In probably the first study to link smoking with severe COVID-19 risk, a team of researchers now claim that people with chronic obstructive pulmonary disease (COPD) and people who currently smoke have higher level of an enzyme that is the ‘entry point for new coronavirus in lungs. Previous research shows that the molecule, called angiotensin converting enzyme II (ACE-2) which sits on the surface of lung cells, is the ‘entry point’ that allows coronavirus to get into the cells of the lungs and cause an infection.
The new study, published in the European Respiratory Journal, showed that levels of ACE-2 in former smokers are 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. 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,” explained lead researcher Dr Janice Leung from the University of British Columbia and St. Paul’s Hospital, Vancouver, Canada.
The team studied samples taken from the lungs of 21 COPD patients and 21 people who did not have COPD. “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,” said Dr Leung. Patients with COPD should be counselled to strictly abide by social distancing and proper hand hygiene to prevent infection. “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,” the authors wrote.
Professor Tobias Welte, an infections expert from the European Respiratory Society and is a coordinator for the national German COVID-19 task force, said that the study gives some 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,” explained Welte. (IANS)
