Severe Hypersensitivity Dermatitis and Liver Dysfunction Induced by Occupational Exposure to Trichloroethylene

Xu, Xinyun; Rong-xing, Yang; Wu, Nan; Zhong, Ping; Ke, Yuebin; Zhou, Li; Yuan, Jun; Ge-yi, LI; Huang, Haiyan; Wu, Bin

doi:10.2486/indhealth.47.107

Cited by 51 publications

(45 citation statements)

References 16 publications

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“…Human TCE exposure (both occupational and environmental) has been linked to several autoimmune diseases (scleroderma, systemic lupus erythematosus, hepatitis and diabetes [3][4][5][6][7][8][9][10][11]) and hypersensitivity disorders [12][13][14]. By using a female MRL+/+ mouse model, we have shown that chronic exposure to TCE during adulthood promotes autoimmune hepatitis that corresponds to idiopathic autoimmune hepatitis in humans, that is, T-cell infiltration of the liver and development of antibodies specific for liver microsomal proteins [15,16].…”

mentioning

confidence: 99%

Chronic Exposure to Water Pollutant Trichloroethylene Increased Epigenetic Drift in CD4 ⁺ T cells

et al. 2016

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Aim: Autoimmune disease and CD4+ T-cell alterations are induced in mice exposed to the water pollutant trichloroethylene (TCE). We examined here whether TCE altered gene-specific DNA methylation in CD4 + T cells as a possible mechanism of immunotoxicity. Materials & methods: Naive and effector/memory CD4 + T cells from mice exposed to TCE (0.5 mg/ml in drinking water) for 40 weeks were examined by bisulfite next-generation DNA sequencing. Results: A probabilistic model calculated from multiple genes showed that TCE decreased methylation control in CD4 + T cells. Data from individual genes fitted to a quadratic regression model showed that TCE increased gene-specific methylation variance in both CD4 subsets. Conclusion: TCE increased epigenetic drift of specific CpG sites in CD4 + T cells.

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confidence: 99%

Chronic Exposure to Water Pollutant Trichloroethylene Increased Epigenetic Drift in CD4 ⁺ T cells

et al. 2016

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“…Xu et al [2009] conducted a study with 21 patients with TCE-induced skin disorders that worked at 3 separate factories from 2003-2005 with an average exposure duration of 38 days. These patients were exposed during cleaning and degreasing operations and did not wear gloves, and were also possibly exposed via inhalation [Xu et al 2009]. The patients reported neurological symptoms (headache, dizziness), skin effects, and liver dysfunction [Xu, et al 2009].…”

Section: Systemic Toxicity From Skin Exposure (Sk: Sys)mentioning

confidence: 99%

“…These patients were exposed during cleaning and degreasing operations and did not wear gloves, and were also possibly exposed via inhalation [Xu et al 2009]. The patients reported neurological symptoms (headache, dizziness), skin effects, and liver dysfunction [Xu, et al 2009]. Gash et al [2008] reported 3 workers that were exposed to TCE both through chronic inhalation and dermal contact for 25 years or greater had Parkinson's disease (PD).…”

Section: Systemic Toxicity From Skin Exposure (Sk: Sys)mentioning

confidence: 99%

“…In occupational exposures that involved inhalation of the vapor, percutaneous penetration, or both, TCE caused skin irritation and rashes, central nervous system effects, and/or eye effects after repeated exposure [El Ghawabi et al 1973;Bauer and Rabens 1974;Xu et al 2009]. Xu et al [2009] reported skin irritation in 21 patients diagnosed with a TCE-induced skin disorder, and symptoms included skin erythema, rashes, and blistering.…”

Section: Direct Effects On Skin (Sk: Dir)mentioning

confidence: 99%

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NIOSH skin notation (SK) profile: trichloroethylene (TCE) [CAS No. 79-01-6].

2017

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“…Due to its frequent use, there is increasing evidence to demonstrate that exposure to TCE causes several adverse health effects in human and animals, including severe skin lesions, as well as immune-related renal and liver injury (Khan et al 2009;Xu et al 2009;Yu et al 2012). Clinical data indicates that renal injury is an important cause of death in patients exposed to TCE.…”

Section: Introductionmentioning

confidence: 99%

Plasma Kallikrein-Kinin system mediates immune-mediated renal injury in trichloroethylene-sensitized mice

Wang

Zhang

et al. 2016

Journal of Immunotoxicology

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Trichloroethylene (TCE) is a major environmental pollutant. An immunological response is a newlyrecognized mechanism for TCE-induced kidney damage. However, the role of the plasma kallikreinkinin system (KKS) in immune-mediated kidney injury has never been examined. This study aimed to explore the role of the key components of the KKS, i.e. plasma kallikrein (PK), bradykinin (BK) and its receptors B1R and B2R, in TCE-induced kidney injury. A mouse model of skin sensitization was used to explore the mechanism of injury with or without a PK inhibitor PKSI. Kidney function was evaluated by measuring blood urea nitrogen (BUN) and creatinine (Cr) in conjunction with histopathologic characterization. Plasma BK was determined by ELISA; Renal C5b-9 membrane attack complex was evaluated by immunohistochemistry. Expression of BK and PK in the kidney was detected by immunoFuorescence. mRNA and protein levels of B1R and B2R were assessed by real-time qPCR and Western blot. As expected, numerous inflammatory cell inEltration and tubular epithelial cell vacuolar degeneration were observed in TCE-sensitized mice. Moreover, serum BUN and Cr and plasma BK were increased. In addition, deposition of BK, PK and C5b-9 were observed and B1R and B2R mRNA and proteins levels were up-regulated. Pre-treatment with PKSI, a highly selective inhibitor of PK, alleviated TCE-induced renal damage. In addition, PKSI attenuated TCEinduced up-regulation of BK, PK and its receptors and C5b-9. These results provided the first evidence that activation of the KKS contributed to immune-mediated renal injury induced by TCE and also helped to identify the KKS as a potential therapeutic target for mitigating chemical sensitization-induced renal damage.ARTICLE HISTORY

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Severe Hypersensitivity Dermatitis and Liver Dysfunction Induced by Occupational Exposure to Trichloroethylene

Cited by 51 publications

References 16 publications

Chronic Exposure to Water Pollutant Trichloroethylene Increased Epigenetic Drift in CD4 ⁺ T cells

Chronic Exposure to Water Pollutant Trichloroethylene Increased Epigenetic Drift in CD4 ⁺ T cells

NIOSH skin notation (SK) profile: trichloroethylene (TCE) [CAS No. 79-01-6].

Plasma Kallikrein-Kinin system mediates immune-mediated renal injury in trichloroethylene-sensitized mice

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Severe Hypersensitivity Dermatitis and Liver Dysfunction Induced by Occupational Exposure to Trichloroethylene

Cited by 51 publications

References 16 publications

Chronic Exposure to Water Pollutant Trichloroethylene Increased Epigenetic Drift in CD4 + T cells

Chronic Exposure to Water Pollutant Trichloroethylene Increased Epigenetic Drift in CD4 + T cells

NIOSH skin notation (SK) profile: trichloroethylene (TCE) [CAS No. 79-01-6].

Plasma Kallikrein-Kinin system mediates immune-mediated renal injury in trichloroethylene-sensitized mice

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Chronic Exposure to Water Pollutant Trichloroethylene Increased Epigenetic Drift in CD4 ⁺ T cells

Chronic Exposure to Water Pollutant Trichloroethylene Increased Epigenetic Drift in CD4 ⁺ T cells