benzofurans and Acne-Vulgaris

Chloracne is an acneiform skin eruption that is still the most sensitive indicator of systemic poisoning caused by chemicals belonging to the group of chlorinated polycyclic aromatic hydrocarbons. Generally these chemicals are known as dioxins, dibenzofuranes, and PCBs. The cause of chloracne is probably interference of these chemicals with vitamin A metabolism in the skin, resulting in disturbances of the epithelial tissues of the pilosebaceous duct. A study of workers in a factory where chloracne is endemic is described. The product manufactured, pentachlorophenol, a wood preservative, was found to be contaminated with dioxins (congeners of TCDD) and dibenzofuranes. Blood levels of these chemicals in affected workers are given, along with supporting evidence of disturbances in vitamin A (retinoid) metabolism as demonstrated in skin biopsies.

Topics: Acne Vulgaris; Benzofurans; Dermatitis, Occupational; Dioxins; Humans; Hydrocarbons, Chlorinated; Occupational Exposure; Polychlorinated Biphenyls

Chloracne, an acneform eruption resulting from poisoning by halogenated aromatic compounds, has been a considerable problem over the last 40 years. The condition is always a symptom of systemic poisoning and should be familiar to all practitioners, particularly dermatologists. It is difficult to treat and can last for long periods without known additional exposure to chloracnegens. Some chloracnegens are capable of causing a variety of systemic signs and symptoms and may be oncogenic. Although there are probably fewer than 4,000 persons with chloracne worldwide, those found with the disorder should be evaluated medically on a regular basis and followed, if possible, throughout their lives.

Topics: 2,4-Dichlorophenoxyacetic Acid; 2,4,5-Trichlorophenoxyacetic Acid; Acne Vulgaris; Agent Orange; Aniline Compounds; Animals; Azo Compounds; Benzofurans; Biphenyl Compounds; Chemical Phenomena; Chemistry; Dibenzofurans, Polychlorinated; Dioxins; Drug Contamination; Halogens; Humans; Hydrocarbons, Chlorinated; Naphthalenes; Neoplasms; Polychlorinated Dibenzodioxins

In rhesus macaques (Macaca mulatta), consumption of food containing commercial polychlorinated biphenyl (PCB) mixtures, some pure polychlorobiphenyl congeners, 2,3,7,8- tetrachlorodibenzo-p-dioxin (TCDD), and 2,3,7,8-tetrachlorodibenzofuran (TCDF) caused the same clinical toxic manifestations and histopathologic lesions, although the potencies of the toxicants covered a range of five orders of magnitude. Recovery from poisoning by 3,4,3',4'-tetrachlorobiphenyl (34TCB) or TCDF was rapid, whereas recovery from poisoning by Aroclor 1242, 3,4,5,3', 4', 5'-hexachlorobiphenyl (345HCB) or TCDD was protracted, if it occurred at all. 34TCB did not appreciably accumulate in body fat, but the level of 345HCB in fat rose steadily during ingestion. In one monkey, 25% of TCDD stored in fat after a single dose was still present after 2 years. Among the symmetrical tetra-and hexachlorobiphenyl isomers tested, subacute oral toxicity could be demonstrated only for those without ortho chlorine substitutions. 34TCB and 345HCB were toxic at dietary levels of less than 1 ppm, but ingestion of food containing 2,5,2',5'- tetrachlorobiphenyl at 5 ppm, or 2,4,5,2',4',5'-, 2,4,6,2',4',6'-, or 2,3,6,2',3',6'-hexachlorobiphenyl at 15 or 65 ppm, caused no discernible deleterious effects. The principal demonstrable histopathological lesions, bone marrow excepted, were metaplasias in some specialized epithelial structures, such as sebaceous glands, nail beds, gastric mucosa, ameloblast, and thymic corpuscles. These changes were interpreted as toxicant-induced, reversible redirection of differentiation. This aberration was wholly reversible. TCDD and 34TCB caused abortions when given in one or a few oral doses early in pregnancy. At the total doses used (1 or 5 micrograms/kg of body weight for TCDD, 3 or 0.6 mg/kg of body weight for 34TCB), maternal toxicity was frequently apparent subsequent to the abortion.

Topics: Abortion, Spontaneous; Acne Vulgaris; Animals; Benzofurans; Cell Differentiation; Dioxins; Epithelium; Female; Fetus; Gastric Mucosa; Isomerism; Macaca mulatta; Male; Nails; Polychlorinated Biphenyls; Polychlorinated Dibenzodioxins; Pregnancy; Structure-Activity Relationship

During January 10-11, 1978 in Lyon, France, a joint National Institute of Environmental Health Sciences/International Agency for Research on Cancer ad hoc Working Group considered and discussed the feasibility of coordinating epidemiological studies on the long-term hazards associated with the chlorinated dibenzo-p-dioxins and chlorinated dibenzofurans (PCDDs and and PCDFs). Nineteen invited scientists from eight countries presented introductory working papers summarizing the most up-to-date and relevant information available from their individual programs. This report represents the collective views and scientific opinions of the Working Group. The greater part of this document comprises epidemiological studies related to episodes of human exposures. The review begins with a brief section concerning possible routes of human exposure, an overview of the pertinent chemical characteristics, and the salient toxicological properties of the structurally similar PCDDs/PCDFs. The Working Group report ends with recommendations for future activities.

Topics: Abnormalities, Drug-Induced; Accidents, Occupational; Acne Vulgaris; Animals; Benzofurans; Chemical and Drug Induced Liver Injury; Chickens; Dioxins; Female; Guinea Pigs; Haplorhini; Humans; Male; Mice; Occupational Diseases; Polychlorinated Dibenzodioxins; Rats; Structure-Activity Relationship

Topics: Acne Vulgaris; Azo Compounds; Benzofurans; Diagnosis, Differential; Dioxins; Environmental Exposure; Herbicides; Humans; Hydrocarbons, Halogenated; Naphthalenes; Polybrominated Biphenyls; Polychlorinated Biphenyls

In 1968, many people developed dioxin poisoning (Yusho) in Japan. Ingestion of 2,3,4,7,8-pentachlorodibenzofuran (2,3,4,7,8-PeCDF) was considered to be the cause of this poisoning. Although some patients had high concentrations of 2,3,4,7,8-PeCDF in their blood, individuals' half-lives of 2,3,4,7,8-PeCDF were long.. To evaluate the relationship between clinical and laboratory parameters and the individual half-life of 2,3,4,7,8-PeCDF in blood.. Clinical and laboratory data were collected during annual check-ups from 2001 to 2008. We enrolled 71 patients, who were measured more than 3 times, and who had 2,3,4,7,8-PeCDF concentrations in blood >50pgg(-1) lipid. The half-life of 2,3,4,7,8-PeCDF for each patient was estimated using linear regression. Moreover, relationships between clinical and laboratory parameters and individual half-life were investigated by linear regression.. A shortened individual half-life for 2,3,4,7,8-PeCDF was significantly correlated with an increased red blood cell count, increased viscous secretions from the meibomian glands, existing black comedones, and severe cedar pollen allergy.. Symptoms that accelerate excretion of lipids from the body, such as viscous secretions from the meibomian glands, may lead to a shorter half-life of 2,3,4,7,8-PeCDF. Red blood cells are related to the half-life of 2,3,4,7,8-PeCDF. However, further studies are required to investigate the excretory mechanism of 2,3,4,7,8-PeCDF.

Topics: Acne Vulgaris; Adult; Aged; Aged, 80 and over; Benzofurans; Erythrocyte Count; Fatigue; Female; Half-Life; Humans; Japan; Male; Middle Aged; Porphyrias; Rhinitis, Allergic, Seasonal

Chloracne is caused by exposure to certain halogenated polycyclic hydrocarbons such as polychlorinated dibenzodioxins (PCDDs) and dibenzofurans (PCDFs). In chronic exposure it is not known what level of intoxication, represented by the level in blood lipids, is sufficient to cause chloracne. Blood levels of the congeners of PCDD/Fs were determined in four groups of humans. One group had clinically visible chloracne due to exposure in a hexachlorobenzene workshop of a large chemical factory. A second group was exposed in the same workshop, but had no skin changes. There were two control groups: one non-exposed group of maintenance workers from the same chemical factory, and one group of healthy individuals living elsewhere. Blood levels were converted to toxicity equivalents of tetrachlorodibenzo-p-dioxin (TCDD). In the chloracne group blood levels in toxicity equivalents (TEQs) ranged from 1168 to 22,308 pg/g blood lipid. In the exposed without chloracne this ranged from 424 to 662 pg/g. It is concluded that the level to develop chloracne is between 650 and 1200 pg/g TEQ. The contribution of TCDD was rather small, and the main causative congeners were the hexachlorinated dibenzodioxins and dibenzofurans (HxCDD/Fs); lipid-based blood levels in absolute amounts that may cause chloracne are in the range of 2-3.5 ng/g HxCDD, and 2-5 ng/g HxCDF.

Topics: Acne Vulgaris; Benzofurans; Case-Control Studies; Dermatitis, Occupational; Dioxins; Humans; Lipids

1. All members of a Spanish family (father, mother and six children) developed chloracne. 2. The causative agent was found to be the family's stock of olive oil, which had become contaminated with polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), pentachlorophenol, and hexachlorobenzene. 3. The more highly chlorinated PCDDs, in particular octachlorodibenzo-p-dioxin, were the predominant congeners in the oil. 4. Three members of the family exhibited either an overt or a sub-clinical disturbance of kidney function. The father also had a chronic respiratory problem. These changes could not be unequivocally attributed to the PCDDs. 5. Experimental toxicity of the oil was limited to the development of an hepatic porphyria in mice. 6. A serum sample, taken 5 years after consumption of the oil ceased, contained high levels of the PCDDs and PCDFs. Extrapolation back to ingested dose was used to validate dosage estimates. 7. The use of toxicity equivalence factors (TEFs) provided estimates of cumulative dosage to produce chloracne as 0.13-0.31 micrograms 2378-TCDD kg-1 (using EPA TEFs) or 6.7-16 micrograms 2378-TCDD kg-1 (using Nordic/NATO TEFs). 8. This is the first incident in which human toxicity is related primarily to ingestion of PCDDs and for which estimates of dosage can be made.

Topics: Acne Vulgaris; Adult; Animals; Benzofurans; Chickens; Child; Child, Preschool; Female; Food Contamination; Humans; Infant, Newborn; Male; Mice; Olive Oil; Plant Oils; Polychlorinated Dibenzodioxins; Polymers; Spain

Topics: Accidents, Home; Acne Vulgaris; Adult; Benzofurans; Child; Child, Preschool; Dioxins; Family; Female; Hexachlorobenzene; Humans; Hydrocarbons, Chlorinated; Infant; Male; Oils; Pentachlorophenol

Topics: Acne Vulgaris; Azo Compounds; Benzofurans; Dermatitis, Occupational; Humans; Naphthalenes; Polychlorinated Biphenyls; Polychlorinated Dibenzodioxins