cleaning agents, and degreasers. Exposed and control subjects were studied with a neurobehavioral evaluation protocol that included clinical tests, nerve conduction studies, blink reflex measurements, and extensive neuropsychological testing. The blink reflex indicates the physiological integrity of the afferent and efferent circuitry of the Vth (trigeminal) and VIIth (facial) cranial nerves. A physician using electromyographic equipment, quantitatively evaluated reflex latency responses with an automated oscilloscope for several modalities of stimulation. Highly significant differences were detected between the two groups, with a level of significance of 0.0001. Feldman et al. (1990) conclude that the blink reflex measurement appears useful in evaluating a population group with a history of chronic low-dose exposure to TCE, providing a sensitive method for evaluating subclinical neurotoxic effects on the Vth-VIIth cranial nerve circuitry.

While not commonly thought of as constituting markers, neurobehavioral tests can provide a diverse range of measures of toxic exposures and effects. A battery of neurobehavioral tests has been applied to the study of persons exposed to materials that occur at hazardous-waste sites (Table 7-1). This battery includes numerous expressions of neurotoxic central and peripheral neuropathy and covers a wide array of functions. A comprehensive review of developing techniques in neurobehavioral assessment found consistent and significant neurobehavioral effects and a range of other subtle neurological alterations in persons exposed to metals, solvents, and insecticides, with some indication of greater effects in those with greater estimated exposures (White et al., 1990). Animal studies reveal that TCE inhalation also induces a range of neurotoxic effects in rodents (Dorfmueller et al., 1979).

As discussed in Chapter 6, biologic monitoring for neurotoxic chemicals such as TCE has also identified specific markers of exposure. Levels of metabolites of TCE in urine have been determined in persons exposed environmentally and in human volunteers. About 60 percent of TCE is metabolized and excreted in the urine as one of three compounds, di- and trichloroacetic acid, trichloroethanol, and trichloroethanol glucuronide; a small amount (about 10 percent) is exhaled by the lungs as TCE. The typical kinetics and compartments for excretion or uptake of the remaining 30 percent of TCE are unknown, according to studies that have used human volunteers (Monster et al., 1979). There is no evidence of saturation in humans, that is, an exposure above and beyond which there is no uptake; but studies in mice and rats exposed to TCE in water or air indicate metabolic saturation in those species (ATSDR, 1989). Dichloroacetic acid (DCA) is both a by-product of chlorine disinfection of water containing natural organic material and a key metabolite

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