By Rebecca J. Dearman, Ian Kimber
Overview of breathing hypersensitivity and bronchial asthma attributable to publicity to chemical substances and proteins within the place of work. contains an outline of breathing hypersensitive reaction, medical facets of respiration sensitization, and possibility administration. for college kids and researchers. 7 individuals, 2 U.S.
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Additional info for Toxicology of Chemical Respiratory Hypersensitivity
A. T. (1989) Cellular events in the bronchi in mild asthma and after bronchial provocation. American Review of Respiratory Disease, 139, 806–817. B. R. (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.
Non-specific bronchial hyperresponsiveness (NSBH) has also been evaluated as a risk factor for developing occupational asthma. Prospective data in the western red cedar industry indicate that NSBH occurs as the result of chemical exposure and/or allergic sensitization and does not appear to be a pre-existing risk factor for developing OA. In general, gender, age and race have not been determined to be risk factors for workers developing work-related respiratory diseases (Becklake, 1993). , 1993).
P. (1994a) Bronchial biopsy evidence for leucocyte infiltration and upregulation of leucocyte-endothelial cell adhesion molecules 6 hours after local allergen challenge of sensitized asthmatic airways. Journal of Clinical Investigation, 93, 1411–1421. H. T. (1994b) Circulating adhesion molecules in asthma. American Journal of Respiratory and Critical Care Medicine, 149, 1149–1152. J. B. (1991) Expression of mRNA and immunoreactivity for the granulocyte/macrophage colony-stimulating factor (GMCSF) in activated human eosinophils.