Exposure to respirable desert dust entering indoors prompts quick oxidative-stress and inflammatory responses in the airways of chronic heart failure patients

A significant portion of the population is exposed to airborne PM₁₀ levels exceeding WHO guidelines, particularly during desert dust events, which are increasing due to climate change. Cardiovascular mortality has been linked to PM₁₀ exposure, but most studies rely on outdoor air quality data that may not reflect indoor exposure. This study, DESERT HEART, examines whether indoor PM₁₀ exposure during dust events influences airway inflammation and oxidative stress in 40 patients with stable chronic heart failure (HF). Sputum samples were collected weekly for three weeks, and biomarkers (IL-8, MDA, MMP-9, TGF-ß1, CRP) were analyzed. Indoor PM₁₀ levels were monitored at patients' homes. Mixed regression models assessed the impact of PM₁₀ ≥ 90 µg/m³ on biomarkers. Analysis of 120 sputum samples and 720 days of air quality data showed that exposure significantly increased biomarker levels on the first day: IL-8 (+ 6.9 ng/gwt, p = 0.032), MDA (+ 1.3 nmol/gwt, p = 0.014), MMP-9 (+ 222.4 ng/gwt, p = 0.09), TGF-ß1 (+ 4.1 ng/gwt, p = 0.058), and CRP (+ 2 ng/gwt, p = 0.02), followed by a sharp decline. These findings suggest that indoor PM₁₀ exposure from desert dust events acutely exacerbates airway inflammation and oxidative stress in HF patients, highlighting the need for targeted interventions.