بسم الله الرحمن الرحیم Silicosis By : F. Movasatian

Introduction: Most common pneumoconiosis in world(occupational exposure to crystalline silica) Silica (silicon dioxide) :  Free: 1-Crystalline (Quartz,Cristobalite,Tridymite) 1-Crystalline (Quartz,Cristobalite,Tridymite) 2-Amorphous(Diatomite) 2-Amorphous(Diatomite)  Combined(silicates): Asbestos,Talk,Kaoline.

Workers at risk : -Miners or tunnelers -Millers -Quarry workers & stone workers -Foundry workers -Sandblasters -Pottery workers -Glass makers

History History  Length of employment  Exp measurements  Effective respiratory protection

Pathogenesis:  Particles <5 μm deposit in alveoli.  Particles <1 μm the most fibrogenic.  80% of silica dust cleared quickly  Particles interact with alveolar MQ Lung inflammation, fibrosis, silicotic nodules (histo. Hallmark)

Silicosis:  simple silicosis  complicated or conglomerate s. (progressive massive fibrosis) (progressive massive fibrosis)  accelerated silicosis  acute silicosis

Simple Silicosis:  No chest symptoms, productive cough.  P/E: coarse sounds  CXR: Rounded opacities(1-10mm) +hilar LAP with distinctive calcification (Eggshell calcification)  p (up to 1.5 mm)  q (1.5-3 mm)  r (3-10 mm)

Cont. Simple Silicosis  HRCT is not more sensitive than CXR in early detection.  PFT: No significant impairment.

Progressive massive fibrosis:  PMF is result of conglomeration of small rounded opacities.  Chronic productive cough / exertional dyspnea to respiratory failure.  P/E: decrease lung sounds.  CXR: nodules >1cm in upper zone +emphysema in lower zone  A (>10mm, 10mm, <50mm)  B (>A but no > right upper zone)  C (> right upper zone)  Pulmonary impairment

Cont. PMF Progression of silicosis depends on:  Duration of exp.  Concentration of silica  Amount of silicosis in CXR.  Mycobacterium infection

Accelerated silicosis:  Time from silica exp., to X-Ray & PFT changes is much shorter.  Rapid progression to progressive massive fibrosis. massive fibrosis.

Acute silicosis:  Short duration of exp. to very high concentration of (fine,freshly cut ) silica  Rapid onset of chest symp. (1-3 yr)and respiratory failure Death(<2yr)  CXR: diffuse alveolar infiltration, air bronchogram, ground glass, cavity(small rounded opacities arenot seen)

Silica exp. & TB  Incidence of TB is greater in accelerated or acute Silicosis  Silica exp. in the absence of silicosis is risk factor for TB  Silica exp. Risk for TB  Radiographic changes in silicosis frequency of TB frequency of TB  Silica exp. & TB Death 4 yrs earlier than TB alone

Cont. TB & silicosis Cont. TB & silicosis  DX : rapid worsening of CXR, decline in lung function suspicion for TB  regular PPD skin test (yearly )  PPD(+) without active TB,indicated at least 1 yr INH prophylaxis.

Diagnosis Diagnosis 1-History of silica exp. 2-Chest radiography consist with silicosis. 3-R/O other illness that mimic silicosis.  HRCT & Lung biopsy (open) if …

Prevention  Product substitution of silica with less toxic particles  Engineering control of dust concentration  Appropriate use of respiratory protective devices  Medical screening: questionnaire, CXR, spirometry

WHO recommendation:  CXR : At baseline, after 2-3 years of exposure, At baseline, after 2-3 years of exposure, then every 2-5 years. then every 2-5 years.  Spirometry + questionnaire : At baseline, then annually or at the same frequency as CXR. At baseline, then annually or at the same frequency as CXR.

Management  Diagnosis of silicosis Remove  Regular CXR and PPD skin test  Steroid helpful in Acute S. or autoimmune dis. (INH prophylaxis)  Whole lung lavage for acute silicosis ?  Tetrandrine  Lung trasplantation

 Crystalline silica (quartz, cristobalite) is carcinogen (group 1 IARC)  Silicosis is associated with autoimmune dis. (RA, SLE, Scleroderma)