Does the food processing contaminant acrylamide cause developmental neurotoxicity? A review and identification of knowledge gaps

• Published in: Reproductive toxicology (Elmsford, N.Y.) N.Y.), 2021-04, Vol.101, p.93-114
• Main Authors: Lindeman, Birgitte, Johansson, Ylva, Andreassen, Mathilda, Husøy, Trine, Dirven, Hubert, Hofer, Tim, Knutsen, Helle K., Caspersen, Ida H., Vejrup, Kristine, Paulsen, Ragnhild E., Alexander, Jan, Forsby, Anna, Myhre, Oddvar
• Format: Article
• Language: English
• Subjects: Acrylamide; Developmental neurotoxicity; Developmental origins of health and disease; Glycidamide; Human neuronal stem cells; MoBa; Neurological; Physiologically based toxicokinetic (PBTK); The Norwegian mother father and child cohort; The Norwegian mother father and child cohort (MoBa)
• ISSN: 0890-6238; 1873-1708; 1873-1708
• DOI: 10.1016/j.reprotox.2021.02.006

•AA causes developmental neurotoxicity (DNT) in animal studies and in vitro models.•Foetal AA exposure is associated with impaired growth and reduced head circumference.•DNT studies of neural function postnatally in AA-exposed humans are lacking.•Causal mechanisms of AA-induced DNT are incompletely understood.•Available experimental data do not allow estimation of a threshold dose for DNT. There is a worldwide concern on adverse health effects of dietary exposure to acrylamide (AA) due to its presence in commonly consumed foods. AA is formed when carbohydrate rich foods containing asparagine and reducing sugars are prepared at high temperatures and low moisture conditions. Upon oral intake, AA is rapidly absorbed and distributed to all organs. AA is a known human neurotoxicant that can reach the developing foetus via placental transfer and breast milk. Although adverse neurodevelopmental effects have been observed after prenatal AA exposure in rodents, adverse effects of AA on the developing brain has so far not been studied in humans. However, epidemiological studies indicate that gestational exposure to AA impair foetal growth and AA exposure has been associated with reduced head circumference of the neonate. Thus, there is an urgent need for further research to elucidate whether pre- and perinatal AA exposure in humans might impair neurodevelopment and adversely affect neuronal function postnatally. Here, we review the literature with emphasis on the identification of critical knowledge gaps in relation to neurodevelopmental toxicity of AA and its mode of action and we suggest research strategies to close these gaps to better protect the unborn child.