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News
Genes and pollution make a harmful combination for developing lungs. A new study finds that babies born with a higher genetic risk for COPD show measurable differences in lung function development — but only when they grow up in areas with elevated air pollution. The findings suggest that environmental exposure may be a key factor that interacts with inherited respiratory risk in early childhood.
A study presented at the European Respiratory Society (ERS) annual congress in Barcelona reveals that a genetic predisposition to COPD doesn't act in isolation — it appears to interact with air pollution exposure to shape how children's lungs develop from infancy through early childhood.
Researchers from the University of Bern analyzed lung function data from 484 infants in the Basel-Bern Infant Lung Development cohort, tracking them from 44 weeks of age through age 6. They found that a higher COPD polygenic risk score (PRS) was associated with reduced lung function measures — but only in children exposed to the highest levels of fine particulate matter (PM2.5) and nitrogen dioxide (NO2). Children in lower pollution zones showed no significant association.
Why it matters: These findings highlight that genetic respiratory risk and environmental pollution are not independent threats — they compound each other. For clinicians and public health officials, this underscores the importance of early identification of at-risk infants and prioritizing clean air interventions in communities where genetically vulnerable children live.
