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

**Authors:** Stéphane Tuffier, Efstathios Vryonidis, Thorhallur Ingi Halldorsson, Anne Ahrendt Bjerregaard, Damian Chandia-Poblete, Dorte Rytter, Bodil Hammer Bech, Tine Brink Henriksen, Thorkild I.A. Sørensen, Sjurdur Frodi Olsen, Margareta Törnqvist, Marie Pedersen

PMC · DOI: 10.1016/j.envint.2025.110000 · Environment International · 2026-01-01

## TL;DR

Prenatal exposure to acrylamide may be linked to higher waist circumference and LDL cholesterol in young adults, based on a Danish cohort study.

## Contribution

This study is the first to examine the long-term metabolic health effects of prenatal acrylamide exposure in humans.

## Key findings

- Higher prenatal acrylamide exposure was associated with increased waist circumference at 20 years of age.
- Prenatal acrylamide exposure was linked to elevated LDL cholesterol levels in young adults.
- No significant associations were found between prenatal acrylamide exposure and most other metabolic health outcomes.

## Abstract

•Hemoglobin adducts of AA measured in pregnant women reflect prenatal exposure to AA from multiple sources.•Prenatal exposure to AA were associated with higher waist circumference and LDL cholesterol levels at 20 years of age.•Absence of associations between prenatal AA and other metabolic health outcomes.•More studies are needed to understand the potential role of prenatal exposure to AA in adult health.

Hemoglobin adducts of AA measured in pregnant women reflect prenatal exposure to AA from multiple sources.

Prenatal exposure to AA were associated with higher waist circumference and LDL cholesterol levels at 20 years of age.

Absence of associations between prenatal AA and other metabolic health outcomes.

More studies are needed to understand the potential role of prenatal exposure to AA in adult health.

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.

## Linked entities

- **Chemicals:** acrylamide (PubChem CID 6579), glycidamide (PubChem CID 91550)
- **Diseases:** metabolic syndrome (MONDO:0000816)

## Full-text entities

- **Genes:** ADIPOQ (adiponectin, C1Q and collagen domain containing) [NCBI Gene 9370] {aka ACDC, ACRP30, ADIPQTL1, ADPN, APM-1, APM1}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}
- **Diseases:** obesity (MESH:D009765), adiposity (MESH:D018205), intrauterine growth restriction (MESH:D005317), overweight (MESH:D050177), metabolic syndrome (MESH:D024821)
- **Chemicals:** glycidamide (MESH:C071834), HbAA (-), carbohydrate (MESH:D002241), blood glucose (MESH:D001786), lipid (MESH:D008055), AA (MESH:D020106)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

64 references — full list in the complete paper: https://tomesphere.com/paper/PMC12819368/full.md

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Source: https://tomesphere.com/paper/PMC12819368