
A new study has found that people with chronic obstructive pulmonary disease (COPD) have much higher levels of carbon deposits—similar to soot—in certain lung cells than smokers who do not have the disease.
These black particles, which can enter the lungs through cigarette smoke, air pollution, or diesel exhaust, may play a larger role in COPD than previously understood.
The research, published on June 10 in ERJ Open Research, was led by Dr. James Baker and Dr. Simon Lea from the University of Manchester in the UK. They focused on special immune cells in the lungs called alveolar macrophages.
These cells normally protect the lungs by capturing harmful particles and bacteria. However, when overloaded with carbon, the study shows these cells grow larger and trigger more inflammation—possibly damaging the lungs further.
To investigate this, the team analyzed lung tissue samples from 43 people who had undergone surgery for suspected lung cancer. The samples didn’t contain any cancer cells. Among them, 28 patients had COPD and 15 were smokers without COPD.
When scientists looked at the alveolar macrophages under a microscope, they found something striking: the cells from COPD patients had more than three times the amount of carbon buildup compared to those from smokers without COPD.
Additionally, the macrophages packed with carbon were noticeably larger in size. These larger, soot-filled cells were also linked to worse breathing performance, measured using a test called FEV1%. This test checks how much air a person can exhale in one second—a key indicator of lung function. The lower the FEV1%, the harder it is for a person to breathe properly.
To confirm their observations, researchers also exposed healthy macrophage cells to carbon particles in the lab. Just like in COPD patients, the lab-exposed cells grew bigger and began producing more proteins that are known to cause inflammation in the body.
This suggests that carbon alone can change how these protective lung cells behave—making them part of the problem rather than the solution.
Dr. Lea explained that their findings suggest it’s not just smoking itself causing this issue. “As we compared cells from COPD patients with those from smokers, we saw the difference wasn’t just from cigarette smoke,” he said.
“There’s something different happening in the lungs of people with COPD. Either their bodies can’t clear out the carbon properly, or they may have been exposed to more of it in the first place, possibly from pollution or other sources.”
The study opens up new questions about how COPD develops. Are some people more sensitive to pollution? Do their lungs have a harder time clearing out tiny particles? Could carbon buildup even be part of what causes COPD in the first place?
Professor Fabio Ricciardolo from the University of Torino in Italy, who was not involved in the study, called the findings important.
“This research shows that people with COPD seem to gather a lot more carbon in their lung cells. These cells also look and act differently, causing more inflammation and worsening breathing,” he said. “It also helps explain why air pollution might contribute to COPD or make it worse.”
While more research is needed to understand how this carbon builds up over time and exactly how it affects the lungs, the study supports what doctors already know: exposure to air pollution and cigarette smoke is dangerous, especially for people with lung problems.
That’s why scientists and health experts continue to call for better air quality and stronger support to help people quit smoking.
In summary, this research suggests that carbon buildup in the lungs may be more than just a side effect of pollution—it could be a key factor in how COPD develops and worsens. Understanding this could lead to better ways to prevent and treat the disease in the future.
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The research findings can be found in ERJ Open Research.
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