Commercial Polychlorinated Biphenyls Mixture Research Articles

Vitamin E and genistein generate a cytoprotective effect on polychlorinated biphenyl- induced oxidative stress in testicular Leydig cells

Polychlorinated biphenyls (PCBs) are industrial substances which were widely used in industrial applications starting from the 1930s until the mid-1970s. Aroclor 1242 (A1242) is a commercial PCB mixture with 42% chlorine manufactured by the Monsanto Chemical Company in St. Louis, Missouri, USA. Previous studies suggested that PCBs have inhibitory effect on reproductive function, developmental abnormality, and impaired reproductive ability. PCBs may also affect the endocrine system by reducing the testosterone synthesis and the activity of steroidogenic enzymes in Leydig cells. This study was performed to investigate the specific effects of A1242 on the viability of Leydig cells, oxidative damage, and the profile of steroidogenic enzymes in an in vitro culture. The therapeutic effects of vitamin E (VitE) and genistein (Gen), as two antioxidants, in mitigating the damage produced by A1242 were also evaluated. TM3 Leydig cells were exposed to 10-8 and 10-6 M of A1242 and VitE (50µM) and Gen (10µM) as antioxidant for 24 h. After the exposure period, the Leydig cells were assessed to determine their viability using a cell viability assay. Measurements were performed for lipid peroxidation, reactive oxygen species (ROS), and steroidogenic enzymes. The results showed that cell viability was reduced after A1242 exposure, while lipid peroxidation and ROS increased. Steroidogenesis was interrupted in a concentration-dependent manner. Following A1242 exposure, administrations of VitE or Gen as an antioxidant reduced hazardous effects of A1242 on Leydig cells. Our results showed that exposure to A1242 may impair Leydig cell function and cause toxicity in Leydig cells and that VitE and Gen treatment exhibited therapeutic effects against this toxicity.

Experimental study of catalytic hydro-dechlorination (HDC) of Aroclor 1232

Polychlorinated biphenyls (PCBs) is a group of persistent organic pollutants that still requires remediation and reduction long after the production is discontinued. Aroclor 1232 is a commercial PCB mixture that has been much less studied. To address this void, this paper presented catalytic hydro-dechlorination (HDC) of Aroclor 1232 using palladium on activated carbon (Pd/AC) at atmospheric pressure. Experimental variables studied including three mild temperatures, 22.5 °C, 50 °C, and 80 °C, and four different co-catalyst loadings. This batch of Aroclor 1232 constituted of more than 83% of mono-, di-, and tri-, chlorinated biphenyls (CB), in addition to biphenyl, tetra- and penta CBs. HDC efficiency increased with temperature, and reached 99.9% within 4 h of reaction at 80 °C. HDC efficiency also increased with co-catalyst loading. HDC efficiencies followed the trend of para > meta > ortho positions among isomers. The increase of temperature and Et3N dosage are especially effective in dechlorination at ortho and meta positions. The apparent activation energy of Aroclor 1232 HDC was estimated as 25.57 kJ/mol based on pseudo-first order assumption, indicating that the reaction may be diffusion limited. Given the modest reaction conditions used, the HDC of Aroclor 1232 can potentially be a low-cost process.

Structure-Activity Relationship of Lower Chlorinated Biphenyls and Their Human-Relevant Metabolites for Astrocyte Toxicity.

Exposure to polychlorinated biphenyls (PCBs) is associated with developmental neurotoxicity and neurodegenerative disorders; however, the underlying mechanisms of pathogenesis are unknown. Existing literature has focused mainly on using neurons as a model system to study mechanisms of PCB-mediated neurotoxicity, overlooking the role of glial cells, such as astrocytes. As normal brain function is largely astrocyte-dependent, we hypothesize that astrocytes play an important role in PCB-mediated injury to neurons. We assessed the toxicity of two commercial PCB mixtures, Aroclor 1016 and Aroclor 1254, and a non-Aroclor PCB mixture found in residential air called the Cabinet mixture, all of which contain lower chlorinated PCBs (LC-PCBs) found in indoor and outdoor air. We further assessed the toxicity of five abundant airborne LC-PCBs and their corresponding human-relevant metabolites in vitro models of astrocytes, namely, the C6 cell line and primary astrocytes isolated from Sprague-Dawley rats and C57BL/6 mice. PCB52 and its human-relevant hydroxylated and sulfated metabolites were found to be the most toxic compounds. No significant sex-dependent cell viability differences were observed in rat primary astrocytes. Based on the equilibrium partitioning model, it was predicted that the partitioning of LC-PCBs and their corresponding metabolites in biotic and abiotic compartments of the cell culture system is structure-dependent and that the observed toxicity is consistent with this prediction. This study, for the first time, shows that astrocytes are sensitive targets of LC-PCBs and their human-relevant metabolites and that further research to identify mechanistic targets of PCB exposure in glial cells is necessary.

Source apportionment of polychlorinated biphenyls (PCBs) using different receptor models: A case study on sediment from the Portland Harbor Superfund Site (PHSS), Oregon, USA

Multivariate modelling techniques are used by a wide variety of investigations in environmental chemistry. It is surprisingly rare for studies to show a detailed understanding of uncertainties created by modelling or how uncertainties in chemical analysis impact model outputs. It is common to use untrained multivariate models for receptor modelling. These models produce a slightly different output each time they are run. The fact that a single model can provide different results is rarely acknowledged. In this manuscript, we attempt to address this by investigating differences that can be generated using four different receptor models (NMF, ALS, PMF & PVA) to perform source apportionment of polychlorinated biphenyls (PCBs) in surface sediments from Portland Harbor. Results showed that models generally had a strong agreement and identified the same main signatures that represented commercial PCB mixtures, however, subtle differences were identified by; different models, same models but with a different number of end members (EM), and the same model with the same number of end members. As well as identifying different Aroclor-like signatures, the relative proportion of these sources also varied. Depending on which method is selected it may have a significant impact on conclusions of a scientific report or litigation case and ultimately, allocation on who is responsible for paying for remediation. Therefore, care must be taken to understand these uncertainties to select a method that produces consistent results with end members that can be chemically explained. We also investigated a novel approach to use our multivariate models to identify inadvertent sources of PCBs. By using a residual plot produced from one of our models (NMF) we were able to suggest the presence of approximately 30 different potentially inadvertently produced PCBs which account for 6.6 % of the total PCBs in Portland Harbor sediments.

Occurrence, origin and potential ecological risk of dissolved polycyclic aromatic hydrocarbons and organochlorines in surface waters of the Gulf of Gabès (Tunisia, Southern Mediterranean Sea)

We investigated the occurrence, origin, and potential ecological risk of dissolved polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyl (PCBs) and organochlorine pesticides (OCPs) in 27 surface water samples collected from a highly anthropized and industrialized area in the Gulf of Gabès (Tunisia, Southern Mediterranean Sea) in October–November 2017. The results demonstrated a wide range of concentrations (ng L−1) with the following decreasing order: Ʃ16 PAHs (17.6–71.2) > Ʃ20 PCBs (2.9–33.7) > Ʃ6 DDTs (1.1–12.1) > Ʃ4 HCHs (1.1–14.8). Selected diagnostic ratios indicated a mixture of both pyrolytic and petrogenic sources of PAHs, with a predominance of petrogenic sources. PCB compositions showed distinct contamination signatures for tetra- to hepta-chlorinated PCBs, characteristic of contamination by commercial (Aroclor) PCB mixtures. The dominant OCP congeners were γ-HCH, 2,4′-DDD and 2,4′-DDE, reflecting past use of Lindane and DDTs in the study area. Agricultural, industrial and domestic activities, as well as atmospheric transport are identified as potential sources of PAHs, PCBs and OCPs in surface waters of the Gulf of Gabès. Toxic equivalents (TEQs) suggested a low carcinogenic potential for PAHs in seawater samples (mean of 0.14 ng TEQ L−1). Evaluation of risk coefficients revealed low risk for PAHs and PCBs, and moderate to severe risk for OCPs.

Effect of microplastics on microbial dechlorination of a polychlorinated biphenyl mixture (Aroclor 1260)

Microplastics (MPs) and polychlorinated biphenyls (PCBs) generally coexist in the environment, posing risks to public health and the environment. This study investigated the effect of different MPs on the microbial anaerobic reductive dechlorination of Aroclor 1260, a commercial PCB mixture. MP exposure inhibited microbial reductive dechlorination of PCBs, with inhibition rates of 39.43%, 23.97%, and 17.53% by polyethylene (PE), polypropylene (PP), and polystyrene (PS), respectively. The dechlorination rate decreased from 1.63 μM Cl− d−1 to 0.99–1.34 μM Cl− d−1 after MP amendment. Chlorine removal in the meta-position of PCBs was primarily inhibited by MPs, with no changes in the final PCB dechlorination metabolites. The microbial community compositions in MP biofilms were not significantly different (P > 0.05) from those in suspension culture, although possessing greater Dehalococcoides abundance (0.52–0.81% in MP biofilms; 0.03–0.12% in suspension culture). The co-occurrence network analysis revealed that the presence of MPs attenuated microbial synergistic interactions in the dechlorinating culture systems, which may contribute to the inhibitory effect on microbial PCB dechlorination. These findings are important for comprehensively understanding microbial dechlorination behavior and the environmental fate of PCBs in environments with co-existing PCBs and MPs and for guiding the application of in situ PCB bioremediation.

The occurrence and sources of polychlorinated biphenyls (PCBs) in agricultural soils across China with an emphasis on unintentionally produced PCBs.

In addition to being historically intentionally manufactured as commercial products, polychlorinated biphenyls (PCBs) can be unintentionally released as by-products from industrial processes. Recent studies have emphasized the importance of unintentionally produced PCBs (UP-PCBs) and have even identified them as major contributors to atmospheric PCBs. However, little is known about contributions of UP-PCBs in current soils. In this study, all 209 PCB congeners were analyzed in agricultural soils on a national scale to investigate the influence of unintentional sources on Chinese soil. The concentration of Σ209PCBs in soils across China was in the range of 64.3-4358pg/g. Four non-Aroclor congeners, i.e., PCB11, PCB44+47+65, PCB68, and PCB209, were dominant among all PCBs, averagely accounting for 26.3%, 8.83%, 3.03%, and 2.80% of total PCBs, respectively. PCB11 and PCB209 were found to be higher in East China, while PCB44+47+65 and PCB68 were higher in South China. Their spatial distributions were largely dependent on local sources. The results of source apportionment indicated that the legacy of historically produced and used commercial PCB mixtures was the dominant contributor to seven indicator PCBs in Chinese agricultural soils, especially high-chlorinated congeners. However, unintentional sources (i.e., pigment/paint, combustion-related sources, and polymer sealant), which contributed 57.4% of the total PCBs, are controlling PCB burdens in agricultural soils across China.

A novel analytical method for determining total polychlorinated biphenyl concentrations in fish and shellfish using a simple and rapid clean-up followed by GC–MS/MS

We developed an analytical method for determining total (sum of all 209 congeners) polychlorinated biphenyl (PCB) concentrations in fish and shellfish using a newly developed clean-up method and gas chromatography tandem mass spectrometry. The clean-up involved passing a sample extract through a column containing silica gel and sulfuric-acid-treated silica gel and then a column containing alumina and silver-modified alumina. This gave a short clean-up time and required less organic solvent. No marked losses of any of the 209 PCB congeners were found during clean-up. The trueness and repeatability of the analytical method for total PCBs and seven indicator PCBs in fish and shellfish spiked with a commercial PCB mixture were 92 %–94 % and 93 %–105 %, with relative standard deviations of <0.9 % and <3.1 %, respectively. A certified reference fish sample was analyzed, and the measured concentrations of the certified congeners were within the uncertainty limits of the certified concentrations. The concentration ratios for total PCB and the indicator PCBs in fish determined by the new method and the conventional method using high-resolution gas chromatography high-resolution mass spectrometry were 0.9–1.1 and 0.9–1.2, respectively. The results indicate that the developed method will be very useful for rapidly determining total PCB concentrations in fish and shellfish.

Developmental polychlorinated biphenyl exposure influences adult zebra finch reproductive behaviour.

Polychlorinated biphenyls (PCBs) are worldwide chemical pollutants that have been linked to disrupted reproduction and altered sexual behaviour in many organisms. However, the effect of developmental PCB-exposure on adult passerine reproductive behaviour remains unknown. A commercial PCB mixture (Aroclor 1242) or an estrogenic congener (PCB 52) were administered in sublethal amounts to nestling zebra finches (Taeniopygia guttata) in the laboratory to identify effects of developmental PCB-exposure on adult zebra finch reproductive parameters. Results indicate that although traditional measures of reproductive success are not altered by this PCB dosage, PCBs do alter sexual behaviours such as male song and nesting behaviour. Males treated with PCB 52 in the nest sang significantly fewer syllables than control males, while females treated with Aroclor 1242 in the nest showed the strongest song preferences. PCB treatment also caused an increase in the number of nesting attempts and abandoned nests in the Aroclor 1242 treatment relative to the PCB 52 treatment, and offspring with control fathers fledged significantly earlier than those with fathers treated with Aroclor 1242. Behavioural differences between males seem to best explain these reproductive effects, most notably aggression. These findings suggest that sublethal PCB-exposure during development can significantly alter key reproductive characteristics of adult zebra finches, likely reducing fitness in the wild.

Evidence Implicating Non-Dioxin-Like Congeners as the Key Mediators of Polychlorinated Biphenyl (PCB) Developmental Neurotoxicity.

Despite being banned from production for decades, polychlorinated biphenyls (PCBs) continue to pose a significant risk to human health. This is due to not only the continued release of legacy PCBs from PCB-containing equipment and materials manufactured prior to the ban on PCB production, but also the inadvertent production of PCBs as byproducts of contemporary pigment and dye production. Evidence from human and animal studies clearly identifies developmental neurotoxicity as a primary endpoint of concern associated with PCB exposures. However, the relative role(s) of specific PCB congeners in mediating the adverse effects of PCBs on the developing nervous system, and the mechanism(s) by which PCBs disrupt typical neurodevelopment remain outstanding questions. New questions are also emerging regarding the potential developmental neurotoxicity of lower chlorinated PCBs that were not present in the legacy commercial PCB mixtures, but constitute a significant proportion of contemporary human PCB exposures. Here, we review behavioral and mechanistic data obtained from experimental models as well as recent epidemiological studies that suggest the non-dioxin-like (NDL) PCBs are primarily responsible for the developmental neurotoxicity associated with PCBs. We also discuss emerging data demonstrating the potential for non-legacy, lower chlorinated PCBs to cause adverse neurodevelopmental outcomes. Molecular targets, the relevance of PCB interactions with these targets to neurodevelopmental disorders, and critical data gaps are addressed as well.

Levels and characteristics of polychlorinated biphenyls in surface sediments of the Chaobai river, a source of drinking water for Beijing, China.

We collected surface sediments from the Chaobai river, the dominant source of drinking water for Beijing, China, to assess the status of contamination by polychlorinated biphenyls and evaluate their sources. Total concentrations of polychlorinated biphenyls in the sediments ranged from 0.125 to 70.6ng/g dry weight and correlated with the locations relating to painting operation such as printing factories and construction material markets. Dioxin-like polychlorinated biphenyls were present and corresponded with constituents of commercial polychlorinated biphenyl mixtures. Principal component analysis indicated two dominant sources of polychlorinated biphenyls in the sediments-deposition from airborne emissions and point-source pollution from factories. An ecological risk assessment concluded that there was only slight polychlorinated biphenyl pollution in the sediments of the Chaobai river, which was not likely to induce adverse biological effects. Our findings provide information for polychlorinated biphenyl risk assessment and recognition of the dominant sources of these compounds in drinking water in China.

Adolescent exposure to environmental level of PCBs (Aroclor 1254) induces non-alcoholic fatty liver disease in male mice

Polychlorinated biphenyls (PCBs) are persistent organic pollutants found in various environmental media, and there is growing evidence that PCBs may contribute to the pathogenesis of non-alcoholic fatty liver disease (NAFLD). The purposes of this study were to investigate whether environmental level of Aroclor 1254 (a commercial mixture of PCBs) exposure to adolescent male mice could induce the development of NAFLD and the mechanisms involved. Twenty-one-day-old male C57BL/6 mice were exposed to Aroclor 1254 (0.5–500 μg/kg body weight) by oral gavage once every third day for 60 days. The results showed that exposure to Aroclor 1254 increased body weight and decreased the liver-somatic index in a dose-dependent manner. Aroclor 1254 administration increased lipid accumulation in the liver and induced the mRNA expression of genes associated with lipogenesis, including acetyl-CoA carboxylase 1 (Acc1), acetyl-CoA carboxylase 2 (Acc2) and fatty acid synthase (Fasn). Moreover, Aroclor 1254 decreased peroxisome proliferator-activated receptor alpha (PPARα) signaling and lipid oxidation. In addition, we found that Aroclor 1254 administration induced oxidative stress in mouse liver and elevated the protein level of cyclooxygenase 2 (COX-2), an inflammatory molecule, possibly via the endoplasmic reticulum (ER) stress inositol-requiring enzyme 1α-X-box-binding protein-1 (IRE1α-XBP1) pathway, but not the nuclear factor-κB (NF-κB) pathway. In summary, adolescent exposure to environmental level of PCBs stimulated oxidative stress, ER stress and the inflammatory response and caused NAFLD in male mice. This work provides new insight into the idea that adolescent exposure to environmental level of PCBs might induce the development of NAFLD under the regulation of ER stress in males.

Atmospheric deposition of polychlorinated biphenyls to seasonal surface snow at four glacier sites on Svalbard, 2013-2014.

During spring 2014 we collected annual surface snow from four glacial sites on Svalbard, an archipelago in the European Arctic. The sampling sites are 230 km apart from west to east, but are at varying elevations, affecting local atmospheric contaminant inputs. Samples were analyzed for 209 polychlorinated biphenyl (PCB) congeners. The western sites, Holtedahlfonna and Kongsvegen, had the highest ∑PCB flux (26.7 pg cm-2 yr-1 at Kongsvegen) while the lowest was at Lomonosovfonna, in central Svalbard (14.4 pg cm-2 yr-1). The greatest difference between sites was the trichlorobiphenyl homologue which was nearly four times greater at Kongsvegen than the eastern site at Austfonna. The most concentrated congeners at each site were PCB-52, 70+74, 95, 101, 110 comprising 32-39% of ∑PCB, similar to Clophen 40 which is comprised 27% of these congeners. Similar variance of these congeners in samples and Clophen 40 was verified by principal components analysis. Air mass back trajectories from likely source areas for all sites were similar, indicating no difference in frequency or distribution of PCB from long-distances, suggesting local PCB sources contributing to Kongsvegen. We found 2,3-DiCB (PCB-5) and 3,3'-DiCB (PCB-11) at all sites; neither was found in western commercial PCB mixtures. PCB-5 may be from the Russian PCB product "Trichlorobiphenyl" or is residue from production of pigment violet 23. PCB-11 may come from waste incineration in northern Europe containing various pigments. These results, in comparison to earlier data from Lomonosovfonna, suggest that PCB inputs are variable and are not declining over time.

Proteomic Analysis Reveals Novel Mechanisms by Which Polychlorinated Biphenyls Compromise the Liver Promoting Diet-Induced Steatohepatitis.

Environmental pollution contributes to fatty liver disease pathogenesis. Polychlorinated biphenyl (PCB) exposures have been associated with liver enzyme elevation and suspected steatohepatitis in cohort studies. Male mice treated with the commercial PCB mixture, Aroclor 1260 (20 mg/kg), and fed high fat diet (HFD) for 12 weeks developed steatohepatitis. Receptor-based modes of action including inhibition of the epidermal growth factor (EGF) receptor were previously proposed, but other mechanisms likely exist. Objectives were to identify and validate the pathways, transcription factors, and mechanisms responsible for the steatohepatitis associated with PCB and HFD coexposures. Comparative proteomics analysis was performed in archived mouse liver samples from the aforementioned chronic exposure study. Pathway and transcription factor analysis (TFA) was performed, and selected results were validated. Liver proteomics detected 1103 unique proteins. Aroclor 1260 upregulated 154 and downregulated 93 of these. Aroclor 1260 + HFD coexposures affected 55 pathways including glutathione metabolism, intermediary metabolism, and cytoskeletal remodeling. TFA of Aroclor 1260 treatment demonstrated alterations in the function of 42 transcription factors including downregulation of NRF2 and key nuclear receptors previously demonstrated to protect against steatohepatitis (e.g., HNF4α, FXR, PPARα/δ/γ, etc.). Validation studies demonstrated that Aroclor 1260 significantly reduced HNF4α protein levels, while Aroclor 1260 + HFD reduced expression of the HNF4α target gene, albumin, in vivo. Aroclor 1260 attenuated EGF-dependent HNF4α phosphorylation and target gene activation in vitro. Aroclor 1260 reduced levels of NRF2, its target genes, and glutathione in vivo. Aroclor 1260 attenuated EGF-dependent NRF2 upregulation, in vitro. Aroclor 1260 indirectly activated hepatic stellate cells in vitro via induction of hepatocyte-derived TGFβ. PCB exposures adversely impacted transcription factors regulating liver protection, function, and fibrosis. PCBs, thus, compromised the liver by reducing its protective responses against nutritional stress to promote diet-induced steatohepatitis. The identified mechanisms by which environmental pollutants influence fatty liver disease pathogenesis require confirmation in humans.

Effects of quercetin on Aroclor 1254-induced expression of CYP450 and cytokines in pregnant rats

The present study aimed to investigate the protective effect of quercetin on polychlorinated biphenyls (PCB)-induced liver and embryo damage in pregnant Sprague–Dawley rats. Pregnant rats were divided into five groups, and then were orally gavaged daily with peanut oil (vehicle) or a commercial PCB mixture (Aroclor 1254) — with or without co-treatment with 75, 150, or 300 mg/kg quercetin — on gestation days (GD) 4–7. At GD 9, all rats were euthanized, and their blood, liver, and uterus were collected. Expressions of CYP450 mRNA and protein in liver, cytokines (IFNγ, IL-2, IL-4, and IL-6) and IFNγ/IL-4 ratios in liver and sera, liver morphology, and the status of implanted embryos were analyzed. The results showed Aroclor 1254 treatment alone caused hepatic cord damage (i.e. cell disorganization, swelling, decreased cytoplasm, vacuolization), and that quercetin co-treatment appeared to mitigate this damage. Similarly, levels of CYP1A1 and CYP2B1 mRNA in livers of Aroclor 1254-only-treated rats were significantly higher than those in rats co-treated with quercetin. Hepatic and sera levels of IFNγ, IL-2, IL-6, and IFNγ/IL-4 ratios, and the ratio of delayed-development embryos, all increased in Aroclor 1254-treated rats, but were relatively decreased as a result of quercetin co-treatments. IL-4 levels were decreased by Aroclor 1254 and tended to increase back to normal when quercetin was used. The results indicated that quercetin imparted a protective effect against Aroclor 1254-induced toxicity in pregnant rats, in part, by modulating levels of important pro-inflammatory cytokines and reducing induced CYP1A1 and CYP2B1 expression.

Effective degradation of polychlorinated biphenyls by a facultative anaerobic bacterial consortium using alternating anaerobic aerobic treatments

Polychlorinated biphenyls (PCBs) are synthetic mixtures of chlorinated hydrocarbon compounds that were widely used in the past and still found in the environment due to their highly recalcitrant nature. A combination of anaerobic dechlorination and aerobic oxidation is essential to degrade these PCB mixtures into less toxic products. It was hypothesized that due to the complexity of PCB mixtures, a consortium of carefully selected suitable microbial species will perform better than the application of individual microbes. In the present study, biodegradation of the commercial PCB mixture, Aroclor 1260, was studied under two different combined anaerobic-aerobic conditions, namely, alternating (AN) and two stage (TS). The facultative anaerobic bacterial consortium consisted of naturally occurring Achromobacter sp. NP03, Ochrobactrum sp. NP04 and Lysinibacillus sp. NP05. These bacteria were found capable as individuals of solubilizing and degrading PCBs under both anaerobic and aerobic conditions. 49.2 ± 2.5% total reduction of the original 50 mg/L Aroclor 1260 mixture was achieved after 2 weeks in AN treatment whereas the reduction was only 24.44 ± 2.46% in TS treatment. At the end of week 6, a yield of 17.63 ± 0.91 mg/L chloride released was measured under AN condition compared to 11.79 ± 1.28 mg/L measured under TS condition. The overall results suggested that the microbial consortia capable of degrading and utilizing PCBs under both, anaerobic and aerobic conditions achieved better PCB degradation by repeated exposure to short periods of anaerobic and aerobic conditions alternatingly rather than the conventional two stage anaerobic-aerobic conditions.

KONSENTRASI POLYCHLORINATED BIPHENYLS (PCBS) DAN POLYCHLORINATED DIBENZO-P-DIOXINS/POLYCHLORINATED DIBENZOFURANS (PCDDS/FS) DALAM AIR DARI DAERAH PERKOTAAN JABODETABEK

Determination of polychlorinated biphenyls (PCBs) and polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDDs/Fs) in water samples from Jabodetabek urban area was conducted. In the results, a unique pattern were found interestingly in Ciliwung river, Pluit, Jakarta, where decachlorinated biphenyl (PCB IUPAC #209), and dichlorinated biphenyl (PCB IUPAC #11) were detected at relatively high concentrations as 406.77 ng/L and 6.38 ng/L, respectively. This congener pattern is different with commercial PCB mixtures, such as arochlor, kanechlor, or chlophen. Octachlorinated dibenzo-p-furan (OCDF) was also detected at a significant concentration in this water as 3.10 ng/L. Decachlorinated biphenyl (PCB IUPAC #209) and OCDF were associated with industrial by-products. Meanwhile, dichlorinated biphenyl (PCB IUPAC #11) was associated with colour pigment which widely used in consumer goods, such as paint and printed ink. Thus, PCBs and PCDD/Fs contamination might have arisen from industrial by-products where various industries located near sampling point. Keywords: polychlorinated biphenyls (PCBs), polychlorinated dibenzodioxins /polychlorinated dibenzo-p-furans (PCDDs/Fs), waters, Jabodetabek, industrial by-products.

Behaviorally active environmental chemicals target genes of cell-autonomous control of neural progenitors and interneuron development in hippocampus. Possible microRNA involvement

Exposure to persistent organic pollutants, including polychlorinated biphenyls (PCBs) is correlated with multiple vascular complications including endothelial cell dysfunction and atherosclerosis. PCB-induced activation of the vasculature subsequently leads to oxidative stress and induction of pro-inflammatory cytokines and adhesion proteins. Gene expression of these cytokines/proteins is known to be regulated by small, endogenous oligonucleotides known as microRNAs that interact with messenger RNA. MicroRNAs are an acknowledged component of the epigenome, but the role of environmentally-driven epigenetic changes such as toxicant-induced changes in microRNA profiles is currently understudied. The objective of this study was to determine the effects of PCB exposure on microRNA expression profile in primary human endothelial cells using the commercial PCB mixture Aroclor 1260. Samples were analyzed using Affymetrix GeneChip® miRNA 4.0 arrays for high throughput detection and selected microRNA gene expression was validated (RT-PCR). Microarray analysis identified 557 out of 6658 microRNAs that were changed with PCB exposure (p < 0.05). In-silico analysis using MetaCore database identified 21 of these microRNAs to be associated with vascular diseases. Further validation showed that Aroclor 1260 increased miR-21, miR-31, miR-126, miR-221 and miR-222 expression levels. Upregulated miR-21 has been reported in cardiac injury while miR-126 and miR-31 modulate inflammation. Our results demonstrated evidence of altered microRNA expression with PCB exposure, thus providing novel insights into mechanisms of PCB toxicity.

Concentrations and Source Identification of Polycyclic Aromatic Hydrocarbons (PAHs) and Polychlorinated Biphenyls (PCBs) in Agricultural, Urban/Residential, and Industrial Soils, East of Oran (Northwest Algeria)

ABSTRACTThe aim of this study is to determine potential sources and concentrations of polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs) in surface soils devoted to different land uses in northwest Algeria. Microwave-assisted extraction (MAE) and gas chromatography/mass spectrometry (GC–MS) methods were applied to quantify 16 PAHs and 7 PCB congeners in surface soils. The sum of the 16 US-EPA priority PAHs and the 7 European indicator PCBs ranged from 133.7 to 2068.0 ng g−1 and from n.d. to 19.34 ng g−1, respectively. PAHs with four to six fused rings were predominant in soils, and their concentrations ranged from 110.1 to 1768.0 ng g−1. Principal component analysis (PCA) and isomeric ratios showed that pyrogenic processes and petrogenic contributions were the main sources of PAHs, while commercial mixtures of PCBs (Aroclor 1254 and 1260) were sources of PCBs in urban/residential and industrial sites. This is a first screening of data about PAHs and PCBs in soils around a Mediterranean city (Oran, North Africa), and a first step toward a better understanding of the impact of anthropogenic activities on land uses.

Perinatal exposure to organohalogen pollutants decreases vasopressin content and its mRNA expression in magnocellular neuroendocrine cells activated by osmotic stress in adult rats

Polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) are environmental pollutants that produce neurotoxicity and neuroendocrine disruption. They affect the vasopressinergic system but their disruptive mechanisms are not well understood. Our group reported that rats perinatally exposed to Aroclor-1254 (A1254) and DE-71 (commercial mixtures of PCBs and PBDEs) decrease somatodendritic vasopressin (AVP) release while increasing plasma AVP responses to osmotic activation, potentially emptying AVP reserves required for body-water balance. The aim of this research was to evaluate the effects of perinatal exposure to A1254 or DE-71 (30mgkg/day) on AVP transcription and protein content in the paraventricular and supraoptic hypothalamic nuclei, of male and female rats, by in situ hybridization and immunohistochemistry. cFOS mRNA expression was evaluated in order to determine neuroendocrine cells activation due to osmotic stimulation. Animal groups were: vehicle (control); exposed to either A1254 or DE-71; both, control and exposed, subjected to osmotic challenge. The results confirmed a physiological increase in AVP-immunoreactivity (AVP-IR) and gene expression in response to osmotic challenge as reported elsewhere. In contrast, the exposed groups did not show this response to osmotic activation, they showed significant reduction in AVP-IR neurons, and AVP mRNA expression as compared to the hyperosmotic controls. cFOS mRNA expression increased in A1254 dehydrated groups, suggesting that the AVP-IR decrease was not due to a lack of the response to the osmotic activation. Therefore, A1254 may interfere with the activation of AVP mRNA transcript levels and protein, causing a central dysfunction of vasopressinergic system.