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XYLENE

BACKGROUND INFORMATION

PHYSICAL AND CHEMICAL PROPERTIES*

 

o-Xylene

m-Xylene

p-Xylene

CAS number:

1330–20–7

1330–20–7

1330–20–7

Chemical formula:

C6H4(CH3)2

 

C6H4(CH3)2

C6H4(CH3)2

Molecular weight:

106.16

106.16

106.16

Boiling point (760 mm Hg):

144.411°C

139.103° C

138.351°C

Freezing point:

−25.182°C

−47.872°C

13.263°C

Density (25°C):

0.87596 g/ml

0.85990 g/ml

0.85669 g/ml

Vapor density (air=1):

3.7

3.7

3.7

Flash point (closed cup):

17.2°C

25°C

25°C

Vapor pressure (25°C, 760 mm Hg):

6.6

8.39

8.87

Conversion factors for three isomeric xylenes:

1 ppm=4.34 mg/m3

1mg/m3 =0.23 ppm

 

 

General characteristics:

Clear flammable liquid; aromatic hydrocarbon odor; commercial form is mixture of three isomers, with meta form usually principal component; insoluble in water; miscible with organic solvents

OCCURRENCE AND USE

The xylenes are major commodity chemicals in this country and around the world. The National Research Council report The Alkyl Benzenes (1981) showed that in the United States the annual production of xylenes over the last decade averaged approximately 2.7 million metric tons; about 15.3 million metric tons has been used per year by the chemical industries. Because of the impetus to remove lead from gasoline and the excellent antiknock properties of these compounds, they are found in increasing concentrations in gasoline. In a gasoline sample reported in the NRC document, m- and p-xylenes constituted 6.73% and o-xylene 2.86% by weight. Reports on the use of these compounds in solvents have suggested that as much as 500,000 metric tons of xylenes is used for this purpose per year. Because of their high volatility and ubiquitous use, these compounds pervade the environment; one result is extensive human exposure. Xylenes are monitored as possible contaminants of submarine atmosphere.

*  

Adapted from NRC, 1980.



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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 XYLENE BACKGROUND INFORMATION PHYSICAL AND CHEMICAL PROPERTIES*   o-Xylene m-Xylene p-Xylene CAS number: 1330–20–7 1330–20–7 1330–20–7 Chemical formula: C6H4(CH3)2   C6H4(CH3)2 C6H4(CH3)2 Molecular weight: 106.16 106.16 106.16 Boiling point (760 mm Hg): 144.411°C 139.103° C 138.351°C Freezing point: −25.182°C −47.872°C 13.263°C Density (25°C): 0.87596 g/ml 0.85990 g/ml 0.85669 g/ml Vapor density (air=1): 3.7 3.7 3.7 Flash point (closed cup): 17.2°C 25°C 25°C Vapor pressure (25°C, 760 mm Hg): 6.6 8.39 8.87 Conversion factors for three isomeric xylenes: 1 ppm=4.34 mg/m3 1mg/m3 =0.23 ppm     General characteristics: Clear flammable liquid; aromatic hydrocarbon odor; commercial form is mixture of three isomers, with meta form usually principal component; insoluble in water; miscible with organic solvents OCCURRENCE AND USE The xylenes are major commodity chemicals in this country and around the world. The National Research Council report The Alkyl Benzenes (1981) showed that in the United States the annual production of xylenes over the last decade averaged approximately 2.7 million metric tons; about 15.3 million metric tons has been used per year by the chemical industries. Because of the impetus to remove lead from gasoline and the excellent antiknock properties of these compounds, they are found in increasing concentrations in gasoline. In a gasoline sample reported in the NRC document, m- and p-xylenes constituted 6.73% and o-xylene 2.86% by weight. Reports on the use of these compounds in solvents have suggested that as much as 500,000 metric tons of xylenes is used for this purpose per year. Because of their high volatility and ubiquitous use, these compounds pervade the environment; one result is extensive human exposure. Xylenes are monitored as possible contaminants of submarine atmosphere. *   Adapted from NRC, 1980.

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 SUMMARY OF TOXICITY INFORMATION EFFECTS ON HUMANS Evidence of brain hemorrhages and axonic anoxia was observed in a person who died as a result of exposure to xylene at approximately 10,000 ppm over an 18-h period (Morley et al., 1970). In another case, a man was exposed at 60–350 ppm to mixed solvents containing 75% xylene and experienced giddiness, anorexia, and vomiting (Glass, 1961). In a similar report of exposure to a mixed solvent containing 80% xylene, a person who apparently suffered from latent epilepsy displayed seizures; that suggested that xylene might exacerbate seizures in susceptible people (Goldie, 1960). In each of these instances, either mixtures were involved or the extent of exposure was not well documented. Neither flicker fusion* nor reaction time was affected in 23 volunteers exposed at 100 or 200 ppm for 3–7 h (Ogata et al., 1970). In a similar study, Gusev (1968) reported changes in brain electric activity at 0.07 ppm, but not at 0.05 ppm. Fifteen male subjects were exposed to xylene vapor at approximately 100 or 300 ppm for 70 min (Gamberale et al., 1978). No noticeable change in test performance (numerical ability, reaction time, short-term memory, and critical flicker fusion) was seen. However, subjects exposed to xylene at 300 ppm for 70 min when the exposure period began with 30 min of exercise on a bicycle showed significant impairment of performance in tests for numerical ability, short-term memory, and choice reaction time. The difference was apparently due to an increase in the uptake of xylene in subjects that exercised during the first part of the exposure period. Savolainen et al. (1979b), Riihimaki and Savolainen (1980), and Savolainen et al. (1980) exposed six volunteers to m-xylene at 100 or 200 ppm, 6 h/d, 3 d/wk for 2 wk. In one part of the experiment, constant exposure concentrations were used; in another, the concentration was varied so that peak concentrations of 400 ppm were obtained. During the first week, significant increases in reaction time and some impairment of equilibrium were observed at 100 ppm, but these effects were transient, perhaps because tolerance developed. The effects reappeared during the second week at the higher concentration. No changes in manual dexterity or visual functions were observed. The authors suggested that light exercise reverses the effects of xylene. At 200–400 ppm, the report suggested, the subjects displayed decreased vigilance, as indicated by EEG changes. Carpenter et al. (1975) studied the odor threshold for mixed xylenes. They estimated it to be about 1 ppm. They suggested that discomfort and dizziness would ensue at 460 ppm and concluded that 110 ppm would be tolerable for working. *   Flicker fusion refers to the frequency at which a flickering light no longer appears to flicker.

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 EFFECTS ON ANIMALS Cameron et al. (1938) reported that, in rats and mice, the lethal doses by subcutaneous injection were 5–10 ml/kg for p- and m-xylenes and 2.5–5.0 ml/kg for o-xylene. The lethal doses by intraperitoneal injection were 2–2.5 ml/kg for p- and m-xylenes and 1.5–2 ml/kg for o-xylene. The acute LD50 in male rats receiving a single peroral administration of 95% pure xylene (19% o-, 52% m-, and 24% p-) was 4.3 g/kg (Wolf et al., 1956). The impurities were not identified. Repeated skin contact with the undiluted xylene solution led to erythema and slight necrosis in rabbits. Instillation into the rabbit eye led to conjunctival irritation and very slight, transient corneal injury. Exposure of rats and mice to o- and m-xylenes (separately) by inhalation at 2,000–3,000 ppm (8.7–13.0 g/m3) for 24 h resulted in deaths, and mice were reportedly more sensitive than rats to m-xylene (Cameron et al., 1938). Deaths were not observed in either rats or mice that had been exposed to o-xylene at 4,912 ppm (21.3 g/m3) for 24–28 h, but they did occur after exposure at 19,650 ppm (85.3 g/m3) for 12 h. Exposure of rats to the various pure isomers of xylene separately at 1,000–1,500 ppm (4.3–6.5 g/m3) 8 h/d for 14 d produced no deaths, and no specific organ changes were observed on autopsy. It should be noted that, generally, only small groups of animals were studied in this relatively early report, and the source and purity of the compounds used were not specified. In a later study (Carpenter et al., 1975), the LC50 in male rats for a 4-h inhalation exposure to a mixture of xylenes was 29 (22–37) g/m3. Pathologic findings in the 16 rats that died after exposure at 43 g/m3 included atelectasis, hemorrhage, and interlobular edema of the lung (two cases each). At concentrations as low as 5.8 g/m3, the investigators observed transient irritation, protraction of the eyes, and lack of coordination of the extremities. Rats exposed at 4 g/m3 displayed a slight loss of coordination by the second hour of exposure. No unusual effects were observed after exposures at approximately 2 g/m3. Respiratory-tract irritation, as evidenced by a decrease of 50% or more in respiratory rate, was observed in mice exposed at 5.6 g/m3 or more for 1 min. This did not occur at 2 g/m3 or during the 15-min period after exposure. Exposure of cats at 41 g/m3 for 2 h resulted in a classic nervous-system effect: the sequential development of salivation, ataxia, tonic and clonic spasms, anesthesia, and death. Pathologic examination revealed no lesions that were obviously related to the exposure. Dogs exposed at approximately 4 g/m3 experienced an increase in lacrimation that began after 1 h and persisted throughout the 4-h exposure period. LC50s of 5,267 ppm (22.8 g/m3) for m-xylene, 4,595 ppm (19.9 g/m3) for o-xylene, and 3,907 ppm (17 g/m3) for p-xylene were reported in mice (Bonnet et al., 1979). Carpenter et al. (1975) exposed 4 male beagles and 25 male rats at 3.5, 2.0, or 0.77 g/m3 or to control air 6 h/d, 5 d/wk, for up to 66 d. There was no evidence of toxicity of xylene.

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 Jenkins et al. (1970) exposed rats, guinea pigs, monkeys, and dogs to o-xylene at either 780 ppm (3358 mg/m3) for 8 h/d, 5 d/wk for 30 exposures or 78 ppm (389 mg/m3) continuously for 90 d. Mortality was 3 of 15 rats, none of 15 guinea pigs, none of 2 dogs, and 1 of 4 monkeys. One dog was tremulous and one rat died during the continuous exposure. Hematologic studies and evaluation of necropsy material did not show any effect of o-xylene. Male guinea pigs were given intraperitoneal injections of American Chemical Society reagent-grade xylene (isomer not specified) at 1,000 mg/kg (DiVincenzo and Krasavage, 1974). The investigators observed an increase in serum ornithine carbamoyl transferase, which is said to be an indicator of hepatocellular damage. Histologic examination revealed a moderate degree of hepatic lipid accumulation, but no tissue necrosis. After intraperitoneal injections at 2,000 mg/kg, three of four guinea pigs died. In behavioral studies, Battig and Grandjean (1964) failed to detect alterations in a conditioned-avoidance protocol with rats exposed to xylene by inhalation at 800 ppm initially and then 550–750 ppm for the balance of the 2.5-h exposure. Desi et al. (1967) injected xylene into rats at 0.02, 0.05, or 0.1 ml/100 g of body weight subcutaneously and compared them with control animals for ability to run a maze. Treatment continued for 28 d, after which the rats given the highest dose died. Other treated animals lost weight. The authors concluded that xylene prevents the acquisition of learned behavior, but does not facilitate loss of acquired behavior. The authors’ conclusions require substantiation. Carpenter et al. (1975) exposed rats to mixed xylenes at 2,800 ppm (12.2 g/m3 and reported irritation and prostration within 2–3 h. Exposure at 1,300 ppm (5.6 g/m3) led to ataxia. Exposure of dogs and rats at 580 ppm did not produce these effects. Batchelor (1927) had previously reported that exposure at 980 and 620 ppm (4.3 and 2.7 g/m3) caused no central effects. Lazarev (1929) reported that the production of narcosis in mice by o-, m-, and p-xylenes required 3,846, 1,923, and 7,885 ppm, (16.7, 8.3, and 34.2 g/m3), respectively. Intravenous infusion of a 10% solution of m-xylene (commercial-grade) as a lipid emulsion into rabbits produced a concentration of 30 ppm (0.130 g/m3) in blood and caused positional nystagmus, but no vestibular effects, at a steady-state blood content of 10 ppm (Aschan et al., 1977). Savolainen et al. (l979a) studied behavioral and neurochemical changes in young rats exposed to xylene at 300 ppm (1.3 g/m3) 6 h/d, 5 d/wk, for 5–18 wk with and without simultaneous ingestion of ethanol. Although the xylene alone had no behavioral effects, the mixed exposure resulted in increases in preening and ambulation, which suggested a synergistic effect; when ethanol was given alone, there was a transient decrease in preening. Minor changes in brain enzymes were observed, including an increase in superoxide dismutase activity after 14 wk of exposure to xylene alone and an increase in brain proteolytic activity in animals given both ethanol and xylene at 9–14 wk. There was no indication of a cause-effect relation between the enzyme changes and changes in preening and ambulation, nor was there evidence that these minor changes in enzyme activity constituted serious toxic impairment.

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 Savolainen and Pfaffli (1980) studied neurochemical changes in rat brain after inhalation of m-xylene at 48.8, 393, and 739 ppm (0.21, 1.7, and 3.2 g/m3) 6 h/d, 5 d/wk, for 2 wk. Xylene in brain and peripheral fat increased from the first to the second week. Brain content of NADPH diaphorase increased, whereas brain superoxide dismutase decreased. Biochemical analyses on rats withdrawn from exposure for 2 wk indicated that the biochemical effects were largely abolished within that time, although cerebral RNA was above the control value at the two higher exposures. The latter data disagree with the results of the earlier study, however, and the difference in duration of exposure may account for the discrepancy. The most important finding was the increase in brain RNA, which persisted after the termination of the treatment period. Andersson et al. (1981) exposed rats to commercial xylene and to its component o−, m−, and p-xylenes and ethylbenzene at 2,000 ppm (8.7 g/m3) 6 h/d for 3 d. Within 16–18 h after exposure stopped, they found increases in norepinephrine turnover in the hypothalamus caused by all the compounds and increases in dopamine in the median eminence of the forebrain caused by all but ethylbenzene and o-xylene. Ethylbenzene selectively reduced norepinephrine in the paraventricular region of the hypothalamus. Prolactin secretion was reduced by p- and o-xylenes. Although no overt behavioral signs were found in these experiments, the authors suggested that xylene (by disturbing dopamine neurotransmission) can produce motor disturbances and motivational deficits. A connection between the occurrence of sacral aplasia and occupational exposure to organic solvents has been demonstrated by Kucera (1968), who also observed a developmental malformation analogous to sacral aplasia in chick embryos treated with an unspecified concentration of xylene, which was positively correlated with time of exposure and negatively correlated with embryonic age. Krotov and Chebotar (1972) did not find any developmental defects in fetuses of rats that had inhaled xylene. Hudak and Ungvary (1978) evaluated the embryotoxic effects of xylene (a mixture of 10% o-xylene, 50% m-xylene, 20% p-xylene, and 20% ethylbenzene) at 230 ppm (1 g/m3) given by inhalation to rats for 24 h/d on days 1–21 of pregnancy. Untreated groups of animals that inhaled pure air served as controls. No evidence of teratogenicity was found, but skeletal anomalies (extra ribs and fused sternebrae) increased, although they were not significant (p < 0.05 for both). Mirkova et al. (1983) studied the effect of daily exposure (6 h/d, 5 d/wk) to xylene at 10, 50, and 500 mg/m3 on pregnant white Wistar rats during days 1 through 21 of gestation. The authors observed that concentrations of 50 and 500 mg/m3 exerted pronounced embryotoxic and teratogenic effects. Xylene increased the incidence of anomolies of internal organs (hydroephalus, microphthalmia, intracerebral hematomas and hemorrhages in the liver). It impaired the processes of ossification of sternum and skull. At concentrations of 50 and 500 mg/m3, xylene causes disturbances in postnatal development of the F1 generation. Xylene was not mutagenic in a battery of short-term tests: a test for mitotic gene conversion in yeast Saccharomyces cerevisiae D4, gene-mutation tests in bacteria (with Salmonella typhimurium strains TA 98, TA 100, TA 1535, TA 1537, and TA 1538) with and without activation,

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 and specific-locus forward-mutation Induction in the L5178Y thymidine kinase Fischer mouse lymphoma cell assay. Xylene did not produce significant Increases in chromosomal aberrations in rat bone marrow cells at 0.044, 0.157, and 0.441 ml/kg (Litton Bionetics, 1978). PHARMACOKINETICS All the xylene isomers enter the body rapidly by inhalation and less rapidly by absorption from the gastrointestinal tract (Gerarde, 1960) or through the skin (Dutkiewicz and Tyras, 1968). The blood-to-gas partition ratio for xylene has been calculated to be 29:1 (Astrand, 1975) and 42:1 (Sherwood, 1976). The rate at which xylene is absorbed through human skin that is immersed in liquid xylene has been estimated to be 4.5–9.6 mg/cm2 per hour (Dutkiewicz and Tyras, 1968). Xylene is distributed rapidly into all tissues of the body, especially into the adrenals, bone marrow, brain, spleen, and adipose tissue (Fabre et al., 1960). The pharmacokinetics of m-xylene in rats and mice fit a three-compartment model (Bergman, 1979), and more than 90% of an administered dose should be eliminated within 24 h (NRC, 1981). Comparable studies have not been conducted in humans, but Sedivec and Flek (1976) reported that only 5% of a dose of a mixture of xylenes was exhaled. Their finding that 95% of the urinary metabolites was excreted within 10 h indicates that the total body clearances of the xylenes are rather high. The xylenes undergo side-chain oxidation to methylbenzoic acids, which in turn are conjugated with glycine and excreted into urine as toluic acids in all mammals studied, including dogs, humans, rabbits, rats, and guinea pigs. In addition to side-chain oxidation, the xylenes undergo ring hydroxylation, but only to a minor extent (Bakke and Scheline, 1970). In rats, approximately 1% of a dose (100 mg/kg) of p-xylene was converted to 2,5-xylenol, 0.9% of m-xylene was converted to 2,4-xylenol, and 0.1% of o-xylenol was converted to 3,4-xylenol. Pretreatment of rats with phenobarbital or 3-methylcholanthrene markedly increased the activity of the hepatic enzyme that converts p-xylene to p-methylbenzyl alcohol, but did not alter the activity of the enzyme in the lungs (Harper et al., 1977). Patel et al. (1978, 1979) reported that pretreatment of mice with individual xylene isomers did not alter the activity of cytochrome P-450 in the liver. However, the administration of p-xylene to rabbits inactivated cytochrome P-450 in the lung. INHALATION EXPOSURE LIMITS The American Conference of Governmental Industrial Hygienists (1980, 1983) recommended a TLV-TWA of 100 ppm and a 15-min TLV-STEL of 150 ppm. It believed that irritant effects will be minimal, and that no substantial degree of narcosis or chronic injuries will result from continued occupational exposure at 100 ppm. OSHA (1983) recommended a PEL of 100 ppm. Other recommendations were as follows: ANSI (1970), 100 ppm; West Germany (1974), 200 ppm; Sweden (1975), 100 ppm; Czechoslavakia (1969) and East Germany (1973), 45 ppm; and USSR (1972), 11 ppm (ACGIH, 1980).

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 COMMITTEE RECOMMENDATIONS The Committee on Toxicology suggested limits for exposure to xylene in 1966: a 60-min EEL of 200 ppm, a 24-h EEL of 100 ppm, and a 90-d CEL of 50 ppm. The Committee on Alkyl Benzene Derivatives (NRC, 1981) reviewed the toxicologic data on xylene and included the following statement in its report: The acute toxicity of the xylenes predominantly reflects effects on the central nervous system similar to those produced by other alkyl benzenes and related compounds. Irritant effects on mucous membranes have been reported, particularly upon direct contact. There is negligible evidence of acute or chronic effects in organ systems other than the central nervous system. Xylene is a major commodity solvent and component of gasoline, and the potential for human exposure is large. The major effects are on the central nervous system and appear to be reversible. There is no indication of genetic toxicity or carcinogenesis. The lowest doses at which any biologic effects have been observed in humans were reported by Ogata et al. (1970) and Gusev (1968), who detected changes in electric activity of brain in humans exposed at 0.05–0.07 ppm. These changes were not related to any functional impairment. Although Savolainen et al. (1979b), Riihimaki and Savolainen (1980), and Savolainen et al. (1980) described changes in psychophysiologic functions, such as reaction time and body balance, that were also accompanied by EEC changes in humans exposed to xylene at 90–200 ppm, one of the authors (Seppolainen, personal communication) has questioned the wisdom of using these results to set exposure limits. Chronic exposure does not seem to increase sensitivity to these effects. The available evidence does not warrant revision of the exposure limits recommended in 1966. The present Committee’s recommended EELs and CEL for xylene and the limits proposed in 1966 are shown below.   1966 1984 60 min EEL 200 ppm 200 ppm 24-h EEL 100 ppm 100 ppm 90-d CEL 50 ppm 50 ppm

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 REFERENCES American Conference of Governmental Industrial Hygienists. 1980. Trichlorofluoromethane. Documentation of the Threshold Limit Values. 4th ed. Cincinnati, Ohio: American Conference of Governmental Industrial Hygienists. p. 439–440. American Conference of Governmental Industrial Hygienists. 1983. TLVs(R): Threshold Limit Values for Chemical Substances and Physical Agents in the Work Environment with Intended Changes for 1983–1984. Cincinnati, Ohio: American Conference of Governmental Industrial Hygienists. 93 p. American Petroleum Institute. 1978. Mutagenicity Evaluation of Xylene. Washington, D.C.: American Petroleum Institute. Med. Res. Publ. 26–60018. 150 p. Andersson, K., Fuxe, K., Nilsen, O.G., Toftgård, R., Eneroth, P., and Gustafsson, J-A. 1981. Production of discrete changes in dopamine and noradrenaline levels and turnover in various parts of the rat brain following exposure to xylene, ortho-, meta-, and para-xylene, and ethylbenzene. Toxicol. Appl. Pharmacol. 60:535–548. Aschan, G., Bunnfors, I. Hydén, D., Larsby, B., Odkvist, L.M. and Tham, R. 1977. Electronystagmographic and gas chromatographic studies in rabbits. Acta Otolaryngol. 84:370–376. Åstrand, I. 1975. Uptake of solvents in the blood and tissues of man: A review. Scand. J. Work Environ. Health 1:199–218. Bakke, O.M., and Scheline, R.R. 1970. Hydroxylation of aromatic hydrocarbons in the rat. Toxicol. Appl. Pharmacol. 16:691–700. Batchelor, J.J. 1927. The relative toxicity of benzol and its higher homologues. Am. J. Hyg. 7:276–298. Battig, K., and Grandjean, E. 1964. Industrial solvents and avoidance conditioning in rats. A comparison of the effects of acetone, ethyl alcohol, carbon disulfide, carbon tetrachloride, toluene, and xylene on acquisition and extinction. Arch. Environ. Health 9:745–749. Bergman, K. 1979. Whole-body autoradiography and allied tracer techniques in distribution and elimination studies of some organic solvents: Benzene, toluene, xylene, styrene, methylene chloride, chloroform, carbon tetrachloride and trichloroethylene. Scand. J. Work Environ. Health 5(Suppl 1):1–263. Bonnet, P., Raoult, G., and Gradiski, D. 1979. Lethal concentration of 50 main aromatic hydrocarbons. Arch. Mal. Prof. Med. Trav. Secur. Soc. 40:805–810. (in French)

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 Cameron, G.R., Paterson, J.L.H., DeSaram, G.S.W., and Thomas, J.C. 1938. The toxicity of some methyl derivatives of benzene with special reference to pseudocumene and heavy coal tar naphtha. J. Pathol. Bacteriol. 46:95–107. Carpenter, C.P., Kinkead, E.R., Geary, D.L., Jr., Sullivan, L.J., and King, J.M. 1975. Petroleum hydrocarbon toxicity studies. V. Animal and human response to vapors of mixed xylenes. Toxicol. Appl. Pharmacol. 33:543–558. Dési, I., Kovács, F., Zahumenszky, Z., and Balogh, A. 1967. Maze learning in rats exposed to xylene intoxication. Psychopharmacologia 11:224–230. DiVincenzo, G.D., and Krasavage, W.J. 1974. Serum ornithine carbamyl transferase as a liver response test for exposure to organic solvents. Am. Ind. Hyg. Assoc. J. 35:21–29. Dutkiewicz, T., and Tyras, H. 1968. Skin absorption of toluene, styrene, and xylene by man. Br. J. Ind. Med. 25:243. Fabre, R., Truhaut, R., and Laham, S. 1960. Recherches sur le métabolisme comparé des xylènes ou dimethylbenzènes. Arch. Mal. Prof. Med. Trav. Secur. Soc. 21:314–328, (in French) Gamberale, F., Annwall, G., and Hultengren, M. 1978. Exposure to xylene and ethylbenzene. III. Effects on central nervous functions. Scand. J. Work Environ. Health 4:204–211. Gerarde, H.W. 1960. Toxicology and Biochemistry of Aromatic Hydrocarbons. New York: Elsevier Publishing Co. 329 p. Glass, W.I. 1961. Annotation: A case of suspected xylol poisoning. N.Z.Med. J. 60:113. Goldie, I. 1960. Can xylene (xylol) provoke convulsive seizures? Ind. Med. Surg. 29:33–35. Gusev, I.S. 1968. Comparative toxicity studies of benzene, toluol, and xylol by the reflex activity method. Pp. 60–67 in Levine, B.S., U.S.S.R. Literature on Air Pollution and Related Occupational Diseases. Volume 17. Springfield, VA.: National Technical Information Service. PB-180 522-T. Harper, C., Drew, R.T., and Fouts, J.R. 1977. Benzene and p-xylene: A comparison of inhalation toxicities and in vitro hydroxylations. Pp. 302–311 in Jollow, D.J., Kocsis, J.J., Snyder, R., and Vainio, H., eds. Biological Reactive Intermediates: Formation, Toxicity, and Inactivation. Proceedings of an International Conference on Active Intermediates: Formation, Toxicity, and Inactivation, held at the University of Turku, Turku, Finland, July 26–27, 1975. New York: Plenum Press.

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 Hudák, A., and Ungváry, G. 1978. Embryotoxic effects of benzene and its methyl derivatives: Toluene, xylene. Toxicology 11:55–63. Jenkins, L.J., Jr., Jones, R.A., and Siegel, J. 1970. Long-term inhalation screening studies of benzene, toluene, o-xylene, and cumene on experimental animals. Toxicol. Appl. Pharmacol. 16:818–823. Krotov, Yu.A., and Chebotar, N.A. 1972. Embryotoxic and teratogenic action of some industrial substances formed during production of dimethyl terephthalate. Gig. Tr. Prof. Zabol. 16(6):40–43. Kucera, J. 1968. Exposure to fat solvents: A possible cause of sacral agenesis in man. J. Pediatr. 72:857–859. Lazarev, N.W. 1929. Toxicity of various hydrocarbon vapors. Arch. Exp. Pathol. Pharmakol. 143:223–233. Mirkova, E., Zaikov C., Antov, G., Mikhailova, A., Khinkova, L., and Benchev, I. 1983. Prenatal toxicity of xylene. J. Hyg. Epidemiol. Microbiol. Immunol. 27:337–343. Morley, R., Eccleston, D.W., Douglas, C.P., Greville, W.E.J., Scott, D.J., and Anderson, J. 1970. Xylene poisoning: A report on one fatal case and two cases of recovery after prolonged unconsciousness. Br. Med. J. 3:442–443. National Research Council. 1980 The Alkyl Benzenes. Washington, D.C.: National Academy Press. 384 p. Ogata, M., Tomokuni, K., and Takatsuka, Y. 1970. Urinary excretion of hippuric acid and m− or p−methylhippuric acid in the urine of persons exposed to vapours of toluene and m− and p-xylene as a test of exposure. Br. J. Ind. Med. 27:43–50. Patel, J.M., Harper, C., and Drew, R.T. 1978. The biotransformation of p-xylene to a toxic aldehyde. Drug Metab. Dispos. 6:368–374. Patel, J.M., Wolf, C.R., and Philpot, R.M. 1979. Interaction of 4-methylbenzaldehyde with rabbit pulmonary cytochrome P-450 in the intact animal, microsomes, and purified systems. Destructive and protective reactions. Blochem. Pharmacol. 28:2031–2036. Riihimaki, V., and Savolainen, K. 1980. Human exposure to m-xylene. Kinetics and acute effects on the central nervous system. Ann. Occup. Hyg. 23:411–422. Savolainen, H., Pfaffli, P., Helojoki, M., and Tengén, M. 1979a. Neurochemical and behavioural effects of long-term intermittent inhalation of xylene vapour and simultaneous ethanol intake. Acta Pharmacol. Toxicol. 44:200–207.

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2 Savolainen, H., Riihimaki, V., and Linnoila, M. 1979b. Effects of short-term xylene exposure on psychophysiological functions in man. Int. Arch. Occup. Environ. Health 44:201–211. Savolainen, H., Riihimaki, V., Seppäläinen, A.M., and Linnoila, M. 1980. Effects of short-term m-xylene exposure and physical exercise on the central nervous system. Int. Arch. Occup. Environ. Health 45:105–121. Savolainen, H., and Pfaffli, P. 1980. Dose-dependent neurochemical changes during short-term inhalation exposure to m-xylene. Arch. Toxicol. 45:117–122. Sedivec, V., and Flek, J. 1976. The absorption, metabolism, and excretion of xylenes in man. Int. Arch. Occup. Environ. Health 37:205–217. Sherwood, R.J. 1976. Ostwald solubility coefficients of some industrially important substances. Br. J. Ind. Med. 33:106–107. Wolf, M.A., Rowe, V.K., McCollister, D.D., Hollingsworth, R.L., and Oyen, F. 1956. Toxicological studies of certain alkylated benzenes and benzene. Experiments on laboratory animals. AMA Arch. Ind. Health 14:387–398.

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