The reliability of 2,3,7,8-tetrachlorodibenzo-p-dioxin and toxicity equivalence measurements in Missouri residents

This study evaluates the reliability of serum measurements of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and toxicity equivalence (TEQ) in individuals with no prior exposure to TCDD or dioxin-like compounds above background levels. Reliability was measured over three time-periods in the same individuals. TCDD and TEQ were measured in 127 and 128 participants. The values declined during the testing periods. Reliability coefficients for TCDD was 0.69 and for TEQ 0.91 but increased to 0.79 and 0.92, respectively, after removal of three outlying cases. Study results show good reliability over 22 months suggesting a consistency in the uptake and excretion of TCDD and other dioxin-like compounds.     

Concentrations of dioxin-like PCB congeners in unweathered Aroclors by HRGC/HRMS using EPA Method 1668A

We have determined the congener compositions of nine commercial Aroclor products of polychlorinated biphenyls (PCBs) to the sub-part-per-million level using high-resolution gas chromatography combined with high-resolution mass spectrometry according to US Environmental Protection Agency (EPA) Method 1668A. These Aroclor composition data should allow improved characterization and risk assessment of PCB contamination at hazardous waste sites, particularly for dioxin-like PCB congeners. By combining the data on the concentrations of each dioxin-like congener with its World Health Organization toxicity equivalency factor, we have established dioxin toxic equivalent concentrations for each pure Aroclor product.     

Dioxin incinerator emissions exposure study Times Beach, Missouri

PURPOSE: To determine whether living in the vicinity of a hazardous waste incinerator that was burning material contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increased TCDD and toxicity equivalencies (TEQ) in individuals living near the incinerator. METHODS: Participants were randomly chosen from an area close to the incinerator and compared to participants outside of the exposure area. TCDD and related compounds were measured in blood serum before incineration, four months after incineration started, and at the end of incineration. RESULTS: Lipid adjusted serum levels of TCDD and TEQ decreased from pre-incineration to four months after incineration, and decreased further by the end of incineration. CONCLUSION: Incineration of TCDD did not result in any measurable exposure to the population surrounding the incinerator.     

Predicting the sensitivity of fishes to dioxin-like compounds: possible role of the aryl hydrocarbon receptor (AhR) ligand binding domain

Dioxin-like compounds are chronically toxic to most vertebrates. However, dramatic differences in sensitivity to these chemicals exist both within and among vertebrate classes. A recent study found that in birds, critical amino acid residues in the aryl hydrocarbon receptor (AhR) ligand binding domain are predictive of sensitivity to dioxin-like compounds in a range of species. It is currently unclear whether similar predictive relationships exist for fishes, a group of animals at risk of exposure to dioxin-like compounds. Effects of dioxin-like compounds are mediated through the AhR in fishes and birds. However, AhR dynamics are more complex among fishes. Fishes possess AhRs that can be grouped within at least three distinct clades (AhR1, AhR2, AhR3) with each clade possibly containing multiple isoforms. AhR2 has been shown to be the active form in most teleosts, with AhR1 not binding dioxin-like compounds. The role of AhR3 in dioxin-like toxicity has not been established to date and this clade is only known to be expressed in some cartilaginous fishes. Furthermore, multiple mechanisms of sensitivity to dioxin-like compounds that are not relevant in birds could exist among fishes. Although, at this time, deficiencies exist for the development of such a predictive relationship for application to fishes, successfully establishing such relationships would offer a substantial improvement in assessment of risks of dioxin-like compounds for this class of vertebrates. Elucidation of such relationships would provide a mechanistic foundation for extrapolation among species to allow the identification of the most sensitive fishes, with the ultimate goal of the prediction of risk posed to endangered species that are not easily studied.     

Dioxin-like potencies and extractable organohalogens (EOX) in medical, municipal and domestic waste incinerator ashes in Japan

Ash samples collected from medical, municipal and small-scale domestic incinerators in Japan were tested for dioxin-like activity using bioassay technique (ethoxyresorufin-O-deethylase: EROD assay) and for extractable organohalogens (EOX) using instrumental neutron activation analysis in order to estimate potential toxicity and responsible chemicals in those samples. Crude extracts and fractions cleaned-up for dioxin analysis from the samples were used for the analysis. The ranges of dioxins in the ashes were between 2.23 and 12.29 ng TEQ/g (dry weight). Relative potency ranges estimated by EROD assay in the medical incinerator ashes were 3.8-17.6 times higher than the results of conventional chemical analysis. EOX analysis suggested that ash samples contained plenty of organochlorine compounds apart from chlorinated dioxins. In addition, medical waste incinerator ashes were considered to have relatively higher amount of organoiodine compounds. In the cleaned-up fractions, bioassay potency ranges were lower than those in the crude extracts. However, some samples still exhibited higher potency than expected from chemical analysis. Though some polycyclic aromatic hydrocarbons were found in the fractions, the amounts were relatively low (0.39-10.56 ng/g). The results imply that some bioactive organohalogens that cannot be detected in the conventional chemical analysis might have potential for dioxin-like toxicity, and contribute to higher bioassay activities. The combination of the chemical analysis with the bioassay and EOX provides rough figure of dioxin-like toxicity and suggests types of organohalogen compounds that should be identified as a part of dioxin analysis for control emission from an incineration plant.     

A technical mixture of 2,2',4,4'-tetrabromo diphenyl ether (BDE47) and brominated furans triggers aryl hydrocarbon receptor (AhR) mediated gene expression and toxicity

Polybrominated diphenyl ethers (PBDE) are found as ubiquitous contaminants in the environment, e.g., in sediments and biota as well as in human blood samples and mother's milk. PBDEs are neuro- and developmental toxins, disturb the endocrine system and some are even carcinogenic. Structural similarities of PBDEs with dioxin-like compounds, e.g., 2,3,7,8-tetrachloro-dibenzodioxin (TCDD), have raised concern about a possible "dioxin-like" action of PBDEs. TCDD exerts its toxicity via binding to and activation of the aryl hydrocarbon receptor (AhR). AhR ligands are in contrast to PBDEs usually coplanar compounds. Thus, PBDEs are not likely to be strong AhR agonists. The aim of this study was to analyze the effects of the most abundant PBDE congener, 2,2',4,4'-tetrabromo diphenyl ether (BDE47), on AhR activity and signaling. Initially, we measured cytochrome P450 1A1 (Cyp1A1) induction as a readout for AhR activation by BDE47. Low grade purified BDE47 increased CYP1A1 levels in transformed and primary rat hepatocytes and human hepatoma cells. Chemical analysis of the BDE47 sample identified trace contaminations with brominated furans such as 2,3,7,8-tetrabromo dibenzodioxin (TBDF), which most likely were responsible for the observed activation of AhR. Subsequently, the BDE47 mixture was studied for its effect on AhR mediated toxicity and global gene expression. Indeed, in rat hepatoma cells and in zebrafish embryos the BDE47 mixture provoked changes in gene expression and toxicity similar to known AhR agonists. In addition to the dioxin-like actions, the BDE47 sample enhanced Cyp2B and Cyp3A expression suggesting that commercial PBDE mixtures, which also often contain brominated furans, may disturb cellular homeostasis at multiple levels.     

Fate of ah receptor agonists during biological treatment of an industrial sludge containing explosives and pharmaceutical residues

GOAL, SCOPE AND BACKGROUND: Sweden is meeting prohibition for deposition of organic waste from 2005. Since 1 million tons of sludge is produced every year in Sweden and the capacity for incineration does not fill the demands, other methods of sludge management have to be introduced to a higher degree. Two biological treatment alternatives are anaerobic digestion and composting. Different oxygen concentrations result in different microbial degradation pathways and, consequently, in a different quality of the digestion or composting residue, It is therefore necessary to study sludge treatment during different oxygen regimes in order to follow both degradation of compounds and change in toxicity. In this study, an industrial sludge containing explosives and pharmaceutical residues was treated with anaerobic digestion or composting, and the change in toxicity was studied. Nitroaromatic compounds, which are the main ingredients of both pharmaceutical and explosives, are well known to cause cytotoxicity and genotoxicity. However, little data are available concerning sludge with nitroaromatics and any associated dioxin-like activity. Therefore, we studied the sludge before and after the treatments in order to detect any changes in levels of Ah receptor (AhR) agonists using two bioassays for dioxin-like compounds. METHODS: An industrial sludge was treated with anaerobic digestion or composting in small reactors in a semi-continuous manner. The same volume as the feeding volume was taken out daily and stored at -20 degrees C. Sample preparation for the bioassays was done by extraction using organic solvents, followed by clean up with silica gel or sulphuric acid, yielding two fractions. The fractions were dissolved in DMSO and tested in the bioassays. The dioxin-like activity was measured using the DR-CALUX assay with transfected H4IIE rat hepatoma pGudluc cells and an EROD induction assay with RTL-W1 rainbow trout liver cells. RESULTS AND DISCUSSION: The bioassays showed that the sludge contained AhR agonists at levels of TCDD equivalents (TEQs) higher than other sludge types in Sweden. In addition, the TEQ values for the acid resistant fractions increased considerably after anaerobic digestion, resulting in an apparent formation of acid resistant TEQs in the anaerobic reactors. Similar results have been reported from studies of fermented household waste. There was a large difference in effects between the two bioassays, with higher TEQ levels in the RTL-W1 EROD assay than in the DR-CALUX assay. This is possibly due to a more rapid metabolism in rat hepatocytes than in trout hepatocytes or to differences in sensitivities for the AhR agonists in the sludge. It was also demonstrated by GC/FID analysis that the sludge contained high concentrations of nitroaromatics. It is suggested that nitroaromatic metabolites, such as aromatic amines and nitroanilines, are possible candidates for the observed bioassay effects. It was also found that the AhR agonists in the sludge samples were volatile. CONCLUSIONS: The sludge contained fairly high concentrations of volatile AhR agonists. The increase of acid resistant AhR agonist after anaerobic digestion warrants further investigations of the chemical and toxic properties of these compounds and of the mechanisms behind this observation. RECOMMENDATION AND OUTLOOK: This study has pointed out the benefits of using different types of mechanism-specific bioassays when evaluating the change in toxicity by sludge treatment, in which measurement of dioxin-like activity can be a valuable tool. In order to study the recalcitrant properties of the compounds in the sludge using the DR-CALUX assay, the exposure time can be varied between 6 and 24 hours. The properties of the acid-resistant AhR agonists formed in the anaerobic treatment have to be investigated in order to choose the most appropriate method for sludge management.     

Six interaction profiles for simple mixtures

The Agency for Toxic Substances and Disease Registry (ATSDR) has a program for chemical mixtures that encompasses research on chemical mixtures toxicity, health risk assessment, and development of innovative computational methods. ATSDR prepared a guidance document that instructs users on how to conduct health risk assessment on chemical mixtures (Guidance Manual for the Assessment of Joint Toxic Action of Chemical Mixtures). ATSDR also developed six interaction profiles for chemical mixtures. Two profiles were developed for persistent environmental chemicals that are often found in contaminated fish and also can be detected in human breast milk. The mixture included chlorinated dibenzo-p-dioxins, hexachlorobenzene, dichlorodiphenyl dichloroethane, methyl mercury, and polychlorinated biphenyls. Two profiles each were developed for mixtures of metals and mixtures of volatile organic chemicals (VOCs) that are frequently found at hazardous waste sites. The two metal profiles dealt with (a) lead, manganese, zinc, and copper; and (b) arsenic, cadmium, chromium, and lead; the two VOCs mixtures dealt with (a) 1,1,1-trichloroethane, 1,1-dichloroethane, trichloroethylene, and tetrachloroethylene; and (b) benzene, ethylbenzene, toluene, and xylenes (BTEX). Weight-of-evidence methodology was used to assess the joint toxic action for most of the mixtures. Physiologically based pharmacokinetic modeling was used for BTEX. In most cases, a target-organ toxicity dose modification of the hazard index approach is recommended for conducting exposure-based assessments of noncancer health hazards.     

Dioxin-like compounds in Australian sewage sludge--review and national survey

An Australian survey of dioxin-like compounds in sewage sludge was conducted in two parts (a) a national survey, and (b) a time-study. All sewage sludge samples analysed as part of these studies had low overall concentrations of dioxin-like compounds. Out of 37 samples, all except one, were within the reported concentration range of soil within the Australian environment. The mean concentration of dioxin-like compounds in the Australian sewage sludge survey of 2006 was found to be 5.6 (s.d. 4.5) ng WHO(05) TEQkg(-1) (n=14) and were within the range of 1.2-15.3 ng WHO(05) TEQ kg(-1). All the Australian sewage sludge samples cited in these studies were below the Victorian EPA "investigation limit" of 50 ng WHO(98) TEQ kg(-1), and well below the European proposed guidelines of 100 ng I-TEQ kg(-1). The burden of dioxin-like compounds in Australian sewage sludge is low and its land application as biosolids is not likely to pose a problem. A general positive relationship was found between population of the town producing the waste and both dioxin-like PCDD/Fs and dioxin-like PCBs. The one exception to this trend was sludge from a town that had a history of smelting and had a relatively high burden of dioxin-like compounds. Sludge from one rural WWTP also had a higher burden of dioxin-like compounds. The treatment plant services a geographically isolated town with a low population and no known emitters of dioxin-like compounds. However, this sample also had a relatively high burden of dioxin-like PCBs, which could be the source of the dioxin-like PCDD/Fs found in this sludge. The time study analyzing sludges from three WWTP from the same city between the years 2002 and 2006 found no apparent difference between WWTPs, but a statistically significant decline of 1.49 ng WHO(05) TEQ kg(-1) per year. Also, a comprehensive review of the scientific literature, presents typical levels and sources of dioxin-like compounds in international sewage sludges.     

Levels of hexachlorobenzene and other organochlorine compounds in cord blood: exposure across placenta

Hexachlorobenzene (HCB) is an organochlorine compound widespread in the environment, highly lipophilic, that accumulates in biological systems. It has been suggested that it should be classified as a dioxin-like compound. Newborns are exposed to organochlorine compounds across the placenta and through breastfeeding. Although HCB is one of the most common organochlorine compounds, the transplacental transference of HCB from mother to fetus during pregnancy has been scarcely documented. This study reports the levels of HCB, dichlorodiphenyl trichloroethane (DDT) and its metabolite p,p'DDE, polychlorinated biphenyls (PCBs), and beta-hexachlorocyclohexane (beta-HCH) in 72 maternal blood samples at delivery and in 69 cord blood samples, from which 62 corresponded to mother infant pairs born between May 1997 and September 1999 in a rural area highly exposed to HCB. Results show that all newborns presented detectable levels of HCB, PCBs, and p,p'DDE, and, to a lesser extent, of beta-HCH, the HCB levels being the highest. The geometric mean of HCB was 1.1 ng/ml, ranging from 0.3 to 5.7 ng/ml. Concentrations of HCB levels in cord blood (log ng/ml) were positively associated with concentrations in maternal blood (log ng/ml) (coefficient = 0.45, P < 0.01). Gestational age was not associated with the transplacental transfer of HCB. Maternal p,p'DDE and beta-HCH levels were also associated with newborn levels, but levels of PCBs were not. We conclude that HCB, similar to other organochlorinated compounds, has a transplacental transfer.     

Development of human dermal epithelial cell-based bioassay for the dioxins

None of bioassays is complete for assessing biological impact in humans upon the xenobiotic exposure due to species and organ-specific responsiveness. Thus, it is speculated that the human cell-based bioassay may be more appropriate system because of its direct relevance to humans. Here, we have developed a human epidermal cell-based bioassay for the dioxins and related compounds. The AD12-SV40-immortalized human keratinocyte cell line was stably transfected with a recombinant expression vector which contains the luciferase gene under dioxin-inducible control of four DREs. The tansfectants showed a consistent dose-response of luciferase activity upon dioxin exposure even after 120 passages. The maximal half effective dose (EC50) was 200 pM with a maximum of 32-fold induction of luciferase activity at 5 nM. The minimum detection limit was 10 pM. Optimal exposure time for the assay was 24h. When cells were treated with aryl hydrocarbon receptor agonists of different toxic equivalent factor (TEF) values, the shape of the dose-response curve for each compound was parallel to that of TCDD and the maximum response was similar, indicating that this bioassay system can be applied to generate the total toxic equivalency (TEQ) estimate from the samples. When relative induction potency of luciferase activities for each compound was calculated, it was similar to WHO-TEF values within an order of magnitude. This human cell system can be used as an efficient screening tool to quantify the TEQ values of dioxin-like chemicals in the samples and may help understand the interspecies difference between humans and animals.     

Revised relative potency values for PCDDs, PCDFs, and non-ortho-substituted PCBs for the optimized H4IIE-luc in vitro bioassay

While the World Health Organization 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) equivalency factors are useful estimates of relative potencies of mixtures when conducting risk assessments, they are not useful when comparing the results of bioassays such as the H4IIE-luc to concentrations of TCDD equivalents calculated from instrumental analyses. Since there are thousands of dioxin-like compounds (DLCs), one use of screening assays is to determine if all of the aryl hydrocarbon receptor (AhR) active DLCs in a mixture have been accounted for in instrumental analyses. For this purpose, bioassay-specific relative potency (ReP) values are needed. RePs of 21 polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, and dioxin-like polychlorinated biphenyls that exhibit effects mediated through the AhR were determined by use of the H4IIE-luc assay. Different values of RePs are derived, depending on the statistical, curve-fitting methods used to derive them from the dose–response relationships. Here, we discuss the various methods for deriving RePs from in vitro data and their assumptions and effects on values of RePs. Full dose–response curves of 2,3,7,8-TCDD and other representative DLCs were used to estimate effective concentrations at multiple points (e.g., EC20-50-80), which were then used to estimate ReP of each DLC to 2,3,7,8-TCDD.     

Systematic analysis and overall toxicity evaluation of dioxins and hexachlorobenzene in human milk

A systematic method for analyzing dioxins (PCDDs, PCDFs and dioxin-like PCBs), hexachlorobenzene (HCB), heptachlor epoxide and beta-hexachlorocyclohexane (HCH) in human milk was developed to determine the residual amount of HCB in human milk and to evaluate the overall toxicity of both dioxins and HCB in human milk. The fractionation behavior of HCB on chromatography with silica gel, alumina, and activated carbon/silica gel, and the concentrated sulfuric acid decomposition method, which is widely used as a dioxin cleanup method, were studied in order to make the preprocessing operation for HCB measurement compatible with that for conventional dioxin measurement. HCB was found to be eluted in the 2% dichloromethane (DCM)/hexane 60 ml fraction from an alumina column. Heptachlor epoxide and a part of beta-HCH were eluted in the 10% DCM/hexane 50 ml fraction from a silica gel column, while the remaining beta-HCH was eluted in the 25% DCM/hexane 60 ml fraction from an activated carbon/silica gel column. Moreover, HCB showed significant correlation with dioxin congeners having high toxicity equivalence factors (TEFs). The results suggest that the exposure route to HCB and its accumulation behavior in the human body are similar to those of the dioxins.     

Evaluation of age, gender and regional concentration differences for dioxin-like chemicals in the Australian population

The results of this study provide a measure of the levels of dioxin-like compounds (polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans and polychlorinated biphenyls) in pooled blood serum collected throughout Australia in 2003. De-identified samples selected from surplus pathology samples were stratified on the basis of gender, region and age. In total 9090 samples were collected and analysed as 96 pools. Dioxin-like chemicals were detected in all strata. The mean and median levels expressed as TEQ values for all pooled samples were 10.9+/-1.0 pg TEQ g(-1) lipid and 8.3 pg TEQ g(-1) lipid. For males and females the mean levels were 10.4+/-0.6 pg TEQ g(-1) lipid and 11.5+/-1.5 pg TEQ g(-1) lipid, respectively. A direct relationship of increasing dioxin-like chemical levels with increasing age was observed and could be described by the following equation: Levels in blood expressed as pg TEQ g(-1) lipid = 3.3 exp(0.0251 age) (r2 = 0.87). No significant differences were observed in the levels of dioxin-like chemicals in samples collected from males and females. In addition, the levels of dioxin-like chemicals across the five regions were similar within each age range. In summary, the levels of dioxin-like chemicals in the Australian population are low compared to international levels and are similar across all regions of Australia within each designated age range. The levels of these chemicals increase with age and can be estimated if the age of an individual is known.     

Biomonitoring of persistent organochlorine pesticides, PCDD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993 to 2003

In the context of a monitoring program, persistent organic pollutants (POPs) were quantified in the blood of 10 year old children at four different demographic regions in Baden-Wuerttemberg, a highly industrialised federal state in South West Germany. DDE, HCB, PCB 138, PCB 153 and PCB 180 were measured in 1996/1997, 1998/1999, 2000/2001 and 2002/2003 in individual samples of about 400 children per year. PCDD/PCDFs and some relevant coplanar PCBs were determined in pooled samples from children in seven cycles from 1993 to 2003. Blood concentrations of the investigated compounds decreased in that time period by a factor of 2-4 with the exception of most PCDFs. The concentrations of POPs in the blood of the children were distinctly lower than the concentrations reported for adults. Breast feeding was associated with about 30% higher median concentrations of DDE, HCB, PCBs and a 30% increase for mean PCDD/PCDF concentrations. Concerning demographic differences, significant lower concentrations of HCB, PCBs and PCDD/PCDFs could be seen in children from Mannheim compared to the region of Aulendorf. About 10-20% higher concentrations were found in boys compared to girls for HCB, indicator PCBs and PCDD/PCDFs. The pattern of non-ortho and mono-ortho PCBs in the blood of children was similar to the pattern reported for mother's milk, and PCB 126 and PCB 156 contributed about 70% to the toxicity of dioxin-like PCBs and about one-third to total TEQ including PCDD/PCDFs.     

Congener-specific egg contribution of polychlorinated biphenyls to nestlings in two passerine species

Quantifying polychlorinated biphenyl (PCB) residues in nestlings of avian species is a common method for assessing trophic transfer and risk at PCB-contaminated sites. The proportion of nestling PCB mass due to maternal transfer is often accounted for by subtracting total PCB mass in eggs from nestlings. However, variation in physicochemical properties and metabolism among congeners may lead to differences between egg contribution based on total PCBs and dioxin-like congeners. We examined congener-specific variation in contribution of PCBs from eggs to nestlings in tree swallows and European starlings. Egg contribution of total PCB mass was 14.3 and 16.2%, respectively, whereas contribution based on dioxin-like congeners was 14.8 and 13.6%, respectively. These data suggest that using total PCB mass in eggs to adjust estimates of PCB accumulation in nestlings may not reflect patterns for dioxin-like congeners, potentially over or under-estimating the risk of toxicity of PCBs.     

A Comparison of Organic Emissions from Hazardous Waste Incinerators Versus the 1990 Toxics Release Inventory Air Releases

Incineration is often the preferred technology for disposing of hazardous waste and remediating Superfund sites. The effective implementation of this technology is frequently impeded by strong public opposition to hazardous waste incineration (HWI). One of the reasons cited for this opposition is the perception that the emission of organics pose an unreasonable threat to human health. While numerous risk assessments for these facilities have demonstrated that the risks from the inhalation of HWI emissions are very low, this has not totally allayed some of the concerns. In order to put organic emissions in perspective, the mass of these emissions from the incineration of hazardous waste on a national scale has been estimated using “reasonable worst-case” assumptions and compared to the 1990 Toxics Release Inventory (TRI) air releases. Comparisons were made for 15 carcinogenic organic compounds and 17 non-carcinogenic organic compounds. Ratios for all but one of these compound-specific HWI emissions to their corresponding TRI air releases ranged from 0.0003 to 0.678 percent. The total mass emissions (110.5 tons) of all 32 specific organics from HWIs was less than 0.03 percent of the corresponding 1990 TRI air releases (431,586 tons).     

Emission profiles of polychlorinated dibenzodioxins, polychlorinated dibenzofurans (PCDD/Fs), dioxin-like PCBs and hexachlorobenzene (HCB) from secondary metallurgy industries in Portugal

This paper reports, for the first time, a study of dioxin emissions from 10 siderurgies and metallurgies, secondary copper, aluminum and lead metallurgies, in Portugal. The study reports the emission factors and total emission amounts of PCDD/Fs, dioxin-like PCBs and hexachlorobenzene (HCB). The congener patterns were characterized and are discussed. The results showed that the total amount of PCDFs is higher than PCDDs in flue gas of each industrial unit. The toxic equivalent emission factors of pollutants emitted are 3098-3338 ngI-TEQt(-1) for PCDD/Fs and 597-659 ng I-TEQt(-1) for dioxin-like PCBs in siderurgies production (total estimated emission amounts released to atmosphere of 3.9-4.5 g I-TEQyr(-1)), 50-152 ng I-TEQt(-1) for PCDD/Fs and 24-121 ng I-TEQt(-1) for dioxin-like PCBs in ferrous foundries production (total estimated emission amounts released to atmosphere of 0.0010-0.0016 g I-TEQyr(-1)) and 5.8-5715 ng I-TEQt(-1) for PCDD/Fs and 0.49-259 ng I-TEQt(-1) for dioxin-like PCBs in non-ferrous foundries production (total estimated emission amounts released to atmosphere of 0.00014-0.12 g I-TEQyr(-1)). The HCB emission from siderurgies production is 0.94-3.2 mg t(-1) (total estimated emission amounts released 0.94-3.8 g yr(-1)), being much smaller, residual, in the emissions of the other types of plants (0.0012-0.026 mg t(-1) production and total estimated emission amounts released to atmosphere of 0.013-1.7 mg yr(-1)).     

The use of environmental risk assessment methodologies for an indoor air quality investigation

The authors of this paper chose several target compounds that have been found in average US homes, applied the current United States Environmental Protection Agency (USEPA) Superfund risk assessment methodologies to indoor air quality, and produced risk numbers for hazard quotients and predicted increases in incidence of cancer which would be unacceptable at US hazardous waste sites. The calculations were made for the average child and adult with USEPA default exposure values. Calculations were also made for a worst case scenario using maximum concentrations and exposure estimates defined by the USEPA as describing the reasonable exposure (RME). Significant cancer risks and non-cancer hazard quotients were predicted.     

Polychlorinated dibenzo-p-dioxins and dibenzofurans in marine mammals in the Canadian North

Polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) were determined in pooled samples of ringed seal (Phoca hispida) blubber, beluga (Delphinapterus leucas) blubber and polar bear (Ursus maritimus) liver and fat from several areas throughout the Canadian north and compared to mean PCB and HCB levels in the same samples. All seal samples, and all but one polar bear sample, had detectable 2,3,7,8-TCDD at concentrations ranging from 2 to 37 ng/kg, but TCDD was not found in beluga blubber (< 2 ng/kg). All seal samples and one of three beluga samples contained 2,3,7,8-TCDF at levels of 2 to 7 ng/kg, but TCDF was not found in any bear sample. TCDF must therefore be cleared rapidly by polar bears. No other PCDF congeners were found at detection limits of 4 to 8 ng/kg. OCDD concentrations in seal blubber and polar bear samples ranged from not detected (< 8 ng/kg) to 43 ng/kg. No apparent biomagnification of TCDD, OCDD or TCDF occurred from seal to bear fat, similar to previous findings for DDT, and unlike SigmaPCBs and HCB which biomagnified 6- to 17-fold. Highest concentrations of 2,3,7,8-TCDD and OCDD in seals and bears were found in the central Canadian Arctic Archipelago, and lowest were found in Hudson Bay, the reverse of PCB concentration distribution. The reason for higher levels of TCDD and OCDD in the Arctic than in the sub-Arctic is suggested to be trans-polar movement of aerosols with combustion-related origins in Eurasia. Levels of 2,3,7,8-TCDF were more evenly distributed throughout the North, and were positively correlated with PCB, but not with HCB or 2,3,7,8-TCDD levels in seals.