Trichloroethylene Hypersensitivity Syndrome Is Potentially Mediated through Its Metabolite Chloral Hydrate

Background We documented previously the entity of trichloroethylene (TCE) hypersensitivity syndrome (THS) in occupational workers. Objectives To identify the culprit causative compound, determine the type of hypersensitivity of THS, and establish a screening test for subjects at risk of THS. Methods TCE and its main metabolites chloral hydrate (CH), trichloroethanol (TCOH) and trichloroacetic acid (TCA) were used as allergens at different concentrations in skin patch tests. The study included 19 case subjects diagnosed with occupational THS, 22 control healthy workers exposed to TCE (exposure >12 weeks), and 20 validation new workers exposed to TCE for <12 weeks free of THS. All subjects were followed-up for 12 weeks after the patch test. Results The highest patch test positive rate in subjects with THS was for CH, followed by TCOH, TCA and TCE. The CH patch test positive rate was 100% irrespective of CH concentrations (15%, 10% and 5%). The TCOH patch test positive rate was concentration-dependent (89.5%, 73.7% and 52.6% for 5%, 0.5% and 0.05%, respectively). Lower patch test positive rates were noted for TCA and TCE. All patch tests (including four allergens) were all negative in each of the 22 control subjects. None of the subjects of the validation group had a positive 15% CH patch test. Conclusions Chloral hydrate seems to be the culprit causative compound of THS and type IV seems to be the major type of hypersensitivity of THS. The CH patch test could be potentially useful for screening workers at risk of THS.

[1]  G. Cooper,et al.  Human Health Effects of Dichloromethane: Key Findings and Scientific Issues , 2014, Environmental health perspectives.

[2]  M. Tohyama,et al.  Occupational trichloroethylene hypersensitivity syndrome: human herpesvirus 6 reactivation and rash phenotypes. , 2013, Journal of dermatological science.

[3]  K. Guyton,et al.  Human Health Effects of Trichloroethylene: Key Findings and Scientific Issues , 2012, Environmental health perspectives.

[4]  W. Zhou,et al.  Cytokine expression in trichloroethylene-induced hypersensitivity dermatitis: an in vivo and in vitro study. , 2012, Toxicology letters.

[5]  Xingfen Yang,et al.  Upregulation of Calprotectin and Downregulation of Retinol Binding Protein in the Serum of Workers with Trichloroethylene‐induced Hypersensitivity Dermatitis , 2012, Journal of occupational health.

[6]  Hailan Wang,et al.  [Studying the changes of the related serum complement immune indexes in patients with occupational medicamentosa-like dermatitis induced by trichloroethylene and workers occupationally exposed to trichloroethylene]. , 2012, Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational diseases.

[7]  Z. Ikezawa,et al.  Evaluation of serum cytokine levels in toxic epidermal necrolysis and Stevens–Johnson syndrome compared with other delayed‐type adverse drug reactions , 2011, The Journal of dermatology.

[8]  B. K. Park,et al.  Immune pathomechanism of drug hypersensitivity reactions. , 2011, The Journal of allergy and clinical immunology.

[9]  P. Friedmann,et al.  Patch testing in drug allergy , 2010, Current opinion in allergy and clinical immunology.

[10]  M. Tohyama,et al.  Occupational Trichloroethylene Hypersensitivity Syndrome with Human Herpesvirus-6 and Cytomegalovirus Reactivation , 2010, Dermatology.

[11]  M. Pirmohamed,et al.  Characterization of p-phenylenediamine-albumin binding sites and T-cell responses to hapten-modified protein. , 2010, The Journal of investigative dermatology.

[12]  H. Han-lin Research progress on immune injury resulted from occupational medicamentose-like dermatitis induced by trichloroethylene , 2010 .

[13]  Jie Liu Clinical analysis of seven cases of trichloroethylene medicamentose-like dermatitis. , 2009, Industrial health.

[14]  E. Phillips,et al.  A review of drug patch testing and implications for HIV clinicians , 2008, AIDS.

[15]  S. Leng,et al.  HLA-B*1301 as a Biomarker for Genetic Susceptibility to Hypersensitivity Dermatitis Induced by Trichloroethylene among Workers in China , 2007, Environmental health perspectives.

[16]  N. Hisanaga,et al.  Occupational trichloroethylene exposure as a cause of idiosyncratic generalized skin disorders and accompanying hepatitis similar to drug hypersensitivities , 2007, International archives of occupational and environmental health.

[17]  T. Yoshikawa,et al.  Human Herpesvirus 6 Reactivation in Trichloroethylene‐exposed Workers Suffering from Generalized Skin Disorders Accompanied by Hepatic Dysfunction , 2006, Journal of occupational health.

[18]  E. Barletta,et al.  Expression of cytokines and chemokine receptors in the cutaneous lesions of erythema multiforme and Stevens–Johnson syndrome/toxic epidermal necrolysis , 2006, The British journal of dermatology.

[19]  Huang Han-li Editorial explanation for Diagnostic Criteria of Occupational Medicamentosa-like Dermatitis induced by Trichloroethylene , 2006 .

[20]  Xiao Lihua A clinical observation on hepatic dysfunction in epispasis-like dermatitis patients due to trichloroethylene , 2004 .

[21]  D. Shin,et al.  Exfoliative Dermatitis and Toxic Hepatitis Associated with Occupational Exposure to Trichloroethylene , 2003 .

[22]  D. Gawkrodger Patch testing in occupational dermatology , 2001, Occupational and environmental medicine.

[23]  P. Wattanakrai,et al.  Fever, skin rash, jaundice and lymphadenopathy after trichloroethylene exposure: a case report. , 1997, Journal of the Medical Association of Thailand = Chotmaihet thangphaet.

[24]  T. Takano,et al.  Generalized eruption with severe liver dysfunction associated with occupational exposure to trichloroethylene , 1988, Contact dermatitis.

[25]  C. Goh,et al.  Stevens‐Johnson syndrome associated with occupational exposure to trichloroethylene , 1984, Contact dermatitis.

[26]  L. Condé‐Salazar,et al.  Subcorneal pustular eruption and erythema from occupational exposure to trichloroethylene * , 1983, Contact dermatitis.

[27]  S. Ohmori,et al.  Metabolism of trichloroethylene. , 1980, Biochemical pharmacology.