System trichloroethylene

Of the solvent systems, trichloroethylene is the most efficient. The inserts are first tumbled in the solvent to remove the majority of the organic contaminants. To obtain a surface that is free from oils and grease, a vapour phase degrease is then used. When the inserts are flooded with vapour, the solvent immediately begins to condense on the insert surface and then run off, carrying with it in solution the last traces of organic contaminants. The volume of condensate, per insert, depends on ... 

Goh and Ng (1988) reported of a patient with recurrent localized erythematous xerotic plaques, which became parched and fissured on the arms and trunk of a patient with trichloroethylene. Biopsy showed superficial perivascular lymphohistiocytic infiltrate. The epidermis shows parakeratosis. The route of entry of trichloroethylene was from the respiratory tract and it was believed to be a form of systemic trichloroethylene toxicity in a sensitized individual. 

AH volatile organic solvents are toxic to some degree. Excessive vapor inhalation of the volatile chloriaated solveats, and the central nervous system depression that results, is the greatest hazard for iadustrial use of these solvents. Proper protective equipment and operating procedures permit safe use of solvents such as methylene chloride, 1,1,1-trichloroethane, trichloroethylene, and tetrachloroethylene ia both cold and hot metal-cleaning operations. The toxicity of a solvent cannot be predicted from its chlorine content or chemical stmcture. For example, 1,1,1-trichloroethane is one of the least toxic metal-cleaning solvents and has a recommended threshold limit value (TLV) of 350 ppm. However, the 1,1,2-trichloroethane isomer is one of the more toxic chloriaated hydrocarboas, with a TLV of only 10 ppm. 

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. 

Halogenated hydrocarbons depress cardiac contractility, decrease heart rate, and inhibit conductivity in the cardiac conducting system. The cardiac-toxicity of these compounds is related to the number of halogen atoms it increases first as the number of halogen atoms increases, but decreases after achieving the maximum toxicity when four halogen atoms are present. Some of these compounds, e.g., chloroform, carbon tetrachloride, and trichloroethylene, sensitize the heart to catecholamines (adrenaline and noradrenaline) and thus increase the risk of cardiac arrhythmia. 

Inhalant intoxication dehrium can occur as a consequence of disturbances in dopaminergic, glutamatergic, and GABAergic neu to transmission secondary to acute, high-level exposure to psychoactive ingredients in solvents such as toluene, trichloroethane, and trichloroethylene. Systemic effects of solvent inhalation such as cerebral hypoxia and/or metabolic acidosis may also be involved (Rosenberg 1982). Under these circumstances, inhalant intoxication dehrium develops over a short period of time (usually hours to days) and tends to fluctuate during the course of the day. Usually, the delirium resolves as the intoxication ends or within a few hours after cessation of use. 

The prepared photocatal3rsts were tested to know the reactivity and quantum efficiency in the aqueous solution with trichloroethylene(TCE) as a reactant in photocatalytic batch reactor. Also these results were compared the reactivity to the case of P25 catalyst. The liquid phase photocatalytic reaction system was shown in Fig. 1. 

EPA has set a drinking water standard of 5 parts of trichloroethylene per one billion parts of water (ppb). One ppb is 1,000 times less than 1 ppm. This standard became effective on January 9, 1989, and applies to community water systems and those that serve the same 25 or more persons for at least 6 months. EPA requires industries to report spills of 1,000 pounds or more of trichloroethylene. It has been proposed that this level be reduced to 100 pounds. 

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. 

Animal experimentation has revealed inhaled concentrations that result in death following acute, intermediate, and chronic exposure. An LC50 value for acute exposure in rats was reported as 12,500 ppm for a 4-hour exposure (Siegel et al. 1971). Two out of 10 mice died after a 4-hour exposure to 6,400 ppm trichloroethylene (Kylin et al. 1962). Death was often caused by the central nervous system depression that... 

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. 

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... 

Respiratory Effects. One study suggested increased respiratory disorders (asthma, bronchitis, pneumonia) in children with chronic exposure to a solvent-contaminated water supply (Byers et al. 1988). Two municipal wells in eastern Woburn, Massachusetts, were found to contain several solvents including trichloroethylene (267 ppb) and tetrachloroethylene (21 ppb). The increased susceptibility to infection may be secondary to effects on the immune system. Accurate chemical-specific exposure levels for individuals could not be determined because the water distribution system was designed to use water from different wells at different rates and times. Other limitations of this study are described in Section 2.2.2.8. 

Immunological abnormalities were reported in 23 adults in Woburn, Massachusetts, who were exposed to contaminated well water and who were family members of children with leukemia (Byers et al. 1988). These immunological abnormalities, tested for 5 years after well closure, included persistent lymphocytosis, increased numbers of T-lymphocytes, and depressed helper suppressor T-cell ratio. Auto-antibodies, particularly anti-nuclear antibodies, were detected in 11 of 23 adults tested. This study is limited by the possible bias in identifying risk factors for immunological abnormalities in a small, nonpopulation-based group identified by leukemia types. Other limitations of this study are described in Section 2.2.2.8. A study of 356 residents of Tucson, Arizona, who were exposed to trichloroethylene (6-500 ppb) and other chemicals in well water drawn from the Santa Cmz aquifer found increased frequencies of 10 systemic lupus erythematosus symptoms, 5 (arthritis, Raynaud s phenomenon, malar rash, skin lesions related to sun exposure, seizure or convulsions) of which were statistically significant (Kilbum and Warshaw 1992). 

Sato et al. (1991) expanded their earlier PBPK model to account for differences in body weight, body fat content, and sex and applied it to predicting the effect of these factors on trichloroethylene metabolism and excretion. Their model consisted of seven compartments (lung, vessel rich tissue, vessel poor tissue, muscle, fat tissue, gastrointestinal system, and hepatic system) and made various assumptions about the metabolic pathways considered. First-order Michaelis-Menten kinetics were assumed for simplicity, and the first metabolic product was assumed to be chloral hydrate, which was then converted to TCA and trichloroethanol. Further assumptions were that metabolism was limited to the hepatic compartment and that tissue and organ volumes were related to body weight. The metabolic parameters, (the scaling constant for the maximum rate of metabolism) and (the Michaelis constant), were those determined for trichloroethylene in a study by Koizumi (1989) and are presented in Table 2-3. 

Distribution. Once inside the body, trichloroethylene is easily absorbed into and distributed through the circulatory system. The amount that is not absorbed initially on inhalation is expired unchanged (see Section 2.3.1.1). Absorption from the gastrointestinal tract often leads to a first pass through the liver, where toxic metabolites can form (see Section 2.3.3). Trichloroethylene and its metabolites may form adducts with blood proteins, and the metabolite glyoxylate may become incorporated into amino acids (Stevens et al. 1992), thus facilitating their distribution. The ability of these compounds to traverse membranes accounts for then-generalized systemic effects. 

Route Dependent Toxicity. The toxicity of trichloroethylene does not seem to be heavily dependent upon its route of entry. Inhalation and ingestion are the primary exposure routes, and the liver, heart, and central nervous system are the primary targets for both routes (Candura and Faustman 1991). Renal toxicity results principally from oral exposure, and dermal exposure generally confines its toxic effects to the skin, although broad systemic effects can be induced imder conditions of high exposure (Bauer and Rabens 1974). Attributing such effects solely to dermal exposure, however, is difficult because inhalation exposure is often a factor in these cases as well. 

The liver is an organ that shows variable effects from trichloroethylene among species, and this can probably be attributed to interspecies differences in metabolism (see Section 2.4.2.1). Specifically, the apparent difference in susceptibility to trichloroethylene-induced hepatocellular carcinoma between humans and rodents may be due to metabolic differences (see Section 2.4.2.3). Kidney effects are also variable among species. Humans and mice are less sensitive than rats. In rats exposed chronically to trichloroethylene, toxic nephrosis characterized as cytomegaly has been reported (NTP 1988). The kidney effects in rats do not seem to be related to an increase in alpha-2 -globulin (Goldsworthy et al. 1988). Effects on the nervous system appear to be widespread among species, presumably due to interactions between trichloroethylene and neuronal membranes. 

In the past, trichloroethylene was used as a human anesthetic. Trichloroethylene has also been used by individuals who intentionally inhale it for its narcotic properties. Therefore, most of the information regarding the effects of trichloroethylene in humans comes from case studies and experiments describing effects of trichloroethylene after inhalation exposure. These studies indicate that the primary effect of exposure to trichloroethylene is on the central nervous system. Effects include headache, vertigo, fatigue, short-term memory loss, decreased word associations, central nervous system depression, and anesthesia. 

Some members of a community that were exposed to trichloroethylene along with a variety of other solvents in their drinking water complained of respiratory disorders, but the complaints could not be attributed specifically to trichloroethylene (Byers et al. 1988). This effect may have been due to immune system impairment resulting in increased susceptibility to infection. A study in mice in which inhalation exposure to trichloroethylene increased the susceptibility to pulmonary infection with Streptococcus zooepidemicus (Aranyi et al. 1986) provides evidence that trichloroethylene may result in adverse respiratory effects through effects on the immune system. 

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... 

Alcohol can affect the metabolism of trichloroethylene. This is noted in both toxicity and pharmacokinetic studies. In toxicity studies, simultaneous exposure to ethanol and trichloroethylene increased the concentration of trichloroethylene in the blood and breath of male volunteers (Stewart et al. 1974c). These people also showed "degreaser s flush"—a transient vasodilation of superficial skin vessels. In rats, depressant effects in the central nervous system are exacerbated by coadministration of ethanol and trichloroethylene (Utesch et al. 1981). 

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