Chlorierte aromatische zyklische �ther als Ursache der sogenannten Chlorakne

Kimmig, J; Schulz, K. H.

doi:10.1007/bf00630959

Cited by 56 publications

(8 citation statements)

References 1 publication

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The biologically most active congener, and in experimental studies the one with the highest toxic potency, is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, or "Seveso-dioxin"), for which the largest data base exists. Its connection with chloracne was revealed already in 1957 [7].…”

Section: Introductionmentioning

confidence: 94%

Reflections on the assessment of the toxicity of “dioxins” for humans, using data from experimental and epidemiological studies

Neubert

1997

Teratog. Carcinog. Mutagen.

View full text Add to dashboard Cite

"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.

show abstract

Section: Introductionmentioning

confidence: 94%

Reflections on the assessment of the toxicity of “dioxins” for humans, using data from experimental and epidemiological studies

Neubert

1997

Teratog. Carcinog. Mutagen.

View full text Add to dashboard Cite

show abstract

“…It produces chloracne in man and rabbits (Kimmig and Schulz, 1957;Jones and Krizek, 1962) and causes several pathologic changes in the liver of different species (Gupta et al, 1973;Jones and Butler, 1974;Vos et al, 1974). Edemas were reported in chickens (Schwetz et al, 1973), in mice (Vos et al, 1974) and in rat fetuses after maternal treatment (Khera and Ruddick, 1973).…”

Section: Introductionmentioning

confidence: 99%

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on early life stages of the pike (Esox lucius L.)

Helder

1980

Science of The Total Environment

View full text Add to dashboard Cite

Freshly fertilized pike eggs were exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) at concentrations of 0.1, 1.0 and 10 ppt (ng/liter) for 96 hours. At all concentrations examined egg development was retarded by 23%, and the growth of fry was also significantly retarded for a long period after exposure. A dose-related mortality was observed. Highest mortality rates occurred during resorption of the yolk and reached almost 100 percent at a concentration of 10 ppt. Death was preceded by development of severe generalized edemas.Histopathologically edemas and hemorrhages were observed, together with alterations of bloodvessel walls. In the liver, two stages of pathological changes were distinguished. The first was characterized by a dilation of sinusoids and a slight swelling of hepatocyte nuclei; in the second stage the nuclei were enlarged up to twice the normal diameter. Hepatocytes were degenerated and varied in size and shape and liver architecture was a almost completely lost.

show abstract

“…'-3 The agent most likely to have caused these responses was not determined until 1957 when 2,3,7,8-tetrachlorodibenzop-dioxin (TCDD) was chemically identified as a byproduct of trichlorophenol production and was shown to be a potent inducer of chloracne. 4 As well as the clinical reports, follow up studies were conducted to evaluate the mortality experience of exposed employees.56 The eventual study population included persons who assisted in demolishing the autoclave portion of the unit in 1968-9 as well as those assigned to prior assessment and clean up activities. Although other materials were produced by the unit after the accident, trichlorophenol production was not resumed.…”

mentioning

confidence: 99%

Morbidity follow up study of BASF employees exposed to 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) after a 1953 chemical reactor incident.

Zober¹,

Mg²,

Messerer³

1994

Occup Environ Med

107

View full text Add to dashboard Cite

show abstract

Chlorierte aromatische zyklische �ther als Ursache der sogenannten Chlorakne

Cited by 56 publications

References 1 publication

Reflections on the assessment of the toxicity of “dioxins” for humans, using data from experimental and epidemiological studies

Reflections on the assessment of the toxicity of “dioxins” for humans, using data from experimental and epidemiological studies

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on early life stages of the pike (Esox lucius L.)

Morbidity follow up study of BASF employees exposed to 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) after a 1953 chemical reactor incident.

Contact Info

Product

Resources

About