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Divisions of 1 Respiratory Medicine, 2 Clinical Immunology and Allergy, Dept of Medicine, Karolinska Hospital and Institutet, 3 Occupational and Environmental Dermatology, Dept of Medicine, Karolinska Institutet and Stockholm County Council, 4 Workplace Air, National Institute for Working Life and ITM, Stockholm University, Stockholm, and 5 Clinical Science, Astra Zeneca, Lund, Sweden
CORRESPONDENCE: J. Grunewald, Dept of Medicine, Lung Research Laboratory L2:01, Karolinska Hospital, S-171 76 Stockholm, Sweden. Fax: 46 851775451. E-mail: johan.grunewald@medks.ki.se
Keywords: bronchoalveolar lavage, cornstarch glove powder, eosinophil granulocytes
Received: March 25, 2002
Accepted November 29, 2002
This study was supported by the Swedish Council for Work Life Research (RALF), the Swedish Heart-Lung Foundation, the King Oscar II Jubilee Foundation, the Swedish Foundation for Health Care Sciences and Allergy Research and Karolinska Institutet.
Starch is a main component of wheat flour, which, besides being an occupational allergen can also induce irritative symptoms in the airways. A purified starch product (cornstarch glove powder) was used to investigate whether starch alone could induce airway inflammation. The aim of the study was to investigate a role for starch in wheat flour-induced airway inflammation.
Ten healthy individuals were exposed to cornstarch glove powder in a whole-body exposure chamber. Bronchoscopy with bronchoalveolar lavage (BAL) was performed 23 weeks before and 1 day after exposure, and the BAL cells were counted differentially. In addition, the expression of activation, adhesion and subset markers on alveolar macrophages and BAL T-cells were investigated using flow cytometry.
A three-fold increase in BAL cell concentrations was found, with a selective accumulation and activation of eosinophilic granulocytes, as well as an influx of nonactivated monocytes and polyclonal CD4+ T-cells into the airways.
The results show that inhalation of cornstarch glove powder leads to the development of a subclinical inflammation in the airways, with an accumulation of eosinophilic granulocytes. The authors suggest that such exposure may be an interesting model for studying factors contributing to lung accumulations of eosinophil granulocytes in humans.
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