• National Exposure Registry
• Benzene
• Dioxin
• Journal Articles
• Trichloroethylene(TCE)
• Trichloroethane(TCA)
• Registry Data

SECTION 2

THE SELECTION OF TCE AS A PRIMARY CONTAMINANT

In 1988, TCE was selected as the primary chemical for the first subregistry of the National Exposure Registry. In keeping with the general procedures for chemical selection (1), the factors that led to the selection of TCE included: the ubiquitousness of TCE in the environment; published evidence of TCE toxicity in worker populations and in toxicologic studies(1); and the paucity of information on low-level, long-term exposures to TCE. Each of these three factors suggested that the Registry could contribute significantly to the detection of an excess in adverse human effects, should they exist, following long-term, low-level exposure to TCE in the environment.

ENVIRONMENTAL INFORMATION

At the time of its selection, TCE was the most prevalent contaminant found at National Priorities List (NPL) sites.(2) Figure 2-1 shows that TCE was identified at 37% (n = 355) of all NPL sites. TCE was a groundwater contaminant at 91% (n = 322) of the TCE sites.

Local communities were using the TCE-contaminated groundwater as a source of drinking water at 87% (n = 279) of the groundwater sites. Of the groundwater sites, 33% (n = 91) had private well systems, 33% (n = 93) had municipal systems, and 34% (n = 95) used both private and municipal systems to provide residents with drinking water. Last, 11% (n = 31) of the TCE-contaminated groundwater sites also used TCE-contaminated surface water as a drinking water source (3).

HUMAN DATA

As of 1988, the year the subregistry was established, the available literature indicated that TCE was toxic to humans and animals. A brief synopsis of the literature follows; a more detailed discussion, along with current information, is given in Section 8. For humans (5), research reported in the literature indicated that the principal targets following TCE exposure were the central nervous system (CNS), liver, kidney, and hematologic system. Because of the paucity of relevant study information and the uncertainties in interpreting the study findings reported in the literature, neither the lowest observable adverse effect levels (LOAELs) nor the no observable adverse effect levels (NOAELs) for most effects in humans could be specified.

Figure 2-1.Number and types of TCE sites in 1988.

For example, there was limited information regarding lethality in humans resulting from inhalation or oral exposure to TCE (Figure 2-2) (5). Reports of acute exposures were poorly quantified or not quantified at all. Data were available for CNS effects in humans resulting from acute and chronic inhalation exposures, but threshold concentrations for acute exposures and effect levels for chronic exposures were inadequately defined. Reports of acute oral and inhalation exposures indicated hepatic and renal effects, but exposure and dose data were not available. Although these studies were considered inconclusive, they indicated that there might be an association between ingestion of water contaminated with TCE and other chlorinated compounds, and developmental effects and leukemia in humans. Little information was available for effects in humans with dermal exposure to TCE.

ANIMAL DATA

Studies of animals were also limited in 1988, but they too indicated some possible adverse health effects following TCE exposure. Ingesting or breathing levels of TCE that were much higher than typical environmental levels could possibly produce numerous adverse outcomes: nervous system damage; liver and kidney damage; effects in the blood; tumors of the liver, kidney, lung, and male sex organs; and cancer of tissues that form white blood cells

Figure 2-2.--Availability of information on health effects of TCE (human data).

(leukemia). Results of a few studies in pregnant animals exposed to TCE in air or in food showed varied effects on unborn animals or newborns. These effects are discussed further in Chapter 8.

Figure 2-3 (5) summarizes the available information gleaned from animal studies. These studies (5) identified the general range of lethality and principal toxic effects of inhalation and oral exposure to TCE, but did not fully characterize exposure- or dose-effect relationships. Threshold and no-effect concentrations or doses were lacking for many of the toxic effects, and some of the effects (for example, immunosuppression and hematologic effects) needed additional characterization.

Animal data were also insufficient to determine the health effects resulting from acute and chronic exposures. Inhalation studies (6,7) indicated that TCE was a developmental toxicant, but a NOAEL had not been identified and an evaluation of malformations associated with oral exposure had not been conducted. The effects of oral exposure on fertility or reproductive performance in rodents had been adequately characterized (8,9), but the threshold for fetal effects had not been defined. Little information was available for effects in animals following dermal exposure to TCE.

In summary, the TCE Subregistry was created in response to the pervasiveness of TCE in the nation's waste sites; the relative lack of information on human health outcomes associated with long-term, low-level exposure to TCE; and the knowledge of adverse health outcomes

Figure 2-3.--Availability of information on health effects of TCE (animal data).

among people experiencing different types of TCE exposure (for example, short term at high concentrations). Subsequent new knowledge concerning TCE exposure and human health, available since the selection of TCE and the establishment of the subregistry, further supports the establishment and maintenance of a TCE Subregistry.

1. 1 At the time of its selection, TCE was one of the 25 chemicals on the Hazardous Substance Priority List (2).

2. 2 At the time of its selection, TCE was listed as present at more than 355 sites in an ATSDR database called VIEW (3). A more recent ATSDR environmental database, HAZDAT (4), lists TCE as being present at 887 (25.5%) of 3,468 active sites in the file, and at 806 (59.3%) of the 1,357 NPL sites.