Speaker: Yutong Cai
Asthma and chronic obstructive pulmonary disease (COPD) are prevalent respiratory disorders that often share common symptoms, including shortness of breath and chest tightness. While most asthma patients do not progress to COPD, approximately 10-31% may develop COPD over time, known as asthma-COPD overlap (ACO). Identifying risk factors for this progression is crucial. Environmental factors such as poorly controlled asthma, tobacco smoke, and air pollution are significant contributors to the development of COPD in asthma patients. Traffic-related air pollutants, specifically particulate matter (PM2.5) and nitrogen dioxide (NO2), are of particular interest. Genetic susceptibility also plays a role, with higher genetic risk scores exacerbating the effects of these pollutants. A study using the UK Biobank cohort analyzed the impact of traffic-related air pollution on the risk of asthma patients developing COPD. Genetic risk scores, derived from a genome-wide association study (GWAS), were categorized into high, medium, or low risk. The study employed cross-sectional hazard regression analysis, adjusting for various individual-level risk factors. The results indicated that increased exposure to traffic-related air pollutants correlates with a higher risk of progression from asthma to COPD. Specifically, each interquartile increase in PM2.5 and NO2 was associated with a 6% and 10% increased risk, respectively. Adverse effects were observed at relatively low concentrations (8 microgram/m3 for PM2.5 and 12 microgram/m3 for NO2), highlighting that pollution levels in many urban environments could exacerbate these risks.
Gene-environment interactions revealed that individuals with high genetic risk are particularly susceptible to the adverse effects of air pollution. No significant associations were found with larger particulate matter (PM10), indicating that fine particulate matter and NO2 are more pertinent in this context. Limitations of the study include reliance on baseline exposure data, which may not reflect long-term exposure accurately. Changes in smoking status and body mass index (BMI) over time were not considered, and the lack of clinical data limits the ability to differentiate between various ACO phenotypes. Future research should focus on collecting detailed clinical data and comparing asthma patients with healthy controls to better understand these dynamics.
In conclusion, increased exposure to PM2.5 and NO2 significantly heightens the risk of asthma progressing to COPD, particularly among individuals with high genetic susceptibility. Future studies should aim to incorporate comprehensive clinical data and investigate the comparative risk in healthy controls to enhance understanding and management of ACO.
European Respiratory Society Congress 2024, 7–11 September, Vienna, Austria