Silicosis Workup

  • Author: Basil Varkey, MD, FCCP; Chief Editor: Zab Mosenifar, MD   more...
 
Updated: Jan 26, 2011
 

Laboratory Studies

Although various serologic abnormalities have been noted in patients with silicosis, they are not diagnostic of the disease, and tests to detect these abnormalities are not indicated routinely (see Other Tests).

Humoral immune system abnormalities observed in silicosis include increased incidence and titer of rheumatoid factor, antinuclear antibodies, and immune complexes. No consistent abnormality is noted in the cell-mediated immune system.

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Imaging Studies

Chest radiograph

Radiographic studies of the chest are essential to the diagnosis of silicosis. While some chest radiographic findings of silicosis may be nonspecific, others are sufficiently characteristic of the disease.

Bilateral alveolar filling and a ground-glass appearance mimicking alveolar proteinosis are observed in silicoproteinosis.

Simple silicosis manifests as multiple small (< 10 mm) nodules that are scattered diffusely throughout the lungs but may be more prominent in the upper lung fields. These radiographic findings have been found to correlate well with pathologic findings. Chest radiographic findings in persons with simple silicosis have a high degree of sensitivity and specificity. Calcification of the hilar lymph nodes, particularly in the rim of the nodes (ie, eggshell calcification) is very characteristic of silicosis. However, eggshell calcifications are observed only in a minority of cases of silicosis. Other causes of eggshell calcification include sarcoidosis, histoplasmosis, and irradiation. Rarely, the pulmonary nodules also may show calcification.

Progressive massive fibrosis (PMF) manifests as bilateral upper lobe masses, which are formed by the coalescence of nodules. Cavitation may be seen. As these masses retract toward the hilum because of fibrosis, the lower lung fields may appear overinflated. Hilar calcifications may be present.

CT scan

A high-resolution CT scan has more sensitivity than chest radiography in discerning the nodules of simple silicosis but is unnecessary if the chest radiographic appearance shows characteristic nodules.

In progressive massive fibrosis, a CT scan provides more detail of emphysematous changes, pleural thickening, and the confluent masslike lesions (eg, the presence of cavitation) than a chest radiograph. Although cavitation in silicosis can occur without a mycobacterial infection, such a possibility should be considered when cavitation is observed.

Although pleural effusions are quite rare, pleural thickening is not an unusual finding.

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Other Tests

Pulmonary function test (spirometry) results may be normal in simple silicosis. However, silicosis is associated with an excessive decline in lung function. In more advanced disease, airflow obstruction or a mixed pattern of obstruction and restriction is observed. In smokers with airflow obstruction, separating the effect of silicosis from the confounding factor of tobacco smoke is difficult. Progressive massive fibrosis causes severe restriction, decreased compliance, and hypoxemia.

A tuberculin skin test using purified protein derivative (PPD) is indicated in all persons with silicosis. If the test result is positive (ie, 10 mm or more of induration at the site), treatment for latent or active infection is indicated. In individuals who have a positive skin test result, sputum samples should be examined for acid-fast bacilli (AFB) by microscopy and cultured for AFB to identify active disease.

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Procedures

Bronchoscopy rarely is needed. The rare indication is in a cavitary or mass lesion when mycobacterial disease or lung cancer is suspected and examination of sputum samples is nondiagnostic.

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Histologic Findings

The diagnosis of silicosis is based on history of exposure, chest radiographic appearance consistent with silicosis, and an absence of other diagnoses that simulate the radiographic abnormalities of silicosis. Clinical manifestations, symptoms, and physical examination findings provide support to the diagnosis. Thus, examination of lung tissue is seldom warranted.

The initial histopathologic changes of silicosis are pigmented macrophages and reticulin fibers in peribronchial, paraseptal, and perivascular areas.

The characteristic histopathologic finding is the silicotic nodule mostly located near the respiratory bronchiole. The nodule is composed of refractile particles of silica surrounded by whorled collagen in concentric layers, with macrophages, lymphocytes, and fibroblasts in the periphery. Emphysematous blebs surround the silicotic nodule, especially in the subpleural area. Birefringent crystals of silica in the center of a silicotic nodule may be identified by polarized light microscopy. For definitive identification, scanning electron microscopy combined with x-ray spectroscopy may be needed.

In PMF, the masslike areas may show cavitation caused by a necrotic process.

Acute silicosis silicotic nodules are seldom seen and the histology is similar to pulmonary alveolar proteinosis with alveolar filling with proteinaceous material that stains with periodic acid-Schiff stain.

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Contributor Information and Disclosures
Author

Basil Varkey, MD, FCCP  Professor Emeritus, Department of Internal Medicine, Division of Pulmonary and Critical Care, Medical College of Wisconsin; Consulting Pulmonologist, Froedtert Memorial Lutheran Hospital

Basil Varkey, MD, FCCP is a member of the following medical societies: American Association of Physicians of Indian Origin and American College of Chest Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Anita B Varkey, MD  Assistant Professor, Department of Medicine, Loyola University Medical Center; Associate Program Director, Internal Medicine Residency; Medical Director, General Internal Medicine Clinic, Loyola Outpatient Center

Anita B Varkey, MD is a member of the following medical societies: American College of Physicians and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Gregory Tino, MD  Director of Pulmonary Outpatient Practices, Associate Professor, Department of Medicine, Division of Pulmonary, Allergy, and Critical Care, University of Pennsylvania Medical Center and Hospital

Gregory Tino, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Om Prakash Sharma, MD, FRCP, FCCP, DTM&H  Professor, Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Southern California Keck School of Medicine

Om Prakash Sharma, MD, FRCP, FCCP, DTM&H is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Osler Society, American Thoracic Society, New York Academy of Medicine, and Royal Society of Medicine

Disclosure: Nothing to disclose.

Timothy D Rice, MD  Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, St Louis University School of Medicine

Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD  Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, professor and Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center.David Geffen School of Medicine at UCLA.

Zab Mosenifar, MD, is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society

Disclosure: Nothing to disclose.

References
  1. Centers for Disease Control and Prevention. Silicosis-related years of potential life lost before age 65 years--United States, 1968-2005. MMWR Morb Mortal Wkly Rep. Jul 18 2008;57(28):771-5. [Medline].

  2. Rosenman KD, Reilly MJ, Kalinowski DJ, Watt FC. Silicosis in the 1990s. Chest. Mar 1997;111(3):779-86. [Medline].

  3. Sonnenberg P, Murray J, Glynn JR, Thomas RG, Godfrey-Faussett P, Shearer S. Risk factors for pulmonary disease due to culture-positive M. tuberculosis or nontuberculous mycobacteria in South African gold miners. Eur Respir J. Feb 2000;15(2):291-6. [Medline].

  4. Caplan A, Payne RB, Withley JL. A broadened concept of Caplan's syndrome related to rheumatoid factors. Thorax. 1962;17:205-209.

  5. Yucesoy B, Vallyathan V, Landsittel DP, et al. Polymorphisms of the IL-1 gene complex in coal miners with silicosis. Am J Ind Med. Mar 2001;39(3):286-91. [Medline].

  6. Verma DK, Vacek PM, des Tombe K, et al. Silica exposure assessment in a mortality study of vermont granite workers. J Occup Environ Hyg. Feb 2011;8(2):71-9. [Medline].

  7. Chaudhury N, Phatak A, Paliwal R, Raichaudhari C. Silicosis among agate workers at Shakarpur: An analysis of clinic-based data. Lung India. Oct 2010;27(4):221-4. [Medline]. [Full Text].

  8. Linch KD. Respirable concrete dust--silicosis hazard in the construction industry. Appl Occup Environ Hyg. Mar 2002;17(3):209-21. [Medline].

  9. Centers for Disease Control and Prevention. Silicosis in dental laboratory technicians--five states, 1994-2000. MMWR Morb Mortal Wkly Rep. Mar 12 2004;53(9):195-7. [Medline].

  10. Goodman GB, Kaplan PD, Stachura I, Castranova V, Pailes WH, Lapp NL. Acute silicosis responding to corticosteroid therapy. Chest. Feb 1992;101(2):366-70. [Medline].

  11. Gupta R, Vats M, Dadhich P, et a. Steroid pulse therapy in silicosis. Chest. 2003;124:2155.

  12. Sharma SK, Pande JN, Verma K. Effect of prednisolone treatment in chronic silicosis. Am Rev Respir Dis. Apr 1991;143(4 Pt 1):814-21. [Medline].

  13. American Thoracic Society, Centers for Disease Control and Prevention, Infectious Diseases Society of America. Treatment of tuberculosis. MMWR Recomm Rep. Jun 20 2003;52:1-77. [Medline].

  14. Rosenman KD, Moore-Fuller M, Reilly MJ. Connective tissue disease and silicosis. Am J Ind Med. Apr 1999;35(4):375-81. [Medline].

  15. Mulloy KB. Silica exposure and systemic vasculitis. Environ Health Perspect. Dec 2003;111(16):1933-8. [Medline].

  16. Hogan SL, Cooper GS, Savitz DA, et al. Association of silica exposure with anti-neutrophil cytoplasmic autoantibody small-vessel vasculitis: a population-based, case-control study. Clin J Am Soc Nephrol. Mar 2007;2(2):290-9. [Medline].

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