• Investigating the Association Between Acrylamide Exposure and Cancer Risk: A Targeted Review and Translational Perspective
  • Arezoo sadeghi,1,*
    1. Msc of Molecular Genetic Department of Genetics, Zanjan Branch, Islamic Azad University, Zanjan, Iran.


  • Introduction: Acrylamide (AA) is a small, water-soluble industrial monomer that can also form in carbohydrate-rich foods during high-temperature processing. AA is metabolized to glycidamide, a reactive epoxide capable of binding DNA, which has raised long-standing concern about carcinogenic potential. Evidence from multiple experimental systems suggests tumorigenic effects, yet translating this to human risk has been challenging due to exposure misclassification and confounding. The aim of this submission is to synthesise concise, decision-relevant evidence on AA and cancer risk across animal bioassays and human studies, and to outline translational implications for exposure reduction and biomonitoring.
  • Methods: A targeted literature search was conducted in PubMed, Scopus, and Web of Science using combinations of “acrylamide”, “glycidamide”, “carcinogenicity”, and “cancer risk”. Inclusion prioritised: (i) two-year rodent bioassays and mechanistic papers on AA→glycidamide metabolism/DNA adducts; (ii) human cohort or case-control studies using either dietary assessment or hemoglobin/albumin adduct biomarkers; and (iii) reviews from authoritative agencies. English-language, peer-reviewed sources were screened by relevance to exposure–response; no quantitative meta-analysis was performed here.
  • Results: Animal evidence consistently shows multi-organ tumor responses after AA exposure, with patterns compatible with a genotoxic mode of action via glycidamide. These bioassay findings, combined with DNA-adduct data, establish biological plausibility. In humans, studies relying on diet-based exposure estimates are mixed—largely because food-frequency questionnaires introduce non-differential error and smoking-related confounding. By contrast, studies using internal dosimetry (hemoglobin or serum adducts) tend to show tighter exposure–response relationships for selected cancer sites, although sample sizes remain modest and heterogeneity persists. Mechanistic investigations indicate that glycidamide-DNA adduct formation, perturbation of endocrine signalling, and neuronal pathway effects may contribute to tumor development. Overall, the weight of evidence supports carcinogenicity in rodents and suggests potential human cancer risk at sufficient exposures. Where modeling or simulation is referenced in this work, it is clearly labeled as simulated and is used only to contextualise plausible exposure ranges; no simulated values are presented as measured data. These insights point to biomarker-anchored exposure assessment as the most reliable approach for risk evaluation and for targeting public-health interventions.
  • Conclusion: The totality of evidence supports rodent carcinogenicity of acrylamide and indicates a plausible human cancer risk, justifying continued mitigation of dietary and occupational exposures. Priority next steps include harmonised cohorts employing adduct biomarkers, improved control of confounders (notably smoking and diet quality), and transparent, pre-registered analytical plans. Such advances will clarify dose–response at human-relevant exposures and strengthen the translational basis for risk communication and regulatory guidance.
  • Keywords: Acrylamide; Glycidamide; Carcinogenicity; Cancer risk; Biomarkers