Centrilobular emphysema is the most common form of emphysema, a condition where the tiny air sacs in your lungs are permanently destroyed. It specifically targets the center of each small unit of lung tissue, called a lobule, starting with the smallest breathing tubes (respiratory bronchioles) and expanding outward. It overwhelmingly affects the upper portions of the lungs and is strongly tied to cigarette smoking.
If this term appeared on your CT scan report, here’s what it means, how it differs from other types, and what it tells you about your lung health going forward.
How It Damages the Lungs
Your lungs are organized into thousands of tiny functional units called secondary lobules. Each lobule has a central core of small airways and blood vessels, surrounded by clusters of air sacs (alveoli) where oxygen enters your blood. In centrilobular emphysema, the destruction begins right at the center of these lobules, in the respiratory bronchioles, while the outer portions of each lobule may initially remain intact.
This pattern is distinct because it doesn’t just destroy air sacs. Research comparing lung tissue samples shows that regions dominated by centrilobular emphysema have significantly fewer terminal bronchioles (the smallest conducting airways) per volume of lung tissue compared to mildly affected areas. The remaining airways also have narrower openings and thicker walls. In other words, both the airways feeding air into the lobule and the air sacs themselves are damaged, which is why this form tends to cause more breathing impairment than some other types.
The destruction is typically uneven. The severity differs from one lobule to the next, creating a patchy appearance on imaging. It concentrates in the upper lobes and the top portions of each lobe, a pattern that helps distinguish it from other forms of emphysema.
Why Smoking Is the Primary Cause
Cigarette smoking is the dominant risk factor. Each puff delivers roughly 4,000 chemicals into the lungs, and these compounds trigger a chain of damage: they chemically alter proteins in lung tissue, generate oxidative stress, provoke chronic inflammation, and cause lung cells to self-destruct through a process called apoptosis. The immune system’s response to this ongoing assault, particularly the infiltration of inflammatory cells, plays a central role in breaking down the walls of the air sacs.
The reason centrilobular emphysema favors the upper lungs likely relates to how inhaled smoke deposits in the airways. The central portions of each lobule receive the most direct exposure to inhaled particles, which explains why the destruction starts there rather than at the edges.
That said, smoking doesn’t account for every case. CDC data from 2017 found that about one in four adults with COPD (the broader disease category that includes emphysema) had never smoked. The overall prevalence of COPD among current smokers was 15.2%, compared to 2.8% among people who never smoked. Occupational dust exposure, air pollution, and genetic susceptibility all contribute, but smoking remains by far the leading cause of the centrilobular pattern specifically.
What It Looks Like on a CT Scan
Centrilobular emphysema is diagnosed on high-resolution CT (HRCT) scanning, where it appears as small dark spots scattered through the center of lobules, called low attenuation areas. These dark areas represent destroyed lung tissue that now holds only air, without the normal network of blood vessels and air sac walls.
Radiologists classify these spots into three patterns based on CT-pathologic studies:
- Type A: Small round or oval dark spots with sharp borders, surrounded by normal-looking lung. This represents early, mild disease.
- Type B: Irregularly shaped spots less than 5 mm across with blurry borders, still surrounded by normal lung.
- Type C: Irregular spots 5 mm or larger with indistinct borders, indicating more advanced destruction where damaged areas are merging together.
The progression from A to C reflects increasingly severe tissue loss. Your radiology report may also grade the emphysema as trace, mild, moderate, or severe, which describes how much of the lung is affected overall.
How It Differs From Other Emphysema Types
There are three main patterns of emphysema, and they differ in where the damage occurs within each lobule, which parts of the lung they favor, and what causes them.
Centrilobular (centriacinar) emphysema destroys the center of each lobule, concentrates in the upper lungs, and is primarily caused by smoking. The destruction varies unevenly between lobules.
Panlobular (panacinar) emphysema destroys the entire lobule uniformly, from the smallest airways all the way out to the alveoli. It predominates in the lower lungs and is classically linked to alpha-1 antitrypsin deficiency, a genetic condition where the body lacks a protein that protects lung tissue. The lungs tend to be more overinflated than in centrilobular disease, and the airways are more uniformly narrowed.
Paraseptal (distal acinar) emphysema destroys the edges of lobules, particularly near the outer lining of the lung (the pleura) and along the upper back surface. It’s often limited in extent and frequently associated with scarring. Importantly, research shows that paraseptal emphysema does not cause the same loss of small airways that centrilobular emphysema does. Within the same set of lungs, regions with severe paraseptal emphysema had terminal bronchiole counts no different from mildly affected areas, while centrilobular regions showed significant bronchiole loss.
Many people have more than one type simultaneously, but the dominant pattern matters for understanding prognosis.
How It Affects Breathing
Emphysema reduces your lungs’ ability to move air and transfer oxygen in two ways. First, the destruction of air sac walls means less surface area for oxygen to cross into your blood. Second, the loss and narrowing of small airways creates resistance to airflow, especially during exhalation.
Two key measurements capture this. The ratio of how much air you can blow out in one second compared to your total forced breath (FEV1/FVC) drops below 0.70 in obstructive disease. The diffusing capacity test (DLCO) measures how efficiently oxygen passes from your lungs into your bloodstream. A normal DLCO falls between 75% and 140% of the predicted value for your age, sex, and height. Values below 40% of predicted indicate severe impairment.
Centrilobular emphysema has a particularly strong effect on diffusing capacity over time. A study published in CHEST found that moderate or more severe centrilobular emphysema was associated with an accelerated decline in diffusing capacity across multiple disease stages, something not seen with paraseptal emphysema. This progressive gas exchange impairment is what gradually worsens shortness of breath, first during exertion and eventually at rest.
Prognosis and Disease Progression
Not all emphysema carries the same outlook. The centrilobular pattern, when moderate or severe, is more consequential than paraseptal emphysema in terms of both lung function decline and survival.
Data from long-term follow-up of COPD patients showed that moderate or more severe centrilobular emphysema was associated with additional decline in FEV1 and higher 10-year mortality among patients with severe airflow obstruction (GOLD stage 3 or higher). Paraseptal emphysema, by contrast, was not associated with worsening lung function or increased mortality in any disease stage.
This means the severity grading on your CT report carries real prognostic weight. Trace or mild centrilobular emphysema in someone with good lung function numbers is a very different situation from moderate or severe centrilobular emphysema in someone already experiencing significant airflow limitation. The combination of CT findings and breathing test results together gives the clearest picture of where the disease stands and how quickly it may progress.
Treatment and Management
Centrilobular emphysema is managed under the broader framework of COPD treatment, since emphysema is one component of that disease. The destroyed air sacs cannot be regenerated, so treatment focuses on slowing further damage, relieving symptoms, and maintaining function.
Quitting smoking is the single most effective intervention for slowing progression. Nothing else comes close in terms of preserving remaining lung function. Inhaled medications that open the airways (bronchodilators) are the cornerstone of symptom relief. For people with frequent flare-ups, combination inhalers that include an anti-inflammatory component may be added. Current guidelines recommend considering triple therapy (two types of bronchodilators plus an inhaled anti-inflammatory) for patients with elevated flare-up risk and higher blood eosinophil counts.
Pulmonary rehabilitation, a structured program of exercise training and education, consistently improves exercise tolerance and quality of life. For people whose oxygen levels drop significantly, supplemental oxygen during activity or sleep helps maintain organ function. In select cases of severe upper-lobe-predominant emphysema, lung volume reduction surgery or bronchoscopic valve procedures can improve breathing mechanics by removing or deflating the most damaged portions of lung, allowing healthier tissue to expand more fully. Because centrilobular emphysema concentrates in the upper lobes, some patients are well suited to these procedures.