Silica: The Deadly Dust

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Silica (Silicon Dioxide - SiO₂)

• Crystalline silica occurs naturally in the earth’s crust
• Earth’s most abundant mineral
• Three most common forms
  • Cristobalite
  • Tridymite
  • Quartz – most abundant component of soil & rock
    

• Respirable particles of silica (<5 µ in diameter) produced when crystalline silica-containing rock and sand is used or processed
  • Mining, milling, and stone work
  • Quarrying and tunnel operations
  • Foundry and boiler work
  • Sandblasting and drilling
  • Pottery and glass making

• Occupational exposure associated with respiratory diseases
  • Silicosis (chronic, accelerated, acute)
  • Progressive pulmonary fibrosis
  • Chronic obstructive pulmonary diseases
  • Lung cancer
  • Increased risk for TB

• Occupational exposure associated with other diseases
  • Systemic autoimmune diseases
    • Rheumatoid arthritis, SLE, scleroderma, small vessel vasculitides
  • Renal Disease
    • Glomerulonephritis, nephrotic syndrome, end-stage renal disease

Silica – Historical Overview

• Silicosis
  • First reported by ancient Greeks
• Prevalence
  • Peaked in the industrial countries in the last half of the 19th century
  • Disease still prevalent in the developing world and not eliminated from the developed world

• Largest industrial disaster in US history
  • Gauley Bridge, WV – 1930-1932
• Tunnel construction
  • Silica content of the rock - >90%
• >475 workers died
• 1,500 were disabled from chronic silicosis
  

View of Gauley Bridge, WV circa 1930
Source: The Hawk’s Nest Incident, Cherniak M, 1986

View of Hawk’s Nest tunnel interior, March 13, 1932
Source: The Hawk’s Nest Incident, Cherniak M, 1986

Silicosis: Crude mortality rates by state, U.S. residents age 15 and over, 1987-1996

Silicosis

• A pulmonary disease caused by inhalation of dust particles of respirable size
• Three presentations and severity of the disease
  • Classic silicosis
  • Accelerated silicosis
  • Acute silicosis

• Chronic (classic) silicosis
  • 20+ years of exposure to low-medium dust levels
• Accelerated silicosis
  • 5-10 years of higher dust exposure
• Acute silicosis
  • <1-3 years exposure to extremely high levels of free crystalline silica

Pathogenesis

Pathogenesis: Chronic Silicosis (Classic and Accelerated)
Source: ACCP Pathology Slide Set, No. 36-2

Pathogenesis: Acute Silicosis
Source: Silicosis. Weber and Banks. In: Textbook of Clinical Occupational & Environmental Medicine. Rosenstock & Cullen, eds., 1994, page 270.

Chronic Classic Silicosis

• Simple silicosis
  • Development predominantly in the upper lobes
  • Rounded opacities < 1cm in diameter seen on chest x-ray
  • Enlarged hilar lymph nodes with peripheral calcification - eggshell calcification
    
    
    

• Progressive Massive Fibrosis
  • A massing of small rounded opacities in upper lobes
  • Large opacities > 1 cm
  • Hila retract upward & lower zones become hyper-inflated & appear emphysematous
    
    
    
    

Source: Pathology of Occupational Lung Disease, 2nd ed. A Churg, FHY Green, 1998, pg. 163

Accelerated Silicosis

• Characterized by same features as chronic classic silicosis
• Time from initial exposure and development of radiographic findings and symptoms and change in pulmonary function much shorter
• Rapid progression to PMF with severe respiratory impairment

Acute Silicosis

• Radiographic Evidence
  • Diffuse alveolar infiltrate
  • Air bronchograms
  • Ground glass appearance
  • Hilar & mediastinal lymphadenopathy
  • Bullae formation
  • Air trapping
  • Volume loss
  • Cavity formation
    
    
    Source: Environmental & Occupational Medicine, 2nd ed., Rom W, 1992, pg. 353.
    
    
    Source: Diagnosis of Diseases of the Chest, Fraser & Pare, 1970, pg. 923.
    

 

Chronic silicosis

Simple silicosis

• Symptoms
  • Often no symptoms
  • Chronic productive cough may be due to industrial bronchitis from dust exposure
• Physical exam
  • Normal breath sounds
  • Course breath sounds with co-existing bronchitis

Progressive Massive Fibrosis

• Symptoms
  • Range from chronic productive cough to exertional dyspnea
• Physical exam
• Diminished breath sounds
• Prolonged expiration
• Clubbing rare

Acute silicosis

• Symptoms
  • Irritative cough - sometimes productive
  • Weight loss
  • Fatigue
  • Dyspnea
• Physical exam
  • Crackles heard on auscultation

 

Chronic silicosis

Pulmonary Function Testing

• Simple silicosis
  • Normal lung function
• PMF
  • Severe restriction
  • Mixed obstructive/restrictive defect
  • Loss of pulmonary compliance
  • Hypoxemia

Diagnosis

The Occupational History

• What kind of work do you do?
• Do you think your health problems are related to your work?
• Are your symptoms better or worse when you are at home or at work?
• Are you now or have you previously been exposed to dust, fumes, chemicals, radiation or loud noises?

• History of silica exposure
• Radiographic evidence consistent with silicosis
• Absence of other illnesses that mimic silicosis
  (LS Newman. N Engl J Med 1995; 333:1129)

Silicotuberculosis

• Prevalence
  • 5.3% in workers with x-ray evidence of silicosis
  • 25% in workers with acute or accelerated silicosis
  • As high as 75% among South African gold miners

• Diagnosis difficult
  • TB infection can be walled off in the lung by the silica induced fibrosis
  • False negative acid-fast-staining sputum smear may occur
• Radiographic changes seen with TB infections can mimic advanced cases of silicosis

• Diagnosis
  • Presence of chest x-ray changes of a worker with silicosis over a short period of time indicates superimposed TB infection until proven otherwise
  • Annual PPD
• If results become positive without clinical evidence of active TB, the patient should be treated with 1 year of INH

Silica Exposure & Cancer

• Crystalline silica deposited in lungs causes epithelial & macrophage injury and activation and persistent inflammation
• Human subjects exposed to dust containing crystalline silica showed an increase in the levels of sister chromatid exchange and chromosomal aberrations in peripheral blood lymphocytes
• Animal studies have shown gene mutations and tumor formation as a result of marked and persistent inflammation and epithelial proliferation

• IARC
  • Crystalline silica inhaled in the form of quartz or cristobalite from occupational sources is carcinogenic to humans (Group 1)

Silica Exposure & Autoimmune Disease

• First described in 1953 by Caplan
  • Unusual radiologic changes in the lungs of Welsh coal miners who had pneumoconiosis
• Since then the autoimmune disease linked with crystalline silica exposure
  • Rheumatoid arthritis, scleroderma, SLE, some small vessel vasculitides

• Inhalation of crystalline silica particles leads to chronic immune activity and fibrosis
• Studies have shown that crystalline silica can be mobilized from lungs to other organs - lymph nodes, spleen, and kidney
• Silicosis has been linked to an increase in autoantibodies, immune complexes, and excess production of immunoglobulins, even in the absence of a specific autoimmune disease

• Possible Mechanisms
  • May be result of adjuvant (a substance that enhances an immune response to an antigen) effect on antibody production
  • Cell death by necrosis and apotosis (an active process involved in gene regulation)
  • Host susceptibility and genetic differences may explain why all workers exposed to silica do not develop immune disorders may

Silica Exposure & Renal Disease

• Epi studies
  • Statistical significance between silica exposure and several renal diseases
  • An increasing standardized rate ratio for acute and chronic renal disease with increasing cumulative crystalline silica exposure and an excess of end-stage renal disease incidence (highest for glomerulonephritis)

• Intensity of exposure to silica dust may be more important than cumulative exposure or duration in the development of autoimmune diseases
• Study crystalline silica exposure most strongly associated with ESRD and median exposure was below the OSHA permissible exposures levels

Treatment

• Prevention/ Prevention/Prevention
• Workers at risk for progression of disease and TB infection
• Yearly chest x-ray and PPD Flu and pneumococcal vaccine
• Aggressive treatment of TB infections
• Dyspnea treated with inhaled bronchodilators
• O₂ for cor pulmonale, hypoxemia, pulmonary hypertension

Prevention

• Occupational Health Surveillance
  • Gather information on cases of occupational illness and injury and workplace exposures
  • Condense, refine, and analyze the data
  • Disseminate analyzed data to workers, unions, employers, governmental agencies, public
  • Plan and execute interventions - primary prevention - based on the analyzed data
• Occupational Sentinel Health Event
  • "A disease, disability, or untimely death which is occupationally related and whose occurrence may: 1) provide the impetus for epidemiologic or industrial hygiene studies; or 2) serve as a warning signal that materials substitution, engineering control, personal protection, or medical care may be required"
• State-based Surveillance
  • Sentinel Event Notification Systems for Occupational Risk (SENSOR)
  • Many state based silicosis surveillance projects
  • May help in case investigations
  • Many states have a legal requirement to report a case of silicosis to the appropriate state agency

• Hierarchy of Controls
• Engineering
  • Substitution, control hazard at source (wet process), improved ventilation
• Administrative
  • Rotating workers
• Personal Protective Equipment
  • Respirators

Prevention - Regulation

• Federal Coal Mine Health and Safety Act of 1969 (Coal Act)
• Federal Mine Safety and Health Act of 1977 (Mine Act)
  • MSHA
• Occupational Safety and Health Act of 1970
  • NIOSH
  • OSHA
• Current OSHA PEL for respirable silica
  • 10 mg/m³ / %SiO₂ + 2 for 8-hour TWA
• Current NIOSH REL for respirable silica
  • 50 µg/m³ TWA for up to 10 hours/day during a 40 hour workweek
    
    
    
    
    

SIlica: The Deadly Dust

Any Questions?

"The way to dusty death. Out, out, brief candle!
Life's but a walking shadow, a poor player
That struts and frets his hour upon the stage
And then is heard no more."

- Shakespeare, Macbeth, Act V, Scene V

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