Statins, the widely used class of drugs for cholesterol management, are now showing promising results in slowing smoking-induced lung damage. In a new study presented at CHEST 2006, the 72nd annual international scientific assembly of the American

"Until now, no medication has shown to slow smoking-induced lung damage," said Walid G. Younis, MD, University of Oklahoma Medical Center, Oklahoma City, OK. "Our study is the first to show that statins may decrease the decline in lung function in smokers and former smokers, and, therefore, prevent millions from developing debilitating diseases that could eventually lead to death." Younis and colleagues from the University of Oklahoma Medical Center compared the effects of statins on the management of 182 current smokers and 303 former smokers, with a mean age 66.1 +/- 2.1 years, seen at the Oklahoma City Veterans Hospital. Patients had at least two pulmonary function tests, with the time between the first and the last test being 2.7 +/- 1.6 years. Patients were categorized by initial level of lung impairment, with 319 having obstructive lung disease, 99 having restrictive lung disease, and 67 patients having normal lung function. Of the patients, 238 were on statin for an average of 2.7 +/- 1.8 years, while the remaining patients did not receive statins (control group). Over the study follow-up period, the decline in FEV1 was 12.8 percent in the control group and 2.5 percent in the statin group. The decline in FVC was 10.3 percent in the control and 1.3 percent in the statin group. Both differences were highly significant. This beneficial effect of statin remained significant, irrespective of the type of lung disease and regardless of whether the patient continued or stopped smoking. Furthermore, statin use in patients with obstructive lung diseas e led to a 35 percent decline in the rate of respiratory-related emergency department visits and hospitalizations. Researchers note that it is not known whether decreasing the rate of decline in lung function or whether preventing emphysema, an independent risk factor of lung cancer, could translate into a reduction of lung cancer. "It is conceivable that long-term statin therapy could be used in smokers and former smokers to prevent and slow the progression of lung diseases," said Dr. Younis. "Even though statins may help with lung function, they have no effect on preventing a patient from the major smoking-related killer, which is lung cancer. Therefore, smokers should never lose their incentive to quit smoking." "Smoking is the number one cause of lung cancer and chronic lung diseases in the world. Although statins may reduce the incidence of lung damage in smokers, patients must still be urged to stop smoking as the best way to maintain and improve their health," said Mark J. Rosen, MD, FCCP, President of the American College of Chest Physicians. CHEST 2006 is the 72nd annual international scientific assembly of the American College of Chest Physicians, held October 21-26 in Salt Lake City, UT. ACCP represents 16,500 members who provide clinical respiratory, critical care, sleep, and cardiothoracic patient care in the United States and throughout the world. The ACCP's mission is to promote the prevention and treatment of diseases of the chest through leadership, education, research, and communication. For more information about the ACCP, please visit the ACCP Web site at

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