Clinical and immunologic evaluations of reactive dye-exposed workers.

Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Journal of Allergy and Clinical Immunology (Impact Factor: 12.05). 04/1991; 87(3):639-49. DOI: 10.1016/0091-6749(91)90382-X
Source: PubMed

ABSTRACT To evaluate type 1 hypersensitivity to reactive dyes, its prevalence, and its relationship to respiratory dysfunction, we studied clinical and immunologic features, including skin prick tests. RAST, and bronchoprovocation tests, of 309 employees working in a reactive-dye industry. Our survey revealed that 78 (25.2%) employees had work-related lower respiratory symptoms associated with or without nasal, skin, or eye symptoms. Among these employees, 38 (48.7%) had nonspecific bronchial reactivity. Thirteen demonstrated immediate (6), dual (6), or late only (1) asthmatic responses after inhalation of four kinds of reactive-dye solutions. Twenty-five employees demonstrated immediate skin responses to black GR dye, and 21 reacted to orange 3R. Fifty-three employees (17%) had specific serum IgE antibody against black GR and orange 3R-human serum albumin conjugate. Specific IgE was detected more frequently in symptomatic employees (30%) and smokers (100%). No association was found between atopy and specific IgE binding. The RAST-inhibition tests of black GR revealed significant inhibitions by black GR-human serum albumin conjugate and minimal inhibitions by unconjugated black GR. Orange 3R RAST-inhibition tests revealed significant inhibitions by conjugated forms of black GR and orange 3R and some inhibitions by two unconjugated dyes, suggesting an immunologic cross-reactivity between these dyes. These findings suggested that reactive dyes could induce immunologic responses, most likely IgE-mediated.

  • Archives des Maladies Professionnelles et de l Environnement 06/2010; 71(3):459-469. · 0.22 Impact Factor
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    ABSTRACT: BACKGROUND: Respiratory irritants represent a major cause of occupational obstructive airway diseases. We provide an overview of the evidence related to irritative agents causing occupational asthma or occupational COPD. METHODS: We searched MEDLINE via PubMed. Reference lists of relevant reviews were also screened. The SIGN grading system was used to rate the quality of each study. The modified RCGP three-star system was used to grade the body of evidence for each irritant agent regarding its causative role in either occupational asthma or occupational COPD. RESULTS: A total of 474 relevant papers were identified, covering 188 individual agents, professions or work-sites. The focus of most of the studies and the predominant diagnosis was occupational asthma, whereas occupational COPD arose only incidentally.The highest level assigned using the SIGN grading was 2+ (well-conducted systematic review, cohort or case--control study with a low risk of confounding or bias). According to the modified RCGP three-star grading, the strongest evidence of association with an individual agent, profession or work-site ("**") was found for 17 agents or work-sites, including benzene-1,2,4-tricarboxylicacid-1,2-anhydride, chlorine, platinum salt, isocyanates, cement dust, grain dust, animal farming, environmental tobacco smoke, welding fumes or construction work. Phthalic anhydride, glutaraldehyde, sulphur dioxide, cotton dust, cleaning agents, potrooms, farming (various), foundries were found to be moderately associated with occupational asthma or occupational COPD ("*[+]"). CONCLUSION: This study let us assume that irritant-induced occupational asthma and especially occupational COPD are considerably underreported. Defining the evidence of the many additional occupational irritants for causing airway disorders will be the subject of continued studies with implications for diagnostics and preventive measures.
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