Farmer's Lung in Chile: Symptoms, Causes & Treatment | aihealz
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Farmer's Lung.Care & specialists in Chile
In Chile, farmer's Lung is managed by occupational medicines. Farmer's lung is a hypersensitivity pneumonitis caused by inhalation of thermophilic actinomycete and fungal antigens released from moldy hay, grain, silage, or compost. The dominant antigen is Saccharopolyspora rectivirgula, which thrives in damp organic material heated to 40-60 °C.
aliases · Farmer's lung (agricultural hypersensitivity pneumonitis)· Farmer's lung· Poumon du fermier· Pulmón del granjero· reviewed May 14, 2026
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Reviewed by AIHealz Medical Editorial Board · Occupational MedicineLast reviewed May 13, 2026
Farmer's lung (ICD-10: J67.0) is the prototypical agricultural form of hypersensitivity pneumonitis (HP), an immune-mediated interstitial lung disease caused by repeated inhalation of organic dust containing thermophilic actinomycetes (chiefly Saccharopolyspora rectivirgula, formerly Micropolyspora faeni and Thermoactinomyces vulgaris) and fungi (Aspergillus, Penicillium, Wallemia sebi). Inhaled antigens trigger a combined IgG-mediated immune complex deposition and T-cell-mediated granulomatous response in the small airways and alveoli. The ATS/JRS/ALAT 2020 guideline redefined HP into two clinical phenotypes — non-fibrotic (inflammatory) and fibrotic — replacing the older acute/subacute/chronic classification. Non-fibrotic disease is reversible with antigen avoidance and corticosteroids; fibrotic HP behaves like a slowly progressive fibrosing interstitial lung disease and carries substantial mortality.
key facts
Prevalence
1-19% of exposed farmers depending on climate and farming practice (Quirce 2016); annual incidence of clinical disease 5-30 per 100,000 in farming populations
Demographics
Male predominance (4:1) reflecting traditional farming work distribution; peak age 40-60; dairy farmers in temperate, humid climates highest risk
Avg. age
Acute episodes typically age 30-50; fibrotic chronic disease often diagnosed age 50-70 after years of exposure
Global cases
Hypersensitivity pneumonitis affects an estimated 1-2 per 100,000 in the general population; farmer's lung historically the most common occupational HP, though pigeon-breeder lung now matches or exceeds it in some regions
Specialist
Occupational Medicine
§ 02
How you might notice it
The key symptoms of Farmer's Lung are: Fever, chills, myalgia, and malaise developing 4-8 hours after exposure to moldy hay, grain, silage, or compost — the classic acute farmer's lung episode., Dry cough that becomes productive of scanty sputum, often described as paroxysmal and worse during or shortly after farming activities., Progressive exertional breathlessness, initially with strenuous work and ultimately at rest in advanced fibrotic disease., Tight chest and inspiratory crackles at the lung bases on auscultation (positive in 60-80% of chronic cases), sometimes with mid-inspiratory squeaks suggesting bronchiolitis., Weight loss of 5-15 kg over months in chronic disease, often initially attributed to working hard and eating less., Unintended episodes resembling 'recurrent pneumonia' that respond partially to antibiotics — a major diagnostic clue when occurring in the same farmer multiple times., Clubbing of the fingers and toes in 20-50% of long-standing fibrotic farmer's lung patients, similar in appearance to that seen in idiopathic pulmonary fibrosis..
01Fever, chills, myalgia, and malaise developing 4-8 hours after exposure to moldy hay, grain, silage, or compost — the classic acute farmer's lung episode.
02Dry cough that becomes productive of scanty sputum, often described as paroxysmal and worse during or shortly after farming activities.
03Progressive exertional breathlessness, initially with strenuous work and ultimately at rest in advanced fibrotic disease.
04Tight chest and inspiratory crackles at the lung bases on auscultation (positive in 60-80% of chronic cases), sometimes with mid-inspiratory squeaks suggesting bronchiolitis.
§ 03
How it’s diagnosed
diagnosis
Diagnosis of farmer's lung follows the ATS/JRS/ALAT 2020 algorithm combining exposure history, clinical features, imaging, bronchoalveolar lavage, and serology. A compatible occupational history is essential — quantifying years of farming, types of fodder, storage conditions, ventilation, and timing of symptoms relative to specific tasks. The Lacasse 2003 clinical prediction criteria support diagnosis when 6 of the following are met: known antigen exposure, positive precipitating IgG antibodies, recurrent episodes of symptoms, inspiratory crackles, symptoms 4-8 hours after exposure, and weight loss. Pulmonary function tests typically show restrictive ventilatory defect with reduced total lung capacity, reduced diffusing capacity for carbon monoxide (DLCO), and resting or exertional hypoxia. High-resolution CT (HRCT) is the imaging cornerstone. Non-fibrotic disease shows ground-glass opacities, ill-defined centrilobular nodules, and mosaic attenuation with expiratory air-trapping (the 'three-density sign'). Fibrotic disease adds reticulation, traction bronchiectasis, and sometimes honeycombing, typically in mid- and upper-lung zones — differentiating it from the basal predominance of IPF. Bronchoalveolar lavage with cell count and differential is recommended in most cases: a CD8-predominant lymphocytosis above 30% (often above 50%) is characteristic. Specific IgG antibody panels against Saccharopolyspora rectivirgula, Thermoactinomyces vulgaris, Aspergillus, and Penicillium support exposure but are not specific for disease. Lung biopsy (transbronchial cryobiopsy or surgical) is reserved for ambiguous cases and shows poorly formed non-necrotizing granulomas, lymphocytic bronchiolitis, and giant cells. Multidisciplinary discussion with radiology and pathology improves diagnostic confidence.
Key tests
01
Detailed exposure history and symptom diaryIdentifies the temporal relationship between farming tasks and respiratory symptoms; quantifies antigen exposure
02
High-resolution CT thorax (inspiratory and expiratory)
§ 04
Treatment & cost
medical treatments
✓Oral prednisolone (0.5-1 mg/kg/day, taper over 8-12 weeks)
✓Mycophenolate mofetil (1-3 g/day) or azathioprine (1.5-2.5 mg/kg/day)
✓Nintedanib (150 mg twice daily)
✓Pirfenidone (2,403 mg/day in three divided doses)
surgical options
Lung transplantation (single or double)1-year survival 80-85%; 5-year survival 50-55%; recurrence of HP in transplanted lung is rare with confirmed antigen avoidance
The dominant thermophilic actinomycete causing farmer's lung. Proliferates in damp organic material heated to 40-60 °C by microbial fermentation — typical of moldy hay stored wet. Spores 1 µm in diameter reach the alveoli and trigger immune complex and granulomatous lung injury.
Thermoactinomyces vulgaris and Streptomyces species
Additional thermophilic actinomycetes implicated in farmer's lung, particularly in arable farming with bagged compost and mushroom cultivation. Often coexist with Saccharopolyspora in heavily moldy material.
Aspergillus, Penicillium, and Wallemia fungi
Mesophilic fungi colonizing grain, hay, and silage in cooler regions or after wet harvests. Wallemia sebi has been identified as a major antigen in modern farmer's lung in some northern European studies.
Storage of damp hay, grain, or silage
The single most important practice that produces high antigen exposure. Hay baled at over 20% moisture, grain stored above 14% moisture, or wet silage develops thermophilic actinomycete proliferation. Modern haylage and anaerobic silage storage reduce risk.
Cleaning silos, grain bins, and feed troughs
Discrete heavy exposure events producing acute farmer's lung episodes. Dust clouds released during cleaning can deliver tens of millions of spores per cubic meter.
Cattle and pig sheds with poor ventilation
Indoor livestock environments concentrate organic dust, particularly during winter when animals are kept indoors. Inadequate ventilation, high stocking density, and bedding mold contribute to year-round exposure.
risk factors
Occupational farming exposure
§ 06
Living with it
01Dry hay to below 18% moisture content before baling to prevent thermophilic actinomycete proliferation.
02Use anaerobic silage and sealed bunker storage to limit fungal and actinomycete growth.
03Mechanize loading and unloading of fodder to reduce direct human exposure during high-dust tasks.
04Improve ventilation in livestock sheds; install extraction fans and well-designed bedding management.
05Use NIOSH-approved N95 respirators or powered air-purifying respirators during silo cleaning, bagged-fodder handling, and hay loading.
06Provide regular occupational health surveillance with annual symptom screening and spirometry for at-risk farmers.
07Comply with national agricultural occupational health programs and report suspected cases for compensation and prevention.
recommended foods
•Mediterranean dietary pattern to support general lung health and reduce systemic inflammation
§ 07
When to seek help
why see an occupational medicine
Pulmonology, occupational medicine, and an interstitial lung disease (ILD) multidisciplinary clinic should jointly manage farmer's lung. Pulmonology directs investigation and pharmacotherapy; occupational medicine quantifies exposure, supports antigen avoidance, and certifies fitness-for-work and compensation claims. Radiology and pathology contribute to multidisciplinary discussions that establish diagnosis and progression patterns. Lung transplant programs assess severe fibrotic disease.
Non-fibrotic (inflammatory) farmer's lungPredominantly inflammatory disease with ground-glass opacities, centrilobular nodules, and mosaic attenuation on high-resolution CT. Often follows discrete exposure episodes. Reverses with antigen avoidance and corticosteroids in 70-85% of cases.
Fibrotic farmer's lungEstablished lung fibrosis with reticulation, traction bronchiectasis, and honeycombing on CT, often in mid- and upper-lung zones. Follows years of unrecognized exposure. Carries 5-year mortality of 27-40% and may progress despite antigen removal.
Acute farmer's lung episodeSelf-limited febrile illness 4-8 hours after heavy antigen exposure (cleaning a silo, handling moldy hay). Resolves within 24-72 hours of removal from exposure; recurrence on re-exposure.
Mixed fibrotic-inflammatory patternCombined HRCT features of inflammation and fibrosis. Treatment combines antigen avoidance, immunosuppression, and consideration of antifibrotic therapy depending on progression.
Living with Farmer's Lung
Timeline
Acute episodes resolve within 24-72 hours of removal from exposure and symptom-directed steroids. HRCT ground-glass opacities clear over 4-12 weeks. Lung function recovery follows over 3-6 months. Fibrotic disease does not regress; antifibrotic therapy aims to slow further decline, with measurable benefit by 6-12 months in FVC trajectory. Pulmonary rehabilitation produces walking-distance gains within 8-12 weeks.
Lifestyle
01Eliminate or minimize ongoing exposure to identified antigens — usually moldy hay, silage, grain dust, or animal bedding.
02Quit smoking — smoking accelerates fibrosis and worsens HP outcomes despite paradoxical lower incidence in active smokers.
03Receive annual influenza vaccination, pneumococcal vaccination (PCV20 and PPSV23), and COVID-19 boosters.
04Attend pulmonary rehabilitation and maintain exercise capacity through walking, cycling, or supervised programs.
05Use prescribed oxygen with portable concentrators during activity if exertional desaturation is documented.
06Carry an exposure history and medication list to all healthcare appointments including emergency presentations.
Daily management
01Follow antigen avoidance plan agreed with occupational medicine team
Complementary approaches
Respiratory protective equipment (N95 or PAPR)Powered air-purifying respirators reduce inhaled antigen by over 95% when properly fitted and used during high-exposure tasks. Used when complete avoidance is impossible; not a substitute for environmental changes.
Modern dry hay handling and anaerobic silageDrying hay below 18% moisture content before baling and using sealed anaerobic silage reduce thermophilic actinomycete growth. Modern bunker silos and round-bale silage have substantially lowered farmer's lung incidence in some regions.
Choosing a doctor
Choose a pulmonologist or ILD specialist at a center with multidisciplinary ILD review, HRCT expertise, and access to bronchoalveolar lavage, antifibrotic prescribing, and pulmonary rehabilitation. For occupational compensation, an occupational physician familiar with national agricultural disease schemes is essential. Where lung transplantation is contemplated, refer early (FVC under 80% with progression) to a high-volume transplant center.
BLF / Asthma + Lung UK — Farmer's Lung →Patient-facing UK resource on farmer's lung and other occupational lung disease, including occupational health and compensation advice.
Farmer's lung is an allergic lung disease caused by breathing in molds and bacteria from damp hay, grain, or silage. The immune system overreacts and inflames the lungs, causing fever, cough, and breathlessness 4-8 hours after exposure. Continued exposure can lead to permanent scarring.
What causes farmer's lung?▾▴
The main cause is inhaling Saccharopolyspora rectivirgula and related thermophilic actinomycetes that grow in damp moldy hay, grain, or silage. Aspergillus, Penicillium, and Wallemia molds also contribute. Repeated exposure triggers immune-complex and granulomatous inflammation in the alveoli.
Is farmer's lung the same as hypersensitivity pneumonitis?▾▴
Farmer's lung is the agricultural form of hypersensitivity pneumonitis (HP). Other forms include pigeon-breeder lung, hot-tub lung, mushroom worker lung, and humidifier lung. All share the same immune mechanism but differ by causative antigen and exposure setting.
What are the symptoms of farmer's lung?▾▴
Acute symptoms include fever, chills, dry cough, breathlessness, and chest tightness 4-8 hours after exposure to moldy hay or grain. Chronic disease causes progressive breathlessness, weight loss, fatigue, and inspiratory crackles on examination. Severe disease produces clubbing and resting hypoxia.
How is farmer's lung diagnosed?▾▴
Diagnosis combines a compatible farming exposure history, high-resolution CT showing centrilobular nodules and mosaic attenuation, bronchoalveolar lavage with lymphocytosis over 30%, specific IgG antibody to actinomycetes, and pulmonary function tests showing restriction and reduced gas transfer.
Can farmer's lung be cured?▾▴
Non-fibrotic farmer's lung often resolves completely when exposure stops and corticosteroids are given. Established fibrotic disease cannot be reversed but can be stabilized with antigen avoidance, immunosuppressants, and antifibrotic therapy. Continued exposure roughly doubles 5-year mortality.
Do I have to stop farming if I have farmer's lung?▾▴
Complete antigen avoidance gives the best long-term outcome. Some farmers can continue work with engineering controls (dry hay, mechanized handling, ventilation) and respiratory protection (N95 or powered air-purifying respirators). Occupational medicine input is essential to balance livelihood and disease risk.
What is the role of corticosteroids?▾▴
Oral prednisolone 0.5-1 mg/kg/day for 4-8 weeks tapered over months relieves acute symptoms in 80-90% of patients. It is not a substitute for antigen avoidance. Long-term low-dose steroids may be needed in chronic or refractory disease, with prophylaxis against bone loss and infection.
Are antifibrotic drugs useful in farmer's lung?▾▴
Yes. The INBUILD trial showed nintedanib slows annual FVC decline by approximately 100 mL in progressive fibrotic interstitial lung disease including chronic hypersensitivity pneumonitis. Pirfenidone is used as an alternative when nintedanib is not tolerated. Antifibrotics complement antigen avoidance.
Can farmer's lung kill you?▾▴
Established fibrotic farmer's lung has a 5-year mortality of 27-40%, similar to other progressive fibrosing interstitial lung diseases. Non-fibrotic disease has a much better prognosis. Acute exacerbations of fibrotic disease carry a 5-month mortality above 50% and require urgent treatment.
Can farmer's lung come back after treatment?▾▴
Yes. Symptoms recur with every re-exposure to the causative antigen, even years after recovery. The disease is not curative — it is an immune-mediated response to an environmental trigger. Complete avoidance is the only reliable way to prevent recurrence.
How is farmer's lung different from IPF?▾▴
Idiopathic pulmonary fibrosis (IPF) has no identifiable cause, typically affects older non-farmer adults, and shows basal honeycombing on CT. Fibrotic farmer's lung has a clear exposure history, often mid- and upper-zone fibrosis, mosaic attenuation, and lymphocytic bronchoalveolar lavage.
Does smoking protect against farmer's lung?▾▴
Paradoxically, current smokers have lower farmer's lung incidence than non-smokers, likely due to suppressed immune responses. However, smokers who do develop the disease have worse outcomes and faster progression. All patients with farmer's lung should stop smoking.
Can family members of farmers get farmer's lung?▾▴
Yes, if they are exposed to the same antigens. Spouses and adolescent children who handle hay or work in livestock sheds can develop the disease. Family clustering may also reflect shared HLA susceptibility. Household exposure assessment is part of occupational evaluation.
Which respirators work for farmer's lung?▾▴
NIOSH-approved N95 filtering facepiece respirators block over 95% of airborne particles when properly fitted. Powered air-purifying respirators offer higher protection and better comfort for sustained tasks. Disposable surgical masks do not provide adequate protection against actinomycete spores.
How quickly do symptoms appear after exposure?▾▴
Acute farmer's lung produces fever, cough, and breathlessness 4-8 hours after antigen exposure, distinguishing it from immediate asthma reactions (within minutes to 2 hours). Chronic disease develops insidiously over months to years of repeated low-level exposure.
Is bronchoalveolar lavage needed for diagnosis?▾▴
Bronchoalveolar lavage with cell count is recommended in most cases and shows a CD8-predominant lymphocytosis above 30% (often above 50%) in active hypersensitivity pneumonitis. It supports diagnosis, distinguishes HP from IPF and sarcoidosis, and helps multidisciplinary teams reach diagnostic confidence.
Can children get farmer's lung?▾▴
Yes, but rarely. Children working in family farms with heavy fodder handling can develop hypersensitivity pneumonitis. Diagnosis is the same as in adults, with attention to growth, development, and school attendance. Antigen avoidance and education of the whole farming family are key.
What vaccines should I have?▾▴
Annual influenza vaccination, pneumococcal vaccination with PCV20 and PPSV23, and current COVID-19 boosters are recommended for all patients with chronic lung disease. Patients on long-term immunosuppression should avoid live vaccines and discuss specific scheduling with their pulmonary team.
Can lung transplantation help?▾▴
Lung transplantation is considered for severe fibrotic farmer's lung with FVC under 50% predicted, hypoxia, pulmonary hypertension, or rapid progression in patients under 65 without contraindications. Antigen avoidance must be confirmed pre-transplant. 5-year survival is approximately 50-55%.
Is farmer's lung a recognised occupational disease?▾▴
Yes. Farmer's lung is a recognized occupational lung disease in most countries with agricultural workforces and is covered by occupational compensation schemes in the UK (IIDB), US (workers' compensation), and most EU states. Confirmed diagnosis triggers reporting and benefit applications.
05Weight loss of 5-15 kg over months in chronic disease, often initially attributed to working hard and eating less.
06Unintended episodes resembling 'recurrent pneumonia' that respond partially to antibiotics — a major diagnostic clue when occurring in the same farmer multiple times.
07Clubbing of the fingers and toes in 20-50% of long-standing fibrotic farmer's lung patients, similar in appearance to that seen in idiopathic pulmonary fibrosis.
08Cyanosis at rest or on minimal exertion in advanced disease with type 1 respiratory failure.
09Symptoms that worsen during winter when livestock and fodder are kept indoors and improve during summer when outdoor work dominates.
10Anosmia, headache, and general systemic illness during heavy antigen exposure events such as silo unloading.
early warning signs
•Mild flu-like illness with cough and breathlessness on the evening of a day spent handling moldy fodder
•Recurrent 'chest infections' over multiple winters in the same dairy or arable farmer
•Unexplained weight loss and exertional breathlessness in an active middle-aged farmer
•Inspiratory crackles at the lung bases of a farmer with no smoking history and clear chest X-ray
•Subtle restriction or reduced diffusing capacity for carbon monoxide (DLCO) on routine occupational spirometry
● emergency signs
•Severe breathlessness, hypoxia (SpO2 below 90%), and bilateral infiltrates after a heavy exposure — exclude acute respiratory distress syndrome and admit for oxygen and corticosteroids
•Rapidly progressing breathlessness with weight loss and clubbing over weeks to months — exclude acute exacerbation of fibrotic HP, which carries 5-month mortality above 50%
•Fever, productive cough with greenish sputum, and consolidation on chest X-ray in a known HP patient — superimposed bacterial pneumonia or invasive aspergillosis
•Sudden chest pain and breathlessness — exclude pneumothorax, which complicates 5-10% of fibrotic disease
Imaging cornerstone — characterizes ground-glass opacities, centrilobular nodules, mosaic attenuation, fibrosis, and the three-density sign
03
Pulmonary function tests including DLCOQuantifies restriction, gas-transfer impairment, and exertional desaturation; tracks response to treatment
04
Bronchoalveolar lavage with cell count and differentialDetects characteristic CD8-predominant lymphocytosis (often above 30-50%) supporting HP diagnosis
05
Specific IgG antibody panel (Saccharopolyspora, Thermoactinomyces, Aspergillus, Penicillium)Demonstrates immunologic exposure to relevant antigens; supports but does not confirm diagnosis
06
Specific inhalation challenge (research and selected centers)Confirms causal antigen by controlled re-exposure with monitored physiology
07
Transbronchial or surgical lung biopsyReserved for ambiguous cases; demonstrates poorly formed granulomas, lymphocytic bronchiolitis, and giant cells
Outlook
Outcome depends primarily on disease phenotype, exposure status, and adherence to antigen avoidance. Non-fibrotic farmer's lung managed with complete antigen avoidance plus corticosteroids has excellent prognosis: 70-85% achieve full lung function recovery and 5-year mortality is comparable to age-matched controls. Fibrotic farmer's lung carries a 5-year mortality of 27-40%, similar to or slightly better than idiopathic pulmonary fibrosis when antigen avoidance is achieved. Continued exposure roughly doubles 5-year mortality versus successful avoidance. Predictors of worse outcome include older age, lower baseline FVC and DLCO, honeycombing on HRCT, low BAL lymphocyte percentage, ongoing antigen exposure, and progression in spite of treatment. The INBUILD trial showed antifibrotic therapy slows lung function decline in progressive fibrotic HP; transplant offers a second window of treatment for end-stage disease with 5-year post-transplant survival 50-55%.
modifiable
Dairy and arable farming carry the highest risk. Mushroom cultivation, malthouses, and cheese aging are related occupations with similar antigen exposure. Cumulative exposure dose correlates with both incidence and severity.
Damp climate and traditional hay storageenvironmental
Northern European, northeast US, and Canadian dairy regions historically reported the highest incidence. Modern handling (haylage, anaerobic silage) has reduced incidence in many regions.
Genetic HLA polymorphisms (HLA-DRB1*1305, MHC class II)genetic
Specific HLA class II alleles predispose to immune response against thermophilic actinomycete antigens. Family clustering of HP in farming households is recognized but multifactorial.
Female sex (paradoxical protection in fibrotic disease)non-modifiable
Although fewer women have occupational exposure, those with disease tend to have less fibrotic and better prognosis profiles in published series.
Non-smoker statusnon-modifiable
Paradoxically, current smokers have lower incidence of farmer's lung than non-smokers — likely due to suppression of immune responses — but smokers with HP have worse outcomes.
Viral respiratory infectionsenvironmental
Concurrent viral lower respiratory tract infection may amplify the inflammatory response in HP and trigger acute episodes. Modeled to increase severity through cytokine cross-talk.
Repeated low-level exposure without antigen avoidancemodifiable
Continued exposure after first acute episode is the strongest predictor of progression to fibrotic disease. Full antigen avoidance halts progression in 70-85% of non-fibrotic cases.
•Adequate protein intake (1-1.2 g/kg/day) during corticosteroid treatment to limit muscle loss
•Calcium and vitamin D supplementation during long-term corticosteroid use (1,000 mg calcium, 800-1,000 IU vitamin D daily)
•Hydration with 1.5-2 L water daily to support secretion clearance
foods to avoid
•Alcohol excess, which interacts with corticosteroids and antifibrotics
•Sugary diet contributing to steroid-induced hyperglycemia
•Self-administered herbal supplements without disclosure to the pulmonary team — many interact with antifibrotics
•Grapefruit and grapefruit juice while on nintedanib (CYP3A4 interaction)
Corticosteroid complications: osteoporosis, diabetes mellitus, hypertension, weight gain, cataracts, infection — mitigated by lowest effective dose and prophylaxis.
choosing the right hospital
01Pulmonology service with interstitial lung disease (ILD) subspecialty
02High-resolution CT thorax with inspiratory and expiratory protocols
03Bronchoscopy and bronchoalveolar lavage with cell-count reporting
04Multidisciplinary ILD discussion forum with radiology and pathology
Take medications including corticosteroids, antifibrotics, and inhalers on schedule
03Use peak-flow meter or home spirometer to track lung function weekly during dose changes
04Monitor oxygen saturation with pulse oximeter if prescribed oxygen
05Attend scheduled pulmonary review every 3-6 months during stable disease
06Keep a symptom and exposure diary for review at follow-up appointments
Exercise
Structured pulmonary rehabilitation followed by maintenance exercise is recommended for all patients with breathlessness or exercise limitation. Aim for 150 minutes per week of moderate aerobic activity (walking, cycling, swimming) with resistance training twice weekly. Patients with exertional desaturation should use prescribed oxygen during exercise. Avoid working in high-antigen-density environments even when feeling well.