Occupational Lung Disease

Pneumoconiosis

• Term used to describe the non-neoplastic lung diseases related to workplace exposure

 

General pathogenesis

• The following factors determine the outcome of inhalation;
• The amount of dust retained
• Depends on the original concentration, duration of exposure and effectiveness of clearance mechanisms
• The size, shape and buoyancy of the particles
• Particles larger than 5μm are filtered in the upper airways, those smaller than 1μm remain suspended and are exhaled. Particles between 1 and 5μm tend to reach the terminal small airways and airsacs
• The physiochemical reactivity and solubility of particles
• Quartz may directly injure cells via free radicals on the particle surface
• Highly soluble particles may rapidly cause toxicity whereas other particles may resist dissolution and by persisting can induce a chronic fibrotic reaction

 

Coal workers’ pneumoconiosis (CWP)

 

• The range of pulmonary effects of carbon dust include;
  • Anthracosis – small, harmless accumulation of macrophage containing carbon pigment in the lungs of urban dwellers and smokers
  • Simple CWP – more prominent, numerous aggregates of coal dust laden macrophages forming coal macules.
    • Clinical features include cough and blackish sputum but not significant lung dysfunction
  • Progressive massive fibrosis (PMF) or complicated CWP – manifests as severe fibrosis and scarring in areas of dust accumulation resulting in disabling respiratory insufficiency

 

• Factors involved in determining the progression of simple to complicated CWP include duration and magnitude of exposure and secretion of fibrogenic factors by coal dust laden macrophages

 

Morphology

• In simple CWP coal macules and larger coal nodules composed of dust filled macrophages are diffusely present particularly in the lobar upper zones
• In due coarse dilation of adjacent alveoli occurs resulting in centrilobular emphysema
• Complicated CWP large blackened scars replace substantial portions of the lung, especially in the upper zones

 

Clinical

• In most cases there is little lung dysfunction
• In 10% of cases PMF develops resulting in increasing lung dysfunction, pulmonary hypertension and cor pulmonale

 

 

Silicosis

 

• Lung disease caused by inhalation of crystalline silicon dioxide (silica)
• Currently the most prevalent occupational disease in the world
• Sources of exposure include mining, quarrying, sandblasting, metal grinding and ceramics manufacture
• Macrophage ingestion of silica leads to activation with release of oxidants, cytokines and growth factors that ultimately cause fibroblast proliferation and collagen deposition

 

Morphology

• Distinct collagenous nodules start as small lesions in the upper lung becoming larger and more diffuse with disease progression. Lesions can coalesce to form large areas of dense scar
• The lesions may be surrounded in calcification
• Histologically the nodular lesions consist of concentric layers of hyalinized collagen surrounded by a dense capsule or more condensed collagen
• Examination of the nodules by polarised light microscopy reveals the birefringent silica particles

 

Clinical

• Patients only develop shortness of breath late in the course
• The disease is slow to kill but can seriously restrict lung function
• It is associated with increased susceptibility to TB

 

Asbestos-related diseases

 

• Occupational asbestos exposure is linked to;
  • Localised fibrous plaques
  • Pleural effusions
  • Parenchymal interstitial fibrosis (asbestosis)
  • Lung carcinoma
  • Mesothelioma
  • Laryngeal and perhaps other extrapulmonary neoplasms e.g. colon carcinomas

 

Pathogenesis

• There are two forms of asbestos;
  • Serpentine (curly flexible fibres) – e.g. chrysotile
  • Amphibole (straight, stiff fibres) – e.g. crocidolite
• Amphiboles are more pathogenic as they reach the deep lung more than serpentine fibres
• However both amphiboles and serpentine fibres are fibrogenic and increasing doses are associated with a high incidence of asbestos related disease however only amphibole fibre exposure correlates with mesothelioma
• The possible mechanisms by which asbestos causes lung injury and progressive fibrosis are;
• Enzyme or toxic free radical release by macrophages and neutrophils
• Fibrinogenic cytokines and growth factors released by macrophages after fibre ingestion
• Direct stimulation of fibroblast collagen synthesis by asbestos

 

 

Morphology

• Asbestosis is marked by diffuse interstitial fibrosis and the presence of asbestos bodies
• Asbestos bodies are brown beaded rods with a translucent centre and consist of asbestos fibres coated with an iron containing proteinaceous material. They arise when macrophages attempt to phagocytose the fibre
• The pattern of fibrosis itself is very similar to UIP
• In contrast to CWP and silicosis, asbestosis begins in the lower lobes and subpleurally
• The scarring may trap and narrow pulmonary arteries and arterioles leading to pulmonary hypertension and cor pulmonale
• Pleural plaques are well circumscribes plaques of dense collagen that occur on the parietal pleura in people exposed to asbestos

 

Clinical

• Clinical findings similar to other interstitial diseases
• Dyspnoea usually accompanied by a sputum producing cough
• Manifestations appear 10-20 years after first exposure
• Disease may progress to respiratory failure, cor pulmonale and death