Analysis of Acrylamide, a Carcinogen Formed in Heated Foodstuffs

Abstract

Reaction products (adducts) of acrylamide with N termini of hemoglobin (Hb) are regularly observed in persons without known exposure. The average Hb adduct level measured in Swedish adults is preliminarily estimated to correspond to a daily intake approaching 100 microg of acrylamide. Because this uptake rate could be associated with a considerable cancer risk, it was considered important to identify its origin. It was hypothesized that acrylamide was formed at elevated temperatures in cooking, which was indicated in earlier studies of rats fed fried animal feed. This paper reports the analysis of acrylamide formed during heating of different human foodstuffs. Acrylamide levels in foodstuffs were analyzed by an improved gas chromatographic-mass spectrometric (GC-MS) method after bromination of acrylamide and by a new method for measurement of the underivatized acrylamide by liquid chromatography-mass spectrometry (LC-MS), using the MS/MS mode. For both methods the reproducibility, given as coefficient of variation, was approximately 5%, and the recovery close to 100%. For the GC-MS method the achieved detection level of acrylamide was 5 microg/kg and for the LC-MS/MS method, 10 microg/kg. The analytic values obtained with the LC-MS/MS method were 0.99 (0.95-1.04; 95% confidence interval) of the GC-MS values. The LC-MS/MS method is simpler and preferable for most routine analyses. Taken together, the various analytic data should be considered as proof of the identity of acrylamide. Studies with laboratory-heated foods revealed a temperature dependence of acrylamide formation. Moderate levels of acrylamide (5-50 microg/kg) were measured in heated protein-rich foods and higher contents (150-4000 microg/kg) in carbohydrate-rich foods, such as potato, beetroot, and also certain heated commercial potato products and crispbread. Acrylamide could not be detected in unheated control or boiled foods (<5 microg/kg). Consumption habits indicate that the acrylamide levels in the studied heated foods could lead to a daily intake of a few tens of micrograms.

Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake, smoking habits and gender

“…A temperature-dependent formation of AA in human foodstuffs during cooking (at temperatures above 120º C) was demonstrated and carbohydrate-rich foods, particularly potatoes, showed very high AA levels (up to mg per kg) [2]. Follow-up studies verified the findings (e.g.…”

“…The finding that the industrial chemical substance acrylamide (AA) is formed in high amounts during cooking of food [1,2] led to concerns about exposure and health risk for the general population [3]. AA is a known neurotoxic and clastogenic substance, shown to be carcinogenic in animals and, therefore, classified as a probable human carcinogen [4,5].…”

Associations between estimated acrylamide intakes, and hemoglobin AA adducts in a sample from the Malmö Diet and Cancer cohort

“…Previously, drinking water and tobacco were considered the main sources of exposure to the general population. However, a few years ago, research at Stockholm University revealed that AA is formed when foods are heated at high temperatures, and that certain carbohydrate-rich foods, particularly potatoes, could contain high levels of AA (Tareke et al, 2000(Tareke et al, , 2002. This was later confirmed by others (Rosén and Hellenäs, 2002;World Health Organisation, 2002).…”

Hazardous effects of fried potato chips on the development of retina in albino rats

“…Reports from laboratory studies have provided insight into the biochemical mechanism of acrylamide (ACR) formation. As a neurotoxic chemical, ACR can be generated during the heating of specific foodstuffs as a result of Millard reaction between amino acids and sugars [18,19] . In particular, ACR is formed when the amino acid asparagine in the presence of sugar is heated above 100 曟.…”

“…Early morphological studies suggested that ACR neurotoxicity was mediated by nerve damage classified as a central-peripheral distal axonopathy [19] . However, other contemporary researches demonstrated that ACR can produce neurological toxicity in the absence of axonopathy, whereas equivalent neurotoxicity can be induced by intoxication over a wide range of daily dose-rates (e.g.…”