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Occupational and Environmental Lung Disease |

Pneumoconiosis in Rush Mat Workers Exposed to Clay Dye “Sendo” Dust*: Clinical, Radiologic, and Histopathologic Features in Seven Patients

Kiminori Fujimoto; Nestor L. Müller; Seiya Kato; Hiroshi Terasaki; Junko Sadohara; Toru Rikimaru; Naofumi Hayabuchi
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*From the Departments of Radiology (Drs. Fujimoto, Terasaki, Sadohara, and Hayabuchi), Pathology (Dr. Kato), the First Internal Medicine (Dr. Rikimaru), Kurume University School of Medicine, Kurume, Japan; and the Department of Radiology, Vancouver General Hospital and the University of British Columbia (Dr. Müller), Vancouver, BC, Canada.

Correspondence to: Kiminori Fujimoto, MD, PhD, Department of Radiology, Kurume University School of Medicine, 67 Asahi-machi, Kurume, 830-0011, Japan; e-mail: kimichan@med.kurume-u.ac.jp



Chest. 2004;125(2):737-743. doi:10.1378/chest.125.2.737
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Study objectives: The purpose of this study was to describe the clinical, chest radiographic, high-resolution CT, and histopathologic features of clay dye “sendo” dust pneumoconiosis in seven rush mat (“tatami”) workers.

Patients: Seven patients with a history of occupational exposure to sendo dust and radiographic changes suggestive of pneumoconiosis were retrospectively reviewed.

Results: The duration of exposure ranged from 15 to 45 years (median, 30 years). Three patients had cough, and four patients had abnormal pulmonary function test results. Chest radiographs showed nodular opacities < 3 mm in diameter (types p and q) in all patients. The standard International Labor Office profusion score ranged from 0/1 to 1/1 (median, 1/0). High-resolution CT demonstrated small nodular opacities (types p and q) in all seven patients. In four patients, high-resolution CT demonstrated branching centrilobular structures, airway ectasia, airway wall thickening, and emphysematous changes. None of the patients had conglomerate nodules, large opacities, honeycombing, pleural effusion, or lymphadenopathy. Microscopic examination of the specimens obtained by open lung biopsy or transbronchial lung biopsy revealed nodular fibrosis with accumulation of dust-laden macrophages, but no silicotic nodules. Needle-like particles of 1 to 20 μm in length were evident among the dust deposits, and birefringent crystals were identified under polarizing microscopy. Four of seven patients showed intra-alveolar fibroblastic foci similar to Masson bodies, accompanied by dust deposition.

Conclusion: Rush mat workers’ sendo dust pneumoconiosis is caused by dust containing free silica. The radiographic and high-resolution CT findings consist of small nodular opacities < 3 mm in diameter and bronchial and bronchiolar abnormalities.

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