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Factors affecting the toxicity of dioxin-like toxicants: a molecular approach to risk assessment of dioxins.

The numerous toxic responses of dioxin-like compounds are mediated by the intracellular Ah (aryl hydrocarbon) receptor. It has been suggested that the regulation of dioxins and similar substances could be placed on a molecular foundation by considering the proportion of Ah-receptor sites occupied by toxicant molecules. The present work has shown that the following formation not yet available would be needed in order to develop this approach: correlation between dioxin exposure and human tissue levels; accurate determination of the association constants for human Ah-receptor with toxicant, and for human receptor-ligand complex with DNA; and knowledge of the intracellular concentrations of both receptor binding sites and DNA binding sites. Furthermore, since not all dioxin-like substances behave identically, this information would need to be gathered for a wide variety of substances.

Animals↗

Dioxin and dioxin-like PCB impurities in some Japanese agrochemical formulations.

The profile and amount of dioxin impurity in agrochemicals were studied through detailed analysis of historic Japanese formulations. The chemicals analyzed include pentachlorophenol (PCP), 2,4,6-trichlorophenyl-4'-nitrophenyl ether (chloronitrofen, CNP), 2,4-dichlorophenyl-4'-nitrophenyl ether (nitrofen, NIP), tetrachloro-iso-phthalonitrile (chlorothalonil, TPN), 2-methyl-4-chloro-phenoxyacetic acid (MCP) and 2,4-dichlorophenoxyacetic acid (2,4-D). Among the six, two herbicides, PCP and CNP, produced during the 1960s and 1970s, contained very high concentrations of PCDD/DFs and TEQ. Others contained relatively low concentrations of PCDD/DFs. Dioxin-like PCB concentrations in all chemicals studied were low and their contributions to TEQ were negligible. The total dioxin emissions from the use of agrochemicals in Japan during the past 40 years (1955-1995) were estimated to be about a few hundred thousand kg of PCDD/DFs and 250 kg of WHO-TEQ from PCP and 190 x 10(3) kg of PCDD/DFs and 440 kg of WHO-TEQ from CNP. The major dioxin congeners present in PCP formulations were highly chlorinated PCDD/DFs that can be formed by the coupling of PCP and/or 2,3,4,6-tetrachlorophenol, and those in the CNP formulations were tetra- to hexa-chlorinated PCDD/DFs that can be formed from 2,4,6-trichlorophenol and/or 2,3,4,6-tetrachlorophenol.

Agriculture↗

Estimation of effects of dioxins and dioxin-like PCBs on wildlife population--a case study on common cormorant.

We presented a method for quantitatively evaluating the effects of chemical pollutants in the environment on a wildlife population. We expressed the effects of exposure to dioxins and dioxin-like PCBs in Tokyo Bay sediment on a common cormorant (Phalacrocorax carbo) population in two ways. One was the changes in the intrinsic growth rate, and the other was the changes in the gross population size. The effects of exposure to the compounds were estimated by using the method of population ecology and available field data. Common cormorant population at Shinobazu Pond in Tokyo, Japan during 1974-1986 was selected as the target population. Intrinsic growth rate or gross size of the population based on the calculated residual level of dioxins and dioxin-like PCBs in the period was estimated to decrease to 89% or 85% of that without exposure to the compounds, respectively.

Animals↗

Dietary intakes of polychlorinated dibenzo-p-dioxins, dibenzofurans and dioxin-like polychlorinated biphenyls in Spain.

Congener-specific analyses of seventeen 2,3,7,8-substituted PCDD/Fs, three non-ortho and 8 mono-ortho dioxin-like polychlorinated biphenyls (PCBs) were performed on 258 Spanish foodstuff samples, mainly of animal origin, for 2000--03. Daily dietary intakes of PCDD/Fs and PCBs, expressed as toxic equivalents (WHO-TEQs), were estimated by combining food consumption data from the Spanish National Institute Statistics survey and concentration levels measured in individual samples, using upper bound determination values (not detectable = limit of detection). The calculated dietary intake of PCDD/Fs for a person weighing 70 kg was 1.35+/-0.11pg WHO-TEQs kg(-1) bw day(-1), and 3.22+/-0.75 pg WHO-TEQs kg(-1) bw day(-1) if dioxin-like PCBs (non- and mono-ortho PCBs) were included, showing the importance of their inclusion in monitoring studies. Both values were within the range of tolerable daily intake (TDI) proposed by the WHO (1-4pg WHO-TEQs kg(-1) bw day(-1)). The current levels are lower than earlier intakes estimates conducted in Spain. Meat and meat products accounted for more than 35% of the intake, followed by milk and milk products (29%), vegetables oils (19%), fish and seafood (11%) and eggs (4%). Dioxin-like PCBs are an important component in the total WHO-TEQs in foodstuffs. This is particularly true for the fish food group, where the total WHO-TEQs is dominated by dioxin-like PCBs (up to 80% of WHO-TEQs in some cases).

Benzofurans↗

Dioxin residues in the edible tissue of finishing pigs after dioxin feeding.

The aim of this study was to determine the contamination of finishing pigs with polychlorinated dibenzodioxins and dibenzofurans (PCDD/Fs) after feeding either uncontaminated feed or feed contaminated with 0.75, 2 or 4 ng/kg toxic equivalents (TEQ; calculated by multiplying individual congener concentrations by congener-specific toxicity equivalency factors). The feed was mixed with pure substances of PCDD/Fs to get the intended contamination. Five groups of six piglets each were fed contaminated feed, one group of five piglets served as control. One group was fed contaminated feed (4 ng TEQ/kg) only for the rearing period (6 weeks), and another group for the first 8 weeks of the fattening period (4 ng TEQ/kg feed). The other groups received the contaminated feed during the 12-weeks fattening period. After slaughtering, the edible parts of the belly, loin and fore-end were collected and homogenized. The samples of group 2 and 4a were investigated uncooked as well as roasted. Fattening yield and feed conversion (kg feed/kg weight gain) of the animals of all groups were in the normal range (final weight 109.7 kg; feed conversion 2.55-2.69 kg). The PCDD/F-content in 1 kg fat of the belly, loin and fore-end in relation to the intake was between 0.016 (4 ng TEQ/kg feed for a 6-weeks rearing period) and 1.39% (fore-end; 2 ng TEQ/kg feed for 12-weeks fattening period). There was a decrease in dioxin residues after a 12-weeks period but not after a 4-weeks period of feeding an uncontaminated feed. When feed contaminated with 0.75, 2 and 4 ng TEQ/kg was given for a 12-weeks fattening period, the residue concentrations of PCDD/F-TEQ in 1 kg belly was 0.455, 1.07 and 1.55 ng, in 1 kg fore-end 0.04 ng, 0.32 ng and 0.34 ng and in 1 kg loin 0.015 ng, 0.07 ng and 0.30 ng respectively. Roasting had no influence on the dioxin-residues. The residues per g belly fat exceed the maximum limits for dioxin in food of 0.6 pg WHO-PCDD/F-TEQ/g fat (EC Recommendations 2002/201/EC), when feed containing 0.75 ng PCDD/F-TEQ/kg is given for 12 weeks. When feed containing 0.4 ng TEQ (maximum content; EC recommendations 2002/201/EC) is given for 12 weeks, approximately 0.55 pg TEQ/g fat can be expected in the food. This value is within the action level of 0.6 pg/g fat of porks. In conclusion, the results of the study allow prediction of dioxin residues in the edible tissue of pork, if the feed contamination is known and the amount of feed intake can be estimated.

Animal Feed↗

Dioxin-like and non-dioxin-like toxic effects of polychlorinated biphenyls (PCBs): implications for risk assessment.

Polychlorinated biphenyls (PCBs) are persistent, bioaccumulative and toxic contaminants in the environment. Individual PCB congeners exhibit different physico-chemical properties and biological activities which result in different environmental distributions and toxicity profiles. The variable composition of PCB residues in environmental matrices and their different mechanisms of toxicity, complicate the development of scientifically based regulations for the risk assessment. Various approaches for the assessment of risks of PCBs have been critically examined. Recent developments in the toxic equivalency factor (TEF) approach for the assessment of toxic effects due to dioxin-like PCBs have been examined. PCB exposure studies which describe non-dioxin-like toxic effects, particularly neuro-behavioral effects and their effective doses in animals were also considered. A comparative assessment of effective doses for dioxin-like and non-dioxin-like effects by PCBs was made to evaluate the relative significance of non-ortho and ortho-substituted PCBs in risk assessment. Using mink as an example, relative merits and implications of using TEF and total PCB approaches for assessing the potential for toxic effects in wildlife was examined.

Animals↗

Using the dioxin receptor-CALUX in vitro bioassay to screen marine harbor sediments for compounds with a dioxin-like mode of action.

The presence of dioxin-like compounds in sediments from harbors and reference sites along the Dutch coast was investigated using the dioxin receptor-chemically activated luciferase gene expression (DR-CALUX) bioassay. The DR-CALUX response varied between 0.2 and 136 ng/kg dry weight expressed in units of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) toxic equivalency quotients (TEQ). The highest CALUX-TEQ values (> 50 ng TEQ/kg dry wt) were found in sediments from the center of the Port of Rotterdam and from the North Sea canal near Amsterdam. The DR-CALUX activity of harbor sediments was classified by setting guideline values. None of the 257 harbor sediment samples investigated exceeded the maximum value of 1,000 ng TEQ/ kg, while 94% of the samples fail the target value of 2 ng TEQ/kg. Threshold values (25 and 50 ng TEQ/kg) are intended as pass/ fail criteria for offshore disposal of dredged material and were exceeded in 12 and 3% of the samples, respectively. DR-CALUX response did not always match with contamination of polychlorinated biphenyls (PCBs) as determined in bulk sediments (sigma7-PCB ranging from < 1 to 456 microg/kg dry wt). Concentrations of planar PCBs, polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated-dibenzofuranes (PCDFs), polybrominated biphenyls (PBBs), and polybrominated-diphenylethers (PBDEs) were determined in 20 selected sediment extracts. On average, PCDD/Fs explained 50% of the DR-CALUX activity and planar PCBs 6%. Further research is needed to elucidate the unexplained part of the DR-CALUX response. The DR-CALUX is a highly sensitive and reproducible bioassay that can usefully complement standard PCB analysis, improving the hazard assessment of the disposal of dredged material in the North Sea.

Animals↗

Persistent brominated and chlorinated dioxin blood levels in a chemist. 35 years after dioxin exposure.

This is the first report on occupational health hazards to dioxin chemists associated with laboratory exposure to 2,3,7,8-tetrabromodibenzodioxin (TBrDD), and further characterizes the human response to 2,3,7,8 tetrachlorodibenzodioxin (TCDD). In this case study the chemist was exposed on two separate occasions. In March 1956, after synthesizing 10 g of TBrDD, the chemist suffered from mild and transient chloracne of the neck and wrists; in September 1956, after synthesizing 16 g of TCDD, he suffered severe chloracne of the entire body, headaches, backache, and leg pain on exertion. His measured 2,3,7,8-TBrDD in 1991 was 625 parts per trillion (ppt) in whole blood lipid, 35 years after initial exposure and 18 ppt TCDD, an elevated level in comparison with the mean 2,3,7,8-TCDD level of 5 ppt in the US population. This is the first reported detection of a brominated dioxin in human tissue. The total halogenated dioxin body burden in September 1956 is estimated to have been between 13,005 ppt and 146,726 ppt. This amount can be considered to be, at least in this person, a strong chloracnegenic dose, and a dose causing human nervous system and muscular or circulatory system responses. This uptake demonstrates an occupational hazard to chemists and chemical workers, and the usefulness of human tissue dioxin measurements to document absorption.

Adult↗

Structure-activity relationships and dose responses of polychlorinated dibenzo-p-dioxins for short-term effects in 2,3,7,8-tetrachlorodibenzo-p-dioxin-resistant and -sensitive rat strains.

Dose responses of the characteristic short-term effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 1,2,3,7,8-pentachlorodibenzo-p-dioxin (PeCDD), 1,2,3,4,7,8-hexachlorodibenzo-p-dioxin (HxCDD), and 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (HpCDD) were compared in the resistant Han/Wistar (Kuopio) (H/W) rats and the sensitive Long-Evans (Turku/AB) (L-E) rats. The resistance of H/W rats is linked to the altered H/W-type aryl hydrocarbon receptor (AHR). Exceptionally, in terms of acute lethality, the most potent congener for H/W rats is HxCDD, followed by HpCDD, PeCDD, and TCDD. The study objectives were to find out if this exceptional sensitivity of H/W rats also holds for nonlethal toxic endpoints and to compare potency and efficacy (magnitude of effect) of PCDDs between L-E and H/W rats. Dose responses for several endpoints were determined, modeled, and used for ED50 and relative potency (REP) calculations. For all endpoints measured, TCDD was the most potent congener, followed by PeCDD, HxCDD, and HpCDD in both strains, and the REP estimates were consistent with the current toxic equivalency factors (TEFs). For most endpoints, H/W rats showed smaller responses to all congeners than L-E rats, and this difference was due to lower efficacy rather than lower potency. H/W rats showed lower efficacy to body weight loss, serum aspartate aminotransferase activity, and serum concentrations of total bilirubin, free fatty acids, and thyroxine. In contrast, effects on cytochrome P4501A1 induction, thymus atrophy, and dental defects were similar in both strains. In conclusion, the results are in agreement with the current WHO-TEFs and imply that relative potency values derived from mortality are not necessarily valid for other endpoints. The results support our previous observations about two different types of AHR-mediated mechanisms. Type I effects are similar in both strains, and type II effects show decreased efficacy of toxic response in relation with the altered H/W-type AHR.

Animals↗

Phorbol esters inhibit the dioxin receptor-mediated transcriptional activation of the mouse Cyp1a-1 and Cyp1a-2 genes by 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Tetradecanoyl phorbol acetate (TPA) has been shown to inhibit 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced mouse P450IA1 benzo[a]pyrene hydroxylase activity (Raunio, H., and Pelkonen, O. (1983) Cancer Res. 43, 782-786). When we co-administered TPA and TCDD to C57BL/6 mice, the accumulation of TCDD-inducible liver P450IA1 and P450IA2 mRNA, as well as kidney P450IA1 mRNA, was greatly inhibited. When nuclear run-on assays were conducted, maximal levels of transcriptional activation were achieved for both liver Cyp1a-1 and Cyp1a-2 with 1 micrograms/kg (approximately equal to 3.0 nmol/kg) TCDD. TCDD elicited a dose-dependent increase in the rates of gene transcription, which paralleled the induction of P450IA1 and P450IA2 mRNA. Only Cyp1a-1 gene transcription was elevated in kidney. When these experiments were repeated following the co-administration of TPA with TCDD, the levels of TCDD-mediated transcriptional increases in liver Cyp1a-1 and Cyp1a-2 and P450IA1 and P450IA2 mRNAs were dramatically inhibited. The reduction in Cyp1a gene transcription by TPA could be accounted for by reduced DNA binding of the dioxin receptor to the xenobiotic-responsive element (XRE) sequences, as measured by gel-retardation analysis. Analysis of nuclear [3H]TCDD dioxin receptor by sucrose density gradients demonstrated that the inhibition of Cyp1a gene transcription and DNA binding by TPA resulted from a reduction in nuclear dioxin receptor concentration.

Animals↗

A histochemical study of the liver lesion induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) in rats.

A histochemical study of plasma-membrane associated enzymes in rat liver demonstrated a significant lesion 3 days after a single oral dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin). The complete loss of canalicular ATPase reaction in the parenchymal cells of the centrilobular zone remained the prominent feature of the liver throughout the 6-wk period studied. Involvement of the periportal and midzonal regions occurred in moribund animals and improvement in the health of two surviving animals at 9 mth was associated with a normal distribution of ATPase in the liver. Qualitative changes in 5-nucleotidase and acid phosphatase were secondary to the parenchymal cell damage. This lesion supports the morphological evidence, reported previously, that the parenchymal cell plasma-membrane is a specific subcellular site of the toxic action of dioxin.

Acid Phosphatase↗

Decreased hepatic phosphoenolpyruvate carboxykinase gene expression after 2,3,7,8-tetrachlorodibenzo-p-dioxin treatment: implications for the acute toxicity of chlorinated dibenzo-p-dioxins in the rat.

Decreased activity of the rate limiting gluconeogenic enzyme, phosphoenolpyruvate carboxykinase (PEPCK), has been recently suggested to be the critical lesion in the acute toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). We now show that other toxicologically relevant chlorinated dibenzo-p-dioxins (CDDs), with chlorine substituents in the crucial 2-,3-,7-, and 8-positions, exert the same effect on PEPCK activity. The doses required to cause this enzyme inhibition are within the acutely toxic range for each homologue, suggesting the same mechanism of action for these compounds. To further investigate the mechanism whereby dioxins decrease PEPCK activity, Northern analysis was performed using a cDNA probe complementary to a portion of the PEPCK mRNA. We could demonstrate that after TCDD treatment hepatic PEPCK mRNA was decreased by as much as 90% compared to pair-fed control animals (day 8 after dosing). This decrease in PEPCK mRNA was paralleled by a decrease of the amount of PEPCK protein and enzymatic activity. These results indicate that the physiological changes which occur in TCDD-treated animals (decreased feed consumption, low plasma insulin and elevated plasma corticosterone levels) which under normal conditions increase PEPCK gene expression and enzyme activity, are not effective in stimulating PEPCK synthesis in TCDD-treated animals.

Animals↗

Levels of dioxins and dioxin-like PCBs in food samples on the Greek market.

Food intake is the main source of exposure to dioxin-like compounds for humans. The results of a surveillance programme on polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs) and co-planar polychlorinated biphenyls (co-PCBs) in 77 food samples from the Greek market and producers are presented. The study included the analyses of milk and dairy products, meat and meat products, fish, vegetable oil, eggs, fruit, vegetable and rice collected between August and December 2002. After extraction, extracts were cleaned up on a series of carbon column chromatography, silica gel, alumina chromatography, and then analysed by high resolution gas chromatography/high resolution mass spectrometry. All samples had a dioxin content far below the EC Regulation (2375/2001/EC) limits.

Benzofurans↗

Selective pressurized liquid extraction of polychlorinated dibenzo-p-dioxins, dibenzofurans and dioxin-like polychlorinated biphenyls from food and feed samples.

Selective pressurized liquid extraction (PLE) of polychlorinated dibenzo-p-dioxins/dibenzofurans (PCDD/Fs) and dioxin-like polychlorinated biphenyls (dl-PCBs) from various food and feed samples was performed with a selective PLE method previously developed for bulk PCBs. The method utilizes sulfuric acid impregnated silica inside the extraction cell to oxidize coextracted fat. Extractions were performed at 100 degrees C with n-heptane for 5 min in two cycles. Data obtained by selective PLE combined with gas chromatography/high-resolution mass spectrometry (GC-HRMS) were compared to concentrations derived from reference laboratories applying conventional sample preparation and GC-HRMS. Experiments performed on spiked vegetable oil, naturally contaminated crude fish oil and oil containing compound feed samples showed good results for these relatively simple matrices. The accuracy was generally +/-20% as compared to spiked levels or to values obtained by the reference laboratories. The precision, measured as the relative standard deviation (RSD) for 2,3,7,8-tetrachlorodibenzo-p-dioxin toxic equivalency values (TEQs), was below 10% in all cases. The method was also tested on naturally contaminated herring tissue, chicken tissue, pork tissue and sepiolitic clay, which all caused some trouble. It was observed that sufficient amounts of sodium sulfate should be used for dehydration of tissue samples and additionally, the cells should not be packed too dense in order to avoid suppressed extraction efficiency. Once this was attended to, satisfactory data could be obtained, except for sepiolithic clay. This study demonstrates that selective PLE can be applied with success to a number of food and feed matrices in analysis of PCDD/Fs and dl-PCBs. Since the fat removal step is on-line, the selective PLE method will reduce time and solvent consumption for sample preparation as compared to traditional clean-up.

Benzofurans↗

Levels of polychlorinated dibenzo-p-dioxins and dibenzofurans in primipara breast milk from Taiwan: estimation of dioxins and furans intake for breastfed infants.

Postnatal exposure to dioxins in breastfed infants occurs mainly during breast-feeding. The exposure to a substantial amount of endocrine disruptors in the early days of life may cause long-term health effects. Test subjects were healthy and primiparous mothers with a mean age of 28 (S.D. = 3.8) in 2001. The PCDD/F congeners were analyzed in the breast milk using gas chromatograph/high resolution mass spectrometry. The mean level of PCDD/Fs was 7.4 pg-WHO-TEQ/g lipid, which is significantly lower than the level found in individuals from other countries. The total PCDD WHO-TEQ levels in breast milk had a significant positive association with maternal age and a slightly negative association with perinatal BMI (body mass index of the period before and after the delivery). The estimated daily intake of 10.5 pg-WHO-TEQ/kg/day from individual breast milk was predicted for a breastfed infant at 6 months of age with proper assumption of 8 kg body weight, 854 milk per day of consumption, 95% of dioxin absorption rate, and linear decline of dioxin during lactation. Based on the lower WHO-TEQ levels in the breast milk, breast-feeding should still be encouraged and continued in Taiwan.

Adult↗

Estimating the human health risks from polychlorinated dioxins and furans in stack gas emissions from combustion units: implications of USEPA's dioxin reassessment.

Shortly after promulgation of the Hazardous Waste Combustor MACT rule established regulatory limits for polychlorinated dioxins and furans (dioxins/furans) in incinerator stack gas, the US Environmental Protection Agency (USEPA) announced that facilities could still be required to demonstrate that stack emissions do not present an unacceptable risk to human health and the environment. Guidance for conducting this risk assessment activity, which was to be required under RCRA omnibus authority, was developed by the agency and released in 1998. The guidance represented an increase in complexity over previous documents developed by the agency and contains multiple chemical, fate and transport, and toxicological parameters which are to be used as default deterministic parameters in a complex series of algorithms which ultimately lead to numerical estimates of risk. As these changes were occurring, USEPA was also moving towards completion of its reassessment of dioxin. That series of documents has been the subject of considerable controversy and has, in several of its various drafts, proposed a number of changes, including modification of the existing toxic equivalency factor (TEF) approach and of the cancer potency factor of 2,3,7,8-tetachlorodibenzo-p-dioxin. At this time it is unclear what the impact of these changes will be on facilities progressing through the permitting process, because it is not intuitively obvious how changes in the risk assessment input parameters will impact the magnitude of the dioxinlfuran risk. In this paper, the receptor usually associated with the highest potential risk from dioxins/furans in a combustion risk assessment, the Subsistence Farmer, will be subjected to a sensitivity analysis to determine which of the multiple default input parameters will have the greatest influence on the potential cancer risk.

Algorithms↗

Butter as an indicator of regional persistent organic pollutant contamination: further development of the approach using polychlorinated dioxins and furans (PCDD/Fs), and dioxin-like polychlorinated biphenyls (PCBs).

The potential for use of butter as a widely available, relatively uniform lipid-rich matrix for the determination of spatial distributions of persistent organic pollutants has already been demonstrated. The present study determines the contributions to toxicity equivalence (TEQ) from polychlorinated dioxins and furans (PCDD/Fs) and polychlorinated biphenyls (PCBs) using butter samples from 24 countries world wide. Concentrations of PCDD/Fs and dioxin-like PCBs ranged from 0.07 to 5.69 pg SigmaWHO-TEQ g(-1) lipid. For most samples, PCDD/F TEQ fell within ranges reported for European dairy products over the last decade (0.3-2 pg x g(-1) lipid I-TEQ), though a single sample from Spain was a notable exception. Other than this sample, the highest values were recorded for samples from the Netherlands and Italy, with those from India, China and Tunisia also being relatively high. The contribution from non-ortho-PCBs was particularly significant in samples from Germany, Austria, Italy, the Czech Republic, Tunisia, India and Argentina. Although overall TEQs were generally highest in European and Mediterranean butters, elevated levels were also apparent in industrializing regions of Asia (India, China) and Latin America (Argentina). More detailed regional studies would be necessary to identify likely dioxin and PCB sources in each case. Nevertheless, this study supports the utility of butter as a monitoring matrix that may be especially applicable in regions for which monitoring programmes are currently lacking.

Animals↗

The use of dioxin isomer group ratios to identify sources and define background levels of dioxins in the environment.

Environmental samples containing a mixture of dioxins of which there are seventy-five isomers, show a characteristic composition indicative of their source and the destruction reactions taking place in the environment. Expressed in terms of isomer group ratios, the study shows that thermochemical reactions rearrange the isomer content to form specific ratios characteristic of the source itself, and upon release to the environment a shift in the ratios to a new and constant set of ratios characteristic of the environment into which thery are released. The observed shift is easily modeled, independent of the source, and presumably caused by oxidation reactions in the atmosphere. The reduction/oxidation reactions needed to account for such an observation is demonstrated in a laboratory unit where a single type of dioxin (octachlorodibenzo-p-dioxin) is transformed into all isomer group species during incineration.

Dioxins↗