Environmental tobacco smoke effects on lung surfactant
Creators: name: University Of California Office Of The President
Publisher: name: University of California Office of the President
publisherIdentifier: https://ror.org/00dmfq477
publisherIdentifierScheme: ROR
Year: 2024

description: The specific risks posed by environmental tobacco smoke (ETS) to non-smokers are not particularly well known at the physiological level, although quantifying these risks is an important public health and policy concern. A causal association between ETS exposure and lung cancer appears to exist; for example, nonsmokers married to smokers have a statistically significant higher risk of developing lung cancer than other nonsmokers. In addition to major diseases such as lung cancer, associations have been found between passive smoking at the workplace and chronic respiratory symptoms such as wheezing and cough; the severity of which depends on the extent of exposure. Respiratory effects of ETS are especially significant in infants and children exposed to parental smoking. Epidemiological studies have shown that children raised in homes with smokers have more coughing, wheezing, and respiratory illness compared to children raised in homes without smoking. However, these epidemiological studies cannot provide an explanation of how ETS affects various organs or processes in the body. 
 
 
 
 
 
 This proposal is designed to determine the effects of controlled exposure to environmental tobacco smoke on the chemical and morphological features of human lung surfactants. The surfactant lining of the alveoli, the small gas exchange sacs within the lung, plays an important part in proper lung function. Lung surfactant helps to minimize the energy required to breathe, helps to insure uniform lung inflation and deflation, and helps to clear the deep lung of chemical and particulate contaminants. Lung surfactant works by forming a thin layer that varies from one to no more than 10 molecular layers thick, at the interface between the liquid layer lining the alveolus and the air. This surfactant layer, just like the surfactants used to wash dishes or clean clothes, acts to lower the surface tension at this interface. As the alveolus expands and contracts, it works against the surface tension of this interface; without the surfactant layer to lower the tension, the lung could not inflate. Lung surfactant is unique in that it can almost eliminate surface tension entirely when you exhale, making breathing almost effortless. The unique mix of lipids and proteins in lung surfactant work together to create this film and the near zero surface tension. 
 
 
 
 
 
 Our previous work has shown that rather small changes in the lipid and protein composition of lung surfactant can lead to dramatic changes in surface tension. As ETS comes into contact with the surfactant layer, it is important to determine what ETS can do to the chemistry and morphology of the surfactant. We plan to measure surface tension and determine the morphology of lung surfactant monolayers on model liquids designed to mimic the fluid lining of the alveolus. We will expose these model liquids to various concentrations of side-stream smoke using a system developed at the Institute of Toxicology and Environmental Health at UC Davis. Lung surfactant monolayers will be spread over this smoke-conditioned liquid and the surface tension, viscosity, phase behavior, and morphology of the monolayer will be compared to control monolayers. Detailed chemical analysis of the lipids and proteins in lung surfactant will be conducted to help isolate the species in surfactant most susceptible to damage by ETS. We hope to be able to provide direct evidence of the effects of ETS on the lung surfactant system, and how these changes can lead to changes in respiratory health.