ReviewArchives of toxicology2026
Immune effects of trichloroethylene: key findings of occupational hypersensitivity syndrome and its pathogenesis.
Review in Archives of toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
5 authors.
Funding
Abstract
Trichloroethylene (TCE) remains a versatile organic solvent used globally. In recent years, immunological occupational diseases such as hypersensitivity syndrome (HS) and systemic sclerosis (SSc) have attracted attention in terms of the number of patients and the life-threatening consequences. This review summarizes mechanisms underlying HS pathogenesis based on the available literature. TCE-HS is a disease attributable to anti-CYP2E1 autoantibodies and HLA-B13:01 as susceptibility gene and is characterized by systemic skin lesions, severe-to-moderate liver damage, fever above 38 °C, leukocytosis, lymphadenopathy, and human herpesvirus 6 (HHV6) reactivation with elevated inflammatory cytokines, which are all similar to the characteristics of drug-induced HS. TCE-HS occurs on average 1 month after the commencement of exposure to TCE, which is shorter than the corresponding period for SSc. Recent epidemiological and animal studies have clarified the mechanism of pathogenesis: the oxidative metabolites chloral hydrate, dichloroacetyl chloride, and trichloroethanol, which are produced by CYP2E1, amplify the methylation of CD4
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.