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Acrylamide is a low molecular weight, highly water soluble, organic compound. Heightened concerns about exposure to acrylamide arose in 2002 when it was discovered that it forms when certain foods are prepared at temperatures usually above 120 °C and low moisture, such as in the case of baked or fried carbohydrate-rich foods, including French fries, potato crisps, breads, biscuits, and in coffee beans. It is formed, at least in part, due to a reaction between certain amino acids (the constituents of proteins), such as asparagine, and reducing sugars. This is called the ‘Maillard reaction’, and it is what gives browned food it is distinctive color and taste. Acrylamide is also present in cigarette smoke.
Estimation of human exposure to acrylamide revealed that infants, toddlers and other children were the most exposed population groups.
In its exposure assessment, the CONTAM Panel (Panel on Contaminants in the Food Chain of EFSA) evaluated a total of more than 43000 analytical results from food products collected and analysed since 2010 by 24 European countries and six food associations. Data provided gave overall consistent and complementary information. Based on those measures and on typical diets that were constructed by survey data for each age group, an estimated level of exposure was calculated.
The main contributor to the total acrylamide exposure of infants was ‘Baby foods, other than processed cereal-based’ followed by ‘Other products based on potatoes’ and ‘Processed cereal-based baby foods’. The main contributor to the total exposure of the population of toddlers, other children and adolescents, was ‘Potato fried products (except potato crisps and snacks)’ representing up to half the total exposure, followed by ‘Soft bread’, ‘Breakfast cereals’, ‘Biscuits, crackers, crisp bread’, ‘Other products based on cereals’ and ‘Other products based on potatoes’. These foods groups were also the main contributors to the total exposure of adults, elderly and very elderly together with ‘Coffee’.
Depending on the survey and age group, exposure of children was estimated to be on average between 0.5 and 1.9 µg/kg b.w. per day, and between 1.4 and 3.4 µg/kg b.w. per day for the top 5% of the group exposed (the so-called 95th percentile). For adolescents, adults, elderly and very elderly, the exposure was estimated to be on average between 0.4 and 0.9 µg/kg b.w. per day and the top 5% of the group exposed to between 0.6 and 2.0 µg/kg b.w. per day depending on the survey and age group.
Scenarios designed in order to assess the influence of specific behaviours (e.g. preference for particular products, places of consumption, home-cooking habits) on the total dietary exposure to acrylamide showed for example that on home cooking behaviours, the degree of bread toasting resulted in variations of less than 8 %, while depending on the conditions of potato frying the total dietary exposure to acrylamide could be increased up to 80 %.
For the preference for particular potato crisps and coffee products the variation of the total dietary exposure to acrylamide resulted only in a variation of less than 4 % and 14 %, respectively.
Acrylamide was found at the highest concentrations in (dry) ‘Coffee substitutes’ (average levels of 1 499 µg/kg) and ‘Coffee (dry)’ (average levels of 522 µg/kg). However, due to dilution effects, lower concentrations are found in ‘Coffee beverages’ and ‘Coffee substitutes beverage’ as consumed by the population. High levels were also found in ‘Potato crisps and snacks’ (average level of 389 µg/kg) and ‘Potato fried products (except potato crisps and snacks)’ (average level of 308 µg/kg).
Lower acrylamide levels were found in ‘Processed cereal-based baby foods’ (average level of 73 µg/kg), ‘Soft bread’ (average level of 42 µg/kg) and ‘Baby foods, other than cereal-based’ (average level of 24 µg/kg). However, measurements of acrylamide levels in more than 40 000 samples of fresh sliced potato crisps from a dataset of manufacturers’ of 20 European countries showed a substantial downward trend for mean levels of acrylamide, from about 760 µg/kg in 2002 to about 360 µg/kg in 2011. A similar downward trend was not observed for other food categories.
An important initiative to reduce acrylamide in various food categories is the development of the FoodDrink Europe ‘Acrylamide toolbox’. The aim of the toolbox is to provide national and local authorities, manufacturers and other relevant bodies, with brief descriptions of intervention steps, which may prevent and reduce formation of acrylamide in specific manufacturing processes and products.
In both experimental animals and humans upon oral intake, the part of acrylamide that is not chemically bound to components of the food matrix is extensively absorbed from the gastrointestinal tract. After reaching the systemic circulation, acrylamide is rapidly distributed to the tissues.
Acrylamide is also able to cross the placenta and is transferred to a small extent into human milk. Acrylamide is transformed (metabolised) into other molecules, and one of the metabolic products is glycidamide. Acrylamide and glycidamide can also react with proteins such as haemoglobin and this represents an important biomarker of acrylamide exposure.
Both acrylamide and glycidamide are metabolised to mercapturic acids, which are then excreted via urine. The level of these mercapturic metabolites can be used to determine the level of exposure to acrylamide.
The common adverse effects reported in repeated dose toxicity studies of acrylamide in rats, mice, monkeys, cats and dogs consisted of loss of body weight and effects on the nervous system. Rats were more sensitive to the neurotoxic effects than mice.
Rats and mice studies have demonstrated adverse effects of acrylamide on male reproductive parameters including reduced sperm counts and effects on sperm and testis morphology with a no-observed-adverse-effect level (NOAEL) of approximately 2 mg/kg b.w. per day. This is a concentration 1000 times higher than that from the common dietary exposure in humans.
At exposure levels that in some cases are also associated with maternal toxicity, these experimental studies have shown some signs of developmental toxicity: increased incidence of skeletal variations, slightly impaired body weight gain, histological changes in the central nervous system, and neurobehavioural effects. . The lowest no-adverse-effect-level (NOAEL) reported for developmental toxicity in studies with rats exposed during gestation and after birth was 1.0 mg/kg b.w. per day.
The genetic toxicity of acrylamide and glycidamide has been extensively studied. In vitro genotoxicity studies indicate that acrylamide is a weak mutagen in mammalian cells but an effective clastogen (clastogens cause damage to chromosomes). Glycidamide is a strong mutagen and also a clastogen.
Acrylamide is carcinogenic in multiple tissues in both male and female mice and rats. A similar spectrum of tumours is observed when equivalent concentrations of glycidamide were administered to rats and mice.
For hormonal and endocrine effects of acrylamide, evidence from the available studies is equivocal. This is particularly true for changes in hormone levels in acrylamide-treated animals reported in some studies. Local endocrine effects of acrylamide, which may explain tumour formation in certain target tissues, lack experimental proof.
Associations between cancer risk and acrylamide exposure through diet were analysed in at least 36 publications, including 16 epidemiological (human). They showed no consistent indication for an association between acrylamide exposure and increased cancer risk.
The evidence of an increased risk for renal cell and endometrial (in particular in never-smokers) and ovarian cancer suggested by a few studies, was limited and inconsistent. Two studies specifically focused on occupational exposure to acrylamide did not indicate an increased cancer risk.
Regarding birth weight and other markers of fetal growth, two studies reported an inverse relation with acrylamide exposure but whether the association between dietary acrylamide exposure and these outcomes is causal or not has not been established.
An increased risk of neurological alterations was observed among workers occupationally exposed to acrylamide, including mostly the peripheral but also the central nervous system. However, in most cases, these symptoms were reversible.
Comparing the highest levels of exposure at which no health effects were observed in animal experiments to the estimated human exposure calculated from diet, a margin of exposure (MOE) can be calculated. Across surveys and age groups, the MOE values ranged from 425 to 89 for the mean exposure estimates, decreasing to 283 and 50 for the 5% of most exposed people (95th percentile).
For substances that are carcinogenic and genotoxic, since the MOEs calculated are all substantially lower than the value of 10 000 (which is the margin of safety that would be of low concern from a public health point of view according to the EFSA Scientific Committee), the CONTAM Panel of EFSA concluded that the MOEs across surveys and age groups indicated a concern with respect to neoplastic effects, even if the available human studies have not demonstrated acrylamide to be a human carcinogen.
The CONTAM Panel noted also that acrylamide is a mutagen for germ cell and that there are at present no established procedures to assess a risk using this endpoint.
Six points are more particularly highlighted by the reports regarding ways to improve the evaluation of acrylamide hazards and risks:
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