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Fears of second-hand smoke confirmed

July 29, 2003 -- Bethesda, MD -- Cigarette smoke is the major cause of pulmonary emphysema. This disease involves severe damage to the walls of the air sacs (alveoli), causing the lungs to lose their capacity to expand and contract (loss of elasticity). At that point, the air sacs are unable to completely deflate and are therefore unable to fill with fresh air for adequate ventilation. Two of every 1,000 Americans develop this disease. Scientists know smokers are significantly more likely to develop emphysema compared with nonsmokers, and the seriousness of the disease is directly correlated with the amount of cigarette smoking.

But why cigarette smoke leads to this disease is still open to speculation. Now, a team of researchers from Italy has found that cigarette smoke is a potent source of oxidative stress, DNA damage, and apoptosis for HFL-1 (fibroblast) cells, and is most likely the trigger leading to the development of pulmonary emphysema in smokers' lungs.

Their findings confirm the fears of many in a work and social environment that exposure to second-hand smoke can lead to a deadly and debilitating disease.

Background

Among the different toxic effects of cigarette smoke on human tissues, oxidation of structural and functional molecules and modulation of cell turnover play a major role. One study has hypothesized that cigarette smoke may act by decreasing the expression of vascular endothelial growth factor (VEGF) and its type 2 receptor, thus resulting in lung septal endothelial cell death. Because fibroblasts (stellate or spindle-shaped cells with cytoplasmic processes present in connective tissue) play a pivotal role in remodeling of pulmonary tissue, researchers have exposed fibroblasts to cigarette smoke and have studied two important processes: oxidative stress and apoptosis.

Oxidative stress is a disturbance in the oxidant-antioxidant balance, resulting in potential cell damage. It is involved in many biolog
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Contact: Donna Krupa
djkrupa1@aol.com
703-527-7357
American Physiological Society
29-Jul-2003


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