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Table 3 Association between SNPs and NIHL risk

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

SNP

Genetic model

Genotype

Controls, n (%)

Cases, n (%)

P

OR(95%CI)a

rs1049216

Additive

CC

173(64.3)

195(72.5)

 

1.0

  

CT

82(30.5)

68(25.3)

0.050

0.609(0.372–1.000)

  

TT

14(5.2)

6(2.2)

0.032

0.246(0.069–0.886)

 

Dominant

CC

173(64.3)

195(72.5)

 

1.0

  

CT + TT

96(35.7)

72(27.5)

0.014

0.551(0.343–0.885)

 

Recessive

CC + CT

258(94.8)

266(97.8)

 

1.0

  

TT

14(5.2)

6(2.2)

0.047

0.277(0.078–0.986)

rs6948

Additive

AA

177(65.8)

198(73.6)

 

1.0

  

AC

79(29.4)

65(24.2)

0.050

0.607(0.369–1.000)

  

CC

13(4.8)

6(2.2)

0.089

0.328(0.091–1.185)

 

Dominant

AA

177(65.8)

198(73.6)

 

1.0

  

AC + CC

92(34.2)

71(26.4)

0.020

0.568(0.352–0.916)

 

Recessive

AA + AC

256(95.2)

263(97.8)

 

1.0

  

CC

13(4.8)

6(2.2)

0.128

0.373(0.105–1.327)

Risk genotypeb

0

91(33.8)

71(26.4)

 

1.0

  

1

6(2.2)

3(1.1)

0.701

0.684(0.098–4.779)

  

2

172(63.9)

195(72.5)

0.018

1.787(1.104–2.892)

  1. aadjusted for age, sex, education, marriage status, income, working time, noise exposure time, noise intensity exposure, CNE, telephone using time, music listening time, and time go to sleep
  2. brs1049216 CC and rs6948 AA genotypes were classified as high-risk genotypes; the number represents the numbers of the two genotypes within the combined genotypes