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Key Event Title
|Level of Biological Organization|
Key Event Components
Key Event Overview
AOPs Including This Key Event
|AOP Name||Role of event in AOP||Point of Contact||Author Status||OECD Status|
|Lung surfactant function inhibition leading to decreased lung function||KeyEvent||Brendan Ferreri-Hanberry (send email)||Open for comment. Do not cite||Under Development|
|All life stages||High|
Key Event Description
At the end of expiration, the alveoli are at their minimum volume, and the surface tension is at its lowest. If the surface tension is not sufficiently low at this point, the forces pulling the walls of the alveoli together during expiration cannot be overcome, and the alveoli might collapse (Notter and Wang 1997). Collapsed alveoli may however be re-opened by the force of air drawn into the lungs during inhalation. As breathing is continuous, the same alveoli can collapse and re-open repeatedly. The consequence of alveolar collapse can be observed as atelectasis upon histological examination, or can be indirectly inferred by reduced tidal volume or perfusion/ventilation mismatch (further details in the “Measurements of alveolar collapse” section).
How It Is Measured or Detected
There are approximately 480 million alveoli in the lungs (Ochs, Nyengaard et al. 2004). Alveolar collapse and re-opening can only happen in intact lungs in a living organism and thus cannot be measured in vitro. Further, because of their small diameter of approximately 200 µm in diameter (Ochs, Nyengaard et al. 2004), it is virtually impossible to measure the collapse and re-opening at the level of individual alveoli with any certainty. However, areas of atelectasis can be observed in experimental animals after staining of lung tissue from exposed animals (Jefferies, Kawano et al. 1988, Yamashita and Tanaka 1995, Nørgaard, Larsen et al. 2010).
Domain of Applicability
The applicability domain is restricted to the groups of organisms where the structure and the functioning of the pulmonary system, including the alveoli, are conserved and relevant.
Jefferies, A. L., T. Kawano, S. Mori and R. Burger (1988). "Effect of increased surface tension and assisted ventilation on 99mTc-DTPA clearance." J Appl Physiol (1985) 64(2): 562-568.
Notter, R. H. and Z. D. Wang (1997). "Pulmonary surfactant: Physical chemistry, physiology, and replacement." Reviews in Chemical Engineering 13(4): 1-118.
Nørgaard, A. W., S. T. Larsen, M. Hammer, S. S. Poulsen, K. A. Jensen, G. D. Nielsen and P. Wolkoff (2010). "Lung damage in mice after inhalation of nanofilm spray products: the role of perfluorination and free hydroxyl groups." Toxicol Sci 116(1): 216-224.
Ochs, M., J. R. Nyengaard, A. Jung, L. Knudsen, M. Voigt, T. Wahlers, J. Richter and H. J. Gundersen (2004). "The number of alveoli in the human lung." Am J Respir Crit Care Med 169(1): 120-124.
Yamashita, M. and J. Tanaka (1995). "Pulmonary Collapse and Pneumonia Due to Inhalation of a Waterproofing Aerosol in Female Cd-1 Mice." Journal of Toxicology-Clinical Toxicology 33(6): 631-637.