Acrylamide Exposure And Oxidative Dna Damage, Lipid Peroxidation, And Fasting Plasma Glucose Alteration: Association And Mediation Analyses In Chinese Urban Adults

OBJECTIVE Acrylamide exposure from daily-consumed food has raised global concern. We aimed to assess the exposure-response relationships of internal acrylamide exposure with oxidative DNA damage, lipid peroxidation, and fasting plasma glucose (FPG) alteration and investigate the mediating role of oxidative DNA damage and lipid peroxidation in the association of internal acrylamide exposure with FPG. RESEARCH DESIGN AND METHODS FPG and urinary biomarkers of oxidative DNA damage (8-hydroxy-deoxyguanosine [8-OHdG]), lipid peroxidation (8-iso-prostaglandin-F2 alpha [8-iso-PGF2 alpha]), and acrylamide exposure (N-acetyl-S-[2-carbamoylethyl]-l-cysteine [AAMA], N-acetyl-S-[2-carbamoyl-2-hydroxyethyl]-l-cysteine [GAMA]) were measured for 3,270 general adults from the Wuhan-Zhuhai cohort. The associations of urinary acrylamide metabolites with 8-OHdG, 8-iso-PGF2 alpha, and FPG were assessed by linear mixed models. The mediating roles of 8-OHdG and 8-iso-PGF2 alpha were evaluated by mediation analysis. RESULTS We found significant linear positive dose-response relationships of urinary acrylamide metabolites with 8-OHdG, 8-iso-PGF2 alpha, and FPG (except GAMA with FPG) and 8-iso-PGF2 alpha with FPG. Each 1-unit increase in log-transformed level of AAMA, AAMA + GAMA (sigma UAAM), or 8-iso-PGF2 alpha was associated with a 0.17, 0.15, or 0.23 mmol/L increase in FPG, respectively (Pand/orPtrend < 0.05). Each 1% increase in AAMA, GAMA, or sigma UAAM was associated with a 0.19%, 0.27%, or 0.22% increase in 8-OHdG, respectively, and a 0.40%, 0.48%, or 0.44% increase in 8-iso-PGF2 alpha, respectively (PandPtrend < 0.05). Increased 8-iso-PGF2 alpha rather than 8-OHdG significantly mediated 64.29% and 76.92% of the AAMA- and sigma UAAM-associated FPG increases, respectively. CONCLUSIONS Exposure of the general adult population to acrylamide was associated with FPG elevation, oxidative DNA damage, and lipid peroxidation, which in turn partly mediated acrylamide-associated FPG elevation.