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Trichloroethylene studies

Testing effects of chloral after pretreatment with trichloroethylene Study involves use of metabolic activators. [Pg.158]

Trichloroethylene is acutely toxic, primarily because of its anesthetic effect on the central nervous system. Exposure to high vapor concentrations is likely to cause headache, vertigo, tremors, nausea and vomiting, fatigue, intoxication, unconsciousness, and even death. Because it is widely used, its physiological effects have been extensively studied. [Pg.25]

It is estimated that concentrations of 3000 ppm cause unconsciousness in less than 10 minutes (39). Anesthetic effects have been reported at concentrations of 400 ppm after 20-min exposure. Decrease in psychomotor performance at a trichloroethylene concentration of 110 ppm has been reported in one study (33), whereas other studies find no neurotoxic effects at concentrations of 200 ppm (40—43). [Pg.25]

Efforts to identify the specific compounds responsible for the psychotropic effects of volatile solvents are complicated by the fact that many of these products contain more than one potentially psychoactive ingredient. Another factor obscuring the identity of the psychoactive ingredients of these agents is that patients addicted to these compounds frequendy seek the effects not of the product s primary ingredient but of a secondary ingredient such as the propellant gas (e.g., nitrous oxide). To date, the best-studied psychoactive compounds identified in volatile solvents include toluene, 1,1,1-trichloroethane, and trichloroethylene. However, other less well studied compounds, such as benzene, acetone, and methanol, also appear to have significant psychoactive effects. [Pg.272]

Although catalytic wet oxidation of acetic acid, phenol, and p-coumaric acid has been reported for Co-Bi composites and CoOx-based mixed metal oxides [3-5], we could find no studies of the wet oxidation of CHCs over supported CoO catalysts. Therefore, this study was conducted to see if such catalysts are available for wet oxidation of trichloroethylene (TCE) as a model CHC in a continuous flow fixal-bed reactor that requires no subsequent separation process. The supported CoOx catalysts were characterized to explain unsteady-state behavior in activity for a certain hour on stream. [Pg.305]

In another study of trichloroethylene exposure from well water, increased numbers of children... [Pg.17]

A study in Massachusetts found that exposure was associated with leukemia in children. In studies with people, there are many factors that are not fully understood. More studies need to be done to establish the relationship between exposure to trichloroethylene and cancer. [Pg.18]

The primary purpose of this chapter is to provide public health officials, physicians, toxicologists, and other interested individuals and groups with an overall perspective on the toxicology of trichloroethylene. It contains descriptions and evaluations of toxicological studies and epidemiological investigations and provides conclusions, where possible, on the relevance of toxicity and toxicokinetic data to public health. [Pg.22]

Musculoskeletal Effects. No studies were located regarding musculoskeletal effects in humans after inhalation exposure to trichloroethylene. Trichloroethylene exposure can result in nervous system effects that result in secondary effects on muscle strength, especially in the face (Leandri et al. 1995). See Section 2.2.1.4 for further discussion of nervous system effects following trichloroethylene exposure. [Pg.42]

Inhalation of trichloroethylene for acute or intermediate periods can cause liver enlargement in laboratory animals. Usually this effeet is reversible when exposure eeases. Histological changes were observed in some studies but not in others. Liver weight and plasma butyryleholinesterase (BuChE) aetivity were increased in various strains of mice exposed to 37-300 ppm eontinuously for 30 days (Kjellstrand et al. 1983a, 1983b). [Pg.44]

Renal Effects. Triehloroethylene may have effeets in the kidney however, studies in humans are limited by having poor or no exposure data and by concomitant exposure to other chemicals. There was no evidence of kidney damage in 250 neurosurgery patients who underwent prolonged trichloroethylene anesthesia (Brittain 1948), nor in 405 women who had caesarean sections and were exposed to trichloroethylene anesthesia (Crawford and Davies 1975). [Pg.45]

Endocrine Effects. No studies were located regarding endocrine effects in humans after inhalation exposure to trichloroethylene. [Pg.46]

Stevens-Johnson syndrome, a severe erythema, was seen in five people occupationally exposed to trichloroethylene for 2-5 weeks at levels ranging from 19 to 164 ppm (Phoon et al. 1984). The study authors suggested that the erythema was caused by a hypersensitivity reaction to trichloroethylene. An exfoliative dermatitis (Goh and Ng 1988) and scleroderma (Czirjak et al. 1993), also thought to have an immune component, have been reported in persons occupationally exposed to trichloroethylene. [Pg.46]

Experimental exposure studies have attempted to associate various neurological effects in humans with specific trichloroethylene exposure levels. Voluntary exposures of 1 hours resulted in complaints of drowsiness at 27 ppm and headache at 81 ppm (Nomiyama and Nomiyama 1977). These are very low exposure levels, but the results are questionable because of the use of only three test subjects per dose, lack of statistical analysis, sporadic occurrence of the effects, lack of clear dose-response relationships, and discrepancies between the text and summary table in the report. Therefore, this study is not presented in Table 2-1. No effects on visual perception, two-point discrimination, blood pressure, pulse rate, or respiration rate were observed at any vapor concentration in this study. Other neurobehavioral tests were not performed, and the subjects were not evaluated following exposure. [Pg.48]

Effects noted from exposures of 2-2.5 hours at 1,000 ppm include impaired visual-motor coordination (measured by groove-type hand steadiness, depth perception, and pegboard tests) (Vernon and Ferguson 1969) and, at 200 ppm, an increase in heart and breathing rates when trichloroethylene was inhaled simultaneously with ethanol ingestion (Windemuller and Ettema 1978). This latter study found no effect without ethanol ingestion. An 8-hour exposure (two 4-hour exposures separated by 1.5 hours) to 110 ppm... [Pg.48]

A study that examined the interaction between exposure concentration and time of exposure on nervous system function found that concentration, rather than time of exposure, was more important in determining effects (Bushnell 1997). Rats were trained to press two levers for food reward one lever when a light flashed, the second lever produced food when there was no signal. The trained rats were exposed to 0,400, 800, 1,200, 1,600,2,000, or 2,400 ppm trichloroethylene for 0.33, 0.67, or 1 hour. Response times were signiflcantly increased only at 2,400 ppm at 0.67 and 1 hour. Sensitivity was significantly decreased at 2,400 ppm at all exposure times. At 0.33 hour, sensitivity was not affected at the other concentrations. At 0.67 hour, sensitivity was significantly decreased at 2,000, and 1,200 ppm, and at 1 hour, sensitivity was... [Pg.52]

After 10 days of exposure, reduced social behavior and reduced exploratory behavior were observed in rats exposed to 100 ppm trichloroethylene 6 hours per day 5 days per week for a total of 5 weeks (Silverman and Williams 1975). In rats exposed to 50 or 100 ppm trichloroethylene 8 hours/day, 5 days/week for 6 weeks, effects on sleep patterns were observed (Arito et al. 1994a). At 50 ppm decreased wakefulness was observed during the exposure. Effects remaining at 22 hours after the end of the 6-week exposure included decreased heart rate during sleep at 50 ppm and decreased wakefulness after exposure of 100 ppm (Arito et al. 1994a). Based on the 50-ppm LOAEL identified in the Arito et al. (1994a) study, an intermediate-duration inhalation MRL of 0.1 ppm was calculated as described in the footnote in Table 2-1. [Pg.53]

An increased level of exploratory activity immediately after exposure, attributed to reduced anxiety on the part of the rats, was also observed in this study. Decreased avoidance was observed in rats exposed to 125 ppm trichloroethylene 4 hours per day, 5 days per week for 30 days (Goldberg et al. 1964a). Changes in visually evoked potentials (Blain et al. 1992) and electroretinal responses to flash stimulation (Blain et al. 1994) were seen in rabbits exposed to 350 ppm trichloroethylene for 12 weeks (4 days/week, 4 hours/day). The study authors suggested that binding of trichloroethanol to blood proteins may enable it to reach the visual cortex. [Pg.54]

A retrospective case-control study conducted in humans compared spontaneous abortion rates among women who had been exposed occupationally or nonoccupationally to trichloroethylene and other solvents to rates among women without solvent exposure (Windham et al. 1991). The authors observed approximately three times the risk of spontaneous abortion with exposure to trichloroethylene. This risk increased further when women with less than a half hour of exposure to trichloroethylene each week were excluded from the analysis. However, a consistent dose-response relationship was not observed, and most of the women were exposed to a variety of solvents, not just trichloroethylene. [Pg.55]

Mice exposed to 2,000 ppm of trichloroethylene, 4 hours/day for a 5-day period, had a significant increase in abnormal sperm morphology of 1% 28 days after the exposure (Land et al. 1981). No effect was seen at 200 ppm. A 6% increase in abnormal sperm was observed 4 weeks, but not 4 days or 10 weeks, after mice were exposed to 100 ppm trichloroethylene 7 hours per day for 5 days (Beliles et al. 1980). Based on the time after exposure at which sperm were affected, the study authors indicated that trichloroethylene damages sperm precursor cells but that spermatogonia were either unaffected or were capable of recovery. Reproductive performance was not tested in these studies. Another mouse study tested the effects of a 5-day exposure (6 hours/day) on spermatid micronuclei frequency no effects were observed at exposure levels of up to 500 ppm, the highest concentration tested (Allen et al. 1994). These results were interpreted as evidence that trichloroethylene did not cause meiotic chromosome breakage or loss. No treatment-related reproductive effects were seen in female rats exposed to 1,800 ppm trichloroethylene for 2 weeks (6 hours/day, 7 days/week) before mating (Dorfmueller et al. 1979). [Pg.55]


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