Occupational interstitial lung diseases from inhaled inorganic dusts.
Also known as: silicosis, asbestosis, coal worker's pneumoconiosis, CWP, black lung, berylliosis, pneumoconiosis
Overview
Group of interstitial lung diseases caused by chronic inhalation of inorganic mineral dusts in occupational settings. Major forms: silicosis (silica), asbestosis (asbestos fibers), coal worker's pneumoconiosis (coal dust), and chronic beryllium disease (beryllium — granulomatous, sarcoid-like).
Epidemiology
Resurgence of accelerated silicosis among young engineered stone (quartz) countertop workers in US/Australia. Asbestosis declining due to bans but legacy exposures persist. CWP persists in coal mining regions globally. Berylliosis in aerospace, electronics, ceramics workers.
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Berylliosis: aerospace, nuclear, electronics, ceramic and dental laboratory work
Cumulative exposure duration and intensity drive risk; smoking synergistic for malignancy
Pathophysiology
Inhaled mineral particles reach alveoli; alveolar macrophages phagocytose but cannot digest them → chronic inflammation, fibrogenic cytokine release (TGF-beta, TNF-alpha), fibroblast proliferation, collagen deposition. Silica is the most cytotoxic and fibrogenic. Asbestos fibers (amphiboles especially) cause pleural plaques, fibrosis, and malignancy. Beryllium triggers a delayed-type hypersensitivity (CD4 T-cell) granulomatous response indistinguishable histologically from sarcoidosis.
Clinical presentation
Symptoms
Progressive exertional dyspnea (most common across all forms)
Cough — often non-productive; productive with chronic bronchitis in CWP
Chest discomfort
Constitutional symptoms in advanced disease
Asbestos: long latency (20-40 years from first exposure)
Acute silicosis: rapidly progressive dyspnea after heavy short-term exposure (engineered stone, sandblasting)
Pulmonary rehabilitation, supplemental oxygen for hypoxemia
Treat comorbid airflow obstruction (bronchodilators, ICS) in CWP
Annual TB screening (IGRA) in silicosis; treat LTBI; consider 4-drug therapy if active
Chronic beryllium disease — corticosteroids (prednisone 20-40 mg/day) for symptomatic disease, similar to sarcoidosis
Second-line / adjunct
Lung transplantation for end-stage disease in select patients
Surveillance for malignancy in asbestos-exposed: low-dose CT screening, especially with concomitant smoking; awareness for mesothelioma (insidious chest pain, pleural effusion, pleural thickening)
Whole-lung lavage for severe acute silicosis (anecdotal, specialized centers)
Antifibrotic therapy (pirfenidone, nintedanib) — emerging role for progressive pulmonary fibrosis phenotype, including occupational ILDs (PF-ILD)
Workers' compensation and occupational disease reporting
Complications
Progressive massive fibrosis (silicosis, CWP)
Tuberculosis and atypical mycobacterial infection (especially silicosis)
Lung cancer (all pneumoconioses, multiplied by smoking)
Mesothelioma (asbestos — even brief exposure; latency 20-40 years)
Engineered stone (quartz) countertops have caused a global epidemic of accelerated silicosis in young workers — high silica content + dry cutting.
Eggshell calcification of hilar lymph nodes is the classic silicosis finding.
Pleural plaques (often calcified diaphragmatic) are pathognomonic for asbestos exposure but do not require asbestosis; mesothelioma can occur without asbestosis.
Silicosis dramatically increases TB risk — screen annually with IGRA; consider isoniazid prophylaxis even with intermediate risk.
ATS 2010 — ATS Statement on Occupational Contribution to the Burden of Airway Disease (Am J Respir Crit Care Med 2003)
MMWR 2019 — Severe Silicosis in Engineered Stone Fabrication Workers — California, Colorado, Texas, and Washington, 2017-2019 (Rose et al., MMWR 2019)
Helsinki Criteria 2014 — Asbestos, Asbestosis, and Cancer — Helsinki Criteria for Diagnosis and Attribution 2014 (Wolff et al., Scand J Work Environ Health 2016)
ATS 2014 — Chronic Beryllium Disease — ATS Official Statement (Balmes et al., Am J Respir Crit Care Med 2014)
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