Acrylonitrile exposure in the general population following a major train accident in Belgium: A human biomonitoring study

Smedt, Tom De; Cremer, Koen De; Vleminckx, Christiane; Fierens, Sébastien; Mertens, Birgit; Overmeire, Ilse Van; Bader, Michael; Paepe, Peter De; Göen, Thomas; Nemery, Benoît; Schettgen, Thomas; Stove, Christophe; Oyen, Herman Van; Loco, Joris Van; Nieuwenhuyse, An Van

doi:10.1016/j.toxlet.2014.09.009

Cited by 25 publications

(12 citation statements)

References 14 publications

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“…The LLOQ's (lower limit of quantification) were respectively 0.5 (Lab I), 4.0 (Lab II) and 2.0 (Lab III) pmol/g globin. When receiving the first results from the labs at the end of July, some CEV concentrations showed to be strongly increased, especially in the residents (>1000 pmol/g globin, De Smedt et al (2014), this issue). To verify the results, we decided to carry out an extra inter-laboratory performance test at that moment on a sub sample of the residents and emergency responders who participated in the human biomonitoring study.…”

Section: Adduct and Cotinine Analysesmentioning

confidence: 97%

Acrylonitrile exposure assessment in the emergency responders of a major train accident in Belgium: A human biomonitoring study

Nieuwenhuyse¹,

Fierens²,

Smedt³

et al. 2014

Toxicology Letters

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Emergency responders involved in the on-site management of the train accident were clearly exposed to ACN from the accident. However, the extent of exposure remained relatively moderate with CEV concentrations staying within the ranges described in literature as background for a smoking population. Moreover, the exposure was less pronounced in the emergency responders as compared to that in the local population.

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Section: Adduct and Cotinine Analysesmentioning

confidence: 97%

Acrylonitrile exposure assessment in the emergency responders of a major train accident in Belgium: A human biomonitoring study

Nieuwenhuyse¹,

Fierens²,

Smedt³

et al. 2014

Toxicology Letters

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“…For example, smoking results in elevated levels of several albumin and haemoglobin adducts, rendering it impossible to distinguish moderate exposure to certain toxicants from the contribution by smoking. 137,138 Although adduct monitoring has already successfully been applied for a number of compounds listed in Table 1, this approach has not yet been widely applied for assessing (the absence or extent of) occupational exposure. 135,137,139,140 The occupational history and, when available, the result of workplace monitoring and biomonitoring, are crucial for formulating a presumptive diagnosis.…”

Section: Assessment Of Exposurementioning

confidence: 99%

EASL Clinical Practice Guideline: Occupational liver diseases

Colombo¹,

Vecchia²,

Lotti³

et al. 2019

Journal of Hepatology

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A variety of chemicals have been linked to occupational liver diseases, including several solvents and mixtures thereof, pesticides, and metals. Workplace exposures have been associated with virtually the entire spectrum of acute and chronic liver diseases. However, their prevalence is inadequately quantified and their epidemiology limited. Occupational liver diseases may result from high accidental or from prolonged lower level exposures. Whereas the former is uncommon and easily recognised, the latter are relatively more frequent but often overlooked because they may display normal values of conventional markers, have an insidious onset and be asymptomatic or be obfuscated and confounded by concurrent conditions. In addition, specific tests of toxicity are not available, histopathology may not be revealing and the assessment of internal dose of chemicals is usually not decisive. Given these circumstances, the diagnosis of these liver disorders is challenging, one of exclusion and often requires an interdisciplinary approach. These recommendations offer a classification of the type of liver injuries associated with occupational exposures-based in part on the criteria for drug-induced liver injury-a grading of their severity, and the diagnostic and preventive criteria for chemically induced occupational liver disease.

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“…Globally, more than 10 billion pounds of AN are produced annually; AN is included on the hazardous air pollutant list developed by the United States Environmental Protection Agency and was ranked 269 on the 2019 substance priority list issued by the Agency for Toxic Substances and Disease Registry (ATSDR, 2019). The potential health threat posed to humans by AN exposure cannot be ignored, especially with acute AN poisoning incidents having recently been reported (De Smedt et al, 2014;Leng and Gries, 2014). Acrylonitrile epoxidation to cyanoethylene oxide (CEO) via cytochrome P450 2E1 (CYP2E1) and its subsequent metabolism to yield cyanide are responsible for AN-induced acute adverse effects including mortality (Thier et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Type 2 diabetes mellitus potentiates acute acrylonitrile toxicity: Potentiation reduction by phenethyl isothiocyanate

et al. 2021

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Acrylonitrile (AN) is a known animal carcinogen and suspected human carcinogen. Recently, occupational exposure to AN has considerably increased. Previously, we demonstrated that streptozotocin-induced diabetes potentiates AN-induced acute toxicity in rats and that the induced cytochrome P450 2E1 (CYP2E1) is responsible for this effect. In the present study, we examined whether induction of CYP2E1 is also the underlying mechanism for the potentiation of AN-induced acute toxicity in type 2 diabetes in db/db mice. The effect of phenethyl isothiocyanate (PEITC) in reducing potentiation was also investigated. The mice were randomly divided into the normal control, diabetic control, AN, diabetes + AN, PEITC + AN, and diabetes + PEITC + AN groups. PEITC (40 mg/kg) was orally administered to rats for 3 days, and 1 h after the last PEITC gavage, 45 mg/kg AN was intraperitoneally injected. Time to death was observed. The CYP2E1 level and enzymatic activity, cytochrome c oxidase (CCO) activity, and reactive oxygen species (ROS) levels were measured. The survival rate was decreased in AN-treated db/db mice compared with that in AN-treated wild-type mice. The hepatic CYP2E1 level and enzymatic activity remained unaltered in db/db mice. Phenethyl isothiocyanate alleviated AN-induced acute toxicity in db/db mice as evident in the increased survival rate, restored CCO activity, and decreased ROS level in both the liver and brain. The study results suggested that CYP2E1 may not be responsible for the sensitivity to AN-induced acute toxicity in db/db mice and that PEITC reduced the potentiation of AN-induced acute toxicity in db/db mice.

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Acrylonitrile exposure in the general population following a major train accident in Belgium: A human biomonitoring study

Abstract: The train derailment resulted in a highly atypical sequence-of-events. In addition to exposure in the direct vicinity of the site of the train derailment, exposure also occurred via the sewage system, into which acrylonitrile had entered shortly after the accident.

Cited by 25 publications

References 14 publications

Acrylonitrile exposure assessment in the emergency responders of a major train accident in Belgium: A human biomonitoring study

Acrylonitrile exposure assessment in the emergency responders of a major train accident in Belgium: A human biomonitoring study

EASL Clinical Practice Guideline: Occupational liver diseases

Type 2 diabetes mellitus potentiates acute acrylonitrile toxicity: Potentiation reduction by phenethyl isothiocyanate

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