Human Toxic Chemical Exposure - Trichloroethylene

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Reference Summary

Trichloroethylene (TCE) is a chlorinated hydrocarbon solvent, which is still in fairly widespread use as a metal degreaser, and solvent. Because of concerns about its carcinogenicity it is being used less; 1,1,1-trichloroethane is often used instead. Trichloroethylene has the following structure:



Symptoms of acute exposure to TCE include headache, dizziness, vertigo, tremors, nausea and vomiting, irregular heartbeat, fatigue, blurred vision, and intoxication similar to that of alcohol. Further, alcohol may heighten the symptoms of TCE overexposure. TCE addiction and peripheral neuropathy have been reported (1).

Chronic, low-level exposure is known to cause decreased memory and impairment of the central nervous system (%). Epidemiologic studies have also demonstrated that TCE may be carcinogenic in humans (3).

The American Conference of Governmental and Industrial Hygienists (ACGIH) recommends 100 ppm in air as so exposure limit for an 8-hour workday. NIOSH recommends that peak exposure never exceed 150 ppm. It is important to note that these values are based upon information derived from acute, high-level exposure incidents, not long-term, low-level exposures.

Uptake and Metabolism

TCE is absorbed well by the lungs during inhalation of the vapor. About 30 to 50 percent of the inhaled vapor is absorbed into the bloodstream (4). Not surprisingly during exercise the absorption of the solvent can increase by a factor of 2 or 3 (5).

Skin contact is also a fairly efficient route of exposure. Immersion of one hand in TCE: is equivalent to breathing about 50 ppm of the vapor (6). There is some storage of TCE in the fat; thus, repeated exposures give rise to higher levels of the solvent and its metabolites than do single exposures (7-9).

TCE is metabolized more than most of the other chlorinated solvents. Up to 90% of an inhaled dose is metabolized. It is first converted to an epoxide, then to chloralhydrate (''knock-out drops''), and finally to trichloroethanol or Trichloroacetic acid (TCA).

TCE itself is eliminated fairly rapidly from the bloodstream. Within 5 days of industrial exposure, blood levels are under 10-ppb (10). Within 3 days of a single 6-hour exposure, blood levels drop below 20-ppb (11). However, after repeated exposures, the half-life of the TCE in the blood is longer.

Biological Monitoring

I. Trichloroacetic Acid in Plasma
Due to its efficient binding to serum albumin, trichloroacetic acid has a half-life in the blood of about 3 days; this is longer than the half-life of the parent compound (4). The attached graph of TCA levels in plasma indicates that the levels rise with repeated exposure to TCE.

Lauwerys has suggested a "Tentative Maximum Permissible Level'' for TCA in the plasma of 50 ppm, designed to keep total uptake of TCE below levels found to be safe in resting volunteers (12). Impairment of some central nervous system functions can be found in this exposure range (13-16), although some investigators have not been able to detect such adverse effects (17-18). Again, workers doing strenuous exercise or who have significant skin contact may well be at risk even if they are exposed to "legal" levels of TCE.

An important factor in assessing TCA levels is whether or not the exposed individual has used alcohol during the time of exposure. Alcohol interferes with the metabolism of TCE to TCA. Thus, in a person who has been drinking alcohol, a low TCA level cannot be used to rule out an overexposure to TCE.

A further complicating factor is that there is some evidence from studies in Japanese workers that some persons have a limited capacity to metabolize trichloroethylene to TCA. Exposure levels nearing 100 ppm in air appear to saturate their metabolism (19). Thus, in such persons, exposure over 100 ppm may not give rise to higher levels of TCA than would be found in exposure under 100 ppm. Whether or not Caucasian workers metabolize Trichloroethylene differently than Japanese workers is unknown.

The ACGIH (20) has called for the adoption of a Biological Exposure Index (BEI) for monitoring trichloroethylene exposure. Measuring TCA in urine at the end of the end of the workweek. They suggest that the level of TCA in the urine not exceed 100 mg/l. Although Droz (21) has argued that urinary TCA is a fairly insensitive index of overexposure to trichloroethylene, adoption of this BEI for urinary TCA would likely require that concentrations of TCE in air be kept well below 100 ppm.



II. Trichloroethanol in Urine
Droz has proposed a fairly sensitive way of determining overexposure to TCE by measuring trichloroethanol in urine both before a shift starts and the next morning 21). Comparing these two levels gives a very specific determination of the average airborne TCE concentration during the shift.

The German Research Society has published a recommendation for a "Biological Tolerance Value” for trichloroethanol concentration in the blood, aimed at assuring that exposures to TCE are kept under 50 ppm in the air. Their recommendation is that the trichloroethanol blood level drawn at 5:00 p.m. on Friday afternoon ("end-of-shift/end of week" specimen) be kept under 5 mg/liter (22).

For information on sampling procedures, please see the Pacific Toxicology Laboratories collection instructions.

References

1. Sittig. M., Handbook of Toxic and Hazardous Chemicals, Noyes Publications, 1981.

2. Axelson, O., ct. al., Current Aspects of Solvent Related Disorders. In Developments in Occupational Medicine. (ed. Carl Zenz), Yearbook Medical Publishers Inc., Chicago, Pp. 237-59, 1977.

3. Apfeldorf, R. and Infante, P., Review of epidemiologic study results of vinyl chloride related compounds, Environ. Health Perspect. 41: 221-26, 1981.

4. Monster, A.C., Trichloroethylene, in Biological Monitoring and Surveillance of Workers Exposed to Chemicals, Eds. Aitio A., Riihimaki, V., and Vainio, H., McGraw-Hill. 1984.

5. Vesterberg, 0. and Astrand, I., Exposure to trichloroethylene monitored by analysis of metabolites in blood and urine, J. Occupational Medicine 18:224-226, 1976.

6. Sato, A. and Nakajima, T., Differences following skin or inhalation exposure in the absorption and excretion kinetics of trichloroethylene and toluene, Br. J. Industrial Medicine 25:43-49, 1981.

7. Savolainen, H., Phamzacokinetics, ppharmacodynamics, and aspects of neurotoxic effects of four inhaled aliphatic chlorohydrocarborn solverzts as relevant in man, Eur. J. Drug Metab. Pharmacokin. 6:85-90, 1981.

8. Ertle, T., Henschler, D., Muller, G. and Spassovski, M., Metabolism of trichloroethylene in man, Arch. Toxicol. 29: 171-188, 1972.

9. Fernandez, J.G., Droz, P.O., Humbert, B.E. and Caperos, J.R., Trichloroethylene exposure: simulation of uptake, excretion and metabolism using a mathematical model, Br. J. Indust. Med. 34:43-55, 1977.

10. Monster, A.C., Boersma, G., and Duba, W.C., Kinetics of trichloroethylene in relocated exposure to volunteers, Int. Arch. Occup. Environ. Health 42:283-292, 1979.

11. Muller, G., Spassovski, M. and Henschler, D., Metabolism of trichloroethylene in man, Arch Toxicol 32:283-295, 1974.

12. Lauwerys, R.R., Industrial Chemical Exposure: Guidelines for Biological Monitoring, Biomedical Publications, Davis, p. 138, 1983.

13. Grandjean, E., et. al., Investigations into the effects of exposure to trichloroethylene in mechanical engineering, Br. J. Industr. Med. 12:131-1421 19.55.

14. Lilis, R., Stanescu, D., Muica, N. and Roventa, A., Chronic effects of TCE exposure, Med. Lav. 60: 595-601, 1969.

15. Saivini, M., Minaschi, S., and Riva, M.1 Evaluation of the psychophysiological functions in humans exposed to trichloroethylene, Br. J. Industr. Med. 28:293-295, 1971.

16. Gun, R.T., Grygorcewicz, C. and Nettelbeck, T.J., Choice reaction time in workers using trichloroethylene, Med. J. Aust. 1:535-536, 1978.

17. Vernon, R.J. and Ferguson, R.K., Effects of trichloroethylene on visual-motor performance, Arch. Environ. Health 18:894-900, 1969.

18. Triebig, G., Easing, H.G., Schaller, K.H. and Valentin H., Biochemical and psychological examinations of trichloroethylene-exposed volunteers, Zbl. Bakt. Hyg., I Abt. Orig. B 163:383-416, 1976.

19. Ikeda, M., Metabolism of trichloroethylene and tetrachloroethylene in human subjects, Environ. Health Perspect. 21:239-245, 1977.

20. American Conference of Governmental Industrial Hygienists, Biological Exposure Indices, BEI-25, Cincinnati, 1984.

21. Droz, P.O. and Fernandez, J.G., Trichloroethylene exposure: biological monitoring by breath and urine analysis, Br. J. Industr. Med. 35:35-42, 1978.

22. German Research Council (Deutsche Forschungsgemeinschaft), Maximum Concentrations at the Workplace and Biological Tolerance Values for Working Materials, p. 76, Verlag Chemie: Weirtheim, 1984.

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