Acrylamide risk assessment
Risk assessment
Overview
Acrylamide (CH2=CH-CONH2) is a white crystalline material with a molecular weight of 70.08. It has been widely used as a precursor for the production of polyacrylamides for chemical products since 1950. Polyacrylamide is mainly used for the purification of water, the processing of pulp and the inner coating of pipes. In the EU, the annual production of acrylamide is approximately 8-10 million tons.
In April 2002, Swedish National Food Administration (NFA) and Stockholm University researchers first reported that in some fried and barbecued starchy foods, such as French fries, potato chips, cereals, and bread, etc. Acrylamide was produced; similar results were reported successively in Norway, the United Kingdom, Switzerland, and the United States. Due to the potential neurotoxicity, genotoxicity and carcinogenicity of acrylamide, the contamination of acrylamide in food has attracted the attention of the international community and governments. To this end, on June 25, 2002, the World Health Organization (WHO) and the Food and Agriculture Organization of the United Nations (FAO) jointly convened an expert advisory meeting on acrylamide contamination in foods to discuss the food safety of acrylamide in foods. In February 2005, the 64th meeting of the Joint Food Additives Expert Committee (JECFA) of the Food and Agriculture Organization of the United Nations (FAO) and the World Health Organization (WHO) systematically exposed acrylamide in foods based on new information from the past two years. Evaluation.
Contact route
The human body can contact acrylamide through various routes such as digestive tract, respiratory tract, skin and mucous membranes. Drinking water is one of the most important ways of exposure. For this reason, WHO limits the acrylamide content in water to 1 μg/L. In April 2002, Stockholm University reported that the content of acrylamide in French fries was more than 500 times higher than the maximum allowed in drinking water recommended by WHO. Therefore, food is considered to be the main source of human acrylamide. In addition, the body may also be exposed to acrylamide through smoking and other routes.
Absorption and metabolism
Acrylamide can be absorbed by the body through a variety of ways, among which the fastest absorption by the digestive tract, widely distributed in the body, including breast milk. Rats were given orally 0.1 mg/kg bw of acrylamide with an absolute bioavailability of 23-48%. About 90% of the acrylamide that enters the body is metabolized, and only a small amount is excreted in the urine through the prototype. After acrylamide enters the body, active glycidamide is produced by the action of cytochrome P4502E1. The epoxy propionamide binds more readily to guanine in DNA than acrylamide to form an adduct, resulting in genetic damage and gene mutation; therefore, it is considered to be the main carcinogenicly active metabolite of acrylamide. Studies reported that after administration of acrylamide to large mice, glycidamide was detected in liver, lung, testis, leukocyte, kidney and rat liver, thyroid, testis, breast, bone marrow, white blood cells, and brain. Purine adducts. No evidence of DNA adduct formation after exposure to human acrylamide has been reported.
In addition, acrylamide and epoxypropionamide can also form adducts with hemoglobin. Hemoglobin adducts are detected in the body of animals given acrylamide and ingested foods containing acrylamide. It is recommended that the hemoglobin adduct be used as contact. Biomarkers to estimate population exposure levels of acrylamide.
Risk assessment
For risk assessment of non-genotoxic substances and non-carcinogens, the usual method is to add NOAEL to the safety factor to generate the daily tolerable intake (ADI) or the weekly tolerable intake (PTWI), By comparing the actual level of intake of the population with ADI or PTWI, the population's risk to the population can be assessed. For genotoxic carcinogens, previous risk assessments suggest that exposure to these substances should be avoided as much as possible, without considering the relationship between the intake of such substances and the intensity of carcinogenic effects, and that there is no acceptable threshold dose tolerance, so managers cannot In order to determine the focus of the supervision of pollutants and preventive measures, and managers are very much in need of assessors to provide information on the different health risks that different intakes may cause. Therefore, when assessing the risk of such substances internationally, it is recommended to use the dose response model BMDL and the exposure limit (MOE) for assessment. BMDL is the low-side confidence limit for eliciting 5% or 10% of tumors. Exposure limit (MOE) is the BMDL divided by the population's estimated intake. The smaller the MOE, the greater the risk of cancer of the substance, and vice versa.
The non-carcinogenic effects of acrylamide were evaluated and the NOAEL value resulting in a neuropathologically altered animal test result was 0.2 mg/kg bw. Based on an average human intake of 1 μg/kg bw/day and a high consumer of 4 μg/kg bw/day, the population average and high intake of MOE are 200 and 50, respectively; acrylamide causes reproduction. With a toxic NOAEL value of 2 mg/kg bw, the population average and high intake MOE were 2000 and 500, respectively. JECFA believes that the risk of such side effects can be ignored by taking into account the estimated intake, but for people with high intakes, the possibility of causing neuropathological changes is not excluded.
The risk assessment of acrylamide focuses on the assessment of carcinogenic effects. Because epidemiological data and animal and human biomarker data are not sufficient for evaluation, based on animal carcinogenicity test results, carcinogenic effects were analyzed using eight mathematical models. The most conservative estimate is that the BMDL causing animal breast tumors is estimated to be 0.3 mg/kg bw/day, based on an average human intake of 1 μg/kg bw/day and a high consumer of 4 μg/kg bw/day. The MOE of the intake and high intake groups were 300 and 75, respectively. JECFA believes that for a genotoxic carcinogen, its MOE value is low, that is, the gap between the induced carcinogenic dose and the human maximum possible intake is not large enough, is close, and its potential harm to human health Attention should be given and it is recommended to take reasonable measures to reduce the content of acrylamide in the food. Some food production companies in Europe have achieved very good results in reducing the production of acrylamide in food processing.
In the risk assessment of acrylamide, the BMDL data deduced from animal experiments, population intake assessment, and the difference in the activation intensities of metabolism between humans and animals are uncertain. Therefore, several evaluations of the long-term animal experiments on acrylamide to be carried out should be carried out again. It is necessary to take into account the conversion of acrylamide into glycidamide in the body, as well as the data on the intake of acrylamide in developing countries and the human body. Biological markers were evaluated in connection with intake and toxicity end-point results.
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