Hypersensitivity Pneumonitis 
Overview
Also known as: Extrinsic Allergic Alveolitis; Farmer's lung; Mushroom pickers disease; Humidifier or air-conditioner lung; Bird breeder's lung; and many others – see table.
Responsibilities:
Hospital: Report by phone, fax, or mail
Lab: Report by phone, fax, or mail
Physician/Health care providers: Report by phone, fax, or mail
Medical Examiners: Report by phone, fax, or mail
Poison Control Centers: Report by phone, fax, or mail
Occupational Nurses: Report by phone, fax, or mail
Local Public Health Agency (LPHA): No follow-up required, unless outbreak occurrence
Report to the IDPH Division of Environmental Health:
Iowa Department of Public Health
Division of Environmental Health
Lucas State Office Building
321 E. 12th Street
Des Moines, Iowa 50319-0075
Phone (Mon-Fri 8 am - 4:30 pm): 800-972-2026
Fax: 515-281-4529
24-hour Disease Reporting Hotline: (For use outside of EH office hours) 800-362-2736
Web: https://idph.iowa.gov/ehs/reportable-diseases
Report Form: Environmental & Occupational Report Form on web
A. Agent
Hypersensitivity pneumonitis is a syndrome of cough, dyspnea, and fatigue caused by sensitization and subsequent hypersensitivity to environmental antigens, frequently related to occupational exposures. ICD-10 codes J67.0-J67.9 refer to hypersensitivity pneumonitis due to organic dust, and exclude pneumonitis due to inhalation of chemicals, gases, fumes or vapors (J68.0)
These dusts can be derived from a variety of sources, such as dairy and grain products, animal dander and protein, wood bark, and water reservoir vaporizers. Over 300 antigens have been identified as triggers for hypersensitivity pneumonitis, although farming, birds, and water contamination account for about 75% of cases. The most common antigens are thermophilic Actinomycetes species and avian proteins; the most common diseases are farmer’s lung and bird fancier's lung.
Hypersensitivity Pneumonitis Syndrome – Various Types and Sources
Syndrome Names
|
Antigen or Agent
|
Exposure Source
|
Bagassosis
|
Thermophilic actinomycetes
|
Moldy bagasse (sugar cane)
|
Cheese worker or washer’s lung
|
Aspergillus clavatus; Penicillium casei; Penicillium roqueforti
|
Moldy cheese
|
Coffee worker’s lung
|
Coffee bean dust
|
Coffee beans
|
Compost lung
|
Aspergillus sp
|
Compost
|
Farmer’s lung
|
Fungi, especially Aspergillus sp; Thermophilic actinomycetes
|
Vegetable compost (moldy grain, hay, silage)
|
Mushroom worker’s lung
|
Hypsizigus marmoreus
Thermophilic actinomycetes
|
Mushroom compost
|
Potato riddler’s lung
|
Aspergillus sp
Thermophilic actinomycetes
|
Moldy hay around potatoes
|
Tobacco grower’s lung
|
Aspergillus sp
Scopulariopsis brevicaulis
|
Tobacco plants
|
Tobacco grower’s lung
|
Botrytis cinerea
|
Moldy grapes
|
|
|
|
WATER
|
|
|
Hot tub lung
|
Cladosporium sp
Mycobacterium avium complex
|
Contaminated mist and mold
on ceilings and around tub
|
Humidifier lung
|
Aureobasidium sp;
Candida albicans;
Thermophilic actinomycetes
|
Contaminated water in air-conditioning or humidification
systems
|
Sauna taker’s lung
|
Aureobasidium sp
|
Contaminated sauna water
|
Sewer worker’s lung
|
Cephalosporium sp
|
Contaminated basements
(sewage); sewers
|
Tap water lung
|
Unknown
|
Contaminated tap water
|
|
|
|
BIRDS
|
|
|
Bird fancier’s lung, including: hen worker’s lung, pigeon breeder’s lung, turkey handler’s lung; feather plucker’s lung; duck fever
|
Parakeet, pigeon, chicken, turkey, and duck proteins
|
Bird droppings or feathers
|
|
|
|
ANIMALS
|
|
|
Fish food lung
|
Unknown
|
Fish food
|
Fish meal worker’s lung
|
Fish meal dust
|
Fish meal dust
|
Furrier’s lung
|
Animal fur dust
|
Animal pelts
|
Laboratory worker’s hypersensitivity pneumonitis
|
Rodent proteins
|
Male rat urine and fur
|
Mummy handler’s lung
|
Unknown
|
Cloth mummy wrappings
|
Pituitary snuff taker’s lung
|
Animal proteins
|
Heterologous (bovine, porcine)
pituitary snuff
|
Sausage worker’s lung
|
Penicillium nalgiovense
|
Dry sausage mold
|
|
|
|
GRAINS
|
|
|
Malt worker’s lung
|
Aspergillus sp
|
Moldy barley
|
Miller’s lung, Wheat weevil lung
|
Sitophilus granaries (wheat weevil)
|
Infested wheat flour
|
|
|
|
MILLING AND
CONSTRUCTION
|
|
|
Sequoiosis
|
Aureobasidium sp; Graphium sp
|
Redwood sawdust
|
Thatched-roof worker’s disease
|
Saccharomonospora viridis
|
Dried grass and leaves
|
Wood pulp worker’s disease
|
Penicillium sp
|
Oak and maple tree pulp
|
Wood trimmer’s disease
|
Rhizopus sp; Mucor sp
|
Contaminated wood trimmings
|
Woodworker’s lung
|
Alternaria sp; Bacillus subtilis
|
Oak, cedar, pine, spruce, and
mahogany dusts
|
|
|
|
INDUSTRY
|
|
|
Chemical worker’s lung
|
Isocyanates
|
Polyurethane foam, varnishes,
lacquer
|
Detergent worker’s lung
|
Bacillus subtilis
|
B. subtilis enzymes in detergent
|
Vineyard sprayer’s lung
|
Copper sulfate
|
Copper sulfate use
|
|
|
|
OTHER
|
|
|
Byssinosis (brown lung)
|
Mill dust
|
Cotton, flax, and hemp dust
|
Lycoperdonosis
|
Spores from puffball
(Lycoperdon) mushrooms
|
Alternative medicine or
recreational use (mistaking
puffballs for hallucinogenic
mushrooms)
|
Table reference: Merck Manuals, 2016 http://www.merckmanuals.com/professional/pulmonary-disorders/interstitial-lung-diseases/hypersensitivity-pneumonitis
B. Clinical Description
Hypersensitivity pneumonitis is a syndrome of cough, dyspnea, and fatigue caused by prior sensitization over a period of time resulting in subsequent hypersensitivity to organic environmental antigens. Only a small proportion of exposed people develop symptoms.
Symptoms and onset: Hypersensitivity pneumonitis is categorized as acute, subacute, or chronic disease.
- Acute hypersensitivity pneumonitis: The acute form may develop 4-8 hours after heavy exposure to antigenic materials. Patients abruptly develop fever, chills, malaise, cough, chest tightness, dyspnea, and headache. Anorexia, nausea, and vomiting may also be present.Symptoms often resolve spontaneously within 12 hours to several days upon cessation of exposure.
- Subacute (intermittent) hypersensitivity pneumonitis: similarly to patients with acute disease, but that are less severe and last longer.
- Chronic hypersensitivity pneumonitis: Patients with chronic low-level antigen exposure, which is more common with bird owners, often lack a history of acute episodes. Disease muscle wasting and weight loss. Clubbing has been observed in 50% of patients. Tachypnea, respiratory distress, and inspiratory crackles over lower lung fields often are present..Removing exposure sources results in only partial improvement.
Complications: Pathologic changes are completely reversible if detected early and if antigen exposure is eliminated. Patients may develop complications of underlying medical problems during acute disease episodes. Acute disease is self-limiting with antigen avoidance; symptoms usually lessen within hours. Chronic disease has a more complicated prognosis: fibrosis is usually irreversible, but may not progress if the patient is no longer exposed to the antigen.
Diagnosis: Diagnosis requires a high index of suspicion in patients with compatible symptoms and a compatible occupational, avocational, or domestic exposure history. Chest x-ray, high-resolution CT (HRCT), and pulmonary function tests are done routinely. Bronchoalveolar lavage and biopsy may be necessary if results are inconclusive. The differential diagnosis is broad and includes environmental pulmonary diseases, sarcoidosis, bronchiolitis obliterans, connective tissue–associated pulmonary disease, and other interstitial lung diseases. Referral to a pulmonologist is recommended.
Clues in the history include
- Recurring atypical pneumonias
- Symptom onset after moving to a new job or home
- A hot tub, a sauna, a swimming pool, or other sources of standing water or water damage in the home or regular exposure to them elsewhere
- Having birds as pets
- Exacerbation and relief of symptoms in and away from specific settings
Examination often is not useful in making the diagnosis, although abnormal lung sounds and clubbing may be present.
C. Reservoirs
Environmental reservoirs can be found wherever the host for the antigenic material is present. Areas with conditions that are conducive to fungi and mold growth, indoor and confined spaces with limited ventilation, and storage areas are more likely to concentrate allergenic materials.
D. Modes of Transmission
Transmission is usually through airborne inhalation of allergenic particles.
E. Incubation period
Not an infectious agent; see symptoms and onset, above
F. Period of Communicability or Infectious Period
Not an infectious agent, although antigenic particles can be transferred on clothing and equipment to other locations, which could theoretically cause an allergenic reaction in a susceptible individual if enough antigenic material was present.
G. Epidemiology
Serological testing supports the clinical diagnosis of hypersensitivity pneumonitis by detecting antibodies to a number of different environmental antigens. However, the presence of antibodies does not necessarily indicate hypersensitivity pneumonitis. Antibodies may be detected in normal individuals.Studies have found up to 85% of farmers have antibodies to common allergens but show no evidence of disease.
Frequency - United States: Incidence varies considerably. Studies document 8-540 cases per 100,000 persons per year for farmers and 6,000-21,000 cases per 100,000 persons per year for pigeon breeders. High attack rates are documented in sporadic outbreaks. Approximately 52% of office workers exposed to an infected humidifier were infected, and 27% of workers at a molding plant for polyurethane foam parts were infected.
Prevalence varies by region, climate, and farming practices. Hypersensitivity pneumonitis affects 0.4-7% of the farming population. Reported prevalence among bird fanciers is estimated to be 20-20,000 cases per 100,000 persons at risk.
Mortality/Morbidity: Most patients recover completely after the inciting exposure ceases. Bird fancier's disease has a worse prognosis than farmer's lung. The outcomes of other varieties of hypersensitivity pneumonitis are more variable.
Sex: One epidemiological study revealed a male to female ratio of 1.2:1.
Age: Hypersensitivity pneumonitis is usually seen in the fourth to sixth decade of life. One study looking at 85 consecutive patients with hypersensitivity pneumonitis found a mean age of 53 +/- 14 years.
H. Bioterrorism Potential
None
I. Additional Information
References
Merck Manual. http://www.merckmanuals.com/professional/pulmonary-disorders/interstitial-lung-diseases/hypersensitivity-pneumonitis
American Lung Association. http://www.lung.org/lung-health-and-diseases/lung-disease-lookup/hypersensitivity-pneumonitis/
Dusts From Decayed Grain, Hay, and Silage. 1992. National Agricultural Safety Database. nasdonline.org/document/1630/d001504/dusts-from-decayed-grain-hay-and-silage.html
CDC/NIOSH Health Hazard Evaluation Report HETA 92-0122-2570. 1996. www.cdc.gov/niosh/hhe/reports/pdfs/1992-0122-2570.pdf
NIOSH Request for Assistance in Preventing Organic Dust Toxic Syndrome, Publication 94-102, April 1994 www.cdc.gov/niosh/docs/94-102/
University of Iowa Hospitals and Clinics: https://uihc.org/health-library/hypersensitivity-pneumonitis
Updated 2/2018