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Polybrominated diphenyl ethers (PBDEs) have been used for many years as flame retardants. Due to their physicochemical and toxicological properties, they are considered to be persistent organic pollutants (POPs). BDE-209 is the main component of deca-BDE, the one PBDE commercial mixture currently approved for use in the European Union. The aim of this study was to analyse BDE-209 in surface soil samples from Warsaw and surrounding areas (Poland) as an indicator of environmental pollution with PBDEs, and to characterise the associated health risk. A total of 40 samples were analysed using gas chromatography with electron capture detection (GC-µECD). Concentrations of BDE-209 in soil ranged from 0.4 ng g−1 d.w. (limit of quantification) to 158 ng g−1 d.w. Overall, 52.5% of results were above the method's limit of quantification. The highest levels were found at several locations with heavy traffic and in the vicinity of a CHP plant in the city. The lowest concentrations were observed in most of the samples collected from low industrialized or green areas (<0.4 to 1.68 ng g−1 d.w.). Exposure to BDE-209 was estimated for one of the most sensitive populations, i.e., young children. The following exposure routes were selected: oral and dermal. No risk was found to young children's health. [ABSTRACT FROM AUTHOR]

In the article, we assess the impact of the regulatory framework on banks' funding models in the European Union in the period 2011–2018. We put particular emphasis on the capital requirements captured by two different types of regulatory measures: individual and sectoral. Moreover, we include a country‐level regulatory variable to assess if the overall lawmaking conditions impact banks' funding models. Our estimates indicate that after the Global Financial Crisis, all regulatory measures had a significant impact on the deposits to total assets ratio, which we assume to be the best proxy for banks' funding models. Having divided the sample of the EU banks into four subsamples according to their specialization (i.e. commercial, cooperative, savings, and investment banks), we identified significant differences in strength and direction of regulatory variables' impact on banks' funding model within selected subsamples. In particular, due to the specific nature of investment banks, prudential regulations contribute to a change in the funding model towards safer deposit funding. Moreover, our results indicate that in the case of the non‐euro area banking sector, the regulatory environment measured by the regulatory quality index has an adverse impact on the Deposits to total assets ratio in comparison with both the entire sample as well as the euro area banking sector. [ABSTRACT FROM AUTHOR]

In our paper, we analyse the impact of funding structure on banking sector stability in EU countries. Our findings show that after the global financial crisis (GFC) there are four main funding models in the EU banking sectors. We document that funding structure is an important factor influencing the banking sector stability. We report that there are also some other banking business model characteristics as well as macroeconomic indicators which have impact on banking sector risk. [ABSTRACT FROM AUTHOR]

We investigated the relationship between dibutyl phthalate (DBP)-induced hypomethylation of the c-Myc promoter region (as evident in our early study) and the expression of c-Myc and DNMT1 genes (at messenger RNA (mRNA) and protein level) in the rat liver. Male Wistar rats received DBP in 1, 3, or 14 daily doses of 1800 mg kg−1 body weight. Levels of DNMT1, c-Myc mRNA, and proteins were detected using real-time polymerase chain reaction and Western blot analysis, respectively. Our findings indicate that DBP caused an increase in mRNA levels of c-Myc at all time points. The results showed that protein levels of c-Myc in rat liver also increased significantly by DBP treatment, which were more pronounced at last time point (after 14 doses). Furthermore, overexpression of DNMT1gene have been found after one dose of DBP, which was confirmed at the protein level by Western blot analysis. Reduced levels of DNMT1mRNA and proteins (3 and 14 doses) were coordinated with depletion DNA synthesis (reported previously). Based on our previous results and those presented here, the following conclusion could be drawn: (1) DBP exerted biological activity through epigenetic modulation of c-Myc gene expression; (2) it seems possible that DBP-induced active demethylation of c-Myc gene through mechanism(s) linked to generation of reactive oxygen species by activated c-Myc; and (3) control of DNA replication was not directly dependent on c-Myc transcriptional activity and we attribute this finding to DNMT1gene expression which was tightly coordinated with DNA synthesis. [ABSTRACT FROM AUTHOR]

ABSTRACT The aim of the study was to investigate the early effect of acute dichlorodiphenyltrichloroethane (DDT) exposure on the methylation status of the promoter region of two tumor suppressor genes: p53 and p16INK4a ( p16) in rat liver. We analyzed their transcript and protein expression profiles concurrently with the examination of transcriptional and protein expression levels of DNA (cytosine-5)-methyltransferase 1 ( Dnmt1). Male Wistar rats were treated with a single dose of DDT (57 mg kg−1 of body weight) and the methylation status of p53 and p16 genes was examined after 24 h using methylation-sensitive restriction analysis-MSRA. The obtained results indicate that DDT induced alternations in methylation of the promoter region in both p53 and p16 genes. In all the tested samples, the promoter CpG islands of p53 (−261, −179, and −450) were methylated within 100% as compared to control samples (0%). The methylation status of the p16 promoter (−11 and +77) was also altered due to exposure to DDT. Methylated cytosines were detectable in 75% of the tested DNA samples. The Real-time PCR and western blot analyses showed a decrease in mRNA and protein levels of p53, respectively, which was related to the increase in DNA synthesis. These relationships were also observed for mRNA and protein expressions of p16, although to a slighter extent. We also showed that hypermethylation in the promoter region of both tumor suppressor genes was consistent with an increased Dnmt1 mRNA level, and this relationship was further confirmed at the protein level of DNMT1. Concluding, our data suggests that epigenetically mediated changes in gene expression may play an important role in the mechanism of DDT toxicity, including carcinogenic action. © 2014 Wiley Periodicals, Inc. Environ Toxicol 31: 584-592, 2016. [ABSTRACT FROM AUTHOR]

Introduction and Objective: Polybrominated diphenyl ethers (PBDEs) are a class of flame-retarding synthetic compounds. They may cause a potential threat to human health due to their bio-accumulative and toxicological properties, and ubiquitous presence in the environment. Food, and ingested dust constitute principal sources of human exposure to PBDEs. The aim of this study was to assess the potential human exposure to selected polybrominated diphenyl ethers measured in dust found in cars and airplane cabins to characterize the health risk., Material and Methods: 31 samples of car dust and 14 samples of airplane dust were collected and concentrations of BDE-47, BDE-99, BDE-153 and BDE-209 congeners were determined by gas chromatography with micro-electron capture detector (GC-μECD). Exposures were estimated for infants (0-1 year), toddlers (1-3 years) and adults (>18 years). The Hazard Quotients (HQs) were calculated by comparing the estimated exposure values to reference doses (RfD) established by the US EPA., Results: The study found that BDE-209 levels were much higher in the majority of samples than in the remaining PBDEs The estimated values of average and reasonable maximum exposure (P95) in each age group ranged from <0.001 ng kg -1 b.w. day -1 to 382 ng kg -1 b.w. day -1 and from <0.001 ng kg -1 b.w. day -1 to 1.2 μg kg -1 b.w. day -1 , respectively (considering the individual analysed PBDE congeners). Additionally, the exposure of infants and toddlers was estimated using the highest PBDE concentration reported in the study and the maximum daily dust intake values. All the HQ values were lower than 1, in the majority of cases 2 orders of magnitude lower than 1., Conclusions: The levels of tested PBDE congeners measured both in car and aircraft dust did not indicate health risk for these selected populations resulting from ingestion of dust.

Background: The changes in DNA methylation are considered as one of the early events in hepatocarcinogenesis., Objective: We evaluated the ability of phenobarbital (PB) – the most widely used anticonvulsant worldwide and classical rodent liver carcinogen – to cause the promoter region of the c-myc protooncogene hypomethylation as well as changes of mRNA level of this gene. Moreover, the expression of Dnmt1 protein in rat treated with this compound was analyzed., Material and Methods: Male Wistar rats received PB in daily oral doses of 92.8 mg kg-1 b.w. day-1 (at 24-h intervals; for one, three and fourteen days). Methylation of the c-myc promoter region was measured by PCR-based methylationsensitive restriction enzyme analysis (MSRA). Levels of mRNA for c-myc and protein Dnmt1 were assayed using Real-Time PCR and Western Blot, respectively., Results: The study showed that phenobarbital stimulated persistent changes in DNA methylation, i.e. loss of methylation in the promoter region of the c-myc gene and up-regulated its mRNA level. In addition, a significant increase in protein level of Dnmt1 in the c-myc over-expressing liver cells was observed., Conclusion: The oppose relationship between Dnmt1 activity and methylation status of c-myc gene was demonstrated. The c-myc over-expression by demethylation might represent an important, early events in the mechanism of action (MOA) of phenobarbital.

The aim of the study was to investigate the early effect of acute dichlorodiphenyltrichloroethane (DDT) exposure on the methylation status of the promoter region of two tumor suppressor genes: p53 and p16(INK4a) (p16) in rat liver. We analyzed their transcript and protein expression profiles concurrently with the examination of transcriptional and protein expression levels of DNA (cytosine-5)-methyltransferase 1 (Dnmt1). Male Wistar rats were treated with a single dose of DDT (57 mg kg(-1) of body weight) and the methylation status of p53 and p16 genes was examined after 24 h using methylation-sensitive restriction analysis-MSRA. The obtained results indicate that DDT induced alternations in methylation of the promoter region in both p53 and p16 genes. In all the tested samples, the promoter CpG islands of p53 (-261, -179, and -450) were methylated within 100% as compared to control samples (0%). The methylation status of the p16 promoter (-11 and +77) was also altered due to exposure to DDT. Methylated cytosines were detectable in 75% of the tested DNA samples. The Real-time PCR and western blot analyses showed a decrease in mRNA and protein levels of p53, respectively, which was related to the increase in DNA synthesis. These relationships were also observed for mRNA and protein expressions of p16, although to a slighter extent. We also showed that hypermethylation in the promoter region of both tumor suppressor genes was consistent with an increased Dnmt1 mRNA level, and this relationship was further confirmed at the protein level of DNMT1. Concluding, our data suggests that epigenetically mediated changes in gene expression may play an important role in the mechanism of DDT toxicity, including carcinogenic action., (© 2014 Wiley Periodicals, Inc.)

Background: Polybrominated diphenyl ethers (PBDEs) as other persistent organic pollutants like polychlorinated biphenyls (PCBs) and organochlorine pesticides (OCPs) pose a significant hazard to human health, mainly due to interference with the endocrine system and carcinogenetic effects. Humans are exposed to these substances mainly through a food of animal origin. These pollutants are globally detected in human matrices which requires to dispose reliable and simple analytical method that would enable further studies to assess the exposure of specific human populations to these compounds., Objective: The purpose of this study was to modify and validate of the analytical procedure for the simultaneous determination of selected PBDEs, PCBs and OCPs in human blood serum samples., Material and Methods: The analytical measurement was performed by GC-µECD following preparation of serum samples (denaturation, multiple extraction, lipid removal). Identity of the compounds was confirmed by GC-MS., Results: The method was characterised by the appropriate linearity, good repeatability (CV below 20%). The recoveries ranged from 52.9 to 125.0% depending on compound and level of fortification. The limit of quantification was set at 0.03 ng mL(-1) of serum., Conclusions: The modified analytical method proved to be suitable for the simultaneous determination of selected PBDEs, PCBs and OCPs in human blood serum by GC-µECD with good precision.

Background: Human exposure to trace levels of pesticide residues present in food of plant origin is inevitable as long as pesticides continue to be applied in agriculture. Since Maximum Residue Levels (MRL) are not toxicological endpoint values, their violation is not by default equivalent to health risk for consumers. However, its essential to provide a health- based risk assessment for each case of MRL non-compliance reported during monitoring and official control of foodstuffs., Objective: To assess the potential short-term risk associated with consumption of food products of plant origin containing pesticide residues above MRL values based on notifications forwarded by the National Contact Point for RASFF in Poland during 2011-2015., Material and Methods: 115 notifications including 127 analytical results non-compliant with respective MRL values were forwarded to provide risk assessment. An internationally accepted deterministic approach based on conservative model assumptions for short-term exposure assessment was applied. The risk was characterized by comparing an estimated dietary intake with respective acute reference dose (ARfD)., Results: Black currant, tea, lettuce, Chinese cabbage and carrot were among the most frequently notified products in years 2011-2015. Among pesticides exceeding respective MRL values, over 90% belonged to fungicides and insecticides/acaricides such as acetamiprid, chlorpyrifos, dimethoate, imidacloprid, dithiocarbamates and procymidone. For 15 and 6 results noncompliant with respective MRL value, a predicted short-term intake exceeded ARfD for children and adults, respectively., Conclusions: Residue levels that could potentially pose a health threat are found incidentally. The science-based and transparent risk assessment process with regard to the data, methods and assumptions that are applied is essential to risk management authorities., Key Words: risk assessment, pesticide residues, MRL, dietary intake, RASFF, food safety.

Background: Our previous studies have shown that short-term treatment with phenobarbital (PB) resulted in cytosine methylation of CpG sites on the p53 gene promoter in male Wistar rats' liver. Furthermore, PB induced DNA-methyltransferases (DNMTs) activity was also demonstrated; being the enzymes that catalyze methyl group transfer to cytosine in CpG dinucleotides., Objective: Since DNA methylation is involved in regulating gene transcription and that DNMT1 is implicated in regulating DNA methylation, this study assessed whether PB-induced hypermethylation of the p53 promoter region was associated with an altered expression of p53 and Dnmt1 genes., Material and Methods: Male Wistar rats received PB in three daily oral doses (at 24-h intervals) of 92,8 mg/kg b.w. x day-1. Levels of mRNA for p53 and Dnmt1 and levels of relevant proteins were respectively examined by Real-Time PCR and Western blot analysis., Results: Gene expression analysis revealed that exposure of Wistar rats to PB caused statistically significant alternations in the expression of tested genes. We found that both mRNA and protein expression of p53 was down-regulated, whereas expression of Dnmt1 (both mRNA and protein) was up-regulated after PB treatment., Conclusions: Suppression of p53 mRNA and protein expression, which is probably a result of epigenetic changes, (in particular aberrant p53 promoter hypermethylation), can be associated with tumour promoting activity of phenobarbital.

Background: Currently, nongenotoxic carcinogens-induced changes in DNA methylation profile are considered as mechanism of their toxicity, including carcinogenic action., Objective: The aim of the study was to determine the effect of dibutyl phthalate (DBP) on the methylation levels of the p53 promoter region, as well as mRNA and protein level of this gene., Material and Method: Male Wistar rats received DBP in one, three or fourteen daily oral doses (at 24-h intervals) of 1800 mg/kg b.w. x day(-1). The methylation level of c-myc gene was determined by PCR-based methylation sensitive restriction enzyme analysis (MSRA). The expression of gene was assessed by Real-Time PCR (at mRNA level) and Western blot (at protein level) analysis., Results: There was observed the hypermethylation of p53 promoter region after short (1 day) exposure of the animals to DBP. No correlation was found between mRNA expression and methylation level of p53 gene. The present study showed decreased level of p53 protein, during the whole period of study., Conclusions: No direct correlation was observed between the methylation and expression level of p53. The decreased protein level might be a consequence of the repressive effect of c-myc, which was involved in signal transduction pathways, the same as p53 protein.

The results of food monitoring studies indicate that humans are constantly exposed to residues ofplant protection products (pesticides) in marketed food products. Hence, assessment of the risk to consumers associated with the consumption of products containing residues of the active substances of pesticides is a key stage in both the registration of pesticides and official control of foodstuffs. However there are frequent cases of exposure not only to individual active substances but also to mixtures of pesticide residues. These levels are usually low, below of effective action, and interaction such as synergism orpotentiation is not expected to occur At the same time, literature data indicate that for mixtures sharing a common MOA (Mode of Action/Mechanism of Action), the probability of additive effects is high, even after adjusting for the low levels of the mixed pesticide residues present. Accordingly, health risk assessment for consumers exposed to such mixtures (cumulative/aggregate risk) has become an issue of topical importance. EU-level initiatives regarding the development of appropriate methodology for the estimation of cumulative/aggregate risk have brought about considerable progress in this area. The article discusses various aspects of estimation of cumulative risk for consumers associated with exposure to mixtures of pesticide residues in food.

Recent changes in the European legislation of chemicals suggest an urgent need for introduction of novel, alternative methods for testing chemical substances. Such possibility is offered by toxicogenomics--a scientific discipline combining knowledge from the field of toxicology, i.e., a science investigating the properties of toxic agents and the negative effects these agents exert on health and environment, with genomics, i.e., a science investigating the structure and function of genomes. New research strategies within the field of toxicology (transcriptomics, proteomics, metabolomics) offer conditions to assess the hazards associated with the effects of chemicals with both established and suspected toxic potentials.