The detection of acrylamide in food gives cause for substantial concern. Acrylamide is a toxic substance, which among other things induces neurotoxic effects and is carcinoge- nic in animals.There is no reason to assume that these effects cannot occur in humans. For an average person in Germany, the daily uptake of acrylamide via food is estimated to be roughly 0.6 µg/kg body weight. Exposure can be several times higher for persons con- suming high amounts of food with high acrylamide content. It is not to be expected that these exposures lead to neurotoxic effects in humans. Due to the mutagenic effects of acrylamide, a non-threshold mode of action is assumed for carcinogenicity. Therefore, a cancer risk cannot be excluded for the consumption of acrylamide-contami- nated food.The acrylamide content in food should be decreased as far as reasonably feasible.
Zusammenfassung Der Nachweis von Acrylamid in Lebensmitteln gibt zu erheblicher Besorgnis Anlass. Acrylamid ist ein toxischer Stoff, der im Tierversuch u. a.neurotoxisch und Krebs erzeugend wirkt; es gibt keinen Anlass anzunehmen, dass diese Wirkungen nicht auch im Menschen auftreten können.Die tägliche Belastung durch Acrylamid in Lebensmitteln wird für den durchschnittlichen Verzehrer in Deutschland auf ungefähr 0,6 μg/kg Körpergewicht geschätzt. Für Personen mit starkem Verzehr hoch belasteter Produkte kann die Acrylamidaufnahme mehrfach höher liegen. Es ist nicht anzunehmen, dass diese Belastungen beim Menschen zu neurotoxischen Wirkungen führen. Für die Krebs erzeugende Wirkung von Acrylamid muss aufgrund der ebenfalls vorhandenen mutagenen Wirkungsweise davon ausgegangen werden, dass kein Schwellenwert vorliegt.Daher kann ein Krebsrisiko durch den Verzehr acrylamidbelasteter Nahrung nicht ausgeschlossen werden.Die Acrylamidbelastung durch Lebensmittel sollte so weit gesenkt werden wie vernünftigerweise möglich.
In the regulation of chemical substances, it is generally agreed that there are no thresholds for genotoxic effects of chemicals, i.e. , that there are no doses without genotoxic effects. When classifying and labelling chemicals, dangerous properties of chemicals are to be identified. In this context, in general, the mode of action (threshold or not) is not considered for genotoxic substances. In the process of quantitative risk assessment, however, determination of the type of dose-effect relationships is decisive for the outcome and the type of risk management. The presence of a threshold must be justified specifically in each individual case. Inter alia, the following aspects may be discussed in this respect: aneugenic activity, indirect modes of action, extremely steep dose-effect relationships in combination with strong toxicity, specific toxicokinetic conditions which may lead to 'metabolic protection' prior to an attack of DNA. In the practice of the regulation of chemical substances with respect to their genotoxic effects, the discussion of thresholds has played a minor role. For notified new substances, there are, in general, no data available that would allow a reasonable discussion. Concerning substances out of the European programme on existing substances, so far 29 have been assessed in our institute with respect to genetic toxicity. Eight out of these have shown considerable evidence for genotoxicity. For two of them, a possible threshold is discussed: one substance is an aneugen, the other one is metabolised to an endogenic compound with genotoxic potential. In the practice of risk assessment of genotoxic substances, the discussion of the mode of action for genotoxicity is frequently associated with the evaluation of potential carcinogenic effects. Here, tissue-specific genotoxic effects in target organs for carcinogenicity are to be discussed. Moreover, the contribution of genotoxicity to the multifactorial process of tumour development should be assessed.
According to regulations in the European Union, new chemical substances must be notified before they can be introduced onto the market. One of the prerequisites for notification is that toxicological properties, including mutagenicity, are examined. In this paper, a report on routine in vitro mutagenicity testing is given for 776 new substances notified in Germany between 1982 and 1997. In general, the methodological quality of testing was in line with internationally accepted guidelines. Bacterial gene mutation tests (Bact) were conducted for nearly all of the substances, 13.4% were positive. Of the Bact-positive substances, 36 were also tested in the in vitro chromosomal aberration test (CAbvit) and the mammalian cell gene mutation test (MCGM). Twenty-six of these (72.2%) were negative in both mammalian cell tests indicating that the genotoxic potentials of the substances are not relevant for man. Of all new substances, 333 were tested in CAbvit, here the percentage of positive findings was 25.2%. More than 80% of the in vitro clastogens were negative in the Bact. With respect to a sensitive detection of genotoxic potentials of substances, the combination `Bact+CAbvit' is appropriate for basic testing. In our database CHL cells were more sensitive to clastogenic effects than other cell types. Only very few clastogens were identified as `high toxicity clastogens'. MCGM tests were performed for 118 substances, quite often as follow-up in case of positive Bact tests. In total, 12.7% of the substances were positive in the MCGM. However, there was a clear difference in the frequencies of positive findings in HPRT tests (5.5%) and mouse lymphoma assays (MLA; 37.0%). None of the MCGM-positive substances was a `unique positive', i.e., negative in Bact and CAbvit.
The detection of acrylamide in food gives cause for substantial concern. Acrylamide is a toxic substance, which among other things induces neurotoxic effects and is carcinoge- nic in animals.There is no reason to assume that these effects cannot occur in humans. For an average person in Germany, the daily uptake of acrylamide via food is estimated to be roughly 0.6 µg/kg body weight. Exposure can be several times higher for persons con- suming high amounts of food with high acrylamide content. It is not to be expected that these exposures lead to neurotoxic effects in humans. Due to the mutagenic effects of acrylamide, a non-threshold mode of action is assumed for carcinogenicity. Therefore, a cancer risk cannot be excluded for the consumption of acrylamide-contami- nated food.The acrylamide content in food should be decreased as far as reasonably feasible.
