Asthma is a respiratory disease. It creates narrowing of the air passages that results in difficult breathing, tightness of the chest, coughing, and breath-sounds such as wheezing.
Occupational asthma refers to asthma that is caused by breathing in specific agents in the workplace. An abnormal response of the body to the presence of an agent in the workplace causes occupational asthma.
The abnormal response, called "sensitization," develops after variable periods of workplace exposure to certain dusts, fumes or vapours.
This sensitization may not show any symptoms of disease or it may be associated with skin rashes (urticaria), hay fever-like symptoms, or a combination of these symptoms.
Not all workers react with an asthmatic response when exposed to industrial agents. Asthma strikes only a fraction of workers. Asthmatic attacks can be controlled either by ending exposure to the agent responsible or by medical treatment.
Asthma is triggered in several ways and most of them are not completely understood. For simplicity, we categorize them into two groups: allergic and non-allergic.
Allergic asthma involves the body's immune system. This is a complex defense system that protects the body from harm caused by foreign substances or microbes. Among the most important elements of the defense mechanism are special proteins called "antibodies." These are produced when the human body contacts an alien substance or microbe. Antibodies react with substances or microbes to destroy them. Antibodies are often very selective, acting only on one particular substance or type of microbe.
But antibodies can also respond in a wrong way and cause allergic disorders such as asthma. After a period of exposure to an industrial substance, either natural or synthetic, a worker may start producing too many of the antibodies called "immunoglobulin E" (IgE). These antibodies attach to specific cells in the lung in a process known as "sensitization."
When re-exposure occurs, the lung cells with attached IgE antibodies react with the substance. This reaction results in the release of chemicals such as "leukotrienes" that are made in the body. Leukotrienes provoke the contraction of some muscles in the airways. This causes the narrowing of air passages which is characteristic of asthma.
Following repeated exposure to an industrial chemical, substances such as leukotrienes are released in the lungs. Again, the leukotriene causes narrowing of air passages typical of asthma. The reasons for such release are still not clear because no antibody reaction seems to be involved.
In certain circumstances, symptoms of asthma may develop suddenly (within 24 hours) following exposure to high airborne concentrations of respiratory irritants such as chlorine. This condition is known as reactive airways dysfunction syndrome (RADS). The symptoms may persist for months or years when the sensitized person is re-exposed to irritants. RADS is controversial because of its rarity and the lack of good information on how the lungs are affected and the range of substances which cause it.
There is no fixed period of time in which asthma can develop. Asthma as a disease may develop from a few weeks to many years after the initial exposure. Studies carried out on some platinum refinery workers show that in most cases asthma develops in 6 to 12 months. But it may occur within 10 days or be delayed for as long as 25 years.
Analysis of the respiratory responses of sensitized workers has established three basic patterns of asthmatic attacks, as follows:
Immediate - typically develops within minutes of exposure and is at its worst after approximately 20 minutes; recovery takes about 2 hours.
Late - can occur in different forms. It usually starts several hours after exposure and is at its worst after about 4 to 8 hours with recovery within 24 hours. However, it can start 1 hour after exposure with recovery in 3 to 4 hours. In some cases, it may start at night, with a tendency to recur at the same time for a few nights following a single exposure.
Dual or Combined - is the occurrence of both immediate and late types of asthma.
The frequency of occupational asthma is unknown, although various estimates are available. In Japan, 15 percent of asthma in males is believed to be occupational. In the United States, two percent of all cases of asthma are thought to be of occupational origin. The number of cases of occupational asthma varies from country to country and from industry to industry. About six percent of animal handlers develop asthma due to animal hair or dust. Between 10 and 45 percent of workers who process subtilisins, the "proteolytic enzymes" like "Bacillus subtilis" in the detergent industry develop asthma. However, preparations of the enzymes in granulated form, which is less readily inhaled, have reduced the likelihood of asthma. Approximately five percent of workers exposed to such chemicals as isocyanates and certain wood dusts develop asthma.
Some workplace conditions seem to increase the likelihood that workers will develop asthma, but their importance is not fully known. Factors such as the properties of the chemicals, and the amount and duration of exposure are obviously important. However, because only a fraction of exposed workers are affected, factors unique to individual workers can also be important. Such factors include the ability of some people to produce abnormal amounts of IgE antibodies. The contribution of cigarette smoking to asthma is not known. But smokers are more likely than nonsmokers to develop respiratory problems in general.
Sufferers from occupational asthma experience attacks of difficult breathing, tightness of the chest, coughing, and breath sounds such as wheezing, which is associated with air-flow obstruction. Such symptoms should raise the suspicion of asthma. Typically these symptoms are worse on working days, often awakening the patient at night, and improving when the person is away from work. While off work, sufferers from occupational asthma may still have chest symptoms when exposed to airway irritants such as dusts, or fumes, or upon exercise. Itchy and watery eyes, sneezing, stuffy and runny nose, and skin rashes are other symptoms often associated with asthma.
Lung function tests and skin tests can help to confirm the disease. But some patients with occupational asthma may have normal lung function as well as negative skin tests.
The diagnosis of work-related asthma needs to be confirmed objectively. This can be done by carrying out pulmonary function tests at work and off work. Specific inhalation challenges can demonstrate the occupational origin of asthma and may identify the agents responsible when the cause is uncertain. Specific inhalation challenge tests require breathing in small quantities of industrial agents that may induce an attack of asthma. But they are safe when performed by experienced physicians in specialized centres.
Although there are drugs that may control the symptoms of asthma, it is important to stop exposure. If the exposure to the causal agent is not stopped, treatment will be needed continuously and the breathing problems may become permanent. People may continue to suffer from occupational asthma even after removal from exposure. For example, a follow-up study of 75 patients with asthma caused by red cedar dust showed that only half the patients recovered. The remaining half continued to have asthmatic attacks for a period of 1 to 9 years after the termination of exposure.
Dust masks and respirators can help to control workplace exposure. However, these protective devices, in order to be effective, must be carefully selected, properly fitted and well maintained. Preventing further exposure might involve a change of job. If a job change is not feasible, relocation to another area of the plant with no exposure may be essential.
The best way to prevent occupational asthma is to replace dangerous substances with less harmful ones. Where this is not possible, exposure should be minimized through engineering controls such as ventilation and enclosures of processes.
Education of workers is also very important. Proper handling procedures, avoidance of spills and good housekeeping reduce the occurrence of occupational asthma.
Some of the occupations where asthma has been seen are listed in the following tables. It should be noted that the lists of occupational substances and microbes which can cause asthma are not complete. New causes continue to be added. New materials and new processes introduce new exposures and create new risks.
| Table 1 |
Causes of Occupational Asthma
- Grains, flours, plants and gums
|Chemists, coffee bean baggers and handlers, gardeners, millers, oil industry workers, farmers||Castor beans|
|Cigarette factory workers||Tobacco dust|
|Drug manufacturers, mold makers in sweet factories, printers||Gum acacia|
|Farmers, grain handlers||Grain dust|
|Gum manufacturers, sweet makers||Gum tragacanth|
|Strawberry growers||Strawberry pollen|
|Tea sifters and packers||Tea dust|
|Tobacco farmers||Tobacco leaf|
|Woollen industry workers||Wool|
|Table 2 |
Causes of Occupational Asthma - Animals, insects and fungi
|Bird fanciers||Avian proteins|
|Field contact workers||Crickets|
|Fish bait breeders||Bee moths|
|Flour mill workers, bakers, farm workers, grain handlers||Grain storage mites, alternaria, aspergillus|
|Laboratory workers||Locusts, cockroaches, grain weevils, rats, mice, guinea pigs, rabbits|
|Mushroom cultivators||Mushroom spores|
|Pea sorters||Mexican bean weevils|
|Zoological museum curators||Beetles|
|Table 3 |
Causes of Occupational Asthma - Chemicals/Materials
|Aluminum cable solderers||Aminoethylethanolamine|
|Aluminum pot room workers||Fluorine|
|Autobody workers||Acrylates (resins, glues, sealants, adhesives)|
|Chemical plant workers, pulp mill workers||Chlorine|
|Dye weighers||Levafix brilliant yellow, drimarene brilliant yellow and blue, cibachrome brilliant scarlet|
|Epoxy resin manufacturers||Tetrachlorophthalic anhydride|
|Foundry mold makers||Furan-based resin binder systems|
|Health care workers||Glutaraldehyde, latex|
|Laboratory workers, nurses, phenolic resin molders||Formalin/formaldehyde|
|Meat wrappers||Polyvinyl chloride vapour|
|Paint manufacturers, plastic molders, tool setters||Phthalic anhydride|
|Photographic workers, shellac manufacturers||Ethylenediamine|
|Refrigeration industry workers||CFCs|
|Solderers||Polyether alcohol, polypropylene glycol|
|Table 4 |
Causes of Occupational Asthma - Isocyanates and metals
|Boat builders, foam manufacturers, office workers, plastics factory workers, refrigerator manufacturers, TDI manufacturers/users, printers, laminators, tinners, toy makers||Toluene diisocyanate|
|Boiler cleaners, gas turbine cleaners||Vanadium|
|Car sprayers||Hexamethylene diisocyanate|
|Cement workers||Potassium dichromate|
|Chrome platers, chrome polishers||Sodium bichromate, chromic acid, potassium chromate|
|Nickel platers||Nickel sulphate|
|Platinum chemists||Chloroplatinic acid|
|Platinum refiners||Platinum salts|
|Polyurethane foam manufacturers, printers, laminators||Diphenylmethane diisocyanate|
|Rubber workers||Naphthalene diisocyanate|
|Tungsten carbide grinders||Cobalt|
|Welders||Stainless steel fumes|
|Table 5 |
Causes of Occupational Asthma - Drugs and enzymes
|Ampicillin manufacturers||Phenylglycine acid chloride|
|Detergent manufacturers||Bacillus subtilis|
|Enzyme manufacturers||Fungal alpha-amylase|
|Food technologists, laboratory workers||Papain|
|Pharmacists||Gentian powder, flaviastase|
|Pharmaceutical workers||Methyldopa, salbutamol, dichloramine, piperazine dihydrochloride, spiramycin, penicillins, sulphathiazole, sulphonechloramides, chloramine-T, phosdrin, pancreatic extracts|
|Poultry workers||Amprolium hydrochloride|
|Process workers, plastic polymer production workers||Trypsin, bromelin|
| Table 6 |
Causes of Occupational Asthma - Woods
|Carpenters, timber millers, woodworkers||Western red cedar, cedar of Lebanon, iroko, California redwood, ramin, African zebrawood|
|Sawmill workers, pattern makers||Mansonia, oak, mahogany, abiruana|
Document last updated on February 8, 2005