Exposure to dusts, gases, vapours and fumes at work can lead to the development of the following types of lung disease:
• Acute bronchitis and even pulmonary oedema from irritants such as sulphur dioxide, chlorine, ammonia or the oxides of nitrogen
• Pulmonary fibrosis due to mineral dust
• Occupational asthma
• Extrinsic allergic bronchiolar alveolitis
• Bronchial carcinoma due to industrial agents (e.g. asbestos, polycyclic hydrocarbons, radon in mines)
The degree of fibrosis that follows inhalation of mineral dust varies. While iron (siderosis), barium (baritosis) and tin (stannosis) lead to dramatic dense nodular shadowing on the chest X-ray, their effect on lung function and symptoms is minimal. Exposure to silica or asbestos, on the other hand, leads to extensive fibrosis and disability. Coal dust has an intermediate fibrogenic effect and accounts for 90% of all compensated industrial lung diseases. Lung fibrosis from exposure to asbestos has become an increasing problem. The term pneumoconiosis means the accumulation of dust in the lungs and the reaction of the tissue to its presence. The term is not wide enough to encompass all occupational lung disease and is now generally used in relation to coal dust and its effects on the lung.
Improved conditions and contraction of the coal industry have led to a considerable reduction in the number of cases of pneumoconiosis to about 2 per 1000 wage earners. The disease is caused by dust particles approximately 2-5 f.Lm in diameter that are retained in the small airways and alveoli of the lung. The incidence of the disease is related to total dust exposure, which is highest at the coal face, particularly if ventilation and dust suppression are poor. Two very different syndromes result from the inhalation of coal.
This simply reflects the deposition of coal dust in the lung. It produces a fine micro nodular shadow on the chest X-ray and is by far the commonest type of pneumoconiosis. It is graded on the chest X-ray appearance according to standard categories set by the International Labour Office (see below). Considerable dispute remains about the effects of simple pneumoconiosis on respiratory function and symptoms, many arguing that the development of the latter is largely due to chronic bronchitis and emphysema, commonly related to cigarette smoking. Categories of simple pneumoconiosis are as follows: 1 Small round opacities are definitely present but are few in number.
2 Small round opacities are numerous but normal lung markings are still visible.
3 Small round opacities are very numerous and normal lung markings are partly or totally obscured. The importance of simple pneumoconiosis is that it may lead to the development of progressive massive fibrosis (PM F) (see below). This virtually never occurs on a background of category 1 simple pneumoconiosis but occurs in 30% of those with category 3. Usually category 2 simple pneumoconiosis, which carries a 7% risk of developing PMF, must be present before benefit may be awarded for disability.
Progressive massive fibrosis
The lesions in this disease are round fibrotic masses several centimetres in diameter, almost invariably in the upper lobes and sometimes having necrotic central cavities. The pathogenesis of PMF is still not understood, though it seems clear that some fibrogenic promoting factor is present in individuals developing the disease. This was thought to be M. tuberculosis, but is now thought to be immune complexes, analogous to the development of large fibrotic nodules in coal miners with rheumatoid arthritis (Caplan’s syndrome). The development of both rheumatoid factor and antinuclear factor in the serum of patients with PMF is common, as it is in those suffering from asbestosis and silicosis. Pathologically there is apical destruction and disruption of the lung, resulting in emphysema and airway damage. Lung function tests show a mixed restrictive and obstructive ventilatory defect with loss of lung volume, irreversible airflow limitation and reduced gas transfer.
The patient with PMF suffers considerable effort dyspnoea, usually with a cough. The sputum can be black. The disease can progress (or even develop) after exposure to coal dust has ceased. Eventually respiratory failure may intervene.
This disease is uncommon though it may still be encountered in workers in foundries where sand used in moulds has to be removed from the metal casts (fettling), in sand blasting, and amongst stone-masons, pottery and ceramic workers.
Silicosis is caused by the inhalation of silica (silicon dioxide). This dust is highly fibrogenic. For example, a coal miner can remain healthy with 30 g of coal dust in his lungs but would be dead if he had inhaled 3 g of silica. Silica seems particularly toxic to alveolar macrophages and readily initiates the fibrogenic mechanism. The chest X-ray appearances and clinical features of the disease are similar to those of PMF. The chest Xray appearance is distinctive: thin streaks of calcification are seen around the hilar lymph nodes (‘eggshell’ calcification).
Asbestos is a mixture of silicates of iron, magnesium, nickel, cadmium and aluminium, and has the unique property of occurring naturally as a fibre. It possesses remarkably resistant properties to heat, acid and alkali, hence its widespread use. Asbestos is mined in southern Africa, Canada and the former USSR. World production is 4 million tons, of which 90% is chrysotile, 6% crocidolite and 4% amosite in type.
Chrysotile or white asbestos is the softest asbestos fibre. Each fibre is often as long as 2 em but only a few micrometres thick. It is less fibrogenic than crocidolite. Crocidolite (blue asbestos) is particularly resistant to chemical destruction. It exists in straight fibres up to 50/-tm in length and 1-2/-tm in width. It is now known that this type of asbestos is by far the most important in the development of all types of asbestosis and particularly of mesothelioma. This may be due to the fact that it is readily trapped in the lung. Its long, thin shape means that it can be inhaled, but subsequent rotation against the long axis of the smaller airways, particularly in turbulent airflow during expiration, causes the fibres to impact. Crocidolite is also particularly resistant to macrophage and neutrophil enzymic destruction. Exposure to asbestos occurred particularly in naval shipbuilding yards and in power stations but its ubiquitous use meant that light exposure was common. Up to 50% of urban dwellers had evidence of asbestos bodies (asbestos fibre covered in protein secretions) in their lungs at post mortem. New regulations in the UK prevent the use of crocidolite and severely restrict the use of chrysotile, and enforce careful dust control measures. These changes should eventually abolish the problem.
There is an important synergistic relationship between asbestosis and cigarette smoking and the development of bronchial carcinoma, usually adenocarcinoma; the risk is increased fivefold. There is also an increased risk in nonsmokers and it is also present in workers exposed to asbestos who do not have clinically recognized asbestosis but who do have pleural plaques or thickening. Workers will continue to be exposed to blue asbestos in the course of demolition or in the replacement of insulation, and it should be remembered that there is a considerable time lag between exposure and development of the disease, particularly mesothelioma (20-40 years). The diseases caused by asbestos are summarized. Bilateral-diffuse pleural thickening, asbestosis, mesothelioma and asbestos-related carcinoma of the bronchus are all eligible for industrial injuries benefit in the UK, but account for only one-quarter of the number of cases of compensation compared to coal-worker’s pneumoconiosis. Asbestosis is the disease most frequently compensated (900 cases per year). This progressive disease is characterized by breathlessness and is accompanied by finger clubbing and bilateral basal endinspiratory crackles. Fibrosis not detectable on chest Xray may be revealed on CT scan. No treatment is known to alter the progress of the disease, though corticosteroids are often prescribed. The number of cases of mesothelioma presenting for compensation has increased fivefold in the last decade to over 400 cases per year. Often open lung biopsy is needed to obtain sufficient tissue for diagnosis. No treatment influences the universally fatal outcome. Although pleural effusions are the commonest presentation of mesothelioma, occasionally they may have a benign origin and may regress spontaneously.
This disease occurs worldwide but is declining rapidly in areas where the numbers of people employed in cotton mills are falling. In the UK the disease is confined to areas of Lancashire and Northern Ireland. The symptoms start on the first day back at work after a break (Monday sickness) with improvement as the week progresses. Tightness in the chest, cough and breathlessness occur within the first hour in dusty areas of the mill, particularly in the blowing and carding rooms where raw cotton is cleaned and the fibres are straightened. The exact nature of the disease and its aetiology remain disputed. Two important features are that pure cotton does not cause the disease, and that cotton dust has some effect on airflow limitation in all those exposed. Individuals with asthma are particularly badly affected by exposure to cotton dust. The most likely aetiology is endotoxins from bacteria present in the raw cotton causing constriction of the airways of the lung. There are no changes on the chest X-ray and there is considerable dispute as to whether the progressive airflow limitation seen in some patients with the disease is due to the cotton dust or to other effects such as cigarette smoking or coexistent asthma.
Beryllium-copper alloy has a high tensile strength and is resistant to metal fatigue, high temperature and corrosion. It is used in the aerospace industry, in atomic reactors and in many electrical devices. Although beryllium is inhaled into the lungs, it causes a systemic poisoning that gives rise to a clinical picture similar to sarcoidosis. The major chronic problem is that of progressive dyspnoea with pulmonary fibrosis. However, strict control of levels in the working atmosphere have made the disease a rarity.