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A 48-year-old nonsmoker man, cotton mill worker, working in the carding department for 27 years, presented with progressively worsening dyspnea on exertion and dry cough for a period of 2 years. He did not give history of work-related exacerbation of symptoms. There were no significant systemic complaints. The baseline and postexercise saturation was 98% and 93%, respectively. Bilateral fine end inspiratory crackles were noted on respiratory system examination. Hematological, biochemical, and sputum examination did not show any significant abnormality. Chest radiograph showed scattered nodular opacities. The high-resolution computed tomography (HRCT) of thorax is shown in Figure 1. The spirometry was suggestive of mild restrictive abnormality with forced vital capacity (FVC) of 3.06 (72% predicted), forced expiratory volume in one second (FEV1) of 2.57 (74% predicted), and FEV1/FVC 84%. The transbronchial lung biopsy showed focal scarring with heavy deposits of anthracotic pigments; patchy peribronchial, alveolar septal thickening, and smooth muscle proliferation [Figure 2].
The variations in presentation from exposure to cotton dust are due to deposition of cotton dust into the different parts of bronchial tree, the duration of exposure, and the exposure to various components of cotton dust-like broken cotton fibers, bracts, pericarps, bacteria, and fungi. Cotton-induced airways disease is common; however, pulmonary fibrosis and pneumoconiosis due to cotton dust is rarely reported. Sano first demonstrated fibrosis and granuloma after endotracheal infusion of organic dust in rats. Later, Ruttner et al. showed pulmonary fibrosis in cotton dust-exposed people on postmortem analysis. Kobayashi et al. in 2004 conclusively demonstrated pneumoconiosis caused by cotton dust. The fibrosis is due to inhalation of cotton dust contaminated with lipopolysaccharide (LPS). LPS causes significant production of nitric oxide (NO) from the alveolar type II epithelial cells and macrophages. NO reacts with superoxide anion to form peroxynitrate, which initiates production of a number of inflammatory cytokines and prostaglandin E2.. These potent inflammatory mediators lead to pulmonary damage and pneumoconiosis. Cotton dust pneumoconiosis generally present with minimal symptoms, HRCT show centrilobular and peribronchovascular interstitial opacities, and biopsy specimens show peribronchial fibrous thickening due to the presence of organic fibers.[7,8]
The standard approach to occupational lung diseases involves measures to reduce exposure to the substance even when symptoms have not developed. It has been shown that cessation of work from cotton textile is associated with significant improvement in lung function. Patients can also be counseled to change their occupation if feasible. Corticosteroids may help in reversal or stabilization of airway and interstitial inflammation.
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