University of South Alabama



Welcome to the University of South Alabama's Center for Lung Biology (CLB). Our Center is comprised of more than 40 faculty members and 25 postdoctoral fellows, clinical fellows, and graduate students representing both basic and clinical science departments, all interested in some aspect of lung biology. The CLB seeks to provide state of the art scientific development in lung biology that advances the understanding of human health and disease, to improve patient care and serve as the foundation for outstanding graduate, post-graduate, and fellowship training.

CLB faculty research interests include Acute Lung Injury, Airways Biology, Nano-scale Respiratory Cell Biology, Pulmonary Endothelial Cell Biology, and Pulmonary Hypertension. Summaries of these research groups can be found at our Scientific Programs site, located on the left-side panel. We provide resource information for scientists interested in cell culture and experimental gene manipulation at our Tissue and Cell Culture Core and Gene Delivery Core sites. Our PercipioTM program is highlighted in the Art in Science section, and our healthy lifestyles program is highlighted in the Running and Walking Club section. Faculty, Post-doc and Clinical Fellows, and Graduate Student research interests and biosketches are available with a click. Stream an interview in our Meet the Professor series, which shares the academic lives and careers of our CLB faculty. Information on how to Contact Us is easily accessible, and training opportunities are shown in the Training Opportunities section.  Our Did You Know... series is highlighted on this homepage, and archives can be retrieved with a click. Explore the interests of our faculty, fellows and graduate students. Again, welcome to the CLB. 




Did You Know

… the pressure inside commercial airline cabins during flight is equivalent to 8,000 feet above sea level?

In 1937, the U.S. Army Air Corps operated the first aircraft with a pressurized cabin for long-range, high altitude military flights over mountainous terrain.  Pressurized cabins were then introduced into a Boeing commercial airplane allowing passengers to fly comfortably at an altitude of 20,000 feet1,2.  Turbofan engines in these aircraft compress intake air to create a cabin altitude, or altitude equivalent to the pressure of air inside the cabin, that is far below the actual flying altitude but still greater than that experienced at takeoff1. Crews and passengers initially flew with cabin altitudes between 10,000 and 16,000 feet, but crashes attributed to a lack of oxygen for pilots prompted the government to establish a cabin altitude ceiling. The Federal Aviation Administration currently mandates that commercial airplanes maintain a cabin altitude of 8,000 feet above sea level3. The cognitive functions of most passengers are not significantly impaired during flight2, but does a cabin altitude of 8,000 feet affect lung function?

Figure 1. Relationship between cabin altitude and calculated alveolar oxygen tension (PAO2) in normal and “at risk” individuals (Adapted from Nicholson and Sznajder)[4,5]).

In a normal healthy adult, an ascent to 8,000 feet results in a 25% reduction in alveolar oxygen tension (Figure 1, red line).  Partial pressure of arterial oxygen declines to roughly 60 mmHg, which is considerably lower than approximately 100 mmHg at sea level4,5. However, healthy passengers are not impaired during flight because they maintain an arterial oxygen saturation of 80% to 90%4,6. These individuals are able to counteract a significant drop in partial pressure of arterial oxygen by increasing minute ventilation. More breaths per minute eliminate the arterial content of CO2 and sustain an alveolar partial pressure of oxygen that results in optimal arterial oxygen saturation. This is not the case for passengers at risk of hypoxia (Figure 1, blue line)7.

Patients with interstitial lung disease, pulmonary hypertension, obstructive sleep apnea, and chronic obstructive pulmonary disease experience alveolar oxygen tensions around 50 mmHg during flight, as demonstrated by the blue line in Figure 1. This yields a partial pressure of arterial oxygen significantly lower than 60 mmHg, reported previously in normal passengers, and a decrease in arterial oxygen saturation. Passengers with pulmonary impairments are not able to acclimate efficiently to the elevated cabin altitude during flight due to diffusion limitation across the blood-gas barrier or ventilation-perfusion mismatching. Hypoxia in such patients can result in respiratory, cardiac, or cognitive symptoms even at rest during air travel. Thus, “at risk” individuals must undergo preflight screenings, which include physical examinations, spirometry, and normobaric hypoxic challenges to assess their fitness for flight7.

More than 736 million passengers take to the air each year in the United States7. The development of the pressurized cabin around the time of World War II has enabled many Americans to fly for business or pleasure at altitudes of 20,000 feet and beyond. The benefits of flying at high altitude include a smoother flight and reduced cost due to decreased drag and less fuel burn2. While a cabin altitude equivalent to 8,000 feet above sea level can be tolerated by healthy passengers, the ascent can be detrimental to those with pulmonary impairments. 


  1. Larson GC. How Things Work: Cabin Pressure. Air & Space Magazine 2002.

  2. McFarland RA. Human factors in relation to the development of pressurized cabins. Aerospace medicine 1971;42:1303-18.

  3. Aviation Maintenance Technician Handbook – Airframe. In: Administration FA, ed. FAA-H-8083-31. US Department of Transportation, Federal Aviation Administration.

  4. Cottrell JJ. Altitude exposures during aircraft flight. Flying higher. Chest 1988;93:81-4.

  5. Ernsting J. Hypoxia in the aviation environment. Proceedings of the Royal Society of Medicine 1973;66:523-7.

  6. Gong H, Jr. Air travel and oxygen therapy in cardiopulmonary patients. Chest 1992;101:1104-13.

  7. Nicholson TT, Sznajder JI. Fitness to fly in patients with lung disease. Annals of the American Thoracic Society 2014;11:1614-22.

Author:  Leslie Blair, June 2015

Chief Editor:  Sarah Sayner, Ph.D.

Co-Editor:  Michael Francis, Ph.D.


Text Only Options

Change the current font size: larger | default | smaller

Current color mode is Black on White, other available modes: Yellow on Black | Black on Cream

Current color mode is Yellow on Black, other available modes: Black on White | Black on Cream

Current color mode is Black on Cream, other available modes: Black on White | Yellow on Black

Open the original version of this page.