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PubMed2005

Polychlorinated dibenzo-p-dioxins, dibenzofurans and 'dioxin-like' PCBs in flue gas emissions from municipal waste management plants.

The aim of this work is to give representative data on polychlorinated dibenzo-p-dioxins (PCDD), polychlorinated dibenzofurans (PCDFs) and polychlorinated biphenyl (PCBs) from stack gas emissions of an urban solid waste management plant which has to comply with the limit of 0.1 ng I-TEQ/Nm3. In particular, the study is focused on 29 target compounds, the seventeen 2,3,7,8-PCDDs/Fs, four non-ortho PCBs and eight mono-ortho PCBs which configure so-called 'dioxin-like' PCBs (DL-PCBs). To this end, emission measurements were performed during one year over the three operating combustion lines in a selected waste management plant. In general, accurate methodology allowed characterizing all target compounds in almost all the samples analyzed. In addition, a typical pattern for DL-PCBs is reported. The pattern presented PCB #118 to be the highest, nevertheless the figures demonstrated DL-PCBs contribution to the total TEQ around 3% being PCB #126 the most important congener due to its TEF of 0.1. Finally, remarkable differences were achieved in comparison with both environmental and biological samples such as soils, sediments, human milk or fish since these matrices may present DL-PCB contribution to the total TEQ up to 77%.

Air Pollutants↗
PubMed2004

The evaluation of dioxin and dioxin-like contaminants in selected food samples obtained from the Belgian market: comparison of TEQ measurements obtained through the CALUX bioassay with congener specific chemical analyses.

A limited number of different foods were analysed for dioxin-like compounds by the CALUX bioassay which is an in vitro luciferase reporter gene assay measuring chemical activation of the aryl hydrocarbon receptor. Sixty-two milk samples were obtained from a surveillance campaign, 34 meat samples and 34 fishery products were purchased from the Belgian market. Bio-analytical and chemo-analytical dioxin toxicity equivalents (TEQ) values of the same milk samples were compared. Spearman's Rank correlation coefficients of 0.72, 0.67, 0.73 were obtained respectively between CALUX-TEQ and PCDD/F-TEQ, DL-PCB-TEQ and PCDD/F+DL-PCB-TEQ. The bioassay limit of detection was 0.1 pg TEQ from 1 g animal lipid, the limit of quantification was 0.4 pg TEQ. The repeatability of the CALUX bioassay (variability of butter fat samples analysed in the same run) showed a coefficient of variation (CV) of 10%, intra laboratory reproducibility based on independent runs of the same butter fat samples showed more variation (CV of 26% for samples above 2 pg TEQ/g lipid). All milk samples with a chemical TEQ value above the current limit value in Belgium showed an elevated CALUX-TEQ concentration, above 6 pg TEQ/g lipid. No false negative results were obtained. Based on the good correlation between CALUX-TEQ and chemically measured TEQ levels, the CALUX bioassay can be recommended as a screening tool for routine measurement of potentially toxic PHAHs in milk samples. Chemical analyses could then largely be restricted to positive samples, in order to identify the nature and to quantify the concentration of the chemicals that give the positive signal. Meat samples showed lower CALUX-TEQ values per gram lipid compared to fish samples. The fish samples showed a wider range of CALUX-TEQ values than the meat samples.

Belgium↗
PubMed2000

Prediction of the retentions of polybrominated dibenzo-p-dioxins (PBDDs) by using the retentions of polychlorinated dibenzo-p-dioxins (PCDDs).

The retention equations In k' = A + B/T of 49 polychlorinated dibenzo-p-dioxins (PCDDs) and 4 polybrominated dibenzo-p-dioxins (PBDDs) in gas chromatography (GC) have been investigated to evaluate the properties of regression coefficients A and B. The quantitative relationships between A and B values of PCDDs and those of PBDDs are found. The regression equations derived have correlation coefficients greater than 0.997. The A, B values of any PBDD can be predicted by using the A, B values of the PCDD according to these relationships. Using these predicted A and B values, the retention times of all PBDDs can be predicted at any temperature program. It is very useful to identify the peak position of any PBDD because at present there are only a few standards of PBDDs available.

Bromine Compounds↗
PubMed1984

A screening assay for the tetrachlorodibenzo-p-dioxin receptor using the [125I]iodovaleramide derivative of trichlorodibenzo-p-dioxin as the binding ligand.

A relatively simple assay method for the putative cytosolic 'receptor' that binds 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds is described. The assay is based on specific binding of [125I]dioxin to cytosol 'receptor' protein. Saturation is ensured by competition experiments in which unlabeled TCDD and other competitors displace the radiolabeled ligand from specific binding sites. This assay has been applied to estimation of levels of 'receptor' in cytosol.

Animals↗
PubMed1988

Organ-specific effects of long term feeding of 2,3,7,8-tetrachlorodibenzo-p-dioxin and 1,2,3,7,8-pentachlorodibenzo-p-dioxin on I-compounds in hepatic and renal DNA of female Sprague-Dawley rats.

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a potent hepatocarcinogen, and 1,2,3,7,8-pentachlorodibenzo-p-dioxin (PCDD) on liver and kidney DNA of female Sprague-Dawley rats were investigated by 32P-post-labeling assay. The compounds were administered by gavage [1 microgram/kg/week in corn oil (5 ml/kg)] to the animals for up to 6 months. No exposure-related 32P-labeled spots indicative of TCDD or PCDD covalent DNA adducts were noted on the chromatograms of kidney or liver DNA nucleotides from the rats exposed to the toxins for 2 and 6 months. Corn-oil treated control animals exhibited the characteristic tissue- and age-specific patterns of 32P-labeled I-spots in liver and kidney DNA which are associated with specific DNA modifications of unknown origin and function. Treatment with either TCDD or PCDD resulted in a substantial reduction of the levels of I-compounds in liver, a target organ for TCDD carcinogenesis. After 6 months of exposure to TCDD the reductions in the amounts of individual hepatic I-compounds ranged from 37 to 77% and decreased levels were also observed after 2 months of treatment. It was apparent that PCDD was not as effective as TCDD in reducing hepatic I-compound levels and this corresponded with the lower aryl hydrocarbon receptor binding activity of the former compound. In contrast, TCDD and PCDD did not cause any significant decrease of I-compounds in the kidney which is not a site of TCDD-mediated carcinogenicity in female Sprague-Dawley rats. Whether I-compound deficiency contributes to TCDD-mediated hepatocarcinogenesis (e.g. by facilitating DNA replication) needs to be investigated.

Aging↗
PubMed2002

Degradation of 2,7-dichlorodibenzo-p-dioxin by wood-rotting fungi, screened by dioxin degrading ability.

One hundred thirty-six strains of wood-rot fungi (74 strains, 66 species of 19 genera, and 62 unidentified strains) were screened for the dibenzo-p-dioxin (DD) decreasing activity. It was observed that 20% of additional DD (1 micromol) disappeared in the cultures of eight strains belonging to four genera (Aleurodiscus (one strain), Ceriporia (one strain), Phanerochaete (one strain), Phlebia (five strains)) and four unidentified strains. These 12 fungal strains were used for the examination of the degradation of [U-14C]2,7-dichlorodibenzo-p-dioxin (2,7-diCDD). The fungi unidentified strain MZ-227, Phlebia sp. MG-60 and Phlebia lindtneri showed higher cumulative 14CO2 evolution rates than the other nine fungi. MZ-227, Phlebia sp. MG-60, and P. lindtneri converted 250 nmol of 2,7-diCDD to 196, 155 and 149 nmol of 14CO2, respectively, during a 30-day incubation period

Biodegradation, Environmental↗
PubMed1999

Removal of dibenzofuran, dibenzo-p-dioxin, and 2-chlorodibenzo-p-dioxin from soils inoculated with Sphingomonas sp. strain RW1.

Removal of dibenzofuran, dibenzo-p-dioxin, and 2-chlorodibenzo-p-dioxin (2-CDD) (10 ppm each) from soil microcosms to final concentrations in the parts-per-billion range was affected by the addition of Sphingomonas sp. strain RW1. Rates and extents of removal were influenced by the density of RW1 organisms. For 2-CDD, the rate of removal was dependent on the content of soil organic matter (SOM), with half-life values ranging from 5.8 h (0% SOM) to 26.3 h (5.5% SOM).

Benzofurans↗
PubMed2004

Dioxin revisited: developments since the 1997 IARC classification of dioxin as a human carcinogen.

In 1997 the International Agency for Research on Cancer (IARC) classified 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; the most potent dioxin congener) as a group 1 carcinogen based on limited evidence in humans, sufficient evidence in experimental animals, and extensive mechanistic information indicating that TCDD acts through a mechanism involving the aryl hydrocarbon receptor (AhR), which is present in both humans and animals. The judgment of limited evidence in humans was based primarily on an elevation of all cancers combined in four industrial cohorts. The group 1 classification has been somewhat controversial and has been challenged in the literature in recent years. In this article we review the epidemiologic and mechanistic evidence that has emerged since 1997. New epidemiologic evidence consists primarily of positive exposure-response analyses in several of the industrial cohorts, as well as evidence of excesses of several specific cancers in the Seveso accident cohort. There are also new data regarding how the AhR functions in mediating the carcinogenic response to TCDD. The new evidence generally supports the 1997 IARC classification.

Accidents, Occupational↗
PubMed1975

[Similarities in the biochemical effects of tetrachloro 2,3,7,8 dibenzo-p-dioxin and tetrabromo-2,3,7,8 dibenzo-p-dioxin on rats].

Screening tests for the study of carcinogenic compounds showed that 2,3,7,8-tetrabromodibenzo-p-dioxin was at least as active as 2,3,7,8-tetrachlorodibenzo-p-dioxin in regard to its effect on the in vivo synthesis of zoxanzolamine hydroxylase and on the arginase activity of the liver. The biological properties of these compounds seem to be due to the symmetry of their m molecular structure.

Animals↗
PubMed1996

Potency of a complex mixture of polychlorinated dibenzo-p-dioxin, dibenzofuran, and biphenyl congeners compared to 2,3,7,8-tetrachlorodibenzo-p-dioxin in causing fish early life stage mortality.

Use of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) toxicity equivalents concentration (TEC) assumes that polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and biphenyls (PCBs) act additively and via a common mechanism to cause toxicity. To test these assumptions, 11 TCDD-like congeners and three non-TCDD-like congeners were combined at ratios typically found in Lake Michigan lake trout. The potency of the mixture, expressed as TEC based on fish-specific toxic equivalency factors, was compared to TCDD for producing lake trout and rainbow trout early life stage mortality. Signs of toxicity following exposure of newly fertilized eggs to the mixture or to TCDD were indistinguishable; sac fry mortality associated with blue-sac disease, and slopes of the dose-response curves for percentage sac fry mortality versus egg TEC or versus egg TCDD were parallel. However, the mixture dose-response curves were significantly shifted to the right of the TCDD dose-response curves by 1.3- and 1.8-fold as illustrated by LD50 values. Following exposure to the mixture or TCDD, LD50S for lake trout early life stage mortality were 97 (89-110) pg TE/g egg and 74 (70-80) pg TCDD/g (LD50, 95% fiducial limits) and for rainbow trout were 362 (312-406) pg TE/g egg and 200 (148-237) pg TCDD/g egg. These data suggest that TCDD-like congeners act via a common mechanism to cause toxicity during trout early development, but may not act strictly additively when combined in a mixture of TCDD- and non-TCDD-like congeners at ratios found in Great Lakes fish. The deviation from additivity, however, is less than current safety factors of 10-fold commonly applied in ecological risk assessments, providing support for the continued use of a TE additivity model for assessing risk posed by complex mixtures of PCDDs, PCDFs, and PCBs to fish.

Animals↗
PubMed1994

Inhibition of intercellular communication by 2,3,7,8-tetrachlorodibenzo-p-dioxin and dioxin-like PCBs in mouse hepatoma cells (Hepa1c1c7): involvement of the Ah receptor.

The effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) and the coplanar 3,3',4,4'-tetrachlorobiphenyl (3,3',4,4'-TCB) and 3,3',4,4',5,5'-hexachlorobiphenyl (3,3',4,4',5,5'-HCB) on intercellular communication (IC) were determined in order to investigate the in vitro tumor promoting potency of these compounds. 2,3,7,8-TCDD and the two coplanar PCBs tested caused a rapid (2 hr) and a sustained inhibition (48 hr) of IC in the mouse hepatoma cell line (Hepa1c1c7) to 20 and 50% of the unexposed control, respectively. Inhibition of IC was dose dependent with an EC50 range of about 50-100 pM for 2,3,7,8-TCDD, 2-5 nM for 3,3',4,4'-TCB, and 10-15 nM for 3,3',4,4',5,5'-HCB, respectively. A comparison of the IC inhibitory effects of 2,3,7,8-TCDD and PCBs with a well-known aryl hydrocarbon receptor (AhR)-mediated response, the induction of ethoxyresorufin O-deethylase (EROD) activity, in the same cells revealed EROD induction by 2,3,7,8-TCDD, 3,3',4,4'-TCB, and 3,3',4,4',5,5'-HCB with EC50 ranges of 100-200 pM, 20-70 nM, and 5-10 nM, respectively. The time course of IC inhibition was paralleled by EROD induction, although the time of onset of the response was earlier for IC (1 hr) than for EROD (2.5 hr). A role of the AhR in the inhibition of IC by 2,3,7,8-TCDD and PCBs was demonstrated by the lack of inhibition in AhR-defective Hepa1c1c7 cells. Transient inhibition of IC was observed in the mutant cells only at early time points (within 2 hr of exposure). These results and the observation that alpha-naphtoflavone (an AhR antagonist) greatly reduced the 2,3,7,8-TCDD-dependent sustained inhibition of IC strongly support a role of the AhR in the sustained inhibition of IC by these compounds. Furthermore, these data suggest that the mouse Hepa1c1c7 cells may be a good model in which to study in vitro tumor promoting capacity of dioxins, PCBs, and related compounds.

Animals↗
PubMed1996

Quantitative analysis of enzyme-altered liver foci in rats initiated with diethylnitrosamine and promoted with 2,3,7,8-tetrachlorodibenzo-p-dioxin or 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin.

A quantitative method based upon a stochastic model was used to estimate rates of initiation (alteration to express the ATPase-deficient phenotype) and of clonal growth of altered cells in an initiation promotion experiment in the livers of female Wistar rats. Diethylnitrosamine (DEN) was used as the initiating agent followed by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (HCDD) as promoters. Two distinct versions of the stochastic model, called Model I and Model II, were fitted to the data. Model I made the assumption that, after the initial phase of acute initiation with DEN, background rates of initiation were equal in animals treated with DEN and controls that were not so treated. Model II, which fit the data substantially better than Model I, assumed that background rates of initiation were different in DEN-treated animals and animals not so treated, even after the acute phase of initiation was over. Both models indicate that the rates of cell division and apoptosis of altered cells are increased during TCDD treatment. In contrast, the rate of division remains more or less constant during treatment with HCDD, but the rate of apoptosis is decreased. The background rate of initiation during treatment with HCDD is equal to that in controls not administered promoters. With TCDD treatment, however, the rate of initiation estimated from the model is substantially increased over controls. The analysis also suggests that there is heterogeneity within foci of the rates of cell division, with cells on the surface of foci dividing faster than cells in the interior.

Adenosine Triphosphatases↗
PubMed2001

Development of a reference material for routine performance monitoring of methods measuring polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans and dioxin-like polychlorinated biphenyls.

Matrix-matched environmental certified reference materials (CRMs) are one of the most useful tools to validate analytical methods, assess analytical laboratory performance and to assist in the resolution of data conflicts between laboratories. This paper describes the development of a lake sediment as a CRM for polychorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs) and dioxin-like polychlorinated biphenyls (DLPCBs). The presence of DLPCBs in the environment is of increased concern and analytical methods are being developed internationally for monitoring DLPCBs in the environment. This paper also reports the results of an international interlaboratory study involving thirty-five laboratories from seventeen countries, conducted to characterize and validate levels of a sediment reference material for PCDDs, PCDFs and DLPCBs.

Benzofurans↗
PubMed1990

Arachidonic acid metabolism by dioxin-induced cytochrome P-450: a new hypothesis on the role of P-450 in dioxin toxicity.

Dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD) is a highly potent inducer of cytochrome P-450. The role of the induced P-450 in TCDD toxicity has been obscure as P-450 neither detoxifies TCDD nor activates it to genotoxic or cytotoxic metabolites. We show, using a chick embryo model, that TCDD causes major increases in the NADPH dependent metabolism of arachidonic acid (AA), a predominant cell membrane fatty acid, that it does so with extremely high potency (ED50, 6.3 pmol per egg) and that this metabolism is catalyzed by TCDD-induced cytochrome P-450 species. Thus, TCDD treatment increased by six to ten fold the P-450 mediated hepatic microsomal metabolism of AA to epoxides and monohydroxyeicosatetraenoic acids, products whose diverse biological activities suggest links to TCDD's toxic effects. In contrast only x and x-1 hydroxy AA, inactive products, were significantly formed by the controls. These findings open a new perspective on how P-450 induction could be related to the diverse toxic effects of TCDD. They lead to the novel hypothesis that TCDD-induced cytochrome P-450 metabolizes an endogenous fatty acid to reactive products that in turn mediate or modulate varied manifestations of TCDD toxicity.

Animals↗
PubMed2004

Separation of seventeen 2,3,7,8-substituted polychlorinated dibenzo-p-dioxins and dibenzofurans and 12 dioxin-like polychlorinated biphenyls by comprehensive two-dimensional gas chromatography with electron-capture detection.

Comprehensive two-dimensional gas chromatography (GC x GC) with electron-capture detection (ECD) has been optimized for the separation of seventeen 2,3,7,8-substituted polychlorinated dibenzo-p-dioxins and dibenzofurans and 12 dioxin-like polychlorinated biphenyls, with emphasis on the selection of the first- and second-dimension, commercially available, columns. When eight second-dimension columns were subsequently combined with a 100% methylpolysiloxane stationary phase (DB-1) in the first dimension to create orthogonal conditions, a complete separation of all congeners with different TEF values was obtained with two column combinations, DB-1 x VF-23 and DB-1 x LC-50. When other types of first-dimension columns were used (and orthogonality was partly sacrificed), a DB-XLB column combined with 007-65HT, VF-23 and LC-50 was found to provide a complete separation of all 29 priority congeners. Next, the potential of these three column combinations for real-life analysis was preliminarily studied. With a spiked and fractionated milk extract, DB-XLB x LC-50 was found to be the most powerful column combination, because of the good separation of the 29 priority congeners from each other as well as from the matrix constituents. Quantitative performance (close to three-order linearity; LODs, 30-150 fg injected; R.S.D.s, 1.5-6.5% (n = 10)) was satisfactory.

Benzofurans↗
PubMed2006

Quantitative relationship of dioxin-responsive gene expression to dioxin response element in Hep3B and HepG2 human hepatocarcinoma cell lines.

Dioxin response element (DRE) is a cis-acting DNA sequence mediating the 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced gene expression. The present study was undertaken to elucidate TCDD-responsive gene expression profiles and their relationships to the number of DREs in liver cancer cells. Hep3B and HepG2 human hepatocarcinoma cells were exposed to 50-nM TCDD for 0, 1, 2 and 4h in culture, after which gene expression profiles were analyzed by the microarray hybridization using a chip containing 24,000 cDNAs prepared from the human liver. The TCDD-responsive expression levels in each gene were calculated by dividing the densitometric values of the hybridization signal for h1, h2 and h4 by that of h0, followed by transformation of the resulting data into a log scale with the base of 2. Up- and down-regulated gene expressions were defined as >0.585 and <-0.585 by the log scale (>1.5 and <1/1.5 arithmetically), respectively, exhibited at any time after h0. Hep3B and HepG2 cells had 27 and 58 TCDD-responsive, up-regulated genes, respectively, of which 78% (21/27) and 62% (36/58) had one or more DREs. Of these 85, 80 genes were up-regulated exclusively in one of the two lines, with CYP1A1 and PPP1R15A being so regulated in both lines. Expression levels of the up-regulated genes at h1, h2 and h4 were correlated with each other (P<0.01) and the mean of these regressed to the number of DRE(s) in both lines (P<0.01). However, expression of a total of 93 TCDD-responsive, down-regulated genes, of which 46% contained DRE(s), had no relation to the number of DRE(s). In conclusion, results suggest that DREs may cooperatively mediate the expression of TCDD-responsive genes in liver cancer cells.

Antigens, Differentiation↗
PubMed2002

Levels of polychlorinated dibenzo-p-dioxins and dibenzofurans in food of animal origin. The Swiss dioxin monitoring program.

Between 1997 and 1999, several cases of dioxin contaminations in foodstuffs of animal origin occurred in Europe due to feed contaminated by several independent sources: citrus pulp pellets, fat containing polychlorinated biphenyls (PCB), and kaolinitic clay as anti-caking agent in feedingstuffs. As a consequence of the latter, a survey on polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/F) in food of animal origin was initiated by the Swiss authorities to assess the extent of PCDD/F contamination and to document the efficiency of the measures taken to ensure the decontamination of the food supply. Investigation of a total of 128 samples of cow's milk, poultry, eggs, and meat revealed several cases of residue levels distinctly above the background exposure limit of approximately 2.5 ng of I-TEQ/kg (fat basis). Particularly, elevated concentrations were found in eggs (maximum 13 ng of I-TEQ/kg), poultry (maximum 3.9 ng of I-TEQ/kg), and pork (maximum 7.5 ng of I-TEQ/kg). On the basis of the observed PCDD/F congener pattern, the contamination could be attributed to PCDD/F-contaminated kaolin that was used as an anti-caking agent in particular feedstuffs.

Animal Feed↗
PubMed2001

Dioxin detection based on immunoassay using a polyclonal antibody against octa-chlorinated dibenzo-p-dioxin (OCDD).

An enzyme-linked immunosorbent assay (ELISA) using a polyclonal antibody against octa-chlorinated dibenzo-p-dioxin (OCDD) is presented. This method is based on a competitive reaction between OCDD and OCDD-HRP (horseradish peroxidase) conjugate against the antibody, whereby OCDD-HRP is detected colorimetrically at 450 nm. The detection limit of OCDD was 0.78 pg mL(-1). Optimizing the reaction conditions of the assay, cross reactivities of some dioxins against the antibody are discussed.

Antibodies, Monoclonal↗