eMedicine Specialties > Pulmonology > Occupational Lung Diseases

Farmer's Lung

Laurianne G Wild, MD, FAAAAI, Acting Chief and Associate Professor of Clinical Medicine, Section of Clinical Immunology, Allergy and Rheumatology, Director, Allergy and Clinical Immunology Fellowship Training Program, Tulane University Health Sciences Center; Director, Allergy and Immunology Clinic, Veteran's Administration Medical Center at New Orleans
Eduardo E Chang, MD, Fellow, Department of Allergy and Immunology, Tulane University

Updated: Apr 16, 2009

Introduction

Background

Farmer's lung is a type of hypersensitivity pneumonitis. Hypersensitivity pneumonitis, also known as extrinsic allergic alveolitis, is an immunologically mediated inflammatory disease of the lung involving the terminal airways. The condition is associated with intense or repeated exposure to inhaled biologic dusts. The classic presentation of farmer's lung results from inhalational exposure to thermophilic Actinomyces species and occasionally from exposure to various Aspergillus species.

The effect of these antigens in farmers was described as early as 1713. In Britain in 1932, Campbell described a disorder of the lung caused by inhalation of dust from moldy hay. In 1964, Ramazzini and Wright^{[1 ]}described workers getting "diseases of the chest."

Thermophilic actinomycetes species include Saccharopolyspora rectivirgula (formerly Micropolyspora faeni), Thermoactinomyces vulgaris, Thermoactinomyces viridis, and Thermoactinomyces sacchari, among others. These organisms flourish in areas of high humidity and prefer temperatures of 40-60°C.

The thermophilic actinomycetes are ubiquitous organisms usually found in contaminated ventilation systems and in decaying compost, hay, and sugar cane (bagasse). Exposure to large quantities of contaminated hay is the most common source of inhalational exposure for farmers who develop farmer's lung; therefore, grain farmers are not at risk for the development of the disease. Farmer's lung is often a disease of dairy farmers who handle contaminated hay during the winter months. Most cases of farmer's lung occur in cold, damp climates in late winter and early spring when farmers use stored hay to feed their livestock.

Exposure to the causative antigens depends on the type of farming, industry, and climate in the area. Note that farming practices are changing with time and that new antigens may be introduced or disappear from a region (eg, the disappearance of bagassosis in Louisiana sugar cane workers,^{[2 ]}the appearance of Pseudomonas fluorescens in machine operator's lung). The dynamic nature of this disease and the changing environment may lead to new challenges for the clinician.

In addition to the inhalational exposure to the organic dusts responsible for the hypersensitivity reaction in farmer's lung disease, allergens, chemicals, toxic gases, and infectious agents must also be considered as potential triggers of airway symptoms in symptomatic farmers. Farming is currently ranked as one of the top 3 most hazardous occupations, along with construction and mining.

Pathophysiology

The pathogenesis of farmer's lung depends on the intensity, frequency, and duration of exposure and on host response to the causative antigen. Both humoral and cell-mediated immune responses seem to play a role in pathogenesis. During acute episodes, acute neutrophilic infiltration is followed by lymphocytic infiltration of the airways. Levels of interleukins 1 and 8 and tumor necrosis factor-alpha are increased.^{[3 ]}These cytokines have proinflammatory and chemotactic properties. They cause the recruitment of additional inflammatory mediators, resulting in direct cellular damage and changes in the complement pathway, which provide the necessary stimuli to increase vascular permeability and migration of leukocytes to the lung.

If the acute exposure is large, a dramatic increase in inflammation leads to increased vascular permeability, which can alter the alveolar capillary units, thus promoting hypoxemia and decreased lung compliance. If the exposure is prolonged and continuous, collagen deposition and destruction of the lung parenchyma occur with resultant decreased lung volumes.

Strong evidence suggests the involvement of immune complex–induced tissue injury (type III hypersensitivity). The timing of development of symptoms after exposure supports this conclusion. The presence of antigen-specific immunoglobulin and complement activation and deposition in the lung also supports immune-complex or type III hypersensitivity in the pathogenesis of farmer's lung.

Cell-mediated, delayed-type hypersensitivity (type IV hypersensitivity) also plays a major role in the pathogenesis of this syndrome. The presence of lymphocytes, macrophages, and granulomas in the alveolar spaces and the interstitium supports this conclusion.

Frequency

United States

Farmer's lung is one of the most frequent types of hypersensitivity pneumonitis.

• Incidence is highly variable and depends on multiple factors, such as intensity, frequency, and duration of exposure, type of farming, and climate.
• An incidence of 8-540 cases per 100,000 persons per year for farmers has been reported.
• Hypersensitivity pneumonitis affects 0.4-7% of the farming population.
• In a 2007 study in the United States, farmer's lung accounted for 11% of cases of hypersensitivity pneumonitis.^{[4 ]}

International

The prevalence of farmer's lung in the United Kingdom has been reported to be 420-3000 cases per 100,000 at-risk persons.

• Epidemiologic surveys in France^{[5 ]}and Sweden^{[6 ]}show a cumulative prevalence of the disease in the range of 2.5-153 cases per 1000 farmers.
• Incidence of farmer's lung in Finland is 0.7%. This figure is calculated from death certificates.^{[7 ]}
• As reported in 2006, farmer's lung appears to be on the decline, at least in some parts of the world. Specifically, the incidence of farmer's lung in Ireland declined from 1997-2002.^{[8 ]}Effective changes in farming practice and an increase in awareness of the disease has contributed to this decline.

Mortality/Morbidity

The mortality rate from farmer's lung is reportedly 0-20%.

• Death usually occurs 5 years after diagnosis.
• Several factors have been shown to increase mortality rates in farmer's lung, including clinical symptoms occurring more than 1 year before diagnosis, symptomatic recurrence, and pulmonary fibrosis at the time of diagnosis.
• Comorbid factors: Although a history of smoking appears to decrease the overall risk for the development of hypersensitivity pneumonitis, a smoking history is the strongest predictor of increased respiratory symptoms once the diagnosis is made. Preexisting bronchial hyperreactivity with airway obstruction is also a factor.

Clinical

History

The clinical syndrome of farmer's lung, as with other types of hypersensitivity pneumonitis, is categorized as acute, subacute, or chronic.

• Acute farmer's lung
  • Acute farmer's lung develops after large exposure to moldy hay or contaminated compost. Symptoms often spontaneously resolve within 12 hours to days if antigen exposure is eliminated or avoided.
  • Acute farmer's lung manifests as new onset of fever, chills, nonproductive cough, chest tightness, dyspnea, headache, and malaise.
  • If the inhalational exposure is large, patients may develop acute respiratory failure.
• Subacute farmer's lung
  • Subacute farmer's lung manifests as chronic cough, dyspnea, anorexia, and weight loss.
  • Subacute disease is insidious in onset and may occur over weeks to months.
• Chronic farmer's lung
  • Chronic farmer's lung results from prolonged and continuous exposure to the antigen.
  • Patients may have irreversible lung damage.
  • Patients may experience severe dyspnea at rest or with exertion.

Physical

• Acute farmer's lung
  • Fever
  • Tachycardia
  • Nonproductive cough
  • Rales
  • Rales that persist after fever subsides
  • Wheezing (rare)
• Subacute farmer's lung
  • Normal examination findings between presentations
  • Anorexia
  • Weight loss
  • Chronic nonproductive cough
  • Generalized fatigue
• Chronic farmer's lung
  • Bibasilar rales
  • Clubbing - More often observed in patients with chronic farmer's lung with long-standing hypoxemia and parenchymal damage
  • Anorexia
  • More severe dyspnea
  • Weight loss
  • Impaired exercise tolerance

Causes

• Thermophilic actinomycetes
  • S rectivirgula (formerly M faeni)
  • T vulgaris
  • T viridis
  • T sacchari
  • Aspergillus species

Differential Diagnoses

Other Problems to Be Considered

Differential diagnosis of farmer's lung depends on the amount, intensity, duration, and frequency of exposure and on the stage of disease at clinical presentation.

• Acute hypersensitivity pneumonitis due to farmer's lung
• Pulmonary edema
• Bronchoalveolar cell carcinoma
• Organic dust toxic syndrome
• Chronic farmer's lung
• Congestive heart failure
• Desquamative interstitial pneumonitis
• Respiratory bronchiolitis - Interstitial lung diseases
• Chemotherapeutic agents
• Radiation
• Inhaled toxins
• Pneumoconioses
• Toxic fume bronchiolitis (eg, caused by sulfur dioxide, nitrogen dioxide, ammonia, chlorine, phosgene, ozone)
• Grain fever
• Chronic bronchitis

Workup

Laboratory Studies

• No single diagnostic or clinical laboratory study is specific to the diagnosis of farmer's lung. The most important diagnostic tool is a detailed environmental history.
  • Leukocytosis with neutrophilia (but not eosinophilia) and elevated erythrocyte sedimentation rate (ESR), C-reactive protein level, and quantitative immunoglobulin level are noted.
  • Precipitating immunoglobulin G (IgG) antibodies confirms past exposure but does not indicate active disease.
  • Precipitating antibodies are present in up to 50% of asymptomatic farmers exposed to the antigen.^{[9 ]}
  • In farmer's lung, negative precipitin results have been reported because of a lack of appropriate antigen selection in serologic commercial testing.
  • Laboratories must select antigens based on knowledge of local climate and agricultural practices rather than reliance on commercially available antigen panels.

Imaging Studies

• Chest radiography^{[10,11 ]}
  • Findings are normal between acute attacks.
  • Findings are abnormal during acute and subacute stages of disease.
  • Diffuse air-space consolidation is typical of acute farmer's lung (with acute antigen exposure).
  • Nodular or reticulonodular pattern is characteristic of the subacute phase.
  • Linear radiodensities may be discovered and indicate areas of fibrosis from previous attacks.
  • Pulmonary apices are often spared on plain chest radiography.
• High-resolution computed tomography^{[12 ]}
  • High resolution CT scanning is a superior diagnostic modality compared with plain radiography.
  • Pulmonary fibrosis with honeycombing is observed in chronic disease.
  • Peri-bronchovascular distribution of nodules with ground-glass attenuation may be observed.
  • A normal finding on high-resolution CT scans eliminates the possibility of active acute or chronic farmer's lung.

Other Tests

• Pulmonary function tests
  • Spirometry findings may be normal between attacks and before the development of chronic disease.
  • Acute, subacute, and chronic forms of farmer's lung have a restrictive ventilatory pattern with reduced forced vital capacity (FVC), reduced total lung capacity (TLC), and preserved airflow.
  • Mild-to-severe hypoxemia at rest or during minimal exercise may be present with active disease.
  • Decreased diffusion capacity is present with active disease.

Procedures

• Bronchoscopy
  • Bronchoscopy is useful to exclude other disease processes in the acute setting and to obtain bronchoalveolar lavage (BAL) fluid samples for cell counts.
  • Transbronchial biopsy may show evidence of peri-bronchovascular granuloma formation supporting the diagnosis, but its yield is limited because of sampling size.
• Open lung biopsy
  • Consider this procedure if noninvasive tests are equivocal or inconclusive.
  • Consider this procedure if the patient's presentation is atypical in the presence of significant clinical evidence for the disease.

Histologic Findings

Chronic interstitial inflammation is present with infiltration of plasma cells, mast cells, histiocytes, and lymphocytes. Small and poorly organized nonnecrotizing granulomas are present, usually adjacent to bronchioles. Interstitial fibrosis is often present in chronic disease. Changes consistent with bronchiolitis obliterans may be evident. Guidelines for diagnosis of farmer's lung are as follows:

• Major criteria
  • Symptoms compatible with hypersensitivity pneumonitis
  • Evidence of exposure to appropriate antigen by history or detection of antigen-specific antibody in serum and/or BAL fluid
  • Characteristic radiographic changes on plain radiographs or high-resolution CT scans
  • Bronchoalveolar lymphocytes (if BAL was performed)
  • Pulmonary histological changes compatible with hypersensitivity pneumonitis (if lung biopsy was performed)
  • Positive natural challenge findings (reproduction of symptoms and laboratory abnormalities after exposure to the probable environment)
• Minor criteria
  • Presence of bibasilar rales
  • Decreased diffusion capacity
  • Arterial hypoxemia either at rest or during exercise

Treatment

Medical Care

Systemic corticosteroid administration and avoidance measures constitute the primary treatment for farmer's lung.

Diet

No dietary restrictions are needed.

Activity

Patients may decrease activity because of cough and dyspnea on exertion. In a patient with acute farmer's lung, pulmonary function improves once antigen exposure is eliminated. Between episodes of acute disease, activity may be unlimited.

Medication

Systemic corticosteroids (combined with avoidance measures) are the primary agents used to treat farmer's lung.

Nonsteroidal anti-inflammatory drugs (NSAIDs) (eg, cromolyn, nedocromil) or systemic immune modulators are not indicated for treatment at this time.

Corticosteroids

Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Prednisone (Deltasone, Orasone, Meticorten)

Immunosuppressant for treatment of autoimmune disorders; may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Prescribed for severe symptoms or significant lung dysfunction despite antigen avoidance.

Dosing

Adult

0.5 mg/kg/d PO for 4-8 wk, then taper

Pediatric

4-5 mg/m²/d PO; alternatively, 0.05 -2 mg/kg PO divided bid/qid; taper over 2 wk as symptoms resolve

Interactions

Coadministration with estrogens may decrease clearance; when used with digoxin, digitalis toxicity secondary to hypokalemia may increase; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Contraindications

Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; bacterial, fungal, or tubercular systemic infections

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, and increased incidence of infection may occur with glucocorticoid use

Follow-up

Further Inpatient Care

• Systemic corticosteroids
• Serum precipitins
• Flexible bronchoscopy to exclude other etiologies
• Transbronchial biopsy may be of limited benefit in patients with acute farmer's lung.
• Open lung biopsy may be indicated to confirm the diagnosis if other diagnostic criteria are not met.

Further Outpatient Care

• Routine spirometry with lung volumes and diffusion capacity
• Arterial PO₂ and arterial-alveolar gradient: Recommend exercise (6-min walk or by ergometer) if the room air PO₂ level is normal.
• Monitor chest radiographs and consider high-resolution CT scans of the chest to seek resolution of infiltrates or presence of ground-glass opacities that may indicate a need for further treatment with corticosteroids and/or continued insult to the lungs by antigen exposure.

Deterrence/Prevention

• Complete avoidance of the antigen is indicated.
• Protective devices (eg, masks) may reduce the amount of antigen; however, again, complete avoidance is recommended.
• Maintaining humidity at less than 60% may discourage microbial growth.
• Keeping hay on farms dry and well protected may discourage growth of bacteria and molds. However, salting of hay, a traditional empirical practice used to prevent molding in hay, does not significantly decrease the amount of actinomycetes, the organisms most commonly involved in farmer's lung disease. Salting of hay may provide a false sense of security that the farmer is protected from developing farmer's lung; this false notion should be dispelled.^{[13 ]}

Complications

• Cor pulmonale
• Hypoxemic respiratory failure
• Pulmonary fibrosis
• Death

Prognosis

• The long-term prognosis of farmer's lung varies and depends on the extent of fibrosis and the amount of irreversible damage to the lung parenchyma.^{[14 ]}
• In some patients, the disease may progress even after the antigen exposure has been eliminated.
• If the diagnosis of farmer's lung is confirmed before irreversible changes have developed, most patients recover with minimal functional abnormalities and few become disabled.
• In the acute stages, restriction with decreased static compliance and diffusing capacity that reverses over several weeks (with antigen avoidance) may occur.
• In subacute disease, bronchiolitis and granuloma formation might be slower to resolve even with corticosteroid therapy.
• Individuals with a ground-glass appearance on high-resolution CT scans of the chest have higher response rates to systemic corticosteroids.
• Patients with honeycombing or pulmonary fibrosis may have less than a 20% response to corticosteroids and a mortality rate greater than 90% at 5 years after diagnosis.
• Predictors of long-term decline in farmer's lung
  • Recurrent acute episodes
  • Allergy to mites, organic dust, and fungal elements
  • Smoking, which promotes deterioration of lung function in patients diagnosed with farmer's lung^{[15 ]}

Patient Education

• Environmental control and complete avoidance of the antigen should be the goal.
• Complete avoidance of the environment or farm may be required to ensure prevention of chronic disease and survival.
• Many farmers have thought that salting the hay can prevent the growth of molds in the hay. However, salting does not prevent the growth of molds. The use of salt does not significantly decrease the amount of Saccharopolyspora rectivirgula (the actinomycetes most commonly involved in farmer's lung disease), or Absidia corymbifera, Eurotium amstelodami, and Wallemia sebi, 3 molds responsible for farmer's lung disease in Europe. Therefore, palatable hay is not safe hay.
• For excellent patient education resources, visit eMedicine's Procedures Center. Also, see eMedicine's patient education article Bronchoscopy.

Miscellaneous

Medicolegal Pitfalls

• Failure to diagnose farmer's lung in children living on farms^{[16 ]}
• Failure to review a patient's work and occupational history with emphasis on progression or improvement of symptoms when the patient is away from the farm
• Failure to recognize farmer's lung when pulmonary function test and radiographic findings are normal between exacerbations
• Failure to recognize the limits of transbronchial biopsy and serum precipitins: Interpretation of these tests is dependent on the size of the sample and proper testing with the correct antigen, respectively.^{[17 ]}
• Making the common mistake of misdiagnosing acute farmer's lung as viral/bacterial pneumonia or acute infection

Special Concerns

• History of recurrent pneumonia should prompt consideration of hypersensitivity pneumonitis.
• A complete environmental and occupational history is the key to prompt diagnosis of farmer's lung.
• Periodic episodes of acute respiratory symptoms without obvious triggers should also clue the clinician to evaluate for farmer's lung.
• Consider recommending the wear of filtration masks. This practice is not the criterion standard and should be considered only as the last resort with the understanding that it may not provide complete protection from the antigen.
• Encourage smoking cessation measures.
• Krebs von den Lungen-6 (KL-6) has been recognized as a marker for the activity of diffuse interstitial lung diseases, and levels may be elevated in patients with farmer's lung.^{[18 ]}
• Consider Penicillium species and subspecies in Canada and Europe. Fatalities from farmer's lung have been associated with Penicillium brevicompactum and Penicillium polivicolor.^{[19 ]}
• Patients with farmer's lung have beta-D-glucan levels in BAL fluid higher than those of healthy volunteers, whereas the patients' beta-D-glucan levels in serum were below the detection levels.^{[3,20 ]}
• The diagnoses of farmer's lung should be taken into account in the work-up of interstitial lung disease and pulmonary fibrosis. Several cases have been reported in which patients presented with advanced pulmonary fibrosis with evidence of cough and dyspnea and they responded to corticosteroids and avoidance techniques.

References

1. Ramazzini B, Wright WC, ed. De Morbis Artificium [Diseases of Workers]. New York, NY: Hafner Publishing; 1964.

2. Lehrer SB, Turer E, Weill H, Salvaggio JE. Elimination of bagassosis in Louisiana paper manufacturing plant workers. Clin Allergy. Jan 1978;8(1):15-20. [Medline].

3. Ashitani J, Kyoraku Y, Yanagi S, Matsumoto N, Nakazato M. Elevated levels of beta-D-glucan in bronchoalveolar lavage fluid in patients with farmer's lung in Miyazaki, Japan. Respiration. 2008;75(2):182-8. [Medline].

4. Hanak V, Golbin JM, Ryu JH. Causes and presenting features in 85 consecutive patients with hypersensitivity pneumonitis. Mayo Clin Proc. Jul 2007;82(7):812-6. [Medline].

5. Depierre A, Dalphin JC, Pernet D, Dubiez A, Faucompré C, Breton JL. Epidemiological study of farmer's lung in five districts of the French Doubs province. Thorax. Jun 1988;43(6):429-35. [Medline].

6. Malmberg P, Rask-Andersen A, Palmgren U, Höglund S, Kolmodin-Hedman B, Stålenheim G. Exposure to microorganisms, febrile and airway-obstructive symptoms, immune status and lung function of Swedish farmers. Scand J Work Environ Health. Aug 1985;11(4):287-93. [Medline].

7. Kokkarinen J, Tukiainen H, Terho EO. Mortality due to farmer's lung in Finland. Chest. Aug 1994;106(2):509-12. [Medline].

8. Arya A, Roychoudhury K, Bredin CP. Farmer's lung is now in decline. Ir Med J. Jul-Aug 2006;99(7):203-5. [Medline].

9. Cormier Y, Bélanger J. The fluctuant nature of precipitating antibodies in dairy farmers. Thorax. Jun 1989;44(6):469-73. [Medline].

10. Arshad M, Braun SR, Sunderrajan EV. Severe hypoxemia in farmer's lung disease with normal findings on chest roentgenogram. Chest. Feb 1987;91(2):274-5. [Medline].

11. Mönkäre S, Ikonen M, Haahtela T. Radiologic findings in farmer's lung. Prognosis and correlation to lung function. Chest. Apr 1985;87(4):460-6. [Medline].

12. Cormier Y, Brown M, Worthy S, Racine G, Müller NL. High-resolution computed tomographic characteristics in acute farmer's lung and in its follow-up. Eur Respir J. Jul 2000;16(1):56-60. [Medline].

13. Roussel S, Reboux G, Dalphin JC, Laplante JJ, Piarroux R. Evaluation of salting as a hay preservative against farmer's lung disease agents. Ann Agric Environ Med. 2005;12(2):217-21. [Medline].

14. Barbee RA, Callies Q, Dickie HA, Rankin J. The long-term prognosis in farmer's lung. Am Rev Respir Dis. Feb 1968;97(2):223-31. [Medline].

15. Ohtsuka Y, Munakata M, Tanimura K, Ukita H, Kusaka H, Masaki Y, et al. Smoking promotes insidious and chronic farmer's lung disease, and deteriorates the clinical outcome. Intern Med. Oct 1995;34(10):966-71. [Medline].

16. Thorshauge H, Fallesen I, Ostergaard PA. Farmer's lung in infants and small children. Allergy. Feb 1989;44(2):152-5. [Medline].

17. Lacasse Y, Fraser RS, Fournier M, Cormier Y. Diagnostic accuracy of transbronchial biopsy in acute farmer's lung disease. Chest. Dec 1997;112(6):1459-65. [Medline].

18. Takahashi T, Munakata M, Ohtsuka Y, Satoh-Kamachi A, Sato R, Homma Y, et al. Serum KL-6 concentrations in dairy farmers. Chest. Aug 2000;118(2):445-50. [Medline].

19. Nakagawa-Yoshida K, Ando M, Etches RI, Dosman JA. Fatal cases of farmer's lung in a Canadian family. Probable new antigens, Penicillium brevicompactum and P olivicolor. Chest. Jan 1997;111(1):245-8. [Medline].

20. Imai K, Ashitani J, Imazu Y, Yanagi S, Sano A, Tokojima M, et al. [Farmer's lung cases of a farmer and his son with high BAL fluid beta-D glucan levels]. Nihon Kokyuki Gakkai Zasshi. Dec 2004;42(12):1024-9. [Medline].

21. Ando M, Suga M. Hypersensitivity pneumonitis. Curr Opin Pulm Med. Sep 1997;3(5):391-5. [Medline].

22. Bouchard S, Morin F, Bédard G, Gauthier J, Paradis J, Cormier Y. Farmer's lung and variables related to the decision to quit farming. Am J Respir Crit Care Med. Sep 1995;152(3):997-1002. [Medline].

23. Cormier Y, Bélanger J. Long-term physiologic outcome after acute farmer's lung. Chest. Jun 1985;87(6):796-800. [Medline].

24. Emanuel DA, Kryda MJ. Farmer's lung disease. Clin Rev Allergy. Dec 1983;1(4):509-32. [Medline].

25. Fink JN. Hypersensitivity pneumonitis. In: Allergy Principles and Practice. 5^th ed. St. Louis, Mo: Mosby; 1998:994-1004.

26. Fink JN. Hypersensitivity pneumonitis. Clin Chest Med. Jun 1992;13(2):303-9. [Medline].

27. Fraser RG, Pare JA. Diagnosis of Diseases of the Chest. 3^rd ed. Philadelphia, Pa: WB Saunders; 1989:1273-90.

28. Gay J, Donham KJ, Leonard S. Iowa Agricultural Health and Safety Service Project. Am J Ind Med. 1990;18(4):385-9. [Medline].

29. Kaltreider HB. Hypersensitivity pneumonitis. West J Med. Nov 1993;159(5):570-8. [Medline].

30. Kline JN, Schwartz DA. Agricultural dust-induced lung disease. In: Rom WN, ed. Environmental Occupational Medicine. Philadelphia, Pa: Lippincott Raven; 1998:565-71.

31. Kokkarinen JI, Tukiainen HO, Terho EO. Recovery of pulmonary function in farmer's lung. A five-year follow-up study. Am Rev Respir Dis. Apr 1993;147(4):793-6. [Medline].

32. Lalancette M, Carrier G, Laviolette M, Ferland S, Rodrique J, Bégin R, et al. Farmer's lung. Long-term outcome and lack of predictive value of bronchoalveolar lavage fibrosing factors. Am Rev Respir Dis. Jul 1993;148(1):216-21. [Medline].

33. Myers ML. Health problems and disease patterns in agriculture. In: Encyclopedia of Occupational Health Safety. Geneva, Switzerland: International Labour Office; 1997.

34. Patel AM, Ryu JH, Reed CE. Hypersensitivity pneumonitis: current concepts and future questions. J Allergy Clin Immunol. Nov 2001;108(5):661-70. [Medline].

35. Patterson R, Greenberger PA, Castile RG, et al. Diagnostic problems in hypersensitivity lung disease. Allergy Proc. Mar-Apr 1989;10(2):141-7. [Medline].

36. Salvaggio JE. Extrinsic allergic alveolitis (hypersensitivity pneumonitis): past, present and future. Clin Exp Allergy. May 1997;27 Suppl 1:18-25. [Medline].

37. Schuyler M, Cormier Y. The diagnosis of hypersensitivity pneumonitis. Chest. Mar 1997;111(3):534-6. [Medline].

38. Schuyler M, Gott K, Edwards B. Experimental hypersensitivity pneumonitis: cellular requirements. Clin Exp Immunol. Jul 1996;105(1):169-75. [Medline].

39. Wiatr E, Radzikowska E, Pawlowski J. [Pulmonary fibrosis in young patients with hypersensitivity pneumonitis]. Pneumonol Alergol Pol. 2004;72(3-4):111-6. [Medline].

40. Wild LG. Hypersensitivity pneumonitis: A childhood disease?. Pediatr Asth Allergy. 2000;14:57-75.

41. Wild LG, Lopez M. Hypersensitivity pneumonitis: a comprehensive review. J Investig Allergol Clin Immunol. 2001;11(1):3-15. [Medline].

Keywords

farmer's lung, farmer lung, farmer's lung disease, extrinsic allergic alveolitis, hypersensitivity pneumonitis, HP, wheezing, dyspnea, maple bark stripper's lung, chicken plucker's lung, bagassosis, byssinosis, humidifier lung, Actinomyces, Aspergillus, actinomycetes, Saccharopolyspora rectivirgula, S rectivirgula, Micropolyspora faeni, M faeni, Thermoactinomyces vulgaris, T vulgaris, Thermoactinomyces viridis, T viridis, Thermoactinomyces sacchari, T sacchari, Krebs von den Lungen-6, KL-6

Contributor Information and Disclosures

Author

Laurianne G Wild, MD, FAAAAI, Acting Chief and Associate Professor of Clinical Medicine, Section of Clinical Immunology, Allergy and Rheumatology, Director, Allergy and Clinical Immunology Fellowship Training Program, Tulane University Health Sciences Center; Director, Allergy and Immunology Clinic, Veteran's Administration Medical Center at New Orleans
Laurianne G Wild, MD, FAAAAI is a member of the following medical societies: Alpha Omega Alpha, American Academy of Allergy Asthma and Immunology, American College of Allergy, Asthma and Immunology, and Association of Subspecialty Professors
Disclosure: Nothing to disclose.

Coauthor(s)

Eduardo E Chang, MD, Fellow, Department of Allergy and Immunology, Tulane University
Disclosure: Nothing to disclose.

Medical Editor

Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St. Boniface General Hospital
Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Gregg T Anders, DO, Medical Director, Great Plains Regional Medical Command , Brook Army Medical Center; Clinical Associate Professor, Department of Internal Medicine, Division of Pulmonary Disease, University of Texas Health Science Center at San Antonio
Gregg T Anders, DO is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.

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