Acrylamide: A Cooking Carcinogen?

TLDR

Acrylamide exposure is monitored by detecting the N‑(2‑carbamoylethyl)valine adduct on hemoglobin using mass spectrometry. The study tested whether the hemoglobin adduct originates from cooking‑derived acrylamide by feeding rats a fried diet for one to two months. Gas chromatography/tandem mass spectrometry confirmed the adduct as CEV and demonstrated that acrylamide formed during feed heating produced adduct levels consistent with the measured Hb adduct. The fried‑diet rats showed a strong increase in the Hb adduct, reaching levels similar to the ~40 pmol g⁻¹ background seen in non‑smokers, indicating that cooking is a major source of acrylamide exposure and poses a considerable cancer risk.

Abstract

Exposure to acrylamide (AA) has been monitored by mass spectrometric detection of the adduct, N-(2-carbamoylethyl)valine (CEV), to the N-termini of hemoglobin (Hb), according to the N-alkyl Edman method. In these studies, a conspicuous background level, about 40 pmol/g of globin, of apparently the same adduct was regularly observed in Hb from persons without known exposure to AA. For testing of the hypothesis that this adduct originates from AA formed in cooking, rats were fed fried animal standard diet for 1 or 2 months. These animals exhibited a strong increase of the level of the studied Hb adduct, compared to control rats fed unfried diet. By gas chromatography/tandem mass spectrometry, the identity with CEV was confirmed by the concordance of the product ion spectrum of the studied adduct with that of a verified standard and by interpretation of the fragment ions. Further support of the chemical structure, at the same time pinpointing AA as the causative reactive factor, was obtained through the demonstration that AA is formed in the heating of the feed and that the level of AA in the fried feed is compatible with the measured levels of the CEV adduct. The raised CEV adduct levels observed in experimental animals are of a magnitude that is similar to the background level in nonsmoking humans. These data render it likely that cooking of food is a major source of the background dose of AA also in humans. An evaluation of cancer tests of AA and available data for its metabolism leads to the estimation that the background dose of AA is associated with a considerable cancer risk.