The Response of Rabbit Skin to Compounds Reported to Have Caused Acneform Dermatitis

Adams, Eliane; Irish, D. D.; Spencer, Howard C.; Rowe, V. K.

doi:10.1080/00968204109343795

Cited by 16 publications

(8 citation statements)

References 8 publications

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“…Rabbit ear model is exquisitely sensitive to dioxin 1 and is widely used for the evaluation of chloracnegenic potency of chemical mixtures and as a detection system for the presence of dioxin in contaminated soil and at commercial workplaces (26,80,81). Surprisingly, this model has never been used for studies of cellular and molecular mechanisms of chloracne development.…”

mentioning

confidence: 99%

Dioxin‐induced chloracne – reconstructing the cellular and molecular mechanisms of a classic environmental disease

Panteleyev

Bickers

2006

Experimental Dermatology

130

120

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: 2,3,7,8‐Tetrachlorodibenzo‐p‐dioxin (TCDD) is among the most toxic pollutants known to date that serves as a prototype for a group of halogenated hydrocarbon compounds characterized by extraordinary environmental persistence and unique ability to concentrate in animal and human tissues. TCDD can elicit a complex array of pleiotropic adverse effects in humans, although chloracne, a specific type of acne‐like skin disease, is the only consistent manifestation of dioxin intoxication, thus representing a ‘hallmark’ of TCDD exposure. Chloracne is considered to be one of the most specific and sensitive biomarkers of TCDD intoxication that allows clinical and epidemiological evaluation of exposure level at threshold doses. The specific cellular and molecular mechanisms involved in pathogenesis of chloracne are still unknown. In this review, we summarize the available clinical data on chloracne and recent progress in understanding the role of the dioxin‐dependent pathway in the control of gene transcription and discuss molecular and cellular events potentially involved in chloracne pathogenesis. We propose that the dioxin‐induced activation of skin stem cells and a shift in differentiation commitment of their progeny may represent a major mechanism of chloracne development.

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mentioning

confidence: 99%

Dioxin‐induced chloracne – reconstructing the cellular and molecular mechanisms of a classic environmental disease

Panteleyev

Bickers

2006

Experimental Dermatology

130

120

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“…This occurrence is followed by plugging of the follicular orifice, which occurs simultaneously with the alteration of the differentiation process of the acinar cells. These cells, which are undifferentiated at the periphery, normally differen- chloracnegens since 1941 and is still widely used (1). Assessment of acnegenicity is made on the basis of clinical examination and histologic examination for epidermal hyperplasia, comedones, and epithelial cysts.…”

mentioning

confidence: 99%

Chloracne, "the hallmark of dioxin intoxication".

Rr¹

1985

Scand J Work Environ Health

119

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, "the hallmark of dioxinintoxication." Scand J Work Environ Health II (1985) 165-171. Clinical experiences and laboratory studies are described involving a population of workers who were exposed in a plant making 2,4,5-trichlorophenoxyacetic acid (2,4,5-T), including a trichlorophenol runaway reaction. Workers werefollowed for a period of four years, and 30 years later a mortality analysis was done on those exposed to runaway reaction material to determine possible increased risks for causes of death. Subsequently, a morbidity study on 436 employees involving three cohorts was carried out to determine the long-term health effects associatedwith the production of 2,4,5-T including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The mortality and morbidity studies demonstrated that the standardized mortality ratio for all causes of death was 69, and for cancer at all sites and cardiovascular disease it was 100and 68, respectively. The most significant observations emerging from the morbidity study werethat 86 0J0 of the exposedpersons developed chloracne at some time and that 52.7 070 still had chloracne on examination 20 to 30 years after the initial exposure. There appeared to be no evidence, on a long-term basis, of increased risks for cardiovascular disease, hepatic disease, renal disease, central and peripheral nerve problems, reproductive problems, or birth defects among the exposed and those who had chloracneamong the exposed. Studieson the cellkineticsand pathogenesisof chloracne indicate that TCDD induces the modulation of undifferentiated sebaceous gland cells to keratinocytes. This action results in a disappearance of sebaceous glands and substitution of closed comedones and keratin cysts. Production workers have the highest frequency and severity of chloracne and systemic effects. Populations of users of 2,4,5-T rarely, if ever, develop chloracne, and there appear to be no welldocumented systemic effects. Among populations which live in accidentally or otherwise contaminated environments, there are only a limited number of chloracne cases and no well-documented systemic effects. Sufficientexposureto TCDD can inducechloracne,but systemic manifestations such as peripheral neuritis and transient hepatic dysfunctionoccur only in associationwith and subsequentto the appearance of chloracne. Chloracne is the hallmark of TCDD absorption and biological response in humans.

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“…Anyone coming out of the building had to do so through a special decontamination room where he had assistance to change. The presence of dioxin on the walls, roof, and other parts of the plant was shown by painting a solution prepared from rubbings taken from different parts of the building on the inner side of rabbits' ears, as first demonstrated by Adams, Irish, Spencer, and Rowe (1941). The results were so consistent that they were checked by testing the plain solvent and even rubbings from new asbestos to demonstrate that these, on their own, could not produce chloracne.…”

Section: Treatment Of the Buildingmentioning

confidence: 88%

Chloracne from the accidental production of tetrachlorodibenzodioxin

May

1973

Occupational and Environmental Medicine

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The Response of Rabbit Skin to Compounds Reported to Have Caused Acneform Dermatitis

Cited by 16 publications

References 8 publications

Dioxin‐induced chloracne – reconstructing the cellular and molecular mechanisms of a classic environmental disease

Dioxin‐induced chloracne – reconstructing the cellular and molecular mechanisms of a classic environmental disease

Chloracne, "the hallmark of dioxin intoxication".

Chloracne from the accidental production of tetrachlorodibenzodioxin

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