Biochemical Changes Associated with Chloracne in Workers Exposed to Tetrachlorazobenzene and Tetrachlorazoxybenzene

Scarisbrick, Douglas; Martin, J.V.

doi:10.1093/occmed/31.4.158

Cited by 13 publications

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“…Three outbreaks of chloracne have occurred among workers following exposure to TCAB (Morse and Baker, 1977; Morse et al, 1979; Scarisbrick and Martin, 1981) in chemical plants manufacturing 3,4-dichloroaniline or its derivatives. Chloracne developed in 34 to 61 percent of the exposed workers.…”

Section: Introductionmentioning

confidence: 99%

Inflammatory and chloracne-like skin lesions in B6C3F1 mice exposed to 3,3′,4,4′-tetrachloroazobenzene for 2 years

Ramot¹,

Nyska²,

Lieuallen³

et al. 2009

Toxicology

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Exposure to dioxin and dioxin-like compounds (DLCs) has been connected to the induction of chloracne in humans and animals. 3,3′,4,4′-Tetrachloroazobenzene (TCAB) is an environmental contaminant that induces chloracne in humans. TCAB has been studied only to a limited extent in laboratory animals. While performing a 2-year gavage study in B6C3F1 mice to evaluate the toxic and carcinogenic effects of TCAB, we also explored potential chloracnegenic properties. Groups of 50 male and 50 female B6C3F1 mice were exposed by gavage to TCAB at dose levels of 0, 3, 10 and 30 mg/kg for 5 days a week for 2 years. The animals developed treatment-related gross inflammatory skin lesions, which were characterized histologically by inflammation, fibrosis, hyperplasia, and ulcers. Additionally, many of the animals developed follicular dilatation and sebaceous-gland atrophy, consistent with chloracne-like lesions. This current 2-year study supports recently published papers showing susceptibility to chloracne in mouse strains other than hairless mice. The chloracne-like lesions were not clinically evident; therefore, our study highlights the need for careful examination of the skin in order to identify subtle lesions consistent with chloracne-like changes in rodents exposed to dioxin and DLCs. Since previous short term studies did not demonstrate any skin lesions, we suggest that reliable assessment of all safety issues involving dioxin and DLCs requires evaluation following chronic exposure. Such studies in animal models will help to elucidate the mechanisms of dioxin-related health hazards.

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Section: Introductionmentioning

confidence: 99%

Inflammatory and chloracne-like skin lesions in B6C3F1 mice exposed to 3,3′,4,4′-tetrachloroazobenzene for 2 years

Ramot¹,

Nyska²,

Lieuallen³

et al. 2009

Toxicology

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“…In the case of the polychlorinated biphenyls, the active acnegenic agent is presumed to be the chlorinated dibenzofurans. In the past five years reports have been published regarding the acnegenicity of chlorinated azobenzene and azoxybenzene compounds (12,23,25). These are also found as contaminants in the preparation of herbicides, in which 3,4-dichloroaniline has been used as in the preparation of the herbicides diuron, linuron, propanil, and neburon.…”

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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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“…The skin manifestations observed following dioxin exposure seem not specific of these compounds. Besides the herbicides and defoliants 2,4-dichlorophenoxyacetic acid and 2,4,5trichlorophenoxyacetic acid, which constituted the Agent Orange used by the US Army during the Vietnam War and contained TCDD as impurity, other chlorinated compounds used in the synthesis of herbicides, such as 3,3′,4,4′-tetrachloroazobenzene and 3,3′,4,4′-tetrachloroazoxybenzene, were shown to produce chloracne-like skin lesions in chemical workers (Kimbrough, 1980;Scarisbrick and Martin, 1981). Gawkrodger et al (2009) reported a case series of seven organic chemists exposed to novel polycyclic halogenated chemicals of the family of triazoloquinoxalines, who developed clinical skin manifestations similar to chloracne, without any other signs of toxicity.…”

Section: Chloracne-like Syndromesmentioning

confidence: 99%

Development of skin diseases following systemic exposure: example of dioxins

Sorg,

Saurat

2023

Front. Toxicol.

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Most skin manifestations of exposure to toxic compounds are a consequence of a direct contact with the toxicants. However, some toxicants may reach the skin following systemic exposure, and promote skin diseases. Good examples of such chemicals are dioxin-like compounds. This family of lipophilic molecules comprises polychlorinated (dibenzodioxins, dibenzofurans and biphenyls). The most potent member of this family is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Following oral ingestion of as little as a few mg TCDD, skin lesions appear in a couple of weeks, starting from the face and diffuse then on the trunk and limbs. This syndrome was historically called “chloracne” and the skin lesions have now been shown to be skin hamartoma induced by TCDD. Sweat glands release their lipid content on the surface of the skin by a holocrine secretion, and so any lost sebocyte should be transmitted to progenitor cells to differentiate and migrate to the sebaceous gland to replace the lost sebocyte. TCDD acts by inducing a switch in this signal and skin hamartoma develop in place of new sebocytes.

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Biochemical Changes Associated with Chloracne in Workers Exposed to Tetrachlorazobenzene and Tetrachlorazoxybenzene

Cited by 13 publications

References 0 publications

Inflammatory and chloracne-like skin lesions in B6C3F1 mice exposed to 3,3′,4,4′-tetrachloroazobenzene for 2 years

Inflammatory and chloracne-like skin lesions in B6C3F1 mice exposed to 3,3′,4,4′-tetrachloroazobenzene for 2 years

Chloracne, "the hallmark of dioxin intoxication".

Development of skin diseases following systemic exposure: example of dioxins

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