Effects of genetic polymorphisms of N-Acetyltransferase on trichloroethylene-induced hypersensitivity dermatitis among exposed workers

Ind Health. 2009 Oct;47(5):479-86. doi: 10.2486/indhealth.47.479.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Arylamine N-Acetyltransferase / genetics*
  • Asian People / genetics
  • Case-Control Studies
  • China / epidemiology
  • Dermatitis, Occupational / epidemiology*
  • Dermatitis, Occupational / etiology
  • Dermatitis, Occupational / genetics*
  • Female
  • Genetic Predisposition to Disease
  • Humans
  • Isoenzymes / genetics*
  • Logistic Models
  • Male
  • Phenotype
  • Polymorphism, Genetic*
  • Risk Factors
  • Trichloroethylene / adverse effects*

Substances

  • Isoenzymes
  • Trichloroethylene
  • Arylamine N-Acetyltransferase
  • N-acetyltransferase 1
  • NAT2 protein, human