Introduction

When considering the human health effects of TCE, it is important to make a distinction between occupational exposures to relatively high levels by inhalation and general environmental exposures to low levels in drinking water and ambient air.

Patient History

An occupational history should be routinely obtained. It should include items such as:

• company name and location
• job title
• description of chemical processes encountered
• known toxic agents used
• workplace investigations
• complaints of co-workers

An environmental history should also be obtained, including:

• location and duration of residence
• proximity to industry
• diet
• daily activities
• type of water supply
• use of consumer products that contain TCE

If a temporal association between symptoms and exposure to certain products is suspected, an attempt should be made to identify the specific chemical ingredients involved. In the situation involving occupational or consumer product exposure, if the product label does not list the chemical ingredients, the regional poison control center may maintain a list of ingredients in consumer and proprietary products. In the U.S.: call 1-800-222-1222, or check http://www.aapcc.org/ for an updated list of U.S. Poison Control Centers. The World Health Organization and the International Program on Chemical Safety maintain an international list of poison control centers: http://www.who.int/ipcs/poisons/centre/directory/en/index.html

In occupational exposures in the U.S., the employer or manufacturer is required by law to provide a material safety data sheet (MSDS), which lists the chemical ingredients and describes their potential toxicity.

Physical Examination

The patient's complaints should be identified in terms of onset, duration, and intensity. Complaints should be investigated by focusing first on major organ systems that are likely to be affected by exposure to TCE (CNS, hepatic, integumentary, cardiovascular, renal), and then on systems unlikely to be affected (respiratory, gastrointestinal, endocrine, skeletal).

Vital signs should be recorded, especially abnormalities of heart rate or rhythm. Eyes, nose, throat, and skin should be examined carefully for inflammation or irritation. The conjunctiva may be injected, and nasal mucosa may be injected and swollen. Repeated inhalation exposures to trichloroethylene can cause defatting of nasal mucosa, leading to a friable condition with drying, cracking, or bleeding. Skin contact may cause dermatitis by irritation and defatting.

The patient's abdomen should be palpated for hepatomegaly and right upper quadrant tenderness.

Patients should receive a complete neurological examination, including a mental status exam and evaluation of the cranial nerves, to detect either peripheral or central nervous system involvement. Cranial neuropathies in patients with a history of TCE exposure are uncommon.

Signs and Symptoms

No unique pattern of symptoms characterizes TCE-induced illness.

Acute Exposure

With inhalation of high concentrations, TCE causes initial CNS excitation followed by CNS depression. Depending on the duration and intensity of exposure, symptoms (Meditext 2004) can include:

• ataxia
• bronchial irritation
• confusion
• dizziness
• drowsiness
• dyspnea
• euphoria
• fatal cardiac dysrhythmias
• fatigue
• headache
• lethargy,
• light-headedness
• pulmonary edema
• renal and hepatic damage
• respiratory depression
• seizures
• stupor
• visual disturbances

Coma and respiratory depression may occur with prolonged, high-level exposure (i.e., above 2,000 ppm). Serious ventricular arrhythmias can develop up to 24 hours after large TCE ingestions (Agency for Toxic Substances and Disease Registry 1997).

Effects from ingestion include:

• abdominal pain
• circulatory collapse
• diarrhea
• dizziness
• dysphagia
• dysrhythmias
• hallucinations or distorted perceptions
• headache
• incoordination
• jaundice
• nausea
• paresthesia
• partial paralysis
• somnolence
• vomiting

The main systemic response is CNS depression (Meditext 2004).

TCE is a skin irritant and may cause defatting dermatitis of the skin. Scleroderma has been linked with TCE exposure. Dermal absorption is not likely to be significant if dermatitis is prevented. Vasodilation and malaise ('degreasers flush') recur in workers who drink ethanol after exposure to TCE (Meditext 2004).

After any type of acute exposure, the clinician should keep in mind that:

• because respiratory depression is the most common serious sequela of acute TCE exposure, the adequacy of ventilation should be carefully assessed,
• because of possible arrhythmias, patients with preexisting cardiovascular disease should be monitored by continuous electrocardiogram and frequent evaluation of vital signs, and
• because hepatic injury may occur, liver function tests should be performed.

Chronic Exposure

The symptoms seen in humans in cases of long-term exposure were similar to those seen in acute exposure, but occurred in more extreme and persistent forms (Kleinfeld and Tabershaw 1954; Fan 1988).

Reported neurological effects associated with chronic workplace exposure to TCE have included nonspecific symptoms such as:

• ataxia,
• decreased appetite
• dizziness
• emotional instability
• fatigue,
• headache,
• impaired judgment
• memory loss
• sleep disturbances
• weakness

WHO (1985) noted that chronic effects such as disturbance of the nervous system can occur following prolonged exposure to TCE concentrations of about 100 ppm (WHO 1985).

Although some CNS symptoms may disappear within several weeks after cessation of exposure, other CNS adverse health effects such as memory loss and mood swings may persist in persons who have been exposed to TCE for long periods (Agency for Toxic Substances and Disease Registry 1997).

Persistent neurological symptoms suggest the possibility of psychiatric disorders and also prompt a search for exposure to neurotoxicants, such as alcohol and other drugs of abuse.

Progress Check