No abstract

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.

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 μg 2378-TCDD kg-1 (using EPA TEFs) or 6.7-16 μg 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.

The consequences of exposure of people to highly chlorinated polychlorodibenzop-dioxins (PCDDs) are much less known than those of TCDD. We report on levels of PCDDs (and PCDFs) in 13 members of two families poisoned by contaminated cooking oil. Originally, all persons displayed chloracne as an early symptom.Persisting hexa-and higher chlorinated PCDDs could be analysed many years after exposure. Highest values found in blood lipids were: OCDD 660,000 pg/g; HpCDD 58,000 pg/g; HxCDDs: 3,500 pg/g. None of the participants exhibited increased TCDD levels at the time of study. During a period of 6 years, HpCDD and OCDD disappeared from the blood lipids much faster in persons exposed as children or young adults, than from lipids of their parents. Surface receptors on blood lymphocytes of the members of the two families and the proliferative capacity of these blood cells in the presence of typical stimulants were analysed. Even in family members with the highest body burdens of hexa-to octachlorinated PCDDs we could not detect pronounced changes from a reference population with respect to the immunological markers. Minor deviations of levels of some receptors in a few, but not all, highly exposed persons suggested a similar trend to those reported in previous studies of persons with body burdens of ≥ 3,000 pg TCDD/g blood lipids. An increase in the number of total blood lymphocytes in some subjects exposed as children may have similarity with highly TCDD-exposed children in Seveso.2