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Epidemiology
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The prevalence of occupational asthma is generally estimated to be 2-15%, depending on the industry type as well as the presence of medical practitioners interested in occupational respiratory allergy. For example, the cumulative incidence of occupational asthma is at least 5% in workers exposed to western red cedar wood or isocyanates, and more than 50% in workers exposed to platinum salts or high concentrations of detergent enzymes.
There have been few South African studies of occupational asthma. One study in a small chemical plant, found that six out of twenty workers exposed to toluene di-isocyanate (TDI) had features suggestive of TDI asthma. A more recent study of 40 workers exposed to hexamethylene di-isocyanate (HDI) showed 25% with clinically significant cross-shift decreases in their FEV1, two workers being diagnosed as having asthma. Studies of grainmill workers have demonstrated a prevalence of 37% of workers fulfilling the criteria for the diagnosis of occupational asthma. Experience suggests that only a minority of these workers are diagnosed, reported and have claims fully processed for compensation. The medical practitioner with an interest in allergy thus has an important role to play in the diagnosis, treatment and prevention of occupational asthma.
This chapter is concerned with the management of patients presenting with symptoms suggestive of occupational asthma. Other aspects such as screening and medical surveillance of workers exposed to sensitising agents will not be covered.
Legislation
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Occupational asthma is compensable under the Compensation for Occupational Injuries and Diseases Act (COIDA) 1993. Another new piece of legislation, the Occupational Health and Safety Act (OHSA) 1993, makes it obligatory for medical practitioners to report all cases of suspected occupational disease.
Definition
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There are many possible connections between asthma and work. There are two major categories of asthma viz. occupational asthma and work-aggravated asthma.
Occupational asthma is characterised by intermittent airway obstruction and/or non-specific bronchial responsiveness due to causes in the workplace environment and not present outside the workplace. The two types of occupational asthma can be differentiated from each other depending on whether a latency period exists between exposure and the development of symptoms. Asthma with a latency period pertains to those cases where an immunologic mechanism has been identified, as is the case with most high molecular weight agents and some low molecular weight ones. Asthma without a latency period occurs with irritant-induced asthma, such as in reactive airways dysfunction syndrome.
Work-aggravated asthma is defined as concurrent asthma worsened by nontoxic irritants or physical stimuli in the workplace. Adults with asthma may complain that their condition is aggravated by some factor at work, such as strenuous effort, a draughty or wet workplace, dust or vapours from the materials they use, or tobacco smoke from co-workers. It is important to note however that a history of childhood asthma or concurrent asthma does not exclude the possibility that occupational asthma may develop after exposure to allergens present in the workplace.
Causative agents
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There are over 300 recognised causes of occupational asthma. The COIDA lists those agents recognised as causing occupational asthma and eligible for compensation in South Africa (Table 1). This list can be used as a guide to diagnosis in our setting. Table 2 lists some of the workplaces in which these substances are found.
Reactive airways dysfunction syndrome (RADS) results when a worker inhales a high concentration of an irritant vapour or gas (eg. chlorine, ammonia, acetic acid, sulphur dioxide etc.), often resulting from an accidental leak in a factory. In such cases recovery from the acute illness may be followed by a persistence of non-specific bronchial responsiveness and symptoms of asthma. This should be treated as a type of asthma caused by a work accident.
Pathophysiology
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Occupational allergens can be broadly divided into two main groups viz. complete antigens and small molecular weight chemicals. To cause sensitisation they need to be in a form which can be capable of inhalation. The small molecular weight chemicals (eg. isocyanates, acid anhydrides) act as haptens by binding to body proteins. Other agents may denature proteins (eg. formaldehyde, glutaraldehyde).
With most complete antigens, as in baker’s (or flour-induced) asthma, the mechanism is a Type I hypersensitivity: the immune response is mediated by IgE antibodies to some antigenic component of flour. These are detectable using the various immunological tests available viz. skin prick tests or the radioallergosorbent test (RAST). With the majority of low molecular weight agents, such as in isocyanate asthma, the mechanism is not properly understood. Although IgE antibodies against isocyanate may be detected by a RAST, this test is positive in only a minority (10-20%) of cases of isocyanate asthma.
The pathophysiology of RADS is unclear. It has been suggested that high level of exposure to an irritant induces massive airway injury, followed by activation of non-adrenergic, non-cholinergic pathways via axon reflexes resulting in neurogenic inflammation.
Table 1:
Sensitising agents causing occupational asthma as listed under Schedule 3 of COIDA
1. Organic dust (wood, grain and grain flour and tobacco)
2. Isocyanates
3. Vapours and fumes of formaldehyde, anhydrides, amines and diamines
4. Metals: platinum, nickel, cobalt, vanadium, chromium salts
5. Soldering and welding fumes
6. Hardening agents, including epoxy resins
7. Acrylic acid and acrylates
8. Substances of animal or insect origin
9. Fungi and spores
10. Proteolytic enzymes
Table 2:
Examples of jobs/industries in which occupational asthma has been observed, with causative agents
Industry/Job Type |
Causative Agent/s |
Animal handlers: laboratory/farm |
Animal matter, insects, moulds |
Bakers, millers |
Flour, grain, mites, moulds |
Detergent manufacture |
Enzymes |
Food processors |
Seafoods, sulphites |
Foundries |
Resins, isocyanates |
Furniture, cabinetry, sawmills |
Wood dust, formaldehyde |
Hairdressing |
Persulphates, henna |
Hospital, medical laboratories |
Latex, formaldehyde, glutaraldehyde |
Metal refining, plating, grinding |
Platinum salts, chrome, nickel, cobalt, mineral oils |
Pharmaceutical manufacture, mixing |
Antibiotics, enzymes |
Plastics, rubber, adhesives: manufacture/forming/application |
Isocyanates, anhydrides, amines, acrylates, epoxy resins |
Soldering, electronics |
Colophony, other fluxes |
Spraypainting, coating |
Isocyanates, hardening agents |
Welding |
Fluxes, metal fumes |
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