Prenatal exposure to acrylamide and metabolic health at 20 years of age A biomarker-based Danish cohort study.

Adult obesity and metabolic health may be influenced by prenatal exposure to acrylamide (AA). AA forms in carbohydrate-containing foods and beverages during high-temperature processing. AA disrupts metabolic homeostasis and induces adiposity in mice offspring following gestational exposure. In humans, AA has been associated with intrauterine growth restriction and childhood overweight. It is unknown if prenatal exposure to AA influences metabolic health in young adults. We examined the associations between prenatal exposure to AA and metabolic health in singletons born in 1988-1989, Denmark. Hemoglobin adducts from AA (HbAA) and glycidamide were measured in maternal blood collected at 30 weeks' gestation together with information on maternal dietary and smoking habits (n = 638). At 20 years of age, offspring waist circumference, weight, height, blood pressure, blood glucose, insulin, leptin, adiponectin and lipid levels were measured at a clinical follow-up. Median HbAA concentration was 85 (interquartile range 63-136) pmol/g Hb. For most outcomes examined, there was no evidence of an association with prenatal exposure to AA. However, higher HbAA levels were associated with a minor increase in the offspring waist circumference of 0.06 cm (95 % confidence interval (CI): -0.07, 0.20) and low-density lipoprotein (LDL) cholesterol concentrations of 0.01 mmol/L (95 % CI: <0.01, 0.03) per 10 pmol/g Hb increments in HbAA. Furthermore, we observed that HbAA levels were associated with increased risk of metabolic syndrome in offspring of non-smokers. We found no overall compelling evidence that prenatal exposure to AA was associated with metabolic health of young adults, but the observations that higher prenatal exposure to AA were associated with higher waist circumference and LDL cholesterol levels in young adults warrants replication.