Shortness of breath in a consturction site worker: occupational lung diseases and fibrosing alveolitis

Respiratory problems for exposure in building sites include

What are the possible causes of dyspnoea in a construction site worker

Interstitial lung diseases

A diverse heterogenous group of chronic non-infective disorders which predominantly affect the architectural lung tissue especially the alveolar walls. All are similar in symptoms, signs, radiological findings, physiological derangements, and complications.

Symptoms in Interstitial lung diseases

Signs in interstitial lung diseases

Lung function parameters in interstitial lung diseases i.e. restrictive defect

Radiology in interstitial lung diseases Depends on the staging of the disease. HRCT more sensitive than plain x-ray. Early: ground glass with alveolar pattern. Late: fibrosis with or without honeycombing

Classification of interstitial lung diseases

  1. Occupational exposure: Inorganic dust: silicosis (¯ in Chinese), asbestosis and many others (pneumoconiosis (hard metal, coal), berylosis, aluminium hydroxide fibrosis). Organic dust (hypersensitivity pneumonitis): bird breeder’s lung, farmer’s lung

  2. Iatrogenic: Can be caused by a large variety of drugs and treatment including antibiotics (furantoin, sulfasalazine), anti-arrythmics (amiodarone, propanolol), anti-inflammatory (gold, penicillamin), and anti-tumour drugs (mitomycin C). Also radiotherapy and oxygen

  3. Connective tissue diseases: rare and can complicate e.g. scleroderma, polymyositis and dermatomyositis, systemic lupus erythematosis, rheumatoid arthritis, mixed CT disease, ankylosing alveolitis.

  4. Interstitial pulmonary fibrosis: rare diseases such as: Sarcoidosis and hundred of others (amyloidosis, lymphagitis, sarcinomatosium, AIDS, bone marrow transplant)

  5. Cryptogenic fibrosing alveolitis

Silicosis

The leading occupational lung disease in Hong Kong and workers usually from construction industry. Caused by inhalation of silica which is highly fibrogenic. There are chronic, accelerated and acute types. Chronic types are usually simple which could progress to progressive massive fibrosis.

Pathology of silicosis

Hallmark is formation of silicotic nodules which are concentric whorls of callagen-rcih fibrotic tissue and located predominantly in the upper lobes. Hilar lymph nodes are usually involved.

Clinical features of silicosis

Acute: heavy exposure in short time (<3 years) and poor prognosis. Chronic: light exposure over decades (10-20y: more common in HK)

Accelerated: moderate exposure over 4-8 years with same clinical features as chronic but greater impairment.

Simple and complicated silicosis

Simple silicosis Complicated silicosis

Asymptomatic Exertional dyspnoea

Relatively normal CXR Coalescence of opacities

No clubbing Might have clubbing

No chest signs Many and cor pulmonale

Upper zone <1cm opacities Opacities merge

Normal to mild restrictive lung function Marked restrictive but may also be obstructive

Dx: adequate exposure Hx, supporting CXR, absence of mimicing disease

Investigations in silicosis

  1. History: detailed occupation and smoking

  2. Chest x-ray: useful diagnostic

  3. Lung function: non-diagnostic (smoking, TB)

  4. HRCT: could be diagnostic

  5. Sputum microbiology and AFB (60-80% silicosis develop TB b/c silica inhibits lymphocyte function)

  6. ECG and blood gas analysis

Complications in silicosis

  1. Tuberculosis: 80% of all cases and may superimpose without acute symptoms. Exclude active TB at all times especially: change in sputum characteristics, haemoptysis, rapid radiological changes, cavitation, and weight loss or other TB symptoms

  2. Respiratory failure

  3. Pneumothorax

  4. Lung cancer

Treatment in silicosis: none effective

    1. Removal of affected workers

    2. Tuberculosis

    3. Associated smoking related COPD

    4. Oxygen for respiratory failure

    5. Cor pulmonale

    6. Social support

Compensation for silicosis -- Controversial and unsatisfactory (disability: need to account for social, intellectual, economic and cultural factors)

No gold standard! Impairment of lung function indices is easy to measure but might be due to non-exposure reasons e.g. smoking and TB. Impairment is not disability and assessment of disability is vastly complicated. Current evaluation for compensation is difficult as there are no study on the correlation between lung function parameters, radiological findings, exercise tolerance assessment, and quality of life parameters

Compensation for Silicosis in Hong Kong

Compensation worked out by a formula that takes accounts of the DOI. Current grading of compensation is by measurement of forced vital capacity (FVC) and then converting this into percent predicted. Almost all non-Govt workers. 249 cases in 1993 (cumulative total 5254). Most mild (15-20%) DOI (degree of incapacity). FVC: effort-dependent, affecting by smo,ing + TB

4th Schedule of Pneumoconiosis Compensation Ordinance

FVC% Degree of Incapacity

>95% 5%

90-94% 10%

85-89% 15%

80-84% 20%

75-79% 30%

70-74% 40%

65-69% 50%

60-64% 60%

55-59% 70%

50-54% 80%

<49% 100%

Prevention of silicosis

  1. Build safely and do not tunnel (do not build!)

  2. Low dust density

  3. Wearing of effective masks

  4. Keep surface wet

  5. Treat complications such as TB earlier

  6. Identify earlier silicosis workers to relocate -- not sack!

Cryptogenic fibrosing alveolitis

An uncommon idiopathic disease in Hong Kong in which the lung parenchyma becomes fibrotic. Development of progressive impairment in gaseous exchange and dyspnoea. Usual onset at middle age and the aetiology of cryptogenic fibrosing alveolitis is unknown. Diagnosed by exclusion of other conditions. Histologically can be identical to other secondary CFA. The pathogenesis of cryptogenic fibrosing alveolitis is via immune mechanisms with lymphocyte infiltration of lung parenchyma. Heterogeneous involvement but lower lobe predominance.

Presenting symptoms: exertional dyspnoea, dry cough. Occasional viral prodrome and is associated with weight loss and malaise. May have primary disease features such as arthritis.

Signs: clubbing or cyanosis are usually late. Bilateral end inspiratory "dry" crackles and cor pulmonale

Chest x-ray in cryptogenic fibrosing alveolitis

  1. Lower lobe predominance (periphery)

  2. Reticular shadow

  3. Lace-like curvilinear opacities (scar tissue)

  4. Reduced lung volume

  5. Ground glass consolidation (early) and honeycombing (late)

Complications in cryptogenic fibrosing alveolitis

    1. Respiratory failure

    2. Cor pulmonale (right heart fails secondary to pulmonary oedema)

    3. Bronchogenic carcinoma (main cause of death in CFA)

    4. Spontaneous pneumothorax

    5. Respiratory infections (¯ mucociliary clearance)

    6. Pulmonary embolism (­ in West)

Treatment in cryptogenic fibrosing alveolitis

  1. Early and high dose corticosteroids (1mg/kg prednisolone)

  2. 40-70% subjective improvement and 10-30% subjective and objective improvement

  3. Cytotoxics for steroid sparing (eg. cyclophosphamide)

  4. Oxygen if respiratory failure (extreme SOBOE)

  5. Physiotherapy

  6. Early antibiotic

Note: some specialists do not Tx early (adopt a wait-and-see attitude ® this is wrong