Farmer's Lung (2024)

Continuing Education Activity

Farmer's lung is a type of hypersensitivity pneumonitis that is caused by precipitants such as moldy hay or straw. This condition’s specificity towards farmers makes it a rare but important disease process to know, especially for primary care clinicians. This activity reviews the evaluation of farmer’s lung disease and highlights the role of the interprofessional team in managing patients with this condition.

Objectives:

Describe the typical presentation of farmer's lung.
Identify the risk factors for farmer's lung.
Review the management for farmer's lung.
Summarize the importance of collaboration and communication amongst the interprofessional team to improve outcomes for patients affected by farmer's lung.

Access free multiple choice questions on this topic.

Introduction

Farmer's lung is considered a type of hypersensitivity pneumonitis that was initially identified in the 1700s by Italian researcher Bernardino Ramazzini. He examined exposure risks across multiple professions and found that the disease process was most abundantly found in breeders and farmers who were exposed to organic dust.[1]Interest and knowledge of the disease were rekindled in 1932 when a county tuberculosis officer identified 5 cases of acute respiratory failure seemingly caused by moldy hay during the springtime.Hypersensitivity pneumonitis, as we understand it today, encompasses a wide breadth of exposures that may illicit a delayed allergic response, specifically in the smaller airways. Farmers, in particular, are exposed to various agents in the fields of their workplace. These include organic agents, inorganic agents, gasses, methane, pesticides, fertilizers, and more. The syndrome has great variability in symptom severity and presentation due in large part to the variable exposure durations and innumerable offending agents. Spread between people is nonexistent, however, common exposure history can lead to similar disease states.[2]

Etiology

Farmer's lung or hypersensitivity pneumonitis is the immunologic reaction that occurs in response to an inhaled antigen.[3]To understand the most common exposures that would contribute to hypersensitivity pneumonitis, and by extension farmer's lung, it is important first to understand that chronic exposure to anything that the host body may find offensive and subsequently trigger an immune response can be a possible source. There are numerous varieties of hypersensitivity pneumonitis, often named after the profession or exposure with which they are associated. Examples include woodworker's lung, sauna taker's disease, and gerbil-keeper's lung, to name a few. Farmer's lung, a subgroup of hypersensitivity pneumonitis, has a variety of pathogens. The most common organism leading to farmer's lung are thermophilic actinomycetes likeMicropolyspora faeni,Thermoactinomyces vulgaris,and fungi likeAspergillus.[4]However, etiology varies greatly from region to region.The degree of regional variation of the dominant organism causing farmer's lung across the world necessitates extensive epidemiological evaluation and corresponding preventive measures.[5]

Epidemiology

Tracking epidemiological data for hypersensitivity pneumonitis and, by extension, farmer's lung remains a technical challenge as the condition is simultaneously underdiagnosed and influenced by a myriad of factors such as geographical conditions, season, local customs, and proximity to industrial exposure.[6]In general, there is a higher prevalence of respiratory symptoms in the agricultural population during non-dry climates in an indoor setting.[7]Region-specific data varies, and the prevalence of farmer's lung was found to be higher in Asian countries as compared to European countries.[8]

Pathophysiology

Inhaled antigens may elicit inflammation in the small airways and interstitial spaces, leading to fever, myalgias, and diffusion limitation leading to hypoxia. This inflammation is mediated by two processes, type III and type IV hypersensitivity reactions. The inhaled antigen initially causes an immune complex-mediated (type III) hypersensitivity reaction, which is responsible for granuloma formation. During ongoing acute exposure, IgG antibodies specific to the inhaled antigen can be detected in the serum in relatively high titers. As exposure to the offending antigen continues and becomes chronic, a T-cell mediated (type IV) hypersensitivity reaction is elicited, which is responsible for fibrosis.[1]

History and Physical

The clinical features of hypersensitivity pneumonitis range from an acute febrile reaction to an insidious onset.[3]The clinical picture varies according to the degree of exposure and chronicity of the disease. During an acute episode, symptoms such as dry cough, shortness of breath, fevers, myalgias, and joint pains can be observed. These symptoms can be mistaken for a viral illness.[9]Though there is not a globally recognized established diagnostic criteria, these findings are included in various diagnostic criteria that speak to the prevalence of these symptoms. A detailed history that includes geographical locations, identifies exposure to risk in a systematic fashion, and chronicity of symptoms is essential in making a diagnosis.[10]

Evaluation

A high index of suspicion, along with exposure history, high-resolution computerized tomography (HRCT) scan, and marked lymphocytosis are the main factors leading to the diagnosis of farmer's lung.[11]HRCT is a useful investigation in evaluating acute and chronic cases. Acute features are diffuse ground-glass opacities, centrilobular nodules, mosaic pattern, and air trapping. Chronic features include septal thickening, ground-glass opacities, fibrosis, bronchiectasis, usually with upper lobe predominance, and signs of pulmonary hypertension. Some patients may present with emphysema, and this may be a confounding feature in smokers.[12]

Treatment / Management

In acute stages, removal of the patient from the surroundings is the most important step. Identifying other insults like pesticide poisoning is essential since treatment may differ. Steroids for the short term might give symptomatic improvement, but no functional improvement is seen in the long term.[20][21]Recent trials of usage of mycophenolate in hypersensitivity pneumonitis have resulted in improvement in DLCO, but further studies are needed.[22]

Chronic cases may need supportive therapy like vaccinations, oxygen supplementation, diuretics, and noninvasive ventilation. The final treatment option would be lung transplantation, which may prolong life expectancy. Preventive aspects are important and grossly underutilized. The powered dust respirator helmet has proved to be useful not only for symptoms but also for functional improvement.[23]Avoidance of work is the best measure but may not be possible in all due to financial issues. The persistence of symptoms in 2/3 of patients even after five years after an acute episode indicates the need for strict primary preventive measures.[21][24]Leaving the farm offers the best possible solution.[14]Patients with five or more symptom recurrences usually have progressive and significant lung damage.[25]

Differential Diagnosis

Differential diagnosis of farmer's lung is broad and challenging.

Clinically acute viral infections, organic dust toxic syndrome may resemble hypersensitivity pneumonitis.[9]
Combined pulmonary fibrosis and emphysema in smokers present a similar picture.[26]
The smoking population can have associated COPD, which needs to be distinguished as this may require specific management.

Prognosis

The prognosis of farmer's lung depends on the stage of identification of the disease as avoidance of further antigen exposure may result in the prevention of progression of the disease. Exacerbations have been shown to occur in 8% of casesafter acute episodes.[21]A mortality rate of 1% has been reported. The average lifespan was eight years after diagnosis.[27]

Complications

The most common clinical features of hypersensitivity pneumonitis are fever, cough, and dyspnea. However, it can result in a myriad of complications. As a worst-case scenario, the patient can present with respiratory failure and shock and require ventilatory support and vasopressors.[3]

Deterrence and Patient Education

The prevalence of farmer's lung can be reduced by the regular application of preventive measures, along with financial incentives. Farmworkers should be educated about processes such as efficient drying of cereals and hay before storage, using silage extensively, improving the ventilation of farm buildings, and introducing mechanical feeding systems. Individual farmworkers should also be taught how to spot the early symptoms of farmer's lung. All farmworkers should be encouraged to wear respirators and masks when handling moldy fodder.[28]

Enhancing Healthcare Team Outcomes

Farmer's lung disease is an occupational illness of dairy and cattle farmers in many countries. The diagnosis of the disease is usually overlooked because of the lack of patient orclinician awareness.[29]It often poses a diagnostic dilemma as the patients may exhibit non-specific signs and symptomssuch as dry cough, shortness of breath, fevers, myalgias, and joint pains during an acute episode. These symptoms can be mistaken for a viral illness.[9]While history and physical exam may point towards interstitial lung disease, the underlying cause is difficult to know without proper imaging studies. The pulmonologist is usually the focal person involved in the treatment of patients with farmer's lung. It is, however, essential to involve an interprofessional team, including a radiologist, laboratory technicians, and nurses. The radiologist plays a vital role in determining the diagnosis.[11]The interprofessional team should work together and coordinate with each other to optimize patient education and treatment. The outcomes of farmer's lung depend on the stage of identification of the disease, and avoidance of further antigen exposure may result in the prevention of progression of the disease.[21]However, to improve outcomes of farmer's lung, consultation with an interprofessional group of specialists should be considered.

Review Questions

References

1.: Riario Sforza GG, Marinou A. Hypersensitivity pneumonitis: a complex lung disease. Clin Mol Allergy. 2017;15:6. [PMC free article: PMC5339989] [PubMed: 28286422]
2.: Dales RE, Munt PW. Farmer's Lung Disease. Can Fam Physician. 1982 Oct;28:1817-20. [PMC free article: PMC2306727] [PubMed: 21286564]
3.: Deschênes D, Provencher S, Cormier Y. Farmer's lung-induced hypersensitivity pneumonitis complicated by shock. Respir Care. 2012 Mar;57(3):464-6. [PubMed: 22005584]
4.: Tao BG, Shen YE, Chen GX, Wu AL, Hong ZR, Yuan JW, Chen BC, Gu XQ. An epidemiological study on farmer's lung among hay grinders in Dafeng County. Biomed Environ Sci. 1988 Jun;1(1):13-8. [PubMed: 3268105]
5.: Husman K, Vohlonen I, Terho EO, Mäntyjärvi RA. Precipitins against microbes in mouldy hay in the sera of farmers with farmer's lung or chronic bronchitis and of healthy farmers. Eur J Respir Dis Suppl. 1987;152:122-7. [PubMed: 3478211]
6.: Lopez M, Salvaggio JE. Epidemiology of hypersensitivity pneumonitis/allergic alveolitis. Monogr Allergy. 1987;21:70-86. [PubMed: 3317002]
7.: Cushen B, Sulaiman I, Donoghue N, Langan D, Cahill T, Nic Dhonncha E, Healy O, Keegan F, Browne M, O'Regan A. High prevalence of obstructive lung disease in non-smoking farmers: The Irish farmers lung health study. Respir Med. 2016 Jun;115:13-9. [PubMed: 27215498]
8.: Liu S, Chen D, Fu S, Ren Y, Wang L, Zhang Y, Zhao M, He X, Wang X. Prevalence and risk factors for farmer's lung in greenhouse farmers: an epidemiological study of 5,880 farmers from Northeast China. Cell Biochem Biophys. 2015 Mar;71(2):1051-7. [PubMed: 25344645]
9.: Mönkäre S. Clinical aspects of farmer's lung: airway reactivity, treatment and prognosis. Eur J Respir Dis Suppl. 1984;137:1-68. [PubMed: 6426996]
10.: Morell F, Villar A, Montero MÁ, Muñoz X, Colby TV, Pipvath S, Cruz MJ, Raghu G. Chronic hypersensitivity pneumonitis in patients diagnosed with idiopathic pulmonary fibrosis: a prospective case-cohort study. Lancet Respir Med. 2013 Nov;1(9):685-94. [PubMed: 24429272]
11.: Hirschmann JV, Pipavath SN, Godwin JD. Hypersensitivity pneumonitis: a historical, clinical, and radiologic review. Radiographics. 2009 Nov;29(7):1921-38. [PubMed: 19926754]
12.: Hanak V, Golbin JM, Hartman TE, Ryu JH. High-resolution CT findings of parenchymal fibrosis correlate with prognosis in hypersensitivity pneumonitis. Chest. 2008 Jul;134(1):133-8. [PubMed: 18403660]
13.: Cano-Jiménez E, Rubal D, Pérez de Llano LA, Mengual N, Castro-Añón O, Méndez L, Golpe R, Sanjuán P, Martín I, Veres A. Farmer's lung disease: Analysis of 75 cases. Med Clin (Barc). 2017 Nov 22;149(10):429-435. [PubMed: 28587854]
14.: Cuthbert OD, Gordon MF. Ten year follow up of farmers with farmer's lung. Br J Ind Med. 1983 May;40(2):173-6. [PMC free article: PMC1009167] [PubMed: 6830713]
15.: Takahashi T, Munakata M, Ohtsuka Y, Satoh-Kamachi A, Sato R, Homma Y, Kawakami Y. Serum KL-6 concentrations in dairy farmers. Chest. 2000 Aug;118(2):445-50. [PubMed: 10936139]
16.: Post W, Heederik D, Houba R. Decline in lung function related to exposure and selection processes among workers in the grain processing and animal feed industry. Occup Environ Med. 1998 May;55(5):349-55. [PMC free article: PMC1757584] [PubMed: 9764113]
17.: Lacasse Y, Fraser RS, Fournier M, Cormier Y. Diagnostic accuracy of transbronchial biopsy in acute farmer's lung disease. Chest. 1997 Dec;112(6):1459-65. [PubMed: 9404739]
18.: Casoni GL, Tomassetti S, Cavazza A, Colby TV, Dubini A, Ryu JH, Carretta E, Tantalocco P, Piciucchi S, Ravaglia C, Gurioli C, Romagnoli M, Gurioli C, Chilosi M, Poletti V. Transbronchial lung cryobiopsy in the diagnosis of fibrotic interstitial lung diseases. PLoS One. 2014;9(2):e86716. [PMC free article: PMC3938401] [PubMed: 24586252]
19.: Ramaswamy A, Homer R, Killam J, Pisani MA, Murphy TE, Araujo K, Puchalski J. Comparison of Transbronchial and Cryobiopsies in Evaluation of Diffuse Parenchymal Lung Disease. J Bronchology Interv Pulmonol. 2016 Jan;23(1):14-21. [PMC free article: PMC4864578] [PubMed: 26705007]
20.: Mönkäre S. Influence of corticosteroid treatment on the course of farmer's lung. Eur J Respir Dis. 1983 May;64(4):283-93. [PubMed: 6861923]
21.: Mönkäre S, Haahtela T. Farmer's lung--a 5-year follow-up of eighty-six patients. Clin Allergy. 1987 Mar;17(2):143-51. [PubMed: 3581462]
22.: Morisset J, Johannson KA, Vittinghoff E, Aravena C, Elicker BM, Jones KD, Fell CD, Manganas H, Dubé BP, Wolters PJ, Collard HR, Ryerson CJ, Ley B. Use of Mycophenolate Mofetil or Azathioprine for the Management of Chronic Hypersensitivity Pneumonitis. Chest. 2017 Mar;151(3):619-625. [PMC free article: PMC6026221] [PubMed: 27816444]
23.: Nuutinen J, Terho EO, Husman K, Kotimaa M, Härkönen R, Nousiainen H. Protective value of powered dust respirator helmet for farmers with farmer's lung. Eur J Respir Dis Suppl. 1987;152:212-20. [PubMed: 3478219]
24.: Kusaka H, Ogasawara H, Munakata M, Tanimura K, Ukita H, Denzumi N, Homma Y, Kawakami Y. Two-year follow up on the protective value of dust masks against farmer's lung disease. Intern Med. 1993 Feb;32(2):106-11. [PubMed: 8507920]
25.: Braun SR, doPico GA, Tsiatis A, Horvath E, Dickie HA, Rankin J. Farmer's lung disease: long-term clinical and physiologic outcome. Am Rev Respir Dis. 1979 Feb;119(2):185-91. [PubMed: 434591]
26.: Soumagne T, Pana-Katatali H, Degano B, Dalphin JC. Combined pulmonary fibrosis and emphysema in hypersensitivity pneumonitis. BMJ Case Rep. 2015 Dec 21;2015 [PMC free article: PMC4691920] [PubMed: 26689249]
27.: Kokkarinen J, Tukiainen H, Terho EO. Mortality due to farmer's lung in Finland. Chest. 1994 Aug;106(2):509-12. [PubMed: 7774328]
28.: Grant IW, Blyth W, Wardrop VE, Gordon RM, Pearson JC, Mair A. Prevalence of farmer's lung in Scotland: a pilot survey. Br Med J. 1972 Feb 26;1(5799):530-4. [PMC free article: PMC1787415] [PubMed: 4501939]
29.: Madsen D, Klock LE, Wenzel FJ, Robbins JL, Schmidt CD. The prevalence of farmer's lung in an agricultural population. Am Rev Respir Dis. 1976 Feb;113(2):171-74. [PubMed: 1247230]

: Disclosure: Azka Zergham declares no relevant financial relationships with ineligible companies.
: Disclosure: Daniel Heller declares no relevant financial relationships with ineligible companies.