Children with a genetic predisposition to chronic obstructive pulmonary disease may experience slower lung growth if they are also exposed to higher levels of air pollution, according to research from Switzerland. The findings, presented at the European Respiratory Society Congress in Barcelona, suggest that COPD may not be solely a disease of aging as previously understood.
COPD is a progressive condition that causes chronic bronchitis and emphysema, leading to persistent airflow limitation, breathlessness, and coughing. While commonly linked to smoking and environmental exposures, the condition becomes more prevalent with age, affecting 12% of U.S. adults over 65 compared to 3.8% of adults over 18.
Study Tracks Children’s Lung Development
Researchers followed 484 children enrolled in the Basel–Bern Infant Lung Development cohort from infancy through approximately six years of age. The team calculated each child’s COPD polygenic risk score and compared it against repeated lung-function measurements over time. They also examined whether the relationship between genetic risk and lung function differed based on exposure to fine particulate matter (PM2.5) and nitrogen dioxide (NO2).
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Among children in the highest third of air pollution exposure, with average PM2.5 levels of 15.3 μg/m³ and NO2 levels of 28.3 μg/m³, a higher genetic-risk score corresponded to greater declines in lung-function scores from infancy through early childhood. This association was not observed in children with lower air-pollution exposure.
“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,” said lead investigator Carla da Silva Sena, PhD, a postdoctoral researcher from University Children’s Hospital Basel.
Implications for Early-Life Interventions
Da Silva Sena noted that COPD can develop either because lungs fail to reach their full growth potential during childhood or because lung function declines faster than expected later in life. Understanding these trajectories from the earliest stages may be key to developing preventive strategies.
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Whether these early differences in lung function translate into clinically significant COPD symptoms in adulthood remains uncertain. The children in this study were followed only to age six, leaving questions about long-term outcomes unanswered. It is possible that some children with slower early lung growth eventually catch up, while others may not. Continued tracking of this cohort into adolescence and beyond would help clarify which children face the greatest risk.
“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,” da Silva Sena said. “It reinforces that protecting air quality in early life may benefit children’s long-term health.”
The research adds to a growing body of evidence suggesting that genetic and environmental factors in early life may contribute to the foundations of respiratory disease. For policymakers, the findings may inform discussions around air quality standards and childhood health interventions in urban areas.
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