Ability of trichloroethylene metabolite to promote immune pathology is strain-specific.

Chronic low-level exposure to the environmental pollutant trichloroethylene has been shown to promote autoimmune disease in association with CD4(+) T-lymphocyte activation in lupus-prone MRL(+/+) mice. One of the primary metabolites of trichloroethylene, trichloroacetaldehyde hydrate (TCAH), was similarly shown to increase the percentage of IFNgamma-producing CD4(+) T-lymphocytes when added to the drinking water of MRL(+/+) mice. In addition, TCAH-treated MRL(+/+) mice developed skin inflammation and alopecia. In the present study TCAH was tested for its ability to accelerate the development of alopecia in C3H/HeJ mice which tend to develop the disorder spontaneously late in life. In contrast to MRL(+/+) mice, C3H/HeJ mice treated with TCAH did not develop alopecia at an increased rate. In addition, TCAH did not promote the expansion of activated IFNgamma-producing CD4(+) T-lymphocytes in C3H/HeJ mice. CD4(+) T-lymphocytes from TCAH-treated C3H/HeJ mice, unlike their MRL(+/+) counterparts, did not become resistant to activation-induced apoptosis following in vivo exposure to TCAH. Taken together, it appears that the ability of TCAH to promote immune-mediated pathology is strain-specific and may require an autoimmune-prone genetic background.