Hypersensitivity Pneumonitis



  • Hypersensitivity pneumonitis (HP) is also called extrinsic allergic alveolitis (EAA).
  • HP is a diffuse inflammatory disease of the lung parenchyma caused by an immunologic reaction to aerosolized antigenic particles found in a variety of environments. Classification depends on time frame involved:
    • Acute: fever, chills, diaphoresis, myalgias, nausea; cough and dyspnea common but not necessarily present; occurs 4 to 12 hours after heavy exposure to an inciting agent. Symptoms subside within 12 hours to several days after removal from exposure. Complete resolution occurs within weeks.
    • Subacute: mainly caused by continual low-level antigen exposure, could have a low-grade fever in 1st week; cough, dyspnea, fatigue, anorexia, weight loss—develops over days to weeks
    • Chronic: from recurrent exposure either acute or subacute cases; prolonged and progressive cough, dyspnea, fatigue, weight loss; could lead to fibrosis and respiratory failure
  • Farmer’s lung is an old term of this disease, a type of HP, particular to the farmer population; causative agent is a bacterium found in moldy hay or straw. Farmer’s lung now has new and different etiologies due to modernization of farming practices.


  • Not well defined; tends to occur in adults as a result of occupation-related exposure, but some home environmental exposures are also seen
  • HP is increasingly recognized as an important cause of fibrotic interstitial lung disease (1).



  • Farmers: 1–19% exposed farmers
  • Bird fanciers: 6–20% exposed individuals
  • Others: 1–8% exposed

Etiology and Pathophysiology

  • Hypersensitivity reaction involving immune complexes: Inhaled antigens bind to IgG, triggering complement cascade (types III and IV immunologic reactions) (1).
  • Cellular-mediated reaction: T cell–mediated immune inflammatory response
  • Farming, vegetable, or dairy cattle workers
    • Moldy hay, grain, silage: thermophilic actinomycetes, such as Faenia rectivirgula
    • Mold on pressed sugar cane: Thermoactinomyces sacchari, Thymus vulgaris
    • Tobacco plants: Aspergillus sp., Scopulariopsis brevicaulis
    • Mushroom worker’s lung: Saccharopolyspora rectivirgula, T. vulgaris, Aspergillus spp.
    • Potato riddler’s lung: thermophilic actinomycetes, T. vulgaris, F. rectivirgula, Aspergillus sp.
    • Wine maker’s lung: Mucor stolonifer
    • Cheese washer’s lung: Penicillium caseifulvum, Aspergillus clavatus
    • Coffee worker’s lung: coffee bean dust
    • Tea grower’s lung: tea plants
  • Ventilation and water-related contamination
    • Contaminated humidifiers and air conditioners: amoebae, nematodes, yeasts, bacteria
    • Unventilated shower: Epicoccum nigrum
    • Hot-tub lung: Cladosporium sp., Mycobacterium avium complex
    • Sauna taker’s lung: Aureobasidium sp.
    • Summer-type pneumonitis: Trichosporon cutaneum
    • Swimming pool lifeguard’s lung: aerosolized endotoxin and M. avium complex
    • Contaminated basement pneumonitis: Cephalosporium and Penicillium spp.
  • Bird and poultry handling
    • Bird fancier’s lung: droppings, feathers, serum proteins
    • Poultry worker’s lung: serum proteins
    • Turkey-handling disease: serum proteins
    • Canary fancier’s lung: serum proteins
    • Duck fever: feathers, serum proteins
  • Veterinary work and animal handling
    • Laboratory worker’s lung: urine, serum, pelts, proteins
    • Pituitary snuff taker’s disease: dried, powdered neurohypophysis
    • Furrier’s lung: animal pelts
    • Bat lung: bat serum protein
    • Fish meal worker’s lung: fish meal
    • Coptic lung: cloth wrapping of mummies
    • Mollusc shell HP: sea snail shell
    • Pearl oyster shell pneumonitis: oyster shells
  • Grain and flour
    • Grain measurer’s lung: cereal grain, grain dust
    • Miller’s lung: Sitophilus granarius
    • Malt worker’s disease: Aspergillus fumigatus, A. clavatus
  • Lumber milling, construction, wood stripping, paper, wallboard manufacture
    • Wood dust pneumonitis: Alternaria sp., Bacillus subtilis
    • Sequoiosis: Graphium, Pullularia, Trichoderma sp., Aureobasidium pullulans
    • Maple bark disease: Cryptostroma corticale
    • Wood trimmer’s disease: Rhizopus sp., Mucor sp.
    • Wood pulp worker’s disease: Penicillium sp.
    • Suberosis: Trogon viridis, Penicillium glabrum
  • Plastic manufacturing, painting, electronics, chemicals
    • Chemical HP: diphenyl diisocyanate, toluene diisocyanate
    • Detergent worker’s lung: B. subtilis enzymes
    • Pauli reagent alveolitis: sodium diazobenzene sulfate
    • Vineyard sprayer’s lung: copper sulfate
    • Pyrethrum pneumonitis: pyrethroids
    • Epoxy resin lung: phthalic anhydride
    • Bible printer’s lung: moldy typesetting water
    • Machine operator’s lung: Pseudomonas fluorescens, aerosolized metal working fluid
  • Textile workers
    • Byssinosis: cotton mill dust
    • Velvet worker’s lung: nylon, tannic acid, potato starch
    • Upholstery fabric: aflatoxin-producing fungus, Fusarium sp.
    • Lycoperdonosis: puffball spores


No evidence of clear genetic susceptibility; possible genetic predisposition involving tumor necrosis factor alpha (TNF-α) and major histocompatibility complex (MHC) class II genes (1)[B]

Risk Factors

  • Contact with organic antigens increases risk of developing HP. Viral infection at time of exposure may increase risk.
  • Nonsmokers have an increased incidence of HP compared with smokers. The mechanisms that account for the “protective” effect of smoking are poorly understood, but nicotine is thought to inhibit macrophage activation and lymphocyte proliferation and function (1).
    • Smokers have a diminished antibody response to inhaled antigens.
    • However, smokers who develop disease tend to have the chronic form, and mortality is higher.

General Prevention

Avoidance of offending antigen and/or use of protective equipment

Commonly Associated Conditions

Constrictive bronchiolitis

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