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Trichloroethylene, occupational exposure

The Occupational Exposure Standards imposed for trichloroethylene are Maximum Exposure Limits of 100 ppm (8 hr TWA) and 150 ppm (15 minute reference period). A skin notation Sk is applicable because of the potential for skin absorption. Because of its volatility, trichloroethylene is not recommended for cold cleaning it is normally used in partially enclosed vapour degreasing equipment provided with local exhaust ventilation. [Pg.141]

Trichloroethylene levels in the workplace are regulated by the Occupational Safety and Health Administration (OSHA). The occupational exposure limit for an 8-hour workday, 40-hour workweek, is an average concentration of 100 ppm in air. The 15-minute average exposure in air that should not be exceeded at any time during a workday is 300 ppm. The OSHA standards are based on preventing central nervous system effects after trichloroethylene exposure. For more information, see Chapter 7. [Pg.20]

Dermal Effects. Humans that were experimentally exposed to 200 ppm of trichloroethylene vapor for 7 hours experienced dry throats (40% of the subjects), begiiming after 30 minutes (Stewart et al. 1970). The subjects experiencing these symptoms did not experience them when exposed in the same manner on 5 other consecutive days. These effects are presumed to be due to direct contact with the vapor. Skin irritation and rashes have resulted from occupational exposure to trichloroethylene (Bauer and Rabens 1974 El Ghawabi et al. 1973). The dermal effects are usually the consequence of direct skin contact with concentrated solutions, but occupational exposure also involves vapor contact. Adverse effects have not been reported from exposure to dilute aqueous solutions. [Pg.46]

In studies designed to examine dermal absorption of trichloroethylene, emersion of the hand (Sato and Nakajima 1978) or thumb (Stewart and Dodd 1964) for 30 minutes was reported to be pairrful. The pain was described as excruciating in one study (Sato and Nakajima 1978), and in another study it was described as mild by one subject and moderately severe by two subjects (Stewart and Dodd 1964). Occupational exposure to trichloroethylene that involved both dermal and inhalation exposure has been reported to result in dizziness, headache, insomnia, lethargy, forgetfulness, and loss of feeling in the hands and feet (Bauer and Rabens 1974 Kohlmuller and Kochen 1994). [Pg.108]

Cardiovascular Effects. Chronic cardiovascular disease has not been reported in workers occupationally exposed to low levels of trichloroethylene (El Ghawabi et al. 1973), although deaths following acute high-level inhalation exposures to trichloroethylene have been attributed to cardiac arrhythmias. Case studies have described cardiac arrhythmias that in some instances led to death after occupational exposure (Bell 1951 Kleinfeld and Tabershaw 1954 Smith 1966), poisoning (Dhuner et al. 1957 Gutch et al. 1965), or... [Pg.142]

Gastrointestinal Effects. Case reports indicate that acute inhalation exposure to trichloroethylene results in nausea and vomiting (Buxton and Hayward 1967 Clearfield 1970 David et al. 1989 DeFalque 1961 Gutch et al. 1965 Milby 1968). Anorexia, nausea, vomiting, and intolerance to fatty foods have also been reported after chronic occupational exposure to trichloroethylene (El Ghawabi et al. 1973 Schattner and Malnick 1990 Smith 1966). Trichloroethylene-induced efiects on the autonomic nervous system may contribute to these effects (Grandjean et al. 1955). Some of the people exposed to trichloroethylene and other chlorinated... [Pg.143]

The National Occupational Exposure Survey (NOES), conducted by NIOSH from 1981 to 1983, estimated that 401,000 workers employed at 23,225 plant sites were potentially exposed to trichloroethylene in the United States (NOES 1990). The NOES database does not contain information on the frequency, concentration, or duration of exposures the survey provides only estimates of workers potentially exposed to chemicals in the workplace. [Pg.222]

Workers involved in the manufacture or use of trichloroethylene as a metal degreaser or general solvent may constitute a group at risk because of the potential for occupational exposure. Occupational exposure to trichloroethylene may also occur during its use as a chemical intermediate in the production of polyvinyl chloride (McNeill 1979). [Pg.223]

Conde-Salazar L, Guimaraens D, Romero LV, et al. 1983. Subcorneal pustular eruption and erythema from occupational exposure to trichloroethylene. Contact Dermatitis 9 235-237. [Pg.258]

Corbett TH, Hamilton GC, Yoon MK et al. 1973. Occupational exposure of operating room persoimel to trichloroethylene. Canad Anaesth Soc J 20 675-678. [Pg.258]

Nagaya T, IshikawaN, Hata H, et al. 1993. Subclinical and reversible hepatic effects of occupational exposure to trichloroethylene. Int Arch Occup Environ Health 64 561-563. [Pg.281]

Nakayama H, Kobayashi M, Takahashi M, et al. 1988. Generalized eruption with severe liver dysfunction associated with occupational exposure to trichloroethylene. Contact Dermatitis 19 48-51. [Pg.281]

N10SH. 1973. Criteria for a recommended standard.Occupational exposure to trichloroethylene. Cincinnati, OH U S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health. [Pg.282]

Schuttmann W. 1970. [Liver damage after occupational exposure to trichloroethylene.] DtschZVerdau Stoffwechselkr 30 43-45. (German)... [Pg.289]

Shipman AJ, Whim BP. 1980. Occupational exposure to trichloroethylene in metal cleaning processes and to tetrachloroethylene in the drycleaning industry in the U K. Ann Occup Hyg 23 197-204. [Pg.290]

Skender LJ, Karacic V, Prpic-Majic D. 1991. A comparative study of human levels of trichloroethylene and tetrachloroethylene after occupational exposure. Arch Environ Health 46 174-178. [Pg.290]

Weiss NS. 1996. Cancer in relation to occupational exposure to trichloroethylene. Occup Environ Med 53 1-5. [Pg.296]

The interaction of /2-hexane with toluene and trichloroethylene has also been examined in volunteers (Baelum et al. 1998). Exposure in these experiments was via a gastric feeding tube at controlled rates equivalent to what the authors stated would be delivered to the liver by inhalation exposure at Danish occupational exposure limits (50 ppm /7-hexane. 50 ppm toluene, and 30 ppm trichloroethylene). Coexposure to toluene and trichloroethylene slightly increased the area under the curve (AUC) representing concentration versus time for end exhaled /2-hexane air concentration, but urinary excretion of 2,5-hexanedione was unchanged. The only statistically significant interaction observed with /2-hexane was an 18% decrease in the urinary excretion of hippuric acid, a toluene metabolite. [Pg.154]

National Institute for Occupational Safety and Health Criteria for a Recommended Standard. .. Occupational Exposure to Trichloroethylene. DHEW (NIOSH) Pub No (HSM) 73-11025, pp 15 K). Washington, DC, US Government Printing Office, 1976... [Pg.697]

NIOSH Criteria for a Recommended Standard "Occupational Exposure to Vinyl Halides," USDHEW/PHS/CDC/NIOSH (1978). NIOSH, Current Intelligence Bulletin. "Trichloroethylene (TCE)," p. 1, DHEW/PHS/CDC (June 6. 1975). 8 pp. 18 ref. [Pg.449]

The potential for unusual health effects of chemical mixtures due to the interaction of chemicals or their metabolites (e.g., metabolites of trichloroethylene and benzene) in or with the biosystem constitutes a real issue in the public health arena. However, toxicity testing to predict effects on humans has traditionally studied one chemical at a time for various reasons convenient to handle, physiochemical properties readily defined, dosage could easily be controlled, biologic fate could easily be measured, and relevant data were often available from human occupational exposures. Chemicals are known to cause disease for example, arsenic and skin cancer, asbestos and lung cancer, lead and decrements of IQ, and hepatitis B predisposes to aflatoxin-induced liver cancer but the link between the extent of human exposure to even well-defined chemical mixtures and disease formation remains relatively unexplored, but of paramount importance to public health. [Pg.1438]

Extended exposure (e.g., occupational exposure) to a chlorinated solvent like trichloroethylene typically... [Pg.2774]

Extrapolation to a practical threshold or subthreshold dose, such as the determination of a reference dose [RfD, e.g., EPA s perchlorate (ERA 2009b)] or tolerable daily intake [TDl, e.g.. The Netherlands s National Institute for Public Health and the Environment or RIVM s trichloroethylene (RIVM 2009)], or development of health-based occupational exposure limits by many gronps [e.g., American Conference of Governmental Industrial Hygienists (ACGIH 2006)]. [Pg.616]

EXPOSURE ROUTES inhalation ingestion eye contact skin contact and adsorption drinking contaminated water occupational exposure automobile exhaust atmospheric decomposition of trichloroethylene... [Pg.271]

A retrospective cohort study of 14,457 aircraft maintenance woikers at Hill Air Force Base, Utah, was undertaken by Spirtas et al. (1991) to determine if occupational exposure to over 20 solvents, including trichloroethylene and tetrachloroethylene, posed an increased risk of mortality. Deaths due to multiple myeloma or non-Hodgkin s lymphoma were elevated in female woikers exposed to tetrachloroethylene for at least 1 year. However, confidenee in these data is low primarily beeause multiple and overlapping exposure to more than one chemieal was considerable. In addition, the levels of tetrachloroethylene to which the workers were exposed were not provided, and lifestyle factors such as smoking and alcohol consumption were not assessed. [Pg.68]

Several methods are available for the analysis of tetrachloroethylene in biological media. The method of choice depends on the nature of the sample matrix required precision, accuracy, and detection limit cost of analysis and turnaround time of the method. Since tetrachloroethylene is metabolized in the human body to trichloroacetic acid (TCA), TCA may be quantified in blood and urine as an indirect measure of tetrachloroethylene exposure (Monster et al. 1983). It should be pointed out that the determination of TCA may not provide unambiguous proof of tetrachloroethylene exposure since it is also a metabolite of trichloroethylene. Trichloroethanol has also been thought to be a metabolite of tetrachloroethylene, identified following occupational exposure (Bimer et al. 1996 Ikeda et al. 1972 Monster et al. 1983). However, rather than being a metabolite of tetrachloroethylene, it is more likely that trichloroethanol is formed from trichloroethylene, which is often found as a contaminant of tetrachloroethylene (Skender et al. 1991). Methods for the determination of trichloroethylene and trichloroethanol are summarized in the Toxicological Profile for Trichloroethylene (ATSDR 1993). [Pg.219]


See other pages where Trichloroethylene, occupational exposure is mentioned: [Pg.40]    [Pg.41]    [Pg.42]    [Pg.49]    [Pg.51]    [Pg.60]    [Pg.107]    [Pg.167]    [Pg.184]    [Pg.444]    [Pg.80]    [Pg.31]    [Pg.1216]    [Pg.882]    [Pg.244]    [Pg.449]    [Pg.1342]    [Pg.3006]    [Pg.784]    [Pg.63]    [Pg.208]    [Pg.655]   
See also in sourсe #XX -- [ Pg.963 ]

See also in sourсe #XX -- [ Pg.963 ]




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Occupational exposure

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