may be due to metabolism of trichloroethylene to chloral, which is a biologically plausible mechanism for humans.
More animal research is needed to clarify the metabolites and modes of action responsible for trichloroethylene-induced autoimmunity and immunosuppression. Epidemiology studies should further examine connective tissue diseases and other autoimmune diseases (including Stevens-Johnson Syndrome) or immunologic alterations (e.g., changes in T cell subsets, incidence of autoantibodies) in populations exposed to trichloroethylene.
Results from mouse studies suggest that choral forms protein adducts that lead to an alteration of self proteins and the production of autoantibodies. CYP2E1, a known human polymorphic enzyme, may play a role in the formation of these protein adducts (Griffin 2000c). Inhibition of CYP2E1 was found to decrease the incidence and severity of autoimmune diseases in mice. Therefore, genetic polymorphisms in CYP2E1 may play a role in exacerbating autoimmune disease.
Genetic polymorphisms that may play a role in the metabolism of trichloroethylene should be further examined to determine sensitivity factors and to characterize potentially sensitive populations.