Once smokers develop chronic obstructive pulmonary disease, quitting may not improve smokers’ lung function; thus, smokers should quit as early as possible to have the greatest chance of reversing lung damage.
New research showing how cigarettes affect the lungs on a cellular level provides further evidence that the sooner smokers quit, the better their chances of having healthier lungs. The study, published in Thorax, suggests that once smokers develop chronic obstructive pulmonary disease (COPD), quitting may not improve smokers’ lung function; thus, smokers should quit as early as possible to have the greatest chance of reversing lung damage.
Investigator Yael Strulovici-Barel and colleagues at Weill Cornell Medical College in New York City sought to determine what happens on a cellular level in the area of the small blood vessels of the lungs (pulmonary capillaries) when smokers quit. It is at the interface between the pulmonary capillaries and the alveoli (tiny sacs where gas exchange occurs in the lung) that respiratory gases are exchanged across a two-cell barrier composed of the epithelial layer of the aveolar wall and the epithelial layer of the pulmonary capillary. Previous research demonstrated elevated plasma levels of circulating microparticles released from the endothelial cells that line the lung’s blood vessels in smokers and people with COPD. These circulating endothelial microparticles (EMPs) are thought to be shed from pulmonary capillaries because of active pulmonary capillary endothelial apoptosis (programmed cell death), evidence of lung destruction.
Pulmonary function and high-resolution CT were assessed in 28 nonsmokers, 61 healthy smokers, and 49 COPD smokers; 17 healthy smokers and 18 COPD smokers successfully quit smoking for 12 months after the baseline visit. Flow cytometry was used to assess total, pulmonary capillary, and apoptotic levels of EMPs in all study participants after 3, 6, and 12 months.
Although both healthy and COPD smokers had elevated levels of apoptotic EMPs compared with nonsmokers, only healthy smokers were positively affected by smoking cessation. When healthy smokers stopped smoking, their levels of apoptotic EMPs dropped back to normal levels, whereas for COPD smokers the EMPs levels did not drop back.
Lead researcher, Ronald G. Crystal, MD, chairman of the Department of Genetic Medicine, Bruce Webster Professor of Internal Medicine, and professor of medicine at Weill Cornell Medical College, said the investigators had purposely observed people with the mildest form of COPD because it allows better insight into the disease mechanism. He noted that the research is also important for the development of COPD biomarkers. The takeaway from the study is that the earlier you can stop smoking before developing COPD, the better chance you will have at healthy lungs, Crystal said.