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.
In modern times, the most commonly occurring variant, apart from asbestosis, is coal workers' pneumoconiosis (CWP), arising from the inhalation of coal dust. There is generally a long time lag between exposure and onset of the disease - 10 years in the case of coal dust and 15-60 years with asbestos - hence, most new cases or deaths from pneumoconiosis reflect the working conditions of the past.
Pneumoconiosis is a notifiable industrial disease - where a patient develops the disease, their doctor must notify their employer in writing with the patient's consent. The employer then is duty-bound to inform the local Health and Safety Executive (HSE). Pneumoconiosis is also a prescribed industrial disease. Financial compensation may be available where an individual is able to show they worked in a job for which their disease is prescribed and that their illness is likely due to the occupational exposure.
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. In the post-industrial UK, exposure is nowhere near the scale found in the 1950s and 1960s. Whilst mining has declined in Western Europe and many parts of the USA, elsewhere in the world, many still depend on it for their living and may have much less statutory protection. Interactions between industrial dust diseases and infection may also be signficant, particularly in low income countries with a high incidence of HIV.
Industrial lung disease has a very marked male preponderance but this is most likely related to occupation rather than inherent susceptibility.
The first deaths attributable to asbestos were described in 1907 and disease from asbestos exposure is now said to account for about 4,000 UK deaths each year. It is the most common cause of death relating to work in the UK. Legislation has existed in the UK since 1931 and asbestos use is now banned but much of the material still exists, particularly in buildings. There is still the potential to kill those who are unknowingly exposed to the fibres in their work, or those who choose to ignore the controls that provide effective protection during work with asbestos.
- In 2007, asbestosis was cited as the prime cause of death on 96 death certificates.
- The annual number of mesothelioma deaths has increased from 153 in 1968 to 2,156 in 2007. This will probably continue to rise until 2015.
- Asbestos-related lung cancer is underdiagnosed since it is indistinguishable from that caused by cigarette smoking. Current estimates (based on the number of excess lung cancer cases in high-risk occupations) ascribe about the same amount of deaths to asbestos-related lung cancer as mesothelioma.
Coal workers' pneumoconiosis:
- There were 230 new assessed cases of coal worker's pneumoconiosis and 85 cases of silicosis in the Industrial Injuries and Disablement Benefit (IIDB) scheme in 2008.
- Chronic bronchitis 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' underground exposure to coal dust. The numbers have fluctuated considerably, based more on publicity and relaxation of criteria to be able to claim rather than upon incidence.
See separate article Asbestos-related Diseases.
Asbestosis is a typical pneumoconiosis and tends to follow heavy exposure with a 5- to10-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 nonsmokers. The presentation and investigation of lung cancer are discussed elsewhere.
See separate article Malignant Mesothelioma.
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 called Caplan'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 is 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. Coal workers' pneumoconiosis (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 chronic bronchitis, 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 tests show 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 chronic obstructive pulmonary disease (COPD). Silicosis and coal workers' pneumoconiosis (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).
Management of suspected industrial dust disease
- Take a good occupational history, going back over many years and looking also at hobbies and pastimes.
- CXR and lung function tests are required. Occupational lung disease cannot be diagnosed by radiology alone, but with the advent of high- resolution CT scans which are more sensitive and specific than X-ray, these are having an increasing role in diagnosis, assessment of disease activity, and evaluation of response to therapy.
- Referral to a chest physician for further diagnostic and management advice.
- There may be considerable financial implications and a tribunal may be required to make a decision, often requiring expert opinion. Note that it is no longer possible to make a claim, based on the presence of pleural plaques, for asbestos-related lung damage.
- None of these diseases is curable. Smoking cessation should be encouraged strongly. Treat/palliate symptoms. Support the patient and their family through the disease and its social/occupational/legal ramifications.
Surveillance and monitoring play an important role. The HSE has a Working Group on the Assessment of Toxic Chemicals (WATCH) to consider the evidence on the occupational exposure and health effects of substances, including whether a maximum exposure limit (MEL) or occupational exposure standard (OES) would be appropriate, and setting limits, where indicated.
It is probably impossible to prevent all industrial dust diseases but they can certainly be reduced by following appropriate safety precautions, including:
- Adequate ventilation.
- Keeping down dust levels in the workplace.
- Wearing of facemasks.
Further reading & references
- Varkey B et al; Asbestosis, eMedicine, Sep 2010
- Dhingra A et al, Coal Worker's Pneumoconiosis, Medscape, Jul 2010
- No authors listed; Diagnosis and initial management of nonmalignant diseases related to asbestos. Am J Respir Crit Care Med. 2004 Sep 15;170(6):691-715.
- Working Group on Action to Control Chemicals (WATCH), Health & Safety Executive
- No authors listed; BTS statement on malignant mesothelioma in the UK, 2007. Thorax. 2007 Nov;62 Suppl 2:ii1-ii19.
- Rees D, Murray J; Silica, silicosis and tuberculosis. Int J Tuberc Lung Dis. 2007 May;11(5):474-84.
- Asbestos related disease statistics, Health and Safety Executive (HSE); Last updated October 2009
- Coalworkers' Pneumoconiosis and Silicosis; Coalworkers' Pneumoconiosis and Silicosis, Health and Safety Executive (HSE)
- O'Reilly KM, Mclaughlin AM, Beckett WS, et al; O'Reilly KM, Mclaughlin AM, Beckett WS, et al; Asbestos-related lung disease. Am Fam Physician. 2007 Mar 1;75(5):683-8.
- Roach HD, Davies GJ, Attanoos R, et al; Asbestos: when the dust settles an imaging review of asbestos-related disease.; Radiographics. 2002 Oct;22 Spec No:S167-84.
- Cohen RA, Patel A, Green FH; Lung disease caused by exposure to coal mine and silica dust. Semin Respir Crit Care Med. 2008 Dec;29(6):651-61. Epub 2009 Feb 16.
- Schreiber J, Koschel D, Kekow J, et al; Rheumatoid pneumoconiosis (Caplan's syndrome). Eur J Intern Med. 2010 Jun;21(3):168-72. Epub 2010 Mar 2.
- Fujimura N; Pathology and pathophysiology of pneumoconiosis. Curr Opin Pulm Med. 2000 Mar;6(2):140-4.
- Ross MH, Murray J; Occupational respiratory disease in mining. Occup Med (Lond). 2004 Aug;54(5):304-10.
- Rushton L; Chronic obstructive pulmonary disease and occupational exposure to silica. Rev Environ Health. 2007 Oct-Dec;22(4):255-72.
- McCleskey TM, Buchner V, Field RW, et al; Recent advances in understanding the biomolecular basis of chronic beryllium Rev Environ Health. 2009 Apr-Jun;24(2):75-115.
- Kreiss K, Day GA, Schuler CR; Beryllium: a modern industrial hazard. Annu Rev Public Health. 2007;28:259-77.
- Jedynak AR et al; Silicosis and coal workers pneumoconiosis, eMedicine, Aug 2010
- Sirajuddin A, Kanne JP; Occupational lung disease. J Thorac Imaging. 2009 Nov;24(4):310-20.
- Pleural Plaques, Ministry of Justice, 2010
|Original Author: Dr Chloe Borton||Current Version: Dr Chloe Borton|
|Last Checked: 19/11/2010||Document ID: 1226 Version: 22||© EMIS|
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