Levels Of Polychlorinated Dibenzo-p-dioxins Research Articles

Levels of PCDDs, PCDFs and PCBs in Belgian and international fast food samples

Congener-specific analyses of polychlorinated dibenzo- p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs) and polychlorinated biphenyls (PCBs) were performed on twenty-eight non-pooled fast food samples collected in Belgium, Switzerland, Czech Republic, United States of America and Australia. PCDD/F and PCB concentrations for the four investigated types of meals were very low. PCDD/F values ranged from non-detected to 1.40 pg WHO-TEQ/g fat and from 0.79 to 2.08 pg WHO-TEQ/g fat for lower and upper bound, respectively. Major contributors to the PCDD/F TEQ were 1,2,3,4,7,8-HxCDD, 1,2,3,6,7,8-HxCDD, 2,3,7,8-TCDF and 2,3,4,7,8-PeCDF. The relative contribution of PCBs to the total TEQ was 68%. For adults, an average estimated intake was 6.7 pg WHO-TEQ/kg bw/month, including consumption of all types of analyzed meals, representing 9.5% of the PTMI. For child, a value of 14.5 pg WHO-TEQ/kg bw/month was obtained, representing 20.6% of the PTMI.

Assessment of dietary exposure to some persistent organic pollutants in the Republic of Karakalpakstan of Uzbekistan.

A 1999 study heightened long-standing concerns over persistent organic pollutant contamination in the Aral Sea area, detecting elevated levels in breast milk and cord blood of women in Karakalpakstan (western Uzbekistan). These findings prompted a collaborative research study aimed at linking such human findings with evidence of food chain contamination in the area. An international team carried out analyses of organochlorine and organophosphate pesticides, polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins (PCDDs), and polychlorinated dibenzofurans (PCDFs) on samples of 12 foods commonly produced and consumed in Karakalpakstan. Analysis consistently detected long-lasting organochlorine pesticides and their metabolites in all foods of animal origin and in some vegetables such as onions and carrots--two low-cost components of many traditional dishes. Levels of PCBs were relatively low in all samples except fish. Analyses revealed high levels of PCDDs and PCDFs (together often termed "dioxins") in sheep fat, dairy cream, eggs, and edible cottonseed oil, among other foodstuffs. These findings indicate that food traditionally grown, sold, and consumed in Karakalpakstan is a major route of human exposure to several persistent toxic contaminants, including the most toxic of dioxins, 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD). Intake estimations demonstrate that consumption of even small amounts of locally grown food may expose consumers to dioxin levels that considerably exceed the monthly tolerable dioxin intake levels set by the World Health Organization. Data presented in this study allow a first assessment of the risk associated with the consumption of certain food products in Karakalpakstan and highlight a critical public health situation.

Polychlorinated dibenzo-p-dioxins and dibenzofurans in River Po sediments.

The River Po is the main Italian river draining one of the most populated and industrialised regions in Italy. As part of a monitoring project to assess environmental quality in the River Po, we measured the concentrations of polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) in bottom sediments collected along the whole course of the river, from the spring to the delta, downstream from the confluence of its main tributaries. The aim was to investigate the level of contamination in the main Italian river and the contribution of contaminant loads from the subbasins. Composite sediment samples were collected in summer and winter surveys in low-flow water conditions and analysed by HRGC-HRMS for PCDD and PCDF homologue groups and for the 2,3,7,8-substituted congeners. The spatial trend observed in the Po River for PCDD and PCDF concentrations varied depending on the load of contaminants received from the tributaries and the processes of sedimentation. The sum of PCDD and PCDF concentrations, and the toxic equivalent content, ranged from 121 to 814 and from 1.3 to 13 ng/kg dry weight sediment, respectively. These levels of contamination seem lower than in the sediments of rivers draining highly industrialised areas. The PCDD and PCDF homologue profiles in all the samples were very similar, suggesting a common source of this contamination in the River Po. Principal component analysis suggested that widespread sources, such as urban runoff and domestic wastewaters, are probably the main cause of these levels of PCDDs and PCDFs.

Polychlorinated dibenzo- p-dioxins and polychlorinated dibenzofurans in sediments from Hong Kong

Concentrations of 2,3,7,8-substituted polychlorinated dibenzo- p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) were determined in 14 sediment samples collected from four sites in the Mai Po Marshes Nature Reserve (within a RAMSAR Site) and from another six sites in Victoria Harbour and along the Hong Kong coastline. Elevated levels of PCDDs, and particularly OCDD, were detectable in all samples collected from the Mai Po Marshes and five of the six sites. In contrast to PCDDs, PCDFs were mainly found in sediment samples collected from industrial areas (Kwun Tong and To Kwa Wan) in Victoria Harbour. PCDD/F levels and congener profiles in the samples from the Mai Po Marshes Nature Reserve in particular show strong similarities to those reported in studies which have attributed similar elevated PCDD concentrations to nonanthropogenic PCDD sources.

Historical PCDD inputs and their source implications from dated sediment cores in Queensland (Australia).

Recent investigations have demonstrated the presence of an unidentified source of polychlorinated dibenzo-p-dioxins (PCDDs) in the coastal zone of Queensland (Australia). The present study provides new information on the possible PCDD sources and their temporal input to this environment. Two estuarine sediment cores were collected in northern Queensland for which radiochemical chronologies were established. Core sections from different depositional ages, up to three centuries, have been analyzed for 2,3,7,8-substituted PCDDs and polychlorinated dibenzofurans (PCDFs). Variations of PCDD concentrations in the sediment cores over several centuries of depositional history were relatively small, and elevated PCDD levels were still present in sediment slices from the early 17th century. PCDD/F isomer patterns and congener profiles in sediments deposited during the last 350 years were almost identical and correlated well to the characteristic profiles observed in surface sediments and soils from the entire Queensland coastline. Profiles were dominated by higher chlorinated PCDDs, in particular octachlorodibenzodioxin (OCDD), whereas PCDF concentrations were below or near the limit of detection. These results indicate the presence of a PCDD source prior to industrialization and production of commercial organochlorine products. Further, the present study demonstrates that PCDD input patterns have been similar along an extensive but localized area over at least several centuries, contributing relatively high concentrations of PCDDs to the coastal system of Queensland.

Comparison between “Yusho” patients and healthy Japanese in contamination level of dioxins and related chemicals and frequency of sister chromatid exchanges

Highly toxic organochlorine chemicals such as polychlorinated dibenzo- p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs) and coplanar polychlorinated biphenyls (CoPCBs) were determined in the peripheral blood and sebum from the face of 16 “Yusho” patients of about 27 yr after the outbreak of Yusho accident, and 39 healthy Japanese people. The mean total toxic equivalent (TEQ) levels of PCDDs, PCDFs and CoPCBs in the blood were still about seven times higher in Yusho patients than in healthy Japanese at the age of 45 yr and more. The sebum excretion of these chemicals seemed proportional to their blood levels in Yusho patients. These toxic chemicals, however, did not enhance frequencies of sister chromatid exchanges (SCEs) in the control and 7,8-benzoflavone (ANF) treated cultures in Yusho patients. Hence, no significant difference was observed in the mean SCE rates between the Yusho patients and general Japanese people of more than 45 yr of age. In this study, the number of Yusho patients examined is limited, so further large-scale investigations are needed to get more conclusive results concerning the genotoxic potency such as SCE induction.

PCDDs and PCDFs in the wastewater from Chinese pulp and paper industry.

Polychlorinated dibenzo-p-dioxins (PCDDs) and Polychlorinated dibenzofurans (PCDFs) in emissions from the pulp-bleaching process was characterized by US EPA as the nation’s third largest dioxin source (Johnson, 1994). Zheng et al. (1997) reported the levels of PCDDs and PCDFs in the bleached pulp from five Chinese paper mills in the north of China which use non-wood plant fibers as raw materials. Many paper mills in China discharge the bleaching wastewater directly into rivers or lakes without any treatment. The wastewater may contain PCDDs and PCDFs and seriously pollute the environment, In this paper we present the detail results of PCDDs and PCDFs levels in the wastewater of different process stages from one of the biggest pulp and paper mills in the south of China.

Polychlorinated dibenzo- p-dioxins and dibenzofurans in great barrier reef (Australia) dugongs ( Dugong dugon)

Fat tissue samples from dugong ( Dugong dugon) carcasses stranded at three sites along the Great Barrier Reef were analysed for polychlorinated dibenzo- p-dioxins (PCDDs) and dibenzofurans (PCDFs). Relatively high levels of PCDDs were determined in all three dugongs. In particular OCDD, the PCDD/F congener that is usually considered the least bioavailable of all 2,3,7,8 substituted congeners, was found at levels higher than reported for other marine mammals. Tissue accumulation of PCDDs by dugongs may be a consequence of sediment and/or seagrass ingestion during feeding, microbial biotransformation of PCDD precursors in the animal's hindgut or, alternatively, the possession of a selective degradation capability for PCDFs.

Serum levels of polychlorinated dibenzo- p-dioxins and dibenzofurans in pulp and paper mill workers

Serum levels of polychlorinated dibenzo- p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) among 46 long-term workers at a pulp and paper mill were compared to the levels in 16 community residents who never worked at the mill. Overall, there were no appreciable differences among the three exposure groups (community resident, low-exposure-potential worker, high-exposure-potential worker) for specific PCDDs or PCDFs. Neither exposure group nor duration in high-exposure-potential-jobs was related to total toxic equivalents (I-TEQ). Serum levels of PCDDs and PCDFs in this study generally were within the range previously reported for persons with no known occupational exposure.

96/05605 Safety and environmental requirements of new refrigerants

Polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and biphenyls belong to a class of compounds, the polyhalogenated aromatic hydrocarbons (PHAHs), which are ubiquitous environmental contaminants. Due to the existence of a common mechanism of action, i.e., binding to the Ah receptor, the activity of members of this class of compounds is generally expressed relative to the prototypical 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as toxic equivalency factors (TEFs). In the present studies we examined the presence of PCDDs and PCDFs in standard laboratory feed and in the liver of untreated rats at three different ages (60, 140, and 200 days) in terms of concentration and in toxic equivalents (TEQs, TEF × concentration). Feed was shown to contain trace amounts of PCDDs and PCDFs and control rat liver was shown to contain several PCDD and PCDF congeners in terms of concentration of congener and concentration of TEQs contributed by that congener. The total concentration of TEQs increased with increasing age in rat liver, going from 20 ppt TEQ at 60 days to 78 ppt TEQ at 200 days of age. This accumulation in dioxin-like activity was due primarily to PCDFs. In particular the congener 2,3,4,7,8-pentachlorodibenzofuran accrued in untreated rat liver accounting for approximately 80% of the total TEQ at 200 days of age. These studies affirm the pervasive presence of PHAHs and suggest prudence in evaluating chronic rat studies in which interference from background levels of PCDDs and PCDFs may be a factor.

Rainbow trout hepatic mixed-function oxygenase induction by polychlorinated dibenzo-p-dioxins (PCDDs) as a function of time and tissue concentration.

Rainbow trout, dosed orally with 0.060-84 micrograms/kg of [3H]-2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), [14C]-1,2,3,4,7,8-hexachlorodibenzo-p-dioxin (HxCDD), or [14C]-1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (HpCDD) showed dose-dependent increases in hepatic ethoxyresorufin O-deethylase (EROD) activity, up to 250-fold, after 2-16 d. Induction of EROD activity was a sensitive and rapid indicator of exposure to PCDDs. The effects of time after exposure were not dramatic, but generally EROD activity after 2 d was lower than EROD activity after 16 d. Slopes of dose-response curves relating EROD activity to hepatic concentrations of PCDDs significantly decreased and intercepts significantly increased with increasing time of exposure. When fish were grouped by oral doses, only the low doses of TCDD and HpCDD exhibited time-dependent EROD induction, with significantly greater activity 16 d after dosing compared to 2 d. In most cases, hepatic and muscle concentrations of PCDDs did not significantly change over time. Concentrations of PCDDs in liver and muscle accounted for up to 7% of the orally administered dose. Hepatic levels of PCDDs ranged from 20-100 pg/g at the lowest doses to about 1000 pg TCDD/g, 2000 pg HxCDD/g, or 40,000 pg HpCDD/g at the highest doses. Of the PCDD in the liver, approximately one-third to one-half was associated with the postmitochondrial supernatant (PMS). PCDD concentrations in muscle did not span as wide a range of concentrations as did PCDD in liver; fish given low doses had 10 pg/g in muscle whereas fish given high doses had several hundred picograms per gram in muscle for all three PCDDs.

Bioassay-based risk assessment of complex mixtures

In order to compare a standard chemical-based risk assessment with in vitro genotoxicity assays, two complex environmental mixtures from a wood-preserving site were analyzed in the Salmonella/microsome and E. coli prophage induction assays. Using GC/MS, sample 003 was found to contain relatively low levels of polycyclic aromatic hydrocarbons (PAHs) and elevated levels of polychlorinated dibenzo- p-dioxins (PCDDs), while sample 005 had higher levels of PAHs and relatively low levels of PCDDs. The complex mixtures were sequentially extracted with methylene chloride and methanol for analysis in Salmonella, or extracted with a 1:1 hexane:acetone mixture for analysis in the E. coli prophage induction assay. At a dose of 1.0 mg/plate in Salmonella strain TA98 with metabolic activation, the methanol extract of sample 003 induced 197 net revertants, while sample 005 induced 436 net revertants. In the prophage induction assay, with activation, the hexane:acetone extract of sample 003 induced a genotoxic response that was slightly lower than that observed with sample 005. The estimated incremental carcinogenic risk for ingestion of PAHs was 1.5E – 3 for sample 003, while for sample 005 the estimated risk was 1.5E – 2. Thus, the sample which induced the maximum response in both bioassays also had the highest estimated cancer risk. However, the frequency of PAH-DNA adducts in both skin and liver tissues was appreciably higher with sample 003 than with sample 005. A combined testing protocol, using both biological and chemical analysis, therefore provides more accurate information from which to assess risk than the use of either method alone.

Accumulation of Polychlorinated Dibenzo-p-dioxins and Dibenzofurans in Liver of Control Laboratory Rats

Polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and biphenyls belong to a class of compounds, the polyhalogenated aromatic hydrocarbons (PHAHs), which are ubiquitous environmental contaminants. Due to the existence of a common mechanism of action, i.e., binding to the Ah receptor, the activity of members of this class of compounds is generally expressed relative to the prototypical 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as toxic equivalency factors (TEFs). In the present studies we examined the presence of PCDDs and PCDFs in standard laboratory feed and in the liver of untreated rats at three different ages (60, 140, and 200 days) in terms of concentration and in toxic equivalents (TEQs, TEF × concentration). Feed was shown to contain trace amounts of PCDDs and PCDFs and control rat liver was shown to contain several PCDD and PCDF congeners in terms of concentration of congener and concentration of TEQs contributed by that congener. The total concentration of TEQs increased with increasing age in rat liver, going from 20 ppt TEQ at 60 days to 78 ppt TEQ at 200 days of age. This accumulation in dioxin-like activity was due primarily to PCDFs. In particular the congener 2,3,4,7,8-pentachlorodibenzofuran accrued in untreated rat liver accounting for approximately 80% of the total TEQ at 200 days of age. These studies affirm the pervasive presence of PHAHs and suggest prudence in evaluating chronic rat studies in which interference from background levels of PCDDs and PCDFs may be a factor.

Dioxins and dibenzofurans in adipose tissue of the general US population and selected subpopulations.

The Environmental Protection Agency's National Human Adipose Tissue Survey (NHATS) was conducted in fiscal year (FY) 1987 to (1) estimate average concentrations of polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) in the adipose tissue of humans in the US population, (2) identify differences in average concentrations among subpopulations, and (3) compare average concentrations with those from the FY 1982 NHATS: Population estimates of the average levels of PCDDs and PCDFs were established on the basis of 865 human adipose tissue specimens collected in FY 1987. Average levels among subpopulations were compared. The average concentration of 2,3,7,8-tetrachlorodibenzo-p-dioxin in the adipose tissue of the US population was 5.38 pg/g, increasing from 1.98 pg/g in children under 14 years of age to 9.40 pg/g in adults over 45. The effect of age was significant for nine compounds. Regional differences in the levels of 2,3,4,7,8-pentachlorinated dibenzofurans were statistically significant, but there were no significant differences associated with sex or race. The survey provides a baseline of average levels of PCDDs and PCDFs in the adipose tissue of humans in the US population.

Accumulation of Polychlorinated Dibenzo-p-dioxins and Dibenzofurans in Liver of Control Laboratory Rats

Polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and biphenyls belong to a class of compounds, the polyhalogenated aromatic hydrocarbons (PHAHs), which are ubiquitous environmental contaminants. Due to the existence of a common mechanism of action, i.e., binding to the Ah receptor, the activity of members of this class of compounds is generally expressed relative to the prototypical 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as toxic equivalency factors (TEFs). In the present studies we examined the presence of PCDDs and PCDFs in standard laboratory feed and in the liver of untreated rats at three different ages (60, 140, and 200 days) in terms of concentration and in toxic equivalents (TEQs, TEF × concentration). Feed was shown to contain trace amounts of PCDDs and PCDFs and control rat liver was shown to contain several PCDD and PCDF congeners in terms of concentration of congener and concentration of TEQs contributed by that congener. The total concentration of TEQs increased with increasing age in rat liver, going from 20 ppt TEQ at 60 days to 78 ppt TEQ at 200 days of age. This accumulation in dioxin-like activity was due primarily to PCDFs. In particular the congener 2,3,4,7,8-pentachlorodibenzofuran accrued in untreated rat liver accounting for approximately 80% of the total TEQ at 200 days of age. These studies affirm the pervasive presence of PHAHs and suggest prudence in evaluating chronic rat studies in which interference from background levels of PCDDs and PCDFs may be a factor.

Promotion of preneoplastic foci in rat liver with 2,3,7,8-tetrachlorodibenzo-p-dioxin, 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin and a defined mixture of 49 polychlorinated dibenzo-p-dioxins.

In a two-stage initiation-promotion experiment the hypothesis was investigated that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) equivalents (TE), calculated from data of CYP1A induction in hepatocytes in primary culture, or international TCDD equivalents (ITE) are useful for evaluating the tumor-promoting potency of 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (HpCDD) and of a defined mixture (M2) of 49 polychlorinated dibenzo-p-dioxins (PCDDs) in comparison with TCDD. Therefore, female Wistar rats were treated with an initiating dose of N-nitrosomorpholine, and subsequently received daily doses of 2, 20 and 200 ng TCDD/kg or equivalent doses of HpCDD or M2, based on TE values. After a promotion phase of 13 weeks, hepatic PCDD levels, CYP1A activity and the relative hepatic volume of adenosinetriphosphatase-negative or glutathione S-transferase P-positive preneoplastic foci were determined. After logarithmic transformation, linear PCDD level-response relationships were obtained for induction of CYP1A activity with TCDD, HpCDD or M2. Based on TE values, inducing potencies of both HpCDD and M2 were over-estimated at higher doses, whereas induction was approximately equivalent at the lowest dose. The best fit of PCDD level-response relationships of relative hepatic volumes of preneoplastic lesions was achieved using a four-parameter logistic model. Significantly different functions were calculated for promotion with TCDD or HpCDD. It is concluded that (i) different PCDD level-response relationships exist for the induction of hepatic CYP1A activity and the promotion of preneoplastic liver foci, and (ii) that TE or ITE factors provide only a rough estimate of the tumor-promoting potency of a PCDD mixture but may overestimate the risk from exposure to higher-chlorinated 2,3,7,8-substituted congeners such as HpCDD.

Determination of polychlorinated dibenzo- p-dioxins and dibenzofurans in tire fire runoff oil

Samples of oily runoff resulting from the accidental combustion of automobile tires were analyzed for polychlorinated dibenzo- p-dioxins (PCDDs)and polychlorinated dibenzofurans (PCDFs). PCDDs and PCDFs were identified in each of the oil samples studied. The total levels of PCDDs and PCDFs were in the low parts per billion (ppb; 10 −9 g of PCDDs or PCDFs per g of oil) range. In all of the samples analyzed, the total PCDD concentration was approximately 10 times greater than the total concentration of PCDFs. The most toxic PCDD, 2,3,7,8-T 4CDD, contributed only a small percentage to the overall level of the PCDDs in the oil samples.

Passive water sampling via semipermfable membrane devices (SPMDS) in concert with bivalves in the Sacramento/San Joaquin River Delta

Freshwater clams ( Corbicula fluminea) and the Huckins et al. (1) semi-permeable membrane sampling device (SPMD) were simultaneously deployed at three sites on the Sacramento and San Joaquin rivers in 1990. Both clams and the SPMDs were analyzed for sequestered pesticides and polychlorinated biphenyls (PCBs) by gas chromatography with electron capture detection (GC/ECD). Polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs) and non- ortho PCBs were quantified by high resolution mass spectrometry (MS). In general, levels of organochlorine compounds were approximately 1.6 times higher in clams on a wet weight basis than in the SPMDs, and trends in accumulation were similar except where biofouling of the SPMD membranes decreased uptake rates. Comparisons between the normalized, average levels of PCDDs accumulated showed that while octachlorodibenzo-p-dioxin (OCDD) was most prevalent in both clams and SPMDs, much higher levels of 2,3,7,8 TCDD were found in the SPMDs than in the clams; 2,3,7,8 TCDD was 32% of the profile relative to the OCDD level for the SPMDs and <1% of the clam OCDD level. PCB levels showed the clams primarily accumulated hexachlorinated PCBs while the pentachlorinated and tetrachlorinated congeners were higher in the SPMDs. Differences in profiles for homologous series among the PCBs reveal that some congeners, especially those with 2,4,5 substitution, are more likely to bioaccumulate than those with lower chlorination or adjacent unsubstituted sites. GC/MS chromatograms indicate the SPMDs also sequestered several polyaromatic hydrocarbons. GC/ECD chromatograms indicate the presence of several unidentified, early eluting compounds in the SPMDs.

A source inventory and budget for chlorinated dioxins and furans in the United Kingdom environment

Polychlorinated dibenzo- p-dioxins (PCDDs) and -furans (PCDFs) are ubiquitous in the environment. This paper estimates the present UK environmental loading of PCDD/Fs in soils, vegetation, air, water and sediments. Greater than 95% of the estimated total PCDD/F loading of 5.7 t in the UK environment is present in surface soils. Annual emissions from known primary sources of PCDDs and PCDFs are estimated. The most important of these include: municipal waste incinerator stack emissions (10.9 kg ΣPCDD/F per annum); industrial (7.7 kg/year) and domestic (5.1 kg/year) combustion of coal; clinical waste incinerators (1.7 kg/year); volatilization from chlorophenol-treated substrates (1.7 kg/year) and combustion of leaded petrol by motor vehicles (0.7 kg/year). These sources are generally easy to define and reasonably reliable national estimates can be obtained. More difficult to quantify are secondary releases from the large UK stock of pentachlorophenol (PCP) and PCP-treated products, which may represent quantitatively one of the most important sources of total PCDD/Fs to the environment. Estimates of homologue-specific emissions indicate that combustion processes represent a far more significant source of tetra and penta CDD/Fs than do chlorophenols, which in turn constitute a greater source of hepta- and octachlorinated congeners. Direct emission of PCDD/Fs into the atmosphere from combustion processes facilitates their atmospheric transport to remote locations. This, coupled with the diffuse nature of combustion processes, means that the effects of PCDD/F contamination originating from anthropogenic combustion are more widespread than those from the use and disposal of chlorophenols. Contamination from chlorophenols will be more localised, owing to the insignificance of direct atmospheric release pathways for this source. Although there is reasonable agreement between the estimated current annual flux and the present UK environmental loading of PCDDs and PCDFs, a large discrepancy exists between the sum of the annual contributions from primary sources and this annual flux. Whilst the existence of an as yet unidentified source or sources or gross underestimates of known sources cannot be excluded, it is proposed that much of this discrepancy may be accounted for by secondary releases from the use and disposal of chlorophenols and the long-range transport, continued remobilisation and subsequent redeposition of PCDDs and PCDFs already present in the environment. Despite limited evidence for a modest decline in levels of PCDDs and PCDFs in some environmental compartments over the last 20 years, the environmental persistence of these chemicals means that they will remain in the UK environment for the foreseeable future despite recent action to curb primary emissions.

Serum levels of PCDDs and PCDFs among workers exposed to 2,3,7,8-TCDD contaminated chemicals

The National Institute for Occupational Safety and Health (NIOSH) collected serum from workers exposed to chemicals contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and from unexposed referents. A subset of serum samples were analyzed for polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs). In addition to a marked difference in serum levels between workers and referents for 2,3,7,8-TCDD, there was a small but significant difference for 2,3,7,8-PnCDF and 1,2,3,4,7,8-HxCDF. Funding was received for this study from the Agency for Toxic Substances and Disease Registry.