Vinyl chloride

Easter, M. D.; Burg, R. von

doi:10.1002/jat.2550140411

Cited by 10 publications

(5 citation statements)

References 54 publications

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“…F 1 generation animals exhibited centrilobular hypertrophy and acidophilic, basophilic, or clear cell foci. Hepatotoxicity occurs by the actions of cytochrome P450 2E1 to metabolize VC into 2-chloroethylene oxide, which covalently binds to nucleic acids and pro- teins to produce genotoxicity (Easter and Von Burg, 1994). Ultimately, this leads to hepatic angiosarcoma.…”

Section: Discussionmentioning

confidence: 99%

“…Organ systems affected following acute or subchronic occupational VC exposure include the respiratory and central nervous (CNS) systems. CNS effects include the anesthesia/narcosis signs of ataxia, drowsiness, visual disturbances, and other CNS effects such as numbness and/or tingling in the extremities (Easter and Von Burg, 1994). Hepatotoxicity is the primary result of chronic occupational VC exposure.…”

mentioning

confidence: 99%

“…Cytochrome P450 2E1 converts VC into the active metabolite 2-chloroethylene oxide. This metabolite covalently binds to nucleic acids and proteins, resulting in genotoxicity that ultimately leads to hepatic angiosarcoma (Easter and Von Burg, 1994).…”

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confidence: 99%

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Embryo-Fetal Developmental and Reproductive Toxicology of Vinyl Chloride in Rats

Thornton

Schroeder²,

Robison³

et al. 2002

Toxicological Sciences

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Vinyl chloride (VC) exposure is primarily via inhalation in the workplace. The primary target organ of VC toxicity is the liver and occupational exposure to VC leads to hepatic angiosarcoma. However, based on epidemiological studies, researchers have been unable to ascertain the effect of occupational VC exposure on embryo-fetal development or reproductive function. A limited number of animal studies available in the literature have examined the effect of VC on embryo-fetal development, however, there are no published studies on the effect of VC exposure on reproductive capability. The current study was designed to assess the potential maternal and/or embryo-fetal developmental and 2-generation reproductive toxicity of inhaled VC in CD(R) Sprague-Dawley rats at exposure levels of 0, 10, 100, and 1100 ppm. In the embryo-fetal/developmental toxicity study, the female rats were exposed to VC daily from gestation day (GD) 6 through 19. In the reproductive toxicity study, the F(0) generation male and female rats were exposed to VC for a 10-week premating and 3-week mating periods. The F(0) generation male rats were exposed to VC until terminal euthanasia. The F(0) generation female rats were exposed from GD 0 through GD 20 and lactation day (LD) 4 through LD 25. Our results indicate that up to 1100 ppm VC exposure did not adversely affect embryo-fetal developmental or reproductive capability over 2 generations in rats. The primary target organ of VC, the liver, was affected as evidenced by an increase in liver weight and/or histologically identified cellular alterations, such as centrilobular hypertrophy at 100 and 1000 ppm. Based on the results of these studies, the no observed adverse effect level (NOAEL) for embryo-fetal/development is 1100 ppm, and the NOAEL for reproduction is 1100 ppm. The results from the current studies, which are a more comprehensive embryo-fetal/developmental and reproduction study, may be incorporated into future risk assessments of occupational exposure to VC where concerns regarding the effects of VC exposure remain.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Embryo-Fetal Developmental and Reproductive Toxicology of Vinyl Chloride in Rats

Thornton

Schroeder²,

Robison³

et al. 2002

Toxicological Sciences

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“…Drinking water also contains a certain amount of VC monomer owing to the use of PVC water pipelines and the presence of chlorinated disinfection by‐products (Walter et al, 2011). VC is a multiorgan and multisystem chemical poison (Hsu & Chuang, 2019; Liang et al, 2018; Quan et al, 2014), and the main target organ is the liver (Easter & Von Burg, 1994). It can cause benign and malignant liver lesions, such as toxicant‐associated fatty liver disease (TAFLD) (Wahlang et al, 2013), hepatocellular carcinoma (Fedeli et al, 2019), and hepatic angiosarcoma (Guido et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Mechanism of subchronic vinyl chloride exposure combined with a high‐fat diet on hepatic steatosis

Jin

Chen

Pan

et al. 2021

J of Applied Toxicology

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Vinyl chloride (VC) is a common industrial organic chlorine and environmental pollutant. In recent years, the dietary structure of residents especially Chinese has gradually shifted to western dietary patterns. VC aggravates dietary fatty acid‐induced hepatic steatosis, but its mechanism is still unclear. And if the risk factors for steatosis persist, more severe diseases such as fibrosis and cirrhosis will occur. Therefore, we studied the effects and mechanisms of VC (160 and 800 mg/m3) and its metabolite (chloroacetaldehyde, 2.25, 4.5, and 9 μM) on hepatic steatosis of high‐fat diet (HFD)‐fed mice and palmitic acid (PA, 100 μM) treated HepG2 cells. Liver and serum biochemical indicators and pathological staining of the liver showed that the hepatic steatosis of VC combined with HFD groups was more severe than that of single‐exposure groups (HFD group, low‐dose VC group, and high‐dose VC group). Moreover, VC enhanced HFD‐induced oxidative stress (OS) and endoplasmic reticulum stress (ERS) and further upregulated the expression of sterol regulatory element‐binding protein 1 (SREBP‐1) and FAS. Besides, antioxidants and ERS inhibitors reduced the steatosis of HepG2 cells induced by VC metabolites and PA. These results suggest that VC exposure can enhance the degree of hepatic steatosis in HFD‐fed mice. VC combined with HFD led to OS and ERS and upregulated the expression of de novo lipogenesis‐related proteins, which may be related to the occurrence of hepatic steatosis. And the increased expression of CYP2E1 induced by VC combined with HFD may be the cause of OS.

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“…VCM is reported to be easily absorbed through the respiratory system causing bronchial irritation, drowsiness, central nervous system (CNS) impairment, unconsciousness, and even death at high doses (Easter and Von Burg, 1994). The chronic effects of VCM exposure in working population were reported to produce Raynaud’s syndrome (Fontana et al, 2006), scleroderma-like changes (Foti et al, 2008), liver fibrosis (Hsiao et al, 2004), liver cancer (Mastrangelo et al, 2004; Sherman, 2009; Wong et al, 2002), lung tumor (Gennaro et al, 2008), hematopoietic neoplasms, and brain cancer (Boffetta et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Exploring a new method for the biological monitoring of plastic workers exposed to the vinyl chloride monomer

et al. 2016

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Vinyl chloride monomer (VCM) is widely used in the production of polyvinyl chloride (PVC) plastics. VCM is recognized as a confirmed human and animal carcinogenic compound. Recent studies have reported poor health of plastic workers, even having exposure at concentrations below the permissible limit to VCM. There has not been any study regarding exposed workers to VCM in Iran. Similarly, no information exists as to the biological monitoring of such workers. The main purpose of this study was to conduct a thorough occupational and biological monitoring of Iranian plastic workers exposed to VCM.A total of 100 workers from two plastic manufacturing plants (A and B) in Tehran along with 25 unexposed workers as controls were studied. The personal monitoring of all nonsmoking workers exposed to VCM at two plastic manufacturing plants (A and B) was performed in the morning shift (8 a.m. to 4 p.m.) according to the National Institute For Occupational Safety And Health method no. 1007.Biological monitoring of workers was carried out through collection of exhaled breath of all exposed and control workers in Tedlar bags and with a subsequent analysis using gas chromatography-flame ionization detector.Not only the mean occupational exposure of workers to VCM at plant A was higher than the respective threshold limit value but also the statistical significance was higher than workers at plant B. Similarly, VCM concentration in exhaled breath of workers at plant A was also statistically significantly higher than at plant B. Correlation of occupational exposure of all workers to vinyl chloride with its concentration in exhaled breath was statistically significant.This is the first study on biological monitoring for exposed plastic workers to VCM using exhaled breath. On the basis of the results in this study, a novel method of biological monitoring of plastic workers was proposed.

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Vinyl chloride

Cited by 10 publications

References 54 publications

Embryo-Fetal Developmental and Reproductive Toxicology of Vinyl Chloride in Rats

Embryo-Fetal Developmental and Reproductive Toxicology of Vinyl Chloride in Rats

Mechanism of subchronic vinyl chloride exposure combined with a high‐fat diet on hepatic steatosis

Exploring a new method for the biological monitoring of plastic workers exposed to the vinyl chloride monomer

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