National Industrial Chemicals Notification and Assessment Scheme
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- 11.1Acute toxicity
- 11.1.2Oral
- 11.2.1Skin
- 11.2.2Eye
11.Human Health EffectsA number of reviews have been published on the health effects of trichloroethylene. This section summarises data from the published reviews and is based mainly on the UK SIAR (United Kingdom, 1996). Articles published recently, that is, since completion of the SIDS report, have been assessed. No unpublished studies were provided for assessment. 11.1Acute toxicityData are available from studies in volunteers, accident reports and from use as an anaesthetic. 11.1.1InhalationThe predominant effect of acute inhalation exposure of humans to trichloroethylene is CNS depression. At very high doses trichloroethylene causes narcosis and has been used as an anaesthetic for short operations at concentrations of 5000 to 10,000 ppm. Generally, there were no adverse effects after the patients had recovered from anaesthesia. Cardiac arrhythmias have been reported during use as an anaesthetic. Cranial neuropathies specially involving the trigeminal nerve have also been observed. The trigeminal palsies were believed to be due to dichloroacetylene, a decomposition product of trichloroethylene. Death has been reported following accidental exposure to high levels of trichloroethylene at work. Death was thought to be due to ventricular fibrillation resulting from sensitisation of the heart by trichloroethylene to endogenous catecholamines. Loss of sensation in the trunk and lower extremities and extensive sensory loss over face with numbness have been reported following accidental exposure to high concentrations of trichloroethylene. Loss of consciousness for varying periods has been observed in workers with exposure to high levels (2800 ppm). Workers have also reported symptoms of CNS depression such as dizziness, lethargy, headache and vertigo. Other effects seen following accidental exposure to high levels were raised serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, hypercalcaemia and hyperglobulinaemia. Kidney damage was reported in one worker with acute renal failure following exposure (David et al., 1989). Several studies in volunteers under controlled conditions have reported acute effects of trichloroethylene on CNS functions at 500 ppm and above. Dizziness, lethargy and lightheadedness have been noted by volunteers. Exposure to 1000 ppm for 2 h resulted in marked changes in performance of a range of tests. These changes were potentiated with exposure to alcohol. No significant signs of CNS depression have been noted at 300 ppm. Some subjective effects such as dizziness and lethargy were reported at lower doses (27 ppm) by volunteers in one study (Nomiyama & Nomiyama, 1971). No significant changes were seen in flicker fusion frequency and two-point discrimination. “Irritant effects” have been reported in this study at 27 ppm, however these effects were not reported in other studies following higher exposures. The results of this study were not considered for NOAEL as only three subjects were involved and the symptoms reported were subjective. Another study (Salvini et al., 1971) indicated that impairment of performance can be induced by exposures to 130 ppm of trichloroethylene. This is in contrast to the effects seen in other studies. However the UK SIAR states that actual data was not given and only a statistical analysis of the results was given. This study involved six subjects and was not included when considering a NOAEL for acute effects. From case reports, the no effect level for single inhalation exposure of humans to trichloroethylene is around 300 ppm and is similar to that in animals. Acute effects of trichloroethylene following accidental exposure and in volunteers under controlled conditions are summarised in Table 27.
Two recently published articles reporting accidental and suicidal ingestion respectively of high doses of trichloroethylene have been reviewed during this assessment. No new data on low dose ingestion was available. Accidental oral ingestion of approximately 29 gms of trichloroethylene by a 58 year old man following a fall into a reservoir bath resulted in disturbed consciousness and markedly oedematous pharynx and larynx. Laboratory examinations showed slightly elevated serum AST and ALT levels but kidney functions were normal. The man also developed respiratory insufficiency, chemical pneumonia and chemical burns to 30% of his body surface. The CNS functions returned to normal by 5 weeks and the man was discharged after 44 days (Yoshida et al., 1996). Ingestion of 70 ml trichloroethylene by a 17 yr old male in a suicide attempt resulted in tremor, general motor restlessness and sinus tachycardia. The person lost consciousness 5 h after poisoning. The highest concentration of trichloroethylene in blood was 4 mg/L and was detected 13 h after ingestion. The metabolites by the oxidative and glutathione pathways were quantified in urine. N-acetyl-S-1,2-dichlorovinyl-L-cysteine excretion increased continuously with a maximum (1.25 nmol/mg creatinine) seen 5 days after poisoning. Several low molecular weight proteins were also detected in the urine 5 days after poisoning indicating renal tubular damage (Bruning et al., 1996a). 11.2Irritation and corrosivity |
