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Cough: Occupational and Environmental Considerations : ACCP Evidence-Based Clinical Practice Guidelines FREE TO VIEW

Susan M. Tarlo, MBBS, FCCP
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Correspondence to: Susan M. Tarlo, MBBS, FCCP, Toronto Western Hospital, EW7–449, 399 Bathurst St, Toronto, ON, M5T 2S8 Canada; e-mail susan.tarlo@utoronto.ca



Chest. 2006;129(1_suppl):186S-196S. doi:10.1378/chest.129.1_suppl.186S
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Objectives: This section of the guideline aims to review the role of occupational and environmental factors in causing and contributing to cough. It also aims to indicate when such causes should be considered in a clinical setting, and a general approach to assessment and management.

Methods: A review was performed of published data between 1985 and 2004 using PubMed. The search terms used included “air pollution,” “sick building syndrome,” “occupational asthma,” “occupational lung disease,” “hypersensitivity pneumonitis” (HP), “cigarette smoke,” and “asthma.” Selected articles were chosen when meeting the objectives, but the extent of articles available and the limited space for this section does not permit a fully comprehensive review of all of these areas, for which the reader is referred to other sections of this clinical practice guideline, the published literature, textbooks of occupational lung disease, or more specific review articles.

Results/conclusions: Almost any patient presenting with cough may have an occupational or environmental cause of or contribution to their cough. The importance of this is that recognition and intervention may result in full or partial improvement of the cough, may limit the need for medication/symptomatic treatment, and may improve the long-term prognosis. Nonoccupational environmental contributing factors for upper and lower airway causes of cough include indoor irritant and allergenic agents such as cigarette smoke, cooking fumes, animals, dust mites, fungi, and cockroaches. Causes of HP indoors include birds and fungal antigens. Outdoor pollutants and allergens also contribute to upper and lower airway causes of cough. Occupational exposures can cause hypersensitivity responses leading to rhinitis and upper airway cough syndrome, previously referred to as postnasal drip syndrome, as well as asthma, HP, chronic beryllium disease, and hard metal disease, as well as irritant or toxic responses. The diagnosis is only reached by initially considering possible occupational and environmental factors, and by obtaining an appropriate medical history to determine relevant exposures, followed by objective investigations. This may require referral to a center of expertise.

Occupational and environmental factors may be a cause of cough or may exacerbate cough that has been initially caused by other mechanisms. Therefore, occupation and environment should be considered as possible factors when evaluating every patient with cough. A detailed discussion of the pathogenesis, diagnosis, and management of every occupational and environmental contributing factor/disease is beyond the scope of this section, and more detail, when needed, can be obtained from other relevant sections of this clinical practice guideline or from more specialized publications. A review was performed of data published between 1985 and 2004 using PubMed. The search terms used included “air pollution,” “sick building syndrome,” “occupational asthma” (OA), “occupational lung disease,” “hypersensitivity pneumonitis” (HP), “cigarette smoke,” and “asthma.” Selected articles were chosen when meeting the objectives.

Pathogenesis

Exposures to allergens (eg, dust mite, animal or cockroach allergens, fungi and pollen) in the home, at school, in other indoor environments, or outdoors can trigger upper or lower respiratory causes of cough (eg, allergic rhinitis, asthma, allergic bronchopulmonary mycoses, or HP). Exposures to respiratory irritant agents, other than cigarette smoke, are generally less than would be encountered in occupational settings. Exposure to tobacco smoke should be assessed in all children and adults with cough. There is evidence of increased risk and severity of asthma in the children of parents who smoke,14 and the airway irritant effects of tobacco smoke will aggravate asthma, both from personal smoking and the inhalation of second-hand smoke, in addition to the other risks associated with tobacco smoking57 such as chronic obstructive lung disease, lung cancer, and cardiac disease, all of which commonly include cough as a symptom. Exposure to indoor biomass, which is widely used for cooking or heating in several developing countries, has also been shown to be a significant risk factor for childhood and adult asthma.89 The term hut lung has been used for the finding of increased respiratory symptoms and lung disease associated with indoor particulate pollution from biomass combustion.13

Exposures to water-damaged homes or buildings have been reported to be associated with increased respiratory symptoms, including cough, which potentially may relate to dampness itself, or to associated exposures to dust mites, endotoxin, or fungal components such as glucans,1416 and the reduction of bioaerosols such as by ultraviolet germicidal lights in buildings may reduce some symptoms.17Mechanisms include IgE antibody-mediated responses to dust mites or fungi causing allergic rhinitis and upper airway cough syndrome, which has previously been referred to as postnasal drip syndrome, or asthma. Alternatively, there may be mucous membrane irritation from endotoxin or fungal glucans causing cough.19 Air pollutants such as nitrogen oxides from gas cooking stoves or outdoor traffic have been linked in some studies, particularly in children,20to increased respiratory symptoms including cough and increased symptoms from respiratory viral infections.2122 Outdoor air pollutants such as ozone can cause cough and can increase airway inflammation, triggering asthma symptoms.2327 The response varies with individual susceptibility, but symptomatic effects are likely to be greater in those persons who have preexisting poorly controlled asthma. There is also the suggestion that chronic, relatively high outdoor ozone exposure may be associated with the increased development of childhood asthma.23 Other outdoor pollutants may also be associated with increases in cough as a component of asthma or chronic bronchitis; an increase in the number of emergency department visits and hospital admissions, and in mortality rates for respiratory diseases have been associated with increases in acid aerosols and particulate air pollutants measured as the coefficient of haze, particulate air pollution of mass mean aerodynamic diameter ≤ 10 μm, and particulate air pollution of mass mean aerodynamic diameter ≤ 2.5 μm.25,2829

Unusual outdoor environmental exposures may trigger cough. “Epidemics” of emergency department visits for asthma have resulted from allergic responses to soya bean dusts from the unloading of soya beans in the harbors in Spain,3031 to grass pollen fragments during thunderstorms in Britain,32and to fungal spores in the midwest of North America.33Fungi can also potentially trigger cough through the induction of HP, as in Japanese summer-type HP, which has been linked to indoor exposure to trichosporon cutaneum.34

Diagnosis

The identification of nonoccupational environmental causes or triggers of cough depends on a detailed exposure history. As with other causes of cough, the anatomic source of the cough needs to be identified by medical history, physical examination, and appropriate investigations as indicated from the medical history and physical examination findings. If an allergic mechanism is suspected, then skin-prick testing or in vitro tests for specific IgE antibodies, including allergen extracts that are suggested from the exposure history, can be helpful. Unfortunately, these tests are of limited value for some allergens, such as several fungal allergens, due to a degree of cross-reactivity between some species and poorly sensitive or specific skin test extracts, since there is variability in expressed allergens under different conditions of fungal growth and different substrates. Objective exposure assessment is also limited for fungi due to a lack of correlation between bulk sampling results and airborne exposures, and the lack of a standard interpretation of air-sampling results. When cough is diagnosed on the basis of an allergic respiratory response that can be objectively documented by abnormalities in pulmonary function or chest radiography, then improvements that occur in these tests after removal from a specific environment or exposure may be helpful in further linking the respiratory disease to the environmental agent. Similarly, short-term deterioration in the results of these tests after specific exposure challenges to these agents either in the environmental setting or in specific controlled challenge tests would provide further diagnostic information. However, such objective confirmation is difficult to obtain in clinical practice for upper respiratory causes of cough and for cough triggered by respiratory irritants, and often the approach taken is to empirically suggest a trial of avoidance of the suspected agent/environment, if feasible. If the exposure is in the outdoor environment, such as during the unloading of soya beans,35 then appropriate public health environmental changes may be needed. In the case of the soya bean unloading in Barcelona, the installation of appropriate filters prevented significant outdoor exposure to the soya bean dust. If avoidance is not practical, or if symptoms are considered to be due to mild upper or lower respiratory irritation, then pharmacologic management is an alternative approach as with non-environmentally triggered diseases.

Pathogenesis

Almost every nonoccupational respiratory disease has an occupational equivalent, which may not be identified unless a good occupational history is taken. Many patients with occupational lung diseases may present with a cough. Relatively common examples include OA (with a differential diagnosis including non-OA and work-related aggravation of asthma), HP, hard metal disease (ie, giant cell interstitial pneumonitis from cobalt) or asbestosis (with differential diagnoses including idiopathic pulmonary fibrosis), chronic beryllium lung disease (with a differential diagnosis including sarcoidosis), occupational bronchitis (with a differential diagnosis including nonoccupational bronchitis), and occupational lung cancer (with a differential diagnosis including nonoccupational causes of lung cancer). Relatively low workplace respiratory irritant exposures may induce cough on the basis of mucous membrane irritation as a presumed mechanism of cough associated with sick building syndrome (possibly related to components of bioaerosols such as endotoxins or fungal glucans) or from upper airway irritation secondary to chemicals such as solvents. In addition, workplace factors can induce or aggravate rhinitis and upper airway cough syndrome. The suggestion has also been made that some high-level occupational irritant exposures might also trigger gastroesophageal reflux as a cause of cough.36Finally, in some patients cough may follow an irritant exposure without any objective explanation; findings in one study37 have suggested that there may be increased capsaicin sensitivity and cough without airway hyperresponsiveness in some cases after exposures that may be expected to irritate the airways.

Pathogenesis and Diagnosis

Occupational rhinitis causing cough as a result of an upper airway cough syndrome is most commonly recognized as allergic occupational rhinitis3840 with or without conjunctivitis, caused by an IgE antibody-mediated response to a workplace sensitizer, and often preceding OA.38,4142 Rhinitis may also accompany OA due to low-molecular-weight chemical sensitizers at work, but it is difficult to diagnose in individual patients since the immunologic mechanism is less commonly IgE-mediated and specific tests to confirm causation are usually not possible to perform clinically. Common work exposures associated with occupational rhinitis include laboratory animal workers with allergic rhinitis from laboratory animal allergy,43or nonallergic rhinitis associated with endotoxin exposure; bakers with allergic rhinitis to wheat, egg, enzymes, or other high-molecular-weight allergens in the bakery;4445 health-care workers exposed to natural rubber latex from powdered gloves,46 enzyme workers,39 and workers exposed to acid anhydrides,47acrylic compounds,48 and diisocyanates.

Prevalence and Pathogenesis

OA is now the most common chronic occupational lung disease in most developed areas and has been estimated to account for approximately 10% of all cases of adult-onset asthma from cross-sectional studies,49with up to 29% and 17%, respectively, attributable fraction among men and women in a Finnish population incidence study.50 Cough is a common presenting symptom in OA, either alone or in combination with wheeze, chest tightness, and shortness of breath, as is the case with non-OA. OA is most commonly induced by sensitization to a workplace substance, either through an IgE antibody-mediated response or other presumed immunologic response, or, less commonly, by an acute high-level irritant exposure (ie, irritant-induced asthma), of which the most clear-cut example is reactive airways dysfunction syndrome (RADS).

Diagnosis

OA cannot be diagnosed without obtaining a thorough medical history. A key component of the history is a full occupational history, with special detail of the occupational exposures at the time of symptom onset, not only substances used by the patient in the workplace, but also substances used by coworkers that may become airborne. Details of the introduction of new materials shortly before the onset of symptoms, and a history of any accidental high-level exposures such as spills, may lead to the suspicion of OA. Other aspects of the medical history that lead to an increased suspicion of OA are a history of improved symptoms when away from work, such as weekends or holidays with recurrence or worsening on a return to the workplace. These historical features, while sensitive, are not specific for OA, however, and need to be assessed with objective investigations to confirm the diagnosis of asthma and its relationship to work.5152 The initial investigations aim to confirm whether asthma is the cause of cough, as in cases of suspected asthma from nonoccupational causes, by means of spirometry before and after bronchodilator therapy, and if the spirometry findings are normal or there is no significant bronchodilator responsiveness, then histamine or methacholine challenge testing is helpful to identify the associated airway hyperresponsiveness. These tests need to be performed within 24 h of symptoms or within 24 h of the suspected causative job exposure, because they may become normal with longer periods away from exposure to a relevant workplace sensitizer and may result in a missed diagnosis in that event. If a diagnosis of asthma is confirmed (from the clinical history and pulmonary function responses), then it is necessary to objectively demonstrate whether a work relationship is present.

Diagnosis

As has been detailed in some guidelines and reviews5152 for OA caused by a specific sensitizer, the relationship of asthma to work may be determined by assessing the variability in airflow limitation in relationship to work by patient self-recorded serial peak expiratory flows or spirometric data (as well as respiratory medication use and symptom scores), which can then be interpreted in relation to workplace exposures. These are best recorded at least four times a day in triplicate, using either inexpensive peak flow meters, electronic hand-held peak flow devices, or spirometers. Recordings should be performed during periods of work weeks as well as periods away from the suspected exposure for comparison, preferably at least 10 days away from the workplace exposure area (ideally when off work). The addition of a measure of airway responsiveness such as methacholine challenge tests performed near the end of a working exposure week (within 24 h of exposure),51 and for comparison at the end of a period away from exposure (ideally 2 to 3 weeks away from work) adds a further objective measure to assess airway changes related to work. A threefold improvement in the provocative concentration of methacholine causing a 20% fall in FEV1 when away from the work exposure supports a diagnosis of OA if the results have not been confounded by other factors such as intercurrent upper or lower respiratory infection, or nonoccupational allergen exposure. If these tests cannot be performed or cannot be clearly interpreted, then specific laboratory exposure challenge tests can be helpful, although they are available in relatively few centers.,53Alternatively, it is sometimes possible to perform a closely monitored “workplace challenge” when a technician supervises hourly spirometry during separate days, with the patient performing work in the suspected occupational setting and in an unexposed environment.54 Immunologic tests, such as skin tests when the exposure at work has included high-molecular-weight allergens such as animal proteins or natural rubber latex, can provide further assistance with the diagnosis; however, these tests, although sensitive, are relatively nonspecific for OA, and the results can be positive in exposed workers who do not have a history of respiratory allergy up to the time of testing.38,55For low-molecular-weight occupational sensitizers, skin testing is only useful to assess sensitization to a few agents such as complex platinum salts and, to a lesser extent, salts of other metals such as nickel and cobalt.5659 Similarly, in vitro immunologic tests can be used to demonstrate the presence of specific IgE antibodies to a workplace sensitizer,63 but the use of such tests for low-molecular-weight sensitizers is limited by their reliable availability for relatively few agents, generally in research laboratories,6469 and by antibody presence in only a minority of patients with OA as a result of exposure to the more common low-molecular-weight sensitizers such as diisocyanates (used in polyurethane products and spray paints)70and plicatic acid (in Western red cedar),71in whom other immunologic mechanisms may also be important.7275

Newer investigations, which have been reported in research studies, include the use of induced sputum to assess changes in sputum eosinophilic inflammation during periods at work vs periods off work. While this appears to add diagnostic accuracy to other investigations such as serial peak flow monitoring,76some cases of OA have been associated with neutrophilic inflammatory airway markers rather than eosinophilic inflammation.77Consequently, further investigation will be needed to clarify the interpretation of findings from induced sputum samples in the assessment of OA. The role of other newer investigations such as exhaled nitric oxide measurements and breath condensate analyses also needs further investigation to determine their possible roles in clinical evaluation of OA.7879

Management

Once a diagnosis is reached, the management of OA that is caused by a specific work sensitizer includes the avoidance of further exposure to that sensitizer and medical management of the asthma. Often, the patient will need to move to a different work environment or change jobs. Outcome is best with early diagnosis and early removal from exposure.

Diagnosis

A diagnosis of OA related to an irritant exposure relies mainly on the documentation of an accidental high exposure to a respiratory irritant agent with the onset of asthma symptoms, persisting for at least 3 months and starting shortly after the irritant exposure, in a patient with no preceding evidence of asthma. An objective diagnosis of asthma after the exposure is reached by evidence of a significant airway bronchodilator response or positive methacholine challenge result. Patients who meet the relatively stringent criteria for RADS, as described by Brooks et al,80most certainly will have a diagnosis of irritant-induced asthma. Other reports8183 have modified these criteria to include less massive exposures, less persistent symptoms, or greater delays in the onset of symptoms after exposures. Such an expansion of the criteria of Brook et al80 may represent true irritant-induced asthma, and increases the frequency of diagnosis but decreases the certainty of a true diagnosis.83

The irritant exposure leading to RADS or irritant-induced asthma has most frequently been reported indoors in enclosed spaces with high fume exposures. However, high outdoor exposures to alkaline dust (largely related to calcium oxide) from the collapse of the World Trade Center were associated with occupational airway irritant responses, leading to “World Trade Center cough” in firefighters and other occupationally exposed groups.36 There was an increase in airway responsiveness associated with this exposure,84 which was reported to have a later onset after exposure than the 24 h used in the criteria Brooks et al.80 The findings of cough and increased airway responsiveness were likely based on the presence of irritant-induced asthma (or RADS), but also in some exposed workers cough was associated with increases in symptoms of rhinitis and gastroesophageal reflux, so the causes of cough may have been multifactorial. Although the New York firefighters underwent preemployment medical assessments and periodic medical surveillance to exclude asthma among the active workers, there were also reports of increased symptoms among asthmatic lower Manhattan residents following the collapse of the World Trade Center that may have resulted from an irritant aggravation of underlying asthma, although, as with the firefighters, other mechanisms may also have played a role.

Those with Irritant-induced asthma may be able to stay in the same workplace with appropriate asthma pharmacotherapy and environmental control measures if provisions are made to prevent further high-level irritant exposures.

In addition to the induction of new-onset asthma, occupational exposures can aggravate preexisting asthma, particularly workplace exposures to dusts, fumes, and sprays, which trigger bronchoconstriction in workers with hyperreactive airways. A similar response can occur in asthmatic patients who at work are exposed to cold dry air or put forth strenuous exertion, and these effects are likely to be greatest in those with poor pharmacologic control of their asthma or in workers with severe airway hyperresponsiveness. A diagnosis of true OA needs to be excluded in such patients by the means discussed above, and management of the condition consists of optimizing environmental control measures and pharmacotherapy, as well as controlling personal workplace exposures to respiratory irritants and triggers (eg, with the use of respiratory protection for short-term potential irritant exposures, and the institution of appropriate ventilation and containment measures for respiratory irritants at work).

Occupationally induced eosinophilic airway inflammation can result in cough with or without sputum production but without other physiologic changes of asthma (ie, an absence of airflow limitation and bronchial hyperresponsiveness). This can be induced by the same workplace sensitizers, which can cause OA, and is a presumed immunologic response. Diagnosis relies on the demonstration of significant eosinophilia in sputum samples, usually obtained by sputum induction, and the presence of ≥ 3% eosinophils in sputum samples obtained at the end of a working week, with reduction in the percentage of eosinophils in sputum during periods off work, has been suggested as the criterion for diagnosis.85 The same management regimen as that for OA from a sensitizer includes the avoidance of exposure to the causative work agent and the use of therapy with inhaled steroids.

Cough is a common symptom of HP in addition to dyspnea, chills, and fever. HP can be caused by a hypersensitivity response to medications, to inhaled environmental high-molecular-weight antigens, or to certain chemicals. The range of inhaled agents is large, including antigens from fungi,8688 mycobacteria,89thermophilic actinomycetes (bacteria),90parasites, and birds.91 Nonoccupational antigenic causes, as covered in a separate section of this guideline, include indoor fungi for Japanese summer HP34 and indoor microbial contamination, including contamination of humidifiers and vaporizers,92 hot tubs (including mycobacterial contamination),89 and swimming pool areas,93 in office settings or homes.

Occupational causes of HP include organic dust exposures, as in farmers exposed to “moldy” hay or to chickens, turkeys, or other birds, or in lifeguards or office workers exposed to water contaminated by microorganisms. Chemical exposures that can trigger HP include diisocyanates, most commonly diphenylmethane-diisocyanate.94Metal-working fluid (coolant) contaminated by microorganisms is also a relatively commonly reported cause of HP in the industrialized workplace.95Key aspects of the diagnosis, as with the diagnosis of OA, include an initial suspicion of an extrinsic cause for any patient with interstitial lung disease, careful history-taking for exposure to birds, areas that may generate fungal or other bioaerosol exposures (eg, barns, contaminated homes, offices, hot tubs, swimming pool areas, or other workplace exposures), and potential work exposure to chemicals that can cause this response. Suspicion is further increased if respiratory findings are intermittent in relation to these exposures and clear up without pharmacologic intervention after a few days away from a particular area. BAL findings of predominant lymphocytosis in a patient with apparent interstitial lung disease and findings of giant cell granulomas on lung biopsy specimens also raise suspicion of an extrinsic cause. The demonstration of specific serum IgG antibodies to the suspected agent further supports the diagnosis, although the standardization of antigen extracts is difficult in some cases. Pulmonary function tests can show restrictive changes with reduced diffusing capacity apparent especially on exercise, but chronic airflow limitation may predominate in patients with chronic HP with bronchiolitis. In patients with the acute form of HP, chest radiograph findings may mimic pneumonia, and in patients with the chronic form of HP the findings may resemble idiopathic pulmonary fibrosis. A high-resolution CT scan showing a ground-glass appearance may be helpful in distinguishing the chronic form of HP.97 Occasionally, a specific challenge may be needed for medicolegal purposes to confirm the diagnosis, especially if the findings of radiographic and other investigations are nonspecific.

Patients with hard metal disease (ie, giant cell interstitial pneumonitis from cobalt) or asbestosis (with differential diagnoses including idiopathic pulmonary fibrosis) also may initially present with a dry cough. As with the previous occupational diseases, the work history is a key component in making the diagnosis, but the patient may not be aware of all occupational exposures, and the physician needs to be aware of the types of work in which such exposures may occur and obtain details from a review of material safety data sheets and any occupational hygiene reports that may be obtained from the workplace. Early identification and removal of the patient from further exposure are key components of treatment.

Beryllium is being used more widely than in the traditional uses in the aerospace industries and nuclear power plant facilities. Current uses include the manufacture of materials from alloys containing beryllium for the production of pen clips, golf clubs, and other products. The presenting symptoms can include cough and dyspnea with chest radiographic findings that are identical to those for sarcoidosis.98Thus, chronic beryllium lung disease should be included in the differential diagnosis of sarcoidosis, and an overt or covert exposure to beryllium should be carefully assessed from a medical history supplemented, where appropriate, by beryllium lymphocyte proliferation tests.99

Other occupational lung diseases in patients who may present with cough include occupational bronchitis (with a differential diagnosis including nonoccupational bronchitis) and occupational lung cancer (with a differential diagnosis including nonoccupational causes of lung cancer). The workplace has been estimated to account for approximately 15% of the burden of chronic obstructive lung disease (a mean estimate from several studies).100 Exposure assessment is necessary in addition to information as to other known contributing factors to assist in estimating the probability of occupational contributions to these diseases.

Cough and other asthma-like symptoms are a relatively common component of sick building syndrome, which has been reported most often in sealed office buildings.1416 Associated factors have included psychosocial stress, poor building maintenance, complaints as to temperature or humidity control, and volatile organic compound exposures. Several studies have shown an association with airborne endotoxin or fungal contamination in buildings, and one study17 showed a significant improvement in symptoms with blinded use of biocidal ultraviolet radiation in a crossover study. A similar syndrome, darkroom disease, occurring in radiograph technologists, has also been associated with greater self-reporting of work conditions that would be expected to be associated with low-level irritant exposures, as well as with psychosocial stressors.101

This syndrome has been described mainly in agricultural settings and may be confused initially with HP because the symptoms are similar. Cough may be a prominent feature, with chest tightness, fever, and malaise starting 4 to 8 h after exposure to contaminated grain dust and usually lasting 36 to 48 h before clearing. Although some exposed workers can have airway hyperresponsiveness, and more typical features of asthma or chronic bronchitis, the acute symptoms are more similar to humidifier fever, polymer fume fever, and metal fume fever. Unlike HP, the chest radiograph and pulmonary function test findings are usually normal, and BAL fluid samples show mainly neutrophils. The cause and mechanisms are not fully understood, but in some cases it has been suggested to relate to the contamination of grain or other organic dust by fungi or endotoxins, triggering neutrophil activation and the release of cytokines. More chronic airway inflammatory effects can also occur from these exposures, with chronic cough and sputum, as can more typical findings of asthma.102104

As noted from the above review, almost any cause of cough may have an occupational or environmental cause or contribution. Therefore, a review of the patient’s occupational and environmental exposures is needed in all patients with cough. The failure to identify and correct an occupational or environmental cause or contribution to cough will lead to an increased need for the pharmacologic management of disease, and may lead to progressive disease despite the use of medications to treat the condition. The most common potentially modifiable nonoccupational environmental causes/triggers are tobacco smoke for children and adults, and indoor allergens, such as from cats or other animals, and dust mites. Exposure to these and an assessment of their relevance in cough should be specifically determined for all patients with rhinitis, asthma, and COPD, while other antigenic triggers such as birds and contaminated humidifiers should be considered for all who may have HP.

Occupational exposures should be considered specifically for all patients with rhinitis, asthma, or HP whose symptoms start during their working life. For those with potential diseases of longer latency, such as chronic beryllium disease and hard metal disease or chronic HP, the medical history should specifically include all previous occupational exposures.

The outcome of many occupational causes of cough improves with an early diagnosis and a change in occupational exposure. Research is needed to determine effective strategies to enable the early recognition of occupational causes and contributions to cough. The role of submassive respiratory irritant exposures needs to be further understood and criteria developed for a diagnosis of these effects. Interactions between occupational sensitizers and irritants also need to be better understood to minimize morbidity from such exposures. Host susceptibility factors need clarification and may eventually permit modification. Methods for identifying new potential respiratory sensitizers prior to their use in the workplace need to be developed and alternative nonsensitizing materials need to be developed. Better exposure assessment is also needed to understand details of the exposures leading to many of the occupational and environmental causes of cough.

1. In every patient with cough, when taking a medical history, ask about occupational and environmental causes. Level of evidence, expert opinion; benefit, substantial; grade of recommendations, E/A

2. In every patient with cough who has potentially significant exposures to suspicious environmental or occupational causes, determine the relationship of these occupational and environmental factors to confirm or refute their role in cough and to modify or eliminate exposure to the relevant agents. Level of evidence, expert opinion; benefit, substantial; grade of recommendations, E/A

3. Because outdoor environmental pollution and occupational exposures can be important factors in causing cough, physicians should play a role in developing and supporting enforceable standards for safe workplace and outdoor air pollution exposure limits. Level of evidence, expert opinion; benefit, substantial; grade of recommendations, E/A

4. In patients with a high suspicion of cough due to environmental or occupational exposures, consider referring the patient to a specialist in this area or consult evidence-based guidelines. Level of evidence, expert opinion; net benefit, substantial; grade of recommendation, E/A

Abbreviations: HP = hypersensitivity pneumonitis; OA = occupational asthma; RADS = reactive airways dysfunction syndrome

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Gordon, SB, Curran, AD, Turley, A, et al Glass bottle workers exposed to low-dose irritant fumes cough but do not wheeze.Am J Respir Crit Care Med1997;156,206-210
 
Archambault, S, Malo, JL, Infante-Rivard, C, et al Incidence of sensitization, symptoms, and probable occupational rhinoconjunctivitis and asthma in apprentices starting exposure to latex.J Allergy Clin Immunol2001;107,921-923
 
Sarlo, K, Kirchner, DB Occupational asthma and allergy in the detergent industry: new developments.Curr Opin Allergy Clin Immunol2002;2,97-101
 
Platts-Mills, TA, Longbottom, J, Edwards, J, et al Asthma and rhinitis related to laboratory rats: use of a purified rat urinary allergen to study exposure in laboratories and the human immune response.N Engl Reg Allergy Proc1987;8,245-251
 
Malo, JL, Lemiere, C, Desjardins, A, et al Prevalence and intensity of rhinoconjunctivitis in subjects with occupational asthma.Eur Respir J1997;10,1513-1515
 
Karjalainen, A, Martikainen, R, Klaukka, T, et al Risk of asthma among Finnish patients with occupational rhinitis.Chest2003;123,283-288
 
Draper, A, Newman, TA, Cullinan, P Estimating the incidence of occupational asthma and rhinitis from laboratory animal allergens in the UK, 1999–2000.Occup Environ Med2003;60,604-605
 
Smith, TA, Parker, G, Hussain, T Respiratory symptoms and wheat flour exposure: a study of flour millers.Occup Med (Lond)2000;50,25-29
 
Brisman, J, Belin, L Clinical and immunological responses to occupational exposure to alpha-amylase in the baking industry.Br J Ind Med1991;48,604-608
 
Tarlo, SM, Sussman, GL, Holness, DL Latex sensitivity in dental students and staff: a cross-sectional study.J Allergy Clin Immunol1997;99,396-401
 
Grammer, LC, Ditto, AM, Tripathi, A, et al Prevalence and onset of rhinitis and conjunctivitis in subjects with occupational asthma caused by trimellitic anhydride (TMA).J Occup Environ Med2002;44,1179-1181
 
Lindstrom, M, Alanko, K, Keskinen, H, et al Dentist’s occupational asthma, rhinoconjunctivitis, and allergic contact dermatitis from methacrylates.Allergy2002;57,543-545
 
Blanc, PD, Toren, K How much adult asthma can be attributed to occupational factors?Am J Med1999;107,580-587
 
Karjalainen, A, Kurppa, K, Martikainen, R, et al Work is related to a substantial portion of adult-onset asthma incidence in the Finnish population.Am J Respir Crit Care Med2001;164,565-568
 
Tarlo, SM, Boulet, LP, Cartier, A, et al Canadian Thoracic Society guidelines for occupational asthma.Can Respir J1998;5,289-300
 
Chan-Yeung, M, Malo, JL, Tarlo, SM, et al Proceedings of the first Jack Pepys Occupational Asthma Symposium.Am J Respir Crit Care Med2003;167,450-471
 
Ortega, HG, Weissman, DN, Carter, DL, et al Use of specific inhalation challenge in the evaluation of workers at risk for occupational asthma: a survey of pulmonary, allergy, and occupational medicine residency training programs in the United States and Canada.Chest2002;121,1323-1328
 
Chan-Yeung, M, McMurren, T, Catonio-Begley, F, et al Occupational asthma in a technologist exposed to glutaraldehyde.J Allergy Clin Immunol1993;91,974-978
 
Tarlo, SM, Wong, L, Roos, J, et al Occupational asthma caused by latex in a surgical glove manufacturing plant.J Allergy Clin Immunol1990;85,626-631
 
Merget, R, Schultze-Werninghaus, G, Bode, F, et al Quantitative skin prick and bronchial provocation tests with platinum salt.Br J Ind Med1991;48,830-837
 
Merget, R, Caspari, C, Dierkes-Globisch, A, et al Effectiveness of a medical surveillance program for the prevention of occupational asthma caused by platinum salts: a nested case-control study.J Allergy Clin Immunol2001;107,707-712
 
Dolovich, J, Evans, SL, Nieboer, E Occupational asthma from nickel sensitivity: I. Human serum albumin in the antigenic determinant.Br J Ind Med1984;41,51-55
 
Kusaka, Y, Yokoyama, K, Sera, Y, et al Respiratory diseases in hard metal workers: an occupational hygiene study in a factory.Br J Ind Med1986;43,474-485
 
Platts-Mills, TA, Longbottom, J, Edwards, J, et al Occupational asthma and rhinitis related to laboratory rats: serum IgG and IgE antibodies to the rat urinary allergen.J Allergy Clin Immunol1987;79,505-515
 
Kim, YK, Oh, SY, Jung, JW, et al IgE binding components inTetranychus urticaeandPanonychus ulmi-derived crude extracts and their cross-reactivity with domestic mites.Clin Exp Allergy2001;31,1457-1463
 
Desjardins, A, Malo, JL, L’Archeveque, J, et al Occupational IgE-mediated sensitization and asthma caused by clam and shrimp.J Allergy Clin Immunol1995;96,608-617
 
Bardy, JD, Malo, JL, Seguin, P, et al Occupational asthma and IgE sensitization in a pharmaceutical company processing psyllium.Am Rev Respir Dis1987;135,1033-1038
 
Shimoda, T Detection of IgE antibodies specific to isonicotinic acid hydrazide and its metabolite by enzyme-linked immunosorbent assay and the mechanism of sensitization by inhalation or ingestion of this compound.Arerugi1990;39,567-576
 
Park, JW, Kang, DB, Choi, SY, et al Heterogeneity of IgE epitopes of vinyl sulphone reactive dye: human serum albumin that react with IgE.Clin Exp Allergy2001;31,1779-1786
 
Park, JW, Kim, CW, Kim, KS, et al Role of skin prick test and serological measurement of specific IgE in the diagnosis of occupational asthma resulting from exposure to vinyl sulphone reactive dyes.Occup Environ Med2001;58,411-416
 
Kramps, JA, van Toorenenbergen, AW, Vooren, PH, et al Occupational asthma due to inhalation of chloramine-T: II. Demonstration of specific IgE antibodiesInt Arch Allergy Appl Immunol1981;64,428-438
 
Howe, W, Venables, KM, Topping, MD, et al Tetrachlorophthalic anhydride asthma: evidence for specific IgE antibody.J Allergy Clin Immunol1983;71,5-11
 
Bernstein, DI, Zeiss, CR, Wolkonsky, P, et al The relationship of total serum IgE and blocking antibody in trimellitic anhydride-induced occupational asthma.J Allergy Clin Immunol1983;72,714-719
 
Son, M, Lee, M, Kim, YT, et al Heterogeneity of IgE response to TDI-HSA conjugates by ELISA in toluene diisocyanate (TDI)-induced occupational asthma (OA) patients.J Korean Med Sci1998;13,147-152
 
Tse, KS, Chan, H, Chan-Yeung, M Specific IgE antibodies in workers with occupational asthma due to western red cedar.Clin Allergy1982;12,249-258
 
Frew, A, Chang, JH, Chan, H, et al T-lymphocyte responses to plicatic acid-human serum albumin conjugate in occupational asthma caused by western red cedar.J Allergy Clin Immunol1998;101,841-847
 
Frew, A, Chan, H, Salari, H, et al Is tyrosine kinase activation involved in basophil histamine release in asthma due to western red cedar?Allergy1998;53,139-143
 
Chan-Yeung, M Mechanism of occupational asthma due to western red cedar (Thuja plicata).Am J Ind Med1994;25,13-18
 
Bernstein, DI, Cartier, A, Cote, J, et al Diisocyanate antigen-stimulated monocyte chemoattractant protein-1 synthesis has greater test efficiency than specific antibodies for identification of diisocyanate asthma 2.Am J Respir Crit Care Med2002;166,445-450
 
Girard, F, Côté, J, Boulet, LP, et al An effective strategy for diagnosing occupational asthma: use of induced sputum.Am J Respir Crit Care Med2004;170,845-850
 
Magni, K, Lemiere, C, Ghezzo, H, et al Airway inflammation after cessation of exposure to agents causing occupational asthma.Am J Respir Crit Care Med2004;169,367-372
 
Lemiere, C Non-invasive monitoring of airway inflammation in occupational lung diseases.Curr Opin Allergy Clin Immunol2002;2,109-114
 
Rahman, I, Kelly, F Biomarkers in breath condensate: a promising new non-invasive technique in free radical research.Free Radic Res2003;37,1253-1266
 
Brooks, SM, Weiss, MA, Bernstein, IL Reactive airways dysfunction syndrome (RADS): persistent asthma syndrome after high level irritant exposures.Chest1985;88,376-384
 
Tarlo, SM, Broder, I Irritant-induced occupational asthma.Chest1989;96,297-300
 
Brooks, SM, Hammad, Y, Richards, I, et al The spectrum of irritant-induced asthma: sudden and not-so-sudden onset and the role of allergy.Chest1998;113,42-49
 
Tarlo, SM Workplace irritant exposures: do they produce true occupational asthma?Ann Allergy Asthma Immunol2003;90,19-23
 
Banauch, GI, Alleyne, D, Sanchez, R, et al Persistent hyperreactivity and reactive airway dysfunction in firefighters at the World Trade Center.Am J Respir Crit Care Med2003;168,54-62
 
Quirce, S Eosinophilic bronchitis in the workplace.Curr Opin Allergy Clin Immunol2004;4,87-91
 
Moreno-Ancillo, A, Padial, MA, Lopez-Serrano, MC, et al Hypersensitivity pneumonitis due to inhalation of fungi-contaminated esparto dust in a plaster worker.Allergy Asthma Proc1997;18,355-357
 
Woodard, ED, Friedlander, B, Lesher, RJ, et al Outbreak of hypersensitivity pneumonitis in an industrial setting.JAMA1988;259,1965-1969
 
Cormier, Y, Israel-Assayag, E, Bedard, G, et al Hypersensitivity pneumonitis in peat moss processing plant workers.Am J Respir Crit Care Med1998;158,412-417
 
Rickman, OB, Ryu, JH, Fidler, ME, et al Hypersensitivity pneumonitis associated withMycobacterium aviumcomplex and hot tub use.Mayo Clin Proc2002;77,1233-1237
 
Duchaine, C, Meriaux, A, Brochu, G, et al Saccharopolyspora rectivirgulafrom Quebec dairy barns: application of simplified criteria for the identification of an agent responsible for farmer’s lung disease.J Med Microbiol1999;48,173-180
 
Zacharisen, MC, Schlueter, DP, Kurup, VP, et al The long-term outcome in acute, subacute, and chronic forms of pigeon breeder’s disease hypersensitivity pneumonitis.Ann Allergy Asthma Immunol2002;88,175-182
 
Ganier, M, Lieberman, P, Fink, J, et al Humidifier lung: an outbreak in office workers.Chest1980;77,183-187
 
Moreno-Ancillo, A, Vicente, J, Gomez, L, et al Hypersensitivity pneumonitis related to a covered and heated swimming pool environment.Int Arch Allergy Immunol1997;114,205-206
 
Baur, X Hypersensitivity pneumonitis (extrinsic allergic alveolitis) induced by isocyanates.J Allergy Clin Immunol1995;95,1004-1010
 
Fox, J, Anderson, H, Moen, T, et al Metal working fluid-associated hypersensitivity pneumonitis: an outbreak investigation and case-control study.Am J Ind Med1999;35,58-67
 
Lacasse, Y, Selman, M, Costabel, U, et al Clinical diagnosis of hypersensitivity pneumonitis.Am J Respir Crit Care Med2003;168,952-958
 
Glazer, CS, Rose, CS, Lynch, DA Clinical and radiologic manifestations of hypersensitivity pneumonitis.J Thorac Imaging2002;17,261-272
 
Newman, LS, Lloyd, J, Daniloff, E The natural history of beryllium sensitization and chronic beryllium disease.Environ Health Perspect1996;104(suppl),937-943
 
Newman, LS, Mroz, MM, Maier, LA, et al Efficacy of serial medical surveillance for chronic beryllium disease in a beryllium machining plant.J Occup Environ Med2001;43,231-237
 
American Thoracic Society Statement.. Occupational contribution to the burden of airway disease.Am J Respir Crit Care Med2003;167,787-797
 
Tarlo, SM, Liss, GM, Greene, JM, et al Work-attributed symptom clusters (darkroom disease) among radiographers versus physiotherapists: associations between self-reported exposures and psychosocial stressors.Am J Ind Med2004;45,513-521
 
Von Essen, S, Fryzek, J, Nowakowski, B, et al Respiratory symptoms and farming practices in farmers associated with an acute febrile illness after organic dust exposure.Chest1999;116,1452-1458
 
Monso, E, Magarolas, R, Radon, K, et al Respiratory symptoms of obstructive lung disease in European crop farmers.Am J Respir Crit Care Med2000;162,1246-1250
 
Spurzem, JR, Romberger, DJ, Von Essen, SG Agricultural lung diseas.Clin Chest Med2002;23,795-810
 

Figures

Tables

References

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Wilson, SR, Yamada, EG, Sudhakar, R, et al A controlled trial of an environmental tobacco smoke reduction intervention in low-income children with asthma.Chest2001;120,1709-1722
 
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Mannino, DM Chronic obstructive pulmonary disease: definition and epidemiology.Respir Care2003;48,1185-1191
 
Mannino, DM COPD: epidemiology, prevalence, morbidity and mortality, and disease heterogeneity.Chest2002;121,121S-126S
 
Mishra, V Effect of indoor air pollution from biomass combustion on prevalence of asthma in the elderly.Environ Health Perspect2003;111,71-78
 
Schei, MA, Hessen, JO, Smith, KR, et al Childhood asthma and indoor woodsmoke from cooking in Guatemala.J Expo Anal Environ Epidemiol2004;14(suppl),S110-S117
 
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Mishra, V Indoor air pollution from biomass combustion and acute respiratory illness in preschool age children in Zimbabwe.Int J Epidemiol2003;32,847-853
 
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Wan, GH, Li, CS Indoor endotoxin and glucan in association with airway inflammation and systemic symptoms.Arch Environ Health1999;54,172-179
 
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Barnes, PJ Air pollution and asthma.Postgrad Med1994;70,319-325
 
Chauhan, AJ, Inskip, HM, Linaker, CH, et al Personal exposure to nitrogen dioxide (NO2) and the severity of virus-induced asthma in children.Lancet2003;361,1939-1944
 
McConnell, R, Berhane, K, Gilliland, F, et al Asthma in exercising children exposed to ozone: a cohort study.Lancet2002;359,386-391
 
Linn, WS, Gong, H, Jr The 21st century environment and air quality influences on asthma.Curr Opin Pulm Med1999;5,21-26
 
Peden, DB Pollutants and asthma: role of air toxics.Environ Health Perspect2002;110(suppl),565-568
 
Romieu, I, Sienra-Monge, JJ, Ramirez-Aguilar, M, et al Genetic polymorphism of GSTM1 and antioxidant supplementation influence lung function in relation to ozone exposure in asthmatic children in Mexico City.Thorax2004;59,8-10
 
Schwartz, J Air pollution and children’s health.Pediatrics2004;113,1037-1043
 
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Anto, JM, Sunyer, J, Rodriguez-Roisin, R, et al Community outbreaks of asthma associated with inhalation of soybean dust: Toxicoepidemiological Committee.N Engl J Med1989;320,1097-1102
 
Anto, JM, Sunyer, J, Reed, CE, et al Preventing asthma epidemics due to soybeans by dust-control measures.N Engl J Med1993;329,1760-1763
 
Davidson, AC, Emberlin, J, Cook, AD, et al A major outbreak of asthma associated with a thunderstorm: experience of accident and emergency departments and patients’ characteristics; Thames Regions Accident and Emergency Trainees Association.BMJ1996;312,601-604
 
O’Hollaren, MT, Yunginger, JW, Offord, KP, et al Exposure to an aeroallergen as a possible precipitating factor in respiratory arrest in young patients with asthma.N Engl J Med1991;324,359-363
 
Yoshida, K, Ando, M, Sakata, T, et al Prevention of summer-type hypersensitivity pneumonitis: effect of elimination ofTrichosporon cutaneumfrom the patients’ homes.Arch Environ Health1989;44,317-322
 
Anto, JM, Sunyer, J, Newman Taylor, AJ Comparison of soybean epidemic asthma and occupational asthma.Thorax1996;51,743-749
 
Prezant, DJ, Weiden, M, Banauch, GI, et al Cough and bronchial responsiveness in firefighters at the World Trade Center site.N Engl J Med2002;347,806-815
 
Gordon, SB, Curran, AD, Turley, A, et al Glass bottle workers exposed to low-dose irritant fumes cough but do not wheeze.Am J Respir Crit Care Med1997;156,206-210
 
Archambault, S, Malo, JL, Infante-Rivard, C, et al Incidence of sensitization, symptoms, and probable occupational rhinoconjunctivitis and asthma in apprentices starting exposure to latex.J Allergy Clin Immunol2001;107,921-923
 
Sarlo, K, Kirchner, DB Occupational asthma and allergy in the detergent industry: new developments.Curr Opin Allergy Clin Immunol2002;2,97-101
 
Platts-Mills, TA, Longbottom, J, Edwards, J, et al Asthma and rhinitis related to laboratory rats: use of a purified rat urinary allergen to study exposure in laboratories and the human immune response.N Engl Reg Allergy Proc1987;8,245-251
 
Malo, JL, Lemiere, C, Desjardins, A, et al Prevalence and intensity of rhinoconjunctivitis in subjects with occupational asthma.Eur Respir J1997;10,1513-1515
 
Karjalainen, A, Martikainen, R, Klaukka, T, et al Risk of asthma among Finnish patients with occupational rhinitis.Chest2003;123,283-288
 
Draper, A, Newman, TA, Cullinan, P Estimating the incidence of occupational asthma and rhinitis from laboratory animal allergens in the UK, 1999–2000.Occup Environ Med2003;60,604-605
 
Smith, TA, Parker, G, Hussain, T Respiratory symptoms and wheat flour exposure: a study of flour millers.Occup Med (Lond)2000;50,25-29
 
Brisman, J, Belin, L Clinical and immunological responses to occupational exposure to alpha-amylase in the baking industry.Br J Ind Med1991;48,604-608
 
Tarlo, SM, Sussman, GL, Holness, DL Latex sensitivity in dental students and staff: a cross-sectional study.J Allergy Clin Immunol1997;99,396-401
 
Grammer, LC, Ditto, AM, Tripathi, A, et al Prevalence and onset of rhinitis and conjunctivitis in subjects with occupational asthma caused by trimellitic anhydride (TMA).J Occup Environ Med2002;44,1179-1181
 
Lindstrom, M, Alanko, K, Keskinen, H, et al Dentist’s occupational asthma, rhinoconjunctivitis, and allergic contact dermatitis from methacrylates.Allergy2002;57,543-545
 
Blanc, PD, Toren, K How much adult asthma can be attributed to occupational factors?Am J Med1999;107,580-587
 
Karjalainen, A, Kurppa, K, Martikainen, R, et al Work is related to a substantial portion of adult-onset asthma incidence in the Finnish population.Am J Respir Crit Care Med2001;164,565-568
 
Tarlo, SM, Boulet, LP, Cartier, A, et al Canadian Thoracic Society guidelines for occupational asthma.Can Respir J1998;5,289-300
 
Chan-Yeung, M, Malo, JL, Tarlo, SM, et al Proceedings of the first Jack Pepys Occupational Asthma Symposium.Am J Respir Crit Care Med2003;167,450-471
 
Ortega, HG, Weissman, DN, Carter, DL, et al Use of specific inhalation challenge in the evaluation of workers at risk for occupational asthma: a survey of pulmonary, allergy, and occupational medicine residency training programs in the United States and Canada.Chest2002;121,1323-1328
 
Chan-Yeung, M, McMurren, T, Catonio-Begley, F, et al Occupational asthma in a technologist exposed to glutaraldehyde.J Allergy Clin Immunol1993;91,974-978
 
Tarlo, SM, Wong, L, Roos, J, et al Occupational asthma caused by latex in a surgical glove manufacturing plant.J Allergy Clin Immunol1990;85,626-631
 
Merget, R, Schultze-Werninghaus, G, Bode, F, et al Quantitative skin prick and bronchial provocation tests with platinum salt.Br J Ind Med1991;48,830-837
 
Merget, R, Caspari, C, Dierkes-Globisch, A, et al Effectiveness of a medical surveillance program for the prevention of occupational asthma caused by platinum salts: a nested case-control study.J Allergy Clin Immunol2001;107,707-712
 
Dolovich, J, Evans, SL, Nieboer, E Occupational asthma from nickel sensitivity: I. Human serum albumin in the antigenic determinant.Br J Ind Med1984;41,51-55
 
Kusaka, Y, Yokoyama, K, Sera, Y, et al Respiratory diseases in hard metal workers: an occupational hygiene study in a factory.Br J Ind Med1986;43,474-485
 
Platts-Mills, TA, Longbottom, J, Edwards, J, et al Occupational asthma and rhinitis related to laboratory rats: serum IgG and IgE antibodies to the rat urinary allergen.J Allergy Clin Immunol1987;79,505-515
 
Kim, YK, Oh, SY, Jung, JW, et al IgE binding components inTetranychus urticaeandPanonychus ulmi-derived crude extracts and their cross-reactivity with domestic mites.Clin Exp Allergy2001;31,1457-1463
 
Desjardins, A, Malo, JL, L’Archeveque, J, et al Occupational IgE-mediated sensitization and asthma caused by clam and shrimp.J Allergy Clin Immunol1995;96,608-617
 
Bardy, JD, Malo, JL, Seguin, P, et al Occupational asthma and IgE sensitization in a pharmaceutical company processing psyllium.Am Rev Respir Dis1987;135,1033-1038
 
Shimoda, T Detection of IgE antibodies specific to isonicotinic acid hydrazide and its metabolite by enzyme-linked immunosorbent assay and the mechanism of sensitization by inhalation or ingestion of this compound.Arerugi1990;39,567-576
 
Park, JW, Kang, DB, Choi, SY, et al Heterogeneity of IgE epitopes of vinyl sulphone reactive dye: human serum albumin that react with IgE.Clin Exp Allergy2001;31,1779-1786
 
Park, JW, Kim, CW, Kim, KS, et al Role of skin prick test and serological measurement of specific IgE in the diagnosis of occupational asthma resulting from exposure to vinyl sulphone reactive dyes.Occup Environ Med2001;58,411-416
 
Kramps, JA, van Toorenenbergen, AW, Vooren, PH, et al Occupational asthma due to inhalation of chloramine-T: II. Demonstration of specific IgE antibodiesInt Arch Allergy Appl Immunol1981;64,428-438
 
Howe, W, Venables, KM, Topping, MD, et al Tetrachlorophthalic anhydride asthma: evidence for specific IgE antibody.J Allergy Clin Immunol1983;71,5-11
 
Bernstein, DI, Zeiss, CR, Wolkonsky, P, et al The relationship of total serum IgE and blocking antibody in trimellitic anhydride-induced occupational asthma.J Allergy Clin Immunol1983;72,714-719
 
Son, M, Lee, M, Kim, YT, et al Heterogeneity of IgE response to TDI-HSA conjugates by ELISA in toluene diisocyanate (TDI)-induced occupational asthma (OA) patients.J Korean Med Sci1998;13,147-152
 
Tse, KS, Chan, H, Chan-Yeung, M Specific IgE antibodies in workers with occupational asthma due to western red cedar.Clin Allergy1982;12,249-258
 
Frew, A, Chang, JH, Chan, H, et al T-lymphocyte responses to plicatic acid-human serum albumin conjugate in occupational asthma caused by western red cedar.J Allergy Clin Immunol1998;101,841-847
 
Frew, A, Chan, H, Salari, H, et al Is tyrosine kinase activation involved in basophil histamine release in asthma due to western red cedar?Allergy1998;53,139-143
 
Chan-Yeung, M Mechanism of occupational asthma due to western red cedar (Thuja plicata).Am J Ind Med1994;25,13-18
 
Bernstein, DI, Cartier, A, Cote, J, et al Diisocyanate antigen-stimulated monocyte chemoattractant protein-1 synthesis has greater test efficiency than specific antibodies for identification of diisocyanate asthma 2.Am J Respir Crit Care Med2002;166,445-450
 
Girard, F, Côté, J, Boulet, LP, et al An effective strategy for diagnosing occupational asthma: use of induced sputum.Am J Respir Crit Care Med2004;170,845-850
 
Magni, K, Lemiere, C, Ghezzo, H, et al Airway inflammation after cessation of exposure to agents causing occupational asthma.Am J Respir Crit Care Med2004;169,367-372
 
Lemiere, C Non-invasive monitoring of airway inflammation in occupational lung diseases.Curr Opin Allergy Clin Immunol2002;2,109-114
 
Rahman, I, Kelly, F Biomarkers in breath condensate: a promising new non-invasive technique in free radical research.Free Radic Res2003;37,1253-1266
 
Brooks, SM, Weiss, MA, Bernstein, IL Reactive airways dysfunction syndrome (RADS): persistent asthma syndrome after high level irritant exposures.Chest1985;88,376-384
 
Tarlo, SM, Broder, I Irritant-induced occupational asthma.Chest1989;96,297-300
 
Brooks, SM, Hammad, Y, Richards, I, et al The spectrum of irritant-induced asthma: sudden and not-so-sudden onset and the role of allergy.Chest1998;113,42-49
 
Tarlo, SM Workplace irritant exposures: do they produce true occupational asthma?Ann Allergy Asthma Immunol2003;90,19-23
 
Banauch, GI, Alleyne, D, Sanchez, R, et al Persistent hyperreactivity and reactive airway dysfunction in firefighters at the World Trade Center.Am J Respir Crit Care Med2003;168,54-62
 
Quirce, S Eosinophilic bronchitis in the workplace.Curr Opin Allergy Clin Immunol2004;4,87-91
 
Moreno-Ancillo, A, Padial, MA, Lopez-Serrano, MC, et al Hypersensitivity pneumonitis due to inhalation of fungi-contaminated esparto dust in a plaster worker.Allergy Asthma Proc1997;18,355-357
 
Woodard, ED, Friedlander, B, Lesher, RJ, et al Outbreak of hypersensitivity pneumonitis in an industrial setting.JAMA1988;259,1965-1969
 
Cormier, Y, Israel-Assayag, E, Bedard, G, et al Hypersensitivity pneumonitis in peat moss processing plant workers.Am J Respir Crit Care Med1998;158,412-417
 
Rickman, OB, Ryu, JH, Fidler, ME, et al Hypersensitivity pneumonitis associated withMycobacterium aviumcomplex and hot tub use.Mayo Clin Proc2002;77,1233-1237
 
Duchaine, C, Meriaux, A, Brochu, G, et al Saccharopolyspora rectivirgulafrom Quebec dairy barns: application of simplified criteria for the identification of an agent responsible for farmer’s lung disease.J Med Microbiol1999;48,173-180
 
Zacharisen, MC, Schlueter, DP, Kurup, VP, et al The long-term outcome in acute, subacute, and chronic forms of pigeon breeder’s disease hypersensitivity pneumonitis.Ann Allergy Asthma Immunol2002;88,175-182
 
Ganier, M, Lieberman, P, Fink, J, et al Humidifier lung: an outbreak in office workers.Chest1980;77,183-187
 
Moreno-Ancillo, A, Vicente, J, Gomez, L, et al Hypersensitivity pneumonitis related to a covered and heated swimming pool environment.Int Arch Allergy Immunol1997;114,205-206
 
Baur, X Hypersensitivity pneumonitis (extrinsic allergic alveolitis) induced by isocyanates.J Allergy Clin Immunol1995;95,1004-1010
 
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    Print ISSN: 0012-3692
    Online ISSN: 1931-3543