Co-exposure to PVC microplastics and cadmium induces oxidative stress and fibrosis in duck pancreas.

PVC microplastics (PVC-MPs) are environmental pollutants that interact with cadmium (Cd) to exert various biological effects. Ducks belong to the waterfowl family of birds and therefore are at a higher risk of exposure to PVC-MPs and Cd than other animals. However, the effects of co-exposure of ducks to Cd and PVC-MPs are poorly understood. Here, we used Muscovy ducks to establish an in vivo model to explore the effects of co-exposure to 1 mg/L PVC-MPs and 50 mg/kg Cd on duck pancreas. After 2 months of treatment with 50 mg/kg Cd, pancreas weight decreased by 21 %, and the content of amylase and lipase increased by 25 % and 233 %. However, exposure to PVC-MPs did not significantly affect the pancreas. Moreover, co-exposure to PVC-MPs and Cd worsened the reduction of pancreas weight and disruption of pancreas function compared to exposure to either substance alone. Furthermore, our research has revealed that exposure to PVC-MPs or Cd disrupted mitochondrial structure, reduced ATP levels by 10 % and 18 %, inhibited antioxidant enzyme activity, and increased malondialdehyde levels by 153.8 % and 232.5 %. It was found that exposure to either PVC-MPs or Cd can induce inflammation and fibrosis in the duck pancreas. Notably, co-exposure to PVC-MPs and Cd exacerbated inflammation and fibrosis, with the content of IL-1, IL-6, and TNF-α increasing by 169 %, 199 %, and 98 %, compared to Cd exposure alone. The study emphasizes the significance of comprehending the potential hazards linked to exposure to these substances. In conclusion, it presents promising preliminary evidence that PVC-MPs accumulate in duck pancreas, and increase the accumulation of Cd. Co-exposure to PVC-MPs and Cd disrupts the structure and function of mitochondria and promotes the development of pancreas inflammation and fibrosis.

Worker studies suggest unique liver carcinogenicity potential of polyvinyl chloride microplastics.

BACKGROUND: Plastic debris pervades our environment. Some breaks down into microplastics (MPs) that can enter and distribute in living organisms causing effects in multiple target organs. MPs have been demonstrated to harm animals through environmental exposure. Laboratory animal studies are still insufficient to evaluate human impact. And while MPs have been found in human tissues, the health effects at environmental exposure levels are unclear. AIM: We reviewed and summarized existing evidence on health effects from occupational exposure to MPs. Additionally, the diverse effects documented for workers were organized by MP type and associated co-contaminants. Evidence of the unique effects of polyvinyl chloride (PVC) on liver was then highlighted. METHODS: We conducted two stepwise online literature reviews of publications focused on the health risks associated with occupational MP exposures. This information was supplemented with findings from animal studies. RESULTS: Our analysis focused on 34 published studies on occupational health effects from MP exposure with half involving exposure to PVC and the other half a variety of other MPs to compare. Liver effects following PVC exposure were reported for workers. While PVC exposure causes liver toxicity and increases the risk of liver cancers, including angiosarcomas and hepatocellular carcinomas, the carcinogenic effects of work-related exposure to other MPs, such as polystyrene and polyethylene, are not well understood. CONCLUSION: The data supporting liver toxicity are strongest for PVC exposure. Overall, the evidence of liver toxicity from occupational exposure to MPs other than PVC is lacking. The PVC worker data summarized here can be useful in assisting clinicians evaluating exposure histories from PVC exposure and designing future cell, animal, and population exposure-effect research studies.

Acute Toxic Encephalopathy in Occupational Exposure with Polyvinyl Chloride (PVC) Fumes: A Case Series.

Background: Toxic encephalopathy is a spectrum of central nervous system disorders caused by exposure to toxins, especially from occupational workplace. Polyvinylchloride (PVC) is a synthetic chemical polymer that is used widely in daily activities of living. PVC is produced by polymerization of monomer units of vinyl chloride. Its manufacturing requires multiple procedures and additives for heat and light stabilization involving heavy metals. Objective: In this novel case series, we present the diverse clinical presentation of 10 patients, working in plastic recycling factory having inhalational exposure to PVC fumes, manifesting as acute toxic encephalopathy. Materials and Methods: All the patients were screened for the causes of acute encephalopathy including heavy metals, methanol poisoning, and organotins along with arterial blood gas analysis, brain imaging, and electroencephalogram. Memory loss, confusion, vertigo, headache, and nausea were complained in all the patients while seizure occurred in three patients. Neurocognitive status was grossly impaired in all the patients. Metabolic acidosis in presence of hyponatremia and/or hypokalemia was observed in nine cases. Five of the patients were having evidence of white matter involvement in brain imaging. The screening for heavy metal, methanol, and organotin were negative. Hemodialysis was done in six patients. Recovery was good in everyone and the average discharge was by 10.8 days (range: 2-25 days). All the patients were symptom-free at 3-months follow-up. Conclusion: Early suspicion and aggressive management can have favorable outcome in PVC toxic encephalopathy. Occupational hazards due to PVC toxicity are increasing in the present industrial era but it is very less identified.

Pulmonary Toxicity of Polystyrene, Polypropylene, and Polyvinyl Chloride Microplastics in Mice.

Globally, plastics are used in various products. Concerns regarding the human body's exposure to plastics and environmental pollution have increased with increased plastic use. Microplastics can be detected in the atmosphere, leading to potential human health risks through inhalation; however, the toxic effects of microplastic inhalation are poorly understood. In this study, we examined the pulmonary toxicity of polystyrene (PS), polypropylene (PP), and polyvinyl chloride (PVC) in C57BL/6, BALB/c, and ICR mice strains. Mice were intratracheally instilled with 5 mg/kg of PS, PP, or PVC daily for two weeks. PS stimulation increased inflammatory cells in the bronchoalveolar lavage fluid (BALF) of C57BL/6 and ICR mice. Histopathological analysis of PS-instilled C57BL/6 and PP-instilled ICR mice showed inflammatory cell infiltration. PS increased the NLR family pyrin domain containing 3 (NLRP3) inflammasome components in the lung tissue of C57BL/6 and ICR mice, while PS-instilled BALB/c mice remained unchanged. PS stimulation increased inflammatory cytokines, including IL-1ß and IL-6, in BALF of C57BL/6 mice. PP-instilled ICR mice showed increased NLRP3, ASC, and Caspase-1 in the lung tissue compared to the control groups and increased IL-1ß levels in BALF. These results could provide baseline data for understanding the pulmonary toxicity of microplastic inhalation.

Toxicity evaluation of microplastics to aquatic organisms through molecular simulations and fractional factorial designs.

Molecular docking, molecular dynamics modelling, and fractional factorial design methodologies were used in the current work to examine the harmful effects of ten microplastic (MPs) such as polystyrene (PS), polyvinylchloride (PVC), polyurethane (PU), polymethyl methacrylate (PMMA), polyamide (PA), polyethylene terephthalate (PET), polyethylene (PE), polypropylene (PP), polychloropene (PCP) and polycarbonate (PC) on the aquatic organism (zebrafish). The toxicity was evaluated based on the docking of the MPs on cytochrome P450 (CYP P450) protein crystals. The binding affinities (ΔG) followed the order, PC (-6.9 kcal/mol) > PET (-6.1 kcal/mol) > PP (-5.8 kcal/mol) > PA (-5.6 kcal/mol) > PS (-5.1 kcal/mol) > PU (-4.1 kcal/mol) > PMMA (-3.9 kcal/mol) > PCP (-3.3 kcal/mol) > PVC (-2.4 kcal/mol) > PE (-2.1 kcal/mol). The primary driving factors for the binding of the MPs and the protein were hydrophobic force, and hydrogen bonding based on the molecular dynamics analysis and surrounding amino acid residues. Furthermore, a 210-5 fractional factorial design method was estimated to identify the main effect and second-order effects of MPs in a composite contamination system on binding affinity/energy to CYP450 receptor protein of zebrafish, combined with a fixed effects model. The findings showed that different MPs combinations had varying impacts on aquatic toxicity; as a consequence, the best combination of MPs with the lowest aquatic toxicity effect could be excluded. The factorial designs showed that the PU-PS and PP-PA combination and single PCP, has the most significant main effect on CYP450 receptor protein of zebrafish which translates to an optimum toxicity level of -4.61 kcal/mol. The investigation offers a theoretical foundation for identifying the hazardous impacts of MPs on aquatic life.

Integrated biomarker responses in European seabass Dicentrarchus labrax (Linnaeus, 1758) chronically exposed to PVC microplastics.

Few studies evaluated long-term effects of polyvinyl chloride (PVC) microplastics (MPs) ingestion in fish. The present study aimed to investigate the integrated biomarker responses in the liver and blood of 162 European seabass, Dicentrarchus labrax, exposed for 90 days to control, virgin and marine incubated PVC enriched diets (0.1 % w/w) under controlled laboratory condition. Enzymatic and tissue alterations, oxidative stress, gene expression alterations and genotoxicity were examined. Additives and environmental contaminants levels in PVC-MPs, control feed matrices and in seabass muscles were also detected. The results showed that the chronic exposure at environmentally realistic PVC-MPs concentrations in seabass, cause early warning signs of toxicological harm in liver by induction of oxidative stress, the histopathological alterations and also by the modulation of the Peroxisome proliferator-activated receptors (PPARs) and Estrogen receptor alpha (ER-α) genes expression. A trend of increase of DNA alterations and the observation of some neoformations attributable to lipomas suggest also genotoxic and cancerogenic effects of PVC. This investigation provides important data to understand the regulatory biological processes affected by PVC-MPs ingestion in marine organisms and may also support the interpretation of results provided by studies on wild species.

Chemical composition and particle size influence the toxicity of nanoscale plastic debris and their co-occurring benzo(α)pyrene in the model aquatic organisms Daphnia magna and Danio rerio.

Little is known about how particle chemical composition and size might influence the toxicity of nanoscale plastic debris (NPD) and their co-occurring chemicals. Herein, we investigate the toxicity of 3 × 1010 particles/L polyethylene (PE, 50 nm), polypropylene (PP, 50 nm), polystyrene (PS, 200 and 600 nm), and polyvinyl chloride (PVC, 200 nm) NPD and their co-occurring benzo(a)pyrene (BaP) to Daphnia magna and Danio rerio. During the 21 days of exposure to PE 50 nm and PS 200 nm, the number of broods produced by D. magna decreased compared to other treatments. Exposure to BaP alone did not produce any effects on the reproduction of the daphnids, however, the mixture of BaP with PS (200 or 600 nm) or with PE (50 nm) reduced the number of broods. Exposure of D. rerio embryos to PE 50 nm, PS 200 nm, and PS 600 nm led to a delay in the hatching. The presence of PS 200 nm and PVC 200 nm eliminated the effects of BaP on the hatching rate of zebrafish. Our findings suggest that data generated for the toxicity of one type of NPD, e.g. PVC or PS may not be extrapolated to other types of NPD.

Cytotoxic Effects of Alcohol Extracts from a Plastic Wrap (Polyvinylidene Chloride) on Human Cultured Liver Cells and Mouse Primary Cultured Liver Cells.

An increasing accumulation of microplastics and further degraded nanoplastics in our environment is suspected to have harmful effects on humans and animals. To clarify this problem, we tested the cytotoxicity of two types of plastic wrap on human cultured liver cells and mouse primary cultured liver cells. Alcohol extracts from plastic wrap, i.e., polyvinylidene chloride (PVDC), showed cytotoxic effects on the cells. Alcohol extracts of polyethylene (PE) wrap were not toxic. The commercially available PVDC wrap consists of vinylidene chloride, epoxidized soybean oil, epoxidized linseed oil as a stiffener and stabilizer; we sought to identify which component(s) are toxic. The epoxidized soybean oil and epoxidized linseed oil exerted strong cytotoxicity, but the plastic raw material itself, vinylidene chloride, did not. Our findings indicate that plastic wraps should be used with caution in order to prevent health risks.

Neurotoxicity, oxidative stress biomarkers and haematological responses in African catfish (Clarias gariepinus) exposed to polyvinyl chloride microparticles.

The aquatic environment is outrageously littered with resin pellets and particles of plastic origin which can jeopardise the health of aquatic organisms. The present study investigated the effect of polyvinyl chloride (PVC) microparticles on blood parameters, leucocytes, lipid peroxidation and antioxidant system (brain and gill) of Clarias gariepinus. C. gariepinus is a fresh water indicator species often used as model for ecotoxicological assay. Fish specimens were exposed to diets spiked with PVC microparticles (95.41 ± 4.23 µm) at the following concentrations; 0.50%, 1.50% and 3.0% and control diet for 45 days, followed by a depuration trial which lasted for 30 days. Blood and tissues (brain and gill) were sampled every 15 days interval for haematology, antioxidant enzymes and lipid peroxidation assay. The result obtained revealed that PVC orchestrated the marked alterations in haematological indices. Mean cell volume and mean cell haemoglobin values reduced significantly in all concentration treated groups and were time-dependent. Neutrophil counts decreased with a corresponding increase in PVC exposure time while lymphocytes and monocytes values showed no significant difference between the control and exposed fish groups. Glutathione peroxidase activity was altered substantially in the brain and gill of the exposed groups compared to the control. Superoxide dismutase activity was inhibited in the brain and gill of the exposed groups compared to the control, as well as the different exposed periods. Catalase activity reduced significantly in the brain of 0.5% PVC exposed groups, and also decreased in a time-dependent manner while its activity in the gill did not change significantly among the exposed groups relative to the control. Lipid peroxidation levels in the brain of PVC exposed groups increased significantly in a dose and time-dependent manner. However, PVC caused no significantly change in the gill lipid peroxidation level of the exposed fish, but elevated the lipid peroxidation levels as the exposure time increased. Acetylcholinesterase activity in the brain and gill of the exposed fish reduced substantially with increase in the exposure time. Variations in haematology, antioxidant enzymes, lipid peroxidation and acetylcholinesterase activities are indicative of oxidative stress and neurotoxicity in fish. C. gariepinus is an indispensable bioindicator to measure environmental impact of PVC microparticles.

Evaluation of partial nitrification efficiency as a response to cadmium concentration and microplastic polyvinylchloride abundance during landfill leachate treatment.

The partial nitrification efficiency response to the presence of cadmium (Cd2+) and microplastics was investigated. Microplastics polyvinylchloride (PVC) abundance was 0-10,000 particles/L, and Cd2+ concentration was 0-10 mg/L. Cd-only inhibited the NH4+-N oxidation rate 1.21, 1.23, and 1.18 times with concentrations at 1, 5, and 10 mg/L, respectively. PVC-only inhibited NH4+-N oxidation rate 1.01, 1.21 and 1.05 times with PVC abundance at 1000, 5000 and 10,000 particles/L, respectively. The ammonia oxidation rate was improved with the co-existence of PVC and Cd2+ at the conditions PVC1000 and PVC5000, which could be attributed to the PVC. PVC at 1000 particles/L could act as carrier and mitigate the negative effect of Cd2+ to the partial nitrification process. Moreover, the partial nitrification process was largely inhibited with PVC abundance at 10,000 particles/L. First-order kinetic models could simulate the NH4+-N, NO2-N, and NO3--N changes in the partial nitrification process.

Lead-based paints and children's PVC toys are potential sources of domestic lead poisoning - A review.

Lead (Pb) both in paints and children's Polyvinyl chloride (PVC) toys is a major public health concern which has attracted attention of the international community. Concentrations of Pb both in lead-based paints and children's PVC toys have been assessed through various studies across the globe. Therefore, the purpose of this article was to summarize the results reported in these studies and provide some comprehension on their implications to human health for law enforcement as well as for awareness raising to the general public. Highlights on identified gaps have been provided to pave ways for further research interventions in order to establish comprehensive information on the subject. Regardless of regulatory limits on the content of lead, both in paints and children's PVC toys existing in different countries in the world, some of the reviewed articles have revealed significant levels of lead in these two items far above the permissible limits. High lead levels in paints have been recorded in China (116,200 ppm), Cameroon (500,000 ppm), South Africa (189,000 ppm), Tanzania (120,862.1 ppm), Uganda (150,000 ppm), Thailand (505,716 ppm) and Brazil (170,258.4 ppm) just to mention a few. Lead poisoning cases in children have been reported in several countries including France, Morocco, South Africa and United States. Countries where high levels of lead in children's PVC toys have been recounted include; China (860,000 ppm), South Africa (145,000 ppm), United States (22,550 ppm), Thailand (4,486.11 ppm), Palestine (6,036 ppm) and India (2,104 ppm). Awareness raising among parents is vital to impart them with knowledge on the matter so that they can take strenuous measures to protect their children from lead poisoning emanating from playing with toys and paint dust. Law enforcement on phasing out lead-based paints and control of lead content in children's PVC toys worldwide is also highly recommended.

The interactions between micro polyvinyl chloride (mPVC) and marine dinoflagellate Karenia mikimotoi: The inhibition of growth, chlorophyll and photosynthetic efficiency.

Microplastics pose a great threat to entire marine ecosystems, but little is known about their impacts on phytoplankton, especially for the harmful dinoflagellates. In this study, effects of micro polyvinyl chloride (mPVC) on the growth, chlorophyll content and photosynthetic efficiency of the dinoflagellate Karenia mikimotoi at different periods (0, 24, 48, 72 and 96 h) were assessed using gradient concentrations (0, 5, 25, 50 and 100 mg L-1) of mPVC with a size of 1 µm. PVC microplastics had dose-dependent adverse effects on K. mikimotoi growth, chlorophyll content and photosynthetic efficiency. The density of algal cell decreased with increasing mPVC concentrations and the highest inhibitory rate (IR) was 45.8% at 24 h under 100 mg L-1 of mPVC. The total chlorophyll content and chlorophyll content in a single algal cell decreased at 96 h and the ФPSⅡ and Fv/Fm decreased 25.3% and 17.1%, respectively. The SEM images provided an intuitive visual method to observe the behaviors and interactions between microplastics and microalgae. It was found from the SEM images that microalgae was wrapped by microplastic beads. The physical blockage and aggregation were also responsible for the cytotoxicity of K. mikimotoi. Our study clarified that PVC microplastics can reduce algal growth, chlorophyll content and photosynthetic efficiency, and it is beneficial to evaluate the possible impact of plastics on aquatic ecosystems.

Joint toxicity of microplastics with triclosan to marine microalgae Skeletonema costatum.

Toxicity of single microplastics on organisms has been reported widely, however, their joint toxicity with other contaminants on phytoplankton is rarely investigated. Here, we studied the toxicity of triclosan (TCS) with four kinds of microplastics namely polyethylene (PE, 74 µm), polystyrene (PS, 74 µm), polyvinyl chloride (PVC, 74 µm), and PVC800 (1 µm) on microalgae Skeletonema costatum. Both growth inhibition and oxidative stress including superoxide dismutase (SOD) and malondialdehyde (MDA) were determined. We found that TCS had obvious inhibition effect on microalgae growth within the test concentrations, and single microplastics also had significant inhibition effect which followed the order of PVC800 > PVC > PS > PE. However, the joint toxicity of PVC and PVC800 in combination with TCS decreased more than that of PE and PS. The higher adsorption capacity of TCS on PVC and PVC800 was one possible reason for the greater reduction of their toxicity. The joint toxicity of PVC800 was still most significant (PE < PVC < PS < PVC800) because of the minimum particle size. According to the independent action model, the joint toxicity systems were all antagonism. Moreover, the reduction of SOD was higher than MDA which revealed that the physical damage was more serious than intracellular damage. SEM images revealed that the aggregation of microplastics and physical damage on algae was obvious. Collectively, the present research provides evidences that the existence of organic pollutants is capable of influencing the effects of microplastics, and the further research on the joint toxicity of microplastics with different pollutants is urgent.

Toxic effects of microplastic on marine microalgae Skeletonema costatum: Interactions between microplastic and algae.

To investigate toxic effects of microplastic on marine microalgae Skeletonema costatum, both algal growth inhibition test and non-contact shading test were carried out, and algal photosynthesis parameters were also determined. The SEM images were used to observe interactions between microplastic and algae. It was found that microplastic (mPVC, average diameter 1 µm) had obvious inhibition on growth of microalgae and the maximum growth inhibition ratio (IR) reached up to 39.7% after 96 h exposure. However, plastic debris (bPVC, average diameter 1 mm) had no effects on growth of microalgae. High concentration (50 mg/L) mPVC also had negative effects on algal photosynthesis since both chlorophyll content and photosynthetic efficiency (ΦPSⅡ) decreased under mPVC treatments. Shading effect was not one reason for toxicity of microplastic on algae in this study. Compared with non-contact shading effect, interactions between microplastic and microalage such as adsorption and aggregation were more reasonable explanations for toxic effects of microplastic on marine microalgae. The SEM images provided a more direct and reasonable method to observe the behaviors of microplastic.

Occupational exposures at a polyvinyl chloride production facility are associated with significant changes to the plasma metabolome.

BACKGROUND: Occupational vinyl chloride (VC) exposures have been associated with toxicant-associated steatohepatitis and liver cancer. Metabolomics has been used to clarify mode of action in drug-induced liver injury but has not been performed following VC exposures. METHODS: Plasma samples from 17 highly exposed VC workers without liver cancer and 27 unexposed healthy volunteers were obtained for metabolite extraction and GC/MS and LC/MS2 analysis. Following ion identification/quantification, Ingenuity pathway analysis was performed. RESULTS: 613 unique named metabolites were identified. Of these, 189 metabolites were increased in the VC exposure group while 94 metabolites were decreased. Random Forest analysis indicated that the metabolite signature could separate the groups with 94% accuracy. VC exposures were associated with increased long chain (including arachidonic acid) and essential (including linoleic acid) fatty acids. Occupational exposure increased lipid peroxidation products including monohydroxy fatty acids (including 13-HODE); fatty acid dicarboxylates; and oxidized arachidonic acid products (including 5,9, and 15-HETE). Carnitine and carnitine esters were decreased, suggesting peroxisomal/mitochondrial dysfunction and alternate modes of lipid oxidation. Differentially regulated metabolites were shown to interact with extracellular-signal-regulated kinase 1/2 (ERK1/2), Akt, AMP-activated protein kinase (AMPK), and the N-Methyl-d-aspartate (NMDA) receptor. The top canonical pathways affected by occupational exposure included tRNA charging, nucleotide degradation, amino acid synthesis/degradation and urea cycle. Methionine and homocysteine was increased with decreased cysteine, suggesting altered 1-carbon metabolism. CONCLUSIONS: Occupational exposure generated a distinct plasma metabolome with markedly altered lipid and amino acid metabolites. ERK1/2, Akt, AMPK, and NMDA were identified as protein targets for vinyl chloride toxicity.

Volatile organic compounds of polyethylene vinyl acetate plastic are toxic to living organisms.

Volatile organic compounds (VOCs) in polyvinyl chloride (PVC) plastic products readily evaporate; as a result, hazardous gases enter the ecosystem, and cause cancer in humans and other animals. Polyethylene vinyl acetate (PEVA) plastic has recently become a popular alternative to PVC since it is chlorine-free. In order to determine whether PEVA is harmful to humans, this research employed the freshwater oligochaete Lumbriculus variegatus as a model to compare their oxygen intakes while they were exposed to the original stock solutions of PEVA, PVC or distilled water at a different length of time for one day, four days or eight days. During the exposure periods, the oxygen intakes in both PEVA and PVC groups were much higher than in the distilled water group, indicating that VOCs in both PEVA and PVC were toxins that stressed L. variegatus. Furthermore, none of the worms fully recovered during the24-hr recovery period. Additionally, the L. variegatus did not clump together tightly after four or eight days' exposure to either of the two types of plastic solutions, which meant that both PEVA and PVC negatively affected the social behaviors of these blackworms. The LD50 tests also supported the observations above. For the first time, our results have shown that PEVA plastic has adverse effects on living organisms, and therefore it is not a safe alternative to PVC. Further studies should identify specific compounds causing the adverse effects, and determine whether toxic effect occurs in more complex organisms, especially humans.

[Cytotoxicity of PVC tubes sterilized in ethylene oxide after gamma radiation exposure]. / Citotoxicidade de tubos de PVC esterilizados em óxido de etileno após exposição à radiação gama.

Do materials sterilized using gamma rays become toxic when re-sterilized in ethylene oxide? This question guided the objective of this study, which was to investigate the potential cytotoxic effect of PVC sterilized by gamma radiation and re-sterilized with EO by the agar diffusion method in cell cultures. Nine PVC tubes were subjected to gamma radiation sterilization and were re-sterilized in EO. The tubes were divided into a total of 81 units of analysis that were tested so as to represent the internal and external surfaces and mass of each tube. It was concluded that the PVC materials sterilized in gamma radiation and re-sterilized in EO are not cytotoxic.

Citotoxicidade de tubos de PVC esterilizados em óxido de etileno após exposição à radiação gama / Cytotoxicity of PVC tubes sterilized in ethylene oxide after gamma radiation exposure / Citotoxicidad de tubos de PVC esterilizados en óxido de etileno luego de exposición a la radiación gamma

Materiais esterilizados em raios gama, ao serem re-esterilizados em óxido de etileno (EO), formam substâncias tóxicas? Esta questão norteou o objetivo deste estudo, que foi investigar o potencial efeito citotóxico do PVC esterilizado em radiação gama e re-esterilizado em EO pelo método da difusão em ágar em culturas celulares. Nove tubos de PVC foram submetidos à esterilização em radiação gama e re-esterilizados em EO. Os tubos foram divididos em um total de 81 unidades de análise, que foram testadas de forma a representar as superfícies internas, externas e massa de cada tubo. Concluiu-se que os materiais de PVC esterilizados em Radiação Gama e consecutivamente re-esterilizados em EO não são citotóxicos.

Do materials sterilized using gamma rays become toxic when re-sterilized in ethylene oxide? This question guided the objective of this study, which was to investigate the potential cytotoxic effect of PVC sterilized by gamma radiation and re-sterilized with EO by the agar diffusion method in cell cultures. Nine PVC tubes were subjected to gamma radiation sterilization and were re-sterilized in EO. The tubes were divided into a total of 81 units of analysis that were tested so as to represent the internal and external surfaces and mass of each tube. It was concluded that the PVC materials sterilized in gamma radiation and re-sterilized in EO are not cytotoxic.

Los materiales esterilizados con rayos gama, al ser re-esterilizados en óxido de etileno (EO), ¿forman substancias tóxicas? Esta pregunta orientó el objetivo del presente estudio, que fue investigar el potencial efecto citotóxico del PVC esterilizado en radiación gamma y re-esterilizado en EO por el método de difusión en agar en cultivos celulares. Nueve tubos de PVC fueron sometidos a esterilización por radiación gamma y re-esterilizados en EO. Se les aplicaron en total 81 unidades de análisis, las cuales fueron testeadas de manera tal de representar las superficies internas, externas y la masa de cada tubo. Se concluyó en que los materiales de PVC esterilizados con Radiación Gamma y, posteriormente, con EO, no son citotóxicos.

Mechanical damage to Escherichia coli cells in a model of amino-acid crystal fermentation.

We investigated the mechanical damage to the Escherichia coli cell caused by polyvinyl chloride particles as a model of amino-acid crystal fermentation. Our results indicated that the glucose-consumption rate and the intracellular ATP concentration temporarily increased by the mechanical damage, and decreased after considerable damage had occurred on cell membrane.

Mortality from liver cancer and leukaemia among polyvinyl chloride workers in Taiwan: an updated study.

OBJECTIVES: To investigate types of cancer caused by occupational exposure to vinyl chloride monomer (VCM) and the temporal mortality trends of these cancers in workers from polyvinyl chloride (PVC) manufacturing factories in Taiwan, with follow-up of the cohort extended by 15 years, from 1980 to 2007. Methods A retrospective cohort study of workers from six PVC factories in Taiwan was conducted. 3336 male PVC workers were enrolled and further linked with the National Mortality Registry and National Household Registry databases. Standardised mortality ratios (SMR) with 95% CIs were calculated and compared to the general Taiwanese male population. Cause-specific mortality between two study periods, 1980-1997 and 1998-2007, was compared. Six-year moving averages of the SMRs were calculated to examine mortality trends. RESULTS: Liver cancer mortality increased during 1989-1994 (SMR 1.90, 95% CI 1.01 to 3.25), reached a peak during 1991-1996 (SMR 2.31, 95% CI 1.39 to 3.61) and became non-significant during 1994-1999 (SMR 1.42, 95% CI 0.80 to 2.34). Leukaemia mortality significantly increased during 1984-1989 (SMR 6.06, 95% CI 1.24 to 17.53), reached a peak during 1985-1990 (SMR 7.56, 95% CI 2.06 to 19.35) and became non-significant during 1991-1996 (SMR 3.24, 95% CI 0.39 to 11.69). The mortality trend for haemolymphopoietic cancer showed a similar pattern to that of leukaemia. CONCLUSIONS: VCM may increase the risk of liver cancer and leukaemia. When VCM exposure was controlled at worksites, mortality from these cancers returned to background levels.