Review
Risk assessment, formation, and mitigation of dietary acrylamide: Current status and future prospects

https://doi.org/10.1016/j.fct.2014.03.037Get rights and content

Highlights

  • The state-of-art understanding of acrylamide (AA) risk assessment is summarized.

  • The application of omics into association of AA with human diseases is proposed.

  • More attentions are required to develop novel technologies to reduce AA in foods.

Abstract

Acrylamide (AA) was firstly detected in food in 2002, and since then, studies on AA analysis, occurrence, formation, toxicity, risk assessment and mitigation have been extensively carried out, which have greatly advanced understanding of this particular biohazard at both academic and industrial levels. There is considerable variation in the levels of AA in different foods and different brands of the same food; therefore, so far, a general upper limit for AA in food is not available. In addition, the link of dietary AA to human cancer is still under debate, although AA has been known as a potential cause of various toxic effects including carcinogenic effects in experimental animals. Furthermore, the oxidized metabolite of AA, glycidamide (GA), is more toxic than AA. Both AA and GA can form adducts with protein, DNA, and hemoglobin, and some of those adducts can serve as biomarkers for AA exposure; their potential roles in the linking of AA to human cancer, reproductive defects or other diseases, however, are unclear. This review addresses the state-of-the-art understanding of AA, focusing on risk assessment, mechanism of formation and strategies of mitigation in foods. The potential application of omics to AA risk assessment is also discussed.

Introduction

Acrylamide (AA) is an important industrial chemical, which has been widely used as a flocculating agent in water treatment, as an ingredient in several cosmetic formulations and as a chemical reagent in molecular biology research (Blank, 2005, Friedman, 2003, Pedreschi et al., 2014). It comes to public and academic attention because of its hazards to humans and animals. The Swedish National Food Administration and the University of Stockholm reported that AA is present in many commonly consumed foods, such as bread, fried foods, and coffee (Rosén and Hellenäs, 2002). Interestingly, no AA was found in raw and boiled foods, indicating that AA formation is associated with food processing. Subsequent studies found that AA is formed in food during high-temperature processing, such as cooking, frying, roasting and baking of carbohydrate-rich foods, through a reaction known as the Maillard reaction between sugars and amino acid asparagine, under low moisture conditions (Mottram et al., 2002, Stadler et al., 2002, Tareke et al., 2002, Yaylayan et al., 2003, Zyzak et al., 2003). The Maillard reaction is responsible for the golden color and tasty flavor of baked, fried and toasted foods, and in this sense, AA formation is an adverse by-product of Maillard reaction.

Due to its genotoxicity and carcinogenicity, AA was classified as a Group 2A carcinogen by the International Agency for Research on Cancer (IARC, 1994) and a Category 2 carcinogen and Category 2 mutagen by the European Union (EC, 2002), which caused worldwide concern (FAO/WHO, 2002). It was put into the list of substances of “very high concern” by the European Chemical Agency in 2010. Therefore, the food industry faces a challenge to modify the processes or to change the product parameters without compromising the quality of their foods. This depends largely on a better understanding of AA formation and mitigation technologies, and toxicological mechanisms as well.

During the past years, many new epidemiological studies have been carried out to investigate the association of dietary AA or occupational AA exposure with cancer in humans (Bongers et al., 2012, Chen et al., 2012, Erdreich and Friedman, 2004, Hogervorst et al., 2007, Hogervorst et al., 2014, Konings et al., 2010, Larsson et al., 2009, Lujan-Barroso et al., 2014, Wilson et al., 2010). These studies have been summarized in several extensive reviews (Pelucchi et al., 2011, Pedreschi et al., 2014, Lipworth et al., 2013, Lipworth et al., 2012). So far, epidemiological studies do not suggest a clear association of cancer with dietary or occupational exposure to AA. Therefore, novel epidemiological studies using large populations with broad exposure contrasts and biomarkers of human diseases include cancers are needed.

The review addresses some critical issues of AA with a focus on risk assessment, formation mechanisms and mitigation technologies. The prospects of AA risk assessment are discussed as well.

Section snippets

AA formation

To control the formation of this potential carcinogen in food, detailed knowledge of its mechanism of formation is of critical importance. So far, there are at least a major pathway and a minor pathway for AA formation. Some critical and direct precursors contributing to the formation of AA include 3-aminopropionamide (3-APA), decarboxylated Schiff base (Zyzak et al., 2003), decarboxylated Amadori product (Yaylayan et al., 2003), acrylic acid (Becalski et al., 2003, Stadler, 2003, Stadler et

AA risk assessment

AA risk assessment is one of the fundamental issues of AA biosafety, which is composed of hazard identification, hazard characterization, exposure assessment, and risk characterization. Based on the risk assessment result, various effective strategies and methods could be developed to substantially reduce the levels of AA in the food, and to prevent the risk of human exposure to AA. As compared with AA formation and detection, less attention has been paid to AA risk assessment, particularly in

AA mitigation

As the production of AA is the by-product of the Maillard reaction that is essential for the color, taste, texture, and flavor of the foods, the major challenge of AA reduction is to reduce food AA as much as possible while maintaining their quality traits. Previous studies found that many exogenous and endogenous factors play important roles in the formation of AA (Anese et al., 2009b, Blank, 2005, Halford et al., 2012, Pedreschi et al., 2014, Rydberg et al., 2003, Surdyk et al., 2004, Taubert

Biomarkers and AA risk assessment

AA and GA bind covalently to amino acids in hemoglobin (Hb), thus, Hb adducts of AA and GA, AA-Hb and GA-Hb adducts, have been used as biomarkers of AA exposure in both rodents and human studies (Fennell et al., 2005, JECFA, 2011, Schettgen et al., 2003). Due to the long half-life of Hb and the fact that Hb adducts are not repaired, the measured adduct levels reflect a time-weighted average over the lifetime of the erythrocyte. Thus, similar levels of adducts can result from a low exposure over

Conclusion and prospective

The natural contents of reducing sugars and free amino acids together with water in the raw materials of food and the processing conditions play important roles in AA formation during heating. Current epidemiological and toxicological studies are insufficient to indicate that AA amounts consumed in the normal diet are likely to result in adverse human health effects, particular cancer. Thus, 10 years after the discovery of AA in food, it is still not possible to quantify the risk of dietary AA.

Conflict of Interest

The authors declare that there are no conflicts of interest.

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Acknowledgements

The authors highly appreciate the financial support from National Basic Research Program of China (2012CB72804) and China National Special Project of International Cooperation in Science and Technology (2012DFG31840). Thanks also to Dr. Aibo Wu, from Institute for Agri-food Standards and Testing Technology, Shanghai Academy of Agricultural Sciences, for his critical reading and constructive suggestions for the revision of the manuscript.

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