NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

Beach J, Rowe BH, Blitz S, et al. Diagnosis and Management of Work-Related Asthma. Rockville (MD): Agency for Healthcare Research and Quality (US); 2005 Nov. (Evidence Reports/Technology Assessments, No. 129.)

  • This publication is provided for historical reference only and the information may be out of date.

This publication is provided for historical reference only and the information may be out of date.

Cover of Diagnosis and Management of Work-Related Asthma

Diagnosis and Management of Work-Related Asthma.

Show details

1Introduction

The Problem of Work-Related Asthma

What is Occupational/Work-Related Asthma?

Occupational asthma (OA) is a heterogeneous clinical syndrome characterized by work-related symptoms, airway inflammation (partially or completely reversible), bronchoconstriction, and hyper-responsiveness induced by workplace exposures (asthmagens). In contrast to non-occupational asthma, the differentiating feature of occupational asthma is the causal asthmagen is a substance in the occupational environment.1 The symptoms of OA are similar to non-occupational asthma and include wheezing, cough, dyspnea, and impaired quality of work and non-work life. More than 250 asthmagens have been implicated and identified as causative agents in the development of OA (e.g., di-isocyanates, western red cedar, enzymes, snow crab, latex, flour, and laboratory animals). However, there are likely a variety of workplace asthmagens that have yet to be identified. An attempt has been made to classify the majority of the known asthmagens into categories based on their molecular weight: high molecular weight (HMW; ≥ 5000 Daltons) versus low molecular weight (LMW; <5000 Daltons) compounds, as this is probably important in their mechanism of action.2 Due to the nature and complexity of workplace exposures, this is not always possible. Examples of HMW asthmagens include flour and latex; common LMW asthmagens are di-isocyanates, metals, and dyes.1

OA can be broadly classified into two categories: OA with latency and OA without latency. Latency periods are observed in all instances of immunologically mediated asthma, even though the immunological mechanism may not yet have been clearly identified.2 The latency period, which represents the time between the first exposure and onset of first symptoms, can range from weeks to years. When a worker has OA with latency, a specific inhalation test with the causal agent will usually be positive and often an immunological response for HMW and some LMW asthmagens is identified with specific skin prick tests (SPT) and/or serum specific IgE antibody testing. Generally, serum specific IgE antibodies, biomarkers for sensitization to the specific asthmagen, have been identified for HMW compounds; serum specific IgE antibodies associated with LMW OA have yet to be fully characterized, as the antibodies have yet to be discovered or occur in only a small portion of workers.2 The need to produce appropriate hapten-protein conjugates is probably a common reason for the failure to detect antibodies to LMW agents. OA with latency for which serum specific IgE antibodies have been identified is referred to as IgE associated.

OA can also exist without a latency period and can occur after a single large exposure to irritant gases, fumes, or chemicals, such as nitrogen oxide, ammonia, and chlorine.3 This type of exposure results in reactive airways dysfunction syndrome, or RADS. Occupational asthma has also been reported to occur in few instances from repeated exposures to lower doses of ‘irritant’ or non-sensitizing agents.4 After exposure to an irritant, the asthmatic reaction occurs within a short time.5 Since there is no sensitization, the battery of diagnostic tests for RADS does not include specific immunological tests, and specific inhalation challenge (SIC) is not used. OA without latency is less common; it is believed to represent between 5 and 15 percent of all OA cases.1, 6, 7

For the purpose of this report, OA with and without latency and work-aggravated asthma were defined in concordance with the American College of Chest Physicians (ACCP) and are described in Table 1:

Table 1. Definitions of work-related asthma.

Table 1

Definitions of work-related asthma.

Through the remaining report, the term OA refers to OA with and without a latency period. This approach is similar to that of the American Thoracic Society guidelines.8 Where possible, we have noted where the results are derived from a RADS population. We recognize that some studies may also include individuals with work-aggravated asthma within their study population, although it is rarely possible to identify if this is so. When the individual studies provide adequate detail, we have included the proportion of workers with a previous history of asthma and this may indicate work-aggravated asthma rather than OA.

Epidemiology of Occupational/Work-Related Asthma

Amongst developed countries, OA has become one of the most prevalent occupational lung diseases.2 The annual incidence of OA is estimated to be 50 per million United Kingdom (UK) workers and 140 per million Finnish workers.9 In France, the mean annual incidence rate was 24 per million workers.10 Among American workers belonging to a Health Maintenance Organization who were at risk for developing OA, the annual incidence of new-onset asthma was 1300 per million.11 A review of 43 attributable risk estimates from 19 counties found the attributable risk of OA to be 9 percent (interquartile range [IQR] 5–19 percent).12 Because of the high prevalence of OA, it has been recommended that OA be considered a diagnostic possibility in all adults undergoing initial asthma evaluation. Surveillance programs indicate that OA accounts for 26–52 percent of reported occupational lung conditions in the UK13 and British Columbia, Canada14. Perhaps of even greater concern is the suggestion that OA is potentially more common than studies have previously reported.15 This seems likely, as several factors make OA identification difficult: 1) most industries expose workers to a number of potential causative agents and exposure may vary widely within the same workplace setting, making exposure assessment complex; 2) OA symptoms are variable and non-specific, with late reactions often occurring after the working day has been completed; 3) specific diagnostic tests have limited availability making exact diagnosis difficult; and, 4) the symptom onset is unpredictable.15

Greater than 250 synthetic and naturally occurring agents in a variety of work settings have been identified as relevant workplace exposures16; one of the most common exposures being di-isocyanates used in the production of coatings, adhesives, and foams in a wide variety of settings. It is estimated that up to 11 percent of workers exposed to di-isocyanates will develop bronchial hyper-reactivity.17 Other commonly reported agents include flour, wood dusts, and latex.2 While a large number of the causative agents have been identified, many more sensitizers and irritants are not well characterized and/or known, thus making the diagnosis of OA even more elusive.

The contribution of work-aggravated asthma cannot be ignored. Work-aggravated asthma occurs in workers with a previous or concurrent history of asthma and is characterized by worsening symptoms at work in response to chemicals or physical stimuli encountered at work, such as dust or cold air.2 Among employed asthmatics in a Finnish city, Saarinen et al. found the prevalence of work-aggravated asthma to be approximately 30 percent.18 In a recent study, the annual incidence rate of work-aggravated asthma among employed workers with current asthma was 3.9 cases per 100,000 each year.19 The highest incidence rate occurred among workers employed in the public administration industry (14.2 cases per 100,000 each year). The most commonly responsible agents were mineral and inorganic dusts.

Because workers often need to be away from work due to their illness, and the cornerstone of treatment is removal from the workplace, OA creates a significant economic burden for individuals, industry, health care providers, and society. Using the human capital method, Leigh et al. calculated the cost of OA in the United States to be $1.6 billion annually.20 Sometimes, impaired lung function does not improve or reverse, even after extended periods away from the causative agent21 and this can result in permanent unemployment. The United Kingdom's Surveillance of Work-related and Occupational Respiratory Disease program found that 30 percent of people reported to have OA between 1989 and 1992 were unemployed when contacted later.22

Diagnosis of Occupational/Work-Related Asthma

An ideal diagnostic test has both a high sensitivity and specificity. Sensitivity refers to the test successfully identifying the proportion of the people who truly have the disease, i.e., the test detects true positives. A test has high sensitivity when it identifies nearly all of the people who truly have the disease. A test has high specificity when it successfully identifies most of the people who truly are disease-free as not having the disease, i.e., the test detects true negatives. In general, the sensitivities and specificities of diagnostic test comparisons are more robust if the test results are reproducible. OA is a difficult diagnosis to make for a variety of reasons. The first step is to determine that the patient has asthma and not a similar syndrome, such as upper respiratory tract irritation or vocal cord dysfunction. Having diagnosed asthma, the next step is to show a causative link with exposure to an asthmagen at work and this process often commences with obtaining a history or completing a questionnaire.

While SIC is often cited as a ‘gold standard’, as yet there is no definitive diagnostic test for OA. The applicability of SIC is currently limited by its availability.23 In addition, the possibilities of false negative and positive results have been recognized.5 For example, a false negative can occur when a worker with OA is exposed to multiple asthmagens and is subsequently challenged with the non-offending asthmagen.2 Further, SIC testing is usually not considered useful in determining a diagnosis of irritant induced OA. As a result, throughout this report we will refer to SIC as a reference standard .

There are several alternative techniques, used in isolation or in combination, which can be used to diagnose occupational and work-related asthma. We have summarized SIC and the alternative techniques in the categories below:

Specific inhalation challenge (SIC). There are several methodologies used to perform SIC; however, in general the approach is designed to expose the worker to a suspected asthmagen in a controlled, non-work, test environment. When a suspected asthmagen is a water-soluble compound, the test subject may inhale it in its nebulized form.24 Initially, low concentrations are administered for safety reasons until a response is obtained or a maximum concentration has been tested. When the asthmagen cannot be nebulized because of low solubility, some have proposed tipping powders of the suspected asthmagen from one tray to another in an attempt to mimic the work environment and generate a dry aerosol.25 More recently standardized techniques have been developed to deliver dry powder aerosols. Another method is to conduct a simulated occupational-type specific provocation test.26 For example, when colophony (e.g., used as a solder flux by electronics workers) is suspected to cause OA, the worker is exposed to simulated work tasks in a controlled laboratory environment while lung function monitoring is conducted in an attempt to determine changes in flow volumes or hyper-responsiveness.

The first step of SIC is to perform a control challenge with a substance similar in physical characteristics to the suspected asthmagen, but not likely to cross-react immunologically. When the fluctuations in forced expiratory volume in one second (FEV1) following the control challenge are less than 10 percent, it is generally considered safe for the worker to undergo formal SIC testing with the suspected agent.27 The duration or intensity of exposure is increased progressively, usually commencing with a small dose. Lung function is measured for a period of time after each incremental challenge dose. When challenging with LMW agents, challenges of increasing time durations should occur on separate days, as LMW agents often produce isolated, late asthmatic reactions. When challenging with an HMW agent several doses may be given on the same day as they more typically produce an early asthmatic reaction.27 Conducting SIC in a blinded fashion and ensuring that the results are reproducible can minimize false positive results. A typical definition of a positive response is a decrease from baseline FEV1 (i.e., control exposure) of 15–20 percent.

The greatest advantage of SIC is that a positive test confirms a diagnosis of OA caused by the particular agent. When the appropriate agent is applied and the test is positive in workers with respiratory symptoms that are thought to be work-related asthma, SIC testing is considered confirmatory. However, there are several disadvantages to SIC. First, the suspected workplace agent may not have been identified, which precludes testing. Second, SIC can only be conducted in specialty facilities and these are rare. For example, a survey conducted in 2000 indicated that only 15 centers capable of performing SIC exist in the USA and Canada.23 Moreover, there are many complexities associated with developing a SIC laboratory. These include the expense of purchasing and operating the laboratory and the ability to generate the appropriate concentrations of the putative asthmagens. Third, SIC can only be performed in relatively stable workers (FEV1 >60–70 percent of predicted and/or >2L28) because SIC may induce a very severe asthma attack.29 A fourth disadvantage is the potential for false positives that can occur when SIC is performed in a worker with unstable asthma or when the worker suffers from marked non-specific bronchial hyper-reactiveness, as the non-specific irritant reaction can masquerade as an early reaction to SIC.27 Finally, SIC testing can take several days. While SIC can be performed as an outpatient procedure, carefully monitoring is required for several hours after the challenge and oxygen, bronchodilators, steroids, and intubation equipment should be available.15

History and questionnaires. There are several questionnaires used to assess respiratory health.3033 Questionnaires and histories may focus on specific job duties and work processes and inquire about improvement during weekends and/or holidays and worsening when returning to work.2 The 1995 ACCP guidelines recommend three components of history taking: 1) history detailing onset of illness, temporal relationship between exposure and exacerbation, description of airway disease, and severity of asthma; 2) medical history describing pre- and co-morbidities and associated symptoms; and, 3) occupational and environmental history.15 In addition, material safety data sheets (MSDSs) can be collected for the chemicals used in the workplace. MSDSs describe the ingredients, concentration, and toxic properties of chemicals in the workplace.

Questionnaires and histories are easily administered. However, respiratory symptoms are a common complaint among all workers, thus questionnaires and histories tend to lack specificity. They may also lack sensitivity. The following circumstances can produce falsely negative results: exposure to the agent is indirect and/or sporadic; workers may be reluctant to disclose symptoms for fear of losing employment; or, the worker does not relate progression of OA to a workplace exposure.5 While the utility of history and questionnaires has been established for surveillance purposes and case finding in the event of symptoms of rhinitis and/or asthma, little research exists that examines their usefulness as a diagnostic test.

History and questionnaires are used to identify patients with relevant symptoms and workplace exposures known to cause OA. These patients will have a higher pre-test probability of testing positive to other tests of OA, as the subsequent test is being conducted in a pre-screened population. This is of importance in the later considerations in this review.

Serial lung function testing. Comparing serial lung function at work and away from work has previously been used to diagnose OA, especially when SIC test is unavailable. Until the advent of modern compact flow based spirometers, there were practical problems with the portability of the required equipment. Modern compact spirometers will allow for the measurement of lung function parameters including FEV1 and forced vital capacity (FVC). One solution to this was to measure serial peak expiratory flow rate (PEFR) as portable and inexpensive equipment to measure this has been available for many years. The current ACCP guidelines recommend that PEFR be measured at least four times each day: upon waking, at noon, at the end of the working day, and at bedtime.15 During each measurement, three PEFR measures are performed and recorded once all three readings are within 20 L/min.15 The optimal duration of PEFR recording appears to be at least 4 weeks with a minimum of eight readings each day and at least 4 consecutive days in each work period.34 However, obtaining records of that quality for that period of time is cumbersome. It is noteworthy that the sensitivity and specificity of this procedure was similar to records that were collected for at least four readings per day and at least 3 consecutive days at work for approximately 18 days.34

Serial lung function testing is an inexpensive diagnostic test that may show a temporal association between lung function and occupational exposure.35 Despite these advantages, serial lung function testing is still associated with a number of difficulties. Unfortunately, this test is dependent upon the worker's effort, requires them to reliably perform a forced expiratory maneuver and record the results accurately, and assumes worker honesty in performing and recording the results of the test.2 Spirometers and peak flow meters incorporating a data recording device have helped with this to some extent. Another disadvantage of serial lung function testing is that it may be difficult to measure lung function for long enough periods while the worker is not at work to exclude OA. It is important the worker understands that late asthmatic reactions may occur several hours after exposure ceases, and they may not be detected during the monitoring period if only cross-shift measurements are made. In addition, serial lung function testing may be of no value among patients who are no longer exposed to the causative agent, as an asthmatic response should not occur, and when a patient has advanced OA, their lung function may become relatively fixed and not substantially improve during fairly short periods away from work. Finally, there are no universally accepted, standardized methods, for interpreting the results.15

Non-specific bronchial provocation (NSBP) testing. There are several different protocols used to measure bronchial hyper-responsiveness (BHR).15 In general, the first step of an NSBP test is to measure baseline lung function. Then, a worker inhales increasing doses of a bronchoconstrictor agent; the most commonly used agent in North America is methacholine.15 Numerous other agents have been used for NSBP testing, including histamine, acetylcholine, hypertonic saline, bethanechol, and distilled water. In the most frequently described test method (used in North America) the inhalation of methacholine or histamine begins at a concentration of 0.03 mg/mL for 2 minutes and is typically increased in a doubling fashion up to 32 mg/mL.15 Following each inhalation, the worker's FEV1 is measured. The predicted concentration causing a 20 percent decrement (PC20) in FEV1 can then be estimated by linear interpolation.36 There is no standardized definition of a positive response; however, a commonly used definition is a decrease from baseline FEV1 of 20 percent or more at a methacholine concentration of 8 mg/mL or less.37 For other techniques, a predicted dose causing a 20 percent decrement (PD20) in FEV1 can be similarly estimated.

When compared to SIC, the main advantages of NSBP testing approaches are that they are reasonably inexpensive, easier to perform, available in a larger number of facilities, and have proven safety records. In addition, the test can usually be completed in an hour, or considerably less if using an abbreviated protocol. However, a positive NSBP test only proves that the worker has hyper-reactive airways, which is typical of asthma due to any cause and it is not a definitive test for OA.27 Serial NSBP testing can be performed at work and away from work. If the test demonstrates airways hyper-reactivity while an individual is at work and a significant reduction after the worker has been away from work for several weeks, then it is more likely the worker suffers from OA. From consensus recommendations, a threefold or greater increase in PC20 or PD20 when away from work as compared to at work is often considered a positive test result for OA38, while a twofold change is suspicious, but not universally accepted as definitive of OA.5

Immunological testing. Classically, asthma is often thought of as a specific IgE mediated disease, most prevalent in atopic individuals. Common immunological tests include SPT and estimation of specific IgE/IgG, which is often measured by using the enzyme-linked immuno sorbent assay (ELISA) or radio allergo sorbent test (RAST) techniques. For SPT, a positive response is often defined as a 3mm or greater wheal reaction to a skin prick.39 SPT can be used to identify responses to common allergens, which would signify atopy, or responses to specific antigens. Similarly, a high total IgE would be used to signify atopy, while increased specific IgE or IgG can also be measured. OA caused by the majority of HMW agents is specific IgE mediated and a positive SPT or raised specific IgE will be present. In contrast, LMW-induced OA is generally not specific IgE mediated, and consequently SPT or a measurement of specific IgE in this situation is not usually helpful40, nor is it useful for irritant induced asthma or work-aggravated asthma.

Further, while specific immunological testing confirms that a worker is sensitized to a particular workplace allergen, sensitization is not synonymous with asthma, since sensitization to a workplace exposure can exist in the absence of OA. A further disadvantage of immunological testing is that few allergens known to cause OA are available in a standardized commercial form to be used for allergy testing. Importantly, there is no immunological test available for the majority of LMW compounds.

Total IgE and atopic status are used as screening tools but are not specific for OA or a particular workplace exposure, but rather identify atopy. Atopy is a risk factor for developing some types of sensitizer-induced OA.41

Measures of airway inflammation. Nitrous oxide is produced by a number of cells located in the respiratory tract, such as inflammatory and epithelial cells, and is detectable in exhaled air.42 It is hypothesized that asthmatic workers have higher levels of exhaled nitrous oxide (eNO) caused by airway inflammation than the normal population. Measuring eNO is a non-invasive procedure; however, it has yet to be fully validated as an effective diagnostic test for OA, as eNO seems to be increased in a number of inflammatory lung disorders.43 Also, eNO testing is confounded by inhaled corticosteroid usage, as workers receiving inhaled steroid treatment tend not to have increased eNO.42, 44 Finally, it is a difficult test to perform for workers, is costly, and its availability in North American is limited. Perhaps, once techniques to measure and record eNO are widely available and fully validated, such a method may be more appealing.

A second measure of airway inflammation is sputum induction with identification of eosinophils and other cells or inflammatory markers in the expectorated material. The direct cellular and chemical evaluation of airway inflammation has traditionally been undertaken using bronchial biopsies and bronchial alveolar lavage. In both these latter techniques, individuals are usually sedated and bronchoscopes are used to sample the airways either through biopsy or saline lavages, respectively. Given the cost, inconvenience, and invasive nature of these tests, other methods of identifying and quantifying airway inflammation have been developed. One alternative is the use of sputum to examine the cellular and chemical agents responsible for inflammation. In many cases, asthmatic workers cannot produce sufficient sputum for examination, and so induction is performed using nebulized saline. Once a sample is expectorated, it is prepared and examined microscopically for cellular composition and chemically analyzed using a variety of techniques. The most important cells in the sputum include eosinophils and neutrophils. Standard normal concentrations of both have been reported45 and these can be used to evaluate the samples.

This technique is safe and the repeatability of the technique has now been shown.46 In the correct setting (qualified technologist, laboratory, and interpretation) this technique has been shown to provide useful information about the underlying inflammatory activities in the airway and may be incorporated into the diagnostic testing options available for OA.47, 48

In OA, induced sputum markers have been used to determine changes in cellular make-up between pre- and post-exposure samples.49 This technique shows some promise for agents or circumstances in which SIC cannot be performed. A significant change in eosinophil and/or neutrophil concentration post-exposure signifies an airway response related to the asthmagen.

Management of Occupational/Work-Related Asthma

Once OA is identified, the general recommendation has been to remove workers from the workplace rather than introduce medications to control their symptoms.15 There are, however, several different approaches used to manage OA. Firstly, workers can be treated pharmacologically in a manner that is similar to those with non-occupationally induced asthma. However, additional lung function deterioration may not be prevented in workers who receive pharmacological treatment and yet remain exposed to the causative agent.50 Secondly, various mechanisms can alter the worker's environment to reduce exposures to an “acceptable” level by using personal protective equipment (PPE), making engineering changes to the workplace (e.g., improved ventilation, changing production materials or processes, etc.), or administrative changes to work tasks. Additionally, the worker can be relocated to a different job, or to a different area of the workplace, or it may be possible to substitute a non-hazardous agent for the causative agent in use. The final, and most drastic, management option is to remove the worker entirely from workplace. Removal from the workplace should ensure that exposure to the causative agent is ended completely which is considered by many to be the cornerstone of therapy; however, workers may not wish to be removed for financial and social reasons. In practice, it seems that many workers need to be removed from the workplace. Within 6 years, approximately one-third of workers are unemployed after their initial confirmed diagnosis of OA.22, 41 For those who are able to return to work, close medical follow-up is required to ensure that lung function does not continue to deteriorate at a rate quicker than would be anticipated as due to age alone.2

Reducing exposure. Reducing workplace exposures may benefit not only workers with OA, but also those that may go on to develop OA in the future40; however, not all workers with OA benefit similarly from this approach. Reducing exposure levels has been hypothesized to be of particular use in irritant-based OA where there is no allergic component and hence a more linear and predictable dose response relationship.40 Workers with OA with latency (i.e., immunologically mediated) may often react to very low concentrations of the aetiological agent, and therefore effective management by reducing exposure levels is questionable.2 The American Thoracic Society analyzed five studies that examined the effects of reducing workplace exposure on occupational and work-related asthma.5 They found that OA improved or remained unchanged in approximately two-thirds of workers when exposure was reduced, while the other workers' asthma worsened.

One method to decrease exposure in the workplace is to reduce or eliminate the use of potential asthmagens from the workplace.8 Compared to engineering changes, this method is advantageous because it does not require mechanical maintenance.8 Examples of this method include using latex-free rubber gloves, latex gloves with lower protein content, or switching to a spray paint that is di-isocyanate-free. However, it is not frequently applicable in practice as the substances used in a workplace rarely have an alternative that can easily be substituted.

Engineering or structural changes can decrease workplace exposure to an asthmagen. Such changes include building an enclosure for the process where the asthmagen is used, or the establishment of local ventilation that clears the asthmagen away from the worker's breathing space.8 Administrative changes, such as job rotation, may also be useful in reducing exposure.

A third way to reduce exposure is to relocate the workers to a new job in an area of the building where the exposure is not present (or present in very low concentrations). The Americans with Disabilities Act recommends that large companies with adequate resources go to considerable effort to relocate workers with OA into an area or job with decreased exposure.51

Finally, exposure concentration can be reduced by the proper use of PPE. In order to be of value, PPE must be correctly worn, safely removed, properly maintained, and replaced as needed.41 By creating a better atmospheric breathing environment for the worker, air-supplying respirators provide the highest level of protection.52 The self-contained breathing respirator can protect against most exposures; however, it is cumbersome, expensive, and can not be comfortably worn for an entire work shift.52 There is general consensus that PPE is more appropriate for managing irritant-induced OA with brief and infrequent exposure than sensitizer-induced OA for the reasons mentioned above.8 PPE will reduce but not eliminate exposure and consequently is only recommended for short-term use.8

Removal from exposure. There have been numerous deaths reported among workers with OA who were not removed from exposure suggesting that complete asthmagen avoidance is important.53 Previous authors have also suggested that for workers suffering from OA with latency (immunologically mediated OA), there is consistent evidence concluding that removal from the exposure results in an improved health outcome.2, 54 In addition, it appears that compared to late removal, earlier removal is associated with greater improvement in lung function and symptoms.55, 56 In contrast, workers with irritant-induced OA are more likely to be able to return to work and manage asthma pharmacologically.5

However, removal from the workplace has significant deleterious effects on the income and financial stability of the individual affected, as well imposing costs on the employer.57, 58 OA claims are also a financial burden to the government; the average accepted claim in Quebec, Canada in the early 1990's was approximately $50,000.59

Pharmacological treatments. Pharmacological treatment of OA does not differ from chronic non-occupational asthma treatment. Asthma is managed through a variety of methods including trigger avoidance (reduction of trigger or complete avoidance), education, and pharmacological measures. Asthma is managed pharmacologically using two large groups of agents: relievers (bronchodilators) and preventers (anti-inflammatory agents).

Relievers. Relievers generally act on the beta-receptors in the airway to dilate the airways and relieve symptoms. Examples of these agents include short-acting beta-agonists (SABA) such as salbutamol (Ventolin®) or terbutaline, long acting beta-agonists (LABA) such as salmeterol (Serevent®) and formoterol (Oxese®, Foradil®), and anticholinergic agents such as ipratropium bromide (Atrovent®) and tiotropium (Spiriva®). These agents may be taken for relief of symptoms or prior to work to avoid the drop in FEV1 that normally occurs in workers suffering from OA. There is some evidence that regular use of LABA agents, when administered with inhaled corticosteroids, can improve chronic asthma control.60 Mono-treatment with LABA is not recommended. There is limited evidence that regular use of anticholinergic agents improve chronic asthma control.61

Preventers. Broadly, there are a number of preventers from which physicians and workers may choose to decide upon for therapy (corticosteroids, combination agents, leukotriene receptor antagonists or modifiers, and mast cell stabilizers):

  • Corticosteroids (CS). Corticosteroids work by reducing inflammation, up-regulating beta-receptors, and decreasing airway edema by reducing capillary permeability. There are a variety of agents and delivery methods and doses of corticosteroids; however, the two main methods of delivery are systemic and inhaled. Systemic corticosteroids are effective in intravenous, intramuscular, and oral forms; oral is clearly the preferred method of delivery due to convenience, cost, and worker's adherence. However, long term systemic CS are associated with severe adverse effects, such as osteoporosis, skin changes, cataracts, impaired glucose regulation, and fluid retention (so called: moon-face and buffalo hump appearance). Prior to the introduction of inhaled corticosteroids (ICS), systemic CS agents were the mainstay for control of moderate-severe asthma. Since the introduction of ICS, these agents have largely replaced systemic CS as a treatment of choice.
  • Combination agents. ICS and LABA agents may be taken separately as individual inhalational agents, or as new combination inhalers. The current recommendation states that LABAs should not be used without an ICS. Fluticasone combined with salmeterol (Serevent®) has been marketed as Advair® (Seritide® in Europe); budesonide in combination with formoterol (Oxese®) has been marketed as Symbicort®. These agents deliver both ICS + LABA in each inhalation and have the benefit of increased compliance and ease of use. In general, these agents are reserved for the treatment of moderate-severe work-related asthma unresponsive to increasing doses of ICS.
  • Leukotriene receptor antagonists (LKTRA) or modifiers. Discovery of the cystenyl leukotriene pathway has been an important advancement in asthma care over the past decade. The pathway is particularly important in the inflammatory cascade involved in asthma, especially for children and in aspirin-sensitive workers. Agents that inhibit or block cystenyl leukotriene pathway, called LKTRA, have been marketed and are available for mild-moderate asthma in adults and children. In general, these agents are restricted to add-on treatment of moderate-severe work-related asthma unresponsive to increasing doses of ICS.
  • Mast cell stabilizers. Infrequently, mast cell stabilizers are used to control asthma. These agents are often used in exercise-induced bronchoconstriction (EIB) and in children, due to their non-steroidal nature. Given the availability of more effective agents, these agents are infrequently used now and generally restricted to EIB and mild asthma in children.
  • Other agents. A variety of other agents are available to treat asthma including methyl-xanthines, antibiotics (especially newer macrolides) and a non-traditional agents. Due to their general lack of effectiveness, these agents will not be described in detail in this report.

Objectives of this Review

OA is a common respiratory disease that is difficult to diagnose and treat. Several societies have created clinical practice guidelines for OA (Table 2). However, many do not address or there is not consensus on the key components identified for this review. In summary; the guidelines do not agree upon the role of SIC testing for diagnosing OA; when removal from work is mentioned, it appears to be the recommended treatment.

Table 2. Summary of occupational asthma guidelines.

Table 2

Summary of occupational asthma guidelines.

The first aim was to review the diagnostic approaches for occupational asthma. Many studies have examined the utility of various diagnostic techniques that attempt to differentiate OA from non-occupational asthma. However, there is variability in study methodology and definitions of what constitutes a positive test, and a systematic review and meta-analysis of the existing literature is required to determine the most appropriate diagnostic technique and identify which workers should be undergoing SIC testing. The objective of this review was not to examine the utility of the different tests in screening for OA, such as might be performed in a working population potentially exposed to an asthmagen, but rather to reflect how the tests might be used in the clinical diagnosis of OA.

Similarly, the best methods for managing OA have yet to be established. As discussed above, there are various techniques for treating OA and many studies have followed cohorts of workers suffering from OA and measured markers of disease progression. Thus far, it is unclear which treatment option best improves lung function and symptoms. Also, it has yet to be established whether complete removal from exposure, with its attendant social and economic consequences, is imperative in all types of OA.

It was our objective to systematically gather the existing evidence to determine which diagnostic methods are effective at determining a case of OA and what the optimal treatment is for such workers.

Key Questions

The American College of Chest Physicians put forth the following four questions:

1.

What is the best diagnostic approach for a patient with suspected occupational asthma? What are the advantages of SIC testing versus peak flow monitoring, serial methacholine challenges, immunological testing, or spirometry in making the diagnosis of occupational asthma?

2.

In what situations would specific inhalation challenge testing provide additional useful diagnostic information?

3.

Which treatment is most effective for asthma that is occupationally caused, such as removal from work environment versus reduced exposure through modification and treatment with optimal asthma anti-inflammatory medications (e.g., inhaled steroids)?

4.

Must patients with asthma that is occupationally caused or aggravated be removed from the workplace environment to control symptoms and/or disease progression?

PubReader format: click here to try

Views

  • PubReader
  • Print View
  • Cite this Page

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...