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Hypersensitivity Pneumonitis

  • Author: Caleb Hsieh, MD, MS; Chief Editor: Ryland P Byrd, Jr, MD  more...
Updated: Jan 20, 2015


Hypersensitivity pneumonitis (HP), or extrinsic allergic alveolitis, is an inflammatory syndrome of the lung caused by repetitive inhalation of antigenic agents in a susceptible host. The syndrome varies in intensity, clinical presentation, and natural history depending on the inciting agent. In most cases, disease can be reversed with prompt diagnosis followed by identification and removal of exposure risks. As such, prognosis is generally very good.

In 1700, Bernardino Ramazzini, an Italian physician, published the first description of HP when he noticed that sifters and measurers of grain experienced acute reactions after repeated exposure to grain dust. This same phenomenon often seen in farmers was noted independently by many subsequent physicians. In 1874, Dr. Jon Finsen of Iceland, provided a more detailed description of “Heykatarr,” now known as Farmer’s lung, in his graduate thesis after noting that men “whose job it is to loosen the hay in the barn and handle it before it is fed to cattle,” became ill after inhalation of the dust.[1]

The antigens responsible for HP come from a variety of sources. In general, these are classified into three major categories: microbes, animal proteins, and low-molecular-weight chemicals. These most commonly manifest as farmer’s lung, bird fancier’s lung, and chemical worker’s lung, respectively.



Hypersensitivity pneumonitis is a spectrum of immune-mediated disorders characterized by diffuse inflammation of interstitial lung, terminal bronchioli, and alveoli. Inflammation is caused by prolonged or frequent exposure of inhaled antigens generally less than 5 µm in size. Although offending antigens are ubiquitous, the incidence of disease is small. Thus, disease is thought to occur via a two-hit mechanism in which genetic predisposition or environmental exposure (first hit) contribute to progression to HP following antigen exposure (second hit). Type III and Type IV hypersensitivity reactions are implicated.[2]

Within the organic dusts responsible for HP, including dusts from dairy and grain products, animal dander and proteins, wood bark, and water reservoir vaporizers (eg, hot tubs, air conditioners), are antigens consisting of spores from thermophilic actinomycetes (eg, Saccharopolyspora rectivirgula) or fungi (eg, Aspergillus species). High- and low-molecular-weight animal proteins, often from bird serum, feces, or feathers are also common antigens. Direct handling of birds may not be necessary as HP has also been described following the use of feather down items. Finally, low-molecular weight molecules and inorganic materials (eg, isocyanates, zinc, and nickel) may serve as haptens, forming antigenic complexes when combined with host proteins.

Most individuals do not react to these antigens, likely secondary to development of immune tolerance. These individuals may develop a mild lymphocytic alveolitis, but generally remain asymptomatic. Tolerance is thought to be mediated by regulatory T cells, which suppress the Th1 and Th2 cell immune responses.

In patients who go on to develop symptoms, HP is classified as acute, subacute (intermittent), or chronic progressive.[3, 4] The mechanisms of disease are incompletely understood. Acute HP is thought to occur primarily via type III hypersensitivity reaction. Most patients show evidence of specific antibodies in their serum and bronchoalveolar lavage studies may demonstrate high levels of proinflammatory chemokines. This is further supported by the finding of complement and immunoglobulin deposition in vessel walls on immunofluorescence.[5]

Subacute and chronic forms of HP are thought to transition more towards type IV, T-cell mediated, hypersensitivity reactions. Antigen presenting cells (ie, dendritic cells and alveolar macrophages) present antigens to CD4+ Th1 and Th17 cells. This triggers an inflammatory cascade with release of many factors including IFN-γ, TNF, IL-17, IL-22. The milieu of cytokines and chemokines ultimately results in sustained infiltration of mononuclear cells, macrophages, and fibroblasts. The apoptosis of lung tissue lymphocytes is inhibited by IL-17 resulting in the high prevalence of lymphocytes in the lung. This in turn results in the pattern of noncaseating granulomas, bronchiolitis seen on pathology. In chronic stages, a CD4+ Th2 cytokine pattern dominates. This correlates with fibrotic progression in late disease.[2, 6, 5]

Histologically, chronic HP is characterized by interstitial inflammation and alveolar destruction (honeycombing). Cholesterol clefts or asteroid bodies are present within or outside noncaseating granulomas. Areas of cellular interstitial pneumonia with giant cells or granulomas surrounding bronchioles may help distinguish chronic HP from usual interstitial pneumonia (UIP) or fibrotic nonspecific interstitial pneumonia (NSIP). Centrilobular fibrosis, peribronchiolar and bridging fibrosis are also important hallmarks.[7, 8, 9]

Features often associated with poorer prognosis include:

  • Predominantly peripheral fibrosis in a patchy pattern with architectural distortion and fibroblast foci similar to UIP
  • Homogeneous linear fibrosis similar to fibrotic NSIP
  • Irregular predominantly peribronchiolar fibrosis



United States

The exact prevalence of HP is unknown. Difficulties determining prevalence arise from uncertainties in detection and misdiagnosis. This is compounded by the lack of standardized epidemiological criteria for diagnosis.[10] That said, estimated prevalence varies by region, climate, and farming practices. A study in New Mexico calculated the yearly incidence of interstitial lung disease (ILD) to be roughly 30 per 100,000. HP accounted for less than 2% of that population.[11] A highly cited 1981 Wisconsin-based study of 1400 individuals estimated prevalence at 4.2%.[12] In other studies, HP is estimated to affect anywhere from 0.5–19.0% of exposed farmers.[10] Again, these figures are likely to have evolved based on changing farming practices and diagnostic criteria.


HP prevalence outside of the United States varies significantly based on type of exposures. Bird fancier’s lung is the most form of HP worldwide given a growing poultry husbandry industry. Other interesting causes described in literature include suberosis (cork worker’s lung, HP-associated with contaminated corks in Spain), mushroom exposures in Asia, and Chrysonilia sitophila HP associated with logging in Canada among others. Farmer’s lung is ostensibly becoming less common due to increased use of protective measures.[13]

The prevalence of farmer's lung in the United Kingdom is reported to be 420-3,000 cases per 100,000 persons at risk, in France is 4,370 cases per 100,000 persons at risk,[14, 15] and in Finland is 1,400-1,700 cases per 100,000 persons at risk.[16]

One epidemiologic study estimated incidence of interstitial lung disease to be 7.6 cases per 100,000 persons per year. Hypersensitivity pneumonitis accounted for 6.6% of those cases.[17, 6]


Morbidity and mortality of HP varies widely based on type, duration, and severity of exposure. Genetic factors may also play a significant role. In general, acute HP and subacute HP without fibrotic changes respond completely or near completely to removal of the inciting exposure. Once fibrotic changes occur, however, prognosis is less favorable.[18]

Widely cited data published from the National Center for Health Statistics suggested an increase in HP related mortality from 0.09-0.29 million from 1980 to 2002.[19] A similar study out of England and Wales showed stable mortality rate from 0.04-0.08 per million from 1968 to 2008.[20]

Rarely, patients may progress to chronic HP despite exposure control and treatment. Similar to chronic HP, emphysema develops initially with progression to irreversible pulmonary fibrosis. Survival at that point is similar to that observed in idiopathic pulmonary fibrosis (IPF). Pulmonary hypertension is seen in 20% of cases of chronic HP and carries worse prognosis.[2]


A clear role for gender has not been defined. Differences in prevalence may be confounded by skewed gender representation in various occupations.[6]


Hypersensitivity pneumonitis is usually encountered in the fourth to sixth decade of life. One study examined 85 consecutive patients with hypersensitivity pneumonitis and found a mean age of 53 +/- 14 years.[21]

Contributor Information and Disclosures

Caleb Hsieh, MD, MS Department of Internal Medicine, Olive View-UCLA Medical Center

Caleb Hsieh, MD, MS is a member of the following medical societies: American College of Physicians, American Medical Association

Disclosure: Nothing to disclose.


Nader Kamangar, MD, FACP, FCCP, FCCM Professor of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Chief, Division of Pulmonary and Critical Care Medicine, Vice-Chair, Department of Medicine, Olive View-UCLA Medical Center

Nader Kamangar, MD, FACP, FCCP, FCCM is a member of the following medical societies: Academy of Persian Physicians, American Academy of Sleep Medicine, American Association for Bronchology and Interventional Pulmonology, American College of Chest Physicians, American College of Critical Care Medicine, American College of Physicians, American Lung Association, American Medical Association, American Thoracic Society, Association of Pulmonary and Critical Care Medicine Program Directors, Association of Specialty Professors, California Sleep Society, California Thoracic Society, Clerkship Directors in Internal Medicine, Society of Critical Care Medicine, Trudeau Society of Los Angeles, World Association for Bronchology and Interventional Pulmonology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Daniel R Ouellette, MD, FCCP Associate Professor of Medicine, Wayne State University School of Medicine; Chair of the Clinical Competency Committee, Pulmonary and Critical Care Fellowship Program, Senior Staff and Attending Physician, Division of Pulmonary and Critical Care Medicine, Henry Ford Health System; Chair, Guideline Oversight Committee, American College of Chest Physicians

Daniel R Ouellette, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, Society of Critical Care Medicine, American Thoracic Society

Disclosure: Nothing to disclose.

Chief Editor

Ryland P Byrd, Jr, MD Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University

Ryland P Byrd, Jr, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Additional Contributors

Michael Peterson, MD Chief of Medicine, Vice-Chair of Medicine, University of California, San Francisco, School of Medicine; Endowed Professor of Medicine, University of California, San Francisco-Fresno, School of Medicine

Michael Peterson, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Thoracic Society

Disclosure: Nothing to disclose.


Marine Demirjian, MD Resident Physician, Department of Internal Medicine, Ronald Reagan University of California in Los Angeles Medical Center

Marine Demirjian, MD is a member of the following medical societies: American College of Physicians, American Medical Association, American Medical Women's Association, and California Medical Association

Disclosure: Nothing to disclose.

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.

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A 60-year-old dairy farmer had an 8-year history of intermittent dyspnea. Chest radiograph shows bilateral reticulonodular interstitial infiltration secondary to subacute hypersensitivity pneumonitis.
Chest radiograph of a patient with chronic hypersensitivity pneumonitis from pigeon breeder's disease. Bilateral reticulonodular densities are present.
High-resolution CT scan of lungs shows ground-glass opacification in the acute phase of hypersensitivity pneumonitis.
The chronic phase of hypersensitivity pneumonitis shows honeycombing in the right upper lung and traction bronchiectasis.
High-resolution chest CT scan of a patient with subacute hypersensitivity pneumonitis demonstrates centrilobular nodules. These nodules are unlike those of sarcoidosis, in which the nodules are subpleural and along bronchovascular bundles.
Light microscopy shows mononuclear infiltration and noncaseating granulomas usually observed in association with acute hypersensitivity pneumonitis, but it also can be observed in subacute and chronic disease.
Giant cells are a characteristic feature of hypersensitivity pneumonitis.
Chronic hypersensitivity pneumonitis shows interstitial inflammation associated with fibrosis.
Table. Selected Etiological Agents for Hypersensitivity Pneumonitis
Disease Source of Exposure Major Antigen
Farmer's lung Moldy hay Saccharopolyspora rectivirgula

(Micropolyspora faeni)

Bagassosis Moldy sugar cane fiber Thermoactinomyces sacchari
Grain handler's lung Moldy grain S rectivirgula,Thermoactinomyces vulgaris
Humidifier/air-conditioner lung Contaminated forced-air systems, heated water reservoirs S rectivirgula, T vulgaris
Bird breeder's lung Pigeons, parakeets, fowl, rodents Avian or animal proteins
Cheese worker's lung Cheese mold Penicillium casei
Malt worker's lung Moldy malt Aspergillus clavatus
Paprika splitter's lung Paprika dust Mucor stolonifer
Wheat weevil Infested wheat Sitophilus granarius
Mollusk shell hypersensitivity Shell dust Sea snail shells
Chemical worker's lung Manufacture of plastics, polyurethane foam, rubber Trimellitic anhydride, diisocyanate, methylene diisocyanate
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