Взаємодія архетипних систем в українських, польських, староанглійських і кельтських загадках(на матеріалі праць І.Я.Франка та Ексетерської книги)

Метою дослідження є порівняти архетипні системи українських, польських, кельтських і англосаксонських загадок періоду раннього християнства. Основний акцент робиться на порівнянні українських і староанглійських загадок

First order risk assessment for nanoparticle inhalation exposure during injection molding of polypropylene composites and production of tungsten-carbide-cobalt fine powder based upon pulmonary inflammation and surface area dose

AbstractInhalation exposure to low toxicity and biodurable particles has shown to induce polymorphonuclear neutrophilia (PMN) in the lungs, which is a strong indicator for lung inflammation. Recently, Schmid and Stoeger (2016; http://dx.doi.org/10.1016/j.jaerosci.2015.12.006) reviewed mice and rat intratracheal instillation studies and assessed the relation between particles dry powder BET surface area dose and PMN influx for granular biodurable particles (GBPs) and transition metal oxides. In this study, we measured workers alveolar lung deposited surface area (LDSA) concentrations (μm2 cm−3) during injection molding of polypropylene (PP) car bumpers and production of tungsten-carbide-cobalt (WCCo) fine grade powder using diffusion chargers. First order risk assessment was performed by comparing the doses calculated from measured LDSA concentrations during an 8-h work day with the NOEL1/100, the one hundredth of no observed effect level, assigned for GBPs (0.11cm2g−1) and transition metal oxide particles (9×10−3cm2g−1). During the injection molding of PP car bumpers, LDSA concentrations varied from 23 to 39.8μm2cm−3. During 8-h exposure PP, particle doses were at a maximum of 1.4×10−3cm2g−1, which was a factor 100 lower compared to the NOEL1/100 assigned for GBPs. In the WCCo fine powder production plant, the LDSA concentrations were below 18.7μm2cm−3, which corresponds to the 8-h dose of 2.7×10−3cm2g−1. This is 3 times lower than the NOEL1/100 assigned for transition metal oxide particles. The LDSA concentrations were generally low compared to urban background levels of 44.2μm2cm−3 in European cities

First order risk assessment for nanoparticle inhalation exposure during injection molding of polypropylene composites and production of tungsten-carbide-cobalt fine powder based upon pulmonary inflammation and surface area dose

AbstractInhalation exposure to low toxicity and biodurable particles has shown to induce polymorphonuclear neutrophilia (PMN) in the lungs, which is a strong indicator for lung inflammation. Recently, Schmid and Stoeger (2016; http://dx.doi.org/10.1016/j.jaerosci.2015.12.006) reviewed mice and rat intratracheal instillation studies and assessed the relation between particles dry powder BET surface area dose and PMN influx for granular biodurable particles (GBPs) and transition metal oxides. In this study, we measured workers alveolar lung deposited surface area (LDSA) concentrations (μm2 cm−3) during injection molding of polypropylene (PP) car bumpers and production of tungsten-carbide-cobalt (WCCo) fine grade powder using diffusion chargers. First order risk assessment was performed by comparing the doses calculated from measured LDSA concentrations during an 8-h work day with the NOEL1/100, the one hundredth of no observed effect level, assigned for GBPs (0.11cm2g−1) and transition metal oxide particles (9×10−3cm2g−1). During the injection molding of PP car bumpers, LDSA concentrations varied from 23 to 39.8μm2cm−3. During 8-h exposure PP, particle doses were at a maximum of 1.4×10−3cm2g−1, which was a factor 100 lower compared to the NOEL1/100 assigned for GBPs. In the WCCo fine powder production plant, the LDSA concentrations were below 18.7μm2cm−3, which corresponds to the 8-h dose of 2.7×10−3cm2g−1. This is 3 times lower than the NOEL1/100 assigned for transition metal oxide particles. The LDSA concentrations were generally low compared to urban background levels of 44.2μm2cm−3 in European cities

Impact of agglomeration state of nano- and submicron sized gold particles on pulmonary inflammation

BACKGROUND: Nanoparticle (NP) toxicity testing comes with many challenges. Characterization of the test substance is of crucial importance and in the case of NPs, agglomeration/aggregation state in physiological media needs to be considered. In this study, we have addressed the effect of agglomerated versus single particle suspensions of nano- and submicron sized gold on the inflammatory response in the lung. Rats were exposed to a single dose of 1.6 mg/kg body weight (bw) of spherical gold particles with geometric diameters of 50 nm or 250 nm diluted either by ultrapure water or by adding phosphate buffered saline (PBS). A single dose of 1.6 mg/kg bw DQ12 quartz was used as a positive control for pulmonary inflammation. Extensive characterization of the particle suspensions has been performed by determining the zetapotential, pH, gold concentration and particle size distribution. Primary particle size and particle purity has been verified using transmission electron microscopy (TEM) techniques. Pulmonary inflammation (total cell number, differential cell count and pro-inflammatory cytokines), cell damage (total protein and albumin) and cytotoxicity (alkaline phosphatase and lactate dehydrogenase) were determined in bronchoalveolar lavage fluid (BALF) and acute systemic effects in blood (total cell number, differential cell counts, fibrinogen and C-reactive protein) 3 and 24 hours post exposure. Uptake of gold particles in alveolar macrophages has been determined by TEM. RESULTS: Particles diluted in ultrapure water are well dispersed, while agglomerates are formed when diluting in PBS. The particle size of the 50 nm particles was confirmed, while the 250 nm particles appear to be 200 nm using tracking analysis and 210 nm using TEM. No major differences in pulmonary and systemic toxicity markers were observed after instillation of agglomerated versus single gold particles of different sizes. Both agglomerated as well as single nanoparticles were taken up by macrophages. CONCLUSION: Primary particle size, gold concentration and particle purity are important features to check, since these characteristics may deviate from the manufacturer's description. Suspensions of well dispersed 50 nm and 250 nm particles as well as their agglomerates produced very mild pulmonary inflammation at the same mass based dose. We conclude that single 50 nm gold particles do not pose a greater acute hazard than their agglomerates or slightly larger gold particles when using pulmonary inflammation as a marker for toxicity

The biological effects of subacute inhalation of diesel exhaust following addition of cerium oxide nanoparticles in atherosclerosis-prone mice

AbstractBackgroundCerium oxide (CeO2) nanoparticles improve the burning efficiency of fuel, however, little is known about health impacts of altered emissions from the vehicles.MethodsAtherosclerosis-prone apolipoprotein E knockout (ApoE−/−) mice were exposed by inhalation to diluted exhaust (1.7mg/m3, 20, 60 or 180min, 5 day/week, for 4 weeks), from an engine using standard diesel fuel (DE) or the same diesel fuel containing 9ppm cerium oxide nanoparticles (DCeE). Changes in hematological indices, clinical chemistry, atherosclerotic burden, tissue levels of inflammatory cytokines and pathology of the major organs were assessed.ResultsAddition of CeO2 to fuel resulted in a reduction of the number (30%) and surface area (10%) of the particles in the exhaust, whereas the gaseous co-pollutants were increased (6–8%). There was, however, a trend towards an increased size and complexity of the atherosclerotic plaques following DE exposure, which was not evident in the DCeE group. There were no clear signs of altered hematological or pathological changes induced by either treatment. However, levels of proinflammatory cytokines were modulated in a brain region and liver following DCeE exposure.ConclusionsThese results imply that addition of CeO2 nanoparticles to fuel decreases the number of particles in exhaust and may reduce atherosclerotic burden associated with exposure to standard diesel fuel. From the extensive assessment of biological parameters performed, the only concerning effect of cerium addition was a slightly raised level of cytokines in a region of the central nervous system. Overall, the use of cerium as a fuel additive may be a potentially useful way to limit the health effects of vehicle exhaust. However, further testing is required to ensure that such an approach is not associated with a chronic inflammatory response which may eventually cause long-term health effects

An Air-liquid Interface Bronchial Epithelial Model for Realistic, Repeated Inhalation Exposure to Airborne Particles for Toxicity Testing.

For toxicity testing of airborne particles, air-liquid interface (ALI) exposure systems have been developed for in vitro tests in order to mimic realistic exposure conditions. This puts specific demands on the cell culture models. Many cell types are negatively affected by exposure to air (e.g., drying out) and only remain viable for a few days. This limits the exposure conditions that can be used in these models: usually relatively high concentrations are applied as a cloud (i.e., droplets containing particles, which settle down rapidly) within a short period of time. Such experimental conditions do not reflect realistic long-term exposure to low concentrations of particles. To overcome these limitations the use of a human bronchial epithelial cell line, Calu-3 was investigated. These cells can be cultured at ALI conditions for several weeks while retaining a healthy morphology and a stable monolayer with tight junctions. In addition, this bronchial model is suitable for testing the effects of repeated exposures to low, realistic concentrations of airborne particles using an ALI exposure system. This system uses a continuous airflow in contrast to other ALI exposure systems that use a single nebulization producing a cloud. Therefore, the continuous flow system is suitable for repeated and prolonged exposure to airborne particles while continuously monitoring the particle characteristics, exposure concentration, and delivered dose. Taken together, this bronchial model, in combination with the continuous flow exposure system, is able to mimic realistic, repeated inhalation exposure conditions that can be used for toxicity testing

Toxicity of copper oxide and basic copper carbonate nanoparticles after short-term oral exposure in rats

Copper oxide (CuO) nanoparticles (NPs) and copper carbonate nanoparticles (Cu2CO3(OH)(2) NPs have applications as antimicrobial agents and wood preservatives: an application that may lead to oral ingestion via hand to mouth transfer. Rats were exposed by oral gavage to CuO NPs and Cu2CO3(OH)(2) NPs for five consecutive days with doses from 1 to 512 mg/kg and 4 to 128 mg/kg per day, respectively, and toxicity was evaluated at days 6 and 26. Both CuO NPs and Cu2CO3(OH)(2) NPs induced changes in hematology parameters, as well as clinical chemistry markers (e.g. increased alanine aminotransferase, ALT) indicative of liver damage For CuO NPs histopathological alterations were observed in bone marrow, stomach and liver mainly consisting of an inflammatory response, ulceration, and degeneration. Cu2CO3(OH)(2) NPs induced morphological alterations in the stomach, liver, intestines, spleen, thymus, kidneys, and bone marrow. In spleen and thymus lymphoid, depletion was noted that warrants further immunotoxicological evaluation. The NPs showed partial dissolution in artificial simulated stomach fluids, while in intestinal conditions, the primary particles simultaneously shrank and agglomerated into large structures. This means that both copper ions and the particulate nanoforms should be considered as potential causal agents for the observed toxicity. For risk assessment, the lowest bench mark dose (BMD) was similar for both NPs for the serum liver enzyme AST (an indication of liver toxicity), being 26.2 mg/kg for CuO NPs and 30.8 mg/kg for Cu2CO3(OH)(2) NPs. This was surprising since the histopathology evidence demonstrates more severe organ damage for Cu2CO3(OH)(2) NPs than for CuO NPs

Pulmonary toxicity in rats following inhalation exposure to poorly soluble particles : The issue of impaired clearance and the relevance for human health hazard and risk assessment

Intensive discussions are ongoing about the interpretation of pulmonary effects observed in rats exposed to poorly soluble particles. Alveolar clearance differs between rats and humans and becomes impaired in rats at higher exposure concentrations. Some have doubted the human relevance of toxic effects observed in rats under impaired clearance conditions and have suggested that experimental exposures should stay below concentrations inducing impaired clearance. However, for regulatory purposes, insight in potential health effects at relatively high concentrations is needed to fully understand the hazard. Many aspects of impaired particle clearance remain unclear, hampering human health hazard and risk assessment. For an adequate evaluation of the impact of impaired clearance on pulmonary toxicity, a clear definition of alveolar clearance is needed that enables to quantitatively relate the level of impairment to the induction of adverse pulmonary health effects. Also, information is needed on the mechanism of action and the appropriate dose metric for the pulmonary effects observed. In absence of these data, human hazard and risk assessment can only be performed in a pragmatic way. Unless available data clearly point out otherwise, rat pulmonary toxicity including lung inflammation and tumour formation, needs to be considered relevant for human hazard and risk assessment

Pulmonary toxicity in rats following inhalation exposure to poorly soluble particles: The issue of impaired clearance and the relevance for human health hazard and risk assessment.

Intensive discussions are ongoing about the interpretation of pulmonary effects observed in rats exposed to poorly soluble particles. Alveolar clearance differs between rats and humans and becomes impaired in rats at higher exposure concentrations. Some have doubted the human relevance of toxic effects observed in rats under impaired clearance conditions and have suggested that experimental exposures should stay below concentrations inducing impaired clearance. However, for regulatory purposes, insight in potential health effects at relatively high concentrations is needed to fully understand the hazard. Many aspects of impaired particle clearance remain unclear, hampering human health hazard and risk assessment. For an adequate evaluation of the impact of impaired clearance on pulmonary toxicity, a clear definition of alveolar clearance is needed that enables to quantitatively relate the level of impairment to the induction of adverse pulmonary health effects. Also, information is needed on the mechanism of action and the appropriate dose metric for the pulmonary effects observed. In absence of these data, human hazard and risk assessment can only be performed in a pragmatic way. Unless available data clearly point out otherwise, rat pulmonary toxicity including lung inflammation and tumour formation, needs to be considered relevant for human hazard and risk assessment