Children with an inherited risk for COPD show slower lung growth when exposed to higher levels of air pollution during early childhood.
RT’s Three Key Takeaways:
- Gene-Environment Interaction: Children carrying a higher genetic risk for COPD exhibited reduced lung function growth between birth and 6 years of age only when exposed to elevated levels of air pollution.
- Early Lung Trajectories: The foundational stages of adult respiratory disease can take shape during infancy and early childhood before any clinical symptoms appear.
- Clean Air Protection: Targeted environmental regulations and air quality protections may prevent vulnerable children with inherited predispositions from developing long-term respiratory impairment.
The origins of COPD may take root decades before clinical diagnosis through early lung development trajectories influenced by environmental exposures, according to findings presented at ERS 2026.
Researchers found that infants born with a higher genetic predisposition for COPD showed reduced lung function growth between birth and age 6, but this trajectory occurred exclusively in children exposed to elevated concentrations of ambient air pollution.
“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,” said Carla da Silva Sena, researcher at University Children’s Hospital Basel UKBB, University of Basel, and Bern University Hospital.
“We believe that COPD can result from lung function ‘trajectories’ established early in life,” said da Silva Sena, researcher at University Children’s Hospital Basel UKBB. “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.”
Tracking Early Lung Growth
The study evaluated 484 children enrolled in the Basel-Bern Infant Lung Development (BILD) study, an ongoing Swiss birth cohort tracking infants born between 1999 and 2020, according to the presentation. Investigators measured baseline infant lung function within the first month of life via tidal breathing tests during sleep, followed by spirometry testing at 6 years of age, the study reported.
Using blood samples, the research team calculated each child’s polygenic risk score based on adult COPD genetic markers, according to the research team. They then paired this genetic data with individual exposure assessments for fine particulate matter (PM2.5) and nitrogen dioxide (NO2) from birth through age 6.
Analysis revealed that higher polygenic risk scores were aligned with significantly diminished lung growth only among children residing in areas with higher PM2.5 levels, averaging 15.3 μg/m³. In contrast, children living in environments with cleaner air showed a substantially weaker association between genetic risk and lung growth suppression, the investigators noted. A similar interaction occurred at higher levels of NO2 exposure, which averaged 28.3 μg/m³, the study found.
“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 da Silva Sena.
“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,” said da Silva Sena.
Implications for Respiratory Healthcare
Investigators plan to track the cohort through adolescence and adulthood to evaluate whether these early developmental discrepancies persist or widen over time, according to the study authors.
The authors acknowledged study limitations, including the necessity of applying statistical techniques to align different lung function testing modalities between newborns and 6-year-olds, as well as relying on a polygenic risk score derived primarily from European cohorts.
“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,” said Barbara Hoffmann, chair of the European Respiratory Society advocacy council.
“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,” said Hoffmann.
“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,” she added.
