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Industrial Dust Diseases

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The term "pneumoconiosis" refers to a group of lung diseases caused by the inhalation and retention in the lungs of dusts. The impact of occupation on health has been known since antiquity - Hippocrates and Pliny referred to silicosis (from the Greek word silex, meaning flint) making it perhaps the oldest known occupational disease.

In modern times, the most commonly occurring variant, apart from asbestosis, is coal workers' pneumoconiosis, arising from the inhalation of coal dust. There is generally a long delay 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). Pneumoconicosis 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.

Epidemiology

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 US, 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.1

Industrial lung disease has a very marked male preponderance but this is most likely related to occupation rather than inherent susceptibility.

Remember there may be a long latency between exposure and the presentation of an industrial lung disease - review past employment history as well as current employment.

The first deaths attributable to asbestos were described in 1907 and disease from asbestos exposure is now said to account for over 4,000 UK deaths each year. It is the commonest 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 2005, asbestosis was cited on 134 death certificates.
  • In 2005, Disablement Benefit for asbestosis was awarded to 835 people. The annual number of mesothelioma deaths has increased from 153 in 1968 to 2037 in 2003. 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.2

Coal workers' pneumoconiosis:

  • There were 1,160 new cases of pneumoconiosis, excluding asbestosis, assessed in the Industrial Injuries Scheme in 2004. These numbers are rising but almost certainly due to publicity about compensation as the mining industry in this country has been in decline for many years and 65% of claimants are over 65 years old.
  • 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.3
Asbestos related diseases4

Asbestos is a strong, flexible, durable fibre whose heat and chemical resistance led to its widespread use.
There are 3 types of asbestos, all of which are dangerous but the blue and brown asbestos are more dangerous than white asbestos. Much of the asbestos found in buildings contains a mixture. Undisturbed asbestos in good condition is not a risk to health but if disturbed, the asbestos fibres can break down into sharp fibres which can then be inhaled. If these fibres lodge in the lungs, they persist and may migrate peripherally where they can trigger the development of several diseases, some of which are fatal. Treatment is symptomatic only.

High risk occupations

Many of those now suffering from asbestos-related disease were exposed to very high levels of asbestos in the more traditional industries such as shipbuilding, construction and boiler work. 25% of the deaths from the disease are in people who have spent some of their working lives in the building and maintenance trades - they are often unaware that they were dealing with asbestos and exposed to risk.
Those who continue to be at risk from exposure to asbestos are those who disturb the fabric of buildings as part of their day to day work and include:

  • Heating and ventilation engineers
  • Gas fitters
  • Roofing contractors
  • Fire and burglar alarm installers
  • Trades people (electricians, plumbers, carpenters, joiners, plasterers, painters and decorators) Demolition workers
  • Telephone and computer installation engineers
  • Site managers and surveyors

Asbestos related diseases include pleural plaques (usually asymptomatic), benign pleural effusions (may be recurrent), bilateral pleural thickening but also:

Asbestosis

Asbestosis tends to follow heavy exposure with a 5-10 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. In smokers, there is a 40 to 50% risk of death from bronchial carcinoma.

Investigations:

  • CXR shows a ground-glass opacification, small nodular opacities, "shaggy" cardiac silhouette, and an ill-defined diaphragmatic contour.5
  • 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.6

Asbestos related lung cancer

Lung cancer is a common disease amongst smokers but it has an increased incidence in those with asbestosis.7 All types can cause the disease with some evidence of more danger from blue and brown. It is commoner amongst those who have smoked but may occur in non-smokers. The presentation and investigation of lung cancer is discussed elsewhere.

Mesothelioma

This malignancy may arise in the chest or abdomen. Disease can be triggered by even light exposure to asbestos but typically has a long latency (typically 20-40 years). There is evidence of increased risk from exposure to blue or brown asbestos fibres. It has a very poor prognosis with median survival time of 6-18 months post diagnosis.
Mesothelioma presents with:

  • Pleuritic pain or a dull ache
  • Shortness of breath
  • Systemic features (fatigue, anorexia, weight loss, fever, sweats)
  • Pleural effusion (common, usually unilateral)
  • Palpable mass (due to direct extension through the chest wall)

Investigations include:

  • CXR - evidence of pleural effusion and thickening with a lobulated outline.
  • CT provides a better image.5
  • Pleural aspiration or pleural biopsy should give a definitive diagnosis.
Coal mining

Coal miners are exposed to a variety of dusts. Coal workers' pneumoconiosis refers to disease from inhalation of coal dust. Silicosis is a particular problem of coal miners but about 10% of cases of silicosis occur in the construction industry. Stonemasons, potters and workers involved in sandblasting may also be at risk.

Tiny particles of coal dust, just 2 to 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. Coal workers' pneumoconiosis is divided into:

  • Simple pneumoconiosis - 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 FEV1 and have additive effects combined with smoking.8
  • Progressive massive fibrosis - symptoms progress from shortness of breath on exertion, cough, 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.

The rate of progression and severity of the diseases is influenced by the amount of silica that is inhaled, the level and duration of exposure and also whether other minerals are present in the inhaled dust. A high percentage of free silica gives a high degree of pulmonary fibrosis.9

Pulmonary siderosis

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 chest x-ray 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).

Berylliosis

This is rare, affecting those working in the aerospace, nuclear, telecommunications, semi-conductor and electrical industries. It causes a granulomatous lung disease, and presents with symptoms similar to sarcoidosis.10

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.
  • 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.
  • 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.
Prevention

Surveillance and monitoring play an important role. The Health and Safety Executive have 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


Document references
  1. Rees D, Murray J; Silica, silicosis and tuberculosis. Int J Tuberc Lung Dis. 2007 May;11(5):474-84. [abstract]
  2. HSE Asbestos related disease statistics - frequently asked questions. Last updated Aug 2007
  3. HSE Coalworkers' Pneumoconiosis and Silicosis, Chronic Bronchitis and Emphysema.
  4. O'Reilly KM, Mclaughlin AM, Beckett WS, et al; Asbestos-related lung disease. Am Fam Physician. 2007 Mar 1;75(5):683-8. [abstract]
  5. 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. [abstract]
  6. Kamp DW, Weitzman SA; Asbestosis: clinical spectrum and pathogenic mechanisms. Proc Soc Exp Biol Med. 1997 Jan;214(1):12-26. [abstract]
  7. Weiss W; Asbestosis: a marker for the increased risk of lung cancer among workers exposed to asbestos.; Chest. 1999 Feb;115(2):536-49. [abstract]
  8. Ross MH, Murray J; Occupational respiratory disease in mining. Occup Med (Lond). 2004 Aug;54(5):304-10. [abstract]
  9. Fujimura N; Pathology and pathophysiology of pneumoconiosis. Curr Opin Pulm Med. 2000 Mar;6(2):140-4. [abstract]
  10. Kreiss K, Day GA, Schuler CR; Beryllium: a modern industrial hazard. Annu Rev Public Health. 2007;28:259-77. [abstract]

Internet and further reading
  • Varkey B; Asbestosis. eMedicine, Nov 2007.
  • Richards JE; Coal workers pneumoconiosis. eMedicine, Sept 2007.
  • Jedynak AR; Silicosis and coal workers pneumoconiosis. emedicine, July 2007; Radiology perspective.
  • 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.
  • HSE Working Group on Action to Control Chemicals (WATCH)
Acknowledgements EMIS is grateful to Dr Chloe Borton for writing this article. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2008.
DocID: 1226
Document Version: 21
DocRef: bgp648
Last Updated: 24 Sep 2008
Review Date: 24 Sep 2010

The authors and editors of this article are employed to create accurate and up to date content reflecting reliable research evidence, guidance and best clinical practice. They are free from any commercial conflicts of interest. Find out more about updating.

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