Search

Background, Aim, and Scope: The main pathway for human exposure to the highly toxic polychlorinated-p-dioxins and polychlorinated furans [polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs)] is via dietary intake. Other exposure pathways may, however, be important in close proximity to point sources, such as wood preservation sites, where PCDD/F contaminated chlorophenols (CP) were previously used. In this study, a heavily PCDD/F contaminated CP saw mill site in Sweden was investigated. Human exposure through a broad spectrum of exposure pathways was assessed. Such studies are in demand since the question whether contaminated sites represent a current or future risk can only be answered by detailed site-specific risk assessments., Materials and Methods: Sampling of exposure media (soil, air, groundwater, raspberries, carrots, potatoes, grass, milk, eggs, and chicken fodder) was made. Exposure media concentrations and congener distribution patterns were used to investigate the mobilization of PCDD/Fs from soil to the environment and to calculate exposure levels for adults. Blood serum levels from site-exposed and control individuals were also analyzed., Results: Congener distribution patterns at the site were generally dominated by a specific marker congener (1234678-HpCDF), which is highly abundant in the polluted soil. The dioxin toxic equivalents (TEQ) concentrations were notably elevated as compared to national reference samples for most exposure media, and the marker congener was a major contributor to increased TEQ levels. There were also indications of soil-to-air volatilization of tetra- and penta-CDD/Fs. People who participated in the restoration of a contaminated building showed higher levels of 1234678-HpCDF compared to controls, and calculated exposure levels suggest that several site-specific exposure routes may be of importance for the daily intake of PCDD/F. CONCLUSIONS, RECOMMENDATIONS, AND PERSPECTIVES: Despite low mobility of higher chlorinated PCDD/Fs, these contaminants were transferred from the polluted soil to the surroundings and into human tissue. The extent of increased exposure from contaminated sites depends on the PCDD/F source strength of the soil, composition of the pollution, human activities, and dietary patterns of the residents. Impact from the contaminated soil on other exposure media was seen also for areas with low to moderate soil contamination. In the future, not only the levels of PCDD/F soil pollution but also the composition must be considered in risk assessments of contaminated sites.

Trace analysis of 2,3,7,8-polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs) and the 12 WHO-PCBs (four non-ortho and eight mono-ortho congeners that have been assigned toxic equivalence factors, TEFs, by the World Health Organisation) was conducted by comprehensive two-dimensional gas chromatography with a micro electron-capture detector (GC x GC-microECD). Four food matrices (fish oil from herring, spiked cows' milk, vegetable oil and an eel extract) were analysed by two GC x GC laboratories, and four GC-HRMS laboratories generated reference values. The two GC x GC laboratories used different column combinations for separating the target analytes. For the first dimension, non-polar DB-XLB and VF-1 columns were used, and for the second dimension, an LC-50 liquid crystalline column with unique selectivity for planar compounds. The congener-specific and total toxic equivalence (TEQ) data obtained using DB-XLB x LC-50 were in good agreement with results obtained by the GC-HRMS laboratories. The WHO-PCB data obtained with the VF-1 x LC-50 combination was also good, but the PCDD/F concentrations were sometimes overestimated due to matrix interferences. GC x GC-microECD using DB-XLB x LC-50 seems to fulfil the European Community requirements of a screening method for PCDD/F and WHO-PCB TEQ in food.

This work compares two lipid extraction methods for determining 24 polychlorinated biphenyls (PCBs), seven dibenzo-p-dioxins (PCDDs) and ten dibenzofurans (PCDFs) in human blood plasma. The first method was based on conventional liquid-liquid partitioning with chloroform-methanol and the other made use of a sorbent (Chem-Elut) to facilitate the partitioning of lipids into a mixture of hexane and 2-propanol. A multi-layer-silica column including acid- and base-impregnated silica gel was used to reduce the amounts of lipid present in the samples before a basic alumina clean-up step and activated carbon fractionation of planar analytes (PCDD/Fs and non-ortho-PCBs) and non-planar analytes (including ortho-chlorinated PCBs). Gas chromatography coupled to high resolution mass spectrometry was used to identify and quantify the analytes in the two fractions. The wet weight based concentrations obtained by the two methods were in agreement but both methods suffer from large organic solvent consumption. The toxic equivalencies derived for PCBs and PCDD/Fs using the two methods were also in agreement. However, the chloroform-methanol method gave slightly higher lipid recoveries, although with greater variation, than the sorbent-assisted method. Nevertheless, despite giving lower lipid recoveries, the sorbent-assisted method has advantages in ease of use and applicability to whole blood samples. The formation of emulsions was avoided with the Chem-Elut method, which probably explains the lower variability in the lipid determinations.

Soils from five agricultural sites, three research sites, and two privately owned farms were analyzed for polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), polychlorinated biphenyls (PCBs), and polybronimated diphenylethers (PBDEs). In soils that had not been treated with sludge (reference soils), the international toxic equivalents (I-TEQs) were 0.6 to 1.5 pg/g dry matter (D.M) for the PCDD/Fs. which are low compared to generally reported background soil levels in Europe. The concentrations of sum of six penta- and hexa-PCBs were 450 to 1,400 pg/g DM. The PBDEs 47 and 99 dominated among the tri- to hepta-PBDEs analyzed (8-80 pg/g DM). The impact of adding 1 to 3 tonnes of sludge (DM) per hectare per year on the concentrations was studied at the three research sites by calculating ratios of the compounds in sludge-treated soil to reference soil (S/R ratio). The concentrations of I-TEQs did not increase in the sludge-treated soil, whereas the S/R ratios for PBDEs were greater than one. Also, although the PCB contents were higher in the sludge-treated soils, the background sources were more important for the concentrations of PCBs than of PBDEs. The largest increase in the S/R ratios was found at a private farm where large amounts of sludge had been used in the past. Accumulation of the compounds in earthworms from the sites also was investigated. The biota-soil accumulation factors (BSAFs) of the tested compounds declined in the following order: ortho-PCBs approximately PBDEs > non-ortho-PCBs > 2.3,7,8-substituted PCDD/Fs. The average BSAF for ortho-PCBs was five (organic matter/lipids), and the lowest BSAFs (0.1-0.8) found were for octachlorodibenzo-p-dioxin. To our knowledge, accumulation of PBDEs in earthworms has not been published previously.

A total of 159 cases of chloracne reported in 1969-1975 in TCDD-contaminated production of the herbicide 2,4,5-T have been followed for mortality and morbidity up to 1996 when blood and urine tests were performed on 50 survivors of these exposed chemical workers and matched controls. In exposed, the most frequent cause of sick leave was chloracne which persisted in 32%. Neurological symptoms were reported frequently (44% sleep disturbance, 32% headache, 30% neuralgia). BSR, leucocytes, gamma-GT, SGOT, and SGPT were significantly higher in exposed than in controls. The effects of exposure (P= 0.002) and alcohol (P= 0.002) on gamma-GT were found to be independent of each other. Comparisons within the chloracne cohort showed significantly exposed TCDD per gram blood lipid in patients with a history of liver disease (mean 801 pg/g) than without (mean 407 pg/g). Other congeners were not found elevated but some higher chlorinated furans and PCBs were found reduced in patients with liver disease. In multiple regression analysis with the factors age, alcohol, and log TCDD, the effects of TCDD and its interaction with age were found significant, indicative of chronic liver damage after high TCDD exposure at a young age. The prevalence of neurological symptoms and signs of chronic liver disease were related to TCDD in blood and abnormal poryphyrins in urine. In 48% coproporphyrin I > III ratio was elevated, this group showing increased TCDD (mean 719 pg/g). These results contribute to the evidence that chloracne is not the only chronic disease which can be related to TCDD exposure, even 23 years after exposure and despite high intersubject variability of TCDD half-life and other exposures.

Nine catfish fillets, three catfish nuggets, two feed samples, and one pond sediment were analyzed for PCDD, PCDF, and PCB. Farm-raised catfish from Mississippi, Alabama, and Arkansas contained significant levels of 2,3,7,8-substituted PCDD and PCDF. In addition, a large number of non-2,3,7,8-substituted congeners were present in all samples. The catfish fillets and catfish nuggets also contained high concentrations of dioxin-like PCB, as well as a number of non-dioxin-like PCB. The TEQ based on PCDD and PCDF ranged from 9.5 to 43.0 pg/g lipid and the TEQ based on PCB ranged from 0.45 to 4.9 pg/g lipid for all catfish samples. The dioxin-like PCB contributed 4-16% to the total TEQ (PCDD/PCDF/PCB) for the catfish samples. The major source for the PCDD, PCDF, and PCB appears to be from feed and not from pond sediment. Immunoreactive CYP1A protein was elevated 2.5 fold in the pond-raised catfish compared to the aquarium-raised one. The results of this study suggest that the PCDD/PCDF are more important than the PCB in the CYP1A induction.

One combined catfish feed sample from Arkansas, USA, and its eight ingredients were analyzed for PCDDs and PCDFs. One of the ingredients, soybean meal, was highly contaminated by PCDDs, especially the toxic 2,3,7,8-substituted congeners, e.g., 7.3 pg/g dry weight or 370 pg/g lipid for the 2,3,7,8-tetra CDD. The I-TEQ value for the soybean meal was 11.4 pg/g dry weight or 576 pg/g fat. The corresponding values for the combined catfish feed concentrations were approximately 3 times lower. The congener pattern, the congener profile and the ratio sigma PCDDs/sigma PCDFs for the soybean meal were quite unique. We are not aware of any environmental sample or technical product with similar characteristics. As a result, natural formation of the PCDDs found in the soybean meal cannot be ruled out.

In 1994, we analyzed 43 foodstuff samples from local supermarkets in southern Mississippi, USA, for PCDD/PCDF. 2,3,7,8-Cl4DD could be quantified in 31 of these samples. On a lipid basis, levels in meat (0.53-1.10 pg I-TEQ/g) and dairy products (0.42-1.10 pg I-TEQ/g) were slightly lower than those reported from other industrialized countries. While levels in dairy samples from the United States and Europe are comparable, there is a difference in the contribution of individual congeners to the I-TEQ: for example, in milk samples from Germany approximately 40% of the I-TEQ is due to the presence of 2,3, 4,7,8-Cl5DF while in the Mississippi samples this congener only contributes 16%. The highest concentrations of PCDD/PCDF in our study were detected in the farm-raised catfish (10.2-27.8 pg I-TEQ/g). A unique finding was that in addition to the 2,3,7,8-substituted PCDD/PCDF the catfish samples contained many non-2,3,7,8-substituted congeners. This is unusual because vertebrate animals selectively eliminate or metabolize the non-2,3,7,8-substituted congeners.