Occupational asthma

Occupational asthma is the commonest occupational lung disease, with an incidence of 3000 cases each year. It is estimated that 10–15% of those with adult‐onset asthma have an occupational cause. Occupational asthma can develop for the first time in an individual exposed to an irritant or sensitizer. Occupational exposure can also exacerbate symptoms in patients who have a known diagnosis of asthma (work‐exacerbated asthma), and the estimated prevalence of this is 21%. A history of atopy or asthma has a poor positive predictive value for developing occupational asthma.

Occupational asthma, just like non‐occupational asthma (see Chapter 6), is characterised by reversible and variable airflow obstruction. Exposure to a variety of substances at work can result in sensitization, resulting in inflammation of the airways and bronchospasm. Non‐immunological agents can irritate the nose and upper airways, resulting in symptoms within minutes or hours of inhalation. The rapidity with which symptoms develop depends on the size of the substance; low molecular weight agents have a shorter latency period. A single exposure to highly soluble toxic gases, for example, sulphur dioxide, ammonia, or chlorine gas, can directly damage the upper airways, and cause reactive airways disease syndrome (RADS), the symptoms of which include persistent dry cough, dyspnoea, and wheeze. More severe or prolonged exposure can result in damage to the alveolar epithelial cells and the development of acute lung injury (ALI) and adult respiratory distress syndrome (ARDS). The long term consequence of this might be the development of bronchiolitis obliterans.

Exposure to immunologic stimuli will result in a period of sensitization and the development of symptoms at a later stage: this latent period may vary from a few weeks to several years. Further exposure to the same agent in a sensitised individual can result in an early (30 minutes) or late (12 hours) response.

Individuals with occupational asthma will develop symptoms of cough, wheeze, chest tightness, and breathlessness while at work, usually within several hours of being in that environment. Their symptoms will generally improve when they are away from the workplace, for example, at weekends or during holidays, and return when they go back to work. This temporal relationship between exposure and symptoms is important in making a diagnosis of occupational asthma. The agent that is likely to be causing the symptoms should be sought by careful evaluation of all the products that the individual is being exposed to. Prolonged and recurrent exposure to the agent could result in chronic asthma and irreversible lung damage, with the individual developing persistent symptoms even when they are away from the workplace.

It is important to remember that other conditions, such as COPD, hypersensitivity pneumonitis and non‐occupational asthma will present with similar symptoms, and will need to be excluded when making a diagnosis of occupational asthma.

Individuals suspected of having an occupational cause for their asthma should have careful monitoring of their peak expiratory flow (PEF) and spirometry at work and when away from work. They may require bronchial hyper‐responsiveness testing using histamine or methacholine in some cases. If these investigations are normal, then occupational asthma is unlikely. Additional investigations that may be useful include skin prick testing and measurement of immunoglobulin E RAST to specific allergens, as discussed in Chapter 6.

Once a diagnosis of occupational asthma has been confirmed, the most important thing is to reduce exposure to the agent provoking it. Ideally, this might mean removing the individual from the workplace altogether. If this is not possible, the employer will have to ensure that safety measures are in place to reduce exposure. This would include adequate ventilation, the wearing of protective masks, screening of other workers, and regular health checks.

Table 15.1 lists some common causes of occupational asthma. This list is not exhaustive. These agents can also result in exacerbation of COPD and other lung diseases.

Asbestosis

Asbestos is a naturally occurring fibre composed of hydrated magnesium silicate. Prior to the recognition that inhalation of asbestos fibres was harmful, asbestos was widely used without any protective measures in a variety of industries, as listed in Box 15.1.

Since the early 1970s, strict regulations in developed countries have resulted in banning the use of asbestos, and the implementation of health and safety measures to reduce exposure in those who might be exposed to it. However, the long lag period between exposure and developing the disease means that patients exposed to asbestos many decades ago are still presenting with asbestosis and mesothelioma. Therefore, it is important to take a full occupational history. In less developed countries, asbestos, which is a cheap material, is still widely used without any regulation.

Asbestos occurs in natural sources, such as rocks, so those living in certain geographical regions are exposed to low levels. Those living or working in a building which contains asbestos, for example, a house or school, are also exposed. Those who breathe in asbestos fibres from the work‐clothes of partners are also at risk. This type of exposure increases the risk of mesothelioma but does not increase the risk of asbestosis.

Asbestos comes in two main forms: serpentine and amphibole. Chrysotile, or white asbestos, is serpentine and accounts for most of the asbestos used commercially. Chrysotile is composed of curly fibres, 2 cm long and 1–2 μm wide. These fibres do not penetrate the lung tissue as much as crocidolite and are therefore less toxic. Crocidolite, blue asbestos, is composed of stiff amphibole fibres, 50 μm long and 102 μm wide. These shorter fibres penetrate the lung tissue, are not easily broken down and result in damage to the lung tissue. Amosite (brown asbestos) and tremolite are also amphiboles but are less prevalent.

Asbestos fibres, which contain iron molecules, have a direct toxic effect on pulmonary parenchymal cells. Alveolar macrophages, neutrophils, lymphocytes, and eosinophils accumulate around the fibres and release proteases, cytokines, reactive oxygen species, and free radicals which damage DNA causing genetic mutations and malignancy. These inflammatory cells also release cytokines that cause fibroblast proliferation and collagen formation. Inhaled asbestos fibres are deposited in the respiratory bronchioles and at the bifurcation of alveolar ducts. Some of the asbestos fibres are removed by mucociliary clearance mechanisms. The remaining fibres are removed by alveolar macrophages and type 1 alveolar cells.

Inhalation of asbestos fibres can cause several types of damage to the lungs. Pleural disease and mesothelioma are discussed in Chapter 10 and bronchogenic carcinoma is discussed in Chapter 9. Asbestosis, which is pulmonary fibrosis resulting from inhalation of asbestos fibres, is a slowly progressive, irreversible disease resulting in respiratory failure and death. The lag period between exposure and development of asbestosis is 10–25 years, which is less than the lag period for developing mesothelioma. Heavy and more intense exposure to asbestos fibres will result in development of fibrosis in a shorter period.

The clinical and radiological presentation is identical to that of other Diffuse Parenchymal Lung Diseases (DPLDs), particularly idiopathic pulmonary fibrosis (IPF), which is discussed in Chapter 7. Patients with asbestosis will have bi‐basal, fine crackles and a third will have finger clubbing. They will become hypoxaemic and, in the late stages, develop cor pulmonale. Pulmonary function tests will show a restrictive picture, with reduced lung volumes (VC and TLC) and reduced diffusing capacity (TLCO), which are the most sensitive measures.

CXR may appear normal in the early stages but will progress to show bilateral, basal, reticulonodular shadowing (Figure 15.1). With progressive disease, these changes will involve the mid and upper zones, and with advanced disease there will be honeycombing. HRCT is more sensitive than CXR at detecting early changes and will show sub‐pleural linear densities, peribronchiolar, intralobular, and interlobular septal fibrosis. The presence of benign pleural plaques on the chest X‐ray is pathognomonic of asbestos exposure (Figure 15.2).Images of pleural plaques are shown in Chapter 10.

If the history of asbestos exposure is clear, and the clinical and radiological features are typical of asbestosis, a histological diagnosis is not required. A bronchoalveolar lavage (BAL) and lung biopsy will be required if there is uncertainty about the diagnosis or if concurrent infection is suspected. Lung biopsy will reveal asbestos bodies which are transparent asbestos fibres coated with iron and protein. The presence of asbestos fibres and asbestos bodies in sputum, a BAL and lung biopsy only indicates asbestos exposure. Patients with asbestosis will have 10–20 times more asbestos fibres than found in normal lung, with more than 1000 asbestos bodies g⁻¹ of lung tissue, which correlates to more than one asbestos body ml⁻¹ of BAL fluid. These ‘ferruginous bodies’, as they are also called, can also be found in individuals exposed to glass, talc, iron, and carbon.

There is no specific treatment for individuals who develop asbestosis. Management is symptomatic and supportive, with long term oxygen therapy (LTOT) and ambulatory oxygen when patients develop respiratory failure. Smoking cessation should be strongly encouraged as smoking is an additional risk factor for developing mesothelioma and asbestosis.

Individuals who develop asbestosis are eligible for compensation, as are those who develop malignant mesothelioma. This is discussed in Appendix 2 of Chapter 10.

Coal worker’s pneumoconiosis

Coal worker’s pneumoconiosis, which results from the inhalation of carbon or coal dust, was a significant problem in the early part of the twentieth century among coal miners, many of whom died from respiratory failure. The risk of developing lung fibrosis is directly related to the amount of exposure to coal dust. Coal dust is taken up by alveolar macrophages in the lungs and cleared by the mucociliary escalator and by lymphatic drainage. If these systems are overwhelmed by the amount of dust inhaled, then the macrophages within the respiratory bronchioles ingest the dust and die, releasing cytokines which induce fibrosis.

In simple coal worker’s pneumoconiosis, there is accumulation of small, < 4 mm particles throughout the lung parenchyma, particularly in the upper lobes, giving a mottled appearance on CXR. These particles contain coal dust, dust‐laden macrophages, and fibroblasts. The individual is not usually symptomatic, despite the abnormal CXR, unless they are concurrent smokers; in smokers, focal emphysema is often present.

Progressive massive fibrosis (PMF) is a serious condition with significant morbidity and mortality. It results in severe breathlessness, and can progress to respiratory failure (Figure 15.3). The CXR will show large (> 1 cm) fibrotic masses in the upper zones of the lung fields composed of collagen and coal dust. These masses may cavitate, resulting in the patient coughing up black sputum, which is called melanoptysis. Lung function tests will demonstrate reduced lung volumes, decreased diffusing capacity, and irreversible airflow obstruction.

Caplan’s syndrome is a pneumoconiosis which occurs in coal miners with rheumatoid arthritis. Less commonly, it can occur after exposure to asbestos and silica. Patients develop multiple nodules, 0.5–2 cm in size, and may have symptoms of breathlessness and cough. Patients may also develop subcutaneous rheumatoid nodules.

Coal miners who develop respiratory disease because of their occupation are eligible for compensation from the Department of Social Security if they have worked for more than 20 years and have abnormal lung function. With fewer people working in the coal industry and the introduction of health and safety measures at work (better ventilation in coal mines and the wearing of protective masks), fewer deaths are associated with this industry these days.

Silicosis

Inhalation of free silica (silicon dioxide) results in lung injury. Box 15.2 lists industries that are associated with silica exposure. As with other pneumoconiosis, stringent health and safety measures in the UK have reduced the incidence of silicosis, although it remains a problem worldwide.