Acrylamide

Acrylamide is a known neurotoxin[1][2] and carcinogen[3], present in heated foods (incl. bread) and cigarette smoke. Environmentally, it may be the result of decomposition of polyacrylamide (in herbicides). Acrylamide is industrially produced for various purposes (eg polymeres). It decomposes in the presence of acids, bases and oxidizing agents, rendering ammonia or nitrogen oxides. Endogenously, acrylamide is metabolized to glycidamide (a DNA-reactive expoxide).

Acrylamide in food

Amides are derivates of ammonia or (carboxylated) amines. Particularly in heated plant foods, acrylamide may be yielded by the reaction of a specific amino acid (asparagine) and carbonyls (eg yielded by lipid oxidation) or reducing sugars (sugars yielding aldehydes; such as glucose in starches, and other aldoses, as well as ketoses and fructose)[4]. Higher levels of reducing sugars results in higher levels of acrylamide.[5] Particularly deep-frying has great consequences, evoking various complex reactions such as oxidation, hydrolysis, isomerization, and polymerization.[6] Some antioxidants (vitamin E) decrease the level of acrylamide produced during food processing.[7]

• Levels of reducing sugar in potatoes vary per season[8], as storing below 10°C increases breakdown of starch to sucrose, ultimately cleaved by acid invertase to produce glucose and fructose[9]. Even though potato crisps contain at least 10 fold more acrylamide (250 to 6700 mcg/kg) than acrolein (26 mcg/kg), 4 to 12 fold more acrolein- than acrylamide-related mercapturic acids are excreted in urine, which may indicate undetected varieties of acrolein.[10] A french study found on average 954 mcg/kg acrylamide in potato chips/crisps.[11]
• Baking temperature and surface color correspond with acrylamide concentration in cookies. Steam-assisted baking results in lower levels.[12] Cookies baked at 150°C  for 25  minutes yielded 75 mcg/kg acrylamide, compared to 236 mcg/kg in cookies baked at 240°C  for 9 minutes.[13] Cookies baked in an oven at 205°C for 11 min yielded 107 mcg/kg acrylamide.[14]
• Soybean-containing commercial bakery products contain higher levels of acrylamide than similar bakery products without soy.[15]

Acrylamide food additives

• AF-2 or furylfuramide; 2-(2-furyl)-3-(5-nitro-2-furyl)-acrylamide (widely used in Japan[16]), was first demonstrated to be mutagenic in Escherichia coli WP-2 and then proved to be carcinogenic in experimental animals [17][18][19] 5-nitro-2-furyl is a radical.
• 5-NFAA; 3-(5-nitro-2-furyl)acrylic acid proved to be more mutagenic than AF-2.[20]

Acrylamide exposure

• In a Californian study, non-cancer benchmarks for acrylamide were exceeded by >95% of preschool-age children, most of the acrylamide coming from chips, cereal, crackers, and other processed carbohydrate foods.[21]
• The exposure of infants aged 6-12 months of life was estimated at the minimum level in the range from 0.41 to 0.62 μg/kg b.w./day, and at the average level - from 2.10 to 4.32 μg/kg b.w./day. For the worst case scenario the exposure ranged from 7.47 to 12.35 μg/kg b.w./day and was more than a dozen times and even several dozen times higher than the exposure estimated for the total Polish population.
• In a french study mean daily acrylamide exposure was assessed to be 0.43 μg/kg of body weight for adults and 0.69 μg/kg for children.[22]

Health effects

• Acrylamide induces hepatic ornithine decarboxylase (ODC)[23] and affects behaviour by influencing hepatic mechanisms or central dopaminergic function.[24]
• Acrylamide crosses the human placenta. Maternal dietary exposure to acrylamide is associated with reduced birth weight and head circumference.[25]
• Acrylamide exposure of 2500 mcg/kg bodyweight in rats caused significant changes in serum hormones, histopathology, testicular gene expression, and cell proliferation.[26]
• In mice, acrylamide altered the morphology and histology of the small intestinal wall, decreasing proliferation, myenteron and submucosal thicknesses, villus length, fractal dimension, crypt depth, crypt number, and the small intestinal absorptive surface. Conversely, apoptosis, hemoglobin adduct levels, intensity of epithelium staining, enterocyte number, villus epithelial thickness, and crypt width and parameters associated with nerve ganglia were increased. These effects were inhibted by potato fiber.[27]
• Epidemiological studies show a lack of relationship between acrylamide intake and various types of cancer.[28] Given the consistent relationship between dietary carcinogenic heterocyclic amines (HCAs) and various types of cancer, and that dietary acrylamide mainly comes from processed plant (starchy) foods, and that dietary carcinogenic HCAs mainly come from processed animal foods, a high plant food intake (vs high animal food intake) is indeed unlikely to increase exposure to dietary carcinogens (acrylamide intake will be the expense of HCA intake).

Acetamide in food

Amides are derivates of ammonia or (carboxylated) amines. Acetamide is a carcinogenic derived from acetic acid, by dehydrating ammonium acetate[29], or by hydrolysis of acetonitrile[30]. Thermal degradation (>200°C) of chitin also yields acetamide.[31] Chitin is a good inducer for defense mechanisms in plants[32], and present in fungi, the exoskeletons of crustaceans such as crabs, lobsters and shrimps, in mollusks, and in the internal shells of squid and octopus. Acetamide is also a byproduct of thermochemical treatment of lignocellulosic biomass.[33]