ABC of Work Related Disorders: OCCUPATIONAL ASTHMA AND OTHER RESPIRATORY DISEASESBMJ 1996; 313 doi: https://doi.org/10.1136/bmj.313.7052.291 (Published 03 August 1996) Cite this as: BMJ 1996;313:291
- Ira Madan
Changing pattern of occupational lung disease
In the United Kingdom, over the past 40 years, there has been a shift away from manufacturing industries and a sharp reduction in the numbers of coal miners. These factors, together with stricter health and safety legislation, have resulted in a substantial decline in the prevalence of silicosis and pneumoconiosis. In contrast, occupational asthma has become increasingly recognised. In developing countries, however, the traditional occupational lung diseases of silicosis, pneumoconiosis, and asbestosis remain common in rapidly industrialising areas.
Our understanding of the epidemiology of occupational lung disease in Britain has been greatly enhanced by the SWORD project (surveillance of work related and occupational respiratory disease), which was established in 1989 sponsored by the Health and Safety Executive. Occupational and respiratory physicians are invited to report new cases of occupational lung diseases together with the suspected agent. The data are regularly analysed and the results published. Further information is available from the Department of Occupational and Environmental Medicine, National Heart and Lung Institute, London.
Occupational asthma is caused by specific sensitising agents inhaled in the workplace—it does not include bronchoconstriction induced by irritants such as exercise and cold air that are encountered at work. There are over 200 known respiratory sensitisers, and more are identified each year. Some sensitisers may not be immediately obvious: thus, it has recently been recognised that workers such as those in health services can develop occupational asthma as a result of wearing latex gloves. The allergen is latex protein, which becomes airborne as the gloves are used.
A comprehensive and detailed occupational history is essential in the initial assessment of a worker thought to have occupational asthma. Coughing at work or at the end of a shift is often the first symptom and precedes wheezing. Concurrent rhinorrhoea, nasal congestion, and lacrimation may be associated with exposure to substances of high molecular weight—such as rat urinary proteins. The symptoms generally improve at weekends and holidays, but at advanced stages the respiratory symptoms may persist. Physical examination is rarely helpful—even in confirmed cases the chest often seems to be normal.
All aspects of a patient's job, including processes in adjacent areas, should be reviewed to identify tasks that could lead to exposure to a sensitising agent. Information about previous jobs should be obtained to determine whether there has been prior exposure to such agents. If a company employs an occupational health service, advice should be sought from the occupational physician, who will have information on the substances that employees are exposed to, including COSHH (control of substances hazardous to health) assessments. The physician may also know whether any other workers have developed occupational asthma.
Patients should record the best of three measurements of peak expiratory flow made every two to three hours from waking to sleeping over a period of one month. Ideally, this period should include one or two weeks away from work. A drop in peak expiratory flow or substantial diurnal variability in peak expiratory flow on working days but not on days away from work supports a diagnosis of occupational asthma. The times of working shifts and use of any drugs must be considered when the records of peak expiratory flow are reviewed.
If there is any doubt about the diagnosis and the patient's company does not have access to an occupational physician, the patient should be referred to a consultant occupational physician or respiratory physician. Further specialist investigations include immunological testing and, if the diagnosis is uncertain, bronchial challenge with the suspected agent.
Although treatment of acute occupational asthma is the same as for asthma generally, it is important to be aware that, once a person has been sensitised to a specific substance, subsequent exposure to even minimal quantities of the substance may precipitate severe bronchoconstriction. A company's occupational physician will be able to advise on suitable areas for redeployment and may be able to arrange this with the employee's manager.
A worker who develops occupational asthma should avoid further exposure to the causative agent. As this often means relocation or loss of current employment, it is essential that the specific cause is accurately identified
Occupational asthma is a prescribed occupational disease. A worker who develops the condition is entitled to “no fault” compensation if the degree of disability is considered to be 14% or over.
Pneumoconiosis is the generic term for the lodgement of any inhaled dusts in the lungs irrespective of the effects (excluding asthma and neoplasia). Sporadic cases of chronic silicosis (fibrosis of the lungs due to inhalation of silicon dioxide) still occur in Britain, usually in people working with slate or granite and in fettlers in foundries. Patients present with increasing dyspnoea over several years, and chest radiographs reveal upper lobe fibrosis or calcified nodules.
The chronic pneumoconiosis of coal miners, due to inhalation of coal dust, produces no symptoms or physical signs: its only danger is that it predisposes to progressive massive fibrosis, which, when sufficiently advanced, causes dyspnoea and cor pulmonale. However, this condition is disappearing in Britain as mines are closed.
Acute silicosis results from a brief but heavy exposure, such as occurs in sandblasting without respiratory protection. Such patients become intensely breathless and may die within months. Chest radiographs show an appearance like pulmonary oedema. As with many other occupational lung diseases, several recent episodes of silicosis could have been avoided if employers had provided satisfactory ventilation in the workplace.
Extrinsic allergic alveolitis
Extrinsic allergic alveolitis is a granulomatous inflammatory reaction caused by an immunological response to inhaled organic dusts or chemicals. Farmer's lung and bird fancier's lung remain the most prevalent forms of the disease. The condition should be suspected if flu-like symptoms occur after exposure to microbial spores, animal proteins, or certain chemicals. Prolonged illness may be associated with considerable weight loss, but symptoms usually tend to improve within 48 hours of removal from the causative agent.
Inspiratory crackles may be heard on examination of the chest, and a chest radiograph may show a ground glass pattern or micronodular shadows. The diagnosis is confirmed by a reduction in lung volumes, impairment of gas transfer, and demonstration of precipitating antibodies (precipitins) to the causal agent in the serum.
Effects of asbestos Non-malignant disorders
Non-malignant asbestos related disorders consist of asbestosis, pleural plaques, diffuse thickening of the pleura, benign pleural effusions, and asbestos corns (callosities on the dorsal and palmar surfaces of the hands, which may be tender to pressure).
Surveys in Finland, where reporting
Occupational groups at greatest risk of developing asbestos related diseases
Carpenters and electricians
Shipyard and rail workers
Asbestos factory workers
Asbestosis is a diffuse interstitial pulmonary fibrosis caused by exposure to fibres of asbestos, and its diagnosis is helped by obtaining a history of regular exposure to any form of airborne asbestos. The presence of calcified pleural plaques on a chest radiograph indicates exposure to asbestos and may help to distinguish the condition from other causes of pulmonary fibrosis.
The malignant asbestos related disorders are bronchial cancer and malignant mesothelioma of the pleura and peritoneum. It is essential to obtain a full occupational history from any patient with a diagnosis of primary lung cancer: if there is evidence of asbestosis or bilateral diffuse pleural thickening and a history of exposure to asbestos at work, the patient may be eligible for compensation from the Department of Social Security. This also applies to patients with primary lung cancer who have evidence of silicosis and who have been exposed to silica dust at work.
Any patient with a history of exposure to asbestos should be encouraged to stop smoking as these two factors have a synergistic effect in development of lung cancer
Most cases of mesothelioma are pleural in origin, and the disease usually develops 20-40 years after exposure to perhaps even small amounts of blue (crocidolite) or brown (amosite) asbestos. The incidence of the disease is still increasing in men born before 1948, and recent research has indicated that deaths from mesothelioma will increase for at least another 15-25 years.
The disease is often insidious—breathlessness and chest pain are the commonest symptoms, and patients usually have a pleural effusion by the time they present to their general practitioner. The diagnosis is made by a history of exposure to asbestos, the clinical picture described, and radiography (including, if necessary, computed tomography).
Treatment is largely palliative as most people die within a year of diagnosis. All cases of mesothelioma in Britain are assumed to be due to occupation, and patients are eligible for industrial injuries benefit from the Department of Social Security provided that the diagnosis is reasonably certain and there is a history of appropriate exposure.
Exposure to gases
Although fatalities from exposure to gases in the workplace are now rare in Britain, inhalation accidents still occur relatively frequently. Asthma may develop within hours of inhaling a toxic chemical in a high concentration. The resulting airway hyperresponsiveness, known as reactive airways dysfunction syndrome, usually resolves spontaneously but can persist indefinitely.
Inhalation of irritant gases such as chlorine may result in pulmonary oedema
On a wider scale, industrial accidents involving the release of a toxic irritant gas may cause pulmonary injury or even death in the surrounding population. One of the worst recent examples was the release of methylisocyanate from the Union Carbide pesticide plant in Bhopal, India, in 1984. Many victims died of acute pulmonary oedema. Survivors suffered from chronic respiratory ill health with chest pain, haemoptysis, and, in the longer term, bronchiolitis obliterans.
The picture of victims of the Bhopal disaster is reproduced with permission of Rex Features.
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