Induction of hepatic cytochrome P4501A1/2B activity and disruption of thyroglobulin synthesis/secretion by mono-ortho polychlorinated biphenyl and its hydroxylated metabolites in rat cell lines

As the active metabolites of polychlorinated biphenyl (PCBs), hydroxylated polychlorinated biphenyls (OH-PCBs) are found in wildlife and human tissues. They have been proposed as main contributors for endocrine disruption of PCBs in living organisms. In this study, mono-ortho PCB 156 and its hydroxylated metabolites 4'-OH-PCB 159, 4'-OH-PCB 121, and 4'-OH-PCB 72 were selected to investigate the toxic effects on rat hepatoma H4IIE cell line and rat thyroid follicle FRTL-5 cell line at concentrations of 1, 10(2), 10(4) nM. 7-Ethoxyresorufin-O-deethylase (EROD) and 7-pentoxyresorufin-O-dealkylase (PROD) activities were determined with micro-EROD/PROD to indicate cytochrome P4501 A1 (CYP1A1) and cytochrome P4502B (CYP2B) induction in the H4IIE cell after exposure for 72 h. To assess thyroid disruption of these compounds, thyroglobulin concentrations also were detected inside FRTL-5 cell with immunocellularchemistry and in its medium with radioimmunoassay after exposure for 24 It. Significant inductions of EROD activity by PCB 156 at 102 and 104 nM (p < 0.05) were observed, but no effects by the three OH-PCBs in H4IIE cell line. 7-Pentoxyresorufin-O-dealkylase activities were induced only by 10(4) nM of PCB156 and the three OH-PCBs (p < 0.05). Meanwhile, significant increases of thyroglobulin concentrations were observed in the medium of FRTL-5 cell exposed to 4'-OH-PCB 121 and 4'-OH-PCB 72 at all of the test concentrations (p < 0.05), but not to the other compounds. The results demonstrated that mono-ortho PCBs mainly could be metabolized to hydroxylated metabolites through CYP1A1 instead of CYP2B. Moreover, after being metabolized, OH-PCBs still sustained the ability to induce PROD activity and did exhibit the disruption on thyroglobulin synthesis/excretion in rat cells.

Polychlorinated Biphenyl DDT And Dieldrin Residues In Grey Seal (Halichoerus-Grypus) Males Females And Mother-Foetus Pairs Sampled At The Farne Islands England During The Breeding-Season

PCB, DDT, DDE, dieldrin and total non-polar organohalogen residues have been determined in the blubber-lipid of grey seals (Halichoerus grypus) sampled during the 1972 breeding season (November) at the Farne Islands off the north eastern coast of England. PCBs were analysed by gas-liquid chromatography linked to a chlorine- and carbon-selective microwave plasma detector and total organohalogen residues were determined by microcoulometry. Total organohalogen residues were negatively correlated with blubber thickness and positively correlated with age in males (aged 1 to 24 y) and females (aged 5 to 38 y). However, the correlation of blubber-lipid residue with age in males depended upon the inclusion of immature (aged < 6 y) animals, and in females reflected only a small residue increment. The mean blubber organohalogen concentration of the males was significantly greater than that of the females. PCB and DDT group residue concentrations were significantly correlated. PCB, DDT, DDE and dieldrin were detected in the liver of mother/foetus pairs demonstrating transplacental movement of these residues. The possibility of the condition of the seals at breeding time influencing residue levels and of these residues influencing the health of the population is discussed.

Microcoulometric Determination Of Total Organo-Chlorinepesticide And Polychlorinated Biphenyl Residues In Grey Seal (Halichoerus-Grypus) Blubber

A procedure for estimating total organochlorine pesticide and PCB residue in seal blubber at concentrations of greater than 1μg g-1 of lipid is described. Lipid is cleaned up by alumina column chromatography, and the halogen concentration of the resulting hexane eluace is determined by combustion and microcoulometry. Results are similar to those obtained by gas chromatographic analysis and can be used to interpolate between results so obtained when data on specific organochlorine compounds is not required for each sample. The organochlorine residues recovered in this manner did not constitute all the halogen determined by combustion and microcoulometry of seal lipid. Analysis by the total halogen procedure was 2.5 tunes faster than the rate achieved with a combination of liquid and gas chromatography operated manually; the requirements for laboratory equipment and space for sample preparation are reduced.

Concentration-dependent half-lives of polychlorinated biphenyl in sera from an occupational cohort.

Polychlorinated biphenyls (PCBs) are carcinogenic. Estimating PCB half-life in the body based on levels in sera from exposed workers is complicated by the fact that occupational exposure to PCBs was to commercial PCB products (such as Aroclors 1242 and 1254) comprised of varying mixtures of PCB congeners. Half-lives were estimated using sera donated by 191 capacitor manufacturing plant workers in 1976 during PCB use (1946-1977), and post-exposure (1979, 1983, and 1988). Our aims were to: (1) determine the role of covariates such as gender on the half-life estimates, and (2) compare our results with other published half-life estimates based on exposed workers. All serum PCB levels were adjusted for PCB background levels. A linear spline model with a single knot was used to estimate two separate linear equations for the first two serum draws (Equation A) and the latter two (Equation B). Equation A gave half-life estimates of 1.74 years and 6.01 years for Aroclor 1242 and Aroclor 1254, respectively. Estimates were 21.83 years for Aroclor 1242 and 133.33 years for Aroclor 1254 using Equation B. High initial body burden was associated with rapid PCB elimination in workers at or shortly after the time they were occupationally exposed and slowed down considerably when the dose reached background PCB levels. These concentration-dependent half-life estimates had a transition point of 138.57 and 34.78 ppb for Aroclor 1242 and 1254, respectively. This result will help in understanding the toxicological and epidemiological impact of exposure to PCBs in humans.

Analysis of a microbial community associated with polychlorinated biphenyl degradation in anaerobic batch reactors

The degradation of polychlorinated biphenyls (PCBs) was investigated under fermentativemethanogenic conditions for up to 60 days in the presence of anaerobic biomass from a full-scale UASB reactor. The low methane yields in the PCBs-spiked batch reactors suggested that the biomass had an inhibitory effect on the methanogenic community. Reactors containing PCBs and co-substrates (ethanol/ sodium formate) exhibited substantial PCB reductions from 0.7 to 0.2 mg mL-1 . For the Bacteria domain, the PCBs-spiked reactors were grouped with the PCB-free reactors with a similarity of 55 %, which suggested the selection of a specific population in the presence of PCBs. Three genera of bacteria were found exclusively in the PCB-spiked reactors and were identified using pyrosequencing analysis, Sedimentibacter, Tissierela and Fusibacter. Interestingly, the Sedimentibacter, which was previously correlated with the reductive dechlorination of PCBs, had the highest relative abundance in the RCS-PCB (7.4 %) and RCS-PCB-PF (12.4 %) reactors. Thus, the anaerobic sludge from the UASB reactor contains bacteria from the Firmicutes phylum that are capable of degrading PCBs.

(Table 1) Polychlorinated biphenyl (PCB) and PCB metabolite concentrations in ringed seals (Phoca hispida) from Svalbard and the Baltic Sea

Polychlorinated biphenyls (PCBs) may induce activity of hepatic enzymes, mainly Phase I monooxygenases and conjugating Phase II enzymes, that catalyze the metabolism of PCBs leading to formation of metabolites and to potential adverse health effects. The present study investigates the concentration and pattern of PCBs, the induction of hepatic phase I and II enzymes, and the formation of hydroxy (OH) and methylsulfonyl (CH3SO2=MeSO2) PCB metabolites in two ringed seal (Phoca hispida) populations, which are contrasted by the degree of contamination exposure, that is, highly contaminated Baltic Sea (n = 31) and less contaminated Svalbard (n = 21). Phase I enzymes were measured as ethoxyresorufin-O-deethylation (EROD), benzyloxyresorufin-O-dealkylation (BROD), methoxyresorufin-O-demethylation (MROD), and pentoxyresorufin-O-dealkylation (PROD) activities, and phase II enzymes were measured as uridine diphosphophate glucuronosyl transferase (UDPGT) and glutathione-S-transferase (GST). Geographical comparison, multivariate, and correlation analysis indicated that sum-PCB had a positive impact on Phase I enzyme and GST activities leading to biotransformation of group III (vicinal ortho-meta-H atoms and <=1 ortho-chlorine (Cl)) and IV PCBs (vicinal meta-para-H atoms and <=2 ortho-Cl). The potential precursors for the main OH-PCBs detected in plasma in the Baltic seals were group III PCBs. MeSO2-PCBs detected in liver were mainly products of group IV PCB metabolism. Both CYP1A- and CYP2B-like enzymes are suggested to be involved in the PCB biotransformation in ringed seals.

Hydroxylated metabolites of polychlorinated biphenyls and their endocrine disrupting mechanism

Hydroxylated polychlorinated biphenyls (OH-PCBs a group of main active metabolites of polychlorinated biphenyl (PCBs) which are typical persistent organic pollutants (Pops) I have been identified in wild animals and human. The endocrine disruption of OH-PCBs has been drawn great attention due to the similarity of their chemical structures to the natural estrogens and thyroid hormones. The metabolic pathways of PCBs, the levels of OHPCBs in organism, the endocrine disruption and other adverse effects of OH-PCBs are reviewed. The further investigation of OH-PCBs will not only reveal the toxicological mechanism of PCBs, but also can lay scientific basis for setting up the risk assessment of POPs contamination and early-warning system in China.

Deposition History of Polychlorinated Biphenyls to the Lomonosovfonna Glacier, Svalbard: A 209 Congener Analysis

A 37 m deep ice core representing 1957–2009 and snow from 2009 to 2010 were collected on the Lomonosovfonna glacier, Svalbard (78.82° N; 17.43° E) and analyzed for 209 polychlorinated biphenyl (PCB) congeners using high-resolution mass spectrometry. Congener profiles in all samples showed the prevalence of tetra- and pentachlorobiphenyls, dominated in all samples by PCB-44, PCB-52, PCB-70 + PCB-74, PCB-87 + PCB-97, PCB-95, PCB-99, PCB-101, and PCB-110. The ∑PCB flux varied over time, but the peak flux, 19 pg cm–2 year–1 from 1957 to 1966, recurred in 1974–1983, 1998–2009, and 2009–2010. The minimum was 5.75 pg cm–2 year–1 in 1989–1998, following a 15 year decline. Peak ∑PCB fluxes here are lower than measured in the Canadian Arctic. The analysis of all 209 congeners revealed that PCB-11 (3,3′-dichlorobiphenyl) was present in all samples, representing 0.9–4.5% of ∑PCB. PCB-11 was not produced in a commercial PCB product, and its source to the Arctic has not been well-characterized; however, our results confirm that the sources to Lomonosovfonna have been active since 1957. The higher fluxes of ∑PCB correspond to periods when average 5 day air mass back trajectories have a frequency of 8–10% and reach 60° N or beyond over northern Europe and western Russia or the North Sea into the U.K

Health consequences of exposure to e-waste : a systematic review

Background The population exposed to potentially hazardous substances through inappropriate and unsafe management practices related to disposal and recycling of end-of-life electrical and electronic equipment, collectively known as e-waste, is increasing. We aimed to summarise the evidence for the association between such exposures and adverse health outcomes. Methods We systematically searched five electronic databases (PubMed, Embase, Web of Science, PsycNET, and CINAHL) for studies assessing the association between exposure to e-waste and outcomes related to mental health and neurodevelopment, physical health, education, and violence and criminal behaviour, from Jan 1, 1965, to Dec 17, 2012, and yielded 2274 records. Of the 165 full-text articles assessed for eligibility, we excluded a further 142, resulting in the inclusion of 23 published epidemiological studies that met the predetermined criteria. All studies were from southeast China. We assessed evidence of a causal association between exposure to e-waste and health outcomes within the Bradford Hill framework. Findings We recorded plausible outcomes associated with exposure to e-waste including change in thyroid function, changes in cellular expression and function, adverse neonatal outcomes, changes in temperament and behaviour, and decreased lung function. Boys aged 8–9 years living in an e-waste recycling town had a lower forced vital capacity than did those living in a control town. Significant negative correlations between blood chromium concentrations and forced vital capacity in children aged 11 and 13 years were also reported. Findings from most studies showed increases in spontaneous abortions, stillbirths, and premature births, and reduced birthweights and birth lengths associated with exposure to e-waste. People living in e-waste recycling towns or working in e-waste recycling had evidence of greater DNA damage than did those living in control towns. Studies of the effects of exposure to e-waste on thyroid function were not consistent. One study related exposure to e-waste and waste electrical and electronic equipment to educational outcomes. Interpretation Although data suggest that exposure to e-waste is harmful to health, more well designed epidemiological investigations in vulnerable populations, especially pregnant women and children, are needed to confirm these associations. Funding Children's Health and Environment Program, Queensland Children's Medical Research Institute, The University of Queensland, Australia.

Assessing infant exposure to persistent organic pollutants via dietary intake in Australia

Persistent organic pollutants (POPs) including polybrominated diphenyl ethers (PBDEs); organochlorine pesticides (OCPs); and polychlorinated biphenyls (PCBs) persist in the environment, bioaccumulate, and pose a risk of causing adverse human health effects. Typically, exposure assessments undertaken by modeling existing intake data underestimate the concentrations of these chemicals in infants. This study aimed to determine concentrations of POPs in infant foods, assess exposure via dietary intake and compare this to historical exposure. Fruit purees, meat and vegetables, dairy desserts, cereals and jelly foods (n = 33) purchased in 2013 in Brisbane, Australia were analyzed. For OCPs and PCBs, concentrations ranged up to 95 pg/g fw and for PBDEs up to 32 pg/g fw with most analytes below the limit of detection. Daily intake is dependent on type and quantity of foods consumed. Consumption of a 140 g meal would result in intake ranging from 0 to 4.2 ng/day, 4.4 ng/day and 13.3 ng/day, for OCPs, PBDEs and PCBs, respectively. PBDEs were detected in 3/33 samples, OCPs in 9/33 samples and PCBs in 13/33 samples. Results from this study indicate exposure for infants via dietary (in contrast to dust and breast milk) intake in Australia contribute only a minor component to total exposure.

Primary cultured cells as sensitive in vitro model for assessment of toxicants-comparison to hepatocytes and gill epithelia

In an effort to develop cultured cell models for toxicity screening and environmental biomonitoring, we compared primary cultured gill epithelia and hepatocytes from freshwater tilapia (Oreochromis niloticus) to assess their sensitivity to AhR agonist toxicants. Epithelia were cultured on permeable supports (terephthalate membranes, "filters") and bathed on the apical with waterborne toxicants (pseudo in vivo asymmetrical culture conditions). Hepatocytes were cultured in multi-well plates and exposed to toxicants in culture medium. Cytochrome P4501A (measured as 7-Ethoxyresorufin-O-deethylase, EROD) was selected as a biomarker. For cultured gill epithelia, the integrity of the epithelia remained unchanged on exposure to model toxicants, such as 1,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), benzo(a)pyrene B[a]P, polychlorinated biphenyl (PCB) mixture (Aroclor 1254), and polybrominated diphenyl ether (PBDE) mixture (DE71). A good concentration-dependent response of EROD activity was clearly observed in both cultured gill epithelia and hepatocytes. The time-course response of EROD was measured as early as 3 h, and was maximal after 6 h of exposure to TCDD, B [alp and Aroclor 1254. The estimated 6 h EC50 for TCDD, B [a]P, and Aroclor 1254 was 1.2x10(-9), 5.7x10(-8) and 6.6x10(-6) M. For the cultured hepatocytes, time-course study showed that a significant induction of EROD took place at 18 h, and the maximal induction of EROD was observed at 24 h after exposure. The estimated 24 It EC50 for TCDD, B[a]P, and Aroclor 1254 was 1.4x10(-9), 8.1x10(-8) and 7.3x10(-6) M. There was no induction or inhibition of EROD in DE71 exposure to both gill epithelia and hepatocytes. The results show that cultured gill epithelia more rapidly induce EROD and are slightly more sensitive than cultured hepatocytes, and could be used as a rapid and sensitive tool for screening chemicals and monitoring environmental AhR agonist toxicants. (c) 2006 Elsevier B.V. All rights reserved.

PCDD/F-s, PCBs, HCHs and HCB in sediments and soils of Ya-Er lake area in China: Results on residual levels and correlation to the organic carbon and particle size

Sediments and soils collected from the Ya-Er Lake area in China were analysed for the polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs), polychlorinated biphenyl (PCBs), hexachlorocyclohexane (HCHs) and hexachlorobenzene (HCB). The results indicated the main pollution problems in the Ya-Er Lake area, which was heavily polluted by HCHs and chlorobenzenes, now is dominantly polluted by PCDD/Fs, PCBs and HCB. The occurrence of PCDD/Fs and PCBs with relatively high levels of HpCDDs, OCDD and low chlorinated-substituted PCBs, is attributed to the discharge of waste water and biodegradation. The vertical distributions of HCH-residues are related with the content of organic carbon and particle size. Copyright (C) 1996 Elsevier Science Ltd

Organochlorine micropollutants in the Jiulong River Estuary and Western Xiamen Sea, China

Organochlorine contaminants including 12 polychlorinated biphenyl (PCB) congeners and 18 insecticides were determined in water, pore water and sediments of the Jiulong River Estuary and Western Xiamen Sea, China. The results showed that the levels of the total PCBs ranged from non-detectable to 1500 ngl(-1) in water, from 209 to 3870 ngl(-1) in pore water, and from 2.78 to 14.8 ng g(-1) dry weight in sediments. Total organochlorine insecticide concentrations were from below the limit of detection to 2480 ngl(-1) in water, from 267 to 33400 ngl(-1) in pore water, and from 4.22 to 46.3 ng g(-1) dry weight in sediments. Concentrations of PCBs and insecticides in pore water were significantly higher than those in surface water, due to the high affinity of these hydrophobic compounds for sediment phase. The PCB congeners with the highest concentrations were CB153, CB180 and CB194, which together accounted for 68-87% of total PCBs in water, pore water and sediment. Among the hexachlorocyclohexane (HCH) compounds, beta-HCH was found to be a major isomer. Analysis of 1,1,1-trichloro-2,2-bis-chlorophenyl-ethane (DDT) and its metabolites showed that 1, 1-dichloro-2[o-chlorophenyl]-2[p-chlorophenyl]-ethylene (DDE) was dominant in the group. In comparison to a 1998 study in the Western Xiamen Sea, levels of organochlorines were enhanced due probably to recent inputs and changes in sediments. (c) 2004 Elsevier Ltd. All rights reserved.

An unrecognized source of PCB contamination in schools and other buildings

An investigation of 24 buildings in the Greater Boston Area revealed that one-third (8 of 24) contained caulking materials with polychlorinated biphenyl (PCB) content exceeding 50 ppm by weight, which is the U.S. Environmental Protection Agency (U.S. EPA) specified limit above which this material is considered to be PCB bulk product waste. These buildings included schools and other public buildings. In a university building where similar levels of PCB were found in caulking material, PCB levels in indoor air ranged from 111 to 393 ng/m3; and in dust taken from the building ventilation system, < 1 ppm to 81 ppm. In this building, the U.S. EPA mandated requirements for the removal and disposal of the PCB bulk product waste as well as for confirmatory sampling to ensure that the interior and exterior of the building were decontaminated. Although U.S. EPA regulations under the Toxic Substances Control Act stipulate procedures by which PCB-contaminated materials must be handled and disposed, the regulations apparently do not require that materials such as caulking be tested to determine its PCB content. This limited investigation strongly suggests that were this testing done, many buildings would be found to contain high levels of PCBs in the building materials and potentially in the building environment. The presence of PCBs in schools is of particular concern given evidence suggesting that PCBs are developmental toxins.