About Industrial Lung Diseases
The term ‘pneumoconiosis’ refers to a group of lung diseases caused by the inhalation and retention of dust in the lung. This causes a range of granulomatous and fibrotic changes. Pneumoconiosis is a notifiable industrial disease – where a patient develops the disease, the employer then is duty-bound to inform the local Health and Safety Executive (HSE). Pneumoconiosis is also a prescribed industrial disease.
Greater understanding of the causes of industrial lung disease, as well as enforcement of legislation by the HSE, have reduced the risk of industrial dust disease. Interactions between industrial dust diseases and infection may also be significant. Industrial lung disease has a very marked male preponderance but this is most likely related to occupation rather than inherent susceptibility.
Coal worker’s pneumoconiosis:
Chronic bronchitis – now chronic obstructive pulmonary disease (COPD) – and emphysema became prescribed diseases in September 1993 for coal miners with a specified level of lung function impairment and a minimum of 20 years of underground exposure to coal dust.
Asbestosis is a typical pneumoconiosis and tends to follow heavy exposure with a 5- to 10-year time interval. It usually presents with:
- Shortness of breath with a dry cough.
- Progressive dyspnoea.
- Repetitive inspiratory basal crackles, sometimes known as ‘velcro crepitations’.
- Clubbing of the fingers (late feature).
The rate of progression depends upon the level of exposure and eventually results in increasing disability and death from cardiorespiratory failure.
- CXR shows a ground-glass opacification, small nodular opacities, ‘shaggy’ cardiac silhouette and an ill-defined diaphragmatic contour.
- Spirometry – restrictive pattern of lung function with reduced volumes/transfer factor.
- Sputum microscopy may show asbestos bodies. These confirm exposure to asbestos but their significance in diagnosing asbestosis is uncertain.
Asbestos-related lung cancer
Lung cancer is a common disease amongst smokers but it has an increased incidence in those with asbestosis (40-50% risk of death from bronchial carcinoma in smokers with asbestosis). All types can cause the disease with some evidence of more danger from blue and brown. Asbestosis-related lung cancer may also occur in non-smokers. The presentation and investigation of lung cancer are discussed elsewhere.
Coal miners are exposed to a variety of dusts including silica. Tiny particles of coal dust, just 2-5 microns in diameter, are retained in the alveoli. They are engulfed by macrophages but, eventually, the system is overwhelmed and an immune response follows. This produces pulmonary fibrosis. If this is associated with rheumatoid arthritis, it is calledCaplan’s syndrome. Morbidity and mortality are related to the type of coal dust and the duration of exposure. Dust that is high in silica increases the risk of fibrosis but the rate of progression and severity of the diseases are also influenced by the presence of other minerals in the inhaled dust. A high percentage of free silica gives a high degree of pulmonary fibrosis. CWP is divided into:
- Simple pneumoconiosis – a nodular interstitial lung disease that is graded according to CXR appearance. Patients are often asymptomatic and the diagnosis is an incidental finding on CXR. There has been much debate as to the effect on lung function – but it does increase the risk of COPD, diminish forced expiratory volume in one second (FEV1) and have additive effects combined with smoking.
- Progressive massive fibrosis – symptoms progress from shortness of breath on exertion, cough and black sputum to respiratory failure. CXR reveals large nodular, fibrotic masses in the upper lobes. Respiratory function testsshow a mixed obstructive and restrictive picture with decreased lung volumes and gas transfer.
This is also known as ‘potter’s rot’ and was recognised by Hippocrates and others in Ancient Greece. Silica exposure occurs beyond coal mining: high levels of exposure may also be found within the construction industry, tunnelling, cement industry, brick manufacturing, pottery and ceramic work, silica sand and granite extraction, gold mining and iron and steel founding.
Prolonged exposure to high levels of silica causes silicosis and increases the risk of developing COPD. Silicosis and CWP are indistinguishable on CXR. Risk varies depending on the presence of other minerals in the dust, particularly clay minerals and the size of the particles and percentage of quartz. The effect of cumulative silica dust exposure on airflow obstruction is independent of silicosis.
Those who work with metal grinding or welding have a risk of inhalation of metallic particles. Iron absorbs X-rays and produces very impressive shadows on CXR but it has little effect on pulmonary function and little long-term morbidity. Tin and barium produce similar clinical and radiological pictures (stannosis and baritosis respectively).
This is rare, affecting those working in the aerospace, nuclear, telecommunications, semi-conductor and electrical industries. It has been recognised as a cause of occupational lung disease since the 1940s and can cause an allergic immune response (beryllium sensitisation), acute beryllium disease (similar to acute pneumonitis) and chronic beryllium disease (a granulomatous lung disease with symptoms similar to sarcoidosis).