Farmer's lung

Farmer's lung (not to be confused with silo-filler's disease) is a hypersensitivity pneumonitis induced by the inhalation of biologic dusts coming from hay dust or mold spores or any other agricultural products.[1] It results in a type III hypersensitivity inflammatory response and can progress to become a chronic condition which is considered potentially dangerous.[2]

Farmer's lung
Hay shed
SpecialtyRespirology

Signs and symptoms

  • Acute Stage: After four to eight hours symptoms such as headache, irritating cough, and shortness of breath upon physical exertion, appear.[3]
  • Subacute Stage: Symptoms persist without further exposure, and increase in severity. Symptoms include: shortness of breath upon exertion, chronic coughing, physical weakness, occasional fever and sweating, decrease in appetite, aches and pains.[3]
  • Chronic Stage: Debilitating effects are now considered long-term. Symptoms include: severe shortness of breath, chronic coughing, physical weakness, occasional fever and sweating at night, decrease in appetite, and general aches and pains.[3]

These symptoms develop between four and eight hours after exposure to the antigens. In acute attacks, the symptoms mimic pneumonia or flu. In chronic attacks, there is a possibility of the victim going into shock and dying from the attack.[4]

Causes

Permanent lung damage can arise due to one's inability to recognize the cause of symptoms.[4] Farmer's lung occurs because repeated exposure to antigens, found in the mold spores of hay, crops, and animal feed, triggers an allergic reaction within the farmer's immune system.[4] The defense mechanisms of the body present as cold and flu-like symptoms that occur in individuals who experience either acute or chronic reactions.[4]

The mold spores are inhaled and provoke the creation of IgE antibodies that circulate in the bloodstream, these types of immune response are most often initiated by exposure to thermophilic actinomycetes (most commonly Saccharopolyspora rectivirgula), which generate IgG-type antibodies. Following a subsequent exposure, IgG antibodies combined with the inhaled allergen to form immune complexes in the walls of the alveoli in the lungs.[5] This causes fluid, protein, and cells to accumulate in the alveolar wall which slows blood-gas interchange and compromises the function of the lung. After multiple exposures, it takes less and less of the antigens to set off the reaction in the lung.[6]

Prevention

Farmer's lung disease is permanent and cannot be reversed, therefore in order to prevent the onset of further stages, farmers should inform their doctor of their occupation and if they have mold in their work environment.[3] Prevention of this respiratory illness can be facilitated through the ventilation of work areas, drying of materials, and the use of a mask when working in confined areas with moldy hay or crops.[4]

Diagnosis

Diagnoses of Farmer's lung is difficult due to its similarity to cold and flu-like symptoms.[7] Doctors diagnose patients with Farmer's lung under the following conditions:

Examination procedures may include:

• taking a blood test[3]

• taking a chest x-ray[3]

• administering a breathing capacity test[3]

• administering an inhalation challenge[3]

• examining lung tissue[3]

• performing an immunological investigation[3]

• performing a lung function test[3]

• reviewing your clinical history [3]

Treatment

Depending on the severity of the symptoms, FLD can last from one to two weeks, or they can last for the rest of one's life. Acute FLD has the ability to be treated because hypersensitivity to the antigens has not yet developed. The main treatment options are: rest and reducing the exposure to the antigens through masks and increased airflow in confined spaces where the antigens are present.[4] Any exposure to the antigens once hypersensitivity can set off another chronic reaction.[4] For chronic FLD, there are no true treatments because the patient has developed hypersensitivity meaning that their condition will last the rest of their life.

Epidemiology

The growth of mold spores occurs when hay is not dried properly.[8] The growth of these mold spores accumulates over time and will infect the host upon release from the source.[9] When in the air, the farmer may inhale the particles and induce an allergic reaction.[9] The hay at risk for increased volumes of spores are found at the bottom of the pile.[9] The presence of Farmer's Lung Disease peaks during late winter and early spring and is mostly seen after the harvest season when symptoms have set in.[10] This disease is most prevalent in damp climates.[10]

References

  1. Enelow RI (2008). Fishman's Pulmonary Diseases and Disorders (4th ed.). McGraw-Hill. pp. 1161–1172. ISBN 0-07-145739-9.
  2. "Farmer's Lung: It Takes Your Breath Away!". Farm Safety Association, Inc.
  3. Grisso R, Gay S, Hetzel G, Stone B (2009). "Farmer's Lung: Causes and Symptoms of Mold and Dust Induced Respiratory Illness" (PDF). Virginia Cooperative Extension: 4.
  4. "National Ag Safety Database - National Ag Safety Database".
  5. Geha R, Rosen F (2008). Case studies in immunology : a clinical companion. Rosen, Fred S. (5th ed.). New York, N.Y.: Garland Science, Taylor and Francis Group. ISBN 9780815341451. OCLC 80460619.
  6. Kahn AP (2004). The encyclopedia of work-related illnesses, injuries, and health issues. New York, N.Y.: Facts on File. ISBN 9780816048441. OCLC 61131489.
  7. Reyes CN, Wenzel FJ, Lawton BR, Emanuel DA (February 1982). "The pulmonary pathology of farmer's lung disease". Chest. 81 (2): 142–6. doi:10.1378/chest.81.2.142. PMID 7035083.
  8. Dyer EL (March 1980). "Farmer's lung: industrial hazard for rural inhabitants". Southern Medical Journal. 73 (3): 353–61, 364. doi:10.1097/00007611-198003000-00024. PMID 7361144.
  9. Dales RE, Munt PW (October 1982). "Farmer's Lung Disease". Canadian Family Physician. 28: 1817–20. PMC 2306727. PMID 21286564.
  10. Grant IW, Blyth W, Wardrop VE, Gordon RM, Pearson JC, Mair A (February 1972). "Prevalence of farmer's lung in Scotland: a pilot survey". British Medical Journal. 1 (5799): 530–4. doi:10.1136/bmj.1.5799.530. PMC 1787415. PMID 4501939.
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