Effects of Genetic Polymorphisms of N-Acetyltransferase on Trichloroethylene-Induced Hypersensitivity Dermatitis among Exposed Workers

被引:13
作者
Dai, Yufei [1 ]
Leng, Shuguang [1 ]
Li, Laiyu [2 ]
Niu, Yong [1 ]
Huang, Hanlin [2 ]
Liu, Qingjun [1 ]
Duan, Huawei [1 ]
Cheng, Juan [1 ]
Liu, Qing [1 ]
Zheng, Yuxin [1 ]
机构
[1] Chinese Ctr Dis Control & Prevent, Natl Inst Occupat Hlth & Poison Control, Beijing 100050, Peoples R China
[2] Hosp Occupat Dis Control Guangdong Prov, Guangzhou 510300, Guangdong, Peoples R China
关键词
Trichloroethylene; Hypersensitivity dermatitis; N-Acetyltransferase; Genetic polymorphisms; Phenotype; GENERALIZED SKIN DISORDERS; PROXIMAL TUBULAR CELLS; OCCUPATIONAL-EXPOSURE; MOLECULAR-GENETICS; PRIMARY CULTURES; CONTACT ALLERGY; NAT1; S-(1,2-DICHLOROVINYL)-L-CYSTEINE; N-ACETYLTRANSFERASE-1; SUSCEPTIBILITY;
D O I
10.2486/indhealth.47.479
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
The hypersensitivity dermatitis induced by trichloroethylene (TCE) exposure was influenced by individual genetic susceptibility factors. In this paper, a case-control study was conducted to investigate effects of various genotypes and phenotypes of N-Acetyltransferases (NATs) on individual susceptibility to the disease. The study consists of 111 patients with hypersensitivity dermatitis and 154 healthy TCE-exposed workers. Polymerase chain reaction-restriction fragment length polymorphism was used to detect the polymorphic sites of NAT1 at nt 1095 and 1088 and the sites of NAT2 at nt 481, 590, and 857. Logistic regression was used to calculate the odds ratios (ORs) and 95% confidence intervals (95%CI). The results reveal that subjects with intermediate or slow acetylators of NAT2 have a 2.01 fold (95%CI=1.14-3.54) higher risk for the disease than subjects with the fast acetylators. When non-fast NAT2 phenotype (intermediate and slow acetylators) and a slow NAT1 phenotype were combined, the risk for the disease was significantly increased (OR=2.71, 95%CI 1.29-5.70) to the level higher than that observed for NAT2 non-fast acetylators phenotype alone. These findings suggest that slow metabolic phenotype of NAT2 maybe one of risk factor for TCE-induced hypersensitivity dermatitis and combined slow acetylator phenotypes of NAT1 and NAT2 further increase such risk.
引用
收藏
页码:479 / 486
页数:8
相关论文
共 42 条
[1]   CUTANEOUS MANIFESTATIONS OF TRICHLOROETHYLENE TOXICITY [J].
BAUER, M ;
RABENS, SF .
ARCHIVES OF DERMATOLOGY, 1974, 110 (06) :886-890
[2]  
BELL DA, 1995, CANCER RES, V55, P5226
[3]   Hepatitis, rash and eosinophilia following trichloroethylene exposure: A case report and speculation on mechanistic similarity to halothane induced hepatitis [J].
Bond, GR .
JOURNAL OF TOXICOLOGY-CLINICAL TOXICOLOGY, 1996, 34 (04) :461-466
[4]   Influence of polymorphisms of GSTM1 and GSTT1 for risk of renal cell cancer in workers with long-term high occupational exposure to trichloroethene [J].
Bruning, T ;
Lammert, M ;
Kempkes, M ;
Thier, R ;
Golka, K ;
Bolt, HM .
ARCHIVES OF TOXICOLOGY, 1997, 71 (09) :596-599
[5]   Functional polymorphism of the human arylamine N-acetyltransferase type 1 gene caused by C190T and G560A mutations [J].
Butcher, NJ ;
Ilett, KF ;
Minchin, RF .
PHARMACOGENETICS, 1998, 8 (01) :67-72
[6]  
CASCORBI I, 1995, AM J HUM GENET, V57, P581
[7]   Metabolism and toxicity of trichloroethylene and S-(1,2-dichlorovinyl)-L-cysteine in freshly isolated human proximal tubular cells [J].
Cummings, BS ;
Lash, LH .
TOXICOLOGICAL SCIENCES, 2000, 53 (02) :458-466
[8]   Cytotoxicity of trichloroethylene and S-(1,2-dichlorovinyl)-L-cysteine in primary cultures of rat renal proximal tubular and distal tubular cells [J].
Cummings, BS ;
Zangar, RC ;
Novak, RF ;
Lash, LH .
TOXICOLOGY, 2000, 150 (1-3) :83-98
[9]   Genetic polymorphisms of cytokine genes and risk for trichloroethylene-induced severe generalized dermatitis: A case-control study [J].
Dai, YF ;
Leng, SG ;
Li, LY ;
Niu, Y ;
Huang, HL ;
Cheng, J ;
Zheng, YX .
BIOMARKERS, 2004, 9 (06) :470-478
[10]   A restriction fragment length polymorphism assay that differentiates human N-acetyltransferase-1 (NAT1) alleles [J].
Deitz, AC ;
Doll, MA ;
Hein, DW .
ANALYTICAL BIOCHEMISTRY, 1997, 253 (02) :219-224