|The work environment can cause lung diseases because of allergy, irritation or a build-up of tiny particles in the lungs. Allergies can occur quite soon after the first time someone is exposed to a substance. They can appear as a runny, irritated nose (rhinitis), inflammation of the airways (asthma) or inflammation in the small airways and air sacs in the lungs (the sacs are called alveoli, and the inflammation is called alveolitis). Other diseases are caused by long exposure to substances that our lungs cannot easily remove. Chronic obstructive pulmonary disease, often called COPD, can be caused by many different dusty jobs. Other diseases can be caused by dust (silicosis), asbestos (asbestosis) and coal dust (coal miner’s pneumoconiosis). Some materials, such as asbestos and chrome, can cause lung cancer. There are two basic strategies employers can use to prevent work-related lung diseases. Primary prevention is when hazards are removed or reduced before anyone becomes ill (an example might be removing a substance from the work environment). Secondary prevention is trying to spot any cases of disease early and acting to prevent more cases.|
Work-related lung diseases are classed as being either chronic or non-chronic, depending on the chances of recovery. Chronic lung diseases may be controlled but cannot be cured, whereas someone who suffers from a non-chronic lung disease has a higher chance of recovery, at least if they are diagnosed promptly and exposure is stopped.
|Occupational COPD||Extrinsic allergic alveolitis|
Work-related asthma and alveolitis are the result of breathing in certain substances at work. Substances that cause these diseases are known as sensitisers, and they can affect anyone who has been exposed to them. The higher the level of sensitiser in the air, the greater the risk of disease. These diseases often occur quite soon after the first exposure to the sensitiser, unlike diseases caused by long exposure. If the sensitiser is removed or replaced, or the worker is moved away from exposure, symptoms should start to decrease. If this cannot be done, employers should ensure that the amount of sensitiser in the air is reduced, by enclosure or local exhaust ventilation.
What is occupational asthma?
Occupational asthma is the commonest work-related lung disease in developed countries. Sufferers’ asthma symptoms are triggered by a particular sensitiser that they breathe in regularly. Many substances can be sensitisers, and occupational asthma can take a short or long time to develop. Symptoms start with coughing, followed by wheezing, a tight chest and difficulty breathing. The sensitisers will often also trigger sneezing and a blocked nose due to rhinitis: sometimes this may precede the asthma and may be a warning the worker is at risk of developing asthma. Symptoms should improve on days away from work or holidays, but some asthma may be permanent, depending on the length of exposure.
What substances can cause occupational asthma?
A wide range of substances can be sensitisers. The most frequently reported agents include flour and grain dust, latex, animals, wood dust, chemicals called isocyanates and aldehydes, colophony, and fluxes. Some sensitisers that cause asthma are also responsible for causing other respiratory diseases.
Here is a list of industries that use sensitisers capable of causing work-related asthma.
|Laboratories||Dust from animals, drugs|
|Farming||Dust from farm animal fur and skin|
|Cleaning||House dust and cleaning products|
|Food||Dust from flour and grain, additives|
|Carpentry, joinery, forestry||Dust from wood|
|Leisure centres||Chlorine in swimming pools|
|Electronics||Fumes from soldering processes|
Can occupational asthma be prevented?
Employers should aim to prevent occupational asthma by removing or reducing exposure to its causes by removing or replacing the substances that cause it. Where this is not possible, they should control workers’ exposure effectively. Regular monitoring of workers’ lung function can detect those affected at an early stage when the condition is more likely to be reversible.
There are different types of occupational asthma
|Work-aggravated asthma||Acute irritant-induced (toxic) asthma|
|Affects workers who already have asthma||Affects workers for the first time after being exposed to a large amount of irritant e.g. during fire|
|Is not due to allergy||Is not due to allergy|
|Symptoms get worse when exposed to an irritant in the work-place e.g. cold air in a cold store||Later exposures should not make the asthma any worse|
|Symptoms should improve once the sensitiser is removed||It may last for years|
Advice for workers who think they have occupational asthma
A worker who thinks they have occupational asthma should visit their occupational health department, if there is one. If not, workers should visit their doctor, to discuss seeing a specialist. It is important to confirm the diagnosis before thinking about changing jobs. If the diagnosis is confirmed, the worker may be able to claim financial assistance to reduce the effect on his or her life. To find out details for a specific country, workers should contact their doctor, government social services or national employment service.
The diagnosis of occupational asthma
Before diagnosing occupational asthma, the doctor will look at the person’s work history and try to identify possible causes of the symptoms. Employers should keep a health and safety record of all substances used in the workplace to make this task easier. To confirm occupational asthma, a patient must use a peak-flow meter (see picture) every few hours over one month, to look for any changes in their lung function. A peak-flow meter is a small hand-held device that measures how fast air comes out of the lungs when a person exhales forcefully. Measurements should also be made when the patient is not at work. If the patient’s lung function drops during the working week, occupational asthma may be diagnosed.
For more information, see www.occupationalasthma.com/workers.aspx (in English).
How to manage occupational asthma
Once a patient has become sensitive to a substance, on-going exposure will cause continuing and worsening asthma. It is better for the patient to move to work in an area where the substance is not present.
Sometimes, a patient may have to change jobs to avoid the substance that has caused their asthma. They should not do this before the diagnosis is confirmed, and they should try to make sure they are dismissed on medical grounds, rather than resigning. Depending on how badly they are affected, and what country they live in, patients may be able to claim financial compensation.
Extrinsic allergic alveolitis
Extrinsic allergic alveolitis is caused by tiny particles that irritate and inflame the small airways and alveoli. It is most commonly found in people who work on farms or keep birds, or people who are exposed to contaminated fine droplets of liquid. It can appear very quickly, with a fever and difficult breathing. Over long periods, it can cause permanent scars in the lungs. An example is farmer’s lung, which is caused by fungal spores in mouldy hay, breathed in repeatedly. The acute form of the disease may cause repeated flu-like symptoms, fever, a tight chest and a dry cough within 12 hours of exposure. How bad the symptoms are is related to the length of exposure. The only symptom of the chronic form is usually weight loss and workers will gradually feel less able to exercise. This form is more common when patients are exposed to a sensitiser all the time (for example when there is a bird in the home).
Work-related lung diseases caused by cumulative exposure
When someone is exposed to a substance again and again over time, the total amount of exposure is called cumulative exposure. Several work-related lung diseases are the result of this.
Chronic obstructive lung disease (COPD)
COPD is very common. The major risk factor is smoking, and, in third world countries, cooking over open fires but scientists think that between 5–15% of COPD cases are caused by work-related exposures. These cases are usually caused by many years spent working in dusty environments, and they can occur in non-smokers as well as smokers. Exposure to a substance at work (such as silica) can increase a smoker’s chances of COPD. The symptoms of occupational COPD do not reduce even when the worker is no longer exposed to the cause. Common causes of occupational COPD include dust (such as coal dust, cotton dust, grain dust and silica), harmful gases and fumes (such as cadmium fumes). Previous studies have shown that specific agents that trigger occupational COPD include:
- Cadmium fume
- Coal dust
To diagnose occupational COPD, the doctor must look at the risks from all the materials the worker has breathed in, including tobacco as well as work-related substances. For this, a full job history of exposures is needed.
Pneumoconiosis occurs when dust or minerals are breathed in and become stuck in the lungs. This can cause changes to the structure of the lungs. Major types of pneumoconiosis are asbestosis, silicosis and coal worker’s pneumoconiosis. Coal worker’s pneumoconiosis usually affects people who have worked underground for many years. Silicosis is caused by exposure to quartz dust and asbestosis is caused by high exposure to any type of asbestos. The European Lung Foundation produces a separate factsheet on asbestos.
Since the decline of coal mining and potteries in Europe, the number of deaths from silicosis and coal worker’s pneumoconiosis has gradually fallen. There is no specific treatment for these diseases except to treat the complications. It is best to avoid any more exposure.
Prevalence of work-related lung diseases in Europe
Data on the causes and distribution of specific work-related lung diseases in Europe are limited because not many countries have the systems required to record information. This makes it difficult to assess the contribution of work-related lung disease to the burden of respiratory disease in Europe.
According to registries and voluntary reporting schemes in Finland, Germany and the United Kingdom, the yearly incidence of work-related lung disease is thought to be between 2–15 cases per 100,000 working individuals and is likely to increase. The table below shows some of the statistics that are known.
|Work-related lung disease||Prevalence in Europe|
|Occupational asthma||The most common lung disorder in industrial countries.|
|Occupational COPD||11.7% of COPD cases in Finland are due to work-related exposures.|
|Extrinsic allergic alveolitis||2-6 per 1000 farmers in Sweden and 5 per 1000 farmers in Finland during the 1980s.|
|Silicosis||In 1995, 4,381 cases were recorded in 15 EU countries. This accounts for 29 cases per million workers. 61% of cases were miners.|
|Asbestosis||Currently, about 125 million people in the world are exposed to asbestos in the work place.|
|Mesothelioma||Mortality rates correlate with past levels of asbestos consumption in industrial countries. It is predicted to kill 250,000 people in Europe between 1995 and 2029|
|Bronchial carcinoma||In Finland, about 24% of lung cancer cases are due to work-related exposures. (lung cancer)|
The contribution of work-related lung disease to the burden of respiratory medicine is often under recognised and under-reported. Further efforts are required to develop a Europe-wide registration system, to produce data on the causes and incidence of these diseases and to try and prevent cases in future years.
This factsheet was prepared by the ELF office with assistance from Professor P.S. Burge, of the Occupational Lung Disease Unit, Birmingham Heartlands Hospital, UK. The material was reviewed and approved by the ERS Advisory Board.
The following sources were used as background information in the compilation of this document:
National Institute of Occupational Safety and Health (NIOSH)
Enviromental Protection Agency
The Health and Safety Executive
European Environment Agency
I. Madan. ABC of work related disorders: occupational asthma and other respiratory diseases.
British Medical Journal 1996; volume 313: pages 291–294.
An article entitled ‘ Occupational exposures and COPD: an ecological analysis of international data’, published in the ERJ in 2009 Eur Respir J 2009; volume 33: pages 298-304.