Table 5 Interactions between PSE and genetic variants on child ADHD risk

From: Prenatal Tobacco Exposure Modulated the Association of Genetic variants with Diagnosed ADHD and its symptom domain in children: A Community Based Case–Control Study

PSE

Genotype

Cases, N(%)

Controls, N(%)

OR(95% CI)

P mul

AP(95% CI)

RERI(95% CI)

ADRA2A rs553668

No

AA

26(16.25)

61(27.11)

1

0.003

0.48(0.09–0.87)

1.88(0.06–4.12)

Yes

AA

14(8.75)

23(10.22)

1.36(0.58–3.22)

   

No

AG + GG

76(47.50)

115(51.11)

1.65(0.93–2.90)

   

Yes

AG + GG

44(27.50)

26(11.56)

3.54(1.73–7.25)

   

DRD2 rs1124491

No

AA

7(4.27)

27(12.16)

1

0.175

−0.55(−1.84–0.73)

−3.34(−11.42–4.74)

Yes

AA

99(60.36)

145(65.32)

5.34(1.64–4.46)

   

No

AG + GG

6(3.66)

6(2.70)

3.99(1.46–0.89)

   

Yes

AG + GG

52(31.71)

44(19.82)

6.04(2.07–7.65)

   

SLC6A4 rs6354

No

TT

74(44.31)

147(63.91)

1

0.234

−0.80(−2.42–0.82)

−1.37(−3.39–0.65)

Yes

TT

44(26.35)

39(16.96)

2.13(1.20–3.78)

   

No

TG + GG

34(20.36)

32(13.91)

1.97(1.10–3.52)

   

Yes

TG + GG

15(8.98)

12(5.22)

1.79(0.75–4.28)

   
  1. Pmul was calculated using the multiplicative interaction term in the logistic regression analysis.
  2. The ORs, 95% CIs, AP and RERI were adjusted by age, gender, pregnancy age of mother, and postnatal smoking exposure.