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JMIR Dermatology Sep 2023Environmental vinyl chloride (VC) exposure may result in serious acute and chronic dermatological conditions. Because existing literature largely focuses on exposures in... (Review)
Review
BACKGROUND
Environmental vinyl chloride (VC) exposure may result in serious acute and chronic dermatological conditions. Because existing literature largely focuses on exposures in occupational settings, a gap persists in our understanding of the medical consequences of large-scale chemical spills.
OBJECTIVE
This study aims to examine the potential dermatological manifestations of VC exposure in the context of industrial spills and other environmental disasters and to highlight the public health and justice implications of such releases.
METHODS
In this narrative review, relevant evidence-based, peer-reviewed scientific sources, gray literature, and media reports were identified via searches of search PubMed and Google using predetermined keyword search terms related to VC, VC spills and releases, train derailment, cutaneous disease, public health, and vulnerable and marginalized populations.
RESULTS
Contact dermatitis and frostbite may arise acutely, highlighting the importance of swift decontamination. Long-term manifestations from chronic VC exposure due to persistence in environmental reservoirs include Raynaud disease, sclerodermatous skin changes, acro-osteolysis, and cutaneous malignancies. The clinical severity of cutaneous manifestations is influenced by individual susceptibility as well as duration, intensity, and route of exposure. Additionally, chemical releases of VC more frequently impact Communities of Color and those of lower socioeconomic status, resulting in greater rates of exposure-related disease.
CONCLUSIONS
With environmental release events of hazardous chemicals becoming increasingly common and because the skin has increased contact with environmental toxins relative to other organs, an urgent need exists for a greater understanding of the overall short- and long-term health impacts of large-scale, toxic exposures, underscoring the need for ongoing clinical vigilance. Dermatologists and public health officials should also aim to better understand the ways in which the disproportionate impacts of hazardous chemical exposures on lower-income and minority populations may exacerbate existing health disparities. Herein, we describe the health implications of toxic releases with particular consideration paid to marginalized and vulnerable populations. In addition to legal and regulatory frameworks, we advocate for improved public health measures, to not only mitigate the risk of environmental catastrophes in the future, but also ensure timely and effective responses to them.
PubMed: 37676716
DOI: 10.2196/48998 -
Journal of Visualized Experiments : JoVE Jan 2020Vinyl chloride (VC), an abundant environmental contaminant, causes steatohepatitis at high levels, but is considered safe at lower levels. Although several studies have...
Vinyl chloride (VC), an abundant environmental contaminant, causes steatohepatitis at high levels, but is considered safe at lower levels. Although several studies have investigated the role of VC as a direct hepatotoxicant, the concept that VC modifies sensitivity of the liver to other factors, such as nonalcoholic fatty liver disease (NAFLD) caused by high-fat diet (HFD) is novel. This protocol describes an exposure paradigm to evaluate the effects of chronic, low-level exposure to VC. Mice are acclimated to low-fat or high-fat diet one week prior to the beginning of the inhalation exposure and remain on these diets throughout the experiment. Mice are exposed to VC (sub-OSHA level: <1 ppm) or room air in inhalation chambers for 6 hours/day, 5 days/week, for up to 12 weeks. Animals are monitored weekly for body weight gain and food consumption. This model of VC exposure causes no overt liver injury with VC inhalation alone. However, the combination of VC and HFD significantly enhances liver disease. A technical advantage of this co-exposure model is the whole-body exposure, without restraint. Moreover, the conditions more closely resemble a very common human situation of a combined exposure to VC with underlying nonalcoholic fatty liver disease and therefore support the novel hypothesis that VC is an environmental risk factor for the development of liver damage as a complication of obesity (i.e., NAFLD). This work challenges the paradigm that the current exposure limits of VC (occupational and environmental) are safe. The use of this model can shed new light and concern on the risks of VC exposure. This model of toxicant-induced liver injury can be used for other volatile organic compounds and to study other interactions that may impact the liver and other organ systems.
Topics: Administration, Inhalation; Animals; Diet, High-Fat; Environmental Exposure; Humans; Liver; Liver Diseases; Mice, Inbred C57BL; Models, Biological; Obesity; Vinyl Chloride
PubMed: 31984951
DOI: 10.3791/60351 -
BMC Gastroenterology Dec 2011Hepatic angiosarcoma (HAS) is a rare type of liver cancer that is often fatal, and arsenic and vinyl chloride monomer (VCM) are two major causal agents. Whereas Taiwan... (Review)
Review
BACKGROUND
Hepatic angiosarcoma (HAS) is a rare type of liver cancer that is often fatal, and arsenic and vinyl chloride monomer (VCM) are two major causal agents. Whereas Taiwan is an endemic area of liver cancer, epidemiologic data on HAS are limited. We reviewed the cases observed at a teaching hospital to evaluate the roles of VCM, arsenic, and viral hepatitis in the occurrence of HAS.
METHODS
We reviewed the medical records of patients with pathological proof of HAS from January 2000 to August 2010 at a teaching hospital which is adjacent to the major VCM processing area in Taiwan and nearby an endemic area of arsenic exposure from drinking water. We also conducted a literature review and included all patients of HAS reported in Taiwan.
RESULTS
Six male and three female cases aged from 56 to 83 years (64.6 ± 8.2 years) were identified at the hospital. The differences in clinical features between men and women were not statistically significant. None of them had exposure to VCM or arsenic in drinking water. Two had evidence of hepatitis C infection, but none had evidence of hepatitis B infection. Five male and four female cases aged 30 to 82 years (58.6 ± 15.5 years) were identified in the literature, including two with arsenic exposure and one with chronic hepatitis B infection.
CONCLUSIONS
HAS is rare in Taiwan, and we found no evidence supporting a major role of VCM, arsenic in drinking water, or viral hepatitis in its occurrence.
Topics: Aged; Aged, 80 and over; Arsenic; Female; Hemangiosarcoma; Hepatitis C; Hospitals, Teaching; Humans; Liver Neoplasms; Male; Middle Aged; Retrospective Studies; Taiwan; Tomography, X-Ray Computed; Vinyl Chloride
PubMed: 22200164
DOI: 10.1186/1471-230X-11-142 -
Environmental Science & Technology Mar 2023A reliable analytical method has been developed to quantify poly(vinyl chloride) (PVC) in environmental samples. Quantification was conducted combustion ion...
A reliable analytical method has been developed to quantify poly(vinyl chloride) (PVC) in environmental samples. Quantification was conducted combustion ion chromatography (C-IC). Hydrogen chloride (HCl) was quantitatively released from PVC during thermal decomposition and trapped in an absorption solution. Selectivity of the marker HCl in complex environmental samples was ensured using cleanup pressurized liquid extraction (PLE) with methanol at 100 °C (discarded) and tetrahydrofuran at 185 °C (collected). Using this method, recoveries of 85.5 ± 11.5% and a limit of quantification down to 8.3 μg/g were achieved. A variety of hard and soft PVC products could be successfully analyzed C-IC with recoveries exceeding >95%. Furthermore, no measurable overdetermination was found for various organic and inorganic matrix ingredients, such as sodium chloride, sucralose, hydroxychloroquine, diclofenac, chloramphenicol, triclosan, or polychlorinated biphenyls. In addition, sediments and suspended particular matter showed PVC concentrations ranging up to 16.0 and 220 μg/g, respectively. However, the gap between determined polymer mass and particle masses could be significant since soft PVC products contain plasticizers up to 50 wt %. Hence, the results of the described method represent a sum of all chlorine-containing polymers, which are extractable under the chosen conditions.
Topics: Plastics; Vinyl Chloride; Microplastics; Gas Chromatography-Mass Spectrometry; Plasticizers; Polymers; Polyvinyl Chloride
PubMed: 36917996
DOI: 10.1021/acs.est.2c06555 -
Cells Jun 2019Vinyl chloride (VC) is a noninfective occupational risk factor. It is found in industrial chemicals, volatile organic compounds, cigarette smoke ingredients, etc. It is...
Vinyl chloride (VC) is a noninfective occupational risk factor. It is found in industrial chemicals, volatile organic compounds, cigarette smoke ingredients, etc. It is a kind of toxic gas that causes many diseases. VC exposure causes an increased risk of liver fibrosis and can result in angiosarcoma of the liver. Previous studies have shown that high-doses of VC exposure in mice resulted in acute death with marked tubular necrosis of the renal cortex. In this study, we assessed the nephrotoxicity of VC in vitro and in vivo. As a result, we demonstrated that VC induced fibrosis-associated protein expression, such as connective tissue growth factor (CTGF), plasminogen activator inhibitor-1 (PAI-1) and collagen 1, and autophagy-associated protein expression, such as Beclin 1 and LC3-II, in kidney cells. The beclin1 siRNA experiments found that autophagy inhibited VC-induced fibrosis. Blood urea nitrogen (BUN) and creatinine levels were increased after VC treatment. Furthermore, VC caused glomerulosclerosis and tubular injury in mouse kidney tissues. Kidney tissue sections showed that VC induced fibrosis and autophagy in mouse kidney tissues. In summary, the results of VC-induced fibrosis suggest that autophagy plays an important role in kidney damage. VC may cause nephrotoxicity, and the results illustrate the importance of considering the toxicological hazards of VC in kidney cells.
Topics: Animals; Autophagy; Biomarkers; Blood Urea Nitrogen; Cell Line; Cell Survival; Creatinine; Fibrosis; Humans; Kidney; Kidney Tubules; Male; Mice, Inbred BALB C; Models, Biological; Vinyl Chloride
PubMed: 31212930
DOI: 10.3390/cells8060601 -
Environmental Health Perspectives Oct 1981Poly(vinyl chloride) resins are produced by four basic processes: suspension, emulsion, bulk and solution polymerization. PVC suspensions resins are usually relatively...
Poly(vinyl chloride) resins are produced by four basic processes: suspension, emulsion, bulk and solution polymerization. PVC suspensions resins are usually relatively dust-free and granular with varying degrees of particle porosity. PVC emulsion resins are small particle powders containing very little free monomer. Bulk PVC resins are similar to suspension PVC resins, though the particles tend to be more porous. Solution PVC resins are smaller in particle size than suspension PVC with high porosity particles containing essentially no free monomer. The variety of PVC resin products does not lend itself to broad generalizations concerning health hazards. In studying occupational hazards the particular PVC process and the product must be considered and identified in the study.
Topics: Chemical Industry; Humans; Particle Size; Polyvinyl Chloride; Polyvinyls; Risk; Vinyl Chloride
PubMed: 7333230
DOI: 10.1289/ehp.8141123 -
Environmental Health Perspectives Oct 1983In 1974, vinyl chloride (VC) was first reported in the open scientific literature to induce angiosarcoma of the liver both in humans and in animals. Additional research... (Review)
Review
In 1974, vinyl chloride (VC) was first reported in the open scientific literature to induce angiosarcoma of the liver both in humans and in animals. Additional research has now demonstrated the carcinogenicity of VC to other organs and at lower concentrations. The target organs for VC now clearly include the liver, brain and the lung, and probably the lymphohematopoietic system. The evidence for a carcinogenic risk has been extended to jobs associated with poly(vinyl chloride) exposure. Cases of liver angiosarcoma have been reported among individuals employed in PVC fabrication facilities and an epidemiological study has demonstrated a significant association between exposure to PVC dust and the risk of lung cancer mortality. Cases of angiosarcoma of the liver also have been reported among individuals living in near proximity to vinyl chloride-poly(vinyl chloride) plants. An association between PVC dust and pneumoconiosis also has been demonstrated. On the basis of findings, prudent control of PVC dust in the industrial setting is indicated.
Topics: Environmental Exposure; Hemangiosarcoma; Humans; Liver Neoplasms; Lung Neoplasms; Male; Middle Aged; Neoplasms; Occupational Diseases; Pneumoconiosis; Polyvinyl Chloride; Polyvinyls; Vinyl Chloride; Vinyl Compounds
PubMed: 6360677
DOI: 10.1289/ehp.835261 -
Cardanol Groups Grafted on Poly(vinyl chloride)-Synthesis, Performance and Plasticization Mechanism.Polymers Nov 2017Internally plasticized poly(vinyl chloride) (PVC) materials are investigated via grafting of propargyl ether cardanol (PEC). The chemical structure of the materials was...
Internally plasticized poly(vinyl chloride) (PVC) materials are investigated via grafting of propargyl ether cardanol (PEC). The chemical structure of the materials was studied by FT-IR and ¹H NMR. The performace of the obtained internally plasticized PVC materials was also investigated with TGA, DSC and leaching tests. The results showed that grafting of propargyl ether cardanol (PEC) on PVC increased the free volume and distance of PVC chains, which efficiently decreased the glass transition temperature (). No migration was found in the leaching tests for internally plasticized PVC films compared with plasticized PVC materials with commercial plasticizer dioctyl phthalate (DOP). The internal plasticization mechanism was also disscussed according to lubrication theory and free volume theory. This work provides a meaningful strategy for designing no-migration PVC materials by introducing cardanol groups as branched chains.
PubMed: 30965920
DOI: 10.3390/polym9110621 -
Frontiers in Microbiology 2021Advanced physicochemical and chemical absorption methods for chlorinated ethenes are feasible but incur high costs and leave traces of pollutants on the site....
Advanced physicochemical and chemical absorption methods for chlorinated ethenes are feasible but incur high costs and leave traces of pollutants on the site. Biodegradation of such pollutants by anaerobic or aerobic bacteria is emerging as a potential alternative. Several mycobacteria including L1, NBB4, JS60, NBB3 and JS623 have previously been described as assimilators of vinyl chloride (VC). In this study, we compared nucleotide sequence of VC cluster and performed a taxogenomic evaluation of these mycobacterial species. The results showed that the complete VC cluster was acquired by horizontal gene transfer and not intrinsic to the genus . These results also revealed the presence of an additional F1 gene that seems to be involved in Coenzyme M biosynthesis, which is ultimately used in the VC degradation pathway. Furthermore, we suggest for the first time that S/N-Oxide reductase encoding gene was involved in the dissociation of the SsuABC transporters from the organosulfur, which play a crucial role in the Coenzyme M biosynthesis. Based on genomic data, L1, NBB4 JS60, NBB3 and JS623 were misclassified and form a novel species within the genus . L1 (CECT 8761 = DSM 6695) was the subject of polyphasic taxonomic studies and showed ANI and dDDH values of 84.7 and 28.5% with its close phylogenetic neighbour, ATCC 33027. Phenotypic, chemotaxonomic and genomic data considering strain L1 (CECT 8761 = DSM 6695) as a type strain of novel species with the proposed name, sp. nov.
PubMed: 35003006
DOI: 10.3389/fmicb.2021.767895 -
Redox Biology Jun 2019Vinyl chloride (VC), an abundant environmental contaminant causes steatohepatitis at high levels, but is considered safe at lower (i.e., sub-OSHA) levels. However, we...
Vinyl chloride (VC), an abundant environmental contaminant causes steatohepatitis at high levels, but is considered safe at lower (i.e., sub-OSHA) levels. However, we have previously shown that even lower VC levels exacerbate experimental nonalcoholic fatty liver disease (NAFLD) caused by high-fat diet (HFD). Mitochondrial oxidative injury and subsequent metabolic dysfunction appeared to play key roles in mediating this interaction. Mitochondrial aldehyde dehydrogenase 2 (ALDH2) serves as a key line of defense against endogenous and exogenous reactive aldehydes. The current study therefore tests the hypothesis that allosteric activation of ALDH2 with Alda-1 will protect against VC-enhanced NAFLD. Mice were exposed to low VC concentrations (<1 ppm), or room air for 6 h/day, 5 days/week for 12 weeks, while on HFD or low-fat control diet (LFD). Some mice received Alda-1 (20 mg/kg i.p., 3 × /week) for the last 3 weeks of diet/VC exposure. Indices of liver injury, oxidative stress, metabolic and mitochondrial (dys)function were measured. As observed previously, low-dose VC did not cause liver injury in control mice; while liver injury caused by HFD was enhanced by VC. VC decreased hepatic ALDH2 activity of mice fed HFD. Alda-1 attenuated oxidative stress, liver injury, and dysmetabolism in mice exposed to HFD+VC under these conditions. Importantly, alterations in mitochondrial function caused by VC and HFD were diminished by Alda-1. Previous studies have indicated that liver injury caused by HFD is mediated, at least in part, by enhanced mitochondrial autophagy (mitophagy). Here, Alda-1 suppressed PINK1/PARKIN-mediated mitophagy. Taken together, these results support the hypothesis that ALDH2 is a critical defense against mitochondrial injury caused by VC in experimental NAFLD. The ALDH2 activator Alda-1 conferred protection against liver damage under these conditions, most likely via increasing clearance of aldehydes and preserving mitochondrial respiratory function.
Topics: Aldehyde Dehydrogenase, Mitochondrial; Animals; Autophagy; Benzamides; Benzodioxoles; Enzyme Activation; Fatty Liver; Male; Mice; Mitochondria; Neutrophil Infiltration; Neutrophils; Non-alcoholic Fatty Liver Disease; Oxidative Stress; Phenotype; Protective Agents; Vinyl Chloride
PubMed: 31026768
DOI: 10.1016/j.redox.2019.101205