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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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Occupational Asthma View online at http://pier.acponline.org/physicians/diseases/d278/d278.html

Module Updated: 2014-05-21

CME Expiration: 2017-05-21

Author

Craig S. Glazer, MD, MSPH

Table of Contents

1. Prevention .........................................................................................................................2

2. Screening ..........................................................................................................................4

3. Diagnosis ..........................................................................................................................6

4. Consultation ......................................................................................................................16

5. Hospitalization ...................................................................................................................17

6. Therapy ............................................................................................................................18

7. Patient Counseling ..............................................................................................................22

8. Follow-up ..........................................................................................................................23

References ............................................................................................................................26

Glossary................................................................................................................................29

Tables ...................................................................................................................................30

Figures .................................................................................................................................45

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1. Prevention Top

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.

Comments

http://journal.publications.chestnet.org/article.aspx?articleid=1044851

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1741012/

http://err.ersjournals.com/content/21/124/105.long

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2092497/

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• People with a laboratory diagnosis of only atopy characterized by positive prick-test results to

common allergens probably should not be removed from their jobs but should be provided with an

individual program of medical prevention (6).

• According to NIOSH, respiratory protection is generally a less effective method of exposure

reduction than elimination, substitution, or engineering controls. Most studies of respiratory

protective devices have examined occupational asthma in circumstances in which workers have

already been sensitized to a particular agent (7). However, these devices are not always successful

in preventing occupational asthma (8).

• National occupational disease surveillance programs have been developed in the U.S. (SENSOR),

Great Britain (SWORD), and other countries (9; 10). SENSOR programs provide workers and

physicians with workplace investigations to facilitate preventive surveillance.

• In the detergent industry, process modification dramatically reduced occupational asthma, using

measures such as encapsulating enzymes, improving ventilation, and screening to detect

sensitization (11).

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2. Screening Top

Screen all patients with asthma for workplace-related asthma.

2.1 Ask all patients with asthma about occupational factors.

Recommendations

• Record occupational history in all patients with asthma.

• Ask whether other workers are similarly affected with asthma.

• Determine whether risk factors (smoking, atopy, occupational rhinitis) for the development of

occupational asthma are present.

• See table Select Agents Associated with Occupational Asthma with or without a Latency.

• See table Questionnaire: Determining Whether Asthma Symptoms Are Work-Related.

Evidence

• The 2007 Expert Panel 3 guidelines on asthma from the National Heart, Lung, and Blood Institute

and National Asthma Education and Prevention Program recommended that clinicians ask all

patients with asthma about occupational exacerbating factors (12).

• A 2003 statement from the American Thoracic Society on the occupational contribution to the

burden of airway disease reviewed the evidence regarding factors that contribute to the

pathogenesis of obstructive airway disease and reported the population attributable risk to range

from 4% to 58%, with a median value of 15% (13).

• A cross-sectional study evaluated the prevalence of occupational rhinitis among 596 individuals

with occupational asthma. Overall, 58.4% of those with occupational asthma had occupational

rhinitis (14).

• A retrospective case series described outcomes after inhalation exposure in 323 patients.

Symptoms lasting 14 or more days were reported by 6% of patients. Risk factors for persistent

symptoms included preexisting lung disease (RR, 2.4 [CI, 14 to 4.2]) and cigarette smoking (RR,

1.7 [CI, 1.3 to 2.2]) (15).

• A prospective study evaluated the prevalence of new-onset occupational asthma in a European

population and identified risk factors. Between 10% and 25% of new adult asthma was attributable

to occupational exposures; risk factors included exposure to a substance known to cause

occupational asthma (RR, 1.6 [CI, 1.1 to 2.3]), a symptomatic inhalation event (RR, 3.3 [CI, 1.0 to

11.1]), and working as a nurse (RR, 2.2 [CI, 1.3 to 4.0]) (16).

• NHANES III showed the prevalence of work-related asthma, defined as an affirmative response to

questions on self-reported, physician-diagnosed asthma and work-related symptoms of rhinitis,

conjunctivitis, and asthma, was 3.7% (CI, 2.88% to 4.52%), and the prevalence of work-related

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 also in smelting, metallurgical, foundry, painting, and lacquering work. Among service workers,

http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf

http://www.atsjournals.org/doi/full/10.1164/rccm.167.5.787

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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 prospective study among subjects exposed to high-molecular-weight occupational allergens

showed that of three potential factors for the development of respiratory symptoms—atopy,

rhinoconjunctivitis, and PC20 (the level of provocational concentration of methacholine causing a

change in FEV1 of 20%)—having a measurable PC20 level was the most significant (20).

• A cross-sectional study of 799 female Finnish dental assistants (response rate, 87%) showed an

increased risk for adult-onset asthma among those with daily methacrylate exposure vs. those with

less than daily exposure (adjusted OR, 2.65 [CI, 1.14 to 7.24]). Nasal symptoms (OR, 1.37 [CI,

1.02 to 1.84]) and work-related cough or phlegm (OR, 1.69 [CI, 1.08 to 2.71]) were also increased

(21).

• A 2006 narrative review discussed six epidemiologic studies on professional cleaners and noted an

increased risk for occupational asthma, even after adjusting for age and smoking history. The

review noted that using bleach, especially in cleaning windows and washing dishes, has been

implicated (22).

• A 2011 narrative review of occupational asthma discussed known environmental risk factors and

possible cofactors, such as exposure to cigarette smoke (23).

Rationale

• Asthma may frequently be related to occupational exposure.

• The identification of a case of occupational asthma may lead to the detection of other cases in the

same work site.

• Smoking has been identified as a risk factor for some types of occupational asthma (lab animal

workers and snow-crab workers).

• Atopic workers are more at risk for the development of IgE-mediated occupational asthma (latex,

lab animal proteins).

• Occupational rhinitis is common among people with occupational asthma and may precede the

development of lower airway disease.

Comments

• A retrospective review of medical records indicated that physicians take incomplete occupational

histories among adults with new-onset asthma. The implications of such underrecognition may

result in underdiagnosis and undermanagement of potentially modifiable workplace exposure (24).

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3. Diagnosis Top

Confirm the diagnosis of occupational asthma through a careful history, a physical exam, and lab testing.

3.1 Ask about classic symptoms of asthma in patients with suspected occupational asthma.

Recommendations

• Ask about the following classic symptoms of asthma:

Cough, particularly if worse at night

Recurrent wheeze

Recurrent difficulty in breathing

Recurrent chest tightness

• Look for symptoms that occur or worsen in the presence of

Exercise

Viral infection

Exposure to allergens, such as animal fur or feathers, dust mites, mold, smoke, or pollen

Changes in weather

Emotional expression (laughing)

Menses

Airborne chemicals, dusts, or other irritants, including those in the workplace

• Look for symptoms that occur or worsen at night, waking the patient.

• See table Diagnostic Criteria for Asthma.

• See module Asthma.

Evidence


and National Asthma Education and Prevention Program recommended criteria for the diagnosis of

asthma. Key indicators for the diagnosis include history of recurrent wheeze, cough (especially if

worse at night), chest tightness, or shortness of breath with worse symptoms in the setting of

exercise, viral infection, allergens (animal fur, mold, smoke, pollen, dust), weather change,

menstruation, or strong emotion (12).







Rationale

• The presence of multiple key indicators increases the probability of a diagnosis of asthma.

• The socioeconomic consequences of occupational asthma can be severe. In addition, the specificity

of history alone is inadequate for the diagnosis of occupational asthma.

3.2 Look for findings on the lung exam consistent with asthma, such as wheezing, prolonged expiratory phase, or chest hyperexpansion, and examine

the skin and nose.



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Recommendations

• 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


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


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.



http://www.atsjournals.org/doi/full/10.1164/ajrccm.161.1.ats11-99#.U1-0zfldWAg

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• Spirometry determines whether there is reversible airflow obstruction; however, normal testing

does not rule out asthma.

• A normal methacholine challenge performed when the patient is still working has a high NPV for

active asthma.

3.4 Ask adult patients with newly diagnosed or worsening asthma about patterns of respiratory symptoms and signs that suggest a relationship to

their work.

Recommendations

• Ask about specific symptom patterns, or use a respiratory questionnaire to record occupational

histories.

• At the completion of the history and physical exam, ask about

The circumstances around the onset of the patient's asthma

The temporal relationships between relevant exposures at the time of symptom onset and with disease

exacerbations

The current severity of the disease

• In patients whose asthma began or worsened during their working life, ask the following:

Were there changes in work processes in the period preceding the onset of symptoms?

Was there an unusual work exposure within 24 hours before the onset of initial asthma symptoms?

Do asthma symptoms differ during times away from work, such as weekends or holidays, or other

extended times away from work?

Are there allergic rhinitis or conjunctivitis symptoms, or both, that are worse with work?

• See table Specific Symptom Patterns and Patterns of Exposure for Occupational Asthma.

Evidence


of work-related asthma recommended screening patients with newly diagnosed or worsening

asthma for work-related factors, including asking about job duties, exposures, use of protective

equipment, and the timing of symptoms in relation to work (1).


and National Asthma Education and Prevention Program recommended that clinicians ask all

patients with asthma about occupational exacerbating factors (12).

• A 2003 statement from the American Thoracic Society on the occupational contribution to the

burden of airway disease reviewed the evidence implicating factors on the pathogenesis of

obstructive airway disease and reported the population attributable risk to range from 4% to 58%,

with a median value of 15% (13).

• A cross-sectional study evaluated the prevalence of occupational rhinitis among 596 individuals

with occupational asthma. Overall, 58.4% of patients with occupational asthma had occupational

rhinitis (14).

• A prospective study evaluated the prevalence of new-onset occupational asthma in a European

population and identified risk factors. Between 10% and 25% of new adult asthma was attributable

to occupational exposures; risk factors included exposure to a substance known to cause

occupational asthma (RR, 1.6 [CI, 1.1 to 2.3]), a symptomatic inhalation event (RR, 3.3 [CI, 1.0 to

11.1]), and working as a nurse (RR, 2.2 [CI, 1.3 to 4.0]) (16).

• NHANES III showed the prevalence of work-related asthma, defined as an affirmative response to

questions on self-reported, physician-diagnosed asthma and work-related symptoms of rhinitis,

conjunctivitis, and asthma, was 3.7% (CI, 2.88% to 4.52%), and the prevalence of work-related



http://www.atsjournals.org/doi/pdf/10.1164/rccm.167.5.787

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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 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

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Phenylcyclohexene

Pesticides, animal materials, mold, and plant materials

Welding fumes

Latex

Ethanolamines

• See the list of agents that can cause occupational asthma, from the UK Health and Safety

Executive.

• See table Select Agents Reported to Be Associated with Reactive Airway Dysfunction Syndrome.

• See table Select Agents Associated with Occupational Asthma with or without a Latency.

Evidence

• A 2012 guideline from the British Thoracic Society on the management of occupational asthma

recommended asking about rhinoconjunctivitis in patients with suspected occupational asthma and

taking a detailed occupational history (30).


of work-related asthma recommended screening patients with newly diagnosed or worsening

asthma for work-related factors, including asking about job duties, exposures, use of protective

equipment, and the timing of symptoms in relation to work (1).

• A population-based study evaluated the association between work and respiratory symptoms in

15,000 adults aged 45 to 64. Overall, 11% reported wheezing and 9% were diagnosed with airway

obstruction. Compared with people with administrative or managerial jobs, those working in food

preparation and service (RR, 1.96 [CI, 1.27 to 3.01]) and as mechanics or repairers (RR, 1.83 [CI,

1.17 to 2.85]) were more likely to have asthma (31).

• From 1993 through 1995 the SENSOR surveillance program in four states (California,

Massachusetts, Michigan, and New Jersey) identified a total of 1101 persons with work-related

asthma. Of these persons, 80% to 89% were classified as having new-onset asthma and 19.1% as

having work-aggravated asthma. The most common industries associated with the condition were

transportation equipment manufacturing (19.3%), health services (14.2%), and educational

services (8.7%) (28).

• A 2000 narrative review of occupational respiratory disease included a list of common causes of

occupational airway disease, which is classified into bronchitis, bronchiolitis, asthma with latency,

asthma without latency, chronic obstructive pulmonary disease, and chronic air flow limitation (32).

Rationale

• Knowledge of the most commonly reported agents causing occupational asthma in general and in

your practice area is important when taking the occupational history.

• Information regarding the extent of exposure, site of exposure, and existent control measures is

essential in making a complete assessment.

Comments

• Work-exacerbated asthma is typically diagnosed by finding a relationship of increased symptoms

with workplace exposure in patients whose asthma was present before the onset of exposure.

• In the U.S., OSHA mandates that material safety data sheets be made available to the employee

upon request.

• The list of agents is adapted from 33.

3.6 In patients with occupational asthma, differentiate between immunologic (sensitizer-induced) and nonimmunologic (or irritant) asthma.

http://www.hse.gov.uk/asthma/substances.htm


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Recommendations

• 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


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

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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

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• 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


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).


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

visual analysis of the PEFR (41).


http://www.ncbi.nlm.nih.gov/books/NBK11926/

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• A retrospective study evaluated agreement between expert interpretation of serial PEFR testing and

readings by a validated diagnostic aid (Oasys-2). For agreement between experts and Oasys-2,

median kappa values were 0.50 to 0.75 (42),

• A case-control study evaluated the accuracy of peak flow monitoring in 81 patients with

occupational asthma and 60 controls with asthma. Taking readings over 4 weeks had a sensitivity

of 81.8% and a specificity of 93.8%; taking readings over 2 weeks had a sensitivity of 70% and a

specificity of 82.4%. The sensitivity and specificity were highest with eight readings per day but

were similar with four per day (43).

Rationale

• In the setting of confirmed asthma, history alone leads to a correct diagnosis of occupational

asthma in, at most, 75% of patients.

• To ensure an accurate diagnosis and avoid the adverse socioeconomic consequences of removal

from work, additional confirmatory testing is recommended.

• Bronchial hyperresponsiveness measured by nonspecific challenge has been shown to worsen when

a patient with sensitizer-induced occupational asthma is exposed to the relevant antigen.

Comments

• As much of the testing described requires the patient to still be working, the clinician should make

every effort not to remove the patient from work until after the evaluation is completed.

• The peak flow meter should be simple to use, inexpensive, and accurate. It also needs to have the

capability to record high flows.

• Immunologic testing is available for about 40 etiologic agents but will not be feasible for most low-

molecular-weight chemical antigens because most do not induce an IgE-mediated response.

• Few of the available antigen preparations are validated and standardized. Variable antigen potency

from different manufacturers can lead to false-negative test results (44).

• Specific antibody responses wane over time, so false-negative results do occur if the patient has

been away from exposure for a prolonged time (45).

• Methacholine challenge testing should be done by a trained individual and is not generally

recommended if the FEV1 is less than 70% of the predicted result, or less than 2 L.

3.8 Consider the differential diagnosis of occupational asthma.

Recommendations

• Consider other diagnoses that may mimic occupational asthma:

Non-work-related asthma

Work-exacerbated asthma

Bronchiolitis obliterans

Hypersensitivity pneumonitis

Metal or polymer fume fever

Organic dust toxic syndrome

Byssinosis

• See table Differential Diagnosis of Occupational Asthma.

Evidence

• A 2000 narrative review of occupational respiratory disease included a list of common causes of

occupational airway disease classified into bronchitis, bronchiolitis, asthma with latency, asthma

without latency, chronic obstructive pulmonary disease, and chronic air flow limitation (32).

• Pulmonary mycotoxicosis is more common than hypersensitivity pneumonitis (46).

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• A 5-year follow-up study compared cotton-thread textile workers with silk-thread textile workers.

The presence of byssinosis at the time of the first survey was 7.3%. An across-shift drop of 5% or

more at the time of the first survey was predictive of a five-year decline in FEV1 (47).

Rationale

• Other conditions can mimic occupational asthma.

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4. Consultation Top

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


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.

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5. Hospitalization Top

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


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

from other patients with asthma.


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6. Therapy Top

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


recommended complete removal of the patient from the exposure (30).


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).


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

exposures through


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Accommodations from the employer for workplace modifications (in the U.S., under the Americans with

Disabilities Act) and to prevent exposures that are even below the permitted NIOSH-ACGIH threshold limits

The use of a mask, respirator, or other protective equipment, especially if such irritants as nuisance dusts trigger bronchospasm

• Recognize that if symptoms continue despite modifications, complete removal of the worker from

irritant exposure is essential.

Evidence


recommended complete removal of the patient from the exposure (30).


of work-related asthma recommended that 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).

Rationale

• Death could occur from persistent exposure to the irritant.

6.3 Use a stepwise approach to asthma therapy in patients with occupational

asthma, and treat those with mild persistent asthma symptoms with inhaled steroids.

Recommendations

• Assess symptom severity in patients with occupational asthma, and classify them as having

intermittent, mild persistent, moderate persistent, or severe persistent disease.

• Prescribe

A β2-agonist as a rescue inhaler

Inhaled steroids for all patients with more than mild symptoms

• See figure Classifying Asthma Severity.

• See figure Stepwise Approach for Managing Asthma Treatment in Youth ≥12 Years of Age and

Adults.

• See table Drug Treatment for Occupational Asthma.

• See module Asthma.

Evidence


recommended treating occupational asthma with the same approach to drug therapy as in

nonoccupational asthma (30).


of work-related asthma recommended treating occupational asthma with the same approach as in

nonoccupational asthma (1).


and National Asthma Education and Prevention Program recommended a stepwise approach to

asthma therapy, starting with a β2-agonist in patients with intermittent asthma and using an

inhaled steroid in patients with moderate persistent (or more severe) symptoms (12).


asthma found few studies of medical therapy in this population (39).


http://www.jacionline.org/article/S0091-6749%2807%2901823-4/journalimage?loc=gr20&src=fig&free=yes&source=imageTab

http://www.jacionline.org/article/S0091-6749%2807%2901823-4/journalimage?free=yes&loc=gr16&source=imageTab&src=fig

http://www.jacionline.org/article/S0091-6749%2807%2901823-4/journalimage?free=yes&loc=gr16&source=imageTab&src=fig





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• A randomized trial compared inhaled beclomethasone with placebo in 32 patients with occupational

asthma. The active therapy group had small improvements in symptoms and lung function

compared with the placebo group (50).

• A randomized trial compared inhaled beclomethasone with placebo in 15 patients with occupational

asthma. During and after treatment, the beclomethasone group had decreased general airway

hyperresponsiveness but did not differ in reactivity to the specific culprit antigen (51).

• In an uncontrolled case series, 10 patients with occupational asthma and ongoing workplace

exposure were treated with beclomethasone dipropionate, 500 mcg twice daily, and salmeterol, 50

mcg twice daily. Lung function and respiratory symptoms were monitored for 3 years. At the end of

the study, no significant differences in any of the morbidity outcomes (FEV1, PC20, PEFR variability,

use of rescue salbutamol, respiratory symptom score) were found as compared with baseline or

run-in values (52).

Rationale

• Clinical trials have shown improvement in clinical and functional measurements and in nonspecific

bronchial hyperresponsiveness in patients treated early with inhaled steroids after removal from

the irritant.

Comments

• Best results are obtained with exposure modification and early (less than 1 year after cessation of

exposure) initiation of therapy with inhaled steroids; however, no cures of occupational asthma

have been documented with medical therapy alone (i.e., without removal from exposure).

• For patients with asthma in general, a 2006 meta-analysis of 19 trials with almost 34,000

participants found increased exacerbations requiring hospitalization (OR, 2.6 [CI, 1.6 to 4.3]) and

life-threatening exacerbations (OR, 1.8 [CI, 1.1 to 2.9]) among users of long-acting β-agonists

compared with placebo. Hospitalizations were also significantly increased with salmeterol (OR, 1.7

[CI, 1.1 to 2.7]) and formoterol (OR, 3.2 [CI, 1.7 to 6.0]) (53).

6.4 Recommend desensitization therapy for appropriate allergens if allergen

avoidance is impossible.

Recommendations

• Consider desensitization therapy in occasional cases of high-molecular-weight antigen-induced

occupational asthma if

Allergen avoidance cannot be accomplished

Standardized allergen extract is available for the responsible antigen

• See table Drug Treatment for Occupational Asthma.

Evidence


of work-related asthma stated that immunotherapy should be considered when there is a clearly

identified allergen that cannot be avoided and for which there is a specific therapy (1).

• A 2010 Cochrane review of injection allergen immunotherapy for asthma included 88 trials

involving a variety of specific allergens. Overall, the immunotherapy had more improvement in

asthma symptom scores (mean difference, -0.59 (CI, -0.83 to -0.35]) and bronchial

hyperreactivity (54).

• A comparative study evaluated the effect of desensitization therapy compared with placebo in

patients with cat-induced asthma and found that treatment resulted in significant reductions in

bronchial sensitivity and prick-test titer compared with control treatment (55).


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• A study compared immunotherapy with placebo in 24 patients with latex allergy (including 16 with

asthma). There were no differences between groups in medication use or bronchial responsiveness

(56).

Rationale

• Alleviation of allergic respiratory symptoms has been shown in animal laboratory and veterinary

workers treated with desensitization therapy.

Comments

• Desensitization therapy has not been studied extensively as a treatment modality for sensitizer-

induced occupational asthma.

6.5 Consider therapy with anti-IgE antibody in patients with IgE-mediated

occupational asthma.

Recommendations

• Consider using anti-IgE antibody in IgE-mediated occupational asthma.

• Consult with an allergist if anti-IgE therapy is considered.

Evidence

• A prospective study in 546 allergic asthmatics taking inhaled steroids showed that compared with a

placebo group, the group receiving anti-IgE antibody (omalizumab) had more than 50% fewer

exacerbations per patient. Anti-IgE antibody therapy has not been evaluated extensively (57).

Rationale

• The frequency of exacerbations and the steroid requirements may be reduced in those with allergic

asthma treated with anti-IgE antibody.

Comments

• Anti-IgE antibodies have not been studied extensively as a treatment modality.

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7. Patient Counseling Top

Inform patients with occupational asthma about the disease and its management.

7.1 Inform the patient about key issues concerning occupational asthma and its causes, treatment, and prognosis.

Recommendations

• Discuss with patients the triggers of their asthma and the importance of recording symptoms,

monitoring peak flow rates, and taking all prescribed medications.

• Stress the importance of avoiding or minimizing exposures to the irritant for patients that have

irritant-induced occupational asthma.

• Inform patients that most patients continue to have respiratory symptoms and increased

nonspecific bronchial hyperresponsiveness even after removal from exposure.

• Explain that it is important to use inhaled steroids early to modify the disease course but that it will

not cure occupational asthma.

• Discuss the rationale for eliminating exposure with patients that have sensitizer-induced

occupational asthma.

Evidence

• A 2003 Cochrane review of self-management education for patients with asthma included 36 trials.

Overall, self-management education improved multiple outcomes, including reducing

hospitalizations (RR, 0.64 [CI, 0.50 to 0.82]) and nocturnal symptoms (RR, 0.67 [CI, 0.56 to

0.79]), and improving quality of life (58).

Rationale

• Patient education is essential for successful management of asthma.

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8. Follow-up Top

Follow up regularly to monitor treatment and response in all patients with occupational asthma.

8.1 Follow patients with occupational asthma regularly after removal from exposure to the causative agent.

Recommendations

• Follow patients with occupational asthma at least every 6 months:

Monitor symptoms, airflow limitation, and nonspecific bronchial hyperresponsiveness

Monitor response to therapy

Monitor adherence to therapy

• Evaluate for permanent impairment or disability after 2 years in patients with continuing severe

symptoms.

Evidence


recommended that patients with confirmed or suspected occupational asthma be followed at a

specialist center every 3 months for a year and every 6 months thereafter, and that patients be

followed for a total of 3 years after removal of the exposure (30).

• Follow-up of patients with some types of occupational asthma showed that after leaving

employment, patients who remained symptomatic had had a longer duration of exposure and

symptoms and greater abnormalities in both pulmonary function and bronchial

hyperresponsiveness at the time of diagnosis (59).

• In one study, workers with occupational asthma to soldering fluxes containing colophony were

followed for 4 years. The study showed that only 10% of affected workers became symptom free

(60).

• When 99 patients with occupational asthma who had been removed from exposure were followed

up, patients removed from exposure for more than 5 years showed significant improvement in

bronchial responsiveness when compared with those removed from exposure for less than 5 years

(P=0.01). Stepwise logistic regression showed that follow-up PC20 could be predicted from baseline

PC20, duration of exposure interval since removal from exposure, and the type of agent. Patients

with occupational asthma due to high-molecular-weight agents had a less favorable outcome

(P=0.04; OR, 0.295 [CI, 0.03 to 1.0]). Treatment with inhaled steroids was not a significant

predictor. (61)

• Thirty-one workers with occupational asthma from snow-crab processing were followed over 5

years after leaving work. Total duration of exposure was approximately 1 year (12.8 months). At

the time of diagnosis, all 31 required medication for asthma. At the end of 1 year, there was a

significant reduction in patients requiring medication; there was also an improvement in FEV1 and

FEV1/FVC percentages, but they reached a plateau thereafter (62).

Rationale

• Regular follow-up is essential to optimal management, determination of impairment, and ability to

work.

8.2 Assess factors that have prognostic significance for recovery.

Recommendations

• Review factors known to have prognostic significance:

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Age

Total duration of exposure

Duration of exposure after onset of symptoms

Evidence

• Among workers with red cedar asthma followed for 3.5 years, those who remained at their jobs

after diagnosis had worsening of symptoms and increased nonspecific bronchial

hyperresponsiveness (63)

• Follow-up of patients with some types of occupational asthma showed that after leaving

employment, patients who remained symptomatic had had a longer duration of exposure and

symptoms and greater abnormalities in both pulmonary function and bronchial

hyperresponsiveness at the time of diagnosis (59).

• A study followed a cohort of 31 workers with occupational asthma caused by snow-crab processing

over a period of approximately 5 years (64.4 ± 6.3 months) after they had left this work. Diagnosis

was established in most workers by specific inhalational challenge. At the initial follow-up at 1 year

(12.8 ± 5.4 months), there was a decrease in the number of participants still requiring medication

who had a significant reduction in FEV1 and a PC20≤16 mg/mL. Interestingly, there was no further

change observed with time. The mean FEV1 and FEV1/FEV percentages improved significantly from

the diagnosis to the first follow-up but did not change thereafter (64).

Rationale

• Complete recovery requires early diagnosis and removal from the source of exposure.

8.3 Monitor all patients who remain continuously exposed to irritants.

Recommendations

• Continuously monitor patients with occupational asthma who remain exposed to the causative

agent.

Evidence

• 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).


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).

• A follow-up study of workers with cedar asthma who were still working in the same industry after

an average of 6.5 years showed that over one third experienced deterioration in their asthma

symptoms (65).

• In one study, workers with occupational asthma to soldering fluxes containing colophony were

followed for 4 years. The study showed that only 10% of affected workers became symptom free

(60).

Rationale

• Affected workers who are continuously exposed do not recover and may deteriorate.

8.4 Recognize the importance of reporting cases of occupational asthma to government agencies.

Recommendations

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• Recognize that under the OSHA act of 1970, physicians are obligated to report cases of

occupational asthma to state and county health departments.

• See table Prevention Measures Instituted by Employers.

Evidence

• Public health surveillance includes the SENSOR program, which NIOSH initiated first as a pilot

project in an effort to improve occupational disease surveillance reporting. Occupational asthma is

a target condition for the SENSOR program. Reporting guidelines and surveillance case definition

have been standardized (9).

• Approaches to the prevention of occupational asthma include primary, secondary, and tertiary

prevention strategies. Such strategies may be employed in sensitizer-induced asthma. Screening

programs have value because early detection may improve long-term prognosis (10).

Rationale

• The diagnosis of occupational asthma in a patient should be regarded as a sentinel event because

the prevalence of asthma can be high in industries where a case of occupational asthma has been

identified.

• Disease surveillance is an integral component in the prevention of occupational asthma by

providing information on how common asthma is in relationship to other occupational lung diseases

and on the relative frequency with which different agents cause asthma.

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References Top

1. Tarlo SM, Balmes J, Balkissoon R, Beach J, Beckett W, Bernstein D, et al. Diagnosis and management of work-related asthma:

American College Of Chest Physicians Consensus Statement. Chest. 2008;134:1S-41S. (PMID: 18779187)

2. Nicholson PJ, Cullinan P, Taylor AJ, Burge PS, Boyle C. Evidence based guidelines for the prevention, identification, and management of occupational asthma. Occup Environ Med. 2005;62:290-9. (PMID: 15837849)

3. Wilken D, Baur X, Barbinova L, Preisser A, Meijer E, Rooyackers J, et al.; ERS Task Force on the Management of Work-related Asthma. What are the benefits of medical screening and surveillance? Eur Respir Rev. 2012;21:105-11. (PMID: 22654082)

4. LaMontagne AD, Radi S, Elder DS, Abramson MJ, Sim M. Primary prevention of latex related sensitisation and occupational asthma: a systematic review. Occup Environ Med. 2006;63:359-64. (PMID: 16469822)

5. Tarlo SM, Liss GM. Prevention of occupational asthma--practical implications for occupational physicians. Occup Med (Lond). 2005;55:588-94. (PMID: 16314329)

6. Górski P. Global Initiative for Asthma 2002—what concerns occupational medicine [Editorial]. Int J Occup Med Environ Health. 2002;15:207-8. (PMID: 12462447)

7. Taivainen AI, Tukiainen HO, Terho EO, Husman KR. Powered dust respirator helmets in the prevention of occupational asthma among farmers. Scand J Work Environ Health. 1998;24:503-7. (PMID: 9988093)

8. Mûller-Wening D, Neuhauss M. Protective effect of respiratory devices in farmers with occupational asthma. Eur Respir J. 1998;12:569-72. (PMID: 9762781)

9. Matte TD, Hoffman RE, Rosenman KD, Stanbury M. Surveillance of occupational asthma under the SENSOR model. Chest. 1990;98:173S-178S. (PMID: 2226005)

10. Venables KM. Prevention of occupational asthma. Eur Respir J. 1994;7:768-78. (PMID: 8005261)

11. Sarlo K. Control of occupational asthma and allergy in the detergent industry. Ann Allergy Asthma Immunol. 2003;90:32-4. (PMID: 12772949)

12. National Asthma Education and Prevention Program. Expert Panel Report 3 (EPR-3): Guidelines for the Diagnosis and Management of Asthma-Summary Report 2007. J Allergy Clin Immunol. 2007;120:S94-138. (PMID: 17983880)

13. Balmes J, Becklake M, Blanc P, Henneberger P, Kreiss K, Mapp C, et al. American Thoracic Society Statement: Occupational contribution to the burden of airway disease. Am J Respir Crit Care Med. 2003;167:787-97. (PMID: 12598220)

14. Ameille J, Hamelin K, Andujar P, Bensefa-Colas L, Bonneterre V, Dupas D, et al.; members of the rnv3p. Occupational asthma and occupational rhinitis: the united airways disease model revisited. Occup Environ Med. 2013;70:471-5. (PMID: 23390199)

15. Blanc PD, Galbo M, Hiatt P, Olson KR. Morbidity following acute irritant inhalation in a population-based study. JAMA. 1991;266:664-9. (PMID: 2072476)

16. Kogevinas M, Zock JP, Jarvis D, Kromhout H, Lillienberg L, Plana E, et al. Exposure to substances in the workplace and new-onset asthma: an international prospective population-based study (ECRHS-II). Lancet. 2007;370:336-41. (PMID: 17662882)

17. Arif AA, Delclos GL, Whitehead LW, Tortolero SR, Lee ES. Occupational exposures associated with work-related asthma and work-related wheezing among U.S. workers. Am J Ind Med. 2003;44:368-76. (PMID: 14502764)

18. Karjalainen A, Kurppa K, Martikainen R, Klaukka T, Karjalainen J. Work is related to a substantial portion of adult-onset asthma incidence in the Finnish population. Am J Respir Crit Care Med. 2001;164:565-8. (PMID: 11520716)

19. Vandenplas O, Ghezzo H, Munoz X, Moscato G, Perfetti L, Lemiere C, et al. What are the questionnaire items most useful in identifying subjects with occupational asthma? Eur Respir J. 2005;26:1056-63. (PMID: 16319335)

20. Gautrin D, Ghezzo H, Malo JL. Rhinoconjunctivitis, bronchial responsiveness, and atopy as determinants for incident non-work-related asthma symptoms in apprentices exposed to high-molecular-weight allergens. Allergy. 2003;58:608-15. (PMID: 12823119)

21. Jaakkola MS, Leino T, Tammilehto L, Ylöstalo P, Kuosma E, Alanko K. Respiratory effects of exposure to methacrylates among dental assistants. Allergy. 2007;62:648-54. (PMID: 17508969)

22. Jaakkola JJ, Jaakkola MS. Professional cleaning and asthma. Curr Opin Allergy Clin Immunol. 2006;6:85-90. (PMID: 16520670)

23. Vandenplas O. Occupational asthma: etiologies and risk factors. Allergy Asthma Immunol Res. 2011;3:157-67. (PMID: 21738881)

24. Shofer S, Haus BM, Kuschner WG. Quality of occupational history assessments in working age adults with newly diagnosed asthma. Chest. 2006;130:455-62. (PMID: 16899845)

25. Pratter MR, Curley FJ, Dubois J, Irwin RS. Cause and evaluation of chronic dyspnea in a pulmonary disease clinic. Arch Intern Med. 1989;149:2277-82. (PMID: 2802893)

http://www.ncbi.nlm.nih.gov/pubmed?term=18779187

























Occupational Asthma


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26. Crapo RO, Casaburi R, Coates AL, Enright PL, Hankinson JL, Irvin CG, et al. Guidelines for methacholine and exercise challenge

testing-1999. This official statement of the American Thoracic Society was adopted by the ATS Board of Directors, July 1999. Am J Respir Crit Care Med. 2000;161:309-29. (PMID: 10619836)

27. Knoeller GE, Mazurek JM, Moorman JE. Work-related asthma among adults with current asthma in 33 states and DC: evidence from the Asthma Call-Back Survey, 2006-2007. Public Health Rep. 2011;126:603-11. (PMID: 21800756)

28. Jajosky RA, Harrison R, Reinisch F, Flattery J, Chan J, Tumpowsky C, et al. Surveillance of work-related asthma in selected U.S. states using surveillance guidelines for state health departments—California, Massachusetts, Michigan, and New Jersey, 1993-1995. Mor Mortal Wkly Rep CDC Surveill Summ. 1999;48:1-20. (PMID: 10421216)

29. McDonald JC, Chen Y, Zekveld C, Cherry NM. Incidence by occupation and industry of acute work related respiratory diseases in the UK, 1992-2001. Occup Environ Med. 2005;62:836-42. (PMID: 16299091)

30. Fishwick D, Barber CM, Bradshaw LM, Ayres JG, Barraclough R, Burge S, et al. Standards of care for occupational asthma: an update. Thorax. 2012;67:278-80. (PMID: 22156958)

31. Mirabelli MC, London SJ, Charles LE, Pompeii LA, Wagenknecht LE. Occupation and the prevalence of respiratory health symptoms and conditions: the Atherosclerosis Risk in Communities Study. J Occup Environ Med. 2012;54:157-65. (PMID: 22157701)

32. Beckett WS. Occupational respiratory diseases. N Engl J Med. 2000;342:406-13. (PMID: 10666432)

33. Work-related lung disease: surveillance report. U.S. Dept of Health and Human Services, Division of Respiratory Disease, NIOSH; 1999:157-8.

34. Brooks SM, Hammad Y, Richards I, Giovinco-Barbas J, Jenkins K. The spectrum of irritant-induced asthma: sudden and not-so-sudden onset and the role of allergy. Chest. 1998;113:42-9. (PMID: 9440566)

35. Malo JL, L’archevêque J, Castellanos L, Lavoie K, Ghezzo H, Maghni K. Long-term outcomes of acute irritant-induced asthma. Am J Respir Crit Care Med. 2009;179:923-8. (PMID: 19234102)

36. Malo JL, Cartier A, Boulet LP, L’Archeveque J, Saint-Denis F, Bherer L, et al. Bronchial hyperresponsiveness can improve while spirometry plateaus two to three years after repeated exposure to chlorine causing respiratory symptoms. Am J Respir Crit Care Med. 1994;150:1142-5. (PMID: 7921449)

37. Aasen TB, Burge PS, Henneberger PK, Schlünssen V, Baur X; EOM Society. Diagnostic approach in cases with suspected work-related asthma. J Occup Med Toxicol. 2013;8:17. (PMID: 23768266)

38. Maghni K, Lemière C, Ghezzo H, Yuquan W, Malo JL. Airway inflammation after cessation of exposure to agents causing occupational asthma. Am J Respir Crit Care Med. 2004;169:367-72. (PMID: 14578217)

39. Beach J, Rowe BH, Blitz S, Crumley E, Hooton N, Russell K, et al. Diagnosis and management of work-related asthma. Evid Rep Technol Assess (Summ). 2005;:1-8. (PMID: 16354102)

40. Leroyer C, Perfetti L, Trudeau C, L’Archevêque J, Chan-Yeung M, Malo JL. Comparison of serial monitoring of peak expiratory flow and FEV1 in the diagnosis of occupational asthma. Am J Respir Crit Care Med. 1998;158:827-32. (PMID: 9731012)

41. Perrin B, Lagier F, L’Archevêque J, Cartier A, Boulet LP, Côté J, et al. Occupational asthma: validity of monitoring of peak expiratory flow rates and non-allergic bronchial responsiveness as compared to specific inhalation challenge. Eur Respir J. 1992;5:40-8. (PMID: 1577147)

42. Baldwin DR, Gannon P, Bright P, Newton DT, Robertson A, Venables K, et al. Interpretation of occupational peak flow records: level of agreement between expert clinicians and Oasys-2. Thorax. 2002;57:860-4. (PMID: 12324671)

43. Anees W, Gannon PF, Huggins V, Pantin CF, Burge PS. Effect of peak expiratory flow data quantity on diagnostic sensitivity and specificity in occupational asthma. Eur Respir J. 2004;23:730-4. (PMID: 15176688)

44. Sander I, Merget R, Degens PO, Goldscheid N, Brüning T, Raulf-Heimsoth M. Comparison of wheat and rye flour skin prick test solutions for diagnosis of baker's asthma. Allergy. 2004;59:95-8. (PMID: 14674940)

45. Brant A, Zekveld C, Welch J, Jones M, Taylor AN, Cullinan P. The prognosis of occupational asthma due to detergent enzymes: clinical, immunological and employment outcomes. Clin Exp Allergy. 2006;36:483-8. (PMID: 16630153)

46. Emanuel DA, Wenzel FJ, Lawton BR. Pulmonary mycotoxicosis. Chest. 1975;67:293-7. (PMID: 46192)

47. Christiani DC, Ye TT, Wegman DH, Eisen EA, Dai HL, Lu PL. Cotton dust exposure, across-shift drop in FEV1, and five-year change in lung function. Am J Respir Crit Care Med. 1994;150:1250-5. (PMID: 7952548)

48. Bartter T, Pratter MR. Asthma: better outcome at lower cost? The role of the expert in the care system. Chest. 1996;110:1589-96. (PMID: 8989082)

49. Vandenplas O, Dressel H, Wilken D, Jamart J, Heederik D, Maestrelli P, et al. Management of occupational asthma: cessation or reduction of exposure? A systematic review of available evidence. Eur Respir J. 2011;38:804-11. (PMID: 21436354)
























Occupational Asthma


of 29

50. Malo JL, Cartier A, Côté J, Milot J, Leblanc C, Paquette L, et al. Influence of inhaled steroids on recovery from occupational

asthma after cessation of exposure: an 18-month double-blind crossover study. Am J Respir Crit Care Med. 1996;153:953-60. (PMID: 8630579)

51. Maestrelli P, De Marzo N, Saetta M, Boscaro M, Fabbri LM, Mapp CE. Effects of inhaled beclomethasone on airway responsiveness in occupational asthma. Placebo-controlled study of subjects sensitized to toluene diisocyanate. Am Rev Respir Dis. 1993;148:407-12. (PMID: 8393638)

52. Marabini A, Siracusa A, Stopponi R, Tacconi C, Abbritti G. Outcome of occupational asthma in patients with continuous exposure: a 3-year longitudinal study during pharmacologic treatment. Chest. 2003;124:2372-6. (PMID: 14665523)

53. Salpeter SR, Buckley NS, Ormiston TM, Salpeter EE. Meta-analysis: effect of long-acting beta-agonists on severe asthma exacerbations and asthma-related deaths. Ann Intern Med. 2006;144:904-12. [Full Text] (PMID: 16754916)

54. Abramson MJ, Puy RM, Weiner JM. Injection allergen immunotherapy for asthma. Cochrane Database Syst Rev. 2010;(8):CD001186. (PMID: 20687065)

55. Ohman JL Jr, Findlay SR, Leitermann KM. Immunotherapy in cat-induced asthma. Double-blind trial with evaluation of in vivo and in vitro responses. J Allergy Clin Immunol. 1984;74:230-9. (PMID: 6206105)

56. Sastre J, Fernández-Nieto M, Rico P, Martín S, Barber D, Cuesta J, et al. Specific immunotherapy with a standardized latex extract in allergic workers: a double-blind, placebo-controlled study. J Allergy Clin Immunol. 2003;111:985-94. (PMID: 12743562)

57. Buhl R, Hanf G, Solèr M, Bensch G, Wolfe J, Everhard F, et al. The anti-IgE antibody omalizumab improves asthma-related quality of life in patients with allergic asthma. Eur Respir J. 2002;20:1088-94. (PMID: 12449159)

58. Gibson PG, Powell H, Coughlan J, Wilson AJ, Abramson M, Haywood P, et al. Self-management education and regular practitioner review for adults with asthma. Cochrane Database Syst Rev. 2003;(1):CD001117. (PMID: 12535399)

59. Chan-Yeung M, Lam S, Koener S. Clinical features and natural history of occupational asthma due to western red cedar (Thuja plicata). Am J Med. 1982;72:411-5. (PMID: 7058838)

60. Burge PS. Occupational asthma in electronics workers caused by colophony fumes: follow-up of affected workers. Thorax. 1982;37:348-53. (PMID: 7112471)

61. Perfetti L, Cartier A, Ghezzo H, Gautrin D, Malo JL. Follow-up of occupational asthma after removal from or diminution of exposure to the responsible agent: relevance of the length of the interval from cessation of exposure. Chest. 1998;114:398-403. (PMID: 9726721)

62. Pisati G, Baruffini A, Zedda S. Toluene diisocyanate induced asthma: outcome according to persistence or cessation of exposure. Br J Ind Med. 1993;50:60-4. (PMID: 8381658)

63. Chan-Yeung M. Fate of occupational asthma. A follow-up study of patients with occupational asthma due to Western Red Cedar (Thuja plicata). Am Rev Respir Dis. 1977;116:1023-9. (PMID: 931178)

64. Malo JL, Cartier A, Ghezzo H, Lafrance M, McCants M, Lehrer SB. Patterns of improvement in spirometry, bronchial hyperresponsiveness, and specific IgE antibody levels after cessation of exposure in occupational asthma caused by snow-crab processing. Am Rev Respir Dis. 1988;138:807-12. (PMID: 3202454)

65. Cote J, Kennedy S, Chan-Yeung M. Outcome of patients with cedar asthma with continuous exposure. Am Rev Respir Dis. 1990;141:373-6. (PMID: 1689129)




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Glossary Top

ACGIH American Conference of Governmental Industrial Hygienists

AHRQ Agency for Healthcare Research and Quality

CI confidence interval

ELISA enzyme-linked immunosorbent assay

FEV1 forced expiratory volume in 1 second

FVC

forced vital capacity

IgE immunoglobulin E

NHANES III Third National Health and Nutrition Examination Survey, 1988-1994

NIOSH

National Institute of Occupational Safety and Health

NPV negative predictive value

OR odds ratio

OSHA U.S. Occupational Safety and Health Administration

PC20 provocative dose causing a 20% fall in FEV1

PEFR peak expiratory flow rate

PPV positive predictive value

RADS

reactive airway dysfunction syndrome

RAST radioallergosorbent

RR relative risk

SENSOR

Sentinel Event Notification System for Occupational Risk

SWORD Surveillance of work-related and occupational respiratory disease (UK)

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Tables Top

Laboratory and Other Studies for Occupational Asthma

Test Sensitivity/Specificity (%) Notes

Pulmonary function tests Easy and inexpensive, but there is no standardized method of

interpretation. Results can vary

Serial peak flow rates over 4 weeks 81.8/93.8 If at least 4 readings per day (though 8 was optimal); based on a

case-control study

Serial peak flow rates over 2 weeks 70-82/82-100 For at least 4 readings per day; based on a case-control study and

a small prospective cohort study

Serial FEV1 over 2 weeks 45-55/56-100 Based on a small prospective cohort study

FEV1 measurement before and after work Low sensitivity

Methacholine challenge test (PC20) 66.7/63.9 Based on pooled data.

Bronchial hyperresponsiveness can also be evaluated with a

histamine challenge test.

The PC20 is defined as the provocative concentration of

methacholine inducing a 20% drop in FEV1

Immunologic tests

Skin-prick test 72.9/86.2 (low-molecular-weight antigen exposure)

80.6/59.6 (high-molecular-weight antigen exposure)

Accuracy differs if exposure was to low-molecular-weight antigens

or high-molecular-weight antigens

Serum IgE testing 31.2/88.9 (low-molecular-weight antigen exposure)

73.3/79 (high-molecular-weight antigen exposure)

Accuracy differs if exposure was to low molecular-weight-antigens

or high–molecular-weight antigens

Chest x-ray May be useful in excluding other or concomitant pulmonary

disorders

FEV1 = forced expiratory volume in 1 second; IgE = immunoglobulin E; PC20 = provocative dose causing a 20% fall in FEV1.

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Differential Diagnosis of Occupational Asthma

Disease Characteristics

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

microorganisms.

Symptoms appear 3-8 hours after exposure


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Drug Treatment for Occupational Asthma

Drug or Drug Class Dosing Side Effects Precautions Clinical Use

Inhaled short-acting β2-agonists Sympathomimetic effects, such as

tremor and tachycardia. Hypokalemia,

hyperglycemia, hypersensitivity

reactions

Caution with CV disease,

hyperthyroidism, diabetes, narrow-

angle glaucoma, seizure disorder

First line for mild, intermittent

symptoms

Albuterol (Proventil HFA, Ventolin HFA,

Proair HFA, Accuneb)

MDI (90 mcg/ inhalation): 2 inhalations

q4-6hr prn. Nebulizer: 2.5 mg q6-8hr

prn. For acute exacerbations, MDI can

increase to 4-8 puffs q1-4hr, or

nebulizer to 2.5-10 mg q1-4hr

Levalbuterol (Xopenex, Xopenex HFA) MDI (45 mcg/ inhalation): 2 inhalations

q4-6hr prn, Nebulizer: 0.63-1.25 mg q8hr. For acute exacerbations, MDI can

increase to 4-8 inhalations q1-4hr, or

nebulizer to 1.25-5 mg q1-4hr

Pirbuterol (Maxair) MDI (200 mcg/ inhalation): 2

inhalations q4-6hr prn. For acute

exacerbations, can increase to 4-8

inhalations q1-4hr

Inhaled corticosteroids Dose depends on previous asthma

therapy

Xerostomia, flushing, cataracts,

glaucoma, oral candidiasis, hoarseness,

purpura. Low incidence of HPA

suppression, bone loss

Caution with diabetes For mild-severe persistent asthma

Beclomethasone (QVAR) Inhaler (40, 80 mcg/inhalation): 40-

160 mcg bid

Budesonide (Pulmicort Flexhaler,

Pulmicort Turbuhaler)

DPI (90, 180 mcg/ inhalation): 360

mcg bid. DPI (200 mcg/inhalation): 200-400 mcg bid

Ciclesonide (Alvesco) MDI (80, 160 mcg/inhalation):80-320 mcg bid

Flunisolide (Aerospan HFA) Inhaler (80 mcg/inhalation): 160 mcg bid

Fluticasone (Flovent HFA, Flovent

Diskus)

MDI (44, 110, 220 mcg/inhalation):

88-440 mcg bid. DPI (50, 100, 250

mcg/inhalation): 100-1000 mcg bid

Mometasone (Asmanex Twisthaler) DPI (110, 220 mcg/inhalation): 220

mcg qd in the PM. Maximum 220-440

mcg bid

Triamcinolone (Azmacort) MDI (75 mcg/ inhalation): 150 mcg tid-

qid or 300 mcg bid. Maximum 1200

mcg total daily dose

Leukotriene modifiers Rare neuropsychiatric events Alternatives for mild-to-moderate

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persistent asthma

Montelukast (Singulair) 10 mg qd in the PM Rare systemic eosinophilia

Zafirlukast (Accolate) 20 mg bid Elevated hepatic enzymes,

hypersensitivity reactions, rare

systemic eosinophilia

Avoid with hepatic disease. Inhibits

CYPs 1A2, 2C8, 2C9 and 3A4.

Increased INR with warfarin

Zileuton (Zyflo CR) Extended-release: 1200 mg bid, within

1 hr after meals

Elevated hepatic enzymes, flulike

syndrome

Avoid with hepatic disease. Check LFTs

at baseline and periodically. Substrate and potent inhibitor of CYP1A2

Respiratory anti-inflammatory

agent

Cromolyn (Intal) MDI (800 mcg/ spray): 2 sprays qid.

Nebulizer: 20 mg qid

Bronchospasm, throat irritation, cough,

severe anaphylactoid reactions

Alternative for mild persistent asthma

Inhaled long-acting β2-agonists Sympathomimetic effects, such as

tremor and tachycardia. Paradoxical

bronchospasm, hypersensitivity

reactions. Rare: hypokalemia,

hyperglycemia

Asthma-related death. Caution with

CV disease, hyperthyroidism, diabetes,

narrow-angle glaucoma, seizure

disorder. Tolerance can occur over time

For moderate to severe persistent

asthma. Must also use an asthma

controller

Formoterol (Foradil Aerolizer) Powder in capsules for use with

Aerolizer: 12 mcg q12hr

Salmeterol (Serevent Diskus) 50 mcg (1 oral inhalation) q12hr

Oral Corticosteroids Long-term use can result in HPA

suppression, immunosuppression,

hypertension, adverse neurologic

effects, glucose intolerance, weight

gain, myopathy, cataracts,

osteoporosis

For acute exacerbations. Not generally

for long-term use

Prednisone 40-80 mg total daily dose, dosed qd-bid, for a total course of 3-10 days

Prednisolone (Prelone, Flo-Pred, Orapred)

40-80 mg total daily dose, dosed qd-bid, for a total course of 3-10 days

Methylprednisolone (Medrol) PO or IV: 40-80 mg total daily dose,

dosed qd-bid, for a total course of 3-10

days

Methylxanthine

Theophylline (Theolair, Theochron,

Theo-24)

Dose must be individualized. Aim for

serum levels between 5 and 15

mcg/mL. IV: 0.2-0.4 mg/kg/hr

Immediate-release: Initially 300 mg

total daily dose, dosed q6-8hr. Can

increase to 400-1600 mg total daily

dose, dosed q6-8hr. Extended-release:

Initially 300 mg total daily dose, dosed

q8-12hr. Can increase to 400-1600 mg total daily dose, dosed q8-12hr.

GI side effects, CV adverse effects Narrow therapeutic index. Many drug

interactions due to CYP450 hepatic

metabolism. Use low dose with:

hepatic disease, HF, elderly. Caution

with cardiac disease, thyroid disease,

peptic ulcer disease, prostatic

hypertrophy, seizure disorder, smoking

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Controlled-release (Theo-24): Initially

300-400 mg q24hr. Can increase to 400-1600 mg total daily dose, dosed

q12-24hr

Inhaled anticholinergics Dry mouth, additional anticholinergic

effects

Caution with: closed-angle glaucoma,

bladder neck obstruction, prostatic

hypertrophy

Ipratropium (Atrovent, Atrovent HFA) MDI (17 mcg/ inhalation): 2-3

inhalations qid. Nebulizer: 500 mcg tid-

qid

May have additive benefit to inhaled

β2-agonists for severe exacerbations

Tiotropium (Spiriva) Powder in capsules for use with

HandiHaler: 18 mcg qd

Anti-IgE antibody

Omalizumab (Xolair) 150-375 mg SC every 2 or 4 weeks.

Dose based on baseline serum IgE and

body weight

CV and cerebrovascular adverse

events, infection, rare systemic

eosinophilia

Anaphylaxis. Caution in patients with

high risk for malignancy, caution with

live virus vaccines

For severe persistent asthma not

controlled with inhaled corticosteroids,

with sensitization to a perennial

airborne allergen

Magnesium sulfate 2 g IV Avoid with AV block. Caution with CKD For severe acute exacerbations

unresponsive to other medication

Combination agents

Corticosteroid/long-acting β2-

agonist

Budesonide/formoterol (Symbicort) 80/4.5 mcg, 160/4.5 mcg; dosed 2

inhalations bid

Mometasone/ formoterol (Dulera) 100/5 mcg, 200/5 mcg; dosed 2

inhalations bid

Fluticasone/salmeterol (Advair Diskus,

Advair HFA)

DPI: 100/50 mcg, 250/50 mcg, 500/50

mcg; dosed 1 inhalation bid. MDI:

45/21 mcg, 115/21 mcg, 230/21 mcg; dosed 2 inhalations bid

= first-line agent; = black box warning; bid = twice daily; CKD = chronic kidney disease; CV = cardiovascular; CYP = cytochrome P450 isoenzymes; DPI = dry powder inhaler; GI = gastrointestinal; HF =

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.

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Select Agents Reported to Be Associated with Reactive Airway Dysfunction Syndrome

Uranium hexafluoride

Hydrazine (35%)

Ammonia (paint spray) fumigating fog

Metal coating remover

Smoke

Floor sealant

Sulfur dioxide

Silo dust

Acetic acid

Anhydrous ammonia

Chlorine

Toluene diisocyanate

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Indications for Peak Flow Monitoring

Patients suspected of having occupational asthma when symptoms and exposures occur

When a new agent is suspected of causing occupational asthma

As a first screening test in establishing work-related problems

When specific challenge testing in the laboratory is not possible

When specific challenge testing result is negative but the history suggests occupational asthma

To document work aggravation of asthma

To determine whether the work environment is safe for the patient

To record when a bronchodilator is used

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Select Agents Associated with Occupational Asthma with or without a Latency

Onset after a Latent Period

Acid anhydrides

Aldehydes (formaldehyde, glutaraldehyde)

Acrylates

Animal proteins

Cobalt

Dusts from flour and grains

Dust from wood

Amines (ethylene diamine, monoethanolamine)

Isocyanates (toluene diisocyanate, hexamethylene diisocyanate)

Latex

Green tea/epigallocatechin

Food and cosmetic coloring/carmine

Freeze-dried raspberry powder

Fungicides/fluazinam and chlorothalonil

Onset without a Previous Latent Period

Contaminants in metalworking fluids

Chlorine gas (pulp from paper mills)

Bleach (sodium hypochlorite)

Strong acids

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Prevention Measures Instituted by Employers*

Primary prevention

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.

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Proper Technique for Recording Portable Peak Flow Rate Recordings

Standing upright position

No nose clip

Firm seal around the mouthpiece

Lungs filled to total capacity at the start of the test

A short forced expiratory maneuver is done as hard and fast as possible

The greatest of three consecutive measurements is recorded

The maximum mean and minimum peak flow rates over each day are plotted

Peak flow rates are recorded at least 4 times per day with 2 recordings at work and 2 away from work

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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)?

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Questionnaire: Determining Whether Asthma Symptoms Are Work Related

Did the symptoms of asthma start after you started a new job or when new materials were introduced at your job?

Do the symptoms of asthma develop within minutes after exposures or with specific activities at work?

Do symptoms occur several hours after exposures or during the evenings on workdays?

Do symptoms occur less often or not at all on days off work or on vacations?

Do symptoms occur frequently on returning to work?

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Diagnostic Criteria for Asthma

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

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Figures Top

Diagnostic Flowchart for Occupational Asthma

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