Acrylamide in food is produced by the same chemical reaction that ‘browns’ food and improves taste during cooking at temperatures above 120°C, especially in foods containing asparagine and reducing sugars. Coffee, fried potato products, biscuits, crackers and crisp breads, soft bread and certain baby foods are key dietary sources of acrylamide, with children being the most exposed age group.
Discussing today's announcement, chair of EFSA’s panel on Contaminants in the Food Chain (CONTAM), Dr Diane Benford, said: “Acrylamide consumed orally is absorbed from the gastrointestinal tract, distributed to all organs and extensively metabolised. Glycidamide, one of the main metabolites from this process, is the most likely cause of the gene mutations and tumours seen in animal studies.”
Benford said currently human studies on acrylamide exposure were “limited and inconsistent” with regards to cancer risk.
The CONTAM Panel evaluated 43,419 results from food commodities collected and analysed since 2010. Of the samples, the report ‘coffee and coffee substitutes’ were found to have the highest content, followed by ‘potato crisps and snacks’ and ‘potato fried products’.
The mean dietary acrylamide exposure across age groups was estimated at 0.6 to 3.4 µg/kg body weight (b.w.) per day, while the 95th 10 percentile was put at around 0.3 to 1.9 µg/kg b.w. per day.
From consumption, acrylamide is absorbed from the gastrointestinal tract and distributed to all organs.
“Acrylamide is extensively metabolised, mostly by conjugation with glutathione but also by epoxidation to glycidamide (GA). Formation of GA is considered to represent the route underlying the genotoxicity and carcinogenicity of acrylamide. Neurotoxicity, adverse effects on male reproduction, developmental toxicity and carcinogenicity were identified as possible critical endpoints for acrylamide toxicity from experimental animal studies,” the panel wrote.
In identifying dose-response assessment, the panel said human data studies were not adequate. However, based on the animal studies, these levels were established as 0.43 mg/kg b.w. per day for peripheral neuropathy in rats and 0.17 mg/kg b.w. per day for neoplastic effects in mice.
“The Panel concluded that the current levels of dietary exposure to AA are not of concern with respect to non-neoplastic effects. However, although the human studies have not demonstrated AA to be a human carcinogen, the margins of exposure across dietary surveys and age groups indicate a concern with respect to neoplastic effects,” it wrote.
Assessing the risks
The panel also considered possible harmful effects of acrylamide on the nervous system, pre- and post- natal development and male reproduction. However, based on current levels of dietary exposure, it concluded that this was not considered to be a concern.
The opinion recommended further human research on acrylamide as well as detection and risk assessment methods for germ cell mutation. “Data collection activities can also be improved, particularly to provide a more accurate indication of acrylamide levels in food produced and consumed at home,” the EFSA assessment said.
The scientific organisation said that once public comments had been considered and the advice had been finalised it would be forwarded to the Commission and member states. It speculated that measures to further reduce consumer exposure to the substance may include advice on eating habits and home cooking, or controls on commercial food production, yet it reiterated that it played no role in this potential phase.