Environmental Toxicology

Review

A Review on Acrylamide in Food: Occurrence, Toxicity, and Mitigation Strategies

Lubna Rifai1 and Fatima A. Saleh2

Abstract Acrylamide (AA) is a food contaminant present in a wide range of frequently consumed foods, which makes human exposure to this toxicant unfortunately unavoidable. However, efforts to reduce the formation of AA in food have resulted in some success. This review aims to summarize the occurrence of AA and the potential mitigation strategies of its formation in foods. Formation of AA in foods is mainly linked to Maillard reaction, which is the first feasible route that can be manipulated to reduce AA formation. Furthermore, manipulating processing conditions such as time and temperature of the heating process, and including certain preheating treatments such as soaking and blanching, can further reduce AA formation. Due to the high exposure to AA, recognition of its toxic effect is necessary, especially in developing countries where awareness about AA health risks is still very low. Therefore, this review also focuses on the different toxic effects of AA exposure, including neurotoxicity, genotoxicity, carcinogenicity, reproductive toxicity, hepatotoxicity, and immunotoxicity.

Keywords acrylamide, toxicity, food, mitigation strategies

Introduction

For thousands of years, people have used heat to cook their

food. Thermal processing has a great importance in terms of

microbiological safety, nutritional quality, and the desired sen-

sory properties, such as color, texture, and flavor; however,

undesirable chemicals have arisen as problems associated with

food processing techniques.1,2 Heating of food induces chem-

ical reactions that lead to the formation of heat-induced toxic

substances, the so-called thermal process contaminants.3 One

such compound that has received much scientific interest over

the recent years is acrylamide (AA).4 Before its discovery in

food, AA was known as an industrial chemical compound used

primarily as a building block in many industrial processes, such

as in the production of plastics, glues, paper, component of

cigarette smoke, and in the treatment of drinking water and

wastewater, including sewage.1 Acrylamide was also found

in consumer products, such as caulking, food packaging, and

some adhesives.5

Although AA has probably been around as long as people

have been baking, roasting, toasting, or frying foods, it was

only in April 2002 when the Swedish National Food Adminis-

tration (SNFA) announced that prolonged heat treatments of

some foods could create significant amounts of AA.6 This dis-

covery by Swedish researchers resulted in the detection of AA

in a wide range of foods, particularly starchy foods such as

potato and grain products when processed at high tempera-

tures.7 Acrylamide does not appear in raw foods themselves;

however, it is formed during the heating process when the

temperature reaches 120�C or higher.8 Maximum limits for

AA in food have not been established, although the World

Health Organization (WHO) guideline for AA in drinking

water is 0.5 mg/L.9 The SNFA and Stockholm University

researchers reported moderate levels (5-50 mg/kg) and high

levels (150-4,000 mg/kg) of AA in heated protein and

carbohydrate-rich foods, respectively.10 Foods that lack AA

are those that are boiled or nonthermally treated.11

Mechanism of AA Formation in Food

A few months following the 2002 announcement by the SNFA,

much attention became focused on the Maillard reaction after it

was reported that AA formation in starchy foods during heating

involves 2 natural components, namely, reducing sugars and

the amino acid asparagine.12 High temperatures and low moist-

ure content in food favor the formation of AA.13 Maillard

reaction is not a single reaction but a complex series of reac-

tions that occur during the thermal processing of food. During

1 Department of Nutrition & Dietetics, Faculty of Health Sciences, Beirut Arab

University, Beirut, Lebanon 2 Department of Medical Laboratory Sciences, Faculty of Health Sciences,

Beirut Arab University, Beirut, Lebanon

Corresponding Author:

Fatima A. Saleh, Department of Medical Laboratory Technology, Faculty of

Health Sciences, Beirut Arab University, Beirut, Lebanon.

Email: [email protected]

International Journal of Toxicology 2020, Vol. 39(2) 93-102 ª The Author(s) 2020 Article reuse guidelines: sagepub.com/journals-permissions DOI: 10.1177/1091581820902405 journals.sagepub.com/home/ijt

this nonenzymatic reaction, reducing sugars (glucose and fruc-

tose) condense with amino acids, mainly asparagine, to pro-

duce N-glycoside that usually rearranges to the Amadori

rearrangement product, which in turn undergoes different steps

to produce melanoidin, where a further decarboxylation of the

Schiff base leads to AA formation (Figure 1).14-16 This reaction

is primarily responsible for the brown color, crust, and char-

acteristic tasty flavor of baked, fried, and toasted foods.17

Research has shown that the reducing sugars are the limiting

factors in potatoes, while asparagine is the limiting factor in

cereal products.18 Recent studies have indicated that one other

compound called 3-aminopropionamide can also be formed

during the Maillard reaction and can be converted to AA

under aqueous conditions.19 This compound has been identi-

fied in cocoa beans, coffee, and cereal products.20 Maillard

reaction is primarily a surface reaction, so AA in bread is

located mainly in the crust with very low amounts in the

crumb.21 In potato crisps, one possible reason for the high

AA content is that the crisp is essentially 2 thin surfaces with

very little matter between them.21 In addition, the darker in

color the food product is (burnt toast, darker chips), the higher

the AA content.21

In conclusion, free asparagine, free reducing sugar, high

temperature (>120�C), and low moisture conditions at the sur-

face of the food are key requirements for AA formation in heat-

processed foods.17

Acrylamide Exposure

Humans can be exposed to AA through oral, dermal, and

inhalational routes.22 Acrylamide is also present in nondietary

sources such as tobacco smoke, which is, therefore, another

source of exposure for both smokers and nonsmokers (through

passive smoking).23 For smokers, it was found that tobacco

smoking is a more prominent source of AA exposure than

food.24 In addition, due to its wide variety of other nonfood

industrial uses, many people can be exposed to AA in the

workplace through dermal absorption or inhalation.25 There-

fore, AA exposure is a combination of exposures from differ-

ent sources such as diet, smoking, drinking water, and

occupational sources.

Dietary Exposure

The presence of AA in heat-processed foods is a worldwide

health concern, since this substance has been classified as a

probable human carcinogen by the International Agency for

Research on Cancer (IARC).26 Acrylamide is primarily formed

in food products derived from raw materials that are rich in

carbohydrates and low in proteins.10,27 Fried, deep-fried, or

baked food items, such as cake, bread, French fries, and chips

are believed to contain the highest levels of AA as shown in

Table 1.13 Despite the fact that AA concentration in coffee is

Figure 1. Main pathway of acrylamide formation in food.

94 International Journal of Toxicology 39(2)

relatively low, it is a major contributor to AA exposure in

adults because of the high amounts of coffee consumed.29

Estimates of the average intake of AA by consumers may

differ between countries and according to dietary habits,

but an average mean intake can be considered to be about

0.4 mg/kg body weight per day (bw/d), and the average intake

for a high-level consumer to be about 1.0 mg/kg bw/d.30 Other

researchers estimated the acceptable daily intake to be

1 mg/AA/d, which is an amount exceeded in many regular

food products.31 The WHO states that AA has no reliably

identifiable threshold of effects, meaning that exposure to low

doses might be followed by a symptom silent period in which

the detrimental effects of the chemical may not be clinically

apparent, but nevertheless morphological and/or biochemical

alterations may be present.32 Tolerable daily intake for neu-

rotoxicity from AA was estimated to be 40 mg/kg/d while that

for cancer was estimated to be 2.6 and 16 mg/kg/d based on

AA or glycidamide, respectively.33

In a study done in Lebanon, the daily consumption of AA

from potato and corn chips was found to be 7- to 40-fold higher

than the risk intake set by WHO but was below the neurotoxic

risk threshold. The cancer risk for the Lebanese population

from AA exposure estimations appears to be significant,

highlighting the need to conduct further epidemiological

studies and to ensure monitoring of AA levels in food prod-

ucts.34 Another Lebanese study on the amount of AA in

caffeinated beverages showed that caffeinated beverages

contributed an average of 29,176 mg/kg of AA, which was

higher than the risk intake for carcinogenicity and neuro-

toxicity set by the WHO.35 This study shows alarming

results that call for the need to regulate the caffeinated

product industry in Lebanon by setting legislations and stan-

dard protocols for product preparation in order to limit the

AA content and protect the consumers.

The Joint Expert Committee on Food Additives had reported

that the major foods contributing to the total AA intake for

most countries are potato crisps (6%-46%), potato chips

(16%-30%), coffee (13%-39%), pastry and sweet biscuits

(10%-20%), and bread (10%-30%).36 Furthermore, food

packages that contain polyacrylamide may lead to indirect

exposure to AA monomer residual.37 Although nonfood expo-

sures may exist, the diet is assumed to be the major source of

AA exposure for the general nonsmoking population, where

around 38% of caloric uptake is provided by food sources that

are known to contain AA.38

Acrylamide Metabolism

After consumption, it is demonstrated that AA is rapidly and

completely absorbed by the gastrointestinal tract in rats via the

circulation and is distributed to the peripheral tissues.39 The

fate of AA in humans seems to be qualitatively similar to that in

rodents.39 One exploratory study in healthy volunteers have

confirmed that AA can cross the blood–placenta barrier in a

human placenta in vitro model as well as the blood–breast milk

barrier in vivo in lactating mothers.40 These studies may sug-

gest that AA is able to reach any human tissue. Once absorbed,

AA is metabolized via at least 2 main pathways. It may be

conjugated to N-acetyl-S-(3-amino-3-oxopropyl) cysteine by

glutathione-S-transferase (GST), or it may be converted to gly-

cidamide in a reaction catalyzed by the cytochrome P450

enzyme complex (CYP450), where this metabolite is known

to be more reactive toward DNA and proteins than the parent

AA compound (Figure 2).41,42

Detoxification of both AA and glycidamide can proceed

through conjugation with glutathione (GSH), mediated by GST

and the GSH adducts thereafter are excreted in urine as by-

products of mercapturic acids.43 The mercapturic acids of AA

and glycidamide represent the major metabolites, and their

urinary excretion levels are proposed to be biomarkers of AA

exposure.43 Additionally, AA and glycidamide can also form

adducts with DNA and amino acids in hemoglobin, and there-

fore, these adducts represent important biomarkers of AA

exposure.44 The importance of AA as a food contaminant was

shown in 2002 when it was observed that feeding rats with fried

feed showed a large increase in the level of a hemoglobin

adduct.1 Moreover, AA was found to be able to cross the

placental barrier where studies showed the presence of

AA-hemoglobin adducts in the neonatal blood.45

Table 1. Acrylamide Levels in Selected Food Groups.a

Food group Food product group

Minimum acrylamide,

mg/kg

Maximum acrylamide,

mg/kg

Potatoes Potato crisps 117 3,770 Chips/French fries 59 5,200 Potatoes (raw) <10 <50

Cereal products

Corn crisps 120 220 Bakery products and biscuits 18 3,324 Gingerbread <20 7,834 Bread <10 130 Bread (toast) 25 1,430 Breakfast cereals 11 1,057

Rice and noodles

Fried noodles 3 581 Fried rice <3 67 Rice crackers, grilled, or

fried 17 500

Fruits and vegetables

Canned black olives 123 1,925 Prune juice 53 267 Fried vegetables 34 34

Nuts Nuts 28 339 Fish and

meat Fish and seafood products,

crumbed, or battered <2 39

Meat/poultry products, crumbed, or battered

<10 64

Cocoa-based products

Chocolate products <2 826 Cocoa powder <10 909

Coffee Coffee (roasted) 45 975 Coffee substitute 116 5,399 Coffee extract/powder 195 4,948

aAdapted from Food and Agriculture Organization/World Health Organization.28

Rifai and Saleh 95

Toxicity of AA

Neurotoxicity

Neurotoxicity is a major consequence of AA exposure, and

considerable attention has been drawn to this area of investi-

gation. This compound is considered to be a cumulative neu-

rotoxicant in rodents as well as in humans.46 In rodent toxicity

studies, exposure to repeated doses of 10 to 50 mg/kg bw/d AA

had been reported to cause neuropathy in most laboratory ani-

mal species, while exposure to single doses of 100 to 200 mg/

kg was fatal in most animals.47 In vitro, AA was shown to

induce apoptosis in rat primary astrocytes and cause mitochon-

drial dysfunction and apoptosis in BV-2 microglial cells.48

Moreover, Chen and Chou showed that AA disrupted the ner-

vous system by inhibiting human neuroblastoma and glioblas-

toma cellular differentiation.49

Acrylamide neurotoxicity in occupationally exposed popu-

lations has been ascertained by various epidemiological stud-

ies.50 General symptoms of neurotoxicity in humans are a

characteristic ataxia, skeletal muscle weakness, weight loss,

distal swelling, and degeneration of axons in the central and

peripheral nervous systems.51,52 A case report from Sweden

described peripheral neuropathy in tunnel workers exposed to

short-term but intensive doses of a grouting agent containing

AA and N-methylolacrylamide.52 There was a significant

dose–response association between peripheral nervous symp-

toms and hemoglobin adducts that were used as biomarkers.52

Genotoxicity and Carcinogenicity

The genotoxicity of AA and its major metabolite glycidamide

had been investigated in several studies. A study by Alzahrani

in mice showed that single doses of AA at 10, 20, and 30 mg/kg

and repeated doses of 10 mg/kg for 1 and 2 weeks significantly

induced DNA damage compared to the control group as shown

by elevation in micronuclei and chromosome aberrations in

mice bone marrow cells.53

Moreover, prolonged exposure of animals to high concen-

trations of AA in the drinking water leads to tumor develop-

ment at multiple sites in both male and female genders.54

Although there is sufficient evidence for the carcinogenicity

of AA in experimental animals, the few epidemiologic studies

conducted to date on occupational and dietary exposure to AA

have found no consistent evidence of its carcinogenic effects in

humans.55,56 Based on the current research, AA is currently

classified as a “probable human carcinogen” by the IARC and

as “reasonably anticipated to be a human carcinogen” by the

US National Toxicology Program.

Two different cohort studies were done on factory workers

being exposed to high levels of AA for many years, but no

statistically significant cancer mortality was reported.57,58

However, other researchers have found some association

between AA-hemoglobin adduct levels and incidence of estro-

gen receptor-positive breast cancer as well as between AA

intake and endometrial and ovarian tumors in postmenopausal

Figure 2. Proposed metabolic scheme of acrylamide.

96 International Journal of Toxicology 39(2)

women.59,60 Herein, it is important to note the need for further

research on this topic to provide information about AA expo-

sure and cancer risk in humans.

Reproductive Toxicity

Reproductive toxicity of AA in humans has not been demon-

strated; however, in rats, the No-observed adverse effect level

for reproductive toxicity was assessed to be 2 to 5 mg/kg/d.54

The administration of 0.5 to 10 mg/kg of AA caused growth

retardation in rats and reduction in epididymal sperm reserves

compared to the control group.54 In addition, repeated injec-

tions of AA (20 mg/kg) to male rats for 20 days caused

decrease in testosterone and prolactin concentrations in a

dose-dependent manner.61 In another study, reproductive toxi-

city was also revealed in AA-treated female mice, where a

decline in the viability of mouse granulosa cells, the number

of corpora lutea, and progesterone production was observed.62

Hepatotoxicity

Although AA is metabolized in the liver, reports of its hepato-

toxicity in humans are still scarce. However, numerous studies

in animals have reported the harmful effects of dietary AA in

the liver due to oxidative stress. A high dose of 25 mg/kg AA

administered for 21 days resulted in significant decrease in

liver GSH level and total antioxidant status in experimental

adult rats. Administration of AA also led to increase in serum

level of liver enzymes (AST, ALT, and ALK) and decrease in

superoxide dismutase and catalase activities, while total oxi-

dant status and malondialdehyde levels increased.63

Immunotoxicity

Studies regarding the adverse effects of AA on the immune

system are limited compared to other end points.54 Neverthe-

less, immunotoxicity of AA was found in female BALB/c

mice, where AA decreased final bw, spleen, and thymus

weights, and lymphocyte counts in addition to causing patho-

logical changes in lymph glands, thymus, and spleen.64 Acry-

lamide was also shown to cross the placenta and reach the fetus,

but no significant associations were found between prenatal

dietary exposure to AA and the investigated immune-related

health outcomes or blood parameters at any age.65

Mechanism of AA Detoxification

Once ingested, AA can be detoxified in the body if it is pro-

cessed through CYP450 and converted into glycidamide or if it

is bound to the sulfur-containing antioxidant glutathione as

shown in Figure 2.66 However, despite the metabolic pathways

assisting in AA detoxification, it is still possible to overload the

detoxification capability of these pathways and create health

risks from excess exposure.67 One way to possibly help lower

the risk of toxicities from AA is to increase glutathione levels

by consuming sulfur-containing foods such as onions, garlic,

and cruciferous vegetables such as broccoli and brussels

sprouts or foods that contain significant amounts of cysteine,

which is an essential substrate for the synthesis of glutathione,

such as onions, garlic, cruciferous vegetables, and red pep-

pers.67,68 Foods such as poultry, yogurt, and eggs also contain

significant amounts of the amino acid cysteine.67

Mitigation Strategies for AA

Since 2002, scientists from all over the world in collaboration

with agencies such as FAO and WHO have been working on

different ways to reduce the levels of AA in foods commonly

consumed with the highest levels of AA such as potato and

cereal products.69,70 Although coffee is also a substantial con-

tributor to the total dietary intake of AA, which is formed

during coffee roasting, currently there are no feasible strategies

to decrease AA levels in coffee. According to the Codex Code

of Practice to reduce AA in foods, it is quoted “no commercial

measures for reducing acrylamide in coffee are currently

available.”38 Nevertheless, work is presently underway to iden-

tify new strategies for AA mitigation without significantly

impacting the significant organoleptic properties and accept-

ability of coffee.71,72 Thus, this review discusses strategies that

have been conducted for reduction of AA in foods such as

potato and cereal products that were categorized into 4 differ-

ent groups based on the effect of raw materials, additives,

processing conditions as well as the effect of pH, water activity,

and fermentation.

Effect of Raw Materials

The formation of AA in foods such as potato and cereal prod-

ucts has been widely studied. The amount of AA formed varies

greatly in the same food items due to variable food composition

(ie, nutrient contents) which is affected by several factors such

as the climate and storage conditions, fertilization, and manu-

facturing.73 Reducing sugars and asparagine content of potato

and cereal products before thermal processing play significant

roles in the formation of AA during later processing stages.74

For example, since the amount of reducing sugars in potatoes is

much higher than that of asparagine, controlling their level in

the initial raw material can decrease AA formation in the fin-

ished fried potato products. Therefore, selecting potato vari-

eties with low content of reducing sugars may help reduce AA,

while maintaining the desirable product qualities. For instance,

potatoes with less than 1 g/kg fresh weight of reducing sugars

should be used for frying or roasting.75 Additionally, lower

levels of AA were detected in French fries made from the

genetically modified potatoes (innate potatoes) than in fries

made from conventional potatoes.76 Innate potatoes were pro-

duced by silencing the asparagine synthetase-1 gene (Asn1) in

the tuber resulting in lower levels of asparagine, which in turn

decreases the formation of AA by 52% to 78% when fried or

baked at high temperatures.77

The reducing sugar content in potato tubers tend to decrease

over the course of the growing period to reach a minimum level

toward the end of the growing season which is a good indicator

Rifai and Saleh 97

to harvest at the right time to reduce the potential for high AA

formation during processing.78 Acrylamide content is also

affected by climatic conditions, where warm weather condi-

tions (above 25�C-30�C) and cold climates (below 8�C-12�C)

tend to increase sugar content of potato tubers and subsequently

increase AA formation upon frying.79 Therefore, it is proposed

that the optimum temperature for tuber growth ranges between

15�C and 20�C.79

Formation of AA is also related to the storage temperature

of potato tubers. Storing potato tubers at 8�C or lower will lead

to phenomenon called “low-temperature sweetening” which

causes an increase in reducing sugar content and enhancement

of the brown pigment during frying and hence higher amounts

of AA.80 For heat processing, potato tubers should be stored at

8�C to 12�C to avoid this increase in reducing sugar content.81

Effect of Additives

Plant antioxidants. The effect of antioxidants and their extracts

on the level of AA in foods has not been investigated satisfac-

torily. Both positive and negative results had been obtained

when food researchers tried to use natural antioxidative

extracts to inhibit AA formation in food. Some antioxidants

were claimed to reduce AA formation, while others did not

show any effect or showed an enhancing effect.82,83

Bioactive products extracted from plants have been shown

to reverse AA toxicity. For example, when rosemary extract,

oil, and dried leaves were added to wheat dough, AA was

reduced by 62%, 67%, and 57%, respectively, compared to

wheat buns without addition of rosemary.82 On the other hand,

grape seed extract added to baked products did not have any

effect on AA formation.83 Similarly, other studies found that

the addition of sesamol, vitamin E, and antioxidants such as

2,6-bis (1.1-dimethylethyl)-4-methylphenol to meat before

heating led to increased AA formation.84 In a model system

based on wheat flour and water, which resembled crackers, the

use of ascorbic acid and ascorbate showed a slight reduction in

AA content.85 Furthermore, the addition of bamboo leaves and

green tea extracts significantly reduced AA formation in an

asparagine–glucose model system.86

In another study, chrysin, which is a natural biologically

active flavonoid compound found in many plants, reduced

AA-induced neurotoxicity in Wistar rats due to its high

antioxidant power.87 Additionally, quercetin, which is a

polyphenolic flavonoid compound, contains a spectrum of

antioxidants that are able to protect against AA-induced

neurotoxicity.88 Berry juices (bilberry, black mulberry, and

raspberry) significantly restored the growth of AA-exposed

yeast cells, Saccharomyces cerevisiae, and decreased the

level of reactive oxygen species.89

Enzymes. The use of asparaginase enzyme is an effective strat-

egy at reducing AA formation in fried potatoes, as it catalyzes

the hydrolysis of asparagine to aspartic acid and ammonia

without affecting the final product aspects.90 This approach

was found to be more significant when the raw material was

blanched prior to enzyme application.91 A study has demon-

strated that soaking of blanched potato strips in an asparaginase

solution at 40�C for 20 minutes reduced AA by 60% when

compared with blanched strips without the enzyme treatment.91

Amino acids. Inhibition of Maillard reaction, thus reducing AA

formation in foods, could occur by using competitive com-

pounds that are able to compete with asparagine for carbonyl

groups. In fact, the addition of amino acids before heat pro-

cessing of foods have been proposed as a possible strategy to

reduce AA formation by competing with asparagine in the

Maillard reaction or reacting with AA after its formation.92

In one study, the formation of AA was reduced by more than

80% in potato slices soaked in 3% solution of either lysine or

glycine prior to frying.93

Vitamins. The formation of AA was reduced by more than

60% after the addition of approximately 1% of vitamin C

and vitamin B1, whereas only 20% to 30% reduction was

found after the addition of 1% vitamin B2 and vitamin B5

in an amino acid/sugar chemical model system.94 Up to 75% reduction in AA formation in french fries was found by

dipping potato cuts in 2% citric acid solutions for 1 hour

before frying; however, there might be concerns about sour

flavors in the resulting products.95

Salt solution. Some mono- and divalent cations (eg, Naþ or

Ca2þ) were reported to effectively mitigate AA formation in

food.96 For example, potatoes dipped in CaCl2 solution showed

95% reduction in the amount of AA formed in fried potatoes

without negatively affecting the sensory characteristics of the

strips.96 These ions interact with asparagine so that the forma-

tion of the Schiff base is inhibited, and thus AA generation

during heating is reduced.96

Effect of Processing Conditions

Frying Time and Temperature

Generally, frying temperature and time have been shown to

significantly affect the amount of AA formed and are consid-

ered to be the most critical factors affecting its content in fried

potato products.97 Higher temperatures and longer duration of

thermal processing are associated with higher AA content.97

Soaking

A simple measure of presoaking potatoes before frying can

reduce the formation of AA.98 Washing raw french fries and

soaking them in water reduced the formation of AA if they

were fried to a lighter color.98 This is because presoaking

causes the glucose content in the potato strips to be reduced

with increased soaking time.98 Therefore, water soaking results

in lower AA content due to the leaching of one important AA

precursor such as glucose.

98 International Journal of Toxicology 39(2)

Blanching

Blanching is also performed in water to reduce the level of

reducing sugars in raw potatoes, which could result in higher

AA content.99 Blanching of potato strips with sunflower oil for

43 seconds at 150�C had a greater reduction effect on the level

of AA precursors (asparagine and reducing sugars) and thus on

the final AA level, relative to soaking in water.100 Moreover,

blanching in hot or warm water was reported to reduce the

amount of AA in french fries.101 As the blanching temperature

and duration increased, more glucose and asparagine are being

leached out leading to french fries with lower AA levels.101

Effect of pH, Water Activity, and Fermentation

Acids

It is widely established that pH levels influence the formation

of AA. Lowering the pH of the soaking solution has been

shown to stop the formation of the Schiff base (the nucleophilic

amine group (NH2) is converted to the non-nucleophilic proto-

nated-NH3þ) that leads to AA formation.102

Water Content

The total amount of water present in foods greatly influences

AA content in food. It has been found that AA is formed in

foods with water activity (aw) between 0.4 and 0.8. When the

water activity is<0.4, the formation of AA is decreased. Water

activity and moisture content are 2parameters that are linked

together, so foods with moisture content <5% are more likely

to follow the Maillard reaction and form AA.97

Fermentation

Formation of AA in food was also found to be affected by

fermentation.103 For instance, lactic acid fermentation was

reported to be suitable in reducing AA formation in potato

products, especially when combined with blanching.104

Conclusion

The report made by the SNFA in April 2002 about the presence

of high levels of AA in carbohydrate-rich foods processed at

high temperature (>120�C) evoked a worldwide health alarm.

This announcement sparked intensive investigations into AA,

its occurrence in foods, and its adverse health effects. At pres-

ent, AA is considered a food-borne toxicant by many interna-

tional organizations such as the Food and Drug Administration

and WHO. Many studies described the potential health risks of

AA; however, there is paucity of information on strategies to

reduce the levels of AA in processed food. This review did not

only present the toxicity of AA including neurotoxicity, muta-

genicity, and carcinogenicity but also focused on various ways

used in mitigating AA levels in food such as soaking, blanch-

ing, fermentation, enzymes, or antioxidant addition.

Author Contributions

Rifai, L. and Saleh, F. contributed to conception and design, drafted

manuscript, critically revised manuscript, gave final approval, and

agree to be accountable for all aspects of work ensuring integrity and

accuracy.

Declaration of Conflicting Interests

The author(s) declared no potential conflicts of interest with respect to

the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, author-

ship, and/or publication of this article.

ORCID iD

Fatima A. Saleh https://orcid.org/0000-0002-3225-3673

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