What Laboratory Tests Can Assist in the Evaluation of Patients Exposed to Trichloroethylene?

Course: WB1112
CE Original Date: November 8, 2007
CE Renewal Date: November 8, 2010
CE Expiration Date: November 8, 2012
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Learning Objectives

Upon completion of this section, you should be able to identify direct and indirect measurements that can assist with diagnosis of TCE exposure.


TCE may be measured to confirm TCE exposure. Significant exposure to TCE may result in elevated values of routine laboratory tests, including renal and liver function tests.

Direct Biological Indicators


Directly testing for TCE in the blood can be used for either immediate exposure or chronic exposure. However there are multiple factors that influence these results, including time when the sample was taken, total body fat, activity level, and enzyme activity of aldehyde and alcohol dehydrogenase (Waksman and Phillips 2004). Detectable plasma levels of TCE in persons without occupational exposure are approximately 0.01 to 0.13 micrograms per deciliter (µg/dL).

TCE Metabolites

Although TCE disappears rapidly from the blood, metabolites (e.g., trichloroacetic acid) can persist in the blood for several weeks and in urine up to three weeks after heavy exposure (Sato, Nakajima et al. 1977; Monster, Boersma et al. 1979). Immediate exposure is best measured by trichloroethanol levels in the blood. Chronic exposure is best measured by urinary trichoroacetic acid (Waksman and Phillips 2004).


The presence of TCE metabolites should be interpreted with caution because some medications (chloral hydrate and disulfiram) and other chlorinated hydrocarbons (1,1,1-trichloroethane and tetrachloroethylene) are also metabolized to trichloroacetic acid and excreted in the urine (Agency for Toxic Substances and Disease Registry 1997).

Indirect Biological Indicators


Urinary excretion of glutathione-S-transferase alpha (Bruning, Sundberg et al. 1999), α1-microglobulin (Bolt, Lammert et al. 2004), β2-microglobulin (Nagaya, Ishikawa et al. 1989) and N-acetyl-β-D-glucosaminidase (Brogren, Christensen et al. 1986; Selden, Hultberg et al. 1993) are used to indicate kidney damage, but neither marker is specific to TCE-induced damage; a number of short-chain halogenated hydrocarbons can produce similar effects (Agency for Toxic Substances and Disease Registry 1997).


Biochemical abnormalities are uncommon after acute TCE exposures. Rarely have elevations of serum hepatic transaminases (serum glutamic-oxaloacetic transaminase (SGOT) or aspartate aminotransferase (AST), serum glutamic-pyruvic transaminase (SGPT) or alanine aminotransferase (ALT)), bilirubin, and creatinine resulted from acute TCE exposure; (Rasmussen, Brogren et al. 1993; Agency for Toxic Substances and Disease Registry 1997) nevertheless, liver and kidney function and serum creatinine tests should be performed to establish baselines.


Electrocardiogram and continuous cardiac monitoring should be considered for heavily exposed persons.


Ingestion of large amounts of TCE, which can cause profuse diarrhea, can produce an electrolyte imbalance.

Nervous System

Because the trigeminal, optic, and facial nerves can be impaired by exposure to dichloroacetylene, changes in the visual fields and trigeminal nerve potentials can be noted (Szlatenyi and Wang 1996).

Immune System

Two studies that may be of value are Kahn and Letz (1989) and American College of Physicians (1989).

If it had been indicated, laboratory evaluation of immunologic host-defense defects would consist of three phases.

The preliminary screening is a complete blood count with differential smear and quantitative immunoglobulin levels. These tests, together with history and physical examination, will identify more than 95% of patients with primary immunodeficiencies.

The second testing phase consists of readily available studies including B-cell function (such as antibodies and response to immunization), T-cell function (skin tests and contact sensitization), and complement levels.

The first two phases combined will detect most immunodeficiencies amenable to conventional treatment with gamma globulin or plasma.

The third phase (in-depth investigation) consists of testing induction of B-lymphocyte differentiation in vitro, stimulated by pokeweed mitogen and histological and immunofluorescent examination of biopsy specimens; T-cell surface markers; assays of T-cell helper or killer cell functions; and functional assays using appropriate target cells. It is inappropriate to perform the latter tests on environmentally exposed patients except for epidemiologic research.

If the patient’s concerns include an increased risk of autoimmune illnesses, general evaluation for autoimmune diseases might include

  • C-reactive protein (CRP)
  • evaluation of the antinuclear antibody (ANA)
  • the erythrocyte sedimentation rate (ESR)

If a specific autoimmune disease is suspected, appropriate serologic markers should be assessed, where available.

Key Points
  • TCE can be detected in the breath and urine up to 16 hours after exposure; metabolites can persist for a week or more.
  • Urinary metabolites are trichloroethanol and trichloroacetic acid.
  • Urinary proteins, liver function tests, a serum creatinine test, and continuous cardiac monitoring should be considered for persons acutely exposed to high levels of TCE.
Page last reviewed: December 10, 2013