Chloracne

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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...

Chloracne is an extremely rare acneiform eruption triggered by exposure to chemicals containing halogenated aromatic hydrocarbons. Unlike acne, which tends to affect areas with a high concentration of sebaceous glands, the most common areas affected by chloracne are the periocular, periauricular, genital, and axillary regions. Histopathology showing characteristic loss of sebaceous glands is supportive of the diagnosis. Numerous open comedones varying in size from small to large and yellow-white inflammatory papules may be appreciated on dermoscopy...

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The legacy of polychlorinated naphthalenes (PCNs) manufactured during the last century continues to persist in the environment, food and humans. Metrological advances have improved characterisation of these occurrences, enabling studies on the effects of exposure to focus on congener groups and individual PCNs. Liver and adipose tissue show the highest retention but significant levels of PCNs are also retained by the brain and nervous system. Molecular configuration appears to influence tissue disposition as well as retention, favouring the higher chlorinated (≥ four chlorines) PCNs while most lower chlorinated molecules readily undergo hydroxylation and excretion through the renal system...

OBJECTIVE: To determine if occupational exposure to dioxins is associated with an increased frequency of t(14;18) translocations. METHODS: A cross-sectional analysis of serum dioxin levels and t(14;18) frequencies in peripheral blood mononuclear cells in 218 former chemical plant workers and 150 population controls. RESULTS: The workers had significantly higher geometric mean serum levels of 2,3,7,8-TCDD (26.2 vs 2.5 ppt) and TEQ (73.8 vs 17...

To determine the cutaneous effects of in utero and lactational exposure to the AHR ligand 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD), pregnant C57BL/6J mice were exposed by gavage to a vehicle or 5 μg TCDD/kg body weight at embryonic day 12 and epidermal barrier formation and function were studied in their offspring from postnatal day 1 (P1) through adulthood. TCDD-exposed pups were born with acanthosis. This effect was AHR-dependent and subsided by P6 with no evidence of subsequent inflammatory dermatitis...

BACKGROUND: Chloracne is a rare skin condition that is caused by systemic exposure to halogenated aromatic compounds. The main characteristic of chloracne is blackhead, and in severe cases, it can be accompanied by systemic symptoms. Sodium 3,5,6-trichloropyridin-2-ol (STCP) is a necessary precursor compound for the production of chlorpyrifos and triclopyr, which are extensively used as a pesticide and herbicide, respectively. STCP is also a chlorophenol that has been associated with chloracne...

The term dioxin is commonly used to describe a group of ubiquitous environmental contaminants: polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDD/Fs, 209 different compounds). The best studied compound among the group in relation to its higher toxicity is 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD). Polychlorinated biphenyls (PCBs) are a group of environmental compounds containing certain substances known as "dioxin-like PCBs (dl-PCBs)" with a similar mechanism of action to dioxins...

BACKGROUND: Although polychlorinated biphenyls (PCBs) have been classified as human carcinogens for their association with melanoma, few data are available for other skin lesions. OBJECTIVES: To investigate the prevalence of skin disorders in a highly PCB polluted area in northern Italy, with locally produced food as the main source of human contamination, and evaluate the association between skin lesions and PCB serum levels, taking account of possible confounders...

Poisoning by high concentrations of dioxin and its related compounds manifests variable toxic symptoms such as general malaise, chloracne, hyperpigmentation, sputum and cough, paresthesia or numbness of the extremities, hypertriglyceridemia, perinatal abnormalities, and elevated risks of cancer-related mortality. Such health hazards are observed in patients with Yusho (oil disease in Japanese) who had consumed rice bran oil highly contaminated with 2,3,4,7,8-pentachlorodibenzofuran, polychlorinated biphenyls, and polychlorinated quaterphenyls in 1968...

Dioxins and dioxin-like compounds are environmental pollutants that are hazardous to human skin. They can be present in contaminated soil, water, and air particles (such as ambient PM2.5 ). Exposure to a high concentration of dioxins induces chloracne and hyperpigmentation. These chemicals exert their toxic effects by activating the aryl hydrocarbon receptor (AHR) which is abundantly expressed in skin cells, such as keratinocytes, sebocytes, and melanocytes. Ligation of AHR by dioxins induces exaggerated acceleration of epidermal terminal differentiation (keratinization) and converts sebocytes toward keratinocyte differentiation, which results in chloracne formation...

The aryl hydrocarbon receptor (AHR) mediates 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) induced toxicity that can lead to chloracne in humans. A characteristic of chloracne, in contrast to acne vulgaris, is shrinkage or loss of sebaceous glands. Acne vulgaris, on the other hand, is often accompanied by excessive sebum production. Here, we examined the role of AHR in lipid synthesis in human sebocytes using distinct classes of AHR ligands. Modulation of AHR activity attenuated the expression of lipogenic genes and key pro-inflammatory markers in the absence of canonical DRE-driven transcription of the AHR target gene CYP1A1...

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Exposure to toxic halogenated polyaromatic hydrocarbons, of which 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is the most potent, induces diverse skin pathologies in humans, including chloracne, hyperkeratosis, hamartomas, etc. While the toxic effects of TCDD have been extensively studied, effective approaches to their treatment are still lacking. Retinoids are commonly used in therapy of acneiform skin diseases. In vitro, retinoids elicit antagonistic effects on keratinocyte differentiation and proliferation, as compared to TCDD, suggesting their potential in treatment of TCDD-induced skin lesions...

2,3,7,8-Tetrachlordibenzo- p-dioxin (TCDD) is an environmental pollutant that can cause various toxic effects, including chloracne, metabolic syndrome, and immune suppression. Most of the toxicity associated with TCDD is mediated through activation of the aryl hydrocarbon receptor (AHR). Recent research has suggested the presence of a wide-range of interindividual variability in TCDD-mediated suppression of the Immunoglobulin-M (IgM) response across the human population. In an attempt to identify putative modifiers of AHR-mediated immunosuppression beyond the AHR, B cells were isolated from a panel of genetically diverse mouse strain to scan for modulators that drive interstrain differences in TCDD-mediated suppression of the IgM response...

Chloracne is the major skin symptom caused by dioxin intoxication. Dioxin activates the aryl hydrocarbon receptor (AHR)⁻cytochrome p450 1A1 (CYP1A1) system, generates oxidative stress, and induces hyperkeratinization of keratinocytes and sebocytes leading to chloracne. Nuclear factor-erythroid 2-related factor-2 (NRF2) is a master switch that induces the expression of various antioxidative enzymes, such as heme oxygenase-1. Cinnamaldehyde is an antioxidant phytochemical that inhibits AHR⁻CYP1A1 signaling and activates the NRF2⁻antioxidative axis...

Aryl hydrocarbon receptor (AHR) is a chemical sensor that is expressed abundantly in epidermal keratinocytes. Oxidative AHR ligands induce the production of reactive oxygen species. However, antioxidant AHR ligands inhibit reactive oxygen species generation via activation of nuclear factor-erythroid 2-related factor-2, which is a master switch for antioxidative signalling. In addition, AHR signalling accelerates epidermal terminal differentiation, but excessive acceleration by oxidative ligands, such as dioxins, may induce chloracne and inflammation...

BACKGROUND: Patients treated with vemurafenib for metastatic melanoma often develop skin lesions similar to those observed after exposure to dioxin-like compounds. We previously called these lesions MADISH (metabolizing acquired dioxin-induced skin hamartoma) when analysing a case of acute dioxin poisoning. OBJECTIVE: We performed a clinical trial aimed at comparing the skin lesions observed under vemurafenib treatment with MADISH in order to bring to light a possible cross-talk between vemurafenib and dioxin pathways...

An 11-year-old boy presented with a 1-year history of multiple comedonal lesions distributed over his body. The lesions (Figure 1) were densely distributed throughout his body. Ophthalmologic examination revealed hyperpigmented conjunctival mucosae and enlarged meibomian glands (Figure 2). His nails were also hyperpigmented. In addition, he had been coughing and had a fever, each present for a month. Significant laboratory studies included mild anemia (hemoglobin 11.6 gm%) and leukocytosis of 20,800. A chest x-ray was suggestive of interstitial lung disease...