AI Article Synopsis

  • Occupational exposure to trichloroethylene (TCE) can lead to trichloroethylene hypersensitivity syndrome (TCEHS), characterized by skin and liver issues.
  • The study used guinea pigs to identify allergens (TCE, its metabolite TCEOH, and TCA) and assess their effects on skin and liver health through specific tests.
  • Results showed TCE as the primary allergen causing significant skin reactions and liver damage, while TCEOH acted as a secondary allergen contributing to the condition.

Article Abstract

Objectives: Occupational exposure to trichloroethylene (TCE) induces trichloroethylene hypersensitivity syndrome (TCEHS), which causes hypersensitivity dermatitis and hepatitis. However, whether TCE itself or its two metabolites, trichloroethanol (TCEOH) and trichloroacetic acid (TCA), are involved in TCEHS remains unclear. Therefore, in this study we explored the allergens causing TCEHS and characterized TCEHS-related liver injury in guinea pigs.

Method: The guinea pig maximization test was performed using TCE, TCEOH, and TCA as candidate allergens. Skin inflammation was scored, and liver function and histopathological changes were evaluated by biochemical tests and hematoxylin and eosin staining, respectively.

Results: The sensitization rates for TCE, TCEOH, and TCA were 90.0%, 50.0%, and 0.0%, respectively. In the TCE and TCEOH experimental groups, the skin showed varying degrees of erythema with eosinophil granulocyte infiltration in the dermis. Additionally, serum alanine aminotransferase and γ-glutamyl transpeptidase levels increased significantly, and histological analysis revealed focal hepatocellular necrosis with inflammatory cell infiltration in the liver.

Conclusions: TCE is the main cause of allergy and TCEOH is a secondary factor for allergy in guinea pigs. TCE and TCEOH can cause immune-mediated skin sensitization complicated by focal hepatic necrosis.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7428806PMC
http://dx.doi.org/10.1002/1348-9585.12142DOI Listing

Publication Analysis

Top Keywords

tce tceoh
16
skin sensitization
8
focal hepatic
8
hepatic necrosis
8
guinea pigs
8
tceoh tca
8
tce
7
tceoh
6
trichloroethylene trichloroethanol
4
trichloroethanol induce
4

Similar Publications

Article Synopsis
  • Occupational exposure to trichloroethylene (TCE) can lead to trichloroethylene hypersensitivity syndrome (TCEHS), characterized by skin and liver issues.
  • The study used guinea pigs to identify allergens (TCE, its metabolite TCEOH, and TCA) and assess their effects on skin and liver health through specific tests.
  • Results showed TCE as the primary allergen causing significant skin reactions and liver damage, while TCEOH acted as a secondary allergen contributing to the condition.
View Article and Find Full Text PDF

The industrial solvent trichloroethylene (TCE) and its two major metabolites trichloroethanol (TCE-OH) and trichloroacetic acid (TCA) cause formic aciduria in male F344 rats. Prior treatment of male F344 rats with 1-aminobenzotriazole a cytochrome P450 inhibitor, followed by TCE (16mk/kg, po), completely prevented formic aciduria, but had no effect on formic acid excretion produced by TCA (8 or 16 mg/kg, po), suggesting TCA may be the proximate metabolite producing this response. Dow and Green reported an increase in the concentration of 5-methyltetrahydrofolate (5-MTHF) in the plasma of rats treated with TCE-OH, suggesting a block in the cycling of 5-MTHF to tetrahydrofolate (THF).

View Article and Find Full Text PDF

Trichloroethylene (TCE) is widely used as a metal degreaser in industrial processes. The present study reports on the effects of TCE exposure on workers employed in the lock industries. To ensure exposure of the workers to TCE, its toxic metabolites, trichloroacetic acid (TCA), dichloroacetic acid (DCA) and trichloroethanol (TCEOH) were detected in the plasma of the subjects through solid phase microextraction-gas chromatography-electron capture detection.

View Article and Find Full Text PDF

Trichloroethylene (TCE) is widely used as a cleaning and decreasing agent and has been shown to cause liver tumours in rodents and a small incidence of renal tubule tumours in male rats. The basis for the renal tubule injury is believed to be related to metabolism of TCE via glutathione conjugation to yield the cysteine conjugate that can be activated by the enzyme cysteine conjugate β-lyase in the kidney. More recently TCE and its major metabolite trichloroethanol (TCE-OH) have been shown to cause formic aciduria which can cause renal injury after chronic exposure in rats.

View Article and Find Full Text PDF

Micronucleus induction by oxidative metabolites of trichloroethylene in cultured human peripheral blood lymphocytes: a comparative genotoxicity study.

Environ Sci Pollut Res Int

December 2013

Petroleum Toxicology Division, Indian Institute of Toxicology Research (IITR), Council of Scientific and Industrial Research, P.O. Box No. 80, Mahatma Gandhi Marg, Lucknow, 226001, India.

The genotoxic effects of oxidative metabolites of trichloroethylene (TCE), namely chloral hydrate, trichloroacetic acid (TCA), dichloroacetic acid (DCA), and trichloroethanol (TCEOH) were examined in human peripheral blood lymphocytes. In this context, lymphocytes were exposed in vitro to 25, 50, and 100 μg/ml concentrations of these metabolites separately for a period of 48 h and examined for micronucleus (MN) induction through flow cytometer. At 50 μg/ml TCE metabolites, TCA (6.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!