Occupational And Environmental-Related Lung Disease
The most common form of occupational and environmental lung disease is asthma (Chapters 24 and 25). The UK government has reported that 750 000 people with asthma work in an environment that triggers their symptoms, and more than 3000 per year develop asthma as a result of workplace substances. While the most common cause of occupational asthma is isocyanates (e.g. paint and plastics), grain and f our dust are not far behind, and secondary smoking is most commonly reported to exacerbate symptoms. It is estimated that elimination of occupational asthma alone could have a benefi of up to £1 billion over 10 years; education and prevention are therefore key targets. Atmospheric pollution in the form of car exhausts, diesel particulates and smoke, particularly by main roads and in cities, exacerbates symptoms of respiratory disease and can lead to increased mortality in the vulnerable and elderly.
Response to acute lung irritants
Inhaled irritants (Fig. 33a) cause exacerbation of asthma and chronic obstructive pulmonary disease (COPD), coughing and dyspnoea through activation of irritant receptors (Chapter 12), and irritation of mucous membranes. Highly soluble agents (e.g. ammonia and sulphur dioxide) cause immediate irritation in the upper airways, whereas less soluble agents (e.g. chlorine and ozone) favour deeper penetration to alveolar epithelial cells, which are particularly susceptible to injury. High concentrations lead to extensive lung injury, primarily by damage to epithelium, consequent inflammatio and pulmonary oedema. Development of acute respiratory distress syndrome (ARDS) is common, and treatment is similar (Chapter 41). Some patients who initially recover from moderate or severe exposure may subsequently develop bronchiolitis obliterans (obliteration of bronchioles by fibrou growth) after 2-8 weeks. Although steroids may slow progression, prognosis is often poor.
Inhalation of mineral dusts (pneumoconiosis) Coal worker’s pneumoconiosis (CWP) is caused by inhalation of coal or carbon dust. In simple CWP, the upper lobes of the lung contain small (<4 mm), round opacities (coal macules) consisting of dust, dust-laden macrophages and fibroblasts These may enlarge to fibrose coal nodules. Weakening of bronchiolar walls leads to focal emphysema, which together with macules is characteristic of CWP. Simple CWP is often described as symptomless, with no change in lung function. It can however develop into progressive massive ﬁbrosis (PMF), with black fibroti masses from 1 cm to several centimetres in diameter, which may have necrotic cavities. Obliteration and disruption of airways result in emphysema. Patients show irreversible airfl w limitation, loss of lung volume and elastic recoil, and reduced DLco, with breathlessness on exertion. Treatment is limited, and similar to other progressive fibroti diseases (Chapter 25). Caplan’s syndrome is a nodular form of CWP associated with the defective immunology of rheumatoid disease; it may also occur with asbestosis or silicosis.
Asbestos is a f brous mixture of silicates that is highly resistant to degradation. The f bres are 1-2 μm wide, but up to 50 μm (blue asbestos-crocidolite) or 2 cm (white asbestos-chrysotile) long. They are thus easily trapped in the lung. Blue asbestos is far more dangerous. Regulations have reduced exposure since the 1980s, but the presence of asbestos in buildings and the long interval between exposure and disease development mean that asbestos-related disease will be encountered for some time. Asbestos bodies (protein-covered f bres) in the lungs are indicative of exposure, but not disease. The type and extent of disease largely depend on exposure. Asbestosis is a f brous lung disease developing up to 10 years after heavy exposure. Patients present with progressive dyspnoea, basal crackles on inspiration and sometimes finge clubbing. There is a restrictive lung function defect and reduced DLco, with diffuse streaky shadows on X-ray and thickening of visceral pleura; honeycomb lung is often prominent in the lower lobes. Prognosis is poor. Mesothelioma (Chapter 32) can develop up to 40 years after light exposure, and is invariably fatal. Milder forms of asbestos-induced pleural disease produce dyspnoea and restrictive defects coupled with pleural thickening and plaques or effusions, with scattered fibrotic foci. No treatment is effective for asbestos-related disease, as the stimulus remains in the lungs. Asbestos-related lung cancer is discussed in Chapter 40.
Silicosis is a fibrotic disease caused by inhalation of silica, with a low prevalence in developed nations. Occupations at risk include mining, stone-working, manufacture of abrasives, foundry work and glass-working. Silica is very toxic to macrophages and thus highly fibrogenic Chronic silicosis (over decades) is characterized by silicotic nodules of collagen around a cell-free core, firs developing in hilar lymph nodes. In acute silicosis due to heavy exposure, severe dyspnoea may develop over months. The clinical features of silicosis are similar to PMF.
Inhalation of organic material
Extrinsic allergic alveolitis (or hypersensitivity pneumonitis) is a diffuse inflammator disease of small airways and alveoli caused by allergens, primarily microbial spores, that are small enough to reach the alveoli (Fig. 33b). The most common example is farmer’s lung, caused by dust from mouldy hay or plants contaminated with thermophilic actinomycetes bacteria, which thrive in warm moist conditions. Typically, symptoms occur several hours after exposure, and include fever, dyspnoea and cough. Although early removal of exposure results in rapid recovery, continuous exposure leads to progressive interstitial ﬁbrosis (Chapter 32), with infiltratio of inflammator cells and formation of granulomas (chronically inflame tissue masses characterized by multinucleate giant cells, see Fig. 29b). Patients present with dyspnoea, restrictive defects and decreased DLco. Fluffy nodular shadowing or ground glass opacity may be shown in CXR, with honey- comb lung (Chapter 32) in severe cases. Detailed histories are required to establish antigens, with confirmatio by precipitating antibodies in serum. Management centres on abolishing antigen exposure. High-dose corticosteroids can regress early disease, but established disease with fibrosi is irreversible and can progress to respiratory failure. Differential diagnosis includes asthma (Chapters 24 and 25), sarcoidosis (Chapter 31), viral and mycoplasma pneumonias (Chapters 36 and 37) and mycobacterial infections.
Byssinosis occurs in workers handling raw cotton, fla and hemp. It is characterized by chest tightness, cough and/or shortness of breath on the f rst day back at work, with recovery as the week progresses. It is primarily due to acute bronchoconstriction, possibly related to contaminating bacterial endotoxins. Long-term exposure causes a disease similar to chronic bronchitis (Chapter 26), with chronic productive cough, progressive decline in lung function and disability.