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  • Author: Kamran Boka, MD, MS; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
Updated: Oct 23, 2014


Emphysema and chronic bronchitis are airflow-limited states contained within the disease state known as chronic obstructive pulmonary disease (COPD). Just as asthma is no longer grouped with COPD, the current definition of COPD put forth by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) also no longer distinguishes between emphysema and chronic bronchitis.[1]

Emphysema is pathologically defined as an abnormal permanent enlargement of air spaces distal to the terminal bronchioles, accompanied by the destruction of alveolar walls and without obvious fibrosis.

The theory surrounding this definition has been around since the 1950s, with a key concept of irreversibility and/or permanent acinar damage. However, new data posit that increased collagen deposition leads to active fibrosis, which inevitably is associated with breakdown of the lung’s elastic framework. An entity known as combined pulmonary fibrosis and emphysema (CPFE) has been shown to exist in a subset of emphysematous patients.[2] This implies an association between fibrosis and the permanence of alveolar damage. The complex mechanism thought to be responsible is the interplay between Notch and Wnt, two signaling pathways playing critical roles in epithelial and mesenchymal precursor cell maintenance and differentiation.[3]

Risk factors

The risk factors thought to be responsible for the development of COPD are all associated with an accelerated decline in FEV1 over time. Leading this list is cigarette smoking: 15-20% of 1 pack-per-day smokers and 25% of 2 pack-per-day smokers develop COPD. Next are cigars and pipe smoke, followed by secondhand and thirdhand smoke. Occupational, inhalational, and environmental exposures, including biomass fuel cooking, also are included on the list.[4]

Women in developing countries who are exposed to biomass cooking of liquids and fuels including wood, crops, animal dung, and coal, are at increased risk of developing COPD. Add to that poor ventilation of the home and dependent family members’ (children and the elderly) risk increases also. Throughout the world, COPD is a disease of occupation and environmental pollutants too, including but not limited to organic and inorganic dusts, isocyanates, and phosgenes.[5]

However, the evolution of disease based on smoke exposure differs widely among people, suggesting genetic factors to be involved. It is not truly known why certain people with a positive smoke exposure develop injury patterns, symptoms, and disease. For instance, the Lung Health Study from 2002 showed that a third of smokers never developed impaired lung function after 11 years despite a baseline study of airway obstruction.[6]

Genetic risk factors for the development of COPD are also thought to exist. The most well-studied is alpha-1-antitrypsin (AAT) deficiency (also known as alpha-1 antiprotease deficiency).

Alpha-1-antitrypsin deficiency

AAT is a glycoprotein member of the serine protease inhibitor family that is synthesized in the liver and is secreted into the blood stream. The main purpose of this 394–amino acid, single-chain protein is to neutralize neutrophil elastase in the lung interstitium and to protect the lung parenchyma from elastolytic breakdown. If not inactivated by AAT, neutrophil elastase destroys lung connective tissue leading to emphysema. Therefore, severe AAT deficiency predisposes to unopposed elastolysis with the clinical sequela of an early onset of panacinar emphysema.

Deficiency of AAT is inherited as an autosomal codominant condition. The gene, located on the long arm of chromosome 14, expresses different phenotypes (serum protease inhibitor phenotype notated Pi type). The most common type of severe AAT phenotype (more than 90%) occurs in individuals who are homozygous for the Z allele. Homozygous individuals (Pi ZZ), usually of northern European descent, have serum levels well below the reference range levels at about 20% of the normal level (2.5 to 7 mmol/L). The normal M allele phenotype is Pi MM, with levels of 20-48 mmol/L.[7]

Lifetime nonsmokers who are homozygous for the Z allele rarely develop emphysema. Hence, cigarette smoking is the most important risk factor for emphysema development. The American Thoracic Society/European Respiratory Society (ATS/ERS) Guidelines[7] recommend screening for AAT deficiency if emphysema is suspected in any patient younger than 45 years and with any of the following:

  • Absence of recognized emphysema risk factors such as smoking or occupational inhalational exposure
  • Unexplained liver disease
  • Family history of AAT deficiency, COPD, bronchiectasis, or panniculitis
  • Positive c-ANCA (anti-neutrophilic cytoplasmic antibody) vasculitis
  • Unclear/idiopathic bronchiectasis
  • Asthma with persistent, fixed-airways obstruction despite therapy


Once innate respiratory defenses of the lung’s epithelial cell barrier and mucociliary transport system are infiltrated by foreign/invading antigens (noxious cigarette ingredients, for instance), the responding inflammatory immune cells (including polymorphonuclear cells, eosinophils, macrophages, CD4 positive and CD8 positive lymphocytes) transport the antigens to the bronchial associated lymphatic tissue layer (BALT). It is here where the majority of the release of neutrophilic chemotactic factors is thought to occur. Proteolytic enzymes like matrix-metalloproteinases (MMPs) are mainly released by macrophages, which lead to destruction of the lung’s epithelial barrier.

Macrophages are found to be 5- to 10-fold higher in the bronchoalveolar lavage fluid of emphysematous pateints.[8] Also, along with macrophages, the release of proteases and free radical hydrogen peroxide from neutrophils adds to the epithelial ruination, specifically with emphasis on the basement membrane. This is why neutrophils are thought to be highly important in the pathogenesis of emphysema at the tissue level, a differentiator to the mainly eosinophilic inflammatory response in airways affected by asthma.

After all, the T lymphocytes in the sputum of emphysematous smokers are mainly CD8 positive cells.[9] These cells release chemotactic factors to recruit more cells (pro-inflammatory cytokines that amplify the inflammation) and growth factors that promote structural change. The inflammation is further amplified by oxidative stress and protease production. Oxidants are produced from cigarette smoke and released from inflammatory cells. Proteases are produced by inflammatory, macrophage, and epithelial cells, which fuel bronchiolar edema from an elastin-destroying protease-antiprotease imbalance. This protease-menace is elastase, released by macrophages, and responsible for breakdown of the lung’s fragile elastic lamina (of which elastin is a structural protein component).[8] This is believed to be central in the development of emphysema. Peptides from elastin can be detected in increased quantities in patients with emphysema and AAT.[10]

The repair process of airway remodeling further exacerbates emphysema’s anatomical derangements with key characters such as vascular endothelial growth factor (VEGF), which is expressed in airway smooth muscle cells and is responsible for neovascularization and expression of increased and possibly abnormal patterns of fibroblastic development. It is these structural changes of mucus hyperplasia, bronchiolar edema, and smooth muscle hypertrophy and fibrosis in smokers’ airways that result in the small airways narrowing of less than two millimeters.


Pathologically defined as permanent enlargement of airspaces distal to the terminal bronchioles, emphysema creates an environment leading to a dramatic decline in the alveolar surface area available for gas exchange. Loss of individual alveoli with septal wall destruction leads to airflow limitation via two mechanisms. First, loss of alveolar wall results in a decrease in elastic recoil, which subsequently limits airflow. Second, loss of alveolar supporting structures is indirectly responsible for airway narrowing, again limiting airflow.[11]

Though the paradigm for classification continues to evolve, the described morphological pathology of region-specific emphysema remains in three types:[12]

  • Centriacinar (centrilobular)
  • Panacinar (panlobular)
  • Paraseptal

Centriacinar emphysema is the most common type of pulmonary emphysema mainly localized to the proximal respiratory bronchioles with focal destruction and predominantly found in the upper lung zones. The surrounding lung parenchyma is usually normal with untouched distal alveolar ducts and sacs. Also known as centrilobular emphysema, this entity is associated with and closely-related to long-standing cigarette smoking and dust inhalation.[13, 14]

Centrilobular emphysema. Courtesy of Dr Frank Gail Centrilobular emphysema. Courtesy of Dr Frank Gaillard, (

Panacinar emphysema destroys the entire alveolus uniformly and is predominant in the lower half of the lungs. Panacinar emphysema generally is observed in patients with homozygous (Pi ZZ) alpha1-antitrypsin (AAT) deficiency. In people who smoke, focal panacinar emphysema at the lung bases may accompany centriacinar emphysema.[13, 14]

Panlobular ephysema. Courtesy of Dr Frank Gaillard Panlobular ephysema. Courtesy of Dr Frank Gaillard, (

Paraseptal emphysema, also known as distal acinar emphysema, preferentially involves the distal airway structures, alveolar ducts, and alveolar sacs. The process is localized around the septae of the lungs or pleura. Although airflow is frequently preserved, the apical bullae may lead to spontaneous pneumothorax. Giant bullae occasionally cause severe compression of adjacent lung tissue.[13, 14]

Paraseptal emphysema. Courtesy of Dr Frank Gaillar Paraseptal emphysema. Courtesy of Dr Frank Gaillard, (
Gross pathology of bullous emphysema shows bullae Gross pathology of bullous emphysema shows bullae on the surface of the lungs.
Gross pathology of emphysema shows bullae on the l Gross pathology of emphysema shows bullae on the lung surface.



United States

The National Health Interview Survey reports the prevalence of emphysema at 18 cases per 1000 persons and chronic bronchitis at 34 cases per 1000 persons.[15] While the rate of emphysema has stayed largely unchanged since 2000, the rate of chronic bronchitis has decreased. This prevalence is based on the number of adults who have ever been told by any health care provider that they have emphysema or chronic bronchitis. This is felt to be an underestimation because most patients do not present for medical care until the disease is in its later stages.


The Burden of Obstructive Lung Disease (BOLD) study showed that the worldwide prevalence of COPD (stage II or higher) was 10.1%.[16] This figure varied by geographic location and by sex with a pooled prevalence among men of 11.8% (8.6-22.2%) and among women of 8.5% (5.1-16.7%). The differences can, in part, be explained by site and sex differences in the prevalence of smoking. These rates are similar to rates observed in the Proyecto Latino Americano de Investigacion en Obstruccion Pulmonar (PLATINO study), which studied 5 countries in Latin America.[17]


A US Centers for Disease Control and Prevention (CDC) Morbidity Mortality Weekly Report study of the National Vital Statistics System reported an age-standardized death rate from COPD in the United States for adults older than 25 years of 64.3 deaths per 100,000 population.[18] This rate varied by location, with the lowest rate in Hawaii (27.1 deaths per 100,000 population) and the highest rate in Oklahoma (93.6 deaths per 100,000 population).


In the past, COPD was more prevalent among men; however, this was attributed to the difference in smoking rates of men versus women. With the increase in smoking among women over the past 30 years, the sex difference has declined. Some studies have suggested women may be even more susceptible to the development of emphysema.[19, 20]

Contributor Information and Disclosures

Kamran Boka, MD, MS Faculty, Division of Critical Care, Department of Internal Medicine, The University of Texas Health Science Center at Houston (UTHealth)

Kamran Boka, MD, MS is a member of the following medical societies: American College of Physicians, American Thoracic Society

Disclosure: Creator of Boka's Notes Internal Medicine Series Apps for: Vagal Thoughts, LLC.


Daniel R Ouellette, MD, FCCP Associate Professor of Medicine, Wayne State University School of Medicine; Chair of the Clinical Competency Committee, Pulmonary and Critical Care Fellowship Program, Senior Staff and Attending Physician, Division of Pulmonary and Critical Care Medicine, Henry Ford Health System; Chair, Guideline Oversight Committee, American College of Chest Physicians

Daniel R Ouellette, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, Society of Critical Care Medicine, American Thoracic Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women's Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society

Disclosure: Nothing to disclose.

Additional Contributors

Helen M Hollingsworth, MD Director, Adult Asthma and Allergy Services, Associate Professor, Department of Internal Medicine, Division of Pulmonary and Critical Care, Boston Medical Center

Helen M Hollingsworth, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American Thoracic Society, Massachusetts Medical Society

Disclosure: Nothing to disclose.


Berj George Demirjian, MD Fellow, Division of Pulmonary/Critical Care Medicine, Cedars-Sinai Medical Center

Berj George Demirjian, MD is a member of the following medical societies: American College of Chest Physicians, American Medical Association, California Medical Association, California Thoracic Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Nader Kamangar, MD, FACP, FCCP, FCCM Associate Professor of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, University of California, Los Angeles, David Geffen School of Medicine, Olive View-UCLA Medical Center; Associate Program Director, Pulmonary and Critical Care Multi-Campus Fellowship Program, Cedars-Sinai/West Los Angeles Veterans Affairs/Los Angeles Kaiser Permanente/Olive View-UCLA Medical Center; Site Director, Pulmonary/Critical Care Fellowship Program, Olive View-UCLA Medical Center

Nader Kamangar, MD, FACP, FCCP, FCCM is a member of the following medical societies: American Academy of Sleep Medicine, American Association of Bronchology, American College of Chest Physicians, American College of Physicians, American Lung Association, American Medical Association, American Thoracic Society, California Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

Disclosure: Nothing to disclose.

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Gross pathology of bullous emphysema shows bullae on the surface of the lungs.
Gross pathology of emphysema shows bullae on the lung surface.
At high magnification, loss of airway walls and dilated airspaces are observed in emphysema.
Chest radiograph shows hyperinflation, flattened diaphragms, increased retrosternal space, and hyperlucency of the lung parenchyma in emphysema.
A CT scan shows emphysematous bullae in upper lobes.
Diffuse emphysema secondary to cigarette smoking.
Pressure-volume curve is drawn for a patient with restrictive lung disease and obstructive disease and is compared to healthy lungs.
Flow-volume curve of lungs with emphysema shows marked decrease in expiratory flows, hyperinflation, and air trapping (patient B) compared to a patient with restrictive lung disease, who has reduced lung volumes and preserved flows (patient A).
Forced expiratory volume in 1 second (FEV1) can be used to evaluate the prognosis in patients with emphysema. The benefit of smoking cessation is shown here because the deterioration in lung function parallels that of a nonsmoker, even in late stages of the disease.
A CT scan showing severe emphysema and bullous disease.
An emphysematous lung shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragms on posteroanterior (PA) film.
An emphysematous lung shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragms on lateral chest radiograph.
The differential diagnosis of unilateral hyperlucent lung includes pulmonary arterial hypoplasia and Swyer-James syndrome. The expiratory chest radiograph exhibits evidence of air trapping and is helpful in making the diagnosis. Swyer-James syndrome is unilateral bronchiolitis obliterans, which develops during early childhood.
Lateral chest radiograph of Swyer-James syndrome may demonstrate some of the features of emphysema.
Paraseptal emphysema. Courtesy of Dr Frank Gaillard, (
Panlobular ephysema. Courtesy of Dr Frank Gaillard, (
Centrilobular emphysema. Courtesy of Dr Frank Gaillard, (
Early stethoscope drawing c 1819. Courtesy of Wikipedia.
Laennec's early stethoscope made of brass and wood c 1820. Courtesy of Wikipedia.
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