A scientific group at the University of Stockholm, headed by Prof. Margareta Törnqvist found, in the year of 2002, that acrylamide is formed during heating of starch-rich foods to high temperatures.
At The Swedish National Food Agency a new and rapid LC/MS/MS-method was developed for the analysis of acrylamide in foods. Analysis has shown that acrylamide is present in a large number of foods, including many regarded as staple foods. The levels of acrylamide differ widely within each food group analysed.
Acrylamide and polyacrylamide are used in the industry for the production of plastics. It has been supposed that the main exposure for acrylamide in the general population has been through drinking water and tobacco smoking. The exposure via drinking water is small and the EU has determined maximum levels of 0.1 microgram per liter water.
Recent analyses have indicated that the exposure to acrylamide is probably considerably higher (for non-smokers) from consumption of certain foods that have been heated.
Acrylamide is water soluble and is quickly absorbed in the digestive tract. The excreation via the urine is fast and half of the acrylamide is cleared from the body in a few hours.
The toxicological effects of acrylamide are well known. It causes DNA damage and at high doses neurological and reproductive effects have been observed. Glycidamide, a metabolite of acrylamide, binds to DNA and can cause genetic damage. Prolonged exposure has induced tumours in rats, but cancer in man has not been convincingly shown. The International Agency for Research on Cancer (IARC) has classified acrylamide as a "probably carcinogenic to humans" (Group 2A).
Acrylamide has been shown to induce gene mutations in cultured animal cells and also in animals treated in vivo. Thus it is assumed that exposure also to very low doses of acrylamide increases the risk for mutation and cancer.
High doses of acrylamide have been applied in the toxicological studies, which is an accepted practice, but at the Swedish Food Agency studies in the laboratory have shown that chromosome aberrations are induced in mice at comparable low doses. The linearity in the dose response curve points to an elevetad risk also at the lowest doses (ref. Abramsson-Zetterberg, 2003).
Among the acrylamide metabolites glycidamide is considered the most likely candidate for causing genetic damage. Glycidamide has been found in mice and rats, and also in humans exposed to acrylamide.
Neurological damage was observed when rats were given acrylamide in their drinking water. The lowest effective dose was 2 mg/kg body weight and day, and the highest no-effect dose was 0.5 mg/kg body weight and day. Also humans exposed to high doses of acrylamide have shown neurological damage, e.g. some workers occupied in the building of the tunnel at Hallandsåsen. It is difficult to assess the highest acrylamide dose in humans that does not cause neurological effects (NOEL). The level is probably several times higher than the average acrylamide intake from food. Decreased fertility was observed in rats exposed to 5-10 mg acrylamide/kg body weight and day, which is a dose level several thousand times higher than the average intake.