Persistent airflow limitation. Eosinophilic inflammation. A history that fits neither diagnosis cleanly. ACO is common, under-recognized, and treatable -- but it requires a specialist who works across both conditions.
For decades, pulmonologists divided obstructive airway disease into two clean categories: asthma (reversible, often allergic, begins young) and COPD (progressive, smoking-related, begins in middle age). Clinical reality has never respected that boundary.
A meaningful proportion of adults with obstructive lung disease -- estimates range from 15% to 25% -- have features of both conditions simultaneously. This group is now referred to as having Asthma-COPD Overlap, or ACO.
ACO patients have worse outcomes than patients with either condition alone: more frequent exacerbations, faster lung function decline, higher hospitalization rates, and greater impairment of quality of life. They also tend to be excluded from the major clinical trials that produced current treatment guidelines, leaving physicians to navigate treatment decisions without direct evidence.
At Advanced Asthma Clinic in Plantation, FL, Dr. Frank Hull has spent more than 20 years managing complex airway disease -- including the growing number of patients whose lungs do not fit a single label. This page explains what ACO is, how it is diagnosed, and what current evidence supports for treatment.
Note: The information on this page is for educational purposes. Asthma-COPD overlap requires individual evaluation. Always consult your physician before changing any aspect of your treatment.
ACO is defined by the coexistence of persistent airflow limitation (the hallmark of COPD, confirmed on spirometry as a post-bronchodilator FEV1/FVC ratio below 0.70) combined with one or more features that are characteristic of asthma:
No international consensus has settled on a single definition, which is part of why ACO remains both clinically confusing and an active research area. GINA (Global Initiative for Asthma) and GOLD (Global Initiative for Chronic Obstructive Lung Disease) issued a joint guidance document acknowledging ACO as a real and important clinical entity, but stopped short of fixed diagnostic criteria.
Calling a patient's condition "ACO" rather than simply "asthma" or "COPD" has direct treatment implications:
| Population | Estimated ACO Prevalence | Notes |
|---|---|---|
| All adults with obstructive airway disease | 15-25% | Varies by diagnostic criteria |
| Adults ≥60 with obstructive disease | 20-30% | Age increases overlap prevalence |
| COPD patients with ≥300 eosinophils/µL | ~25-30% | Type 2 inflammatory subgroup |
| Long-term smokers with prior asthma diagnosis | 40-50% | Highest-risk combination |
| Asthma patients with significant smoking history | 15-20% | Post-bronchodilator FEV1/FVC <0.70 |
| General adult population (≥40 years) | 2-4% | Population-based studies |
These numbers suggest that several hundred thousand South Floridians may have ACO -- many of them undiagnosed or being treated for only one of the two conditions.
Asthma and COPD share the anatomical site -- the bronchial airways and alveoli -- but differ in the primary mechanism of disease:
| Feature | Asthma | COPD | ACO |
|---|---|---|---|
| Primary inflammation | Eosinophilic / Type 2 | Neutrophilic / CD8+ T-cell | Mixed (eosinophilic + neutrophilic) |
| Airflow limitation | Largely reversible | Fixed / progressive | Partially reversible with fixed component |
| Age of onset | Often childhood/young adult | Usually 40+ | Variable (childhood asthma + later COPD) |
| Smoking association | Not required | Primary driver | Present in most but not all |
| Emphysema on CT | Absent | Common | Variable |
| Mucus hypersecretion | Episodic | Chronic (chronic bronchitis subtype) | Common |
| Blood eosinophils | Often elevated | Elevated in ~25-30% | Elevated in majority |
| ICS response | Strong | Partial (eosinophilic subtype) | Good for asthmatic features |
Because no single test diagnoses ACO, evaluation requires integrating multiple data points. At Advanced Asthma Clinic, Dr. Hull uses a systematic approach:
Spirometry establishes the presence and severity of airflow obstruction. A post-bronchodilator FEV1/FVC below 0.70 confirms obstruction meeting GOLD criteria. The degree of reversibility (FEV1 improvement after albuterol) provides the first clue toward asthma -- a ≥12% and ≥200 mL increase is significant.
Impulse oscillometry measures airway resistance and reactance at multiple frequencies, revealing small airway dysfunction that spirometry may miss. IOS is particularly useful in ACO patients where central and peripheral airway disease can coexist.
Fractional exhaled nitric oxide (FeNO) is a biomarker of eosinophilic airway inflammation driven by IL-4 and IL-13. Elevated FeNO in a patient with COPD-pattern obstruction strongly supports an asthmatic (type 2) inflammatory component.
Blood eosinophil count is a key biomarker in ACO. Counts above 300 cells/µL predict both ICS response in COPD and eligibility for several biologics. Counts above 150 cells/µL may still carry clinical significance.
CT identifies emphysema (low attenuation areas, air trapping), bronchial wall thickening, mucus plugging, and gas trapping on expiratory images. The pattern and extent of emphysema guide prognosis and help differentiate COPD-predominant from asthma-predominant disease within the ACO spectrum.
A documented asthma diagnosis before age 40, childhood wheezing, positive allergy skin tests, or a clear family history of atopic disease all favor the asthmatic component. Smoking pack-year history, occupational exposures, and symptom chronology quantify the COPD contribution.
Reduced DLCO indicates emphysema destroying alveolar surface area. In pure asthma, DLCO is typically normal or supranormal. A reduced DLCO in an asthma-pattern patient points toward significant emphysematous COPD co-contribution.
Dr. Hull's practice integrates spirometry, IOS, FeNO, and blood biomarker testing under one roof in Plantation, FL -- enabling same-visit ACO workup rather than multiple referrals across different labs and facilities.
Multiple large registry studies have documented that ACO patients experience worse health outcomes than patients with either asthma or COPD alone:
These outcomes underscore the importance of accurate ACO identification -- and the risk of treating only the asthma component or only the COPD component while missing the other.
ACO treatment combines elements from both GINA asthma guidelines and GOLD COPD guidelines. The following framework reflects current best practice, though individual therapy must be tailored to each patient's phenotype.
Unlike pure COPD -- where ICS monotherapy is no longer recommended except in eosinophilic subgroups -- ACO patients with any asthmatic features should remain on ICS. The asthmatic component of ACO is ICS-responsive, and withdrawal risks severe exacerbations.
Most ACO patients benefit from triple inhaled therapy: ICS + LABA + LAMA (long-acting muscarinic antagonist). This combination addresses both the eosinophilic inflammation (ICS), bronchoconstriction (LABA), and cholinergic-driven mucus/tone (LAMA). Combination single-inhaler devices simplify adherence.
ACO patients with elevated eosinophils or FeNO may qualify for biologic therapy -- and this is where the most significant treatment advances are occurring:
| Biologic | Target | Asthma FDA Approval | COPD FDA Approval | Key ACO Relevance |
|---|---|---|---|---|
| Dupilumab (Dupixent) | IL-4Rα (blocks IL-4 + IL-13) | Yes (≥6 yrs, eos ≥150 or FeNO ≥25) | Yes (COPD + type 2 inflammation) | Only biologic with both asthma AND COPD approval -- directly applies to ACO |
| Benralizumab (Fasenra) | IL-5Rα | Yes (≥12 yrs, eos ≥300) | No (trials ongoing) | Strong data in eosinophilic COPD; ACO patients with eos ≥300 may qualify under asthma label |
| Mepolizumab (Nucala) | IL-5 | Yes (≥6 yrs, eos ≥150) | Yes (COPD with eos ≥300) | FDA-approved for both asthma and eosinophilic COPD; relevant to ACO |
| Tezepelumab (Tezspire) | TSLP | Yes (≥12 yrs, no eos threshold) | Not approved | Works upstream of type 2 cascade; useful in ACO with mixed inflammation |
| Omalizumab (Xolair) | IgE | Yes (allergic asthma, total IgE 30-700) | No | Limited to ACO patients with significant allergic/IgE-mediated component |
Learn more about these agents on our dedicated biologic therapy page.
For ACO patients who smoke, cessation is non-negotiable and the most powerful single intervention. Smoking cessation slows FEV1 decline, reduces exacerbation frequency, and improves biologic treatment response. Pharmacotherapy (varenicline, bupropion, NRT) combined with behavioral support achieves the highest cessation rates.
Structured pulmonary rehabilitation -- supervised exercise training plus education -- improves exercise capacity, reduces dyspnea, and lowers exacerbation rates in both COPD and asthma. ACO patients benefit substantially and should be referred if symptoms limit daily activity.
ACO patients face high exacerbation risk from respiratory infections. Annual influenza vaccination, RSV vaccination (adults ≥60), and pneumococcal vaccination are standard care. COVID-19 vaccination and boosters remain important. Patients with frequent exacerbations should discuss azithromycin prophylaxis with their physician, balancing antibiotic stewardship concerns.
South Florida's climate creates specific ACO aggravants: year-round high humidity, seasonal mold spore surges, wildfire smoke (particularly during dry winter months), and hurricane season air quality events. See our guides on humidity and mold in Florida and wildfire smoke and asthma for detailed mitigation strategies.
Lung Research Florida, the research affiliate of Dr. Hull's practice located in Plantation, FL, is currently enrolling participants in a COPD clinical trial studying an investigational anti-IL-33 therapy. IL-33 is a key alarmin cytokine that drives both COPD-type airway damage and type 2 inflammation -- making it a mechanistically relevant target for ACO patients with both neutrophilic and eosinophilic features.
Participation in clinical trials is voluntary. Eligibility is determined by the research team after screening. This is an investigational therapy not yet approved by the FDA.
Clinical trials represent an opportunity for eligible patients to access investigational therapies, contribute to medical science, and receive close monitoring at no cost for study-related visits and treatments.
Broward County and the broader South Florida region present a specific environmental context for ACO patients:
Dr. Hull's practice at Plantation, FL is centrally located in Broward County, serving patients from Fort Lauderdale, Davie, Hollywood, Pembroke Pines, Miramar, Weston, and Dania Beach.
ACO is a clinical condition in which a patient has persistent airflow limitation (as in COPD) plus significant features of asthma -- such as reversible bronchospasm, eosinophilic inflammation, or a clear history of asthma onset before age 40. ACO is not a single disease but a descriptive label for patients who do not fit neatly into either diagnosis.
Depending on diagnostic criteria used, ACO accounts for 15-25% of adults with obstructive airway disease. Prevalence rises with age: among patients over 60 with obstructive lung disease, roughly one in five has ACO features.
Yes. A lifelong asthmatic who also smoked heavily, or a former smoker who developed asthma late in life, can have persistent airflow limitation from COPD alongside the eosinophilic inflammation and reversibility characteristic of asthma. These patients are said to have ACO.
No single gold-standard test defines ACO. Clinicians use a combination of spirometry (post-bronchodilator FEV1/FVC below 0.70 confirming obstruction), bronchodilator reversibility testing, blood eosinophil counts, FeNO measurement, CT of the chest, and detailed clinical history to identify features of both conditions.
ACO treatment combines elements from both GINA (asthma) and GOLD (COPD) guidelines. Inhaled corticosteroids (ICS) are generally maintained because of the asthmatic component. Long-acting beta-agonists (LABA) and long-acting muscarinic antagonists (LAMA) are added for the COPD component. Biologics targeting eosinophilic inflammation show promise in ACO patients with high eosinophil counts.
No biologic currently carries an FDA label specifically for ACO. However, patients with ACO who meet criteria for severe asthma may qualify for biologic therapy under the asthma indication. Dupilumab is also FDA-approved for COPD with type 2 inflammation, making it relevant to many ACO patients.
Yes. Lung Research Florida (954-520-7296 x1) in Plantation is currently enrolling a COPD clinical trial studying an anti-IL-33 investigational therapy for adults aged 40-80. Patients with COPD features may be eligible. Consult your physician and contact the research team to learn more.
Cigarette smoking is the primary driver of COPD-type fixed airflow limitation. In patients who also have asthma, smoking accelerates lung function decline and can produce a permanently obstructed airway even after smoking cessation. Smoking cessation is the single most important modifiable intervention for ACO patients.
Confirms airflow obstruction and reversibility -- the first step in ACO evaluation.
Detects small airway disease in both asthma and COPD components of ACO.
Identifies eosinophilic inflammation in patients with COPD-pattern obstruction.
Key biomarker for biologic eligibility and ICS response in ACO.
Overview of dupilumab, benralizumab, mepolizumab, tezepelumab, and omalizumab.
The only biologic approved for both severe asthma and COPD with type 2 inflammation.
Foundation of ACO treatment for the asthmatic inflammatory component.
All testing services available at Advanced Asthma Clinic, Plantation FL.
Managing South Florida's year-round environmental triggers for ACO patients.
CRSwNP frequently coexists with ACO in patients with type 2 airway inflammation.
If you or your physician suspects asthma-COPD overlap, Advanced Asthma Clinic offers comprehensive airway evaluation with spirometry, IOS, FeNO, and blood biomarker testing in a single visit. Dr. Frank Hull brings more than 20 years of pulmonary medicine and research experience to the diagnosis and management of complex obstructive airway disease.
We serve patients from Plantation, Fort Lauderdale, Davie, Hollywood, Pembroke Pines, Weston, Miramar, Dania Beach, and across Broward County.
Always consult your physician regarding your individual health situation. The information on this page is for educational purposes and does not constitute medical advice.