Most of the literature involves populations exposed occupationally to those solvents and other industrial chemicals.
Symptoms due to short-term exposures typically resolve within a few hours of exposure. In a study of 50 workers employed from 1 month to 15 years in various industrial cleaning and degreasing operations using TCE, complaints due to chronic exposure included decreased appetite, sleep disturbances, ataxia, vertigo, headache, short-term memory loss, and fewer word associations.
Greater frequency of symptoms were noted in workers exposed to higher 85 ppm than lower 14 ppm mean TCE concentrations.
In the brains of animals chronically exposed to high concentrations of TCE ppm to ppmhistologic changes have been demonstrated, but these changes do not correlate with behavioral abnormalities detected in animals or humans.
Persons who have deliberately abused volatile chlorocarbon solvents have developed cerebellar damage and ataxia. Electrophysiologic studies in humans have not detected significant abnormalities of peripheral nerve conduction.
Mortality studies of TCE-exposed workers do not indicate an increased risk of cardiovascular death. A few susceptible persons who are exposed to near-anesthetic levels during vigorous activity may have increased risk of cardiac dysrythmia.
However, there is no evidence that exposure at high TCE levels causes a predisposition to cardiac toxicity at lower levels. When TCE was administered as an anesthetic agent, serious ventricular dysrhythmias and cardiac arrests were rare and were nearly always associated with hypoxia.
Significant ventricular ectopy would not be expected from TCE exposure at background environmental levels or those currently allowed in the workplace. When swallowed, TCE causes gastrointestinal irritation, with possible inflammation of the GI tract manifested as nausea, vomiting, diarrhea, and abdominal pain.
Hepatotoxicity has been associated primarily with intentional TCE inhalation abuse. In these cases, hepatic histologic examination has revealed centrilobular necrosis with fatty infiltration. Chronic TCE exposures at concentrations currently permissible in the workplace or at those expected in ambient air are not likely to cause liver damage.
Page Share Cite Suggested Citation: Integrating a Missing Element into Medical Education. The National Academies Press. One case involved a long-time metal degreaser who developed acute tubular necrosis confirmed by biopsywhich led to renal failure.
Another case involved a worker exposed to Animals demonstrate little nephrotoxicity after single, high-dose exposures. No increased incidence of congenital malformations has been detected in babies born to mothers occupationally exposed to TCE.
A small cross-sectional study of degreasing workers showed no effect of TCE exposure on male germ cells. Data from animal studies reveal no adverse effects on reproductive system histology, fertility, or other reproductive performance parameters.
TCE crosses the placenta in animals and has been found in human newborns after maternal TCE anesthesia during child-birth.
Human developmental effects were attributed to the ingestion of TCE-contaminated water in one study, but the significance of this finding is questionable because of mixed chemical exposures and methodologic inadequacies of the study.
In animals, abnormalities decreased fetal body weight and ossification anomalies have been reported infrequently.
Inhalation or oral exposure to high doses of TCE produces liver and lung tumors in mice, and renal adenocarcinomas, testicular tumors, and possibly leukemia in rats.
The relevance of the liver tumor data obtained from the mice used in these studies is controversial because the species used tends to form spontaneous liver tumors.
The presence of TCE stabilizers, such as epichlorohydrin, may also confound some of these results.Health effects with positive findings in at least one study that evaluated exposure to TCE and/or PCE: Chonal atresia (nasal passages blocked with bone or tissue) (1, 2) Eye defects (1, 2).
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A study of nurses occupationally exposed by inhalation to trichloroethylene along with other chemicals in operating rooms, and another epidemiological study of women exposed occupationally or nonoccupationally to trichloroethylene and other solvents, have reported increases in the incidence of.
A team of TCE power system experts carried out the study and investigated the following shortlisted probable causes of failure thoroughly: Possibility of moisture ingress due to long term storage of bushings before usage.
Washington, DC: The National Academies Press. doi: / Human developmental effects were attributed to the ingestion of TCE-contaminated water in one study, but the significance of this finding is questionable because of mixed chemical exposures and methodologic inadequacies of the study.
In animals, abnormalities (decreased fetal. May 09, · The study by Raaschou-Nielsen et al. (), having greater statistical power because of its larger cohort size, suggested that both sites are possible targets of TCE toxicity, reporting a standardized incidence ratio (SIR) for primary liver cancer similar to .