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Environmental effects & skin diseases

Environmental effects & skin diseases. By Dr. Shereen Gheida Lecturer of Dermatology & Venereology. Environmental effects& skin disease.

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Environmental effects & skin diseases

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  1. Environmental effects & skin diseases By Dr. Shereen Gheida Lecturer of Dermatology & Venereology

  2. Environmental effects& skin disease Environmental exposure is important in aetiologies of some dermatoses.Most environmental exposure to harmful substances will occur at work, but exposure may occur at home or during normal day-to-day activities.

  3. Chloracne Environmental pollution can result in a variant of acne called chloracne. It is caused by systemic exposure to certain halogenated aromatic hydrocarbons “ chloracnegens”

  4. Chloracne-producing chemicals • Polyhalogenated naphthalenes Polychloronaphthalenes   & Polybromonaphthalenes • Polyhalogenated biphenyls  Polychlorobiphenyls (PCBs)   & Polybromodiphenyls (PBBs) • Polyhalogenated dibenzofurans Polychlorodibenzofurans, especially tri-, tetra-, penta- and hexachloro-dibenzofuran     Polybromodibenzofurans, especially tetra bromodibenzofuran • Contaminants of polychlorophenol compounds—especially herbicides (2,4,5-T and pentachlorophenol) and herbicide intermediates (2,4,5-trichlorophenol) • 2,3,7,8-Tetrachlorodibenzo-p-dioxin(TCDD)  &  Hexachlorodibenzo-p-dioxin • Contaminants of 3,4-dichloroaniline and related herbicides (propanil, methazole, etc.) Tetrachloroazoxybenzene  &  Tetrachloroazobenzene

  5. Dioxin is the most potent environmental chloracnegens.

  6. Chloracne is considered to be one of the most sensitive indicators of systemic poisoning by these compounds.

  7. Most cases of chloracne have resulted from Occuptional Non occuptional

  8. Occuptional chloracne have resulted fromenvironmental exposure in: • Chemical manufacturing. • Rarely from end-use of products.

  9. Non occuptional chloracne mainly resulted from contaminated industrial wastes & contaminated food products

  10. Exposure is usually through Inhalation Ingestion Direct contact

  11. Pathogenesis Chloracnegen Undifferentiated Sebaceous gland cells KCs Disappearance of sebaceous glands Comedones& Keratin cysts Imbalance of epidermal stem cells))

  12. Non inflammatory comedones & straw coloured cysts are 1ry clinical manifestations of chloracne.

  13. The eruption may be mild, involving localized exposure or covered areas of the body or severe, disseeminated with involvement of almost every follicular orifice.

  14. The severity of chloracne is related to : • Dosage of exposed chloracnegens. • Chloracnegenic potency. • Individual susceptibility.

  15. Chloracne appears to be resistant to tested forms of treatment . The only way to control chloracne is to prevent exposure to chloracnegens.

  16. Chemical leukoderma It is defined as hypo or depigmentation of the skin due to industrial exposure to certain chemicals. Certain chemicals, particularly the substituted phenols,are destructive to functional melanocytes.

  17. Chemicals capable of causing occupational leukoderma: • Monobenzylether of hydroquinone • eMonoethylether of hydroquinone(p-ethoxyphenol) • Monomethylether of hydroquinone)p-methoxyphenol) • p-Cresol • p-Isopropylcatechol • P-Methylcatechol • p-Nonylphenol • p-Octylphenolp-Phenylphenol • p-tert-Amylphenol • p-tert-Butylcatechol • p-tert-Butylphenol • N,N',N''-Triethylenethiophosphoramide (thio-TEPA) • Mercaptoamines, e.g. N-2-mercaptoethyl-dimethylamine hydrochloride (MEDA)

  18. Many of these compounds cause permanent depigmentation of the skin resembling vitiligo.

  19. Some of these chemicals are useful as antioxidant and find utility in: • Rubbers. • Plastics. • Food. • As polymerization inhibitors in monomers. • In some bleaching agents.

  20. The mechanism by which depigmentation occurs is probably related to: • Interference with one or more of the many steps of melanin biosynthesis. • It is accompanied by destruction of melanocytes & their organelles.

  21. The diagnosis • The diagnosis of occuptional vitiligo should be suspected if a worker who potentially has been exposed to depigmented chemicals develops leukoderma on the dorsal aspects of the hands or in a more widespread distribution. • There should be particular suspicion if more than one worker is involved.

  22. The treatment • There is no specific treatment . • Removal of the offending chemical may result in partial repigmentation or may not occur at all. • Camouflage cosmetics may be used. • Sunscreens.

  23. Scleroderma like disease Scleroderma-like diseases have been observed increasingly over the last few decades. These comprise diseases that in addition to skin changes similar to those of scleroderma also involve other organ systems, but are not consistent with classical scleroderma.

  24. Scleroderma like disease

  25. A common factor in these diseases is that they generally show definite clinical improvement when exposure to the relevant agent ceases.

  26. Connective tissue diseases related to environmental exposures

  27. Quartz induced scleroderma • Quartz is widely distributed in nature(silicon dioxide,SiO2). • Silicon dioxide is present in over 90% of all minerals. • The principal medical significance of the substance is as the causative agent of pulmonarysilicosis.

  28. Quartz exposure occurs in the following industries& occupation: • Mining • Stone industry. • Rubber industry. • Ceramic & glass industries. • There are many implants made of silicon for medical purpose as cosmetic breast implant, joint implant and cardiac valve replacement.

  29. The exact mechanism by which silica promotes or accelerates the development of autoimmune disease is unknown.

  30. In vitro studies have shown that: • Silica can act as adjuvant stimulating T cell response. • As inducer of apoptosis. • It is also known to cause a relative decrease in the number of regulatory T cells & tend to have cytotoxic effect on macrophage attempting to breakdown internalized silica particles which causes a cascade of events, including:

  31. Oxidative stress. • Induction of proinflammatory cytokines. • Chronic inflammation. • Latent immune stimulation.

  32. Treatment of scleroderma is unsatisfactory as there no specific therapy . • The course is almost always progressive. • Death usually results from general weakness or from renal,myocardial or pulmonary sclerosis.

  33. Vibration white finger • It consists of the episodic appearance of white-finger skin patches(Raynaud´s phenomenon) in response to environmental cold or vibration and is accompanied by secondary loss of sensation caused by vascular ischaemia. • It can be part of but is not synonymous with the hand-arm vibration syndrome.

  34. Vibration white finger

  35. How vibration causes it ? Chronic vibration exposure Disturbing the endothelial-derived relaxing factor-mediating vasodilatory function. Damage of endothelial vasoregulatory mechanisms.

  36. Operatives using vibrating tools • Coal miners. • Road & construction workers. • Lumberjacks.

  37. The diagnosis is usually made by history alone. • The treatment VWF is the same as for Raynaud´s phenomenon. • It is generally believed that symptoms of VWF regress sometime after cessation of exposure.

  38. Skin cancer In 1775, the first cancer of any type to be linked with environmental exposure was scrotal squamouscarcinomas in British chimney sweeps reported by Percival Pott.

  39. Ultraviolet radiation The major environmental carcinogens Ionizing radiation Arsenic Polycyclic hydrocarbons

  40. Occupations with potential exposure to causative agents in environmental skin cancer • Polycyclic hydrocarbons Tar distilling     Coal gas manufacturing     Briquettes manufacturing     Shale oil workers     Refinery workers • Ultraviolet light Outdoor workers     Printers  Laser exposure    • Ionizing radiation Nuclear power plant workers     X-ray technicians    

  41. These chemicals are contained in Tar Greases Lubricating oils

  42. The diagnosis of skin cancer • Similar to that of non-occupational skin cancer. • Generally, the exposed sites are involved. • There may be co-existing signs of exposure prior to or in addition to evidence of skin cancer. Oil folliculitis& hyperkeratoses Tar warts

  43. Prevention of skin cancer • Substitution of carcinogens. • Protection of the skin (protective clothing &machine guarding). • Daily washing is essential. • Surveillance of older or retired workers. • Finally, the skin cancers need to be treated as appropriate.

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