Trichloroethylene: environmental and occupational exposure
Tricloroethylene (TCE) is a clear, non-flammable liquid with a sweet odor similar to that of chloroform. It has a variety of uses, including paint stripping and industrial degreasing (80 percent of TCE is used for degreasing of fabricated metal parts in the automotive and metal industries). It is also a component of many other products, such as typewriter correction fluid, rug cleaners and spot removers. In the past, TCE was used as an anesthetic, analgesic, dry-cleaning solvent, grain fumigant, spice extractant and coffee decaffeinator. Trade names of trichloroethylene products include Benzinol, Circosolve, Flock Flip, Narcogen, Perm-A-Chlor, Tri-Clene and Vestrol.
An estimated 3.5 million U.S. workers have been exposed low levels of TCE and 100,000 of these workers are constantly exposed. In addition to automotive and metal industries, TCE exposure occurs in a variety of settings, including chemical industries that produce polyvinlychloride, pentachloroethane and other polychlorinated aliphatic hydrocarbons, insecticides, disinfectants, pharmaceuticals, dyes, perfumes and soaps. Exposure can also occur as a result of deliberate inhalation of solvents and typewriter correction fluid, a form of substance abuse.
TCE is a common environmental contaminant and has been detected at over one-third of the hazardous waste sites on the national priorities list of the U.S. Environmental Protection Agency (EPA). While TCE becomes volatile rapidly in contact with air, it does not degrade in soil under anaerobic conditions and migrates to groundwater. TCE has become a common contaminant of water supplies, particularly those near landfills or industrial waste-water sites. TCE has been detected in 10 percent of wells tested. TCE is estimated to be in 34 percent of the nation’s drinking water supplies. Although most ground-water contamination occurs at a level below the federal standard of 5 ppb (parts per billion), there have been well-publicized instances of community water supplies with levels of 200 to 400 ppb. These cases have resulted in successful litigation against the industries responsible.
Because of TCE’s volatility, household activities such as bathing or cooking with contaminated water may produce measurable air concentrations. Fortunately, these levels are usually lower than those found in workplace exposures. TCE does not accumulate in the food chain.
Due to the widespread occurence of TCE contamination and the increasing public concern about toxic exposures, family physicians are likely to be asked about the health effects of occupational and environmental exposure to TCE. This article summarizes the current literature on TCE metabolism, exposure limits and known or suspected health effects of occupational and environmental exposure. Recommendations are also provided on how to address patients’ concerns about known or suspected TCE exposure.
Metabolism and Exposure Levels
TCE is readily absorbed orally and by inhalation; dermal exposure in much less efficient. TCE passes through the blood-stream to all organs, especially those that receive a large blood supply (brain, liver and kidneys) and is deposited in the fat cells. TCE also crosses the placenta and enters fetal tissues.
Metabolism of TCE occurs in the liver, and three main metabolites (trichloroethanol, trichloroacetic acid [TCA] and trichloroethanol glucuronide) are excreted in the urine. The half-life of TCE in the body is five hours, and the half-life of TCA is 52 hours; the other metabolites have a half-life of 10 hours. The metabolites, rather than TCE itself, may be responsible for some of the health effect observed in animal studies.
Table 1 lists the recommended limits of TCE exposure in occupational and environmental settings. The amount of TCE involved with different exposures can be quantified by the following example: a body of water 30 ft x 20 ft x 6 ft contaminated with 5 ppb of TCE will contain three drop of TCE; a persons drinking 10 L of water daily contaminated with 200 ppb of TCE will consume 15 mL of TCE in 30 years.
Recommended Limits for TCE Exposure
Type of exposure limits of exposure
Short-term exposure limit (STEL) 200 ppm
Set OSHA; a time-weighted
average that workers can be
exposed to for 15 minutes
four times a day with one hour
Permissible exposure limit (PEL) 50 ppm(*)
Set by OSHA; a time-weighted
average that workers
can be exposed to for an
Drinking water quality criteria 5 ppb
(set by the EPA)
(*) – The California Occupational Safely and Health
Administration has set a PEL of 25 ppm.
Acute Clinical Effects of Exposure
Acute effects of TCE inhalation at levels higher than 200 ppm (part per million) for one to seven hours include nausea, vomiting, drowsiness, headache, dizziness, decreased psychomotor function and confusion. Higher levels of exposure can cause respiratory failure, hepatotoxicity, coma and death. Cardiac arrhythmias may develop in susceptible individuals exposed to very high levels.
TCE air levels higher than 100 ppm can cause dryness of the throat, eye irritation and, possibly, detectable central nervous system depression and decreased ability to perform complex task.[1,2,4]
Effects of Prolonged, Low-Level Exposure
The health effects of prolonged occupational and environmental exposures at low levels are major of controversy.
BIRTH DEFECTS AND REPRODUCTION
Most studies of environmental and occupational TCE exposure have found no increased rate birth defects. Two studies have found an increased risk of congenital heart defects in children of women who have had environmental exposure to TCE.[6,7] TCE has not been found to cause heart defects in animals unless it is injected directly into the uterus or embryonic.[8,10] While cause and effects has yet to be firmly established, TCE may be a cause of congenital heart defects.
Neither paternal nor maternal occupational exposure to TCE appears to have an effects on the rate of spontaneous abortion.[5,11,12]
The EPA has listed TCE as a probable human carcinogen, but the National Toxicology Program and the International Agency for Research on Cancer have not. High levels of TCE exposure have been associated with liver and lung tumors in mice and renal and testicular tumors in rats, although the significance of these findings has been disputed.
Studies of TCE carcinogenicity in humans have been of variable quality and have produced conflicting results. Table 2 summarizes these studies by listing the type of study and the type of cancer found to be increased. In most of these studies, the exposure to TCE was not well documented. Many studies used proportional mortality ratios, which can be affected by an increased or decreased prevalence of other causes of mortality. Many studies examined the prevalence of mortality from all cancers and use P = .05 levels of significance (an increased or decreased mortality will be found for one out of 20 cancers by chance alone). As a result, many studies have found an increased mortality rate for one or tow cancers, with the type of cancer differing from study to study. Because of the inconsistent results, the poor quality of many studies and negative findings in the most rigorously conducted cohort studies using standardized mortality ratios,[13-15] the majority of scientific opinion at this time is that TCE has not been proven to be a human carcinogen.
Summary of Studies Showing Association of TCE and Cancer
Type Number of studies identifying Individual TEC
of cancer an association exposure
Leukemia 1 correlational No
2 case control Yes
Bladder 1 correlational No
Liver 3 case control No
2 cohort using PMRs No
Pancreas 1 case control No
Colon 1 case control Yes
Kidney 2 cohort using PMRs No
Genitals 1 cohort using PMRs No
Lung 2 cohort using PMRs No
Cervix 1 cohort using PMRs No
Esophagus 1 cohort using PMRs No
Skin 1 cohort using PMRs No
Stomach 1 cohort using PMRs No
Nose and 1 cohort using PMRs Yes
PMR = Proportional mortality ratio.
Occupational exposure to various organic solvents has been linked to scleroderma. Although cause and effect have not been confirmed, there are five case reports of scleroderma in worker exposed to high levels of TCE. No evidence exists to link to TCE to scleroderma at lower levels of exposure. One court case involving contaminated who claimed that systemic lupus erythematosus was caused bt TCE. No scientific evidence exists to support or refute this claim.
Since TCE was once used as an obstetric anesthetic and as treatment for facial nerve pain, its long-term effects on the nervous system is of concern. Occupational exposure for prolonged periods may impair performance on visual and motor tests. One study showed an effect at 110 ppm, while other studies have shown minimal effects at levels of 300 ppm but significant effects at higher level.[18,19]One report described two worker who developed a multiple sclerosis-like disease after exposure to TCE and other chemical. It should be noted that case reports cannot prove cause and effect.
The neurologic effects of chronic environmental exposure to TCE are unknown. In one study, delayed blink reflexes were documented in 21 people from a geographical area that had TCE contamination of the water supply, but the study results were tainted by nonrandom selection of cases and inappropriate control subject. No solid evidence support or refutes claims of chronic neurologic effects from environmental exposure to TCE.
In case-control studies in Japan, TCE has been linked to primary pneumatosis cystoides intestinalis, a rare begin disease characterized by multiple gas-filled cysts in the wall of the gastrointestial tract. It usually is manifested by hematochezia. Hepatotoxicity has been associated with intentional TCE inhalation abuse. At concentrations currently found in the workplace, TCE is unlikely to cause liver damage.
While most studies of the long-term health effects of low-dose TCE exposure have been reassuring, large gaps are present in the knowledge base. At this time, the general consensus of scientific opinion is that low-level environmental and occupational TCE exposure is unlikely to cause significant community-wide health effects.
The family physicians is likely to encounter three types of TCE exposure: high-level acute workplace exposure; prolonged, low-dose workplace exposure, and environmental exposure.
ACUTE, HIGH-LEVEL WORKPLACE EXPOSURE
Following acute, high-level exposure, contaminated environment. Any areas of cutaneous contact should be washed with soap and water. A complete physical examination, with emphasis on the neurologic, cutaneous, respiratory and cardiovascular systems, should be performed.
Cardiac and respiratory status may need to be monitored. Liver function tests and serum creatinine determination should be obtained, with follow-up of abnormal results. An occupational history should be obtained, and the potential for effects of co-contaminants should be kept in mind.
Workplace exposed to low level of TCE may have a variety of complaints. A complete occupational history should be obtained as well as details about each complaint. The physical examination should be complete, with emphasis on the neurologic and metal status examinations. Routine laboratory tests ussually not helpful.
TCE measurements may be takenfrom breathand urine samples for up to 16 hours after exposure, and TCA is measurable in the blood and urine for up to three weeks. These tests, however, are difficult to interpret because some medications other chlorinasted hydrocarbons metabolize to TCA. Any suspected workplace exposure exceeding recommended level should be reported to the Occupational Safely and Health Administration (OSHA).
Patients with concerns about environmental TCE exposu pose a difficult problem. Details should be obtained about the location and duration of residence, the location of nearby industries, and the type of water used. Information on TCE levels in local water supplies may be obtained from the local health department or water company.
Specific physical complaints should be investigated and reassurance provided about the lack of documented health effects of most environmental exposures, although the physicians should be candid that current data are not optimal. If the clinical examination is negative, the physician should express willingness to follow and investigate new or deteriorating symptoms. The family physician needs to remember that information provided to patients may be contradicted by advocacy groups and persons involved with litigation.
TCE exposure typifies the type of clinical situations related to toxic chemicals that will be increasingly encountered by family physicians in the future. Cautious investigation of patients’ concerns and complaints, with an open mind about potential health effects of each chemical in question, will best serve the individual patient and the community.
REFERENCES[1.] Barceloux DG. Trichloroethylene toxicity. Atlanta, Ga.: Department of Health and Human Services, 1990. [2.] Trichloroethylene. Rev Environ Contam Toxicol 1988; 106:203-12. [3.] Marshall E. Woburn case may spark explosion of lawsuits [News]. Science 1986;234: 418-20. [4.] Syracuse Research Corporation. Toxicological profile for trichloroethylene. Washington, D.C.: Department of Health and Human Services, 1989. [5.] Olsen J, Hemminki K, Ahlborg G, et al. Low birthweight, congenital malformations, and spontaneous abortions among dry-cleaning workers in Scandinavia. Scand J Work Environ Health 1990;16:163-8. [6.] Goldberg SJ, Lebowitz MD, Graver EJ, Hicks S. An association of human congenital cardiac malformations and drinking water contaminant. J Am Coll Cardiol 1990;16:155-64. [7.] Swan S, Deane M, Harris J, Neutra R. Pregnancy outcomes in relation to water contamination, 1980-81. San Jose, Ca. In: Pregnancy outcomes in Santa Clara Country 1980-82: reports of two epidemiological studies. Berkeley, Calif.: Epidemiological Studies Section, California Department of Health Services, 1985. [8.] Fan AM. Trichloroethylene: water contamination and health risk assessment. Rev Environ Contam Toxicol 1988;101:55-92. [9.] Loeber CP, Hendrix MJ, Diez De Pinos S, Goldberg SJ. Trichloroethylene: a cardiac teratogen in developing chick embryos. Pediatr Res 1988;24:740-4. [10.] Dawson BV, Johson PD, Goldberg SJ, Ulreich JB. Cardiac teratogenesis of trichloroethylene and dichloroethylene in a mammalian model. J Am Coll Cardiol 1990;16:1304-9. [11.] Lindbohm M, Hemminki K, Bonhomme MG, et al. Effects of paternal occupational exposure on spontaneous abortions. Am J Public Health 1991;81:1029-33. [12.] Lindbohm ML, Taskinen H, Sallmen M, Hemminki K. Spontaneous abortions among women exposed to organic solvents. Am J Ind Med 1990;17:449-63. [13.] Axelson O, Anderson K, Hogstedt C, Holmberg B, Molina G, de Verdier A. A cohort study on trichloroethylene exposure an cancer mortality. J Occup Med 1978;20:194-6. [14.] Tola S, Vilhunen R, Jarvinen E, Korkala M. A cohort studt on workers exposed to trichloroethylene. J Occup Med 1980;22:737-40. [15.] Shindell S, Ulrich S. A cohort study of employees of a manufacturing plant using trichloroethylene. J Occup Med 1985;27:577-9. [16.] Haustein UF, Ziegler V. Environmentally induced systemic sclerosis-like disorders. Int J Dermatol 1985;24:147-51. [17.] Salvini M, Binaschi S, Riva M. Evaluation of the phychophysiological functions in humans exposed to trichloroethylene. Br J Ind Med 1971;28:293-5. [18.] Vernon RJ, Ferguson RK. Effects of trichloroethylene on visual-motor performance. Arch Environ Health 1969;18:894-900. [19.] Ettema JH, Zielhuis RL, Burer E, Meier HA, Kleerekoper L, de Graaf MA. Effects of alcohol, carbon monoxide and trichloroethylene exposure on mental capacity. Int Arch Occup Environ Health 1975;35:117-32. [20.] Noseworthy JH, Rice GP. Trichloroethylene poisoning mimicking multiple sclerosis [Letter]. Can J Neurol Sci 1988;15:87-8. [21.] Feldman RC, Chirico-Post J, Proctor SP. Blink reflex latency after exposure to trichloroethylene in well water. Arch Environ Health 1988; 43:143-8. [22.] Sato A, Yamaguchi K, Nakajima T. A new health problem due to trichloroethylene: pneumatosis cystoides intestinalis. Arch Environ Health 1987;42:144-7.
DOUG CAMPOS-OUTCALT, M.D. is assistant professor of family and community medicine at the University of Arizona College of Medicine, Tucson. He graduated from the University of Arizona College of Medicine and received a master’s degree in public administration from Arizona State University. He completed a residency in family medicine at the University of California, Davis, School of Medicine and a residency in preventive medicine at Maricopa County Department of Health Services, Phoenix.
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