Occupational Asthma (OA) is a form of asthma associated with work or a hobby involving inhalation of a chemical, allergen, or irritant which is aerosolized as dust or fumes. Occupational asthma symptoms have been observed among workers (e.g., bakers, grain workers), even dating back to ancient times. OA may only affect a small percentage of the population; however, it is a serious problem which can lead to permanent lung damage.
Occupational asthma affects the bronchial tree, resulting in symptoms that mimic those of bronchial asthma (e.g., coughing, wheezing, dyspnea, and chest congestion) and is associated with airway obstruction and/or airway hyper-responsiveness. These symptoms may also be accompanied by typical allergy symptoms such as itchy eyes, itchy nose and sneezing when OA is IgE-mediated.
There
are many types of OA, and it is now understood that there is more than one
possible mechanism involved in its development.
Unlike
most cases of bronchial asthma (which usually respond to treatment and may be
reversible), OA with long-term exposure to workplace allergens and irritants
can lead to a chronic, irreversible form of asthma that is unresponsive to
medication, even when the patient is no longer exposed to the original
offending agent.
The common form of allergic bronchial asthma is often provoked by common aeroallergens found at home and outdoors during the pollen season. In contrast, OA is associated with the inhalation of specific and potent airborne agents unique to the workplace.
The common form of allergic bronchial asthma is often provoked by common aeroallergens found at home and outdoors during the pollen season. In contrast, OA is associated with the inhalation of specific and potent airborne agents unique to the workplace.
Symptoms
of OA can include:
- coughing
- wheezing
- itchy eyes
- chest tightness
- shortness of breath
- itchy nose
- sneezing
- congestion
In
addition to a new onset of asthma symptoms at work in a previous non-asthmatic
individual, some patients with pre-existing asthma may notice that their symptoms
are triggered or worsened while at work. This may be due to exposure to
non-specific airborne irritants or inhaled allergens to which the patient is
already sensitive.
In addition, asthmatic
patients may also develop new sensitivities or lung damage due to inhaled
environmental agents unique to the workplace.
The following section details the known mechanisms at work in the development of OA.
The following section details the known mechanisms at work in the development of OA.
B. Causes of OA
There are at least two major mechanisms involved in the development of OA:
1. The most common type of OA occurs after prolonged exposure to workplace allergens. During this time, the patient becomes sensitized to the inhaled workplace agent. The initial period in which the patient is symptom-free is called the latency phase, which can sometimes last years. During this period, the patient has no asthma symptoms as the immunologic hypersensitivity to the workplace allergen is developing. The mechanism is mostly IgE-mediated, and the patient may also develop typical allergy-like symptoms that include itchy eyes, itchy nose and sneezing prior to or during the presentation of asthma symptoms. Early in the course of OA, asthma symptoms usually lessen or resolve when the patient is not at work, especially during evenings, weekends, and vacations.
There are at least two major mechanisms involved in the development of OA:
1. The most common type of OA occurs after prolonged exposure to workplace allergens. During this time, the patient becomes sensitized to the inhaled workplace agent. The initial period in which the patient is symptom-free is called the latency phase, which can sometimes last years. During this period, the patient has no asthma symptoms as the immunologic hypersensitivity to the workplace allergen is developing. The mechanism is mostly IgE-mediated, and the patient may also develop typical allergy-like symptoms that include itchy eyes, itchy nose and sneezing prior to or during the presentation of asthma symptoms. Early in the course of OA, asthma symptoms usually lessen or resolve when the patient is not at work, especially during evenings, weekends, and vacations.
Immunologic
sensitization to a workplace agent in this form of OA is mostly due either to high
molecular weight (HMW) agents (e.g., flour, animal protein), or less often,
to low molecular weight (LMW) agents (e.g., chemicals such as
isocyanates). The mechanism for HMW sensitization is usually IgE-mediated,
while the mechanism for LMW sensitization is often a result of T-cell mediation
(cellular hypersensitivity).
2. The less common type of OA results from exposure to high levels of airborne
irritants in the workplace. Symptoms begin soon after entering the new work
environment, with little to no latency period. Since there is no underlying
immunologic mechanism or sensitization (latency) period, symptoms result from
direct irritation or damage to the airway. This presentation is often referred
to as reactive airway dysfunction syndrome (RADS), or irritant-induced asthma
(IrIA), which is mentioned in the next section.
C. Mechanisms of OA
Immunologic: IgE-mediated sensitization
HMW agents (e.g., animal proteins) have the size and molecular weight to act as complete allergens; therefore, they can elicit a specific IgE response to a workplace allergen (for example, baker’s asthma is a specific IgE response to airborne flour). In this example, sensitization is not immediate, but it follows a latency period that can last years. Although IgE sensitization is usually the result of HMW allergen exposure, a few LMW agents, classified as haptens or incomplete allergens (e.g., platinum salts), can also cause a similar reaction. LMW haptens can act as sensitizers when they combine with body proteins to form complete allergens. Such allergens then behave as HMW allergens, thus eliciting the production of specific IgE against the offending workplace allergen.
Immunologic: IgE-mediated sensitization
HMW agents (e.g., animal proteins) have the size and molecular weight to act as complete allergens; therefore, they can elicit a specific IgE response to a workplace allergen (for example, baker’s asthma is a specific IgE response to airborne flour). In this example, sensitization is not immediate, but it follows a latency period that can last years. Although IgE sensitization is usually the result of HMW allergen exposure, a few LMW agents, classified as haptens or incomplete allergens (e.g., platinum salts), can also cause a similar reaction. LMW haptens can act as sensitizers when they combine with body proteins to form complete allergens. Such allergens then behave as HMW allergens, thus eliciting the production of specific IgE against the offending workplace allergen.
Immunologic: Non-IgE
mediated sensitization
LMW chemicals (e.g., isocyanates, plicatic acid/western cedar) that induce OA are not usually associated with specific IgE production. Although IgE and IgG antibodies have been detected against some LMW agents, a cellular immunologic reaction involving T-cell activation appears to be more commonly associated with LMW sensitization to workplace agents.
LMW chemicals (e.g., isocyanates, plicatic acid/western cedar) that induce OA are not usually associated with specific IgE production. Although IgE and IgG antibodies have been detected against some LMW agents, a cellular immunologic reaction involving T-cell activation appears to be more commonly associated with LMW sensitization to workplace agents.
Non-immunologic
Irritant-induced asthma (IrIA) or reactive airway dysfunction syndrome (RADS) can occur after a single dose or multiple exposures to high concentrations of non-specific irritants (e.g., acids). While the exact mechanism is unknown, epithelial damage to the bronchi is common early in the disease process, leading to airway narrowing and typical symptoms of asthma. In other words, a previously non-asthmatic individual can develop OA following a single exposure to a strong irritant or chemical. An example of this would be the first responders present at the collapse of the World Trade Center on 9/11. This often occurs following an intense irritant or chemical exposure, as with a chemical spill.
Irritant-induced asthma (IrIA) or reactive airway dysfunction syndrome (RADS) can occur after a single dose or multiple exposures to high concentrations of non-specific irritants (e.g., acids). While the exact mechanism is unknown, epithelial damage to the bronchi is common early in the disease process, leading to airway narrowing and typical symptoms of asthma. In other words, a previously non-asthmatic individual can develop OA following a single exposure to a strong irritant or chemical. An example of this would be the first responders present at the collapse of the World Trade Center on 9/11. This often occurs following an intense irritant or chemical exposure, as with a chemical spill.
Combined immunologic and
non-immunologic
Some agents (e.g., toluene diisocyanate/TDI) can cause OA through both immunologic and non-immunologic mechanisms, causing epithelial damage in addition to sensitization.
Some agents (e.g., toluene diisocyanate/TDI) can cause OA through both immunologic and non-immunologic mechanisms, causing epithelial damage in addition to sensitization.
D. The OA history
The possibility of OA should always be considered with a new onset of asthma symptoms or a recent worsening of asthma symptoms or recent worsening of asthma. Beyond current employment and hobbies, the physician should consider the patient’s past work history and exposure experiences to assess prior risk of OA.
The possibility of OA should always be considered with a new onset of asthma symptoms or a recent worsening of asthma symptoms or recent worsening of asthma. Beyond current employment and hobbies, the physician should consider the patient’s past work history and exposure experiences to assess prior risk of OA.
Diagnostic
clues
- Type of symptoms (wheezing, etc. prominent in the workplace)
- Relationship of symptoms to workplace
- Risk factors at workplace due to known sensitizers
- Past medical and occupational history
- History of lung disease
- Chemicals, processes, and exposure incidence, as well as potential
agent exposure risks within the profession or industry
- Location of patient within the work environment
Material
safety data (MSD) sheets obtained from the patient’s employer
can help identify the offending agent. However, the MSD is not required by law
in work environments where the offending chemical is present in concentrations
of less than 1%. Therefore, information on a suspected agent must be obtained
directly from its manufacturer.
Identifying
high-risk agents in the work environment may require detective work by the
patient with the guidance of an allergist or other specialist. He/she will need
to gather information regarding the duration and frequency of agent exposure,
concentration of exposure, preventive measures used in the workplace (e.g.,
masks, ventilation methods, air cleaners, etc.), and location of the worker in
relation to agent exposure. These bits of information may offer clues in
detecting the presence of OA.
In
the development of OA, the occurrence of symptoms of allergic rhinitis and
conjunctivitis in the workplace often precede chest symptoms, especially when
HMW agents are involved (e.g., animal protein, grains). Workers with OA
frequently notice that chest symptoms begin early in their shift, progress in
severity during the shift, and later extend into the hours after the shift has
ended. Improvement in asthma symptoms when not at work is suggestive of OA, but
not conclusive.
In
the early stages of OA, symptoms usually resolve during weekends and holidays.
However, with continued exposure to the offending agent, the disease process
and symptoms become chronic, often persisting outside of the workplace.
For
many patients with longstanding OA, symptoms may not resolve even when the
patient discontinues work completely and is no longer exposed to the allergen.
Therefore, early detection of OA and removal of the individual from the
workplace before permanent changes occur may prevent chronic lung symptoms. It
has been reported that early intervention may result in resolution of asthma
symptoms in one third or more of OA patients.
Agent
exposure history may not always be obvious. For example, a bookkeeper in an
office connected to a warehouse or factory may be exposed to high levels of an
allergen or irritant via a common ventilation system. Therefore, such a
clerical worker may develop OA symptoms without awareness of his or her
exposure to a high-risk agent.
In
contrast, awareness of high-risk occupational exposure to agents with the
potential to cause OA (see Tables 1 and 2) will help the physician reach an
early diagnosis in the development of OA symptoms. This is no simple matter
since there are more than 400 known sensitizers or irritants which can cause
asthma in the workplace. One compilation of these triggers can be found at the
following web address: www.remcomp.fr/asmanet/asmapro/agents.htm#start.
About
10% of adult workers with a prior diagnosis of asthma will experience a
worsening of their asthma symptoms in the workplace. Such asthma symptoms may
be due to either non-specific air pollution irritating a hyperreactive airway
or result from allergic sensitivity to the presence of a specific airborne
allergen or agent.
E. Typical onset of OA
For those exposed to HMW allergens, allergy symptoms such as conjunctivitis and rhinitis often precede or accompany the development of coughing, wheezing or dyspnea in cases of OA. The diagnosis may be complicated when exposure to a workplace allergen is intermittent or the patient has a history of asthma and airway hyperreactivity prior to beginning employment. In this latter instance, workplace exposure to non-specific pollution can trigger underlying asthma. On the other hand, the patient can have symptoms resulting from a workplace inhaled allergen, either as a result of a newly acquired sensitization or from prior sensitization.
For those exposed to HMW allergens, allergy symptoms such as conjunctivitis and rhinitis often precede or accompany the development of coughing, wheezing or dyspnea in cases of OA. The diagnosis may be complicated when exposure to a workplace allergen is intermittent or the patient has a history of asthma and airway hyperreactivity prior to beginning employment. In this latter instance, workplace exposure to non-specific pollution can trigger underlying asthma. On the other hand, the patient can have symptoms resulting from a workplace inhaled allergen, either as a result of a newly acquired sensitization or from prior sensitization.
The
latency period for sensitization to a workplace allergen varies with the type
of allergen inhaled. For example, the latency period is generally shorter with
exposure to LMW substances (e.g., isocyanates) and longer with HMW substances
(e.g., flour, animal protein). As discussed earlier, the latency period may
persist for years with HMW sensitization.
F.
Diagnosis of OA
Occupational asthma
diagnosis is based on:
1) History of asthma-related symptoms in the workplace
2) Pulmonary function tests
1) History of asthma-related symptoms in the workplace
2) Pulmonary function tests
A
pulmonary function test performed during or after work that demonstrates an
obstructive pattern with or without significant reversibility supports the
diagnosis of OA.
If spirometric pulmonary
functions do not clearly support the diagnosis of OA, then a methacholine
challenge may be necessary. A positive methacholine challenge will demonstrate
the presence of airway hyperreactivity supporting the diagnosis of OA. In
contrast, a negative methacholine challenge rules out the diagnosis of OA.
These objective clinical studies may aid in creating solid documentation
supporting the diagnosis of OA and the need for modification of the workplace
environment with regard to agent exposure. These studies may also be necessary
for disability claims.
An agent-specific bronchoprovocation challenge with a suspected workplace agent is usually not necessary and should only be carried out in specialized laboratories with experienced personnel. Such centers may be found at Johns Hopkins University Hospital in Maryland, The National Institutes of Health in Maryland, and National Jewish Health Center in Denver, Colorado, and the College of Medicine at the University of Cincinnati, among others.
An agent-specific bronchoprovocation challenge with a suspected workplace agent is usually not necessary and should only be carried out in specialized laboratories with experienced personnel. Such centers may be found at Johns Hopkins University Hospital in Maryland, The National Institutes of Health in Maryland, and National Jewish Health Center in Denver, Colorado, and the College of Medicine at the University of Cincinnati, among others.
Inhalational
challenges to specific agents should be performed in a laboratory equipped to
deliver precisely measured doses of the suspected agent in order to create a
dose response curve. The challenge begins with a very tiny dose in order to
avoid producing an irritant reaction or a serious flare of asthma symptoms.
Specialized equipment—including a dosimeter (which precisely measures the dose
of allergen to be inhaled) and an occupational challenge chamber—are used to
quantify individual doses and provide a safe challenge area for both the
patient and the testing personnel. Bronchoprovocation tests with allergens or
workplace chemicals can result in significant broncho-pulmonary reactions
leading to hospitalization and serious complications. Since most presentations
of OA can be diagnosed accurately by combining history, serial pulmonary
functions, allergy tests and/or evidence of sputum eosinophilia, the risks and
additional benefits of bronchial provocation testing need to be carefully
weighed. Finally, allergy skin testing can also be particularly valuable in
detecting sensitivity to a HMW allergen in the workplace.
G. Objective studies
• Peak flow expiratory rate—Serial measurements of peak flow rates can be performed on a regular basis before, during and after work, 4-6x per day over a few weeks. This should be done similarly for a period when not at work. In OA, peak flows will trend downward during the workday, often improving by the following morning, on weekends, and on vacation. This is not a specific test identifying the cause, but it may help support the diagnosis by demonstrating airway obstruction related to workplace exposure. However, a malingering patient can manipulate these studies.
• Peak flow expiratory rate—Serial measurements of peak flow rates can be performed on a regular basis before, during and after work, 4-6x per day over a few weeks. This should be done similarly for a period when not at work. In OA, peak flows will trend downward during the workday, often improving by the following morning, on weekends, and on vacation. This is not a specific test identifying the cause, but it may help support the diagnosis by demonstrating airway obstruction related to workplace exposure. However, a malingering patient can manipulate these studies.
• Spirometry—Recording
the FEV on workdays and non-workdays is a standard objective study that can
confirm the presence of asthma in the workplace. This test will not identify
the specific agent, but it can support that asthma symptoms are occurring in
the workplace. Although the FEV is the most commonly used spirometric
measurement, the FEF25-75 is actually a more
sensitive measurement and less susceptible to patient manipulation. Another
important advantage of measurement by spirometry versus peak flow measurement
is that it is difficult, if not impossible, for the patient to manipulate the
results without a skilled physician detecting such an attempt.
• Testing for airway hyperreactivity—Another
objective method for identifying changes in the airway induced by workplace
exposure to an allergen or chemical is demonstrating the presence or increase
in bronchial hyperresponsiveness with a methacholine challenge. This study can
be performed at the end of the work period and at the end of a period away from
work. A decrease by 50% or more in the amount of methacholine required to
induce a 20% drop in FEV following work would support the diagnosis of OA by
revealing an increase in airway hyperreactivity.
In
contrast, a lack of bronchial hyper-responsiveness when the subject is at work
with asthma-like symptoms virtually excludes the diagnosis of OA. However, a
negative methacholine challenge when the patient is not at work and
asymptomatic does not rule out OA.
• Allergy
skin testing—Allergy skin test antigens are not available for
documenting hypersensitivity to many occupational agents, since many are of low
molecular weight and therefore unsuitable for skin testing. Allergy extracts
suitable for skin testing can be developed for some HMW antigens, such as
animal dander, insect parts, and plant proteins. While a positive skin test
would support the presence of IgE-mediated sensitization, in order to confirm
an OA diagnosis, there must also be a concomitant history of asthma symptoms
and pulmonary functions demonstrating obstruction and airway hypersensitivity.
However, a negative allergy skin test with suspected HMW allergens (egg, flour
or enzymes) probably rules out that those specific antigens are a cause of OA
symptoms.
• Specific
agent bronchoprovocation challenge—Patients who have asthma symptoms in
the workplace along with normal pulmonary functions in the workplace, negative
methacholine challenges, and eosinophil-free sputum are unlikely to have
occupational asthma as a cause of their symptoms. However, one can finalize a
questionable diagnosis with a specific agent bronchoprovocation challenge. A
negative challenge clearly rules out the presence of OA under these
circumstances.
When the diagnosis of OA is
suspected and yet not clearly defined, specific bronchoprovocation inhalation
testing may be required to objectively finalize the diagnosis. The use of HMW
agents in a bronchial challenge can be carried out in a single day because the
reaction is immediate (IgE mediated). In contrast, LMW agents can induce a
non-immediate or late response and daily challenges of increasing doses on
subsequent days is often required to elicit a response.
In addition to spirometry, demonstration of bronchial hyperresponsiveness at the end of each day of the challenge and/or demonstration of eosinophils in sputum, or an increase in exhaled nitric oxide following the challenge adds support for the diagnosis of OA caused by the specific agent used in the challenge.
In addition to spirometry, demonstration of bronchial hyperresponsiveness at the end of each day of the challenge and/or demonstration of eosinophils in sputum, or an increase in exhaled nitric oxide following the challenge adds support for the diagnosis of OA caused by the specific agent used in the challenge.
In
asymptomatic workers, a positive methacholine challenge or presence of
eosinophils in sputum after antigen exposure may predict the onset of
occupational asthma and allow for an early and sensitive marker for the
potential development of occupational asthma.
• Chest
x-ray—Will either be normal or reveal signs of asthma such as air
trapping in patients with OA. The x-ray or CT scan of the chest in OA will not
reveal signs of fibrosis, while the presence of fibrosis is more typical of
hypersensitivity pneumonitis and other chronic occupational lung diseases
associated with interstitial pulmonary damage.
• Laboratory
studies—In allergy-induced occupational asthma, the eosinophil count
can be elevated in the blood and/or sputum. A RAST assay/Immunocap may be
positive for one sensitized to a HMW allergen.
H.
Common workplace allergens
Examples of HMW agents
causing OA:
• Animal protein (animal lab researchers, veterinarians)
• Animal protein (animal lab researchers, veterinarians)
•
Flour and grains - Cereals (e.g., wheat flour, soya dust used in baking),
enzymes (amylase, cellulose), yeast, and storage mites.
• Latex (healthcare
workers, lab workers)
Airborne latex allergens are often associated with the use of latex gloves. Sensitization to any of several different latex allergens may be involved. Aerosolization of latex often results from latex adhering to glove powder. Frequent changes of gloves will increase aerosolization and exposure to latex.
Airborne latex allergens are often associated with the use of latex gloves. Sensitization to any of several different latex allergens may be involved. Aerosolization of latex often results from latex adhering to glove powder. Frequent changes of gloves will increase aerosolization and exposure to latex.
Examples of LMW agents
causing OA:
• Diisocyanates (automobile painters, plastics manufacturers)
Among the diisocyanates, toluenediisocyanate (TDI) is the most commercially used of these sensitizers. It is often used in the manufacture of automobiles, foam rubber, and molds for insulation. Hexamethylene diisocyanate (HDI) is used in spray paints. This agent can cause OA, RADS, and even hypersensitivity pneumonitis. These chemicals are strong sensitizers and can cause OA in up to 10% of exposed workers.
• Diisocyanates (automobile painters, plastics manufacturers)
Among the diisocyanates, toluenediisocyanate (TDI) is the most commercially used of these sensitizers. It is often used in the manufacture of automobiles, foam rubber, and molds for insulation. Hexamethylene diisocyanate (HDI) is used in spray paints. This agent can cause OA, RADS, and even hypersensitivity pneumonitis. These chemicals are strong sensitizers and can cause OA in up to 10% of exposed workers.
• Wood dust (loggers,
sawmill workers, carpenters)
Exposure to wood dust can cause OA as well as hypersensitivity pneumonitis. A common cause of OA in the Pacific northwestern United States is exposure to western red cedar dust, due to its content of plicatic acid. Plicatic acid as a hapten (LMW agent) can conjugate with body proteins to induce the production of specific IgE which is found in only 20% of exposed patients who developed OA. It appears that cellular hypersensitivity plays a more prominent role in sensitization than does IgE. Sensitization to western red cedar workers occurs in 5 -10% of this population of workers.
Exposure to wood dust can cause OA as well as hypersensitivity pneumonitis. A common cause of OA in the Pacific northwestern United States is exposure to western red cedar dust, due to its content of plicatic acid. Plicatic acid as a hapten (LMW agent) can conjugate with body proteins to induce the production of specific IgE which is found in only 20% of exposed patients who developed OA. It appears that cellular hypersensitivity plays a more prominent role in sensitization than does IgE. Sensitization to western red cedar workers occurs in 5 -10% of this population of workers.
Occupational
asthma must be differentiated from other occupational lung diseases
which can also be immunologically mediated, but by a different mechanism than
that seen in OA. Further, unlike OA in which the bronchi are primarily
affected, other occupational lung diseases usually involve the parenchyma of
the lung.
I.
Three different types of occupational lung disease
Occupational lung disease includes:
- Occupational asthma
- Hypersensitivity pneumonitis
- Pneumoconiosis
- Occupational asthma
- Hypersensitivity pneumonitis
- Pneumoconiosis
Each of these three
occupational lung diseases differs either in the site of lung damage or the
nature of reaction causing the damage. Yet, they share a common element in that
they all result from inhaling allergens, chemicals, or mineral dust in the
workplace.
Occupational asthma is a disease of the bronchial tree resulting in an obstructive pattern on pulmonary function tests. OA is usually associated with symptoms of wheezing, coughing and shortness of breath. Early in the development of OA, symptoms may respond to bronchodilators and the pulmonary function test may reveal partial or total reversibility. In contrast, the two other occupational lung diseases involve damage to the parenchyma of the lung (interstitial tissue) resulting in shortness of breath without wheezing and eventually develop a restrictive pattern on pulmonary function tests.
Occupational asthma is a disease of the bronchial tree resulting in an obstructive pattern on pulmonary function tests. OA is usually associated with symptoms of wheezing, coughing and shortness of breath. Early in the development of OA, symptoms may respond to bronchodilators and the pulmonary function test may reveal partial or total reversibility. In contrast, the two other occupational lung diseases involve damage to the parenchyma of the lung (interstitial tissue) resulting in shortness of breath without wheezing and eventually develop a restrictive pattern on pulmonary function tests.
　
Table 3:
Causes of hypersensitivity related to specific occupations
Causes of hypersensitivity related to specific occupations
J. Treatment
The management of OA consists of limiting the
worker’s exposure to the offending agent to amounts that will not induce
disease. A number of approaches can be taken. For example, the worker can be
moved to another location within the workplace where little or no offending
agent is present. Other techniques include using effective equipment to remove
dust and vapor exposure and improving workplace ventilation so that frequent
air exchange limits agent accumulation. Evaluation of the workplace should be
conducted by a trained industrial hygienist who can measure the degree of agent
exposure. It is important to remember that levels of exposure below the legal
limits are based on toxicity studies and, therefore, the presence of even tiny
amounts of sensitizing agents may still cause immunologic reactions. Face masks
of the filtering type are not especially efficient or well-tolerated. In
contrast, a compressor with a HEPA filter creating a positive air flow through
a mask or head piece can markedly diminish inhalation of airborne dust and
therefore may be helpful when working with HMW agents.
Ideally, the work environment should be designed to limit the concentration of potential sensitizers to safe levels. Since this may be impractical in many manufacturing processes, even in a carefully monitored facility, recommended thresholds may be exceeded. Therefore, total avoidance of the workplace may be the only alternative for some sufferers of OA and may entail retraining and reassigning the employee(s) to another job free of potential exposure to the suspected agent.
Pharmacologic management of OA is rarely helpful in the presence of continued exposure on a chronic basis. Asthma resulting from contact with occupational exposures responds to therapeutic agents such as β-adrenergic agonists, cromolyn sodium, and steroids. As exposure continues, sensitivity may increase, rendering medication less effective.
Immunotherapy has been used with various occupational allergens causing asthma, including treatment of laboratory animal workers, bakers, and oyster gatherers, with reported success.
Ideally, the work environment should be designed to limit the concentration of potential sensitizers to safe levels. Since this may be impractical in many manufacturing processes, even in a carefully monitored facility, recommended thresholds may be exceeded. Therefore, total avoidance of the workplace may be the only alternative for some sufferers of OA and may entail retraining and reassigning the employee(s) to another job free of potential exposure to the suspected agent.
Pharmacologic management of OA is rarely helpful in the presence of continued exposure on a chronic basis. Asthma resulting from contact with occupational exposures responds to therapeutic agents such as β-adrenergic agonists, cromolyn sodium, and steroids. As exposure continues, sensitivity may increase, rendering medication less effective.
Immunotherapy has been used with various occupational allergens causing asthma, including treatment of laboratory animal workers, bakers, and oyster gatherers, with reported success.
K. Prevention
The most important principle of OA management
is prevention, rather than treatment. Educating exposed workers and managers in
high-risk industries is crucial so that affected workers can be recognized
early. Right-to-know legislation should increase awareness of occupational
asthma.
At this time, there are no pre-employment screening criteria that have been shown to be accurate in predicting the eventual appearance of OA. There is conflicting evidence as to whether HLA studies are useful in predicting isocyanate asthma or anhydride asthma. It has been reported that atopy is a predisposing factor for a worker to develop IgE-mediated disease. Further, as many as 25-50% of the work force may have allergy, but it is impractical to avoid hiring such a large portion of the potential work force when only a small number of these individuals may develop OA.
At this time, there are no pre-employment screening criteria that have been shown to be accurate in predicting the eventual appearance of OA. There is conflicting evidence as to whether HLA studies are useful in predicting isocyanate asthma or anhydride asthma. It has been reported that atopy is a predisposing factor for a worker to develop IgE-mediated disease. Further, as many as 25-50% of the work force may have allergy, but it is impractical to avoid hiring such a large portion of the potential work force when only a small number of these individuals may develop OA.
L. Prognosis
Many workers with
occupational asthma do not completely recover, even though they have been
removed from exposure to a sensitizing agent for years. An unfavorable
prognosis has been reported to be associated with a persistent, high level of
specific IgE to the suspected agent, long duration of symptoms (>1 to 2 years),
abnormal pulmonary function test results, and a high degree of airway
hyperreactivity. The obvious conclusion based on these observations is that
early diagnosis and removal from exposure are requisites for the goal of
complete recovery. In workers who remain exposed to offending agents after
being diagnosed with OA, further deterioration of lung function and increased
airway hyperreactivity are likely. It should be understood that
life-threatening attacks and even deaths have been reported with continued exposure
after diagnosis of OA.
POSTED BY ATTORNEY RENE G. GARCIA:
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