Occupational Lung Diseases — Asbestosis, Silicosis, Coal Workers' Pneumoconiosis, Byssinosis and Berylliosis

Pneumoconiosis is any lung disease caused by inhaling organic or inorganic airborne dust or fibres, usually at work, so it is classified as an occupational disease. The commonest are asbestosis, silicosis and coal miner's lung. Particles inhaled at the workplace cause inflammation and fibrosis, which is irreversible; prevention depends on workplace exposure control and health surveillance. Latency is long, so disease often appears years after exposure and the risk rises with length of employment.

Particles smaller than about 5 microns escape mucociliary clearance and deposit in the terminal bronchioles and alveoli. Alveolar macrophages phagocytose them and release IL-1, TNF-alpha, lysosomal enzymes and free radicals; growth factors then stimulate fibroblasts to deposit collagen and matrix, producing scar. The overall picture on imaging is widespread opacities, predominantly in the upper zones, except asbestosis, which prefers the lower zones.

Asbestosis is an interstitial lung disease caused by inhaled asbestos fibres, which are hydrated magnesium silicates. Two forms exist. Serpentine (chrysotile) fibres are curly, flexible, soluble and are largely cleared by the upper airways, so they are less pathogenic. Amphiboles (crocidolite, amosite, tremolite, anthophyllite) are straight, stiff, brittle fibres that align with the airstream, penetrate the interstitium and are more toxic. The disease is dose-dependent, and exposure may be direct (shipyards, mining, aerospace), bystander (electricians, masons, painters) or general community.

• Pathology — interstitial fibrosis with asbestos bodies: golden-yellow rod-like structures with a translucent centre (asbestos fibre coated with iron-containing protein); ferruginous bodies resembling golden-brown dumbbells indicate prior exposure to inorganic dust. Subpleural honeycombing develops in advanced disease.
• Symptoms and signs — progressive exertional dyspnoea, dry cough; bibasal crackles, clubbing (reported in roughly a third to two-fifths of patients) and reduced chest expansion; cor pulmonale in advanced disease.
• Imaging — calcified pleural plaques and pleural thickening are hallmarks; fibrosis is subpleural and lower-zone predominant (a UIP-like pattern), so look for pleural plaques to separate it from IPF. Benign pleural effusion often appears early.
• Lung function — restrictive pattern with reduced FVC and total lung capacity, preserved FEV₁/FVC ratio, and early fall in diffusing capacity.
• Management — no specific treatment; supportive care, smoking cessation, exposure control. Corticosteroids have a low success rate and no proven survival benefit.

Silicosis follows inhalation of crystalline silicon dioxide (quartz, sandstone, granite); the amorphous form is not significantly harmful. Silica generates reactive oxygen species and activates macrophages, releasing IL-1 and TNF-alpha and promoting fibrosis. Silica also impairs the ability of macrophages to inhibit mycobacterial growth, explaining the strong association with tuberculosis.

• Histology — silicotic nodules with a central whorled, acellular hyalinised collagen surrounded by dust-laden macrophages ('onion-skin' pattern); lesions are mainly in the upper zones along the respiratory bronchioles; nodules may be firm, round and black-pigmented.
• Complications — progressive massive fibrosis, tuberculosis and non-tuberculous mycobacteriosis (suspect when nodules enlarge rapidly or cavitate), lung cancer, emphysema, scleroderma and glomerulonephritis in some reports.
• Management — no specific therapy; remove the source of exposure, screen for tuberculosis and treat it as indicated.
• Differential — the main histological mimic is the rheumatoid nodule.

Coal workers' pneumoconiosis (CWP, 'black lung') is caused by prolonged inhalation of coal dust. Dust is deposited throughout the lungs but collects around the respiratory bronchioles, where the airspaces dilate. The characteristic lesion is the coal macule: aggregates of dust-laden macrophages (anthrocytes) with reticulin fibrosis, surrounded by a halo of focal emphysema; larger, more fibrotic coal nodules also occur. Patients may produce black sputum. Radiologically it resembles silicosis, with small nodules in the upper and mid zones.

Simple CWP can progress to progressive massive fibrosis (PMF). On MRI, PMF shows low signal on T2, whereas lung cancer is high signal — a useful discriminator. Pulmonary function shows a restrictive pattern with chronic airflow obstruction, reduced FVC, a preserved or modestly reduced FEV₁/FVC ratio and reduced diffusing capacity.

Caplan syndrome (rheumatoid pneumoconiosis) is the combination of rheumatoid arthritis with pneumoconiosis. It was classically linked to coal dust but is now recognised with silica and asbestos exposure (coal miners, asbestos workers, gold miners, sandblasters, quarrymen). Multiple peripheral lung nodules (0.5–5 cm on CT) appear, histologically necrobiotic rheumatoid nodules with concentric rings of black dust. They develop rapidly over weeks to months, may cavitate or calcify, and then stay stable for years. Diagnosis needs imaging, sometimes biopsy to exclude malignancy.

Byssinosis ('brown lung', cotton worker's lung, Monday fever, mill fever) is caused by inhaling dust from raw cotton and, less commonly, flax, hemp and jute. It is attributed to endotoxin (lipopolysaccharide) from Gram-negative bacteria on the fibre, which triggers inflammation and, over time, fibrosis. The most dust exposure is in the early steps of yarn preparation.

• Early disease — cough, chest tightness, dyspnoea, wheeze within hours of re-exposure, typically at the beginning of the working week ('Monday fever'). Occupational asthma, in contrast, is worse towards the end of the week.
• Chronic disease — symptoms lose their weekly cycle, with persistent cough and sputum, chronic bronchitis, falling FEV₁ and fibrosis.
• Treatment — remove the patient from exposure (FEV₁ may recover if early), inhaled bronchodilators and sometimes inhaled or short-course oral steroids, stop smoking.

Berylliosis, or chronic beryllium disease (CBD), is a granulomatous lung disorder caused by sensitisation to and exposure to beryllium, most often occupational. Beryllium is used in metal machine shops, electronics, defence, ceramics, automotive, aerospace, jewellery, dental-alloy and computer industries. Exposure is by inhalation of fume or dust, and skin absorption is possible.

• Mechanism — a CD4+ T-cell-mediated hypersensitivity; macrophages, CD4+ T cells and plasma cells form non-caseating granulomas that can progress to fibrosis. A HLA-DPB1 Glu69 variant increases the risk of sensitisation and disease.
• Look-alike — histology and imaging mimic sarcoidosis; the distinguishing step is the exposure history and a positive beryllium lymphocyte proliferation test on blood or bronchoalveolar lavage.
• Symptoms — fever, night sweats, weight loss, dry cough, fatigue; latency from 3 months to 30 years.
• Imaging — normal early; later hilar lymphadenopathy, nodules, ground-glass opacities and fibrosis.
• Treatment — avoid further exposure; corticosteroids are the drug of choice, usually in a high starting dose for several months.

Diagnosis rests on three criteria: exposure to the relevant dust at high dose or for a long time, characteristic chest imaging, and exclusion of other diseases that could mimic pneumoconiosis. A lung biopsy is rarely needed. A thorough occupational history, covering the nature and duration of exposure, is the single most important step.

• Primary prevention — dust control at source: wet drilling, enclosure and ventilation, substitution of safer materials, respirators and personal protective equipment, and limiting exposure time.
• Secondary prevention — pre-employment and periodic medical examination with chest radiograph and spirometry; early detection to remove workers from exposure.
• Tertiary prevention — rehabilitation, treating complications such as tuberculosis, smoking cessation and removal from further exposure.