Allergic asthma is the most common phenotype of asthma, defined by chronic airway inflammation driven by Type 2 immune responses to inhaled allergens such as house dust mite, animal dander, mould, and pollen. Roughly 60-80% of children and 50-60% of adults with asthma have an allergic phenotype, and globally an estimated 260 million people live with asthma overall (GBD 2021).
Allergic asthma (ICD-10: J45.0), also called atopic or extrinsic asthma, is a chronic inflammatory disease of the airways triggered by IgE-mediated and Type 2 immune responses to inhaled aeroallergens. Inhaled allergen binds IgE on mast cells and triggers degranulation, releasing histamine, leukotrienes, and prostaglandins that produce immediate bronchospasm. A second, late-phase response 4-8 hours later recruits eosinophils, T-helper 2 lymphocytes, and innate lymphoid cells, releasing interleukins IL-4, IL-5, IL-13, and thymic stromal lymphopoietin (TSLP). Chronic inflammation thickens the airway smooth muscle, increases mucous gland mass, and causes basement membrane fibrosis (airway remodelling).
key facts
Prevalence
Approximately 8-12% of adults and 10-15% of children in high-income countries have asthma; 50-70% have an allergic phenotype
Demographics
Female:male ratio 1.5:1 in adults; male predominance in children before puberty
Avg. age
Onset most commonly age 3-15 years; adult-onset allergic asthma typically presents in the 20s-40s
Global cases
260 million people with asthma worldwide; over 1,000 asthma deaths per day (GBD 2021)
Specialist
Allergy & Immunology
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How you might notice it
The key symptoms of Allergic Asthma are: Episodic dry cough, especially at night or in the early morning, often the first and only symptom in milder allergic asthma., Audible wheeze on exhalation, sometimes also on inspiration, produced by narrowed airways and turbulent airflow., Chest tightness, described as a band or weight on the chest, often worse during exacerbations., Breathlessness on exertion, with cold air, or after laughing — exercise-induced bronchoconstriction occurs in 70-90% of patients., Symptoms triggered or worsened by specific allergens (house dust mite, cat or dog dander, mould, tree, grass, or weed pollen, cockroach)., Seasonal pattern of symptoms matching pollen calendars (spring tree, summer grass, autumn weed, year-round perennial allergens)., Coexisting allergic rhinitis (sneezing, itchy nose, blocked nose, watery eyes) in 70-80% of patients with allergic asthma..
01Episodic dry cough, especially at night or in the early morning, often the first and only symptom in milder allergic asthma.
02Audible wheeze on exhalation, sometimes also on inspiration, produced by narrowed airways and turbulent airflow.
03Chest tightness, described as a band or weight on the chest, often worse during exacerbations.
04Breathlessness on exertion, with cold air, or after laughing — exercise-induced bronchoconstriction occurs in 70-90% of patients.
05
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How it’s diagnosed
diagnosis
Diagnosis combines a typical history with objective evidence of variable airflow obstruction. The classic history includes episodic wheeze, cough, chest tightness, or breathlessness triggered by allergens, exercise, viral infection, or cold air, with day-to-day variability and a personal or family history of atopy. Spirometry is the primary lung function test: a post-bronchodilator increase in FEV1 of 12% and 200 mL (children: 12%) confirms reversible airflow obstruction. If baseline spirometry is normal, alternative objective tests include peak flow variability (more than 10% in adults, 13% in children over two weeks), bronchial challenge with methacholine or mannitol (PC20 <8 mg/mL is positive), or exercise challenge for exercise-induced bronchoconstriction. Type 2 biomarkers refine the phenotype and guide biologic eligibility: blood eosinophils above 150/µL, fractional exhaled nitric oxide (FeNO) above 25 ppb in adults (35 ppb in children 5-12), and total IgE above 30 IU/mL. Allergy assessment with skin-prick testing or serum specific IgE to common aeroallergens identifies modifiable triggers and informs allergen avoidance and allergen immunotherapy. A chest X-ray excludes alternative diagnoses (pneumonia, cardiac failure, malignancy) in adults with new wheeze. Differential diagnoses include COPD, vocal cord dysfunction, hyperventilation syndrome, eosinophilic granulomatosis with polyangiitis, allergic bronchopulmonary aspergillosis, and cardiac failure.
Key tests
01
Spirometry with bronchodilator reversibility testConfirms reversible airflow obstruction (post-bronchodilator FEV1 increase ≥12% and 200 mL)
02
Peak expiratory flow monitoringDetects diurnal variability >10% in adults (13% in children) supporting asthma diagnosis and guiding self-management plans
✓Long-acting muscarinic antagonist (tiotropium 5 mcg once daily)
✓Omalizumab (anti-IgE) 150-375 mg every 2-4 weeks subcutaneously
surgical options
Bronchial thermoplastyAIR2 trial: 32% reduction in severe exacerbations and improved quality of life at 12 months; effects sustained at 5 years; rare procedural complications
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Causes & risk factors
known causes
House dust mite sensitisation
Dermatophagoides pteronyssinus and Dermatophagoides farinae are the dominant indoor aeroallergens worldwide. Mite faecal pellets contain Der p 1 and Der p 2 proteases that drive Type 2 airway inflammation. Year-round exposure in mattresses, carpets, and upholstery sustains chronic disease.
Pet dander sensitisation
Cat (Fel d 1) and dog (Can f 1) allergens are airborne and persist in homes for months after a pet leaves. Sensitisation predicts asthma severity and exacerbation risk independently of mite sensitisation.
Pollen and mould sensitisation
Tree pollens (birch, oak, cedar) in spring, grass pollens in summer, and weed pollens (ragweed, mugwort) in autumn drive seasonal exacerbations. Outdoor moulds (Alternaria, Cladosporium) cause severe asthma and have been linked to thunderstorm asthma epidemics.
Cockroach and rodent allergens
Bla g 1 (cockroach) and Mus m 1 (mouse) sensitisation are particularly prevalent in inner-city housing and predict severe asthma in children. Integrated pest management improves symptom control.
Viral respiratory infections
Rhinovirus, respiratory syncytial virus, and influenza precipitate 60-80% of asthma exacerbations and contribute to asthma inception in early childhood when interacting with allergen sensitisation.
Occupational allergens
More than 300 substances are recognised as causes of occupational asthma — flour and grain, animal proteins, latex, isocyanates, persulphates in hairdressing, and laboratory animals. Sensitisation often follows several years of exposure.
risk factors
Atopy and family history
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Living with it
01Avoid second-hand tobacco smoke and never smoke indoors; in-utero and childhood smoke exposure double asthma risk.
02Encase mattresses and pillows in mite-impermeable covers and wash bedding weekly at 60 °C in mite-sensitised patients.
03Vacuum carpets weekly with a HEPA-filter vacuum and use hard flooring where possible.
04Treat allergic rhinitis with intranasal corticosteroids and antihistamines — uncontrolled rhinitis worsens asthma.
05Vaccinate against influenza annually and ensure pneumococcal and COVID-19 vaccinations are up to date.
06Avoid known occupational sensitisers and use appropriate respiratory protection where exposure is unavoidable.
recommended foods
•Mediterranean-style diet rich in fruits, vegetables, fish, nuts, and olive oil
•Oily fish twice weekly for omega-3 fatty acids
•Foods rich in vitamin D (oily fish, fortified dairy) plus supplementation in deficient patients
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When to seek help
why see an allergy & immunology
Patients with frequent exacerbations (more than two per year), persistent symptoms despite medium-dose ICS-LABA, FEV1 below 70% predicted, oral corticosteroid dependence, or features of Type 2 inflammation should be referred to an allergist or respiratory physician for phenotyping and biologic assessment. Children with frequent symptoms or poor inhaler response benefit from paediatric allergy review.
01Severe exacerbations requiring emergency care, oral corticosteroids, or hospitalisation — drive most asthma costs and a small but significant share of asthma deaths.
02Airway remodelling with fixed airflow obstruction in chronic uncontrolled asthma, particularly in adult-onset disease.
03Side-effects of long-term oral corticosteroids in severe disease — osteoporosis, cataracts, diabetes, hypertension — addressed by steroid-sparing biologic therapy.
04Pneumonia and oropharyngeal candidiasis from inhaled corticosteroid use, mitigated by spacer use and mouth rinsing.
Mild intermittent allergic asthmaSymptoms less than twice per week, brief exacerbations, nocturnal awakening less than twice monthly, normal lung function between episodes. Treated as needed with low-dose ICS-formoterol per GINA Track 1.
Mild persistent allergic asthmaSymptoms more than twice per week but not daily, exacerbations affecting activity, nocturnal symptoms more than twice monthly. Daily low-dose ICS-formoterol or alternative controller required.
Moderate persistent allergic asthmaDaily symptoms, exacerbations more than twice yearly, nocturnal symptoms more than weekly, FEV1 60-80% predicted. Medium-dose ICS-LABA combination needed.
Severe allergic asthma (Type 2 high)Daily symptoms despite high-dose ICS-LABA, frequent exacerbations, FEV1 below 60% predicted, with elevated blood eosinophils (>150/uL), FeNO (>20 ppb), or total IgE >30 IU/mL. Eligible for biologic therapy.
Allergen-induced occupational asthmaOnset after exposure to a specific workplace allergen (flour, latex, animal proteins, isocyanates, persulphates). Diagnosed by serial peak flow recordings at and away from work; treatment includes allergen removal and standard inhaled therapy.
Living with Allergic Asthma
Timeline
Symptomatic improvement begins within hours of initiating ICS-formoterol. FEV1 and FeNO improve over 6-8 weeks. Biologic therapy effects are usually apparent by 4-12 weeks with maximal exacerbation reduction by 6 months. Allergen immunotherapy requires 3-5 years for long-lasting benefit. Step-down to lower controller doses can be considered after 3 months of good control.
Lifestyle
01Use the prescribed maintenance inhaler every day, even when feeling well.
02Carry the reliever inhaler at all times and use a spacer for metered-dose inhalers to improve drug delivery.
03Keep a written personalised asthma action plan and follow yellow/red zone instructions promptly.
04Avoid known allergen and irritant triggers (smoke, strong perfumes, cold air, paint fumes).
05Maintain a healthy body mass index of 18.5-24.9 kg/m2 — weight loss in obesity improves asthma control.
06Exercise regularly with pre-exercise warm-up and reliever inhaler if exercise-induced symptoms occur.
Daily management
01Take the maintenance inhaler at the same time every day; use a spacer for pressurised metered-dose inhalers.
02
Complementary approaches
Allergen-specific immunotherapy (subcutaneous or sublingual)Disease-modifying therapy for selected allergic asthma patients with confirmed single-allergen sensitisation, FEV1 above 70% predicted, and well-controlled disease on ICS. Reduces medication need and may prevent asthma in children with allergic rhinitis.
Vitamin D supplementation in deficient patientsReduces severe exacerbations by 26% in patients with baseline 25-OH-vitamin-D below 25 nmol/L (Cochrane 2016, Jolliffe 2017). Aim for level above 50 nmol/L.
Choosing a doctor
Choose a clinician with subspecialty training in asthma and allergy who has access to spirometry, FeNO, allergy testing, and biologic prescribing. Ask whether the clinic offers a severe asthma multidisciplinary team review including respiratory physiotherapy, allergy nurse specialist, and clinical psychology, and whether they use validated outcome measures (ACT, ACQ).
Allergic asthma is the most common type of asthma, in which airway inflammation is triggered by IgE-mediated immune responses to inhaled allergens such as house dust mite, pet dander, mould, and pollen. It causes episodic wheeze, cough, breathlessness, and chest tightness.
How is allergic asthma different from regular asthma?▾▴
Allergic asthma is the subtype driven by allergen-specific IgE and Type 2 inflammation. Non-allergic asthma can be triggered by irritants, infection, exercise, or unknown causes without identifiable allergen sensitisation. Both share airway inflammation and respond to inhaled corticosteroids.
What are the symptoms of allergic asthma?▾▴
Symptoms include episodic wheeze, dry cough, chest tightness, and breathlessness, often worse at night, with exercise, cold air, or specific allergen exposure. Many patients also have allergic rhinitis (sneezing, blocked nose, itchy eyes) and a personal or family history of atopy.
How is allergic asthma diagnosed?▾▴
Diagnosis combines typical symptoms with objective evidence of variable airflow obstruction on spirometry (post-bronchodilator FEV1 increase ≥12% and 200 mL) or peak flow variability. Allergy assessment with skin-prick test or specific IgE confirms aeroallergen sensitisation.
What triggers allergic asthma?▾▴
Common triggers include house dust mite, cat and dog dander, mould, pollen (tree, grass, weed), cockroach allergens, and occupational sensitisers. Viral upper respiratory infections, air pollution, tobacco smoke, cold air, exercise, and aspirin or NSAIDs can also provoke attacks.
What is the best treatment for allergic asthma?▾▴
Inhaled corticosteroid-formoterol combinations are first-line, used as-needed in mild disease and as maintenance plus reliever in moderate to severe disease. Long-acting muscarinic antagonists are added at higher steps, and biologics (omalizumab, mepolizumab, dupilumab, tezepelumab) are reserved for severe disease.
Are biologics safe for allergic asthma?▾▴
Biologics for asthma (omalizumab, mepolizumab, benralizumab, reslizumab, dupilumab, tezepelumab) have an excellent safety profile in trials and registries. Common side effects include injection-site reactions; rare anaphylaxis with omalizumab occurs in under 0.2% of patients.
Can allergic asthma be cured?▾▴
There is no cure, but most patients achieve excellent control with inhaled therapy. Up to 50% of children with allergic asthma improve substantially or enter clinical remission by adolescence. Allergen immunotherapy can be disease-modifying in selected patients.
Should I get allergy testing for asthma?▾▴
Allergy testing with skin-prick or specific IgE panels is recommended in most patients with allergic features (rhinitis, eczema, family history, suspected trigger). Results guide avoidance, immunotherapy, and biologic selection (omalizumab needs documented sensitisation).
Can children outgrow allergic asthma?▾▴
About 30-50% of children with allergic asthma have substantial improvement or remission of symptoms by late adolescence, but airway hyperresponsiveness may persist. Risk of recurrence in adulthood is higher in those with severe early disease, persistent atopy, or smoking.
Is allergic asthma hereditary?▾▴
Yes. Heritability of asthma is 60-80% in twin studies. A first-degree relative with asthma, eczema, or hay fever increases asthma risk 2-4 fold. Multiple susceptibility loci have been identified including 17q21 (ORMDL3) and IL33.
How can I reduce dust mites at home?▾▴
Encase mattresses, pillows, and duvets in mite-impermeable covers; wash bedding weekly at 60 °C; use hard flooring or low-pile carpet; vacuum weekly with a HEPA-filter device; and maintain indoor humidity below 50%. These measures reduce mite allergen by 50-80%.
Can I exercise with allergic asthma?▾▴
Yes. Regular aerobic exercise improves cardiovascular fitness and asthma control. Use a 10-15 minute warm-up and a pre-exercise reliever (ICS-formoterol or salbutamol) when exercise-induced symptoms occur. Swimming in chlorinated pools may worsen symptoms in some patients.
Is allergen immunotherapy effective?▾▴
Yes, in selected patients. Subcutaneous or sublingual immunotherapy for 3-5 years reduces medication needs and may prevent asthma in children with allergic rhinitis. Best evidence is for house dust mite and grass pollen. Patients need FEV1 above 70% predicted and well-controlled disease.
What is an asthma action plan?▾▴
A personalised written plan describing daily controller medication, what to do for worsening symptoms (yellow zone), and when to seek emergency care (red zone). Action plans reduce hospitalisations by 30-40% and are recommended by GINA for every asthma patient.
Can pregnancy affect allergic asthma?▾▴
Asthma worsens in about a third of pregnancies, improves in a third, and remains stable in a third. Uncontrolled asthma is more harmful to mother and baby than asthma medications. Inhaled corticosteroids, formoterol, salbutamol, and most biologics are considered safe in pregnancy.
How serious is allergic asthma?▾▴
Most allergic asthma is mild to moderate and well controlled with inhaled therapy. Severe asthma affects 5-10% of patients and is associated with frequent exacerbations and reduced quality of life. Worldwide, more than 1,000 people die of asthma every day; access to inhaled corticosteroids reduces deaths dramatically.
When should I see a specialist?▾▴
Refer to allergy or respiratory specialists for frequent exacerbations (more than two per year), persistent symptoms despite medium-dose ICS-LABA, FEV1 under 70% predicted, oral corticosteroid dependence, suspected occupational asthma, or consideration of biologics or immunotherapy.
Can pets stay if I have allergic asthma?▾▴
Removing the offending pet from the home reduces exposure but allergen persists for months. Keeping pets out of bedrooms, weekly washing of the animal, and HEPA air filtration help when removal is not possible. Sensitised patients with severe asthma usually benefit from rehoming.
How does smoking affect allergic asthma?▾▴
Active and second-hand smoking worsen asthma control, reduce ICS effectiveness, accelerate airway remodelling, and increase exacerbations. Smoking cessation rapidly improves lung function and reduces exacerbations and emergency visits.
What is bronchial thermoplasty?▾▴
Bronchial thermoplasty delivers controlled radiofrequency heat via bronchoscopy to reduce airway smooth muscle in severe asthma. Three procedures 3 weeks apart reduce severe exacerbations by 32% at 12 months with effects sustained at 5 years, used in patients failing biologic therapy.
07Coexisting allergic rhinitis (sneezing, itchy nose, blocked nose, watery eyes) in 70-80% of patients with allergic asthma.
08Atopic dermatitis or eczema, food allergy, and family history of atopy in many patients (the atopic march).
09Acute exacerbations triggered by viral upper respiratory infections, second-hand smoke, air pollution, or aeroallergen surges.
early warning signs
•Reduced morning peak flow on a home diary, 20% or more below personal best
•Increased reliever inhaler use (more than two days a week)
•Awakening at night with cough, wheeze, or breathlessness
•Daytime symptoms with usual activities (climbing stairs, brisk walking)
•Recent upper respiratory tract infection in a known asthmatic
● emergency signs
•Severe breathlessness preventing speech in full sentences, peak flow under 50% of personal best, heart rate above 110/min
•Cyanosis, exhaustion, drowsiness, or confusion — features of life-threatening asthma
•Silent chest on auscultation in a deteriorating patient — pre-arrest sign
•Oxygen saturation below 92% on room air with respiratory distress
•No symptomatic relief after 6-8 puffs of salbutamol within 20 minutes — call emergency services
Biomarker of Type 2 airway inflammation; supports the diagnosis and predicts ICS response
04
Allergy assessment (skin-prick test or serum specific IgE)Identifies sensitisation to common aeroallergens to guide avoidance, immunotherapy, and biologic selection
05
Bronchial provocation challenge (methacholine, mannitol, or exercise)Detects airway hyperresponsiveness when spirometry is normal and asthma is suspected
06
Blood eosinophil count and total IgEType 2 inflammatory biomarkers guiding ICS dose and biologic eligibility
Outlook
Most patients with mild to moderate allergic asthma achieve good control on inhaled corticosteroid-formoterol with rare exacerbations and normal life expectancy. About 50% of children with allergic asthma improve substantially or enter clinical remission by adolescence, although airway hyperresponsiveness often persists. Severe allergic asthma now responds to targeted biologic therapy in 60-80% of well-phenotyped patients, with halving of severe exacerbations, halving of oral corticosteroid use, and substantial quality-of-life improvement. Asthma-related mortality has fallen substantially in countries with widespread access to inhaled corticosteroids — UK and US rates now around 1.5 per 100,000 — but remains higher among lower-income and minority populations. The major modifiable risk factors for poor prognosis are non-adherence, smoking, persistent allergen exposure, and untreated comorbid rhinitis or obesity.
genetic
First-degree relative with asthma, eczema, or hay fever increases asthma risk 2-4 fold. Heritability estimates from twin studies are 60-80%.
Childhood RSV or rhinovirus bronchiolitisnon-modifiable
Severe early-life lower respiratory infection doubles the risk of childhood asthma, particularly in genetically predisposed children. Newer nirsevimab prophylaxis may reduce this risk.
Early-life aeroallergen exposureenvironmental
Exposure to high mite, mould, or cockroach allergen loads in early life increases sensitisation and asthma risk; this effect is modified by microbial exposure and breastfeeding.
Maternal smoking and second-hand smokemodifiable
In-utero and childhood tobacco smoke exposure increase asthma incidence by 60-90% and worsen severity. Cessation in pregnancy halves the relative risk.
Air pollution (PM2.5, NO2, ozone)modifiable
Living within 50 m of major roads or in cities with high PM2.5 levels increases asthma incidence and exacerbations. NO2 augments allergen-induced airway inflammation.
Obesity (BMI ≥30 kg/m2)modifiable
Obesity doubles asthma incidence in adults and worsens control. Mechanical effects on lung volumes plus systemic inflammation contribute.
Occupational sensitiser exposuremodifiable
Bakers, hairdressers, healthcare workers, animal handlers, and isocyanate-exposed workers have 3-10 fold higher occupational asthma incidence; early identification and exposure control are protective.
Vitamin D deficiencymodifiable
Low 25-OH-vitamin-D (<25 nmol/L) is associated with more exacerbations in some cohorts; supplementation reduces severe exacerbations in patients with low baseline levels (VIDA, Brehm).
•Adequate hydration to support mucociliary clearance
foods to avoid
•Sulfite-containing foods and drinks (some wines, dried fruits) in sulfite-sensitive patients
•Aspirin and other NSAIDs in patients with NSAID-exacerbated respiratory disease
•Excessive processed and ultra-processed foods that worsen systemic inflammation
•Heavy alcohol use, which worsens sleep and may trigger asthma in some patients
Sudden asthma death, especially in patients with frequent reliever use, previous near-fatal asthma, and poor adherence.
choosing the right hospital
01Spirometry and bronchodilator reversibility testing on-site
02FeNO and total IgE assays available
03Allergy testing with skin-prick and specific IgE panels
04Specialist nurse-led asthma clinic with biologic administration
05Multidisciplinary severe asthma service
Essential facilities
Allergy and immunology clinicsSpecialist respiratory medicine outpatientsPaediatric allergy and respiratory servicesSevere asthma centres with biologic capabilityPulmonary rehabilitation services
Rinse the mouth and spit after each ICS dose to reduce oral candidiasis and hoarseness.
03Check inhaler technique with a healthcare professional at least annually.
04Record symptoms and reliever use; review the action plan when reaching the yellow zone (worsening symptoms or peak flow 60-80% of best).
05Take any prescribed leukotriene receptor antagonist (montelukast) at night.
06Attend annual asthma review including spirometry, biomarker check, and inhaler review.
Exercise
Regular aerobic exercise (150 minutes per week) improves cardiovascular fitness and asthma control. Use a 10-15 minute warm-up to reduce exercise-induced bronchoconstriction; pre-exercise inhaled corticosteroid-formoterol or salbutamol can be added when needed. Swimming in chlorinated pools may benefit some patients but worsens others — try alternatives if symptoms develop after swimming.