Air pollution could play a role in shaping the lungs of children who are genetically more vulnerable to chronic obstructive pulmonary disease (COPD), new research suggests.
The findings raise the possibility that the foundations of a disease usually associated with older age may be laid decades earlier, during childhood lung development.
Researchers found that babies with a higher genetic risk of COPD experienced slower growth in lung function between birth and the age of six. However, the link was strongest among children exposed to higher levels of air pollution.
The research, presented at the European Respiratory Society (ERS) Congress in Barcelona, involved 484 children taking part in the Basel-Bern Infant Lung Development (BILD) study in Switzerland.
The ongoing study has followed children born between 1999 and 2020, allowing researchers to examine how lung function develops from the earliest stages of life.
Lung function was first assessed during the children’s first month, using a test that measures natural breathing while babies are asleep. At six, the children underwent spirometry, a standard test in which they take a deep breath and blow out as hard as they can.
Researchers also estimated the children’s exposure to outdoor air pollution from birth to age six, focusing on PM2.5 and NO2.
Genetic information from blood samples was used to calculate each child’s polygenic risk score for COPD. The score combines many small genetic differences that have previously been associated with the disease.
The researchers found that children with a higher genetic risk had lower growth in lung function during their first six years, but mainly when they had also been exposed to higher levels of PM2.5 pollution.
Among children living in areas with the highest exposure, where average PM2.5 levels were 15.3 μg/m³, the relationship was particularly clear. A similar pattern was observed among children exposed to higher levels of NO2, with an average exposure of 28.3 μg/m³.
Dr Carla da Silva Sena, of University Children’s Hospital Basel, the University of Basel and Bern University Hospital, 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 researchers say their findings do not mean that children with a higher genetic risk will inevitably develop COPD. Instead, they suggest that genes and environmental exposures such as air pollution may interact during a crucial period of lung development.
Dr da Silva Sena said: ‘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.’
The 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.
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.’
Photo: Artyom Kabajev
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