The study, published in the European Respiratory Journal, shows that levels of angiotensin converting enzyme II (ACE-2) --which sits on the surface of lung cells -- in former smokers is lower than in current smokers.
"The data emerging from China suggested that patients with COPD were at higher risk of having worse outcomes from COVID-19," said Janice Leung from the University of British Columbia in Canada.
"We hypothesised that this could be because the levels of ACE-2 in their airways might be increased compared to people without COPD, which could possibly make it easier for the virus to infect the airway," Leung said.
The researchers studied samples taken from the lungs of 21 COPD patients and 21 people who did not have COPD.
They tested the samples to gauge the level of ACE-2 and compared this with other factors, such whether they were from people who never smoked, were current smokers or former smokers.
Not only did they find higher levels of ACE-2 in COPD patients, they also found higher levels in people who were smokers.
The researchers then checked their new findings against two existing study groups, which together contain data on a further 249 people -- some non-smokers, some current smokers and some former smokers.
They found levels of ACE-2 were higher in current smokers but lower in non-smokers and in those who were former smokers.
"We found that patients with COPD and people who are still smoking have higher levels of ACE-2 in their airways, which might put them at an increased risk of developing severe COVID-19 infections.
"Patients with COPD should be counselled to strictly abide by social distancing and proper hand hygiene to prevent infection," said Leung.
"We also found that former smokers had similar levels of ACE-2 to people who had never smoked. This suggests that there has never been a better time to quit smoking to protect yourself from COVID-19," she said.
Professor Tobias Welte, an infections expert from the European Respiratory Society said the study gives interesting insight into why some people may be at risk of more severe COVID-19 symptoms than others.
"What it does not tell us is whether it's possible to manipulate ACE-2 levels to improve survival in patients infected with COVID-19 or whether this would make a difference in COPD patients who contract the infection," said Welte, who was not involved in the study. SARSAR