Toxic chili?
Historical background
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On 9 May 2003, France sent initial information to the European Commission through the rapid alert system for food and feed (RASFF) relating to discovery of the dye Sudan I in hot chilli products originating from India.
In June 2003 the Standing Committee on the Food Chain and Animal Health (SCFCAH) agreed to take emergency measures, and European Commission (EC) notified to member states that products contaminated with Sudan I found in France had been produced in the UK. More recently, other contaminated chilli products were detected in Germany, Italy, Ireland and elsewehere.
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Chilli powder |
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Since 21 January 2004, an EC Decision requires that cargos of dried and crushed or ground chilli and curry powder coming into any EU Member State must be accompanied by a certificate showing they have been tested and found to be free of Sudan I, Sudan II, Sudan III and Sudan IV. The scope of sampling for analysis includes all products made from fruit of the genus Capsicum, but also curry powder, if intended for human consumption.
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Biochemical background
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Sudan I, Sudan II, Sudan III and Scarlet Red (Sudan IV) have been classified as category 3 carcinogens by the International Agency for Research on Cancer (IARC). This means there's no direct evidence that these compounds cause cancer in humans. But Sudan I has recently been shown to cause cancer in rats, mice and rabbits. It has also been found to form DNA adducts with human DNA in specifically engineered human liver cells.
All compounds belong to the monoazo (Sudan I and II) or diazo dyes (Sudan III and IV). They share many biochemical properties, among which the ability to form reactive intermediates upon biotransformation sive metabolic activation in several mammalian species is of special interest.
The acute toxicity of azo dyes, as defined by the EU criteria for classification of dangerous substances, is rather low. Information about acute oral toxicity, including skin and eye irritation, is in form of material safety data sheets available for many commercial azo dyes. Only a few azo dyes showed LD50 values below 250 mg/kg body weight, whereas a majority showed LD50 values between 250-2,000 mg/kg body weight. Massive exposure to aromatic amines may cause methemoglobinemia. The amines oxidise the heme iron of haemoglobin from Fe(II) to Fe(III), blocking the oxygen binding. Other health concerns related to azo dyes is sensitisation and allergy. Azo dyes of the Disperse series have been found especially effective in this regard, but not the Sudan dyes.
A class genotoxicity of Sudan dyes is controversial. In rats, Sudan I or its metabolites, respectively, have been found to form both RNA and DNA adducts and to induce liver nodules upon (repeated) oral administration. Data on the other Sudan dyes is scarce.
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Metabolic activation: The azo linkage is the most labile portion of an azo dye molecule and may easily undergo enzymatic breakdown in mammalian organisms, including man. The azo linkage may be reduced and cleaved, resulting in the splitting of the molecule in two parts. The anaerobic environment of the lower gastrointestinal tract of mammals is well suited for azo-reduction. Several anaerobic intestinal bacteria are capable of reducing the azo linkage. The majority of these bacteria belong to the genera Clostridium and Eubacterium. They contain an enzyme associated with the cytochrome P 450, also termed azo-reductase. It is a non-specific enzyme, found in various micro-organisms and in all tested mammals. Azo-reductase activities are also found in mammalian cells: that of the liver, followed by the azo-reductase of the kidneys possess the greatest enzymatic activity. The majority of azo dyes requires metabolic activation, namely reduction and cleavage of the azo linkage to the component aromatic amines to show mutagenicity in vitro test systems. Therefore the majority of azo dyes, if highly purified, will, at least without metabolic activation, be negative in such tests. There is a strong evidence that aromatic amines require metabolic activation, e.g. in the liver, for carcinogenicity. The first step involves N-hydroxylation and N-acetylation, and the second step involves O-acylation yielding acyloxy amines. These compounds can degrade to form highly reactive nitrenium and carbonium ions. These electrophilic reactants may then readily bind covalently to genetic material, i.e. cellular DNA and RNA.
11:19:29 PM 
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