Chronic obstructive pulmonary disease (COPD) is a serious, incurable lung disease that is common in older people. However, researchers are learning that the origins of the disease may lie decades earlier in how children's lungs grow and develop.
New research, presented at the European Respiratory Society (ERS) Congress in Barcelona, Spain, suggests that babies born with higher genetic risk for COPD showed reduced lung function growth between birth and six years, which could place them on a path to developing the disease. However, researchers only saw this pattern in children who were exposed to higher levels of air pollution.
The research was presented by Dr Carla da Silva Sena from University Children's Hospital Basel UKBB, University of Basel, and Bern University Hospital, Switzerland. She said: "COPD develops through a combination of genetic factors and environmental exposures across the lifespan, leading to an accelerated decline in lung function. While COPD is often associated with smoking, growing evidence suggests that genetic and environmental factors in early life may also contribute to the foundations of the disease, particularly during lung development in infancy and childhood.
"We believe that COPD can result from lung function 'trajectories' established early in life. For example, COPD can develop because the lungs do not reach their full growth potential during childhood or because lung function declines faster than expected later on. Studying these trajectories from the earliest stages of life is key to understanding how COPD develops."
The research included 484 children who were taking part in the Basel-Bern Infant Lung Development (BILD) study. This is an ongoing Swiss birth cohort study that follows children born between 1999 and 2020.
Children's lung function was assessed in the first month of life using the infant tidal breathing test, which records a baby's natural breathing while they sleep. At age six, children took part in a spirometry test, where lung function is assessed by taking a deep breath and blowing out as hard as possible. Researchers estimated each child's exposure to outdoor air pollution, including fine particles (PM2.5) and nitrogen dioxide (NO2), from birth until age six.
Researchers also collected genetic information from children's blood samples. COPD is not caused by a single gene, but the risk of developing COPD has been linked to many small genetic differences that can be combined into a measure known as a 'polygenic risk score'. The researchers examined whether this polygenic risk score, which has been established by studying adult COPD patients, shows an effect on how lung function develops in healthy newborns, even before they display any symptoms.
The researchers found that this genetic risk for developing COPD was aligned with a lower lung function growth in children between birth and six years old, but only in the children who grew up in areas with the highest PM2.5 air pollution (average 15.3 μg/m³). In children from areas with lower air pollution, this effect was much weaker. Researchers found a similar pattern between lung function growth and higher levels of nitrogen dioxide (average 28.3 μg/m³).
These findings suggest that some babies may be born with a higher genetic risk for COPD, and this risk may already begin to show up as differences in lung function growth in early childhood, but only in those who grow up in areas with higher air pollution.
This study adds to the evidence that early-life environment matters for lung health, and not just for children who already have breathing problems, but potentially for how lungs develop over time in seemingly healthy children. It reinforces that protecting air quality in early life may benefit children's long-term health."
Dr. Carla da Silva Sena, University Children's Hospital Basel UKBB, University of Basel, and Bern University Hospital, Switzerland
Researchers plan to follow the children into adolescence and adulthood to see whether the differences they see in the children's lung function persist or grow over time.
A limitation of the study is that it is not possible to use the same lung function test in babies and school-age children. To overcome this problem, the researchers used statistical techniques to make the results comparable between the different tests. The study also relied on a genetic risk score that was developed based on populations of European ancestry. This means the findings may not directly apply to children from other backgrounds.
Professor Barbara Hoffmann, Chair of the European Respiratory Society's Advocacy Council, based at the University of Düsseldorf, Germany, who was not involved in the research said: "This study reveals a genetic risk pathway for COPD that only became apparent when researchers looked at the effects of air pollution in seemingly healthy children. This shows how genes and environment in the early years can combine to set children on a path to lung disease much later in life.
"These findings fit with a broader shift in how COPD is understood, reflected in a 2022 Lancet Commission, which argued that COPD is shaped by risk pathways across life, not just by adult smoking. It may help explain why COPD can also occur in non-smokers.
"Given the potential long-term benefits for children's lung development, this research strengthens the case for clean air policies. Air pollution, unlike genetic risk, is something that can be addressed through the right policy and regulation."
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