A18-03 Personal Pm2.5 Exposure Is an Important Environmental Risk Factor for Sleep Oxygen Desaturation During Sleep in COPD Patients: A Prospective Repeated-measure Study

Abstract Rationale Sleep-related breathing disorders are common in patients with chronic obstructive pulmonary disease (COPD), primarily characterized by decreased oxygen saturation (SpO2) and frequent episodes of hypoxemia. Airborne fine particulate matter (PM2.5) pollution is a primary risk factor for COPD. However, the association between PM2.5 exposure and hypoxemia risk during sleep in COPD patients remains unclear. Methods This prospective repeated-measure study included 96 COPD patients with real-time personal monitoring of PM2.5 and SpO2 during sleep (84,971 observations), aiming to investigate the association of PM2.5 with oxygen desaturation and identify susceptible individuals by smoking and inflammatory phenotypes. Personal exposure levels to PM2.5 were continuously monitored in real-time for 24 hours at 1-min sample intervals. Real-time monitoring of SpO2 during sleep was carried out simultaneously with a ring-type pulse oximeter. SpO2 90% was defined as oxygen desaturation. Non-invasive exhaled breath biomarkers were used to assess airway inflammation in COPD patients. Additionally, based on the counts and percentages of blood neutrophils and eosinophils, systemic inflammatory phenotypes of COPD patients were categorized. Generalized linear mixed model were applied to estimate the association of personal PM2.5 exposure with the risk of oxygen desaturation, respectively. Results Personal PM2.5 exposure was significantly associated with sleep SpO2 decline within hours. From lag 0 to lag 0-7h, the decrease in SpO2 increased from 0.07% (95%CI: -0.10%, -0.05%) to 0.22% (95%CI: -0.25%, -0.20%) for an interquartile range (IQR) increase of 22.4 μg/m3 in PM2.5 concentration, and the odds ratio (OR) for oxygen desaturation increased from 0.96 (95%CI: 0.90, 1.03) to 1.16 (95%CI: 1.08, 1.25). The highest risk of oxygen desaturation associated with PM2.5 was observed in current smokers (OR = 1.53, 95%CI: 1.22, 1.92), followed by former smokers (OR = 1.14, 95%CI: 1.02, 1.28), with no significant effect in never smokers.Notably, current smokers exhibited higher neutrophilic inflammation, and those with higher airway neutrophilic inflammation were more susceptible to PM2.5-related oxygen desaturation (P-interaction0.001). For former smokers, those with higher small-airway eosinophilic inflammation were more susceptible (P-interaction0.001). Both former and current smokers with a systemic mixed granulocyte phenotype were at greater risk of oxygen desaturation. Furthermore, individuals with constant high inflammation are more susceptible to PM2.5-related oxygen desaturation than those without inflammation. Conclusions Airborne PM2.5 is an important risk factor for sleep hypoxia in COPD patients, especially for individuals with smoking history and specific inflammatory phenotypes. This abstract is funded by: This work was supported by the National Natural Science Foundation of China (No. 22376005, 22076006, 82090014, 91543112), the Capital Health Development Research Project (No. 2020-2Z-40917).