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. Author manuscript; available in PMC: 2010 Sep 1.
Published in final edited form as: Toxicol Appl Pharmacol. 2009 Jun 16;239(2):200–207. doi: 10.1016/j.taap.2009.06.007

Table 5.

Analysis of association between AS3MT polymorphisms and the presence of arsenic skin lesions.

Group
N Genotype frequency (%)
Allele frequency (%)
A-477G AA AG GG A G
As-skin lesion 69 26 (38) 33 (48) 10 (14) 85 (62) 53 (38)
Non-lesion 50 21 (42) 21 (42) 8 (16) 63 (63) 37 (37)
Xi2=0.04, p=0.83 Xi2=0.01, p=0.90
OR=1.60a 95%CI (0.6–4.3)
Met287Thr TT TC CC T C

As-skin lesion 71 60 (84.5) 10 (14.1) 1 (1.4) 130 (91.5) 12 (8.5)
Non-lesion 51 47 (92) 4 (8) 0 98 (96) 4 (4)
Xi2=3.22, p=0.055 Xi2=1.32, p=0.25
ORb=4.28a 95%CI (1–18.5)*
T35587C TT TC CC T C

As-skin lesion 71 41 (58) 30 (42) 0 112 (79) 30 (21)
Non-lesion 51 30 (59) 21 (41) 0 81 (79) 21 (21)
Xi2=0.02, p=0.88 Xi2=0.1, p=0.90
OR=0.76a 95%CI (0.3–1.9)

The genotype and allele distributions of the AS3MT polymorphisms in individuals exposed to inorganic arsenic are shown for groups with and without skin lesions.

Two-sided Xi2 test.

a

Logistic regression models adjusted by age, gender and TWE.

b

Comparison between TT and TC+CC;

*

P=0.05.