Acrylamide (AA), an animal carcinogen and neurotoxicant, widely used in industry and present in tabcco smoke and high-temperature processed foods. Ubiquitous exposures to AA have been of great concerns. AA and its active metabolite glycidamide can be detoxified by glutathione transferase and further metabolized to form 3 mercapturic acids, abbreviated as AAMA, GAMA2, and GAMA3. The objective of this paper was to study the effects of the interactions between AA exposures and genetic polymorphisms of phase I and II metabolic enzymes on the urinary levels of the 3 MAs. Total 51 AA-exposed and 34 control workers were recruited. Personal samples, blood, and pre-shift and post-shift urine samples were collected. Airborne AA was analyzed by using an isotope-dilution GC/MS method. Urinary AAMA, GAMA2, and GAMA3 were analyzed with an isotope-dilution LC-MS/MS operated under MRM. The PCR-RFLP method was applied to analyze CYP2E1, GST, and mEH genetic polymorphisms. Chemical analysis revealed that workers were exposed to AA in the range from 0.006 to 0.051 mg/m3 with a mean at 0.023 mg/m3. Statistical analysis demonstrates that AA-exposed workers excreted significantly higher levels of AAMA, GAMA2, and GAMA3 than the control group. Multiple linear regressions show that AA exposures and GSTM1 genotype were significantly associated with the formation of AAMA and GAMAs (GAMA2 + GAMA3). GSTM1 was also significantly associated with the ratios of GAMAs/AAMA (0.005–0.013). These results demonstrate that only a small proportion of AA absorbed is metabolized to glycidamide which can be detoxified by GSTM1 in humans.
