麻豆传媒

Asthmatic smokers who quit the habit can reverse lung damage that exacerbates their breathing difficulties, regardless of how long and how often they smoked in the past, a Dutch study found.

The lungs of asthmatics who stopped smoking were in similar condition to those of asthmatics who never smoked, based on a several measurements of lung health, including goblet cell numbers and mucus-positive epithelium, epithelial thickness, epithelial proliferation rate, and mast cell numbers, according to a report in the Dec. 15 American Journal of Respiratory and Critical Care Medicine.

Asthmatics who continued to smoke showed signs of unhealthy lungs, including lower scores on pulmonary function tests (Forced Expiratory Volume in 1 Second) and lower levels of alveolar and bronchial nitric oxide in their breath than those who never smoked.

Compared to asthmatics who had quit smoking, they had more mucous-producing goblet cells in their epithelium, and the epithelial cell layer contained more mucus protein.

"We show in a large population of patients with asthma that cigarette smoking induces epithelial changes in association with increases in asthma symptoms, such as shortness of breath and phlegm production," Martine Broekema, PhD, of University Medical Center Groningen, and colleagues wrote.

"Cigarette smoking in asthma was associated with lower bronchial eosinophil and higher mast cell numbers. The fact that epithelial changes and higher mast cell numbers were not observed in ex-smokers with asthma suggests that these smoke-induced changes can be reversed by smoking cessation."

Although smoking exacerbates the symptoms of asthma -- coughing, wheezing, sputum production and attack frequency -- the habit is just as common among asthmatics as in the general population, the authors wrote.

But little was known about the underlying pathological processes that deteriorate the lungs of asthmatics who smoke.

So Broekema and colleagues assessed 147 asthmatic patients, determining the severity of their asthma and allergies through clinical examinations.

The patients also answered chronic obstructive pulmonary disease questionnaires about their smoke-induced symptoms and underwent bronchial biopsies to determine the condition of the tissues that line the lungs.

Of those in the study, 66 had never smoked, 46 were ex-smokers, and 35 were current smokers.

Among all the participants, the severity of phlegm production reported on the questionnaire was associated with the number of goblet cells (P=0.034), presence of mucus-positive epithelium (P=0.045) and lung epithelial thickness (P=0.011). The severity of shortness of breath correlated with epithelial thickness (P=0.018).

To determine whether a smoker's history affected the ability of the lungs to rebound after quitting, the researchers included ex-smokers in the study, dividing them into two groups: those with fewer than the median 3.4 pack-year exposure and those with more than 3.4 pack-years.

"Our ex-smoking group had a significantly lower number of pack-years compared with the smoking group, suggesting that differences between these two groups might be due to lower cumulative smoke exposure in ex-smokers," the authors wrote.

"This was not the case because the number of pack-years was not significantly correlated to any of our outcome variables in the ex-smoking group."

The authors cautioned that their study was cross-sectional in design and that longer studies on smoking cessation will be needed to confirm their findings.

"Nevertheless," they concluded, "based on our observations, we speculate that the smoke-related epithelial changes and increase in mast cell numbers are reversible by smoking cessation."