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Evidence Ratings: Practice recommendations in PIER are given a strength of evidence rating (A,B,C):
= Preponderance of data supporting this statement is derived from high quality studies with minimal bias, including treatment issues (randomized
trials and systematic reviews or meta-analyses), diagnostic issues (cohort studies with appropriate reference standards), and prognosis issues
(observational studies with adequate controlling for confounders).
= The preponderance of data supporting this statement is derived from suboptimal quality studies, such as observational data for treatment issue
or others not meeting the criteria above.
= The preponderance of data supporting this statement is derived from non-experimental evidence such as case series or from expert opinion.
Disclosures: Craig S. Glazer, MD, MSPH, current author of this module, has no financial relationships with pharmaceutical companies, biomedical device manufacturers, or health-care related organizations. Deborah Korenstein, MD, FACP, Editor-in-Chief, PIER, has no financial relationships with
pharmaceutical companies, biomedical device manufacturers, or health-care related organizations. Richard B. Lynn, MD, FACP, Editor, PIER, has no
financial relationships with pharmaceutical companies, biomedical device manufacturers, or health-care related organizations.
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Take primary preventive measures and report patients with occupational asthma to surveillance programs to prevent progressive disease and additional cases.
1.1 Take measures to prevent occupational asthma.
Recommendations
• Take primary preventive measures that focus on reducing exposures:
Eliminate potential sensitizers or substitute other substances with lower risk profiles
Implement engineering controls, including improved ventilation or process modification, or both, that
would reduce exposure levels
Consider administrative controls to limit the number of exposed workers or their time in exposure, and improve worker education regarding risks and alarm symptoms for which they should seek medical attention
Provide respiratory protection when the above options fail to eliminate exposure
• Take the following measures once occupational asthma has been identified:
Screen other exposed workers for sensitization (when possible) or early disease
Implement a medical surveillance program. These programs typically include medical screening but also use screening data to define interventions that can reduce exposure and prevent disease
Evidence
• A 2008 guideline from the American College of Chest Physicians on the diagnosis and management
of work-related asthma recommended that work sites with potential exposures to sensitizers
implement secondary prevention, including medical surveillance (1).
• A 2005 guideline from the British Occupational Health Research Foundation on occupational asthma
emphasized the need to reduce workplace exposure as the most important factor in preventing the
development of occupational asthma (2).
• A 2012 systematic review of medical screening and surveillance in the workplace included 72
studies. Overall, the predictive value of pre-employment screening for individual risk factors was
too low to justify excluding those individuals from employment. There were few systematic studies
of medical surveillance programs, but there was some evidence that such programs may prevent
disease (3).
• A 2006 systematic review of primary prevention of latex sensitivity and occupational asthma
included eight studies, most of which were observational. The use of powder-free nonlatex gloves
appeared to reduce the incidence of latex allergy and asthma (4).
• A 2005 literature review of studies of the prevention of occupational asthma highlighted the
importance of various preventive measures in the development and prognosis of occupational
asthma. Primary prevention was effective for occupational asthma related to natural latex and
diisocyanate asthma. Secondary prevention, such as medical health surveillance, has been
effective in occupational asthma related to detergent enzymes, platinum salts, and diisocyanates.
Tertiary prevention is thought to improve the prognosis of workers who already have occupational
asthma (5).
Rationale
• Occupational asthma is a preventable illness. Identifying a case of occupational asthma is a
sentinel health event indicating an opportunity for preventive measures in the workplace.
• Examine the respiratory system, the nose, and the skin:
Look for wheezing during normal breathing, use of accessory muscles of respiration, hyperexpansion of the thorax, and prolongation of forced exhalation
Examine the nose for increased nasal secretion, mucosal swelling, and nasal polyps
Examine the skin for evidence of atopic dermatitis or eczema
• See table Diagnostic Criteria for Asthma.
Evidence
• The 2007 Expert Panel 3 guidelines on asthma from the National Heart, Lung, and Blood Institute
and National Asthma Education and Prevention Program noted that a physical exam for asthma
includes the upper respiratory tract, chest, and skin, and stated that findings that increase the
likelihood of asthma include chest hyperexpansion; wheezing during normal breathing; prolonged
expiratory phase; nasal secretions, swelling, or polyps; and atopic dermatitis or eczema (12).
• A prospective study evaluated the accuracy of history and physical exam findings in 85 patients
with chronic dyspnea. Wheezing on physical exam had a PPV of 33% and an NPV of 72% for
asthma, and spirometry had a PPV of 18% and an NPV of 72% for asthma (25).
Rationale
• The presence of certain physical findings helps confirm the diagnosis of asthma.
Comments
• Wheezing during forced exhalation is not a reliable indicator of airflow limitation. Wheezing may be
undetectable in mild asthma, very severe asthma, or between exacerbations. In general,
physicians have limited ability in assessing the degree of airflow limitation or to predict whether the
obstruction is reversible.
3.3 Use spirometry to confirm a diagnosis of asthma.
Recommendations
• Obtain spirometry to measure inspiratory and expiratory flow curves and establish FEV1 before and
after bronchodilators.
Obtain baseline spirometry to assess the degree of airway obstruction and the severity of the illness
Obtain postbronchodilator FEV1 to confirm the diagnosis
Note that reversible obstruction confirms asthma
• If spirometry is normal, then perform nonspecific airway responsiveness testing (e.g.,
methacholine challenge) to document airway hyperresponsiveness.
• High-value care: Do not diagnose or manage asthma without spirometry.
Evidence
• The 2007 Expert Panel 3 guidelines on asthma from the National Heart, Lung, and Blood Institute
and National Asthma Education and Prevention Program stated that spirometry is essential for the
diagnosis and treatment of asthma (12).
• A 1999 American Thoracic Society guideline discussed the indications for methacholine challenge
testing and described the details of its performance (26).
Rationale
• Confirming bronchial hyperresponsiveness or reversible airflow obstruction is crucial for objective
confirmation of asthma.
• An empiric therapeutic trial with asthma therapy may confound the evaluation for occupational
asthma and is discouraged when occupational asthma is a consideration.
wheezing was 11.46% (CI, 9.87% to 13.05%). The main industries at risk for work-related asthma
and wheeze included the entertainment industry, agriculture, forestry, fishing, construction,
electrical machinery repair services, and lodging places. The population attributable risk for work-
related wheezing was 28.5% (17).
• A large population-based study in Finland combined data from individuals with persistent asthma
with population census data to estimate the attributable fraction of work in adult-onset persistent
asthma. The attributable fraction of occupation in males was 29% (CI, 25% to 33%) and in
females was 17% (CI, 15% to 19%). The risk increased especially in agricultural, manufacturing,
and service work. Among manufacturing jobs, high risks were recorded in food and beverage work
and in smelting, metallurgical, foundry, painting, and lacquering work. Among service workers,
high risks were recorded in hygiene and beauty treatment, pressing, dry cleaning, and laundering
work (18).
• A prospective study evaluated the accuracy of specific questions for the diagnosis of occupational
asthma in 212 patients who underwent challenge testing. Overall, 72 patients (34%) were
diagnosed with occupational asthma. In the multivariate analysis, symptoms at work that were
independently associated with occupational asthma included wheezing (OR, 3.39 [CI, 1.43 to 8.0]),
nasal itching (OR, 3.7 [CI, 1.8 to 7.8]), and eye itching (OR, 2.37 [CI, 1.06 to 5.30]). Loss of voice
at work made occupational asthma less likely (OR, 0.39 [CI, 0.18 to 0.86]) (19).
• A cross-sectional study assessed the prevalence of work-related asthma in 17,637 adults with
asthma and a history of employment from a national sample of U.S. residents. Overall, 9.7% had
work-related asthma. Compared with patients with non-work-related asthma, those with work-
related asthma had lower household income (OR, 2.2 [CI, 1.6 to 3.1] for the lowest income group
compared with the highest income group) and were more likely to be 45 to 64 years old (OR, 1.9
[CI, 1.5 to 2.4] compared with those aged 18 to 44 years) (27).
Rationale
• The occupational history taken by an experienced clinician or by questionnaire either given by an
interviewer or self-administered is a sensitive tool.
• Workplace exposure may worsen bronchial asthma or aggravate subclinical or mild asthma.
• Work-related asthma accounts for a significant portion of adult asthma.
• There are important non-drug interventions for work-related asthma.
Comments
• Several different reporting systems demonstrate incidences of occupational asthma ranging from 1
to 18/100,000 per year (28; 29; 18).
3.5 In patients whose asthma symptoms are related to their work environments, ask about specific exposures.
Recommendations
• Ask patients with apparent occupational asthma about specific exposures.
Focus on exposures at the time the disease began or initially started to worsen
Assess the duration, concentration, frequency, and peak concentration of any exposures
Ask the worker to obtain the material safety data sheets kept on file by the employer, and discuss all the agents to which the worker may be exposed, including data on composition, physical characteristics, and health-related information
• Note that agents that can cause occupational asthma include
Smoke, wood dust, acrylates, and paper dust
Solvents, isocyanates, aldehydes, glues, epoxy resins, and paint
Ammonia, bleach, acids, bases, cleaning materials, metalworking fluid, and oxidizers
• Classify the disease type in patients with occupational asthma:
Ask about a latent period, defined as the period between the onset of exposure and the onset of disease
Note that immunologic (sensitizer-induced) occupational asthma is characterized by the presence of a latent period and that occupational asthma related to an irritant is characterized by a lack of a latent period
Rule out other causes of airway symptoms
• Classify patients with sensitizer-induced occupational asthma according to the molecular weight of
the culprit antigen and the pattern of bronchial reactivity:
Note that low-molecular-weight antigens are less than 5000 kilodaltons and are typically chemicals, and that most do not induce detectable IgE responses
Note that high-molecular-weight antigens are typically proteins of animal, plant, or microbial origin, and
typically induce detectable IgE responses
Determine the pattern of bronchial reactivity:
o Immediate: usually within 1 hour of exposure (or of entering the workplace)
o Isolated late: patients develop bronchial hyperreactivity and symptoms 6 to 8 hours after exposure, generally toward the end of work shifts or in the evening of days worked
o Dual: patients in this group manifest both responses
• In patients with occupational asthma related to an irritant,
Assess whether the patient meets the criteria for RADS (nonimmunological asthma without a latent period), which is found with
o A documented absence of preceding respiratory complaints
o The onset of symptoms after a single specific high exposure
o Exposure to a particular irritating gas, fume, or vapor that was present in high concentrations
o Onset of symptoms occurring within 24 hours after the exposure
o Presence and persistence of nonspecific bronchial hyperresponsiveness (methacholine or histamine challenge test) following the exposure
o Other types of pulmonary diseases ruled out
Classify patients with longer-term irritant exposures or with symptom onset after 24 hours as having irritant-induced asthma or not-so-sudden irritant-induced asthma.
• See the list of agents that can cause occupational asthma, from the UK Health and Safety
Executive.
• See table Select Agents Associated with Occupational Asthma with or without a Latency Period.
• See table Select Agents Reported to Be Associated with Reactive Airway Dysfunction Syndrome.
Evidence
• A 2008 guideline from the American College of Chest Physicians on the diagnosis and management
of work-related asthma presented diagnostic criteria for RADS and described patterns of response
to irritant exposure (1).
• A retrospective study of 86 asthmatic patients showed that 63% had irritant-induced asthma with
two distinct clinical presentations: sudden and not-so-sudden onset. Eighty-eight percent of the
not-so-sudden group showed an atopic-allergic status. Sixteen patients with atopy and presumed
new-onset asthma had preexistent asthma. Preexisting allergic-atopic status or preexisting asthma
were significant contributors to the pathogenesis of not-so-sudden irritant-induced asthma (34).
• In a long-term follow-up study of pulmonary function, quality of life, and psychological status after
an average of 13.6 years (±5.2 years) from the time of acute irritant exposure, all 35 subjects who
had filed for compensation for work-related injuries with the medicolegal agency in Quebec still
reported respiratory symptoms, and 68% were on inhaled steroids. Measures of quality of life and
psychological status indicated that irritant-induced asthma can be a significant cause of long-term
impairment and disability. Subjects with acute irritant-induced asthma were no different from those
with allergic occupational asthma in terms of pulmonary function and markers of inflammation
(35).
• A follow-up study of 20 patients with irritant-induced asthma due to repeated exposure to chlorine
found no change in mean FEV1 after 2.5 years of follow-up; 33% of patients had improved airway
hyperresponsiveness (36).
• A 2013 narrative review discussed a diagnostic approach to suspected work-related asthma (37).
Rationale
• It is important to make the distinction between immunologically induced occupational asthma
(which occurs after a period of sensitization) and irritant-induced occupational asthma (which
occurs rapidly after exposure without sensitization).
• RADS is defined as asthma occurring after a single or multiple exposures to high levels of an
irritating gas, vapor, fume, or smoke; there is no objective test for the diagnosis and no recurrence
of symptoms after reexposure.
Comments
• The latent period can range from months to decades but is usually between 2 and 5 years in
duration.
• In individuals with significant exposure, acute irritant-induced asthma can be a long-term
impairment that may require chronic medical care.
• At the World Trade Center site where rescue workers experienced massive exposure to airborne
particulates, the development and persistence of hyperreactivity and RADS were associated
strongly and independently with exposure intensity. Hyperreactivity demonstrated shortly after
exposure predicted RADS at 6 months in highly exposed workers (1).
• Most high-molecular-weight occupational allergens and some low-molecular-weight occupational
allergens mediate asthma at least partly by a type 1 IgE-dependent mechanism, which results in
immediate symptoms, occurring within minutes but resolving usually within 1 hour; however, some
workers may have an isolated late phase (late-phase asthma) occurring 4 to 6 hours after
exposure or a dual-phase response where the immediate reaction is followed by the late-phase
response. Isolated late responses are more common with low-molecular-weight (i.e., chemical)
antigens.
• Long-term cure rates appear to be similar for acute irritant-induced asthma (17%) and allergic
occupational asthma (27%) (35; 38).
3.7 Perform confirmatory testing using serial measures of pulmonary
function, and consider immunologic testing.
Recommendations
• Measure serial PEFR in patients with occupational asthma who remain in the workplace:
Measure PEFR four times daily for 2 weeks at work and four times daily for 2 weeks outside of work
Instruct the patient to record rescue inhaler use and precipitating exposures
Recognize that patients may not accurately record or report PEFR readings obtained with portable devices (e.g., Wright mini peak flow meter); therefore, whenever possible, use an electronic device that records
PEFR or FEV1 values on a memory chip
Do not change medical therapy during the testing period
Note that positive patterns will show reduced flow or increased diurnal variability in flows, or both, when times at work are compared with times away from work in patients with sensitizer-induced occupational asthma
• Consider serial methacholine or histamine challenge testing if serial PEFR measurements cannot be
obtained or are nondiagnostic:
Do the test on the last working day of the work week and after the patient has been exposed at work for at least 2 consecutive weeks, then repeat after at least 2 weeks away from the exposure
Discontinue bronchodilators, anticholinergic medications, theophyllines, and antihistamines for 24 to 48 hours
Instruct patients to refrain from caffeine-containing beverages for 6 hours and from smoking for 2 hours before testing if methacholine is the agent used
Note that a 3 dilution or greater improvement in the PC20 when away from exposure is consistent with sensitizer-induced occupational asthma
• Consider immunologic testing in patients with suspected sensitizer-induced occupational asthma
without a clearly identified agent of exposure using one of the following:
Skin tests
Immunoassays (RAST, ELISA tests)
• Refer to a specialist for immunologic testing.
• See table Laboratory and Other Studies for Occupational Asthma.
• See table Indications for Peak Flow Monitoring.
• See table Proper Technique for Recording Portable Peak Flow Rate Recordings.
Evidence
• A 2012 guideline from the British Thoracic Society on the management of occupational asthma
recommended measuring serial PEFR at least four times per day for at least 3 consecutive weeks
during a 2-week period outside of work followed by a period after return to work. Serial PEFR
measurement had a sensitivity of 64% and a specificity of 77%. Immunologic testing is not
specific, and serial measures of bronchial responsiveness are neither sensitive nor specific (30).
• A 2008 guideline from the American College of Chest Physicians on the diagnosis and management
of work-related asthma recommended measuring PEFR four times daily for 2 weeks during work
and four times daily outside of work in all patients with suspected occupational asthma. The
guideline recommended that patients with suspected sensitizer-induced occupational asthma
undergo immunologic testing if available (1).
• A 2005 AHRQ systematic evidence report on the diagnosis and management of work-related
asthma included 61 studies assessing the diagnostic accuracy of testing, generally compared with
specific inhalational challenges. A single nonspecific bronchoprovocational challenge test had a
pooled sensitivity of 66.7% and a specificity of 63.9%, and testing for high-molecular-weight
antigens had a pooled sensitivity of 79.3% and a specificity of 59.3%. Skin-prick testing had a
sensitivity and a specificity of 72.9% and 86.2%, respectively, in studies of low-molecular-weight
exposures; 80.6% and 59.6%, respectively, in studies of high-molecular-weight exposures; and
85.1% and 65.2%, respectively, in studies of various exposures. Serum IgE testing had a
sensitivity and a specificity of 31.2% and 88.9%, respectively, for low-molecular-weight agents;
73.3% and 79.0%, respectively, for high-molecular-weight agents; and 85.1% and 61.2%,
respectively, in studies of various agents (39).
• A prospective study evaluated the accuracy of serial PEFR measurements and serial FEV1
measurement in 20 patients with suspected occupational asthma, using inhalation challenge testing
as the reference standard. The sensitivity of flow rate recordings varied based on interpreter
between 73% and 82%, with a specificity between 89% and 100%. The sensitivity of FEV1 varied
between 45% and 55%, and the specificity varied between 56% and 100% (40).
• A prospective study using specific inhalational challenge test results to evaluate PEFR showed that
the best index for comparing results of PEFR with specific inhalational challenge testing was the
Consider consultation for diagnosis in all patients suspected of having occupational asthma and for management in all patients with occupational asthma.
4.1 Consider consultation with a pulmonologist or allergist to help establish
the diagnosis.
Recommendations
• Refer patients suspected of having occupational asthma to a pulmonologist or an allergist for
assistance in the identification of specific etiologic agents and management.
• Recognize that the investigation and diagnosis of occupational asthma include testing for
nonspecific bronchial hyperresponsiveness and peak flow monitoring.
Evidence
• Consensus.
Rationale
• Patients require confirmation of a history that suggests that an occupational or environmental
inhalant is provocative or contributory to asthma.
4.2 Consider referring all patients with occupational asthma to a
pulmonologist or allergist for management.
Recommendations
• Obtain consultation with a specialist (pulmonologist, occupational medicine specialist, allergist) to
improve management in patients with poorly controlled symptoms.
• Consider referral to an allergist for desensitization therapy.
Evidence
• A 2012 guideline from the British Thoracic Society on the management of occupational asthma
recommended that patients with confirmed or suspected occupational asthma be followed at a
specialist center (30).
• A 1996 narrative review of the role of experts in asthma care noted that “expert-based” care
systems are associated with better outcomes (48).
Rationale
• A specialist is experienced in the diagnosis, treatment, or intervention required in the work
environment and in managing patients over a period of time or comanaging with the primary care
provider.
• Desensitization therapy may be helpful in controlling symptoms.
Consider hospitalization for severe occupational asthma.
5.1 Hospitalize patients with severe asthma symptoms. Consider hospitalization using the same determinants as for other types of asthma.
Recommendations
• Admit patients with acute asthma to the hospital if they have
Impending respiratory arrest (admit to the intensive care unit)
Severe exacerbation (peak flow or FEV1 less than 40% of predicted or best) and incomplete or poor response to initial therapy in the emergency department
Moderate exacerbation (peak flow or FEV1 40% to 69% of predicted or best) and incomplete or poor response to initial therapy in the emergency department
• Consider hospitalization in other patients with
History of severe exacerbations or multiple intubations
Medication use at the time of the exacerbation
Poor access to medical care and medications
Inadequate support or poor home conditions
Severe psychiatric illness
Evidence
• A 2008 guideline from the American College of Chest Physicians on the diagnosis and management
of work-related asthma recommended hospitalizing patients with impending respiratory arrest and
those with mild to moderate or severe exacerbations and poor or incomplete response to
emergency department therapy (1).
Rationale
• The factors that govern the hospitalization of patients with occupational asthma are no different
After establishing the diagnosis of occupational asthma, develop a strategy with the patient to reduce or completely avoid exposure to the cause. Consider the use of inhaled steroids and other drugs.
6.1 For patients with sensitizer-induced occupational asthma, plan with the
patient to ensure complete removal from the source of exposure.
Recommendations
• For patients with sensitizer-induced occupational asthma, advise avoidance of all further exposure
to the causative agent through
Substitution or elimination of the causative agent from the work site
Transfer to a different position with the same employer
Job change
Evidence
• A 2012 guideline from the British Thoracic Society on the management of occupational asthma
recommended complete removal of the patient from the exposure (30).
• A 2008 guideline from the American College of Chest Physicians on the diagnosis and management
of work-related asthma recommended removing patients with sensitizer-induced occupational
asthma from the environment, and reducing exposure and optimizing asthma therapy for those
with irritant-induced occupational asthma (1).
• A 2011 systematic review of exposure elimination or reduction for patients with occupational
asthma included 14 studies. Overall, reduction in exposure was associated with a lower rates of
asthma symptom improvement (OR, 0.16 [CI, 0.03 to 0.91]) and recovery (OR, 0.30 [CI, 0.11 to
0.84]) compared with complete exposure avoidance (49).
• A 2005 AHRQ systematic evidence report on the diagnosis and management of work-related
asthma found that workers with continued exposure generally experienced further deterioration in
FEV1 and that those for whom the exposure was eliminated generally had improvements in FEV1
(39).
Rationale
• Most patients with occupational asthma improve or stabilize with exposure removal. Some are
cured, but most will not completely recover after cessation of exposure and will worsen if exposure
is continued.
Comments
• Significant prognostic factors include both the duration of symptoms and the duration of exposure;
death has been reported with persistent exposure.
• Studies show that exposure reduction is not adequate for sensitizer-induced occupational asthma.
6.2 Reduce exposures for patients with irritant-induced occupational asthma or work-exacerbated asthma through workplace modifications.
Recommendations
• For patients with irritant-induced occupational asthma or work-exacerbated asthma, reduce
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Occupational asthma New diagnosis of asthma related to exposure in the workplace. Characterized by worsening of
symptoms during or after exposure to work environment and can be related to an irritant or an
identifiable allergen.
Associated with a wide variety of exposures
Asthma (non-work-related) Reactive airway disease unrelated to work environment. Initial diagnostic testing is the same as for
occupational asthma
Work-exacerbated asthma Preexisting asthma worsened by the work environment. Differentiated from occupational asthma based
on history
Bronchiolitis obliterans Obliterative fibrotic disease of the terminal bronchioles that can follow exposure to toxic irritants,
gases, or fumes.
Associated with ammonia, chlorine, hydrogen sulfide, nitrogen dioxide, phosgene
Hypersensitivity pneumonitis Immunologic inflammatory reaction involving the lung interstitium, terminal bronchioles, and alveoli
that is due to hypersensitivity to antigenic organic dusts encountered in some occupations.
Can also occur after exposure to certain chemicals
Metal fume fever/polymer fume fever Flulike illness occurring up to 12 hours after exposure to fumes from metal oxides (or fumes from heated fluorocarbons [Teflon]).
Symptoms resolve within 36 hours (weekends and vacations). Symptoms include fever (38.9°C
[102°F] to 40.0°C [104°F]), marked chest pains, muscle ache, and extreme weakness, sometimes with
a metallic taste in the mouth. Leukocytosis and normal chest x-ray are characteristic. Repeated attacks
are common
Byssinosis Chest tightness that develops on first returning to work in cotton or flax workers. Associated with a
decline in ventilatory capacity over the first work shift of the week
Organic dust toxic syndrome Flulike illness with symptoms that include fever, myalgia, chest tightness, cough, headache, and
dyspnea, resulting from inhalation of organic dusts or aerosols containing large quantities of
heart failure; HPA = hypothalamic-pituitary-adrenal; IgE = immunoglobulin E; IM = intramuscular; INR = international normalized ratio; IV = intravenous; LFT = liver function test; MDI = metered-dose
inhaler; PO = oral; prn = as needed; q12hr = every 12 hours; q4-6hr = every 4-6 hours; qd = once daily; qid = four times daily; SC = subcutaneous; tid = three times daily.
PIER provides key prescribing information for practitioners but is not intended to be a source of comprehensive drug information.
Elimination of the agent from the workplace either by substitution of the agent or a change in the process
Reduction of exposure through better local exhaust, isolation, and enclosure
Exclusion of susceptible individuals from high-risk workplaces after the preemployment examination
Secondary prevention
Early detection of disease using periodic examinations
Tertiary prevention
Prevention of permanent asthma with early recognition and removal from the source of exposure
* For patients with risk factors for occupational asthma including atopy, smoking, level of exposure, and possibly certain human leukocyte antigen class 2 genes, because these workers may be more
susceptible to the disease. Atopy may be defined as a personal history of allergic respiratory symptoms, cutaneous reactivity, or both to common environmental allergens.
Specific Symptom Patterns and Patterns of Exposure for Occupational Asthma
Respiratory symptoms that may be associated with occupational asthma include
Dyspnea
Wheezing
Dry cough
Chest tightness
Increased breathing effort
Characteristic symptom patterns include
Improvement in symptoms during vacations or days off (may take a week or more)
Initial symptoms may occur after a high level of exposure (spill)
Symptoms may be immediate (<1 minute), delayed (most commonly 2 to 8 hours after exposure), or nocturnal
Patterns of exposure
Do symptoms of asthma develop after a worker starts a new job or after new materials are introduced on a job? (A substantial period may elapse between the initial exposure and the development of
symptoms)
Do symptoms develop within minutes of specific activities or exposure at work?
Do delayed symptoms occur several hours after exposures, during the evenings of work days, or at night?
Do symptoms occur less frequently or not at all on days away from work and on vacations?
Do symptoms occur more frequently on getting to work?
Did symptoms occur initially after a high-level exposure (spill)?
A typical history, clinical features, and course must be recorded as well as a continuing regular use of asthma medication that has lasted for 6 months plus at least one of the following criteria:
A variation of more than 20% diurnal peak expiratory flow recording (reference to maximal value)
An increase of more than 15% in peak expiratory flow or FEV1 with β2 agonist
A decrease of more than 15% in peak expiratory flow or FEV1 in exercise testing