Self-reported symptoms and neuropsychological function among tunnel workers previously exposed to acrylamide and N-methylolacryl­amide

Goffeng, Lars Ole; Alvestrand, Monica; Ulvestad, Bente; Sørensen, Kjell Aage; Skaug, Vidar; Kjuus, Helge

doi:10.5271/sjweh.3083

Cited by 17 publications

(11 citation statements)

References 25 publications

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“…Finally, Goffeng et al (2011) in the same 44 exposed and 49 non-exposed workers, investigated whether self-reported symptoms and neuropsychological test results were different during work and at the time of examination. The retrospectively self-reported prevalence of symptoms like paresthesia in hands and legs and leg cramps during work periods were higher in the exposed workers.…”

Section: Epidemiological Studies: Neurological Alterationsmentioning

confidence: 99%

Scientific Opinion on acrylamide in food

Publication¹

2015

EFS2

329

170

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EFSA was asked to deliver a scientific opinion on acrylamide (AA) in food. AA has widespread uses as an industrial chemical. It is also formed when certain foods are prepared at temperatures above 120 °C and low moisture, especially in foods containing asparagine and reducing sugars. The CONTAM Panel evaluated 43 419 analytical results from food commodities. AA was found at the highest levels in solid coffee substitutes and coffee, and in potato fried products. Mean and 95th percentile dietary AA exposures across surveys and age groups were estimated at 0.4 to 1.9 µg/kg body weight (b.w.) per day and 0.6 to 3.4 µg/kg b.w. per day, respectively. The main contributor to total dietary exposure was generally the category 'Potato fried products (except potato crisps and snacks)'. Preferences in home-cooking can have a substantial impact on human dietary AA exposure. Upon oral intake, AA is absorbed from the gastrointestinal tract and distributed to all organs. AA is extensively metabolised, mostly by conjugation with glutathione but also by epoxidation to glycidamide (GA). Formation of GA is considered to represent the route underlying the genotoxicity and carcinogenicity of AA. Neurotoxicity, adverse effects on male reproduction, developmental toxicity and carcinogenicity were identified as possible critical endpoints for AA toxicity from experimental animal studies. The data from human studies were inadequate for dose-response assessment. The CONTAM Panel selected BMDL 10 values of 0.43 mg/kg b.w. per day for peripheral neuropathy in rats and of 0.17 mg/kg b.w. per day for neoplastic effects in mice. The Panel concluded that the current levels of dietary exposure to AA are not of concern with respect to non-neoplastic effects. However, although the epidemiological associations have not demonstrated AA to be a human carcinogen, the margins of exposure (MOEs) indicate a concern for neoplastic effects based on animal evidence. © European Food SUMMARYFollowing a request from the European Commission, the Panel on Contaminants in the Food Chain (CONTAM Panel) was asked to deliver a scientific opinion on acrylamide (AA) in food. The Panel developed the draft scientific opinion which underwent a public consultation from 1 July 2014 to 15 September 2014. The comments received and how they were taken into account when finalising the scientific opinion were published in an EFSA Technical Report (EFSA, 2015).AA is a low molecular weight, highly water soluble, organic compound. It is used inter alia as an industrial chemical and in the production of polyacrylamides. Heightened concerns about exposure to AA arose in 2002 when it was discovered that it forms when certain foods are prepared at temperatures usually above 120 °C and low moisture. It forms, at least in part, due to a Maillard reaction between certain amino acids, such as asparagine, and reducing sugars. However, several other pathways and precursors have also been proposed to contribute to AA formation. AA forms in numerous baked or fried carbohydrate-rich f...

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Section: Epidemiological Studies: Neurological Alterationsmentioning

confidence: 99%

Scientific Opinion on acrylamide in food

Publication¹

2015

EFS2

329

170

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“…8,9 Both acute and long-term exposure have been shown to damage the nervous system, causing lesions in sensory peripheral nerves and, at higher doses, in the central nervous system. 8,9 Both acute and long-term exposure have been shown to damage the nervous system, causing lesions in sensory peripheral nerves and, at higher doses, in the central nervous system.…”

Section: Introductionmentioning

confidence: 99%

“…Human epidemiological data indicate that ACR is a neurotoxicant. 8,9 Both acute and long-term exposure have been shown to damage the nervous system, causing lesions in sensory peripheral nerves and, at higher doses, in the central nervous system. ACR has been linked to reproductive toxicity and mutagenicity in mammals, both in vivo and in cell culture tests, 10 and is classified as a probable human carcinogen.…”

Section: Introductionmentioning

confidence: 99%

A urinary metabolomics study of rats after the exposure to acrylamide by ultra performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry

Wang

Jin

et al. 2015

Mol. BioSyst.

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Acrylamide (ACR) is known to induce neurotoxicity in humans and occupational exposure to ACR has an effect on human health. Since some animal experiments indicate the metabolic change caused by the ACR based on the metabolomics, increasing concern is the change of metabolite profiles by the low-dose ACR. In the present study, a low-dose of ACR (18 mg kg(-1)) was administered to male Wistar rats for 40 days. Ultra performance liquid chromatography/time of flight mass spectrometry (UPLC-Q-TOF MS) was used to examine urine samples from ACR-dosed and control animals. Multiple statistical analyses with principal component analysis (PCA) were used to investigate metabolite profile changes in urine samples, and to screen for potential neurotoxicity biomarkers. PCA showed differences between the ACR-dosed and control groups 20 days after the start of dosing; a bigger separation between the two groups was seen after dosing for 40 days. Levels of 4-guanidinobutanoic acid and 2-oxoarginine were significantly higher in urine from the ACR-dosed group than in urine from the control group after 10 days (p < 0.05). Receiver operator characteristic (ROC) curve analysis suggested that 4-guanidinobutanoic acid and 2-oxoarginine were the major metabolites. Our results suggest that high levels of 4-guanidinobutanoic acid and 2-oxoarginine may be related to ACR neurotoxicity. These metabolites could, therefore, act as sensitive biomarkers for ACR exposure and be useful for investigating toxic mechanisms. They may also provide a scientific foundation for assessing the effects of chronic low-dose ACR exposure on human health.

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“…In the European Union, acrylamide has been replaced by less toxic alternatives to acrylamide, such as N-methylolacrylamide. Thus, alternatives to acrylamide are needed in Korea, especially for employees of small waterproofing businesses [ 25 ]. Government oversight and regulation of acrylamide use remain important, and there are several related recommendations, such as adequate ventilation to control dust and gas, wearing appropriate personal protective equipment (e.g., a respirator, facial shielding, and impermeable protective gloves), and washing contaminated skin after work.…”

Section: Discussionmentioning

confidence: 99%

Dermal and neural toxicity caused by acrylamide exposure in two Korean grouting workers: a case report

Kim¹,

Lee²,

Rhie³

2017

Ann of Occup and Environ Med

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BackgroundPeripheral neuritis caused by acrylamide is well-known, and many Korean grouting workers are frequently exposed to acrylamide in grouting agents that are injected into cracked concrete. We recently encountered two cases of dermal and neural toxicity in Korean grouting workers with exposure to grouting agents that contained a high concentration of acrylamide.Case presentationThe first case involved a 44-year-old man with 8 years of waterproofing experience. The patient developed peeling skin on both hands while grouting, which progressed to systemic neurological symptoms, such as reduced sensory function and strength. The patient was diagnosed with peripheral neuropathy caused by acrylamide exposure, and fully recovered after conservative treatment and withdrawal of exposure to the grouting agent. The second case involved a 34-year-old man with 10 years of grouting experience. The patient initially experienced weakness in both legs, which progressed to weakness in his arms and uncontrolled phonation. After being hospitalized, he was diagnosed with cerebellar ataxia and peripheral neuropathy caused by acrylamide exposure, and was discharged after conservative treatment. Our follow-up investigation revealed that both workers were recently exposed to grouting agents that contained higher concentrations of acrylamide, compared to the agents that they had previously been using.ConclusionsBoth workers had workplace acrylamide exposure through dermal contact plus inhalation of dust and vapor, which led to the neural toxicity and dermatitis. Therefore, government studies are needed to investigate the current status of workplace acrylamide use, and to protect workers from the hazardous effects of using acrylamide-containing grouting agents.

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Self-reported symptoms and neuropsychological function among tunnel workers previously exposed to acrylamide and N-methylolacrylamide

Cited by 17 publications

References 25 publications

Scientific Opinion on acrylamide in food

Scientific Opinion on acrylamide in food

A urinary metabolomics study of rats after the exposure to acrylamide by ultra performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry

Dermal and neural toxicity caused by acrylamide exposure in two Korean grouting workers: a case report

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Self-reported symptoms and neuropsychological function among tunnel workers previously exposed to acrylamide and N-methylolacryl­amide

Cited by 17 publications

References 25 publications

Scientific Opinion on acrylamide in food

Scientific Opinion on acrylamide in food

A urinary metabolomics study of rats after the exposure to acrylamide by ultra performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry

Dermal and neural toxicity caused by acrylamide exposure in two Korean grouting workers: a case report

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Self-reported symptoms and neuropsychological function among tunnel workers previously exposed to acrylamide and N-methylolacrylamide