Silicosis Clinical Presentation
- Author: Basil Varkey, MD, FCCP; Chief Editor: Zab Mosenifar, MD more...
History
In obtaining a detailed occupational history, the physician should note chronologically the periods of exposure, the type of work exposure, any respiratory protective devices used, and whether other people working in the same environment have any similar symptoms or disease.
The clinical picture of silicosis is variable; acute and chronic forms have been recognized. Acute silicosis follows a relatively brief exposure to silica dust. The more common chronic forms manifest after several years of exposure and may be asymptomatic (recognized by chest radiographic findings) or symptomatic, with indolent symptoms or progressive symptoms.
Acute silicosis follows a large exposure to dust, often in unregulated environments. Symptoms of cough, shortness of breath, and pleuritic pain may develop in days to several weeks, followed by weight loss and fatigue in months to years.
Chronic silicosis can be either simple silicosis or complicated silicosis (also called progressive massive fibrosis), a distinction based on the chest radiographic appearance (see Imaging Studies). Symptoms often manifest only 1-3 decades after initial exposure. Those who develop symptoms within 10 years after initial exposure have an accelerated form of silicosis and are more likely to develop progressive massive fibrosis (PMF).
Patients with simple silicosis may be asymptomatic or may present with exertional dyspnea and cough with sputum production. Differentiating these symptoms from chronic bronchitis and emphysema in a smoker may be difficult. In PMF, dyspnea and productive cough often are accompanied by constitutional symptoms of malaise and weight loss.
Physical
Physical findings vary with the type and extent of the disease.
Physical findings are often unremarkable in simple silicosis. Rhonchi and or rales may be present in some patients. Tachypnea, expiratory prolongation, rhonchi, wheezing, and rales may be present in complicated silicosis. Digital clubbing is uncommon. Cyanosis may be noted in advanced cases of PMF.
In advanced cases with cor pulmonale, characteristic signs may be present, including prominent jugular pulse, a left parasternal heave, loud pulmonary valve closure sound (P2), tender hepatomegaly, and pedal edema.
Causes
Silicosis is a fibronodular lung disease caused by inhalation of dust containing crystalline silica (alpha-quartz or silicon dioxide), which is distributed widely, or its polymorphs (tridymite or cristobalite), which are distributed less widely. The polymorphs of silica naturally present in lava can also be produced if amorphous silica is subjected to very high temperatures, and this has high toxicity to the lungs.
Because of the wide presence of crystalline silica in nature in an undisturbed form, as in rocks and the earth's crust, people in occupations that disturb the natural state or those involved in collecting, refining, or working with the material are at risk of developing silicosis. These occupations include the following:
- Mining or tunneling
- Quarrying[6]
- Drilling
- Crushing stone
- Chipping
- Grinding
- Sandblasting
- Grinding or polishing in pottery or stone work[7]
- Foundry work
- Cement manufacturing
- Glass manufacturing
- Masonry
- Blast furnaces
- Coal mining
- Construction[8]
- Cutting or manufacturing heat-resistant bricks
- Dental laboratory technicians (a few cases have been reported)[9]
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].
Rosenman KD, Reilly MJ, Kalinowski DJ, Watt FC. Silicosis in the 1990s. Chest. Mar 1997;111(3):779-86. [Medline].
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].
Caplan A, Payne RB, Withley JL. A broadened concept of Caplan's syndrome related to rheumatoid factors. Thorax. 1962;17:205-209.
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].
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].
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].
Linch KD. Respirable concrete dust--silicosis hazard in the construction industry. Appl Occup Environ Hyg. Mar 2002;17(3):209-21. [Medline].
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].
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].
Gupta R, Vats M, Dadhich P, et a. Steroid pulse therapy in silicosis. Chest. 2003;124:2155.
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].
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].
Rosenman KD, Moore-Fuller M, Reilly MJ. Connective tissue disease and silicosis. Am J Ind Med. Apr 1999;35(4):375-81. [Medline].
Mulloy KB. Silica exposure and systemic vasculitis. Environ Health Perspect. Dec 2003;111(16):1933-8. [Medline].
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].
Print
