Demonstrates the cytotoxicity of mineral dusts in racehorses, indicating contributions to respiratory health issues and inflammasome activation.
Air quality is key determinant of respiratory health in humans and animals. Within a One Health framework, racehorses represent a valuable sentinel model for studying the effects of mineral dusts originating from soil surfaces, as they share similar environmental exposure conditions and high ventilation rates with humans during intense activity. Lower airway inflammatory conditions are frequently diagnosed in racehorses and are often associated with dust exposure; however, the specific contribution of inorganic mineral dust, such as respirable crystalline silica (RCS), remains largely understudied. This study investigates the physicochemical characteristics and cytotoxic potential of inorganic particulate matter (iPM) derived from seven mineral-rich racetrack soils. Fine soil fractions (<20 µm) were isolated to represent the respirable component. Scanning Electron Microscopy (SEM) revealed that the fine fractions were mainly composed of particles within the respirable size range, while X-Ray Powder Diffraction (XRPD) identified heterogeneous mineral assemblages dominated by silicates, aluminosilicates, carbonates, and Fe–Ti oxides. Surface reactivity tests showed low oxidative potential, whereas haemolysis assays indicated variable membranolytic activity, reflecting compositional differences among samples. In vitro analysis on equine macrophages showed a concentration-dependent reduction in viability, consistent with the membrane damage observed in the haemolysis assay. Similar patterns were observed in adenocarcinomic human alveolar cells (A549 VIM-RFP) using Alamar Blue and Calcein assays, confirming a dose-dependent cytotoxic response. In two of seven soils, cytotoxicity did not correlate linearly with crystalline silica content, suggesting that mineral composition and surface reactivity mutually modulate cytotoxicity effects. Ongoing studies on human macrophages aim to elucidate inflammasome activation and identify early metabolic alterations induced by mineral dust exposure.
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Giuli et al. (2026) studied this question.
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