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Year : 2012  |  Volume : 7  |  Issue : 3  |  Page : 162-164
An unusual interstitial lung disease

1 Department of Pulmonary Medicine, ESI-PGIMSR, New Delhi, India
2 Department of Pulmonary Medicine, B.Y.L. Nair Hospital and T.N. Medical College, Mumbai, India

Date of Submission19-Sep-2012
Date of Acceptance02-Jan-2012
Date of Web Publication21-Jul-2012

Correspondence Address:
Jyotsna M Joshi
Head of Department of Pulmonary Medicine, B.Y.L. Nair Hospital and T.N. Medical College, Mumbai 400008
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1817-1737.98851

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How to cite this article:
Gothi D, Joshi JM. An unusual interstitial lung disease. Ann Thorac Med 2012;7:162-4

How to cite this URL:
Gothi D, Joshi JM. An unusual interstitial lung disease. Ann Thorac Med [serial online] 2012 [cited 2023 Jan 27];7:162-4. Available from:

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)

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Figure 2: Photomicrograph under high power field (400x) magnification of transbronchial lung biopsy

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   Questions Top

  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?

   Answers Top

  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 3]a. 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 3]b. 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 3]c. 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

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    Table 1: Differential diagnosis of nodules on HRCT lung scan[1],[2],[5]

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  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]

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   Discussion Top

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 E 2. 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.

   References Top

1.Raoof S, Amchentsev A, Vlahos I, Goud A, Naidich DP. Pictorial Essay: Multinodular Disease - A high-resolution CT Scan diagnostic algorithm. Chest 2006;129:805-15.  Back to cited text no. 1
2.Lee KS, Kim TS, Han J, Hwang JH, Yoon JH, Kim Y, et al. Diffuse micronodular lung disease: HRCT and pathologic findings. J Comput Assist Tomogr 1999;23:99-106.  Back to cited text no. 2
3.Xing GC. Some opinions on bysinossis in China. Am J Ind Med 1987;12:737-42.  Back to cited text no. 3
4.Redlich CA, Balms JR. Occupational and environmental lung disease In: George RB, Light RW, Matthay MA, Matthay RA, editor. Chest medicine: Essentials of pulmonary and critical care medicine, 5 th Edition. Phladelphia: Lippincott, Williams and Wilkins; 2005. p. 289-315.   Back to cited text no. 4
5.Bhat SP, Ladhani SS, Joshi JM. Lung nodules in a silver polisher. Postgrad Med J 2002;78:628.  Back to cited text no. 5
6.Khan AJ, Nanchal R . Cotton dust lung diseases. Curr Opin Pulm Med 2007;13:137-41.  Back to cited text no. 6
7.Sano T. Pathology and pathogenesis of organic dust pneumoconiosis. J Sci Labour 1967;43:3-18.  Back to cited text no. 7
8.Ruttner JR, Spycher MA, Engeler ML. Pulmonary fibrosis induced by cotton fibre inhalation. Pathol Microbiol (Basel) 1968;32:1-14.  Back to cited text no. 8
9.Kobayashi H, Kanoh S, Motoyoshi K, Aida S. Diffuse lung disease caused by cotton fibre inhalation but distinct from byssinosis. Thorax 2004;59:1095-7.  Back to cited text no. 9
10.Castranova V. Role of nitric oxide in the progression of pneumoconiosis. Biochemistry (Mosc). 2004;69:32-7.  Back to cited text no. 10
11.Shi J, Hang JQ, Mehta AJ, Zhang HX, Dai HL, Su L, et al. Long-term effects of work cessation on respiratory health of textile workers: A 25-year follow-up study. Am J Respir Crit Care Med 2010;182:200-6.   Back to cited text no. 11
12.Beckett WS. Occupational respiratory diseases. N Engl J Med 2000;342:406-13.  Back to cited text no. 12


  [Table 1], [Figure 1], [Figure 2], [Figure 3]

  [Table 2]

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