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Background: We observed an increasing number of patients who presented with facial or retro‐auricular dermatitis after skin contact with plastic spectacles or plastic covered temples. Objectives: To identify the allergens in plastic spectacles that may cause allergic contact dermatitis. Methods: All patients with suspected allergic contact dermatitis to eyewear were tested with Solvent Orange 60 (SO60), four additionally with Solvent Yellow 14 (SY14), and five with scrapings from their own spectacles. In one case, a chemical analysis of the spectacles was performed to uncover the causative allergen. Results: Three patients were allergic to SO60, two patients to SY14, and two patients were allergic to both SO60 and SY14. Conclusion: Patients with suspected allergic contact dermatitis from spectacles should be tested with SO60 and SY14, and based on findings from previous reports, also with Solvent Red 179. [ABSTRACT FROM AUTHOR]

We patch tested the TLC plate as described by Bruze et al.[5] The patient reacted to the yellow band on the TLC plate (see Figure). The patient was then patch tested with a dilution series of CI Solvent Yellow 14, prepared in pet. This case was solved only because of complex chemical analysis combined with patch testing, which requires access to expensive equipment, specialist knowledge, and patients who are willing to appear for patch testing multiple times. [Extracted from the article]

The in vivo genotoxicity of CI Solvent Yellow 14 (Sudan I) was examined using repeated-dose liver and gastrointestinal tract micronucleus (MN) assays in young adult rats. Sudan I is a mono-azo dye based on aniline and 1-amino-2-hydroxynaphthalene. This dye was demonstrated as a rat liver carcinogen in a National Toxicology Program (NTP) bioassay, and genotoxicity was noted in a rat bone marrow micronucleus (BMMN) assay. In the present study, Sudan I was administered orally to rats for 14-days, and the MN frequency in the liver, stomach, colon, and bone marrow were analyzed. The frequency of micronucleated hepatocytes (MNHEPs) was not significantly increased by the administration of the Sudan I. Gastrointestinal tract MNs were also not induced. However, in the BMMN assay, a significant increase in micronucleated immature erythrocytes (MNIMEs) was observed in a dose-dependent manner. While Sudan I has been reported to lack hepatic genotoxicity, it has also exhibited tumor-promoting activities. These results are consistent with the lack of induction of MN in the hepatocytes. The lack of MN induction in cells of the gastrointestinal tract was also logical because azo-compounds are reported to be unlikely to induce DNA damage in the rat gut. The repeated-dose rat liver and gastrointestinal tract MN assays have the potential to be used in the evaluation of the genotoxicity of a chemical in each organ in accordance with its mode of action. [ABSTRACT FROM AUTHOR]