Abstract: 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 m… Show more
“…The poisoning scenario and clinical data for Family 1 were reported previously (Hansson et al, 1995b;Rappe et al, 1998;Rodriguez-Pichardo and Camacho, 1990;Rodriguez-Pichardo et al, 1991). The existence of Family 2 has only been briefly reported before (Rappe et al, 1998).…”
Section: Introductionmentioning
confidence: 76%
“…The data suggest (Rappe et al, 1998;Rodriguez-Pichardo et al, 1991) that higher chlorinated congeners of PCDDs and PCDFs are capable of inducing chloracne. Body burdens predominantly consisted of hepta-and octachlorinated congeners, for which little information is available, and levels of the dioxins were very high (>500,000 ppt OCDD in some cases) although the early measurements closer to the time of exposure, when the skin lesions existed, also showed moderately increased levels of penta-and hexachlorinated congeners in the plasma.…”
Section: Discussionmentioning
confidence: 99%
“…A further son was born a few months after the family were first seen (Rodriguez-Pichardo and Camacho, 1990;Rodriguez-Pichardo et al, 1991). Blood samples from the most severe cases originally, were combined in 1987 and together with the contaminated olive oil analysed for PCDDs and PCDFs.…”
Section: Familiesmentioning
confidence: 99%
“…The father also suffered from severe respiratory problems at the time of presentation and the youngest son developed convulsions soon after birth which did not reoccur after his mother stopped breast feeding. In early years his growth was apparently retarded (Rodriguez-Pichardo et al, 1991). Oil was consumed by use in cooking and as a salad dressing.…”
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
“…The poisoning scenario and clinical data for Family 1 were reported previously (Hansson et al, 1995b;Rappe et al, 1998;Rodriguez-Pichardo and Camacho, 1990;Rodriguez-Pichardo et al, 1991). The existence of Family 2 has only been briefly reported before (Rappe et al, 1998).…”
Section: Introductionmentioning
confidence: 76%
“…The data suggest (Rappe et al, 1998;Rodriguez-Pichardo et al, 1991) that higher chlorinated congeners of PCDDs and PCDFs are capable of inducing chloracne. Body burdens predominantly consisted of hepta-and octachlorinated congeners, for which little information is available, and levels of the dioxins were very high (>500,000 ppt OCDD in some cases) although the early measurements closer to the time of exposure, when the skin lesions existed, also showed moderately increased levels of penta-and hexachlorinated congeners in the plasma.…”
Section: Discussionmentioning
confidence: 99%
“…A further son was born a few months after the family were first seen (Rodriguez-Pichardo and Camacho, 1990;Rodriguez-Pichardo et al, 1991). Blood samples from the most severe cases originally, were combined in 1987 and together with the contaminated olive oil analysed for PCDDs and PCDFs.…”
Section: Familiesmentioning
confidence: 99%
“…The father also suffered from severe respiratory problems at the time of presentation and the youngest son developed convulsions soon after birth which did not reoccur after his mother stopped breast feeding. In early years his growth was apparently retarded (Rodriguez-Pichardo et al, 1991). Oil was consumed by use in cooking and as a salad dressing.…”
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
“…Total estimated TCDD TEQ body burdens were 150 pg or approximately 200-fold greater than the average current level of TCDD TEQs in North American adults (81). In comparison, the estimated chloracneinducing dose in a Spanish family who ingested PCDD/PCDF-contaminated olive oil for approximately 6 to 7 months was 32 to 76 ng/kg/day (82). The discrepancy between the two estimated chloracneinducing doses may be the result of congener patterns; in the rice oil poisonings, PCDFs were more prevalent, but PCDDs were more predominant but in the olive oil example.…”
One of the major goals of the Great Lakes Action Plan is to actively accumulate and assess toxicological information on persistent toxic substances found in the Great Lakes basin.
"Dioxins" (polyhalogenated dibenzo-p-dioxins and dibenzofurans, PHDDs/PHDFs) have gained considerable scientific interest, and (unjustified or justified) also received tremendous political attention. The data pool available on sources, distribution in the environment, kinetics in animals and humans, and on biological and toxic actions in various species (including humans), is one of the largest among all environmental organic substances; but quality and predictive power of the data on possible effects in humans vary widely, from adequate to not acceptable. This fact is often ignorantly or perhaps even deliberately disregarded, and such divergent data are frequently given the same weight in attempted risk assessments. It must be stressed that the quality of the toxicological data on most "environmental compounds" in general is far below today's standards required for preclinical and clinical data on medicinal substances. The crucial question is whether humans constitute an especially vulnerable species for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or the other PHDDs/PHDFs. Since ample data on body burdens and some results of clinical and epidemiological studies on TCDD have become available, answering this question may now be attempted on the basis of a comparison of animal and human data. Quality of the data and the predictive power of the methods used must be considered, dose-response relationships must be critically evaluated, and body burdens achieved in humans and experimental animals must be taken into account. Pitfalls in attempts to extrapolate data from animal studies to humans and limitations of conclusions to be drawn from epidemiological data on humans are discussed in this presentation.
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