Occupational Asthma

Lawrence Martin, M.D., FACP, FCCP

Dr. Martin is a board-certified pulmonary specialist practicing in Cleveland. He is an examiner for the Ohio Bureau of Workers' Compensation on pulmonary-related cases, and Clinical Associate Professor of Medicine at Case Western Reserve University School of Medicine.

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Asthma is a common condition, affecting an estimated 5-10% of the general population (1, 2). It is estimated that one out of 10 adult asthmatics have a work-related connection, i.e., asthma either caused directly by their occupation or with pre-existing asthma reactivated by the job (3).

This article is written from the standpoint of a practicing pulmonary disease specialist who is often asked to evaluate individual claimants. Before discussing work-related asthma it will be necessary to discuss in general. Unlike other lung diseases that are unique to the job (e.g., asbestosis, silicosis), the mere diagnosis of asthma does not provide a link to the worker's occupation.


Asthma symptoms typically manifest as wheezing, chest tightness, cough and shortness of breath. Wheezing is a high pitched sound generated by air going through the constricted passages. Shortness of breath (the medical term is 'dyspnea') is typically felt with exertion, but in severe cases can be at rest.

In most stages asthma is a reversible condition, which means symptoms and air flow obstruction significantly improve with treatment. In mild cases, symptoms may go away without medication. Conversely, in a small percentage of asthmatics the airway obstruction doesn't reverse, and these patients end up with chronic obstructive pulmonary disease (COPD). We see this mainly in patients with repeated severe asthma attacks, particularly when are under-treated.

Asthma is to be distinguished from COPD, although there is often overlap in a given individual. The vast majority of cases of COPD are due to heavy smoking; only a small percentage is from severe/under-treated asthma. Smoking is not the cause of asthma, although it can worsen any asthmatic condition. Smoking is also a predisposing factor for some cases of occupational asthma.

At a basic level the cause of asthma is unknown. Given an individual's predisposition to asthma, variety of factors can trigger symptoms (Table 1). Perhaps the most common trigger in adults is respiratory viral infections, including the common cold. Less common, but very important, are allergens, substances that when inhaled can react with the host's antibodies to generate an "allergic" response. Allergens include various plant pollens, animal furs, excreta from house mites, proteins in shellfish, and some metals. Allergens play a major role in many cases of occupational asthma.

Irritants can also trigger an asthma attack through a non-allergic mechanism, by directly injuring cells within the lungs. Other triggers of an asthma attack include climate changes; exercise, particularly in cold weather; certain medications such as aspirin; and acid-reflux from the stomach. Although everyone is subjected to the types of triggers listed in Table 1, only the 5-10% of people "with asthma" are prone to develop symptoms when so exposed.

Table 1

Some common triggers of symptoms (the "asthma attack") in patients with asthma

  • Respiratory viral infections
  • Allergies (e.g., to pollen, animal fur, grain dust, dust mites, shell fish, diisocyanates, etc.)
  • Irritants (smoke, fumes, gases, other pollutants)
  • Climate changes
  • Exercise (particularly in cold air)
  • Sinus infections
  • Drug reactions, e.g., aspirin
  • Stomach acid reflux

A cardinal feature of asthma is its extreme variability. A patient can be free of symptoms one day and the next day be sick enough to require an emergency room visit or hospitalization. Symptoms can flare in the early morning hours and abate by late afternoon. Or, symptoms can be severe during part of the year (e.g., "allergy season") and be non-existent the rest of the year.

Our bronchial tubes are often compared to pipes, but they are far more fragile and elastic; they are made up of cartilage and connective tissue and lined with millions of tiny hairs (called "cilia") that help cleanse the lungs of inhaled pollutants. During an asthma attack the bronchial lining becomes inflamed; one manifestation of this inflammation is an excess accumulation of mucus in the airways. Products of inflammation lead to narrowing of the bronchial tubes, which in turn inhibits air flow and causes cough and shortness of breath (try breathing through a straw with your nose plugged).

The degree of bronchial tube narrowing reflects severity of the asthma attack. Obviously, if there is little or no air flow, the patient will die. When air flow is down to 50% of normal or less, the asthma attack is classified as severe. However, physicians cannot reliably gauge the degree of bronchial narrowing without an objective test. The basic test for this purpose is called 'spirometry'. Values obtained from spirometry are to asthma what blood sugar measurements are to diabetes: proper diagnosis and management depend on them. Every patient with an occupational asthma claim will have spirometry at least once, and usually more than once.

Spirometry requires a cooperative subject; he or she must take in a deep breath, then blow all the air out quickly and forcefully as possible through a flexible plastic tube, one end of which is held in the mouth. The other end of the tube is connected to the spirometer, which gauges how much air the patient blows out and at what rate.

The total amount of air blown out after a full inhalation is called the forced vital capacity, or FVC. Depending on age, height, and sex, healthy adults have an FVC between 4 and 6 liters, and can blow the air out within 3-4 seconds. Another key component of spirometry is the forced expiratory volume exhaled in the first second, called FEV-1. The ratio of FEV-1 over FVC (FEV-1/FVC) is an important derivative, reflecting severity of the airway obstruction. Normally, adults can blow out 75-80% of their FVC in the first second; anything less reflects airway obstruction.

A fourth key component of the spirometry test is the rate of air flow immediately after exhalation begins; this is called the peak expiratory flow rate, or 'peak flow'. Normal adult peak flow values are also dependent on age, sex and height, and range from about 400 to 700 liters/minute. Consider the following test results in a 27-year-old woman with asthma:

Spirometry values in a 27-year-old woman with asthma

Measurement Baseline values: No symptoms During asthma attack 1 hour after treatment
FVC 5 liters 3 liters 4 liters
FEV-1 4 liters 2 liters 3 liters
FEV-1/FVC 80% 66.7% 75%
Peak Flow 450 liters/min 200 liters/min 300 litesr/min
Comment Normal values Severe airflow obstruction Mild airflow obstruction; excellent response to inhaled medication

Typically (but not always) asthmatics have normal spirometry values when symptom-free, as does this woman; she exhales 80% of her forced vital capacity in the first second and has a peak flow of 450 liters/min. During the asthma attack her FVC and FEV-1 each decreased by two liters; the ratio (FEV-1/FVC) and the peak flow also decreased significantly. Decreases in FEV-1/FVC and peak flow are hallmarks of airway obstruction, and signify that the larger bronchial tubes are narrowed. (Abnormal values like these are also found in patients with other lung diseases, such as emphysema; the difference is that the air flow obstruction is reversible in asthma, but not in the other conditions.)

An hour after treatment (several doses of an inhaled bronchodilator) her values have improved considerably, though not back to baseline. The degree of improvement (33% increase in FVC, 50% increase in FEV- and peak flow) signifies that her bronchial tubes responded well to the medication, and that she is in fact "asthmatic." However, it may take much more medication, and several more days, for her to return to baseline values. (Again, a non-asthmatic with similar abnormal values would not respond with any significant improvement.)

Spirometers should be considered as essential a piece of medical equipment as EKG machines, but they are not nearly so prevalent. Whereas an EKG can be done by just about anyone and the patient does not need to do anything more than lie still, spirometry requires a well-trained technician and an alert, cooperative patient. Another hindrance to widespread use of spirometry is that most physicians are not as well versed in interpreting spirometry values as they are, say, in reading EKGs.

Fortunately, a simpler device can be used to assess asthma severity -- the peak flow meter. A peak flow meter is hand held, easily portable and much less expensive than the typical spirometer. It measures only one aspect of spirometry, the peak expiratory flow rate; this single number is easier to interpret than the multiple values obtained from spirometry. During asthma attacks the peak flow changes along with all other spirometry values, so the peak flow meter is usually adequate for gauging air flow obstruction. This is especially useful in the emergency room and urgent care center, where a quick and reliable assessment of air flow is essential. Also, peak flow can be measured by the patient at home or the work place; if accurately recorded, self-tested values can aid in both diagnosis and management.

Work-related asthma

In 1995 The American College of Chest Physicians published a consensus statement classifying types of asthma found in the workplace (4) (Table 2).

Table 2.


1. Occupational Asthma

Occupational asthma is defined as a disease characterized by variable airflow limitation and/or bronchial hyper-responsiveness due to causes and conditions attributable to a particular working environment and not to stimuli encountered outside the workplace. Two types of occupational asthma are distinguished by whether they appear after a latency period:

  • With a latency period -- encompasses all instances of immunologic asthma for which an immunologic mechanism has been identified and includes most high- and some low-molecular weight agents. For some agents causing this type of occupational asthma, evidence for an immunologic mechanism is still lacking (or may not exist).
  • Without a latency period -- best illustrated by irritant-induced asthma, e.g., reactive airways dysfunction syndrome (RADS).

Under certain exposure conditions, immunologic and non-immunologic mechanisms may coexist. 2. Work-Aggravated Asthma

Work-aggravated asthma is defined as concurrent asthma worsened by nontoxic irritants or physical stimuli in the workplace. A history of childhood asthma or concurrent asthma does not exclude possibility that occupational asthma may develop after an appropriate workplace exposure.

p> This classification distinguishes 'occupational asthma' from 'work-aggravated asthma'; the former is asthma that would not exist were it not for the occupational exposures, while the latter is pre-existing asthma made worse by the occupational exposures. This is a useful dichotomy, and the distinction is often crucial in compensation claims; in some venues work-aggravated may not be compensable (or as compensable) compared to true occupational asthma. In general usage, however, physicians and others involved with claims often lump both categories under the term "occupational asthma". Nonetheless, the ACCP classification points out the importance of clearly detailing each individual's condition.

"Immunologic asthma" is reversible airway obstruction due to an allergic mechanism. In allergic asthma there is a reaction between the offending substance (an antigen) and an antibody produced by the body's immune system; the resultant antigen-antibody reaction can trigger a release of chemicals that cause bronchial inflammation, airway narrowing and asthma symptoms. There is always a latency period (from weeks to years) between time of first contact with the allergen and development of asthma; this is because the subject must first become 'sensitized' to the allergen -- build up an immune response -- before he or she 'reacts' to it.

Many people mistakenly equate all asthma with "allergy", but in fact allergy is only one of the potential triggers of an asthma reac These allergens are typically categorized as high or low molecular weight compounds (1-2, 4-5), but the two groups cannot be distinguished on clinical grounds. Generally, high molecular weight compounds are mostly proteins from animals and plants; low molecular weight compounds include numerous chemicals. Examples of these compounds and the occupations at risk are given in Table 3.

Table 3. Some Antigens Responsible for Work-Related Asthma

animal danders animal handlers
insect scales entolmologists, lab workers
egg white proteins egg producers
grain dusts farmers, grain store workers
wood dusts saw mill workers, carpenters
latex health care workers
diisocyanates workers in printing and painting industry
anhydrides workers in plastics and drug industries
metallic salts tool and dye workers
antibiotics pharmaceutical workers

Low molecular weight diisocyanates are the leading causes of occupational asthma (5); they are used in many different manufacturing processes and their fumes can sensitize the worker. Occupational asthma can also occur in "clean" environments, such as in the pharmaceutical industry, where workers may develop sensitization after repeated exposed to low molecular weight antibiotics.

Another example of occupational asthma in a clean environment is latex allergy. Latex allergy in health care workers appears to be increasing in incidence (6-9). Latex, or natural rubber, is found in many medical products, particularly gloves. (Latex allergy is also seen in patients repeatedly exposed to health care workers' gloves and other latex-containing products.) Reactions range from contact hives (skin reaction only) to asthma and in some extreme cases, shock (anaphylaxis). For this reason many hospitals and dental offices have switched to non-latex gloves and other products. (Latex is not just confined to gloves, but is a component of numerous other hospital products, including intravenous lines and ventilation bags.)

Factors predisposing to latex allergy include a history of other allergies (such as hives or hay fever) and frequent exposure to latex products. 'Sensitization' to latex doesn't happen after a single exposure; instead, the worker becomes sensitized to the latex after repeated exposures, over time. Antibodies gradually build up until there is sufficient amount to produce an antigen (latex)-antibody reaction that produces bronchial inflammation and symptoms. Asthma from latex allergy is thought to arise from repeated inhalation of airborne latex particles that adhere to the cornstarch used to powder gloves (10-11). (Cornstarch is placed in gloves to make them easy to slip on and off.)

Other points bearing emphasis about the ACCP classification (Table 2).

Table 4.

Reactive Airways Dysfunction Syndrome (RADS) (12-13)

  • Exposure to a high concentration of irritant gas, smoke, fume, or vapor
  • Immediate onset of symptoms after single exposure to the irritant, although symptoms may not peak for several hours
  • Documented absence of preceding respiratory complaints
  • Symptoms (cough, wheeze and/or dyspnea) persist at least 3 months
  • Presence of airflow obstruction on pulmonary function testing
  • Presence of non-specific bronchial hyper-responsiveness
  • Other pulmonary diseases ruled out

Occupational asthma is the most prevalent occupational lung disease in developed countries (1), but just how common is it? A recent critical review of available literature found 23 studies that estimated the attributable risk of asthma due to occupational exposures (3). These data were from 17 countries and the estimates varied widely, from 2% to 33%. Using these data, and additional studies that allowed estimation of the attributable risk, the authors wrote that "half of the attributable risk estimates were between 5% and 19%, with a median of 9%." They concluded that "occupational factors are associated with about 1 in 10 cases adult asthma, including new onset disease and reactivation of preexisting asthma." (3)

There are approximately 200 million people in the U.S. age 18 or older (source: www.census.gov). Given a 5-10% prevalence rate of asthma, an estimated 1-2 million U.S. adults have asthma in some way related to work place exposures. (These are prevalence estimates, and do not mean 1-2 million new cases each year.)

Evaluation of work-related asthma

The standard paradigm for evaluating any new patient is: 1) detailed history of the present illness, 2) complete past medical history, 3) physical examination, and 4) selected tests. Clearly, for any condition that may be work-related, a complete occupational and environmental history must be woven into 1) and 2).

As a rule, the most important aspect of evaluating suspected work-related asthma is establishing temporal relationships between exposures and symptoms. A thorough history is paramount. This means a detailed job description (initially from the worker) coupled with the nature and timing of all symptoms. Physical exam and spirometry may be normal when the patient sees his physician. Even if asthma is diagnosed, its clinical features (exam and spirometry) won't distinguish occupational from non-occupational causes. But a detailed accounting of the temporal relationships will usually reveal if there likely is (or is not) a work-related connection. This is true even if the causative agent or agents are not yet identified.

Establishing such relationships may not be easy, especially with allergic reactions. In immunologic asthma, symptoms can occur within minutes of an exposure, but can also occur hours later, after the worker has left the plant and gone to bed (1-2). In most cases temporal relationships by themselves (without testing) can't diagnose work-related asthma, but they can help focus the investigation. An outline of the evaluation process is provided in Table 5.

Table 5

Evaluation of a Patient for Possible Work-related Asthma

Every patient

  • History of the present illness -- emphasis on temporal relationships between job exposures and symptoms; ongoing medical problems; current medications, etc.
  • Documented information about worker's job and work environment (if available): occupational health records; material safety data sheets; industrial hygiene reports; printed job descriptions; co-worker affidavits
  • Worker's past medical and work history -- emphasis on allergies; smoking; other respiratory illnesses, including sinusitis; hospitalizations and doctor visits, including pulmonary function tests; previous work environments
  • Information about current and previous non-work environments
  • Physical examination -- with emphasis on cardiac and respiratory systems
  • Chest x-ray (if none within past year)
  • Spirometry before and after inhaled bronchodilator

Selected patients

  • Bronchoprovocation test (with inhaled non-specific methacholine or histamine)
  • Allergy skin tests
  • Immunologic blood tests
  • Serial peak flow measurements, self-tested by the patient
  • Specific broncho-provocation test with suspected antigen

Much has been written about self-tested, serial peak flow measurements(14-17). The idea behind this strategy is to establish temporal relationships between peak flows and work exposures by having the worker measure his or her own peak flows. The peak flow test is technically simple to do, with each measurement taking only a few seconds.

Typically, the worker checks his or her peak flow every two hours, at work and at home, for a period of about two weeks. A symptom diary is also kept, and in this manner temporal relationships between exposure and air flow obstruction may be established. If the peak flow is seen to fall, say, four hours after entering the work place every day, and to improve on weekends away from work, then a clear temporal relationship is established. Although the idea is a good one, for various reasons self-tested peak flows are rarely used in practice. The test is entirely effort-dependent, record keeping can be onerous, and there is no way to assure that the results recorded are entirely valid (16-17).

Medical management of work-related asthma is no different from asthma unrelated to the job, with one important exception: advice about continued working. If a worker has developed an allergic reaction to something in the environment (i.e., is "sensitized" to it), he or she must leave that environment. The quicker they remove themselves, the better the outcome; studies have shown that continued exposure to the sensitizing agent is associated with further deterioration of lung function (18-19). Masks and other devices to minimize the exposure are of no help, and should not be relied on. Even tiny amounts of allergen can trigger a reaction if the worker is sensitized to it.

On the other hand, if the asthma was due to a one-time irritant exposure, and the irritant is removed completely, than there should be no contraindication to continued working in that environment. One caveat is that other pollutants in the environment may bother the worker more than before, even though the specific agent causing the asthma is removed.

Although stopping exposure generally results in clinical improvement, this is not invariable, particularly if the worker is a smoker or has co-existing sinusitis (which can also trigger asthma exacerbations). Even without these other conditions, the patient may continue to manifest bronchial hyper-responsiveness and require medication for months or years after leaving the job (19).

Work-related Asthma in the Real World

Inevitably, once a physician diagnoses work-related asthma, a claim will be filed on behalf of the Such a claim is for payment of some sort, and often leads to intense debate between opposing parties. In the real world the diagnosis will likely involve the employer, a state workers' compensation agency, claim administrators, lawyers, non-treating physicians hired as medical experts and, if the case goes to trial, a judge and jury. There are four basic reasons why most claims for occupational asthma end up disputed or challenged.

Consider the following cases, each illustrating one of the four points above:


A 36-year-old man had asthma from age 10 to age 16. From age 17 he was symptom free, without need for any asthma medication. He held numerous blue collar jobs until age 35, when he began working in a factory making cardboard boxes. This process involved sawing cardboard cutouts, and applying glue to pieces of cardboard. He smoked about a pack of cigarettes a day, and had done so for 15 years.

At age 36 he developed an upper respiratory infection, with sneezing, coughing and flu-like symptoms; he reported feeling "congested" with "chest tightness" at home, but gradually improved over several days, and returned to work after a week's absence.

After returning to work he noted recurrence of coughing and chest tightness when around the cardboard dust, something he had never experienced before. His symptoms increased each day and by the third day back at work he had to go to an Urgent Care center for treatment. There he was noted to be wheezing, and was sent to a lung specialist. Spirometry testing showed air flow obstruction, with response to inhaled medication. Based on his history and test results, a claim was filed for "occupational asthma".

Several months later the state Workers' Compensation Agency sent him to another lung specialist to evaluate the claim of "occupational asthma." That evaluation revealed air flow obstruction typical of asthma.

Numerous questions are raised by this claim. Did the worker suffer a recurrence of childhood asthma? Was his adult onset of asthma related solely to the upper respiratory infection (a common trigger in the general population)? Did he have underlying airways disease from smoking? Did he have "work-aggravated" asthma, made worse by the dust but not caused by it, or did he develop true "occupational asthma?" Such questions often cannot be answered after a one-time evaluation, but require close follow up and repeated testing. Even then, one often cannot medically assess -- with certainty -- the origin of a patient's asthma.


A 56 year-old man was treated by his family physician for exacerbation of chronic obstructive pulmonary disease (COPD). The patient had a long smoking history, estimated at 40 pack-years (pack a day for 40 years). Some wheezing was heard on the exam. Noting that the patient "works in a foundry," his family physician wrote in the chart:

"Dx. COPD - occupational asthma."

A worker's compensation claim was filed, supported solely by the physician's statement (reiterated on the claim form without any supporting information).

In this case the family physician wanted to give his patient a jump start for his claim, and the sloppily-made diagnosis 'occupational asthma' was all was needed. Two years later the claim was disallowed, after several evaluations by other physicians and documentation that the patient's air flow obstruction was fixed and not reversible, and clearly due to smoking. In other words, not only did this claimant not have occupational lung disease, he did not have asthma.


A 45-year-old female, non-smoking factory worker was exposed to numerous chemicals in her job making plastic molds. She had no prior history of asthma before developing symptoms of wheezing and cough two years into her job. The symptoms abated on weekends away from work and flared again on Mondays back at work. By history and temporal relationships she had developed classic occupational asthma from fumes at her work site. The company hired a pulmonary expert who reviewed the file and the list of chemicals that she was exposed to (from material safety data sheets). Toward the end of his comprehensive report he wrote:

"I know of nothing this patient was exposed to that can cause asthma,"

and denied that she had occupational asthma.

This case is an example of unwarranted expert bias. Over 250 chemicals and compounds have been implicated in occupational asthma (1-2, 4-5), and these are just the substances that have been identified and published in peer-review journals. The list grows yearly (in 1990 it was around 200 chemicals and compounds [24]), and it has never been considered complete. Thus, perusing some material safety data sheets and not finding a published chemical obviously does not rule out occupational asthma. This expert was mis-characterizing the medical literature to counter the claim.

For the individual patient, finding a specific agent is less important than documenting temporal changes in lung function that implicate some causal factor from which the patient can be removed (25). In this case, after the specific temporal relationships and relevant medical literature were cited, the claim was allowed for occupational asthma.


A physician evaluating an asthma patient for "percentage of disability" found the FEV-1 15% below predicted. He wrote that the patient had "15% impairment of the body as a whole," implying a modest degree of fixed impairment and therefore disability. However, he did not address the fact that the patient: a) was taking daily bronchodilator medication, without which the FEV-1 would likely have been much lower; b) had much worse lung function during exacerbations, as documented in emergency department records; and c) was completely disabled for gainful employment because of airway hyper-responsiveness and lack of any skill outside the dusty trades.

In this last case, the physician substituted a precise but limited statement on impairment for a fuller characterization of the patient's true disability from asthma.

Evaluating Claims for Work-related Asthma: A Personal Perspective

For the physician treating a given patient, the goals are straight forward -- first, do no harm, then do what is best for your patient's health. Aside from job counseling, medical management of work-related asthma is no different from managing any other kind.

Apart from the treating physician, however, other physicians often become involved as "experts" when a claim is filed; their job is to assess the claim without treating the patient. Expert physicians may be hired by an impartial government agency, or by a legal team partial to one side or the other. As with any other type of occupational lung disease, physicians should evaluate a work-related claim as objectively as possible no matter who is paying (26). Such a position in no way obviates becoming a paid expert. Indeed, "when called upon on behalf of either defendants or plaintiffs, physicians have an obligation and a duty to participate in the justice system as expert witnesses." (27)

When colleagues in medicine question a diagnosis it is usually in a friendly context. Diagnosis of occupational lung diseases is different. Inappropriate and unsupported claims can expect to be challenged, and when that happens even the most casual declarative statement will come under intense scrutiny (28-29). Other physicians will likely be hired to argue against the diagnosis. The physician may be deposed, his or her background explored, credentials examined, integrity called into question. A physician who takes a medically incorrect or obviously biased stand can actually harm the side he is trying to help, especially if his testimony becomes discredited.

One way physicians can avoid what I call "pitfalls in diagnosis" is to report what they could comfortably defend to their peers. For example, I imagine presenting my report to a group of peers on whose mutual respect I depend. I would look foolish making statements unsupported by any evidence, or statements logically fallacious. Yet many physicians, on both sides of the issue, routinely write reports that seem to flaunt common logic and the extant medical literature (26). In the area of occupational asthma I have encountered many mis-statements by board-certified pulmonary experts, all of whom were writing as paid experts for or against a claim. Examples:

  • 'continued asthma symptoms after a patient has left the workplace rules out occupationally-caused asthma' [not true; see 18-19, 21, 30].
  • 'absence of prior sensitization rules out occupational asthma' [not true; see 12-13].
  • ' blood eosinophilia in asthma is specific for allergy' [not true; see 31].
  • 'antibody to an inhaled compound (e.g., trimellitic acid) is diagnostic of occupational asthma from that compound' [not true; see 32].

Medicine is an art and legitimate controversies exist about many diagnoses, including occupational asthma (29, 33). Physicians live with uncertainty in both diagnosing and attributing causation in this and many other diseases. It is only in the legal world that physicians are asked to state a diagnosis (or its cause) as "more probable than not" and, if need be, affirm this statement under oath.

The fact that work-related asthma -- or any type of occupational lung disease -- also involves the legal profession should not affect one's objectivity or clinical approach. Physicians have an obligation to themselves and to society to help assure that patients deserving compensation get it, and that claimants without a compensable occupational illness are not unjustly rewarded.



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10. Tomazic VJ, Shampaine EL, Lamanna A, et al. Cornstarch powder on latex products is an allergen carrier. J Allergy Clin Immunol 1994;93:751-758.

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17. Malo JL. Assessment of peak expiratory flow in asthma. Curr Opin Pulm Med. 1996;2:75-80.

18. Kuschner WG, Chitkara RK, Sarinas PS. Occupational asthma. Practical points for diagnosis and management. West J Med. 1998 Dec;169(6):342-50.

19. Montanaro A. Prognosis of occupational asthma. Ann Allergy Asthma Immunol 1999 83: 593- 96.

20. Richman SI. Meanings of impairment and disability. The conflicting social objectives underlying the confusion. Chest 1980;78(suppl):367-71.

21. Chan-Yeung M. Evaluation of impairment/disability in patients with occupational asthma. Amer Rev Respir Dis 1987;135:950-51.

22. American Medical Association Guides to the Evaluation of Permanent Impairment, Fourth Edition. American Medical Association, 1993, Chicago.

23. American Thoracic Society: Guidelines for the evaluation of impairment/disability in patients with asthma. Amer Rev Respir Dis 1993;147:1056-61.

24. Chan-Yeung M. Occupational asthma. Chest 1990;98:148S-161S.

25. Cullen MR, Cherniack MG, Rosenstock L. Occupational Medicine. New Engl J Med 1990; 322:594-601.

26. Martin L. Pitfalls in diagnosis of occupational lung disease for purposes of compensation: One physician's perspective. Cleveland State Marshall Law School Journal of Law and Health; Vol 13, Issue 1, 1999. Pages 49-68.

27. ACCP Guidelines for an expert witness. Chest 1990;98:1006.

28. Richman SI. Compensating victims of occupational lung disease: The physician's role in the system. J Occup Med 1989;31:335-38.

29. Richman SI. Legal treatment of the asthmatic worker. A major problem for the nineties. J Occup Med 1990;32:1-27-31.

30. Cockcroft DW, Hargreave FE. Airway hyperresponsiveness. (Editorial). Amer Rev Resp Dis 1990;142:497-500. <

31. Kay AB. Eosinophils and Neutrophils in the Pathogenesis of Asthma. Chapter 23, in: Weiss EB, Segal MS, Stein M, eds. Bronchial Asthma, 2nd edition, Little Brown, Boston, 1985.

32. Patterson, et. al. Use of immunologic technology in the diagnosis of environmental and occupational lung disease. Chest 1990;98(suppl):206S-207S.

33. Bernstein IL, Moira Chan-Yeung M, Jean-Luc Malo JL, editors. Asthma in the Workplace, 2nd ed., 1999; Marcel Dekker, New York.

Copyright 2000 Lawrence Martin, M.D.

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