What is asthma–COPD overlap and how is it different from having both conditions?

Asthma–COPD overlap is a descriptive term for patients with persistent airflow limitation who have significant features of both asthma and COPD. It is not classified as a separate diagnosis — GINA and GOLD now describe it as a clinical descriptor. In practical terms, it refers to patients who don't fit neatly into either category: a long-term smoker who also has atopy and reversible airflow obstruction, or a middle-aged asthmatic who has developed fixed airflow limitation despite optimal inhaled therapy. These patients tend to have more symptoms, more frequent exacerbations, higher hospitalisation rates, and worse quality of life than patients with asthma or COPD alone. The clinical importance is that management needs to address both components — an inhaled corticosteroid for the asthma contribution, plus bronchodilator therapy for the fixed obstruction.

What spirometry pattern suggests asthma–COPD overlap?

ACO is suggested on spirometry when there is both persistent airflow limitation — post-bronchodilator FEV1/FVC less than 0.70 (the COPD criterion) — and significant reversibility after bronchodilator administration — FEV1 increase of ≥12% and ≥200 mL (an asthma feature). The absence of reversibility does not exclude an asthma component, as airway remodelling from longstanding asthma can produce fixed obstruction. Supporting features include peripheral blood eosinophil count ≥300 cells/μL, elevated FeNO (≥50 parts per billion), and positive allergy testing. A full clinical picture combining smoking history, symptom pattern, age of onset, atopy, and spirometry is needed — no single test is diagnostic.

What is the role of eosinophil count in managing airway disease?

Blood eosinophil count is a practical, inexpensive, and increasingly important biomarker for guiding inhaled corticosteroid use in chronic airway disease. A count of ≥300 cells/μL indicates an eosinophilic phenotype that is more likely to respond to ICS — both in asthma and in COPD with eosinophilia. In COPD, this threshold also predicts benefit from stepping up to triple therapy. A count of ≥150 cells/μL is a lower threshold used in some clinical contexts. FeNO (fractional exhaled nitric oxide) ≥50 parts per billion similarly indicates Type 2 airway inflammation. These biomarkers help identify which patients with COPD-like symptoms will benefit from ICS, avoiding both under-treatment (missing the eosinophilic response) and over-treatment (ICS in non-eosinophilic COPD increases pneumonia risk).

Are biologic medications available for asthma–COPD overlap in Australia?

Yes, for patients with the severe Type 2-high (eosinophilic or atopic) phenotype. Biologic agents listed on the PBS Section 100 (Highly Specialised Drugs) program for severe asthma include omalizumab (anti-IgE, for atopic asthma), mepolizumab and benralizumab (anti-IL-5, for eosinophilic asthma), dupilumab (anti-IL-4Rα, for Type 2-high asthma), and tezepelumab (anti-TSLP, severe asthma without eosinophil restriction). Dupilumab has also received PBS approval for COPD with eosinophilia, following the BOREAS and NOTUS trials, which showed reduced exacerbation rates in COPD patients with blood eosinophils ≥300 cells/μL. Access requires specialist (respiratory physician) initiation. These medications are not first-line — they are for patients who remain uncontrolled on optimised triple therapy.

Asthma–COPD overlap

Asthma–COPD overlap: recognising the mixed airway phenotype in general practice

By Dr HB Lo, FACRRM Reviewed 13 June 2026 7 min read

Asthma–COPD overlap (ACO) is persistent airflow limitation with features of both conditions — typically an older smoker with atopy, eosinophilia, or spirometric reversibility. It is a clinical descriptor, not a separate diagnosis, but management differs from either condition alone: never withhold inhaled corticosteroids when asthma features are present.

ICS/LABA combination is first-line; triple therapy adding a LAMA is used when exacerbations remain uncontrolled. Blood eosinophil count guides ICS use. Smoking cessation, pulmonary rehabilitation, and vaccination are cornerstones. Biologic therapy is available for the severe eosinophilic phenotype via specialist referral.

Most patients with chronic airway disease in Australian general practice don’t fit neatly into “asthma” or “COPD.” They are often smokers in their fifties and sixties who grew up with allergies, have reversible but also persistent airway narrowing on spirometry, and whose symptoms don’t respond fully to treatment for either condition alone.

The clinical descriptor asthma–COPD overlap (ACO) captures this group. It is not a separate diagnosis — GINA and GOLD now describe it as a clinical descriptor rather than a disease entity — but it has practical management implications that distinguish it from uncomplicated asthma or COPD.

A. Core clinical — the AU general-practice framework

Who gets ACO

ACO is most common in patients with two or more of the following overlapping features:

Asthma-type features:

Episodic wheeze or breathlessness triggered by allergens, cold air, exercise, viral infections, or NSAIDs
Night or early-morning symptom predominance
Atopy — eczema, allergic rhinitis, food allergy, family history of asthma or atopy
Onset in childhood or early adulthood, sometimes with later remission
Peripheral blood eosinophilia ≥300 cells/μL or elevated FeNO ≥50 ppb

COPD-type features:

Smoking history ≥10 pack-years (current or ex-smoker) or significant occupational dust, chemical, or biomass exposure
Persistent daily dyspnoea and productive cough
Onset typically after age 40; gradual progression
Less reversibility on spirometry; slow decline in FEV1 over time

Epidemiology in Australia: estimates of ACO prevalence range from 15% to 55% of patients with chronic airway disease, reflecting varying definitions. The Lung Foundation’s COPD-X program and the National Asthma Council’s Australian Asthma Handbook both address ACO as a clinically important overlap phenotype. Patients with ACO have higher hospitalisation rates, more frequent exacerbations, and greater symptom burden than those with either condition alone.

Indigenous Australians have a disproportionately high prevalence of COPD at younger ages, with the ACO phenotype common; early identification and access to spirometry and specialist input are priorities.

Spirometry — the central investigation

Post-bronchodilator spirometry is the cornerstone of ACO assessment:

FEV1/FVC below 0.70 post-bronchodilator — confirms persistent airflow limitation (COPD criterion)
FEV1 increase ≥12% AND ≥200 mL post-bronchodilator — significant reversibility (asthma feature)

The absence of reversibility does not exclude ACO — fixed obstruction can develop from years of untreated asthma-driven remodelling.

Supporting investigations:

Peripheral blood eosinophil count — ≥300 cells/μL eosinophilic phenotype; request with routine FBC
FeNO (fractional exhaled nitric oxide) — ≥50 ppb suggests Type 2 airway inflammation; increasingly available in general practice
Total IgE and specific IgE or skin prick testing when atopic contribution needs characterisation
CXR to exclude alternative pathology (malignancy, heart failure, pneumonia)
HRCT chest if bronchiectasis, interstitial lung disease, or malignancy is suspected
Alpha-1 antitrypsin level in patients with COPD onset before age 50 or strong family history of emphysema

Differential diagnosis

The main diagnostic pitfalls in ACO assessment:

Condition	Key distinguishing feature
Asthma only	Fully reversible on spirometry; younger; non-smoker; atopic
COPD only	Smoker; persistent fixed obstruction; no atopy; non-eosinophilic
Bronchiectasis	Chronic productive cough; recurrent infections; HRCT shows dilated airways
Heart failure	Orthopnoea, raised JVP, BNP elevated, responds to diuresis
Vocal cord dysfunction	Inspiratory stridor; normal spirometry; episodic at rest
Eosinophilic granulomatosis with polyangiitis	Multi-system; ANCA; very high eosinophil count
Lung malignancy	Haemoptysis; weight loss; imaging abnormality

B. Evidence appraisal — the ICS rule and triple therapy

Never withhold ICS when asthma features are present

The single most important management principle in ACO is never withhold inhaled corticosteroid therapy when asthma features are present. In patients with genuine asthma, stopping or never starting ICS risks severe and potentially fatal exacerbations. In ACO, the asthma component justifies ICS even when the overall picture also resembles COPD.

This contrasts with uncomplicated non-eosinophilic COPD, where ICS use without a clear indication (eosinophilia, frequent exacerbations, concurrent asthma features) is associated with increased pneumonia risk.

ICS/LABA as the ACO starting point

ICS/LABA combination therapy addresses both the inflammatory (asthma) and bronchodilator (COPD) components simultaneously and is the standard first-line pharmacotherapy for ACO per GINA, GOLD, and eTG. LABA monotherapy — without ICS — must not be used in anyone with ACO or suspected asthma features.

Triple therapy for uncontrolled ACO

The IMPACT trial (Lipson et al., NEJM 2018) showed that single-inhaler triple therapy (ICS/LABA/LAMA) reduced moderate and severe COPD exacerbations more than dual therapy, with the greatest benefit in patients with eosinophil counts ≥150–300 cells/μL. For ACO patients with persistent exacerbations on ICS/LABA, adding a LAMA (long-acting muscarinic antagonist) is the next step.

Biologic therapy for severe Type 2-high ACO

For patients who remain uncontrolled on triple therapy and who have the eosinophilic or atopic phenotype, biologic therapies represent a significant advance. The BOREAS trial (Bhatt et al., NEJM 2023) demonstrated that dupilumab (anti-IL-4Rα) reduced annual exacerbation rate by 34% compared with placebo in COPD patients with blood eosinophils ≥300 cells/μL. This led to PBS approval in Australia for dupilumab in COPD with eosinophilia, in addition to its existing severe asthma indications.

C. Stepping through inhaler choices — the practical AU pathway

PBS-listed ICS/LABA options

Available in Australia and relevant to ACO:

Budesonide/formoterol (Symbicort) — also used as maintenance-and-reliever (SMART) therapy in asthma-dominant ACO
Fluticasone/salmeterol (Seretide)
Fluticasone/vilanterol (Breo Ellipta) — once daily
Mometasone/formoterol (Zenhale)
Beclomethasone/formoterol (Fostair)

PBS-listed triple therapy (ICS/LABA/LAMA)

Single-inhaler triple therapy options:

Fluticasone/vilanterol/umeclidinium (Trelegy Ellipta) — once daily; PBS Authority for COPD with ≥2 moderate exacerbations or 1 severe exacerbation in the prior 12 months
Beclomethasone/formoterol/glycopyrronium (Trimbow) — twice daily; similar indication

Add-on LAMA to existing ICS/LABA is an alternative two-inhaler approach using tiotropium (Spiriva), umeclidinium (Incruse Ellipta), or glycopyrronium (Seebri).

Reliever therapy

Per current GINA recommendations, salbutamol (SABA) is used as a reliever but should not be the only therapy. For asthma-dominant ACO on Symbicort, the SMART regimen — using the same budesonide/formoterol inhaler as both maintenance and reliever — reduces severe exacerbation rates versus SABA-only relievers.

D. Australian operations

MBS items

GP consultations: items 23, 36, 44
Spirometry (pre/post bronchodilator, GP-initiated): item 11506
DLCO (specialist): item 11500
HRCT chest: items 56301–56307
6-minute walk test: item 12203
GPCCMP preparation and review: items 965/967 — ACO with multimorbidity routinely qualifies; allied health referrals (physiotherapist, EP, dietitian, psychology) under items 10950–10970
75+ Health Assessment: item 705 (ACO in older patients)
Mental Health Care Plan: item 2715 — anxiety and depression are common in ACO and undertreated

PBS Section 100 — Highly Specialised Drugs

Biologic agents require specialist initiation and are accessed via Section 100:

Dupilumab — severe uncontrolled asthma (Type 2-high); and COPD with eosinophils ≥300 cells/μL (new 2024 indication)
Mepolizumab, benralizumab — severe eosinophilic asthma
Omalizumab — severe atopic asthma
Tezepelumab — severe asthma without eosinophil restriction

Pulmonary rehabilitation

Pulmonary rehabilitation programs are available through public hospital respiratory departments and community programmes. They are strongly evidence-supported for reducing dyspnoea, hospitalisation, and improving quality of life. Referral via the treating GP is standard; the Lung Foundation Australia maintains a national directory.

Vaccination

Per ATAGI: annual influenza, pneumococcal (PCV20 or PPV23 plus PCV13), COVID-19 per current schedule, and RSV vaccine (Arexvy or mRESVIA, recommended for adults ≥60 from 2024).

E. Special populations

Older smokers. The classic ACO population. Smoking cessation is the single highest-yield modifiable intervention — NPS MedicineWise provides AU prescriber guidance; PBS-listed cessation options include varenicline, bupropion, and nicotine replacement therapy.

Indigenous Australians. COPD prevalence is two to three times higher and appears a decade earlier. The ACO phenotype is common. Care coordination through Aboriginal Community Controlled Health Organisations, telehealth, outreach respiratory services, and culturally appropriate smoking cessation programmes are all relevant.

Rural and remote patients. Limited access to spirometry, FeNO measurement, and respiratory specialist input. Telehealth respiratory consultations and the TSANZ outreach respiratory services are important access points. Biomass (wood smoke) and agricultural dust exposure are additional COPD drivers in these settings.

Women. Women with ACO are more likely to have the atopic/eosinophilic phenotype and may be misdiagnosed with asthma alone. Spirometry confirmation of fixed obstruction is important — particularly in women who smoke — to avoid underdiagnosis of the COPD component.

When to escalate

Refer to or discuss with a respiratory specialist when:

Diagnosis is uncertain after spirometry and clinical assessment
Severe or frequent exacerbations on ICS/LABA
Considering triple therapy or biologic initiation
Suspected significant bronchiectasis, interstitial lung disease, or pulmonary hypertension
Oxygen saturation consistently below 95% at rest — assess for long-term oxygen therapy
Rapid FEV1 decline or progressive disability

Urgent or same-day assessment:

Acute exacerbation with SpO₂ below 92%, use of accessory muscles, or inability to complete a sentence
Suspected PE or pneumothorax

What this article is and is not

This is general health information based on the Australian Asthma Handbook, COPD-X Guidelines, TSANZ, GINA, GOLD, and Therapeutic Guidelines. It does not constitute personal medical advice. Inhaler selection and escalation decisions depend on individual spirometry findings, eosinophil count, exacerbation history, comorbidities, and patient preference — these are made with the treating GP and, in complex cases, a respiratory specialist.

For patient-level information: HealthDirect — COPD, Lung Foundation Australia, and Better Health Channel — Asthma.

Sources cited

Frequently asked questions

What is asthma–COPD overlap and how is it different from having both conditions?

Asthma–COPD overlap is a descriptive term for patients with persistent airflow limitation who have significant features of both asthma and COPD. It is not classified as a separate diagnosis — GINA and GOLD now describe it as a clinical descriptor. In practical terms, it refers to patients who don't fit neatly into either category: a long-term smoker who also has atopy and reversible airflow obstruction, or a middle-aged asthmatic who has developed fixed airflow limitation despite optimal inhaled therapy. These patients tend to have more symptoms, more frequent exacerbations, higher hospitalisation rates, and worse quality of life than patients with asthma or COPD alone. The clinical importance is that management needs to address both components — an inhaled corticosteroid for the asthma contribution, plus bronchodilator therapy for the fixed obstruction.
What spirometry pattern suggests asthma–COPD overlap?

ACO is suggested on spirometry when there is both persistent airflow limitation — post-bronchodilator FEV1/FVC less than 0.70 (the COPD criterion) — and significant reversibility after bronchodilator administration — FEV1 increase of ≥12% and ≥200 mL (an asthma feature). The absence of reversibility does not exclude an asthma component, as airway remodelling from longstanding asthma can produce fixed obstruction. Supporting features include peripheral blood eosinophil count ≥300 cells/μL, elevated FeNO (≥50 parts per billion), and positive allergy testing. A full clinical picture combining smoking history, symptom pattern, age of onset, atopy, and spirometry is needed — no single test is diagnostic.
Which inhaler should someone with asthma–COPD overlap use?

An ICS/LABA combination inhaler is the standard first-line treatment for ACO. Examples PBS-listed in Australia include budesonide/formoterol (Symbicort), fluticasone/salmeterol (Seretide), fluticasone/vilanterol (Breo), mometasone/formoterol (Zenhale), and beclomethasone/formoterol (Fostair). The key principle — derived from both GINA and GOLD guidance — is never to use a LABA alone without ICS in anyone with ACO or suspected asthma features, because LABA monotherapy without ICS increases the risk of severe asthma attacks. When exacerbations remain uncontrolled on ICS/LABA, a third agent (a long-acting muscarinic antagonist, or LAMA) is added. Single-inhaler triple therapy — fluticasone/vilanterol/umeclidinium (Trelegy) or beclomethasone/formoterol/glycopyrronium (Trimbow) — is PBS-listed for COPD with frequent exacerbations.
What is the role of eosinophil count in managing airway disease?

Blood eosinophil count is a practical, inexpensive, and increasingly important biomarker for guiding inhaled corticosteroid use in chronic airway disease. A count of ≥300 cells/μL indicates an eosinophilic phenotype that is more likely to respond to ICS — both in asthma and in COPD with eosinophilia. In COPD, this threshold also predicts benefit from stepping up to triple therapy. A count of ≥150 cells/μL is a lower threshold used in some clinical contexts. FeNO (fractional exhaled nitric oxide) ≥50 parts per billion similarly indicates Type 2 airway inflammation. These biomarkers help identify which patients with COPD-like symptoms will benefit from ICS, avoiding both under-treatment (missing the eosinophilic response) and over-treatment (ICS in non-eosinophilic COPD increases pneumonia risk).
Are biologic medications available for asthma–COPD overlap in Australia?

Yes, for patients with the severe Type 2-high (eosinophilic or atopic) phenotype. Biologic agents listed on the PBS Section 100 (Highly Specialised Drugs) program for severe asthma include omalizumab (anti-IgE, for atopic asthma), mepolizumab and benralizumab (anti-IL-5, for eosinophilic asthma), dupilumab (anti-IL-4Rα, for Type 2-high asthma), and tezepelumab (anti-TSLP, severe asthma without eosinophil restriction). Dupilumab has also received PBS approval for COPD with eosinophilia, following the BOREAS and NOTUS trials, which showed reduced exacerbation rates in COPD patients with blood eosinophils ≥300 cells/μL. Access requires specialist (respiratory physician) initiation. These medications are not first-line — they are for patients who remain uncontrolled on optimised triple therapy.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.

T1 AU primary 6 sources
T2 International primary 2 sources
- GINA 2024 — Global Initiative for Asthma
- GOLD 2024 — Global Initiative for Chronic Obstructive Lung Disease
T3 Named-author reconstruction 3 sources