In silicosis, the pulmonary function worsens with the worsening radiology. Pulmonary function testing (PFTs) are a key component for the diagnosis and to guide the future occupational choices. Typically, spirometry before and after bronchodilator, lung volumes, diffusing capacity for carbon monoxide (DLCO), and resting pulse oxygen saturation are obtained.
Pulmonary function testing (PFTs) are a key component in the diagnosis and follow-up of patients to detect extent of lung involvement, severity of the disease, and guide future occupational choices. Typically, spirometry before and after bronchodilator, lung volumes, diffusing capacity for carbon monoxide (DLCO), and resting pulse oxygen saturation are obtained.
Progressive massive fibrosis is associated with the worst pulmonary function abnormalities including
Decreased compliance,
Decreased FEV1 and FEV1/FVC ratio, and
Decreased diffusing capacity for carbon monoxide (DLCO) .
Pulmonary function, on average, worsens in association with worsening radiographic abnormalities of chronic or accelerated silicosis; cigarette smoking is often contributory.
Spirometry is performed for the evaluation of possible functional lung deterioration
Spirometry shows a mixed picture of obstructive and restrictive ventilatory impairment with decreased FEV1 and FEV1/forced vital capacity (FVC) ratio 
Diffusion capacity is affected in the complicated forms of the disease and is sensitive to the presence of fibrosis.
Static lung volumes can demonstrate a reduction in total lung volume .
Pulse oximetry and arterial blood gases are useful for the detection of respiratory failure (PaO2<60 mmHg with SpO2<90%) in the more advanced cases.
Complete cardiopulmonary exercise testing may be helpful in evaluating patients with respiratory symptoms, particularly exertional dyspnea, who have a history of exposure to silica and whose resting lung function is normal.
Bronchoscopy to confirm the diagnosis is not indicated for most patients. However, bronchoscopic washings, brushing, or bronchoalveolar lavage (BAL) is used to exclude infection, eosinophilic pneumonia, and alveolar hemorrhage when acute silicosis is suspected. In acute silicoproteinosis, BAL yields a thick, opaque (milky) effluent similar to that seen in pulmonary alveolar proteinosis. On cytologic examination, the macrophages in the BAL are foamy and the lipoproteinaceous material stains brightly positive with periodic acid-Schiff (PAS) reagent  In general, transbronchial biopsy is avoided due to the presumed risk for pneumothorax .
A lung biopsy is not necessary in the setting of a definite exposure history and characteristic clinical findings.The histopathology of acute silicosis is different from that of chronic or accelerated silicosis. Silicotic nodules are rarely seen, and, if present, are usually poorly developed. As described for BAL fluid, proteinaceous material fills the alveoli and consists largely of phospholipids or surfactant (or surfactant-like material) and stains with PAS reagent. The interstitium is thickened with inflammatory cells; a minimal amount of pulmonary fibrosis is typically present. Alveoli may be lined with prominent epithelial cells, the majority of which are hypertrophic type II pneumocytes . In addition, desquamated pneumocytes, macrophages, and silica particles are found in the alveolar spaces. The histologic appearance of acute silicosis resembles that of idiopathic alveolar proteinosis
Biomarkers such as Serum NSE and CA125 concentrations would provide valuable clinical information to assess disease severity in silicosis. Research is going on the use of various other biomarkers in silicosis.
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