Table 3.

Genotyping results using archived dried blood spots for control children

Polymorphism (variant genotype or allele)	Hardy- Weinberg Equilibrium^*	Frequency^† Among Controls	Previously Reported Frequency^† Among controls^‡
GSTM1/GSTT1
GSTM1 (Null)	n/a	52.2%	53.1-53.5%[25, 32, 34]
GSTT1 (Null)	n/a	15.4%	15.0-19.7% [25, 32, 34]
Both Null	n/a	10.3%	10.4% [32]

Other polymorphisms^§
GSTP1_I105V (V)	p=0.86	0.42	0.37[25]
CYP2D6 (^*3)	p=1.0	0.018	0.018 [33]
CYP2E1 (^*5)	p=1.0	0.029	0.038 [32]
EPHX1_Y113H (H)	p=0.84	0.29	0.32 [32]
EPHX1_H139R (R)	p=0.81	0.23	0.22 [32]
PON1_C-108T (T)	p=0.38	0.44	0.44-0.62 [28, 29]
PON1_Q192R (R)	p=0.56	0.33	0.24-0.38 [28, 29]
PON1_L55M (M)	p=0.25	0.34	0.28-0.46 [28, 29]
PON2_S311C (C)	p=0.42	0.31	0.20-0.25 [28, 29]

Significant disequilibrium indicated by p<0.05, exact chi square

^†

Genotype frequency (GSTM1 and GSTT1 null) or variant allele frequency (all other polymorphisms)

^‡

Healthy white individuals/control subjects; when available [32], includes genotype/allele frequencies from International Project on Genetic Susceptibility to Environmental Carcinogens (GSEC) database containing information on 12,525 white individuals without cancer

^§

Single nucleotide polymorphisms determined by individual TaqMan assays

Abbreviations: n/a=not applicable; GST=glutathione S-transferase; CYP=cytochrome P450; EPHX=microsomal epoxide hydrolase; PON=paraoxonase