2 Glutathione S-transferase (GST) gene is one of the potential candidate susceptibility genes-because it plays a signiﬁcant role in Cd biotransformation and detoxiﬁcation [5]. The principal function of GST enzymes is conjugations of hy- drophobic and electrophilic compounds with reduced glu- tathione. The intracellular binding reaction with GSH is cat- alyzed by the GSTs and leads to stable GSH-metal conjugates being transported out of the cell and excreted via feces and urine [6]. Seven GSTs gene families (Alpha, Mu, Pi, Theta, Sigma, Omega, and Zeta) have been described and genetic polymorphisms have been reported for GSTM1, GSTP1, and GSTT1, resulting in either decreased or altered enzyme activ- ity [7, 8]. GSTT1 and GSTM1 are particularly important, because they have a deletion polymorphism resulting in impaired catalytic activity, which is associated with greater sensitivity to toxic compounds. The homozygous deleted (null genotype) of GSTT1 and GSTM1 genotypes have been associated with enhanced genotoxicity and are believed to be key factors in determining susceptibility to diseases associated with exposure to xenobiotics such as cancer [9]. Polymorphism of GSTP1 has been found in the coding re- gion. The variant allele of GSTP1 Val105Ile encodes valine (Val) instead of isoleucine (Ile) at codon 105 due to a base pair exchange, where G substitutes A. These substitutions were linked to a change in enzyme activity [8]. Polymor- phisms in GSTT1, GSTM1, and GSTP1 may be associated with increased susceptibility to cadmium toxicity [10]. Given that metabolism and detoxiﬁcation of cadmium (as an electrophile) is mediated by glutathione and GSTs are involved in the complexation of electrophilic substances with glutathione, it is reasonable to hypothesize that genetic polymorphisms in GST genes could result in diﬀerences in sensitivity to cadmium. In recent years, the possibilities of applying molecular techniques to toxicogentics are considerably focused, espe- cially for medical investigations and determinations of fac- tors inﬂuencing chemical poisonings. These include bio- chemical and genetic determinants related to acute and chronic eﬀects. To our knowledge, there are limited data on genetic predisposition inﬂuence on cadmium detoxiﬁcation in the human body. Therefore, this study investigated the association of glutathione S-transferase genes (GSTT1, GSTM1, and GSTP1) polymorphisms and blood cadmium concentration in a nonoccupationally exposed population. 2. Materials and Methods 2.1. Study Subjects. The Electric Generating Authority of Thailand (EGAT) STUDY was the ﬁrst cohort study of chronic disease in Thailand, originally designed in 1985 (known as EGAT 1), and mainly covered multidisciplinary researches related to cardiovascular disease (CVD) risk fac- tors such as nutrition and toxicology. The 370 subjects in this study were participants in the third survey of EGAT 2 in 2009 (the ﬁrst survey started in 1998 and second survey in 2003) [11]. Participants completed a self-administered ques- tionnaire, underwent a physical examination, and provided fasting blood samples. The study was approved by the Journal of Toxicology Committee on Human Rights Related to Researches Involv- ing Human Subjects, Faculty of Medicine, Ramathibodi Hospital, Faculty of Tropical Medicine, Mahidol University, in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki. All participants gave their informed consent prior to their inclusion in the study. Toxicological proﬁle of heavy metals was investigated in both ﬁrst and third surveys of EGAT 2, and further genetic analysis started in 2009. Ten milliliters of blood were collect- ed by venipuncture into EDTA and heparinized tubes from each subject and immediately centrifuged at 2000 g. Buﬀy coat, erythrocytes, and plasma were separated and stored at −20◦C until genotyping analyses and biochemical measure- ment were performed. 2.2. Determination of Cadmium in Blood. Whole blood cad- mium concentrations were measured by graphite furnace atomic absorption spectrometry (GFAAS) with Zeeman background correction after dilution of the blood (1 : 10) with Triton X-100 solution containing diammonium hydro- gen phosphate and nitric acid [12]. The concentration was expressed as micrograms per liter. 2.3. Genotype Analyses. The genomic DNA was extracted from the lymphocytes by a modiﬁed salting out procedure [13] and frozen at −20◦C until analysis. The genetic poly- morphisms of GSTM1, GSTT1, and GSTP1 were performed by real-time polymerase chain reaction (real-time PCR) according to the method of TaqMan SNP Genotyping Assays on an ABI 7500 instrument (Applied Biosystems, Foster City, CA, USA), in 96-well format. The TaqMan Assay included the forward target-speciﬁc polymerase chain reaction (PCR) primer, the reverse primer, and the TaqMan MGB probes labeled with 2 special dyes: FAM and VIC. The concen- trations of probes were 0.04 μM. Ampliﬁcation of 20 ng of DNA was performed during 40 cycles in a reaction volume of 10 μL. TaqMan Universal PCR Master Mix was used for analysis. Thermocycling conditions were 95◦C for 15 seconds follow by 60◦C for 1 minute. Information of speciﬁc probe and primers are available on the National Cancer Institute’s SNP500 database web page at http://variantgps.nci.nih.gov/ [14]. 2.4. Statistical Analysis. Statistical analyses were carried out using the SPSS 16.0 for window software (SPSS, Inc., Chicaco, IL, USA). Cadmium data were log-transformed to achieve normal distribution. The values were expressed as geometric means. The comparisons between variables were examined by the Student’s t-test and analysis of variance (ANOVA). Genotype distribution was analyzed with χ2. The eﬀects of all GSTs gene on blood cadmium were evaluated by linear regression analysis. A P value of 0.05 was used as the criterion for statistical signiﬁcance. 3. Results The subjects of this study consisted of 370 employees of EGAT. The geometric mean of the blood cadmium