Occupational asthma

Occupational asthma is an occupational lung disease and a type of asthma. Like other types of asthma, it is characterized by airway inflammation, reversible airways obstruction, and bronchospasm, but it is caused by something in the workplace environment.^[1]

Symptoms include shortness of breath, tightness of the chest, nasal irritation, coughing and wheezing. The first person to use it in reference to a medical condition was Hippocrates, and he believed that tailors, anglers and metalworkers were more likely to be affected by the disease. Although much research has been done since, the inflammatory component of asthma was recognized only in the 1960s.

Today, asthma affects as much as 15% of the Canadian population,^[2] a statistic reflective of other developed countries, and has increased fourfold in the last 20 years. Various reasons can be identified for this increase, including increase environmental pollution, better diagnostic ability, and greater awareness.

Approximately 21% of the adults affected by asthma report an aggravation of their symptoms while at work and an improvement when away, which implies that they may be suffering from occupational asthma. In the United States, occupational asthma is the most common occupational lung disease.^[3] At present, over 400 workplace substances have been identified as having asthmagenic or allergenic properties.^[4] Their existence and magnitude vary by region and industry and can include diisocyanates, acid anhydrides, plicatic acid, and platinum salts (all low molecular weight agents), and animal protein, enzymes, wheat, and latex (high-molecular weight agents).^[3][1] For example, in France the industries most affected are bakeries and cake-shops, automobile industry and hairdressers,^[5] whereas in Canada the principal cause is wood dust, followed by isocyanates. Furthermore, the most common cause of occupational asthma in the workplace are isocyanates.^[6] Isocyanates are used in the production of motor vehicles.^[7]

Hypersensitivity pneumonitis is a related condition, with many occupational examples (e.g. flock worker's lung, farmer's lung, and indium lung). However, although overlapping in many cases, hypersensitivity pneumonitis may be distinguished from occupational asthma in that it isn't restricted to only occupational exposure, and involves type III hypersensitivity and type IV hypersensitivity^[8] rather than the type I hypersensitivity^[9][10] of asthma. Also, unlike asthma, hypersensitivity pneumonitis targets lung alveoli rather than bronchi.^[11]

Signs and symptoms

Less than five years of exposure or a single exposure to a high-concentration agent can result in symptoms. Coughing, wheezing, nasal irritation, shortness of breath, and chest tightness are the most common symptoms, all of which worsen after work and improve during time away from work. Pre-existing asthma can be exacerbated by similar agents.

Diagnosis

Diagnosis of occupational asthma uses several techniques.^[3]

A non-specific bronchial hyperreactivity test can be used to help diagnose occupational asthma. It involves testing with methacoline, after which the forced expiratory volume in 1 second (FEV₁) of the patient is measured. This test is often used for measuring the intensity of a person's asthma and to confirm that the person needs to be treated for asthma.^[3]

Other non specific tests could require the patient to run for a few minutes at a continuous pace. In this case, the individual’s peak expiratory flow rate (PEFR) is measured, showing how fast a person can exhale.^[12] PEFR can also be measured at work to see if there is a difference from the PEFR in a controlled environment. Measuring PEFR at work is a highly reliable test for occupational asthma.

A skin prick test is usually performed on the inner forearm where a grid is marked and a drop of the allergens to be tested are placed on the arm in the grid. Once this has been done, the skin is pricked through the drop using a lancet. Reactions, if any, occur within 10 to 15 minutes and these results can then be analyzed.^[13]

Immunoglobulin E is an antibody found in human blood and is effective against toxins. Since it can also trigger allergic reactions to specific allergens like pollen, the IgE test is performed to evaluate whether the subject is allergic to these substances.^[14][3]

A spirometer is a device used to measure timed expired and inspired volumes, and can be used to help diagnose occupational asthma.^[15]

Specific inhalation challenges test for reactions to substances found in the workplace. One method is a whole body sealed chamber where the patient is exposed to articles that are present in their workplace. This method has the advantage of being able to assess, albeit highly subjectively, ocular and nasal symptoms as well as a reduction in FEV₁. Another test requires the patient to breathe aerosols of the suspected asthmagens through an oro-facial mask. These asthmagens are aerosolized using closed circuit chambers, and the quantities and concentrations administered are minute and extremely stable, to minimize the risk of exaggerated responses.

Prevention and treatment

Prevention

Prevention of occupational asthma can be accomplished through better education of workers, management, unions and medical professionals. This will enable them to identify the risk factors and put in place preventive measures, including respiratory protection and exposure limits.^[3]

Treatment and Recovery

Recovery is directly dependent on the duration and level of exposure to the causative agent. Depending on the severity of the case, the condition of the patient can improve dramatically during the first year after removal from exposure.

Three basic types of procedures are used for treating the affected workers: reducing a worker's exposure, removing a worker from the environment with the asthma-causing agent, and treatment with asthma medications.^[16][3] Completely stopping exposure is more effective treatment than reducing exposure.^[3] By reducing exposure, the probability of suffering another reaction is lowered. Methods of reducing exposure include transferring an affected worker to a position without the relevant asthmagen, use of respiratory protection, and engineering controls. In 1984 innovator David Cornell discovered and invented effective control equipment in the UK for the removal of many harmful workplace fumes. 'BOFA' extraction products are now found in over 100 countries worldwide.^[17]

People affected by occupational asthma that occurred after a latency period, whether a few months or years, should be immediately removed from exposure to the causative agent. However, this can entail severe socio-economic consequences for the worker as well as the employer due to loss of job, unemployment, compensation issues, quasi-permanent medical expenditures, and hiring and re-training of new personnel. This can be mitigated by transferring the worker within a company.^[3]

Medical and pharmacological treatment

Short-acting beta-agonists like salbutamol or terbutaline or long-acting beta-agonists like salmeterol and formoterol dilate airways which relieve the symptoms thus reducing the severity of the reaction. Some patients also use it just before work to avoid a drop in the FEV₁.

Anti-inflammatory agents like corticosteroids, LKTRA or mast cell stabilizers can also be used depending on the severity of the case.

Society and culture

Compensation

When a person is diagnosed with occupational asthma, it can result in serious socio-economic consequences not only for the workers but also for the employer and the healthcare system because the worker must change positions.^[3] The probability of being re-employed is lower for those with occupational asthma compared to those with normal asthma. The employer not only pays compensation to the employee, but will also have to spend a considerable amount of time and energy and funds for hiring and training new personnel.^[18][19] In the United States, it was estimated that the direct cost of occupational asthma in 1996 was $1.2 billion and the indirect cost $0.4 billion, for a total cost of $1.6 billion.^[20]

Occupations at risk

The following tables show occupations that are known to be at risk for occupational asthma, and main substances involved.^[21]

The occupations most at risk are: adhesive handlers (e.g. acrylate), animal handlers and veterinarians (animal proteins), bakers and millers (cereal grains), carpet makers (gums), electronics workers (soldering resin), forest workers, carpenters and cabinetmakers (wood dust), hairdressers (e.g. persulfate), health care workers (latex and chemicals such as glutaraldehyde), janitors and cleaning staff (e.g. chloramine-T), pharmaceutical workers (drugs, enzymes), seafood processors, shellac handlers (e.g. amines), solderers and refiners (metals), spray painters, insulation installers, plastics and foam industry workers (e.g. diisocyanates), textile workers (dyes) and users of plastics and epoxy resins (e.g. anhydrides)^[22]

Epidemiology

Occupational asthma is the most common occupational lung disease.^[3]

See also

• Asthma
• Chronic obstructive pulmonary disease (COPD)
• Specific inhalation challenge

References

External links

• Asthma in the Workplace
• Occupational Asthma
• Canadian Lung Association
• SCL Medtech
• http://www.asthma.org.uk/knowledge-bank-occupational-asthma/
• Occupational Asthma (UK)
• National Institute for Occupational Safety and Health — Asthma and Allergies Page