Toxicology of Chemical Respiratory Hypersensitivity by Rebecca J. Dearman, Ian Kimber

By Rebecca J. Dearman, Ian Kimber

Overview of breathing hypersensitive reaction and bronchial asthma attributable to publicity to chemical substances and proteins within the office. contains an summary of respiration hypersensitive reaction, medical elements of respiration sensitization, and possibility administration. for college students and researchers. 7 participants, 2 U.S.

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1993). , 1993). , 1987). 1 illustrates a characteristic DAR bronchoprovocation response in a worker with TDI-OA (Bernstein, DI, 1992). It is now well recognized that asthma may persist for years even after removal from further exposure. The prolonged morbidity which may result from OA has been found to correlate directly with the length of time the worker is exposed to the causative chemical agent prior to diagnosis and removal from further exposure (Chan-Yeung, 1993). Histologic features in the airways of patients with OA are similar to those found in individuals with non-occupational asthma (NOA).

1992) Expression of the endothelial leucocyte adhesion molecules ICAM-1, E-selectin and UCAM-1 in the bronchial mucosa in steady state asthma and allergen-induced asthma. Thorax, 47, 852P (Abstract). B. R. (1993) Increases in activated T lymphocytes, eosinophils and cytokine mRNA expression for interleukin-5 and granulocyte/macrophage colony-stimulating factor in bronchial biopsies after allergen inhalation challenge in atopic asthmatics. American Journal of Respiratory Cell and Molecular Biology, 8, 35–42.

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