New Study Finds Another Important Reason Why Smokers Should Keep Their Unhealthy Habit Away From Infants and Children

NEW ORLEANS, LA - Cigarette smoking is well known to cause problems with the pulmonary surfactant system. Millions smoke. Unfortunately, millions more are either exposed to side-stream smoke, that smoke which is produced by a burning cigarette between inhalations, or second-hand smoke, which is the smoke exhaled by the smoker and inhaled by another. There is accumulating evidence that this type of smoke exposure may be just as harmful to the lungs of non-smokers as smoking is to the lungs of smokers.

An investigation into the association between surfactant production and utilization and cigarette smoke exposure to the non-smoker has been conducted by James F. Collins, Ph.D., of the Department of Pediatrics and Steele Memorial Children’s Research Center at the University of Arizona in Tucson, AZ. He will present the results of his study, entitled, "Regulation of Alveolar Type II Cell Sodium-Phosphate Cotransporter Type IIb (NaPi-IIb) Gene Expression by Side-Stream Cigarette Smoke (SSCS) Exposure," during the American Physiological Society’s (APS) annual meeting, part of the "Experimental Biology 2002” conference. More than 12,000 attendees will attend the conference being held at the Ernest N. Morial Convention Center, New Orleans, LA from April 20-24, 2002.

Cotransport proteins are essential in cell biology because they facilitate the movement of nutrient molecules and ions across cell membranes. One such protein is the type IIb sodium-phosphate (NaPi-IIb) cotransporter, a protein which allows cells to intake phosphate along with sodium. This cotransporter can be found in several organs of the body, but it is most highly abundant in the alveolar type II (AII) cells in the lungs.

In the alveoli of the lungs, where gas-exchange occurs, the large, moist alveolar surface area is exposed to inhaled air. The gas exchange between this alveolar surface and the pulmonary blood vessels determine how efficiently the lungs function as a whole. Surfactant, an insoluble film on the surface of the alveolar lining, is produced and secreted by AII epithelial cells. Surfactant effectively reduces the surface tension forces, which tend to favor alveolar and lung collapse, and thus allows the lungs to function normally. Since the lipids and proteins that make up pulmonary surfactant have a very high phosphate content, we surmise that the NaPi-IIb cotransporter is involved in allowing AII cells to intake the high phosphate levels necessary for surfactant production.

Abnormalities in surfactant production and utilization are associated with neonatal and adult (or acute) respiratory distress syndromes. For example, the critical importance of surfactant is evidenced by the clinical problems found in premature infants, before maturation of the surfactant synthesis system has occurred. These infants with severe lung dysfunction are now treated with synthetic surfactant. Surfactant production is also perturbed in smokers and perhaps in those exposed to second hand or side-stream cigarette smoke.

This study was designed to test the hypothesis that AII cell NaPi-IIb cotransporter expression is affected by side-stream cigarette smoke exposure. Thus, rodents were exposed to various levels of sidestream cigarette smoke daily for 60 minutes for 14 consecutive days. Lung tissue was then studied from the exposed and control animals and NaPi-IIb cotransporter gene and protein expression was measured.

The findings of this study revealed that:

Lower levels of cigarette smoke exposure decreased NaPi IIb cotransporter gene and protein expression. This reduction may contribute to disturbances in smoker's surfactant production.

Higher smoke exposure levels in other rodent species lead to increased expression of the NaPi-IIb cotransporter, suggesting a compensatory mechanism for surfactant production.

Overall, these studies suggest that this cotransporter may be involved in surfactant synthesis, since surfactant production is also known to be adversely affected in the lungs of smokers.

It is thought, but not proven, that second-hand and side-stream smoke exposure can damage the lungs of non-smokers. This study finds that exposure of non-smokers to cigarette smoke can effect expression of a key gene possibly involved in the production of pulmonary surfactant, which is necessary for normal lung function. These findings offer another important reason that smokers should keep their unhealthy habit away from children and infants. Further research is required to understand precisely what role this protein plays in surfactant production and utilization, and to determine exactly how its’ expression is effected by cigarette smoke exposure.

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