotoxicity, and spontaneous abortions. Retinal changes and menstrual and ovarian dysfunction reportedly occur at concentrations of less than 3 ppm (Szymankowa, 1968; Vasilyeva, 1973), although sampling and analytical methods were poorly documented and control groups were sometimes lacking in these studies. The Committee is unaware of any report on carcinogenesis or mutagenesis resulting from exposure to CS2. One study (Bariliak et al, 1975), which NIOSH (1977) considered “tentative,” reported a “weak teratogenic effect” in rats after low-concentration exposure (3.2 ppm) to a combination of CS2 and H2S. An English translation of work by Bittersohl et al. (1972) stated that CS2 induces minor symptoms after several hours of exposure at 300 ppm, with distinct signs of poisoning at 400 ppm and severe poisoning after 0.5 h at 1,150 ppm. There is therefore no basis for changing the emergency exposure limits (EELs) previously established by the Committee in 1965. Therefore, the following EELs are recommended: 10-min EEL: 200 ppm 30-min EEL: 100 ppm 60-min EEL: 50 ppm RESEARCH RECOMMENDATIONS Short-term toxicity studies on animals may be useful in ascertaining how concentration and time are related over short periods (up to 24 h). It is suggested that dose-response studies in animals be conducted. If there is a concern over long-term exposure, experimental animal studies are needed to determine whether such exposure to airborne CS2 at low concentrations causes damage to the nervous system (including the retina) and the reproductive, cardiovascular, and renal systems.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 TABLE 11 Effects of Occupational Exposure to Carbon Disulfide plus Hydrogen Sulfidea Workers No. Age Mean or Range, yr Concentration, mg/m3b Duration: Mean or Range, yr Effects Reference CS2 H2S 100 — 450–1,000 — — Polyneuritis in 88%; gastric disturbances in 28% Vigliani, 1954 43 53 30–1,500 — 21 Encephalopathy " 107 32 200–400 — 1–9 Ophthalmic pressure 138/ 110, vs. 115/87 in controls Maugeri et al., 1966 185 25–35 62–174 — 5 Eye burning in 96% of rayon-production workers, 44% of cell-fiber workers; pupillary light reaction abnormal in cell-fiber workers Savic, 1967 100 39 31–137 — 10 Psychomotor and psychologic disturbances Hanninen, 1971 125 47 124 — 13 Coronary heart disease in 5.6%, vs. 1.2% in controls Cirla et al., 1972 33 22 40–81 — 2 Asthenospermia, hypospermia, teratospermia Lancranjan et al., 1969 116 50 62 — 5 Coronary heart disease in 16.5%, vs. 2.7% in controls Locati et al., 1970 28 44 62 — 13 Coronary heart disease in 3.6%, vs. 1.2% in controls Cirla et al., 1972 38 51 29–1 18c — 20 Ocular vascular rigidity Raitta and Tolonen, 1975 100 48 29–118c — 15 Ophthalmic circulation slowed Raitta et al., 1974
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 Workers No. Age Mean or Range, yr Concentration, mg/m3b Duration: Mean or Range, yr Effects Reference CS2 H2S 36 42 29–118c — 6 Peripheral nerve and CNS damage; conduction velocites lowered; EMG abnormal Seppalainen et al., 1972 397 35–64 29–118c — — Coronary heart disease cause of 42% of deaths in highly exposed workers, 24% in moderately exposed, 14% nationally Tiller et al., 1968 630 20–40 13–50 — — Immunologic reactions decreased; job absenteeism increased Kashin, 1965 138 50 22–44 — 10 Arteriosclerotic changes in 30.4%; hypertension in 23.2% Gavrilescu and Lilis, 1967 94 18 12–31 10 1 Hypotension, nervous system excitability Kramarenko et al., 1970 189 30 28 — 3 Spontaneous abortions in 14.3%, vs. 6.8% in controls; premature births in 8.6%, vs. 2.8% in controls Petrov, 1969
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 Workers No. Age Mean or Range, yr Concentration, mg/m3b Duration: Mean or Range, yr Effects Reference CS2 H2S 209 20–40 22 10 — Menstruation irregular, painful, abundant, prolonged Vasilyeva, 1973 60 25 16 — — Muscular power diminished; reflexes slowed Vasilyeva, 1973 500 18–60 9 — 1–30 Retinal degeneration, conjunctival inflammation, temporary corneal opacities, color-vision disturbances Szymankowa, 1968 500 20–40 — 10 — Menstruation abundant, painful, prolonged Vasilyeva, 1973 94 18 3–9 10 1 Hypotension; nervous system excitability Kramarenko et al., 1970 aAdapted from NIOSH (1977). b1 mg/m3=0.321 ppm. cThese studies based on same cohort of workers, exposed to carbon disulfide plus hydrogen sulfide at concentrations averaging 29–88 mg/m3 in 1960, 59–118 mg/m3 in 1950, and higher before 1950. Hydrogen sulfide concentration included in that given for carbon disulfide and estimated to be about 10% of total.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 TABLE 12 Effects on Animals of Exposure to Carbon Disulfide or to Carbon Disulfide Plus Hydrogen Sulfide Concentrationb Species CS2 H2S Duration Effects Reference Rat 2,330 0 6 h/d, 5 d/wk, 10 wk; then 3 d/wk, 2 wk Lethargy; loss of motor control, lowered MCV with no recovery in 12 wk Seppalainen and Linnoila, 1976 Rat 2,330 0 6 h/d, 5 d/wk, 2–5 wk Lethargy; lowered but reversible MCV Seppalainen and Linnoila, 1976 Rat 2,000 0 2 h/d throughout pregnancy Increased fetal mortality, decreased fertility Yaroslavakii, 1969 Rat 1,500 0 5 hr/d, 6 d/wk, 1–15 mo Weakness; paralysis, myelin and neuron degeneration; weight loss Szendzikowski et al., 1973 Rat 12 c 60–110 d before mating and during pregnancy Increased fetal mortality, teratagenesis Bariliak et al., 1975 Rat 1.0 1.0 0.1 0.1 0.1 0 0.1 0 160 d Inflammation of bronchi; weight changes; increased serum aspartate, aminotransferase, and blood cholinesterase activities; most severe with combined exposures Misiakiewicz et al, 1972
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 Concentrationb Species CS2 H2S Duration Effects Reference Mouse 2,000 0 2 h/d throughout Increased fetal mortality; decreased fertility Yaroslavskii, 1969 Rabbit 780–2,300 0 6 h/d 5 d/wk, 38 wk Paralysis; CNS damage; slight liver damage; weight loss Cohen et al., 1958 Rabbit 930 930 0 140 0 140 30 min/d, 120 d Abnormalities of bone marrow, kidneys, and spleen; decreased spermatogenesis; loss of appetite; blood changes; most severe with combined exposure Wakatsuki and Higashikawa, 1959; Wakatsuki, 1959 Rat 78 0 4 mo (every other day)d Testicular lesions; no spermatogenesis Gondzik, 1971 Rat 78 0 2 mo (every other day)d Decreased number of spermatozoa; blood vessels engorged and vessel walls thickened Gondzik, 1971 Rat 39 0 2 mo (every other dayd) No effects Gondzik, 1971 aAdopted from NIOSH (1977). bmg/m3 for inhalation mg/kg for injection; 1 mg/m3=0.321 ppm. Exposure by inhalation, except where noted. cHydrogen sulfide concentration included in that given for carbon disulfide. dExposure intraperitoneal.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 REFERENCES Bariliak, I.R., Vasileva, I.A., and Kalinovskaia, L.P. 1975. Effect of small concentrations of carbon disulfide and hydrogen sulfide on intrauterine development of rats. Arkh. Anat. Gistol. Embriol. 68:77–81. Bittersohl, G., Ehrhardt, W., Grund, W., and Grunewald, A. 1972. Schwefelkohlenstoff. In E.Kersten, ed. Franz Koelsch Handbuch der Berufserkrankungen. Jean, East Germany: VEB Gustav Fischer Verlag. p. 271–273. Cassitto, M.G., Bertazzi, P.A., Camerino, D., Bulgheroni, C., Cirla, A.M., Gilioli, R., Graziano, C., and Tomasini, M. 1978. Subjective and objective behavioural alterations in carbon disulphide workers. Med. Lav. 69:144–150. [Ind. Medicus 19:1673, 1978] Cirla, A.M., Villa, A., Tomasini, M. 1972. A study of the incidence of coronary disease in workers of a viscose-rayon industry, exposed to carbon disulphide. Med. Lav. 63:431–441. Cohen, A.E., Paulus, H.J., Keenan, R.G., and Scheel, L.D. 1958. Skin absorption of carbon disulfide vapor in rabbits. I. Associated changes in blood protein and zinc. AMA Arch. Ind. Health 17:164–169. Dalvi, R.R., and Neal, R.A. 1978. Metabolism in vivo of carbon disulfide to carbonyl sulfide and carbon dioxide in the rat. Biochem. Pharmacol. 27:1608–1609. Delic, V., Graovac-Leposavic, L., Djuric, D., Berkes, I., and Djordjevic, V. 1966. The determination of sulphates in the urine of workers exposed to carbon disulphide. Med. Lav. 57:458–462. Delpech, A. 1856. Memoire sur les accidents que developpe chez les ouvriers en caoutchouc, l’inhalation du sulfure de carbone en vapeur. Bull. Acad. Med. 21:350. DeMatteis, F., and Seawright, A.A. 1973. Oxidative metabolism of carbon disulphide by the rat. Effect of treatments which modify the liver toxicity of carbon disulphide. Chem.-Biol. Interact. 7:375–388. Demus, H. 1967. The mechanism of absorption, metabolism and excretion of carbon disulphide in the human body. In H.Brieger, and J.Teisinger, eds. Toxicology of Carbon Disulphide. Amsterdam: Excerpta Medica Foundation, p. 42–49. Gavrilescu, N., and Lilis, R. 1967. Cardiovascular effects of long-extended carbon disulfide exposure. In H.Brieger, and J. Teisinger, eds. Toxicology of Carbon Disulphide. Amsterdam: Excepta Medica Foundation, p. 165–167.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 Gilioli, R., Bulgheroni, C., Bertazzi, P.A., Cirla, A.M., Tomasini, M., Cassitto, M.G., and Jacovone, M.T. 1978. Study of neurological and neurophysiological impairment in carbon disulphide workers. Med. Lav. 69:130–143. [Ind. Medicus 19:2245, 1978] Gondzik, M. 1971. Histology and histochemistry of rat testicles as affected by carbon disulfide. Pol. Med. J. 10:133–139. [Ind. Medicus 12:1410, 1971] Goto, S., and Hotta, R. 1967. The medical and hygienic prevention of carbon disulphide poisoning in Japan. In H.Brieger, and J. Teisinger, eds. Toxicology of Carbon Disulphide. Amsterdam: Excepta Medica Foundation, p. 219–230. Goto, S., Hotta, R., and Sugimoto, K. 1971. Studies on chronic carbon disulfide poisoning. Pathogenesis of retinal microaneurysm due to carbon disulfide, with special reference to a subclinical defect of carbohydrate metabolism. Int. Arch. Arbeitsmed. 28:115–126. Goto, S., Sugimoto, K., Hotta, R., Graovac-Leposavic, L., Savic, S.M., and Jovicic, M. 1972. Retinal microaneurysm in carbon disulfide workers in Yugoslavia. Prac. Lek. 24:66–70. [Cited in Int. Arch. Occup. Environ. Health 37:1–8, 1976] Guarino, A., and Arciello, G. 1954. Influence of chronic experimental carbon disulfide poisoning on the histology of the coronaries. Folia Med. (Naples) 37:1021–1044. [Chem. Abs. 49:7737h, 1955] Hanninen, H. 1971. Psychological picture of manifest and latent carbon disulphide poisoning. Brit. J. Ind. Med. 28:374–381. Hanninen, H., Nurminen, M., Tolonen, M., and Martelin, T. 1978. Psychological tests as indicators of excessive exposure to carbon disulphide. Scand. J. Psychol. 19:163–174. Hernberg, S., Nurminen, M., and Tolonen, M. 1973. Excess mortality from coronary heart disease in viscose rayon workers exposed to carbon disulfide. Work-Environ. Health 10:93–99. Hildenskiold, R.S. 1959. Limits of allowable concentration of carbon bisulfide in the atmospheric air of residential areas. Gig. Sanit. 24:3–8. Hotta, R., Sugimoto, K., and Goto, S. 1972. Retinopathia sulfocarbonica and its natural history. Acta Soc. Ophthalmol. Jap. 76:1561–1566. Japan Association of Industrial Health 1971. Recommendation for permissable concentrations, etc. (1971). Transl. of: Sangyo Igaku (Jpn. J. Ind. Health) 13:475–484.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 Kashin, L.M. 1965. Overall immunological reactivity and morbidity of workers exposed to carbon disulfide. Hyg. Sanit. 30:331–335. [Transl. from Russian] Knave, B., Kolmodin-Hedman, B., Persson, H.E., and Goldberg, J.M. 1974. Chronic exposure to carbon disulfide: Effects on occupationally exposed workers with special reference to the nervous system. Work-Environ.-Health 11:49–58. Kramarenko, I.B., Yakovleva, I.N., Grishko, F.I., and Litvinova, Yu. A. 1970. Hygienic evaluation of vocational training of young workers in spinning shops of a viscose mill. Hyg. Sanit. 36:379–384. Lancranjan, I., Popescu, H.I., and Klepsch, I. 1969. Changes of the gonadic function in chronic carbon disulphide poisoning. Med. Lav. 60:566–571. Lewey, F.H. 1941. Neurological, medical and biochemical signs and symptoms indicating chronic industrial carbon disulphide absorption. Ann. Intern. Med. 15:869–883. Locati, G., Cirla, A.M., and Villa, A. 1970. Prevalence of coronary heart disease among 253 viscose-rayon workers admitted to the Clinica del Lavoro of Milan from 1947 to 1969. Med. Lav. 61:442–446. Mack, T., Freundt, K.J., and Henschler, D. 1974. Inhibition of oxidative N-demethylation in man by low doses of inhaled carbon disulphide. Biochem. Pharmacol. 23:607–614. Mancuso, T.F., and Locke, B.Z. 1972. Carbon disulphide as a cause of suicide. Epidemiological study of viscose rayon workers. J. Occup. Med. 14:595–606. Maugeri, U., Cavalleri, A., Visconti, E. 1966. The ophthalmodynamography in carbon disulfide occupational poisoning. Med. Lav. 57:730–740. [English summary] Misiakiewicvz, Z., Szulinska, G., Chyba, A. 1972. Effect of a carbon disulfide mixture in the air on white rats during several months of continuous exposure. Rocz. Panstw. Zakl. Hig. 23:465–475. [Chem. Abs. 78:24860s, Feb. 5, 1973] National Institute for Occupational Safety and Health. 1977. NIOSH Criteria for Recommended Standard…Occupational Exposure to Carbon Disulfide. U.S. Department of Health, Education, and Welfare, Public Health Service, Center for Disease Control, Washingtgon, DC: National Institute for Occupational Safety and Health. [186 p.] Paluch, R. 1954. Toksykologia Przemyslowa. PWT, Warszava. p. 351. Pergal, M., Vukojevic, N., Cirin-Popov, N., Djuric, D., and Bojovic, T. 1972a. Carbon disulfide metabolites excreted in the urine of exposed workers. I. Isolation and identification of 2-mercapto-2-thiazolinone-5. Arch. Environ. Health 25:38–41.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 Pergal, M., Vukojevic, N., and Djuric, D. 1972b. Carbon disulfide metabolites excreted in the urine of exposed workers. II. Isolation of thiocarbamide. Arch. Environ. Health 25:42–44. Petrov, M.V. 1969. Course and termination of pregnancy in women working in viscose industry. Pediatr. Akush. Ginekol. 3:50–52. Raitta, C., and Tolonen, M. 1975. Ocular pulse wave in workers exposed to carbon disulfide. Albrecht von Graefes Arch. Klin. Exp. Ophthalmol. 195:149–154. Raitta, C., Tolonen, M., and Nurminen, M. 1974. Microcirculation of ocular fundus in viscose rayon workers exposed to carbon disulfide. Albrecht. Graefes Arch. Klin. Ophthalmol. 191:151–164. Ranelletti, A. 1933. Solfocarbonismo Professionalle. Torino: La Grafica Moderna. Savic, S.M. 1967. Influence of carbon disulfide on the eye. Arch. Environ. Health 14:325–326. Seppalainen, A.M., and Haltia, M. 1980. Carbon disulfide, In P.S. Spencer, and H.H.Schaumburg, eds. Experimental and Clinical Neurotoxicology. Baltimore: Williams and Wilkins. p. 356–373. Seppalainen, A.M., and Linnoila, I. 1976. Electrophysiological findings in rats with experimental carbon disulphide neuropathy. Neuropathol. Appl. Neurob. 2:209–216. Seppalainen, A.M., and Tolonen, M. 1974. Neurotoxicity of long-term exposure to carbon disulfide in the viscose rayon industry. A neurophysiological study. Work-Environ.-Health 11:145–153. Seppalainen, A.M., Tolonen, M., Karli, P., Hanninen, H., and Hernberg, S. 1972. Neurophysiological findings in chronic carbon disulfide poisoning. A descriptive study. Work-Environ.-Health 9:71–75. Societa Italiana di Medicina del Lavoro: Associazione Italiana degli Igienisti Industriali. 1975. Valori Limite Ponderati degli Inquinanti Chimici d Particolati degli Ambienti di Lavoro Per Il. 1975. Med. Lav. 66:361–371. Styblova, V. 1977. Electroencephalography in diagnosis of early cerebral changes due to carbon disulfide. Int. Arch. Occup. Environ. Health 38:263–282. [English summary] Szendzikowski, S., Stetkiewicz, J., Wronska-Nofer, T., and Zdrajowska, I. 1973. Structural aspects of experimental carbon disulfide neuropathy. I. Development of neurohistological changes in chronically intoxicated rats. Int. Arch. Arbeitsmed. 31:135–149. Szymankowa, G. 1968. Studies on the effect of CS2 on visual organ of workers in a synthetic fiber plant. Klin. Oczna 38:41–44.
OCR for page 56
Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 Teleky, L. 1955. Gewerbliche Vergiftungen. Berlin: Springer-Verlag. [414 p.] Tiller, J.R., Schilling, R.S.F., and Morris, J.N. 1968. Occupational toxic factor in mortality from coronary heart disease. Br. Med. J. 4:407–411. Toyama, T., and Sakurai, H. 1967. Ten-year changes in exposure level and toxicological manifestations in carbon disulphide workers. In H. Brieger, and J.Teisinger, eds. Toxicology of Carbon Disulphide. Amsterdam: Excepta Medica Foundation, p. 197–204. U.S. Department of Commerce, U.S. International Trade Commission. 1976. Synthetic Organic Chemicals, United States Production and Sales of Miscellaneous Chemicals, 1974 (preliminary). Washington, D.C.: U.S. International Trade Commission, p. 9 Vasilyeva, I.A. 1973. Effect of low concentrations of carbon disulfide and hydrogen sulfide on the menstrual function of women and the estrual cycle in an experiment. Gig. Sanit. 7:24–27. Vigliani, E.C. 1954. Carbon disulphide poisoning in viscose rayon factories. Br. J. Ind. Med. 11:235–241. Vigliani, E.C. 1961. Vergiftung mit Schwefelkohlenstoff. In E.W. Baader, ed. Handbuch der gesamten Arbeitsmedizin. Band II, Teil 1. Berlin: Urban & Schwarzenberg. p. 313. Wakatsuki, T. 1959. Experimental study on the poisoning by carbon disulfide and hydrogen sulfide. Shikoku Igaku Zasshi 15:671–700. [Chem. Abs. 61:3600h, 1964] Wakatsuki, T., and Higashikawa, H. 1959. Carbon disulfide and hydrogen sulfide poisoning. Histological changes in hemopoietic organs and other internal organs. Shikoku Igaku Zasshi 14:549–554. [Chem. Abs. 58:4960c, 1963] Windholz, M., Budavari, S., Stroumtsos, L.Y., and Fertig, M.N., eds. 1976. The Merck Index: An Encyclopedia of Chemicals and Drugs. 9th ed. Rahway, NJ: Merck & Co., Inc. p. 231. Winell, M. 1975. An international comparison of hygienic standards for chemicals in the work environment. AMBIO 4:34–36. World Health Organization. 1979. Environmental Health Criteria 10: Carbon Disulfide. Geneva: World Health Organization. [100 p.] Yaroslavskii, V.K. 1969. Toxic action of carbon disulfide on the reproductive function and increase of this effect by tryptophan. Bull. Exp. Biol. Med. 68:88–91.
Representative terms from entire chapter: