Several preservatives and fragrances with well-known skin-sensitizing potential were common in the examined product types. Such products may be used several times a day by consumers and workers.
Nickel allergy is by far the most frequent contact allergy, affecting 10-15% of women in the general population, and causing dermatitis and hand eczema. The EU Nickel Directive, aimed at the prevention of nickel allergy, comes fully into force by July 2001. The Directive covers piercing materials, items in contact with the skin, and requirements on resistance to wear. We carried out a study of the prevalence on the market, before the Nickel Directive, of items that release nickel and of nickel in piercing posts. Nickel release, as shown by a positive dimethylglyoxime (DMG) test, was detected in 25% of 725 items intended for direct and prolonged contact with the skin. Of 15 posts intended for use during epithelialization after piercing, 60% contained more than 0.05% nickel. These products do not comply with the requirements of the EU Nickel Directive. It is suggested that experts in contact dermatitis participate in the prevention of nickel allergy by explaining its effects: the r le of skin exposure and which parts of an item are in contact with the skin, and the crucial question of nickel release versus nickel content.
To understand the mechanisms involved in immunological tolerance to skin-associated proteins, we have developed trangenic (Tg) mice that express a model self antigen, membrane-bound ABSTRACTS 125 FS01.3 Disperse (yes), orange (yes), 3 (no): what do we test in textile dye dermatitis?Para-phenylenediamine (PPD), an arylamine dye, is a strong allergen causing allergic contact dermatitis. Cytokines such as TNF-a and IL-1beta are key mediators in the initiation of this reaction. Both cytokines are predominantly produced by stimulated monocytes and macroghages. We investigated the responses of PPD and Bandrowski's base (BB), an autoxidation product of PPD in human monocytes. We isolated monocytes from healthy volunteers and incubated them with the allergens. TNF-a and IL-1beta mRNA expression and protein levels were estimated after 45 min, 2 h, 4 h and 24 h after allergen contact. IL-1beta and TNF-alpha were measured in cell culture supernatants by ELISA (n ¼ 7) and mRNA expression was determined by real-time RT-PCR. We found that PPD reduced TNF-a protein secretion by 20-69.9% (n ¼ 6). Further, IL-1beta levels were decreased by 44-98%. The same tendency was found studying IL-1beta and TNF-a mRNA steady state levels (n ¼ 3; 1 h incubation). These effects were substance-specific and not found for PPD derivatives nor for the autoxidation product BB. These findings suggest that PPD may specifically modify immune responses by directly infering with the cellular proinflammatory cytokine network.
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