IMPACT OF INDOOR AIR POLLUTION ON INFLAMMATORY BIOMARKERS AND CARDIAC AUTONOMIC CONTROL IN HEALTHY SUBJECTS AND PATIENTS WITH CONGESTIVE HEART FAILURE (APICE STUDY)

The present study explores the modifications of cardiac autonomic control (CAC) during sleep and of systemic inflammatory profile associated with exposure to indoor air pollution (IAP) in healthy subjects and patients affected by chronic heart failure (HF). Twenty healthy volunteers and nineteen HF patients were enrolled. Indoor levels of fine particulate matter (PM2.5), nitrogen dioxide (NO2) and volatile organic compounds (VOCs) were monitored using a portable detector for 7 days. Together, a 7-day monitoring was performed through a wireless patch that continuously recorded electrocardiogram, respiratory activity and actigraphy. Indexes of CAC during sleep were derived from the biosignals: heart rate and low-frequency to high-frequency ratio (LF/HF) index of sympathovagal balance with higher values corresponding to a predominance of the sympathetic branch. Cyclic variation of heart rate index (CVHRI events/hour) during sleep, a proxy for the evaluation of sleep apnoea, was assessed for each night. After the monitoring, blood samples were collected to assess the inflammatory profile. Regression and correlation analysis were performed. A positive association between CVHRI during sleep and indoor air pollutants was found, with VOCs affecting healthy subjects (Δ%=+0.2% for 1µg/m3 VOCs, p=0.008) and NO2 impacting patients (Δ =+0.86 events/h for 10% increase in NO2, p=0.022. The CVHRI was also positively associated with LF/HF during sleep, thus higher CVHRI values corresponded to a shift of the sympathovagal balance towards a sympathetic predominance in healthy subjects (r=0.52; p=0.018). Indoor PM2.5 exposure was positively correlated with elevated plasmatic levels of TNF-α in patients (Δ%=17.18 for 10% increase in PM2.5, p=0.006). Indoor NO2 exposure levels were associated with increased plasmatic pro-inflammatory (sTREM-1) and anti-inflammatory (IL-10) biomarkers in healthy subjects (Δ%=+1.2% and Δ%=+2.4%, for 1µg/m3 NO2; p=0.005 and p=0.022, respectively), alongside upregulated expression of pro-inflammatory (IL-6 Δ%=8.94% for 10% increase in NO2, p=0.026; TREM-1 Δ%=6.60% for 10% increase in NO2, p=0.025) and anti-inflammatory (IL-10 Δ%=4.18 for 10% increase in NO2, p=0.037) pathways in patients. The study highlights a possible causal relationship between IAP exposure and higher risk of sleep apnoea events, associated with impaired CAC during sleep, and an altered inflammatory state both in healthy subjects and patients. The findings of this study have significant implications for both clinical practice and public health strategies, particularly in the context of improving cardiovascular health by addressing indoor air quality. The IAP could emerge as a critical and often neglected risk factor for the public health that can be addressed through targeted preventive interventions.