Course Authors

E. Neil Schachter, M.D.

Dr. Schachter reports no commercial conflict of interest.

Estimated course time: 1 hour(s).

Albert Einstein College of Medicine – Montefiore Medical Center designates this enduring material activity for a maximum of 1.0 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

In support of improving patient care, this activity has been planned and implemented by Albert Einstein College of Medicine-Montefiore Medical Center and InterMDnet. Albert Einstein College of Medicine – Montefiore Medical Center is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.

 

Learning Objectives

Upon completion of this Cyberounds^®, you should be able to:

• Discuss the roles of history, physical examination and laboratory testing in the diagnosis of OAD

• Design a management approach for treating the patient with OAD

• Characterize the clinical course of byssinosis.

 

Diagnosis

The diagnosis of occupational airway disease involves two interrelated approaches: the first being the demonstration and characterization of the airway disease (i.e., does the worker indeed have airway disease and what is its nature); the second, and often most demanding, is the establishment of the work-relatedness of the airway disease. Table 1 lists those diagnostic approaches and tests used to delineate occupational airway disease.

All authors reviewing this topic agree that a careful occupational history is essential. This involves an understanding of the nature and variety of workplace agents known or suspected to be airway irritants or sensitizers, as well as a familiarity with the worker's specific workplace exposures.

Both bronchitis and asthma are clinical diagnoses defined by history and confirmed by lung function studies (e.g., reversibility of obstruction by bronchodilator, airway reactivity to methacholine).

Work-relatedness of symptoms and findings is frequently suggested by onset of symptoms within the context of the workplace: specialized settings, such as the cardroom in byssinosis; the absence of previous airway or allergic disease; the improvement of symptoms on weekends, vacations or on job transfer; and the presence of similar symptoms (although not necessarily severe) among co-workers. A physician imposed work restriction with careful follow-up (diaries, peak flow measurements) can be most useful in tracking work-relatedness. In some cases the clinical setting may be pathognomonic. The development of Monday dyspnea, for example, in textile workers or the sudden onset of respiratory symptoms and lab findings of hyperreactivity following a heavy exposure to an irritant (e.g., Reactive Airways Dysfunction Syndrome or RADS).

In many situations, the findings may be confusing, with symptoms often more prominent at the end of a workday or at night (delayed responses, see Figure 1) and confounded by multiple variables (e.g., cigarette smoking, pre-existing allergies). For workers with childhood airway diseases that have subsided in adulthood, this may be a difficult diagnostic problem. In workers presenting with established fixed airway disease (e.g., chronic bronchitis or chronic airway obstruction), workplace associations may be hard to establish and symptoms may persist through weekends, vacations and even into retirement. Knowledge of the natural history of the disease for a specific agent established, in general, by epidemiologic methods, is necessary for the assessment.

History taking involves a careful review of current employment as well as past employment. Each job should be defined as to the nature of the task, the physical setting in which it is performed, the agents used, the by-products of the process (e.g., dusts from grinding, carding or sawing, gases given off by chemical reactions) and related processes that may be occurring contiguously in the work-place. Physical conditions (e.g., temperature), level of activity, environmental pollutants (e.g., tobacco smoke) may be important co-factors or even primary causes of disease.

A latency period is usually experienced before symptoms become prominent -- up to several years for textile workers, months for typical allergens.

Physical examination, chest x-ray and routine spirometry can establish the hallmarks of obstructive lung disease (wheezing, hyperinflation, reversible airway obstruction) but have no specificity for occupational airway disease. They can and should be used to establish the degree of impairment that a worker experiences. Peak flow measurements, accompanied by diary records, can establish diurnal variations, work-relatedness and the response to a changing environment. Airway lability with consistent variation in peak flow of more than 20% between AM and PM measurements suggests the kind of diurnal variations seen with asthma. If the healthcare provider spends time explaining and demonstrating the maneuver to the patient, consistent and reliable readings can be obtained which are well worth the effort.

Non-specific airways challenge(1) testing is frequently used to confirm the presence of airway irritability in workers. Abnormal studies help to confirm the presence of asthma. The development of severe persistent airway hyperreactivity, in the setting of an acute exposure, has been used to define RADS. There are, nevertheless, serious shortcomings in using these tests to validate occupational airway disease. Negative responses do not exclude occupational airway disease.(2),(3) While hyperreactivity may wane in some workers following removal from an offending exposure,(4) this is not always the case, particularly when exposure is great (RADS) or sustained.(5)

Skin testing and serum precipitins may be useful in characterizing occupational airway disease. Atopy can be established by demonstrating positive skin reactions to two or more common allergens. Skin testing with specific occupational antigens may corroborate a highly suspicious case but should not be considered as definitive proof. If the antigen is likely to be seen only in the workplace, the specificity of the test increases (e.g., platinum salts).(6) Skin tests with antigens from animal products,(7) castor bean extract,(8) coffee(9) and flour (10) also produce skin reactions in sensitized workers but are not as specific because of the ubiquitous presence of these agents. The demonstration of IgE antibodies has also been used to confirm sensitization, particularly in response to large molecular weight antigens (lab animals,(11) flour(12) coffee(13). IgE antibodies to low molecular weight compounds have not consistently been found in symptomatic workers (e.g., isocyanates(13) wood dust(14) nickel(15).

Specific inhalation testing is frequently used to confirm that an airway response is linked to a given workplace agent (as opposed to some or multiple agents in the workplace). In contrast to evaluation in the workplace, where the worker is exposed to the suspected agent in the natural setting, laboratory challenges are performed in controlled environments, such as an environmental chamber (see Figure 2). Challenges may be performed with irritants (e.g., gases) or allergens (e.g., antibiotics, extracts of animals or plant products). Because delayed responses may occur with such challenge, it has been recommended that they be performed in specialized facilities and that the patient be monitored for at least 24 hours after challenge. Reasons for performing specific challenge are listed in Table 2. The safety of testing personnel must also be considered.

Specific bronchial provocation is performed using a group of study methods which attempts to duplicate the exposure and the dose experienced by the worker in the workplace. There are several approaches.(16) In some cases, traditional antigen extracts are prepared for nebulization via a standard aerosol generator using the protocol of Chai and co-workers.(17) Bronchial provocation using these standard nebulizers has been frequently criticized as delivering an unrealistic challenge not reflective of the workplace. Occupational materials, such as grain dust or wood dust, can be inhaled as a challenge by pouring workplace dust from one pan to another in an otherwise clean chamber. Fine powders, such as antibiotics or platinum salts, are mixed with a vehicle (e.g., dried lactulose). Soldering can be performed in a specialized environment to recreate workplace vapors associated with colophony.

The dose of standard allergens producing immediate hypersensitivity can be gauged by skin testing. A subthreshold dose, as evaluated by skin testing, can be administered as an aerosol and the dose varied either by concentration or by length of exposure. If skin testing does not yield immediate reactions, the aerosol challenge dose must be evaluated empirically by estimated work exposures or a previous knowledge of an agent's ability to cause bronchospasm.

Delayed responses have been recorded not only the evening or the night following provocation but also on subsequent days.(18),(19) Thus, follow-up of patients, using peak flow meters, is warranted beyond 24 to 48 hours.

Bronchial alveolar lavage (BAL) has been used to characterize the inflammatory response induced by occupational agents(20) but is not, at this point, a diagnostic maneuver of established clinical value.

Workplace studies, exclusive of monitoring lung function in the workplace for a given worker, are most appropriately performed in the context of an epidemiological survey. Limited surveys may be helpful in gaining a better understanding of the relationship between the worker and the suspected agent and in better characterizing the processes by which a worker is exposed.

Therapy

Ideally, for the individual patient found to have impairment as a result of occupational airway disease, removal from the offending agent is the recommended strategy since the disease may involve sensitization, and exposure to even low levels of the agent may aggravate and perpetuate the disease. Management may be complicated by issues related to job seniority or security and any inability of the worker to transfer within or outside of the industry. Some of the options that occur depend on the size of the industry, the prevalence of disease within the industry, and the existence of federal regulations (see Table 3).

Protective devices, job transfer with retention of pay, improving ventilation in the work area may or may not be feasible. Therapy for the symptomatic relief of occupational airway disease is similar to that of standard asthma, although some drugs, such as di-sodium cromoglycate, may have a special role in these syndromes.(21)

Byssinosis: A Case in Point

Byssinosis is an occupational lung disease associated with the inhalation of cotton and other textile dusts. (22),(23) Over 600,000 US textile workers are at risk of developing byssinosis. [The worldwide cohort is difficult to estimate because of the nature of the industry in third world countries, where much of the production is now concentrated, but the number is certainly in the millions.] Cotton processing is by far the largest industry whose workers are at risk of byssinosis. Epidemiologic studies have now extensively documented both acute and chronic effects on the airways of textile workers.

In the early phases of byssinosis, acute reversible symptoms, such as wheezing, chest tightness and shortness of breath, accompany reversible changes in lung function.(24) "Monday dyspnea" is the term used to describe these symptoms that occur on the first day back at work after an absence. The disease may progress to a stage in which symptoms are present throughout the workweek and may eventually result in severe respiratory disability.(25) This has been estimated to occur in 7% of older cotton textile workers.(26)

The characterization of the disease has primarily been based on respiratory symptoms as well as the clinical grading of Schilling(27):

Grade 0: No particular symptoms on first day of working week.

Grade 1/2: Occasional chest tightness or irritation of respiratory tract (e.g., cough) on the first day of working week.

Grade 1: Chest tightness on every first day of working week.

Grade 2: Chest tightness on first and other days of working week.

Grade 3: Grade 2 symptoms accompanied by evidence of permanent incapacity.

Lung function measurements are used clinically and epidemiologically to evaluate the severity of illness and to document acute changes over a work shift. These measurements form the basis for medical surveillance currently mandated in the cotton textile industry.

Inherent in Schilling's clinical grading of byssinosis is the distinction between acute reversible bronchospasm and chronic, debilitating airflow obstruction. While the acute response has been characterized by across-shift changes in lung function and the chronic response identified by the presence of chronic bronchitis and/or impaired lung function, the transition between the two stages of the disease is still poorly understood. Prospective studies in cotton textile workers have documented an accelerated decline in lung function.

The essential dose-relatedness of byssinosis was established in the 1970s by Merchant et al,(28) who showed an increasing prevalence of byssinosis grades with higher dust levels. These relationships form the basis for the current stringent standards established for the regulation of the cotton textile industry in the United States. Additional refinement of these standards may come as more specific surrogates of the byssinotic effect are characterized (e.g., endotoxin (29) and our understanding of the airway active agent(s) in cotton dust becomes known.