Toxicology of chlorinated dibenzo-p-dioxins.

Schwetz, Bernard A.; Norris, Jill M.; Sparschu, G.L.; Rowe, U K; Gehring, P.J.; Emerson, J L; Gerbig, Christoph

doi:10.1289/ehp.730587

Cited by 417 publications

(29 citation statements)

References 12 publications

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“…This condition was first described in German industrial workers in the late 19th century by Von Bettman (14) and later by Herxheimer (15) who suggested that it was caused by chlorine exposure and hence coined the term ‘chloracne’ based on the similarity of its clinical features with acne vulgaris . Later, chloracne was recognized in workers employed in the production of various industrial chemicals including chlorinated phenols (16,17), polychlorinated biphenyls (PCBs) (18,19) and chlorinated naphthalenes (4), while some of these compounds in pure form are not chloracnegenic or possess low chloracnegenic activity (20). Identification of the specific ‘chloracnegenic’ factor in these mixtures remained enigmatic until trace contaminants formed during their manufacture were identified and linked to the disease (9).…”

Section: Chloracne – An Environmental Diseasementioning

confidence: 99%

“…Later, it was suggested that dioxins may be the major chloracnegenic factor in various polyhalogenated chemical formulations (96) and soon thereafter, a series of studies were undertaken to elucidate their chemical and toxic properties (74,97). But it was not until the 1970s that dioxins were studied in detail when extreme toxicity of TCDD became apparent (20) and large numbers of people were exposed to its action in several industrial accidents around the world. This was also abetted by the extensive exposure of American veterans to TCDD‐containing defoliants including Agent Orange during the Vietnam War (e.g.…”

Section: Dioxin – the Most Potent Environmental Chloracnegenmentioning

confidence: 99%

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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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Section: Chloracne – An Environmental Diseasementioning

confidence: 99%

Section: Dioxin – the Most Potent Environmental Chloracnegenmentioning

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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“…Results of these studies are helpful in narrowing the window of sensitivity for rats. Two of these studies reported that exposures during GD 2–20 (Thibodeaux et al 2003) or GD 6–15 (Schwetz et al 1973) induced significant cleft palate development. Several other investigations observed similar effects with narrower windows of exposure such as GD 11–15 (Zangar et al 1989) and GD 12–14 (Springer et al 1986) (Figure 2).…”

Section: Resultsmentioning

confidence: 99%

“…This may be attributed to the longer half-lives of these chemicals and their persistence in the body (ATSDR 1998; 2004). Several studies demonstrated that dose is a critical factor, showing the NOAEL following administration of lower doses and LOAEL following higher doses (Domingo et al 1989; Ema et al 1991; Faqi et al 1997; Hackett et al 1984; Huuskonen et al 1994; Kransler et al 2007; Noda et al 1991; NTP 1983; Schwetz et al 1973). …”

Section: Discussionmentioning

confidence: 99%

Windows of Sensitivity to Toxic Chemicals in the Development of Cleft Palates

Buser

Pohl

2015

Journal of Toxicology and Environmental Health, Part B

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Cleft lip and cleft palate are among the most common birth defects worldwide. There is a genetic component to the development of these malformations, as well as evidence that environmental exposures and prescription drug use may exacerbate or even produce these manifestations. Thus, it is important to understand the underlying mechanisms and when these exposures affect development of the growing fetus. The purpose of this investigation was to critically review the available literature related to orofacial cleft formation following chemical exposure and identify specific time frames for windows of sensitivity. Further, an aim was to evaluate the potential for predicting effects in humans based on animal studies. Evidence indicates that chemical causes of cleft palate development are due to dose and timing of exposure, susceptibility of the species (i.e., the genetic makeup), and mechanism of action. Several studies demonstrated that dose is a crucial factor; however, some investigators argued that even more important than dose was timing of exposure. Data show that the window of sensitivity to environmental teratogens in the development of cleft palates is quite narrow and follows closely the window of palatogenesis in the fetus of any given species.

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“…On ng'dan fazla dioksin içeren yumurtalarda kuluçkadan çıkma engellenmekte, yumurtaların 1.000 ng'dan fazla dioksin içermesi de %80 oranında mortaliteye neden olmaktadır. 51 Serbest dolaşan tavukların dioksinle kontaminasyonu, toprağın yutulması ve dioksin içeren böcek ve solucanların yenmesinden kaynaklanmaktadır.…”

Section: Yumurtada Di̇oksi̇nunclassified

A Public Health Problem: Dioxin Presence in Poultry Products

Kamber¹,

Çil²,

Şireli³

2019

Turkiye Klinikleri J Vet Sci

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ioksinler, toksik özellikte olup maruz kalındığında insanlar için çok ciddi sağlık sorunları oluşturan çevresel kirleticilerdir. Dioksin kelimesi her ne kadar tek bir bileşik ismi olarak algılansa da birçok kimyasal bileşiği ifade eder. İki oksijen köprüsüyle birbirlerine bağlanmış iki Turkiye Klinikleri J Vet Sci. 2019;10(2):71-83 71 Bir Halk Sağlığı Sorunu: Kanatlı Ürünlerinde Dioksin Varlığı Ö ÖZ ZE ET T Dioksinler; kalıcı organik çevresel kirleticiler arasında yer alan, toksik özellikleri nedeniyle insanlar için ciddi sağlık sorunları oluşturan, iki klorlu benzen halkası içeren bileşen grubunun genel adıdır. Özellikle son yıllarda gelişen endüstriyle birlikte klorlu birçok kimyasalın üretimi ve atık yakma sonucunda ara ürün olarak ortaya çıkarak, çevrede yaygın olarak bulunmaktadırlar. Kısa süreli yüksek seviyelerde dioksine maruz kalma, klorakneye, karaciğer fonksiyon bozukluklarına ve cildin şekilsiz kararması gibi deri lezyonlarına sebep olmaktadır. Uzun süreli maruz kalmada ise başta kanser, Tip 2 diyabet ve iskemik kalp hastalığı gibi sağlık sorunlarının olabileceği bildirilmektedir. İnsanlar için dioksinlere maruz kalmanın başlıca yollarından biri de gıdalardır. Dioksinler, kanatlıların besin zincirine birkaç yoldan girdiğinden, özellikle kanatlı etleri ve yumurtalar bu bileşen yönünden risk taşımaktadır. Çevre kirliliğinden etkilenmiş alanlarda üretilen, ev yetiştiriciliği ya da organik besicilik yapan işletmelerden elde edilen yumurta ve kanatlı etlerinde önemli düzeylerde dioksin olduğu tespit edilmiştir. Dioksinlerin zararlı etkilerinden korunmak ve dioksin bakımından güvenli tavuk eti ve yumurta üretimi için çiftlik aşaması başta olmak üzere; üretim, işleme, dağıtım ve satış sırasında kontrol edilmesi gerekir. Tavuk çiftliklerinde tolerans seviyelerinin aşılmasını önlemek için kontaminasyon izleme sistemleri oluşturulmalıdır. Yine kontamine yumurta ve kanatlı etlerinde dioksin düzeylerini tespit etmek ve kontamine ürünleri uzaklaştırmak için çaba gösterilmelidir. Tüketicilerin, kanatlılarda dioksin varlığı ile ilgili bilinci her geçen gün artsa da doğadaki ve gıdalarımızdaki dioksin seviyelerinin arzu edilen değerlere indirilmesinin uzun yıllar alacağı ve dolayısıyla insanlar için bu bileşiğin uzun bir süre daha risk kaynağı oluşturacağı bilinmelidir.A An na ah h t ta ar r K Ke e l li i m me e l le er r: : Dioksin; kanatlı; yumurta; gıda kontaminasyonu; halk sağlığı

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Toxicology of chlorinated dibenzo-p-dioxins.

Cited by 417 publications

References 12 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

Windows of Sensitivity to Toxic Chemicals in the Development of Cleft Palates

A Public Health Problem: Dioxin Presence in Poultry Products

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