Cells taken from the lungs of people with chronic obstructive pulmonary disease (COPD) have a larger accumulation of soot-like carbon deposits compared to cells taken from people who smoke but do not have COPD, according to a study led by University of Manchester researchers.
The study is published today (Wednesday) in ERJ Open Research [1]. Carbon can enter the lungs via cigarette smoke, diesel exhaust and polluted air.
The cells, called alveolar macrophages, normally protect the body by engulfing any particles or bacteria that reach the lungs. But, in their new study, researchers found that when these cells are exposed to carbon they grow larger and encourage inflammation.
The research was led by Dr James Baker and Dr Simon Lea from The University of Manchester, UK, and funded by the North West Lung Centre Charity and the National Institute for Health and Care Research (NIHR) Manchester Biomedical Research Centre (BRC).
Dr Baker, Research Associate within the NIHR Manchester BRC's Respiratory Theme said: "COPD is a complex disease that has a number of environmental and genetic risk factors. One factor is exposure to carbon from smoking or breathing polluted air.
"We wanted to study what happens in the lungs of COPD patients when this carbon builds up in alveolar macrophage cells, as this may influence the cells' ability to protect the lungs."
The researchers used samples of lung tissue from surgery for suspected lung cancer. They studied samples (that did not contain any cancer cells) from 28 people who had COPD and 15 people who were smokers but did not have COPD.
Looking specifically at alveolar macrophage cells under a microscope, the researchers measured the sizes of the cells and the amount of carbon accumulated in the cells.
They found that the average amount of carbon was more than three times greater in alveolar macrophage cells from COPD patients compared to smokers. Cells containing carbon were consistently larger than cells with no visible carbon.
Patients with larger deposits of carbon in their alveolar macrophages had worse lung function, according to a measure called FEV1%, which quantifies how much and how forcefully patients can breathe out.
When the researchers exposed macrophages to carbon particles in the lab, they saw the cells become much larger and found that they were producing higher levels of proteins that lead to inflammation.
Dr Lea, Investigator within the NIHR Manchester BRC's Respiratory Theme said: "As we compared cells from COPD patients with cells from smokers, we can see that this build-up of carbon is not a direct result of cigarette smoking. Instead, we show alveolar macrophages in COPD patients contain more carbon and are inherently different in terms of their form and function compared to those in smokers.
"Our research raises an interesting question as to the cause of the increased levels of carbon in COPD patients' macrophages. It could be that people with COPD are less able to clear the carbon they breathe in. It could also be that people exposed to more particulate matter are accumulating this carbon and developing COPD as a result.
"In future, it would be interesting to study how this carbon builds up and how lung cells respond over a longer period of time."
Professor Fabio Ricciardolo is Chair of the European Respiratory Society's group on monitoring airway disease, based at the University of Torino, Italy, and was not involved in the research. He said: "This set of experiments suggest that people with COPD accumulate unusually large amounts of carbon in the cells of their lungs. This build-up seems to be altering those cells, potentially causing inflammation in the lungs and leading to worse lung function.
"In addition, this research offers some clues about why polluted air might cause or worsen COPD. However, we know that smoking and air pollution are risk factors for COPD and other lung conditions, so we need to reduce levels of pollution in the air we breathe and we need to help people to quit smoking."
[1] Baker J, Booth S, Dungwa J, et al. Alveolar macrophage carbon is associated with COPD severity. ERJ Open Res 2025; in press (https://doi.org/10.1183/23120541.00933-2024).
The paper is available here: https://doi.org/10.1183/23120541.00933-2024
Funding: the North West Lung Centre Charity and the National Institute for Health and Care Research (NIHR) Manchester Biomedical Research Centre (BRC).
