Toxicity of trichloroethylene following inhalation and drinking contaminated water

Abstract

The neurobehavioural effects of trichloroethylene (TCE) were studied in rats following administration of the solvent orally (350, 700 and 1400 ppm in drinking water for 90 days) and through inhalation (376 ppm for 4 h a day, 5 days per week for 180 days). Various aspects of spontaneous locomotor activity were assessed at different periods after exposure through either of the routes. Oral exposure to TCE had no significant effect on spontaneous locomotor activity or cognitive ability, whereas inhalation to the solvent resulted in an increase in the distance travelled and horizontal activity counts at day 30 but a decrease at day 60 of exposure. The time spent in ambulatory and stereotypic movements as well as the number of stereotypic movements were enhanced significantly only at day 30. The resting time was decreased at day 30 but enhanced at day 60 of exposure. The learning ability was not affected significantly up to day 180. The results highlight the neurotoxic potential of inhalation exposure to TCE.

The Role of Environmental Exposures in Neurodegeneration and Neurodegenerative Diseases

“…The neurological effects of TCE have long been known, although the pathological correlates have been somewhat controversial in animals and humans (Schaumburg, 2000). More recent data have shown that inhalation of TCE in the rat after 60 days was found to elicit locomotor impairments (Waseem et al, 2001). Additionally, two recent reports have identified links between long-term TCE exposure and PD in humans and described the creation of a TCE animal model of PD.…”

Genetic Factors in Environmentally Induced Disease

“…Dieldrin ranked second among agricultural chemicals used in the US with a peak in the mid-1960s, with the use of approximately 20 million pounds per year [30]. Recent animal model data show that inhalation of TCE creates motor impairment after 60 days [35]. In addition, studies in animal models have shown that dieldrin exposure replicates many of the neuropathological changes associated with PD [33].…”