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Topic Content

Hypersensitivity Pneumonitis

Hypersensitivity pneumonitis is a syndrome of cough, dyspnea, and fatigue caused by sensitization and subsequent hypersensitivity to environmental antigens, frequently related to occupational exposures. 

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


 

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. 

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 Medical Manuals, 2008 accessed 3/15/11 www.merckmanuals.com/media/professional/pdf/Table_055-5.pdf

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 4-6 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: Subacute disease falls between the acute and chronic forms and manifests either as a productive cough, dyspnea, fatigue, and anorexia that develops over days to weeks or similarly to patients with acute disease, but superimposed on chronic symptoms 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 manifests over months to years as exertional dyspnea, productive cough, fatigue, muscle wasting and weight loss. Clubbing is observed in 50% of patients. Tachypnea, respiratory distress, and inspiratory crackles over lower lung fields often are present.  In advanced cases, pulmonary fibrosis produces signs and symptoms of right heart failure, respiratory failure, or both.  Removing exposure sources results in only partial improvement.
  •  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.

Case classification* – A Diagnostic Criteria for Hypersensitivity Pneumonitis

Category

Specifics

Case Classification

 

Definite

1, 2, and 3

1, 2, and 4a

1, 2a, 3, and 5

2, 3, and 5

Probable

1, 2a and 3

Subclinical

1 and 3a

Sensitization

1 only

Diagnostic Criteria:

 

1. Known exposure to antigen

a. History of exposure

b. Confirmation of antigen in environment by investigation

c. Presence of elevated, specific IgG serum precipitins to an antigen obtained from the patient's environment

2. Clinical, imaging, and pulmonary function test findings

a. Characteristic symptoms and signs (especially after antigen exposure)

b. Characteristic chest x-ray or high-resolution CT findings

c. Abnormal pulmonary function test

results

3. Lymphocytosis in bronchoalveolar lavage fluid

a. CD4+/CD8+ ratio < 1

b. Positive response to lymphocyte transformation testing

4. Recurrence of clinical and pulmonary function test findings with antigen challenge testing

a. Environmental exposure

b. Controlled exposure to antigen extract

5. Histologic findings

a. Noncaseating granulomas

b. Mononuclear cell infiltrate

 

*Source:  Merck Manual Professional, Hypersensitivity Pneumonitis, 2008.  Accessed online March 2011. www.merckmanuals.com/professional/sec05/ch055/ch055e.html 

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.

  • 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.
  • One epidemiological study revealed a male to female ratio of 1.2:1.
  • 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

Hypersensitivity Pneumonitis. Medscape article by Demirjian, M., Kamangar, N., Sharma, S. Updated: May 19, 2010. Accessed March 2011. emedicine.medscape.com/article/299174-overview

Merck Manuals Online Medical Library. Accessed March 2011 www.merckmanuals.com/professional/sec05/ch055/ch055e.html

Dusts From Decayed Grain, Hay, and Silage. National Agricultural Safety Database. Accessed March 2011. nasdonline.org/document/1630/d001504/dusts-from-decayed-grain-hay-and-silage.html

CDC/NIOSH Health Hazard Evaluation Report HETA 92-0122-2570. Accessed March 2011  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/

 A. Purpose of Surveillance and Reporting

  • To quantify the impact of the disease in Iowa
  • To identify and control outbreaks involving groups of people.
  • To help identify high-risk sources (e.g., materials at worksites, workers in a facility with excess dust or other allergen) and recommend interventions to assist in the prevention of additional cases.
  • To monitor the emergence of new types of hypersensitivity pneumonitis or new risk groups.
  • To assist in the development of recommendations for control or prevention.

B. Laboratory and Healthcare Provider Reporting Requirements

 All cases are required to be reported.

Mandatory Reporting is required of health care providers, clinics, hospitals, clinical laboratories, and  other health care facilities; school nurses or school officials; poison control and information centers; medical examiners; occupational nurses. Hospitals, health care providers, and clinical laboratories outside the state of Iowa for confirmed or suspect cases in an Iowa resident.

Additional information and reporting forms can be found in the Iowa Administrative Code [641] Chapter 1, which can be accessed through a link on the IDPH EH Division Web page at www.idph.state.ia.us/eh/reportable_diseases.asp.  Call the IDPH Environmental Health hotline at 800-972-2026 during regular business hours if you have questions.

C.  Local Public Health Agency Follow-up Responsibilities

None; elective involvement in outbreak situations.

A. Isolation and Quarantine Requirements

None

B. Protection of Contacts of a Case

None

C. Managing Special Situations

When Reported Incidence Is Higher than Usual/Outbreak Suspected

If an outbreak is suspected, investigate to determine the type and source of exposure and mode of transmission that may be involved. Clues in the history include recurring atypical pneumonias; symptom onset with a recent history of work or activity involving environments with exposure to allergens known to cause the syndrome (see table); onset after moving to a new job or home; having birds as a hobby or pets; exacerbation of symptoms in specific settings and relief of symptoms away from specific settings.

Consult with the IDPH Environmental Health Occupational Health & Safety Surveillance program staff at (800) 972-2026 to help determine a course of action to prevent further cases, or to provide referral for additional information/action.

D. Preventive Measures

Workers should be protected by preventing or minimizing exposures to airborne contaminants by controlling dust at its source and by using controls such as ventilation and dust suppression.  Exposure to dust and mold can be decreased by providing appropriate mechanical ventilation, wearing a respirator, storing only dried materials to prevent exposure to mold, and wetting materials before moving them to reduce exposure to dust. 

The most important aspect of long-term management is avoidance of exposure to antigens. A complete change of environment is rarely realistic, especially for farmers and other workers, in which case dust control measures (such as wetting down compost before disturbing it) or using air filters or protective masks may be effective. Fungicides may be used to prevent the growth of antigenic microorganisms (e.g., in hay or on sugar cane), but the long-term safety of this approach is unknown. Extensive cleaning of wet ventilation systems, removal of moist carpets, and maintenance of low humidity are also effective in some settings. Patients must be told, however, that these measures may be inadequate in the presence of continued exposure to allergens.