Associations of genetic variation in CASP3 gene with noise-induced hearing loss in a Chinese population: a case-control study

Environ Health. 2017 Jul 24;16(1):78. doi: 10.1186/s12940-017-0280-y.


Background: Noise-induced hearing loss (NIHL) is a complex disease caused by environmental and genetic risk factors. This study explored the relationship between the genetic variations in the CASP gene and the risk of developing NIHL among Chinese workers exposed to occupational noise.

Methods: A case-control study of 272 NIHL workers and 272 normal-hearing workers matched for age, sex and years of noise exposure was conducted. Fifteen single-nucleotide polymorphisms (SNP) in the CASP1, CASP3, CASP4, CASP5, CASP6, CASP8, CASP9, CASP10 and CASP14 genes were genotyped using the polymerase chain reaction-ligase detection reaction method. Using conditional logistic regression models, the adjusted odds ratios (ORs) and 95% confidence intervals (CIs) of genetic variations associated with NIHL risk were calculated.

Results: Two SNPs in the CASP3 gene were associated with NIHL risk. For rs1049216, TT genotype was associated with a decreased risk of NIHL (OR = 0.246, 95% CI = 0.069-0.886) when compared with the CC genotype. For rs6948, the AC and CC genotype were associated with a decreased NIHL risk (OR = 0.568, 95% CI = 0.352-0.916) compared with AA genotype. There were joint effects of working time and CASP3 polymorphisms on NIHL risk (P < 0.05).

Conclusions: Genetic variations in the CASP3 gene and the joint effects of working time and CASP3 polymorphisms may modify the risk of developing NIHL.

Keywords: CASP3; Genetic susceptibility; Noise-induced hearing loss/NIHL; Single-nucleotide polymorphism/SNP.

MeSH terms

  • Adult
  • Case-Control Studies
  • China / epidemiology
  • Female
  • Genotype*
  • Hearing Loss, Noise-Induced / epidemiology
  • Hearing Loss, Noise-Induced / etiology
  • Hearing Loss, Noise-Induced / genetics*
  • Humans
  • Male
  • Noise, Occupational / adverse effects*
  • Occupational Exposure*
  • Polymorphism, Single Nucleotide*
  • Prevalence
  • Young Adult