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PubMed2003

A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany.

Since the formation of acrylamide (AA) in the heating process of starch-containing food could be demonstrated and high contents of this substance were found in commercial food products, there is a great discussion about the possible human health risks connected with this dietary exposure. In order to determine the body burden of the general population in Germany caused by this uptake, we investigated the internal exposure to acrylamide and acrylonitrile in a group of 72 persons using haemoglobin adducts as parameters of biochemical effects. The collective was subdivided into non-smokers and smokers basing on the results of the smoking-specific acrylonitrile adduct (N-cyanoethylvaline, CEV). The median value for the adduct of AA (N-2-carbamoylethylvaline, AAV) in 25 non-smokers was 21 pmol/g globin (approximately 0.6 microgram/l blood) with a 95 percentile of 46 pmol/g globin (approximately 1.3 micrograms/l) (LOD: 12 pmol/g globin). The median level for AAV in smokers (n = 47) was found to be 85 pmol/g globin (approximately 2.3 micrograms/l blood) with a 95 percentile of 159 pmol/g globin (approximately 4.3 micrograms/l blood). Based on these results about 60 micrograms AA/d are taken up by adult non-smoking persons. According to calculations of WHO and US EPA this background exposure would lead to a cancer risk between 6 x 10(-4) and 3.6 x 10(-3). Our results confirm a body burden to AA even in persons from the non-smoking general population in Germany that is most probably caused by dietary uptake. Smoking habits considerably contribute to the level of this adduct.

Acrylamide↗
PubMed2006

Determination of acrylamide in foods by pressurized fluid extraction and liquid chromatography-tandem mass spectrometry used for a survey of Spanish cereal-based foods.

An automated and rapid method for the determination of acrylamide in different food products is presented. The method involves pressurized fluid extraction (PFE) of foods with acetonitrile and precipitation with Carrez reagents. The final extract is analysed by liquid chromatography coupled to electrospray ionization tandem mass spectrometry (ESI-MS-MS). The main parameters affecting the performance of ESI-MS-MS and PFE were optimized using a design of experiments approach. The limit of quantification of the method was 5 microg kg(-1), and recoveries from incurred samples ranged between 93 and 101%. The accuracy was evaluated using the reference test materials FAPAS T3002, T3005 and T3011. Using the optimized method, 62 food samples of potato chips, snacks, biscuits, breakfast cereals and crisp bread sampled from Valencia, Spain, supermarkets were surveyed for acrylamide levels. The levels were similar to those reported in the European Union and USA.

Acrylamide↗
PubMedDate not supplied

Acrylamide: review of toxicity data and dose-response analyses for cancer and noncancer effects.

Acrylamide (ACR) is used in the manufacture of polyacrylamides and has recently been shown to form when foods, typically containing certain nutrients, are cooked at normal cooking temperatures (e.g., frying, grilling or baking). The toxicity of ACR has been extensively investigated. The major findings of these studies indicate that ACR is neurotoxic in animals and humans, and it has been shown to be a reproductive toxicant in animal models and a rodent carcinogen. Several reviews of ACR toxicity have been conducted and ACR has been categorized as to its potential to be a human carcinogen in these reviews. Allowable levels based on the toxicity data concurrently available had been developed by the U.S. EPA. New data have been published since the U.S. EPA review in 1991. The purpose of this investigation was to review the toxicity data, identify any new relevant data, and select those data to be used in dose-response modeling. Proposed revised cancer and noncancer toxicity values were estimated using the newest U.S. EPA guidelines for cancer risk assessment and noncancer hazard assessment. Assessment of noncancer endpoints using benchmark models resulted in a reference dose (RfD) of 0.83 microg/kg/day based on reproductive effects, and 1.2 microg/kg/day based on neurotoxicity. Thyroid tumors in male and female rats were the only endpoint relevant to human health and were selected to estimate the point of departure (POD) using the multistage model. Because the mode of action of acrylamide in thyroid tumor formation is not known with certainty, both linear and nonlinear low-dose extrapolations were conducted under the assumption that glycidamide or ACR, respectively, were the active agent. Under the U.S. EPA guidelines (2005), when a chemical produces rodent tumors by a nonlinear or threshold mode of action, an RfD is calculated using the most relevant POD and application of uncertainty factors. The RfD was estimated to be 1.5 microg/kg/day based on the use of the area under the curve (AUC) for ACR hemoglobin adducts under the assumption that the parent, ACR, is the proximate carcinogen in rodents by a nonlinear mode of action. When the mode of action in assumed to be linear in the low-dose region, a risk-specific dose corresponding to a specified level of risk (e.g., 1 x 10-5) is estimated, and, in the case of ACR, was 9.5 x 10-2 microg ACR/kg/day based on the use of the AUC for glycidamide adduct data. However, it should be noted that although this review was intended to be comprehensive, it is not exhaustive, as new data are being published continuously.

Acrylamide↗
PubMed2003

A physiologically based pharmacokinetic model for acrylamide and its metabolite, glycidamide, in the rat.

Acrylamide is a neurotoxicant and a multisite carcinogen in rats following chronic, high-dose exposures. In an effort to improve risk-based decisions for acrylamide (AMD) and its epoxide metabolite, glycidamide (GLY), a physiologically based pharmacokinetic (PBPK) model was developed for describing AMD and GLY kinetics in the rat. The PBPK model consists of components for both AMD and GLY. AMD is distributed within five compartments (arterial blood, venous blood, liver, lung, and all other tissues lumped together) and is linked to the GLY portion of the model via metabolism in the liver. GLY is distributed within the same five compartments. Dosing of AMD via the intravenous, intraperitoneal, or oral route of exposure is incorporated into the model structure. The model parameters include measured values for rat physiology (tissue volumes, blood flows), estimated tissue partition coefficients based on a published algorithm, and estimated values for metabolism and tissue binding based on fitting the model to tissue kinetic data from four studies. Despite gaps and limitations in the available database, a reliable description of the kinetics of AMD and GLY from existing studies was obtained using a single set of model parameters. The metabolism of AMD via cytochrome P-450 was best described using a Vmax of 1.6 mg/h/kg and a Km of 10 mg/L, while the metabolism of AMD via GST was described using a second-order rate constant of 0.55 L/h-mmol GSH. Similarly, the metabolism of GLY via epoxide hydrolase was best described using a Vmax of 1.9 mg/h/kg and a Km of 100 mg/L, while the metabolism of GLY via GST was described using a rate constant of 0.8 L/h-mmol GSH. These parameters were established based on the proportion of various metabolites found in urine. Future studies will need to focus on the collection of key data for refining model parameters for metabolism and tissue binding and for model validation, as well as for developing a similar model for humans. Completion of these additional studies will result in a validated rat and human PBPK model capable of predicting tissue doses linked to potential mechanisms of toxic effects for AMD and GLY and allow determination of scientifically defensible exposure limits that remain protective of human health.

Acrylamide↗
PubMed1982

Assessment of the effects of acrylamide, methylmercury, and 2,5-hexanedione on motor functions in mice.

Neurotoxic effects of acrylamide, methylmercury, and 2,5-hexanedione were studied in forth female BALB/c mice. The chemicals were dissolved in distilled water and administered via light-tight drinking bottles. Three control groups were used. The first received distilled water, the second received concentrated saccharin solution to assess the effects of reduced water intake, and the third was maintained on a reduced food diet. Motor functions were quantified by measuring landing foot-spread and rotarod performance. Baseline data were collected before dosing started. Mice were placed, twice weekly, on an accelerating rotarod, and their retention time was recorded. In the landing foot-spread test, the experimenter dropped mice from 15 cm onto a flat, smooth surface once a week. The hindlimb splay was then measured by the examiner. Both experimenter and examiner were unaware of the identity of each group (except of the food deprived group, in the case of the experimenter) during the first exposure. Decreased retention time and increased hindlimb splay were observed in mice after 12 d of exposure to acrylamide. Recovery followed treatment cessation. Increased hindlimb splay preceded an obvious decline of rotarod performance in the group receiving the 10 ppm of methylmercury solution. Mice receiving the 20 and 40 ppm of methylmercury solutions did not display any change in these tests before overt signs of toxicity. 2,6-Hexanedione produced a small decline in performance to a constant level after 85 d of exposure. After dosing termination, performance returned to baseline values. Control groups showed no change in performance on either the rotarod or the landing foot-spread test. Our data show that the rotarod and hindlimb splay tests in mice are about equal in sensitivity to the effects of the neurotoxic chemicals tested.

Acrylamides↗
PubMedDate not supplied

Science communication and the Swedish acrylamide "alarm".

On April 24, 2002 the Swedish National Food Administration along with a group of researchers at the University of Stockholm raised an alarm regarding potential health risks associated with eating fried and baked foods such as potatoes and bread. Scientists had found high levels of acrylamide (up to 500 times more acrylamide than that allowed in drinking water by the World Health Organisation), a substance widely believed to cause cancer, in cooked high starch foods. The outcomes of this "alarm" were immediate. In Sweden sales of chips fell by 30-50 percent over a 3-day period following the press conference, and share prices among several fried food manufacturers fell substantially, as stock analysts were fearful that consumption of fried foods would decrease significantly. Four days after the press conference, however, consumers began eating fried food as normal and a number of researchers and journalists in Sweden and elsewhere took the view that the alarm had been both exaggerated and ill placed. In this study, I evaluate the science communication process associated with the scare, based on a content analysis of a select group of Swedish broad sheets from just previous to the April 2002 press conference to the present time (December 2002). In addition, the study is based on interviews with the various Swedish regulators involved in the process itself (in particular at the Swedish National Food Administration) as well as with the scientists responsible for the study at Stockholm University and relevant journalists and politicians.

Acrylamides↗
PubMed1979

Oxygen content determined by acrylamide polymerization: screening of anticancer agents, generation of oxyhemoglobin dissociation curves, and potential applications.

Many investigators have endeavored to accurately measure oxygen content produced or consumed from substrates or tissues. Most of the techniques currently available are time consuming or exceedingly complex. Many require expensive apparatus and demand the skills of a highly trained technician. We have deveoloped a rapid and sensitive method of measuring oxygen content or consumption. This method is based upon the time for polymerization of acrylamide gels. The time of acrylamide polymerization is directly proportional to the oxygen content of the test medium. We have used this method to generate oxyhemoglobin dissociation curves which closely resemble those published by Severinghaus and Duvelleroy, as well as those we determined by the conventional Van Slyke analysis. We have also used this method to measure the oxygen consumption of tumor cells and to evaluate the effects of Actinomycin, cyclohexamide and cytosine arabinoside on Walker 256 ascites tumor. The results correlate with the known in vivo effects of these drugs on this tumor cell line. Therefore, because of its sensitivity and adaptability this method may be useful in a variety of clinical and biological situations.

Acrylamides↗
PubMed1978

Nyloprint-sensitive patients react to NN' methylene bis acrylamide.

Two patients showed occupational contact sensitization to a component present in the Nyloprint photopolymer printing plate. The component could not be identified chemically. It contains an acrylamide group. Both patients gave group-specific reactions to NN' methylene bis acrylamide. This must be a closely realted substance. Possible preventive measures are discussed. The manufacturer should have disclosed the allergic substance and instructed his customer adequately. A "philosophy" concerning this point is being developed.

Acrylamides↗
PubMed1982

Secondary acrylamides in Nyloprint printing plate as a source of contact dermatitis.

Several chemically pure fractions have been isolated from Nyloprint printing plates. 5 of the fractions elicited positive patch test reactions in 7 Nylonprint allergic printers. 4 of the 5 components were analysed by means of nuclear magnetic resonance, infrared spectrophotometry, mass spectrometry and elemental analysis. The fractions were identified as N,N'-methylene-bis-acrylamide. N,N'-[oxybis(methylene)]bis-2-propenamide, N,N'-[1,2-ethanediylbis(oxymethylene)]-2-propenamide, and a new compound N-[(2-hydroxyethoxy)-methyl]-2-propenamide. All of the analysed fractions have the common feature of being secondary acrylamides.

Acrylamides↗
PubMed1978

Excretion of methyl mercury in rat bile: the effect of diethylmaleate, cyclohexene oxide and acrylamide.

Diethylmaleate, cyclohexene oxide and acrylamide administered intraperitoneally to rats, have been shown markedly to inhibit biliary excretion of methyl mercury. Simultaneously the sulphhydryl and sulphide content of the bile decreases. These results probably reflect the conjugation of acrylamide, diethylmaleate and cyclohexene oxide to glutathione in the liver, thereby blocking the biliary excretion of methyl mercury. A high concentration of liver glutathione seems to be a prerequisite for the normal translocation of methyl mercury from liver to bile. These results indicate that methyl mercury is transported from liver to bile as a glutathione complex.

Acrylamides↗
PubMed1978

Qualitative alterations of cytochrome P-450 in mouse liver microsomes after administration of acrylamide and methylmethacrylate.

Cytochrome P-450 in mouse liver microsomes was characterized by SDS-polyacrylamide gel electrophoresis after intraperitoneal injection of 80 mg phenobarbital, 4.5 and 45 mg acrylamide and 60 and 600 mg methylmethacrylate per kg body weight each day for four days. Four different forms of cytochrome P-450 with molecular weights of 47,000, 50,000, 54,000 and 56,000 were identified by staining for peroxidase activity and protein. The amount of cytochrome P-450 with a molecular weight of 47,000 (MLvMcP-450(47) decreased in the phenobarbital group and in both acrylamide groups. After methylmethacrylate treatment, this form increased at the low dose but was totally repressed at the high dose. The cytochrome P-450 form with a molecular weight of 50,000 (MLvMcP-450(50) was significantly increased only in the phenobarbital group. An increase in the total amount of cytochrome P-450 was only observed following treatment with phenobarbital.

Acrylamides↗
PubMed1963

ANTISERUMS PREPARED WITH ACRYLAMIDE GEL USED AS ADJUVANT.

Antiserums to macroglobulins were prepared by a convenient and time-saving procedure in which acrylamide gel was used as adjuvant. After electrophoresis in acrylamide gel, the macroglobulin zone from the gel pattern was homogenized and injected directly into rabbits without intermediate isolation of the purified antigen. The resulting antiserums exhibited high titers of antiserum to macroglobulin and showed only weak cross-reactions with other gamma globulins in serologic tests.

Acrylamide↗
PubMed1975

Acrylamide encephaloneuropathy due to well water pollution.

All five members of a family developed subacutely mental confusion and/or truncal ataxia. Symptoms and signs of polyneuropathy were seen later. The well water in the patients' home contained 400 ppm acrylamide. The present cases are unique in that they are cases of acrylamide poisoning induced by oral intake and percutaneous penetration, and that central nervous system symptoms were prominent.

Acrylamides↗
PubMed1986

Acrylamide cohort mortality study.

The mortality experience of 371 employees assigned to acrylamide monomer and polymerisation operations was examined with particular emphasis on cancers at sites identified from animal studies such as the central nervous system, thyroid gland, other endocrine glands, and mesotheliomas. A total of 29 deaths was observed up until 1982 (38.0 expected). No statistically significant excesses were noted in the total cohort and no deaths were found for the hypothesised sites of cancer. The observed deaths in the total cohort for the all cancers category were somewhat in excess (11 v 7.9); however, this was due entirely to excess cancers of the digestive tract and respiratory system in the subgroup with previous exposure to organic dyes. Among those employees not exposed to organic dyes, four deaths were due to malignancies versus 6.5 expected. This study does not support a cause effect relation between exposure to acrylamide at this work site and overall mortality, total malignant neoplasms, or any specific cancers.

Acrylamides↗
PubMed1977

Acrylamide poisoning.

A small epidemic of acrylamide poisoning amongst workers in the construction industry is described. The clinical features of this condition are reviewed and two cases are described in which residual neurological problems persisted for over 1 year. The literature on acrylamide poisoning is reviewed and it is recommended that this substance should only be handled in the open air or in well ventilated areas. Its use in confined spaces such as tunnels appears to be unduly hazardous.

Acrylamides↗
PubMed2003

A study of tryptophan fluorescence quenching of bifunctional alginate lyase from a marine bacterium Pseudoalteromonas sp. strain No. 272 by acrylamide.

A fluorescence quenching study of a sole tryptophan residue of a bifunctional alginate lyase from Pseudoalteromonas sp. strain No. 272 was done in the presence and absence of substrates, oligomeric guluronic and its C5 isomer mannuronic acid, by a Stern-Volmer plot with a quencher, acrylamide. N-Acetyltryptophanamide and reduced and carboxymethylated alginate lyase showed large quenching constants, on the other hand, the native enzyme had small constants regardless of the presence or absence of the substrates. The result suggests that the tryptophan residue is located in a buried region of the enzyme molecule, but is barely accessible to acrylamide, and that the residue is not masked by the substrates with various degrees of polymerization.

Acrylamide↗
PubMed1996

Conditions for single strand conformation polymorphism (SSCP)analysis with broad applicability: a study on the effects of acrylamide, buffer and glycerol concentrations in SSCP analysis of exons of the p53 gene).

We examined the influence of electrophoretic conditions on the detectability of small sequence alterations in DNA fragments by single strand conformation polymorphism (SSCP) analysis. Three acrylamide concentrations, 7.5, 14 and 20%, were selected, and all three gel types were prepared with four different Tris/borate/EDTA buffer concentrations. In addition, all these twelve gels were prepared both with and without 10% glycerol. All electrophoretic runs were performed at ambient temperature of 20-24 degrees C. The resulting 24 different electrophoretic conditions were used for the SSCP analysis of DNA fragments of exons 5, 7 and 8 of the human p53 gene; the results were evaluated primarily in relation to detectability of mutants. Six out of the 24 conditions permitted the detection of all mutants. For practical reasons, 14% acrylamide, 44.5 mmol/1 Tris, 44.5 mmol/1 boric acid, 1 mmol/1 EDTA, pH 8.0, with and without addition of glycerol was chosen as the most suitable. These "selected conditions" were applied in the SSCP analysis of an arbitrarily chosen set of mutant DNA fragments with single base exchanges,and all but one of seven mutants were detected in the gel system containing glycerol. Our results indicate that the set of "selected conditions" is of broad applicability, permitting the detection of even small sequence differences like single base exchanges with high reliability. It should prove especially useful in screening for unknown mutations.

Acrylamides↗