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Ann Thorac Med. 2012 Jul-Sep; 7(3): 162–164.
PMCID: PMC3425050

An unusual interstitial lung disease

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].

Figure 1
High-resolution computed tomography of thorax (transverse section)
Figure 2
Photomicrograph under high power field (400×) magnification of transbronchial lung biopsy


  1. What does the HRCT (thorax) show?
  2. What are the different types of nodule observed on HRCT thorax? What are the differential diagnoses of various types of nodules on HRCT thorax?
  3. What are various types of cotton-induced lung disease? What are the diagnostic criteria for occupational lung disease? What is the most likely diagnosis in this case?


  1. HRCT of thorax shows multiple, well-defined centrilobular nodules with tree-in-bud appearance.
  2. The nodules observed on HRCT of thorax is a very useful tool in diagnosing and characterizing interstitial lung disease and can be divided into three patterns: centrilobular, perilymphatic, and random.[1] Centrilobular opacities are pathologically regarded as lesions of respiratory bronchiole and are central with respect to the secondary pulmonary lobule [Figure 3a]. They are regularly spaced and do not touch the pleura or fissures, and may have “tree-in-bud” appearance. Perilymphatic nodules are peripheral with respect to the secondary pulmonary lobule [Figure 3b]. These are fissural, subpleural, or along major vessels. They can give an “interface” sign making the adjacent border appear shaggy. Random nodules are fissural but the pattern is random, diffuse, and uniform [Figure 3c]. The differential diagnosis of these nodules is given in Table 1.[1,2]
    Figure 3
    (a) Schematic diagram of centrilobular nodules; (b) Schematic diagram of perilymphatic nodules; (c) Schematic diagram of random nodules
    Table 1
    Differential diagnosis of nodules on HRCT lung scan[1,2,5]
  3. The various types of cotton-induced lung diseases are byssinosis, chronic obstructive pulmonary disease, cotton fever, and pneumoconiosis.[3] The diagnostic criteria for occupational lung disease are listed in [Table 2].[4] As described in Table 1, the centrilobular nodules can be observed in infectious bronchiolitis (e.g., tuberculosis), pneumoconiosis, diffuse panbronchiolitis, vasculitis, vascular metastases, respiratory bronchiolitis, and hypersensitivity pneumonitis.[5] Exposure to cotton dust, presence of centrilobular nodules, transbronchial lung biopsy suggestive of fiber-induced pneumoconiosis, and presence of diagnostic criteria for occupational lung disease indicate the diagnosis of cotton-induced pneumoconiosis.
    Table 2
    Diagnostic criteria for occupational lung disease[4]


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.[3] Cotton-induced airways disease is common; however, pulmonary fibrosis and pneumoconiosis due to cotton dust is rarely reported.[6] Sano first demonstrated fibrosis and granuloma after endotracheal infusion of organic dust in rats.[7] Later, Ruttner et al. showed pulmonary fibrosis in cotton dust-exposed people on postmortem analysis.[8] Kobayashi et al. in 2004 conclusively demonstrated pneumoconiosis caused by cotton dust.[9] 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.[10] 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.[11] Patients can also be counseled to change their occupation if feasible.[12] Corticosteroids may help in reversal or stabilization of airway and interstitial inflammation.


Source of Support: Nil

Conflict of Interest: None declared.


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