The absorption of polychlorinated biphenyls, dibenzo-p-dioxins and dibenzofurans was studied in four breast-fed infants. The absorption was measured by comparing the estimated total intake and the excretion in faeces, during 48 hours, at three different time points; 1, 2 and 3 months post parta. The levels of the analysed compounds in the human milk are typical for Sweden, i.e approximately 20 ppt toxic equivalents for the dibenzo-p-dioxins and dibenzofurans and for the polychlorinated biphenyls approximately 16 ppt toxic equivalents. For most of the congeners the absorption is found to be over 95%. Higher excretion is noticed for heptachlorinated and octachlorinated dioxins.
1. All members of a Spanish family (father, mother and six children) developed chloracne. 2. The causative agent was found to be the family's stock of olive oil, which had become contaminated with polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), pentachlorophenol, and hexachlorobenzene. 3. The more highly chlorinated PCDDs, in particular octachlorodibenzo-p-dioxin, were the predominant congeners in the oil. 4. Three members of the family exhibited either an overt or a sub-clinical disturbance of kidney function. The father also had a chronic respiratory problem. These changes could not be unequivocally attributed to the PCDDs. 5. Experimental toxicity of the oil was limited to the development of an hepatic porphyria in mice. 6. A serum sample, taken 5 years after consumption of the oil ceased, contained high levels of the PCDDs and PCDFs. Extrapolation back to ingested dose was used to validate dosage estimates. 7. The use of toxicity equivalence factors (TEFs) provided estimates of cumulative dosage to produce chloracne as 0.13-0.31 micrograms 2378-TCDD kg-1 (using EPA TEFs) or 6.7-16 micrograms 2378-TCDD kg-1 (using Nordic/NATO TEFs). 8. This is the first incident in which human toxicity is related primarily to ingestion of PCDDs and for which estimates of dosage can be made.
In some regions, including the Baltic Sea, fatty fish such as salmon and herring contain high levels of polychlorinated dibenzodioxins and dibenzofurans. We investigated human exposure to these potentially toxic substances in relation to the consumption of fish from the Baltic Sea.
Plasma levels of 10 different dibenzofurans and 7 dioxins were analyzed in three groups of Swedish men: one group with a high intake of fish (fish eaten almost daily; n = 11), one with a moderate intake of fish (about once per week; n = 9), and one with no consumption of fish (usually because of allergy; n = 9).
Plasma levels of several of the compounds we measured were higher in the men with a high intake of fish than in those who consumed moderate amounts, and the levels were higher in those who ate moderate amounts of fish than in those who ate none. The median amounts of the most toxic dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin) were 8.0 pg per gram of plasma lipid (range, 2.0 to 13) in the high-intake group, 2.6 pg per gram (range, 1.2 to 4.2) in the moderate-intake group, and 1.8 pg per gram (range, 1.0 to 2.5) in the nonconsumers (P = 0.001 and 0.02, respectively). There were consistent and statistically significant associations between the reported amount of fish eaten and the plasma levels of several of the dibenzofurans and dioxins.
Contaminated fish such as those from the Baltic Sea are an important source of exposure to polychlorinated dibenzofurans and dibenzodioxins in persons who eat fish regularly. However, the clinical consequences of such exposure remain uncertain.
M. glutinosa is a cyclostome, living in the mud in seawater of high salinity. It probably is a stationary scavenger feeder. About 28,000 hagfish from the Gullmar Fjord were examined during a 5-year period for the occurrence of tumors. Hepatomas were found to be predominant neoplasm, observed at a frequency that decreased from 5.8% in 1972 to 2.9% in 1973 and finally to 0.6% in 1974--76. Islet cell hamartomas and frank neoplasms decreased from 0.5% in 1972 to less than 0.1% in 1973--76. Occasional subcutaneous and mesenterial neoplasms were also observed during 1972--74. In hagfish caught 12 km out in the open sea, the hepatoma incidence decreased from 2.8% in 1972 to 0.9% in 1974. Given this background, it is possible that pollution of the Gullmar Fjord by carcinogenic substances with low biodegradability has occurred until 1972, and this pollution could be of etiologic significance for these hagfish tumors. In fact, the use of PCBs became prohibited by law in Sweden in 1971--72. Severe restrictions were also introduced for the use of chlorinated pesticides, notably DDT, and associated substances (DDD, DDE). Preliminary analyses for the presence of PCBs, DDT (and its metabolites), and aflatoxins (the notorious hepatocarcinogen) were performed by gas chromatography and thin-layer chromatography. Livers (with and without neoplasms) from hagfish caught inside the threshold of the fjord contained about 5 mg/kg of wet weight of PCBs and about 0.1--0.4 mg/kg of dry weight of DDT, DDD, or DDE, whereas those from hagfish caught in the open sea had a much lower PCB concentration (about 0.2 mg/kg of wet weight). No PCBs and no chlorinated pesticides were found in analyses of the mud at the catching site. High PCB concentrations (3 mg/kg of wet weight) were, however, observed in livers from cod living in the Gullmar Fjord, and it was proposed that bony fish may be the source of hagfish liver PCBs. PCB chromatograms of hagfish livers differed from those of PCB standards and cod liver. This strange pattern, which was not seen in livers from hagfish caught in the open sea, might be explained by an unusual mode of metabolization. The assays for aflatoxins gave completely negative results.
The production of chlorine and vinyl chloride (VCM) is associated with the formation of polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs). The objective of the present study was to determine whether the levels and congener patterns of PCDDs and PCDFs in the blood of workers involved in the production of such substances could be related to their occupational environment. PCDD and PCDF levels in blood plasma from VCM and chloralkali workers and in referents were determined by means of high-resolution gas chromatography/high resolution mass spectrometry (HRGC/HRMS) techniques and the results were evaluated through principal component analysis (PCA). The overall levels of PCDDs and PCDFs were low, but the relative congener distribution detected in the workers differed from that found in the referents. 1,2,3,4,6,7,8-HpCDF, 1,2,3,4,7,8- and 1,2,3,6,7,8-HxCDFs are congeners related to work in VCM and chloralkali industries. Exposure to PCDDs and PCDFs in these industrial environments changes the congener-distribution pattern in the blood of workers as compared with referents. A combination of isomer-specific analysis of PCDDs and PCDFs in blood plasma and PCA is suitable for the differentiation between nonoccupational and occupational exposure and provides a means of assessing workers' exposure situation in different occupational settings.
A cohort study of 142 male Swedish capacitor manufacturing workers was performed. PCB had been used as a dielectricum in power capacitors between 1960 and 1978. Mortality was investigated for the period 1965 to 1982 and cancer incidence from 1965 to 1980. Twenty-one deaths and seven cancers were observed, which was in agreement with the anticipated numbers calculated from national statistics. One person had developed two rare tumors, a slow growing mesenchymal tumor (desmoid) and a malignant lymphoma. The results cannot rule out the possibility of a carcinogenic risk from PCB exposure because of the small size of the cohort and relatively brief follow-up period, but they do not indicate any excess mortality or cancer incidence in this factory so far.
A series of polychlorinated biphenyl (PCB) fires and explosion in PCB-filled capacitors and transformers is discussed. A sampling program followed by isomer specific determination of trace levels of polychlorinated dibenzofurans (PCDFs) and polychlorinated dibenzo-p-dioxins (PCDDs) is described. Data from a series of Swedish PCB accidents are given. In addition to PCDFs and PCDDs, we have also found a series of polychlorinated biphenylenes (PCBPs). Cleaning of contaminated areas was done by vacuum cleaning followed by high pressure washing.