Occupational exposure to trichloroethylene (TCE) is a major cause of dermatitis; however, whether its metabolites are involved in the development of the disease is unclear.

This study aims to evaluate the sensitization of trichloroacetic acid and trichloroethanol and to investigate their roles in the TCE-induced hypersensitive dermatitis (TIHD).

Human myeloid leukemia mononuclear cells (THP-1) were cultured in vitro and exposed to trichloroacetic acid or trichloroethanol at 0, 0.5, 1.0, 2.0, and 4.0mmol·L^-1, respectively. Interleukin-8 (IL-8) was detected by ELISA; inducible nitric oxide synthase (iNOS) was detected by Western blotting. A total of 57 individuals participated in a population-based study, including a TCE non-exposure control group, a TCE exposure group, a TIHD admitted group, and a TIHD discharged group. Peripheral blood mononuclear cells were separated by lymphocyte isolation solution and exposed to 0.5 and 2.0mmol·L^-1 trichloroacetic acid or trichloroethanol. Their survival rates were estimated by CCK-8.

The toxicity of trichloroacetic acid or trichloroethanol on THP-1 cells increased in a dose-dependent manner, and the IL-8 levels in THP-1 cells also increased gradually with the increase of exposure dose in a dose-dependent manner (P< 0.05). Compared with the control group, the IL-8 levels increased by 116.30%, 176.08%, and 541.18% in the 1.0, 2.0, and 4.0 mmol·L^-1 trichloroacetic acid groups and by 176.08%, 366.70%, and 670.48% in the 1.0, 2.0, and 4.0 mmol·L^-1 trichloroethanol groups, respectively (P< 0.05). The results of Western blotting indicated that compared with the control group, the iNOS levels in the 1.0, 2.0, and 4.0 mmol·L^-1 trichloroacetic acid groups increased by 93.73%, 87.08%, and 238.06% (P< 0.05), and the levels in the 1.0, 2.0, and 4.0 mmol·L^-1 trichloroethanol groups increased by 95.99%, 486.29%, and 735.72% (P< 0.05), respectively. In the population-based study, compared with the non-exposure control group, the survival rates of peripheral blood mononuclear cells exposed to 0.5 and 2 mmol·L^-1 trichloroacetic acid increased by 5.81% and 5.64% in the discharged group (P< 0.05), while no cell proliferation was found after trichloroethanol treatment in the discharged group (P< 0.05); the survival rates of peripheral blood mononuclear cells after trichloroacetic acid or trichloroethanol treatment in the TCE exposure group and the TIHD admitted group showed no significant differences with the non-exposure control group (P< 0.05). These results illustrated the presence of trichloroacetic acid antigen-specific mononuclear cells in peripheral blood in the discharged patients.

Both trichloroacetic acid and trichloroethanol could induce cellular sensitization, and trichloroacetic acid may be involved in the development of TIHD as an allergen.