Observational analysis shows increased adhesion of traffic-related particles to red blood cells, highlighting potential systemic transport mechanisms.
Background There is indirect evidence that inhaled traffic-related particulate matter (PM) penetrates into the human circulation. Since nanoparticles readily adhere to red blood cells (RBCs) in vitro , we sought to determine whether a mechanism of systemic transport of translocated traffic-related particles is via adherence to RBCs in vivo . Methods Adult volunteers were exposed to traffic-related emissions from a main road for 1 h. Volunteers were also exposed to emissions wearing a FFP2 mask. Exposure to black carbon PM was assessed by portable aethalometer. The mean area (μm 2 ) of adherent black PM per RBC was determined from unstained blood smears from 3000 cells by light microscopy. Particle composition was determined by scanning transmission electron microscopy and energy dispersive x-ray analyses. The capacity of diesel exhaust particles (DEP) to adhere to human RBCs in vitro was determined, and RBCs were examined after intratracheal instillation of DEP to a mouse model. Results Exposure to traffic-related emissions increased personal black carbon PM (n=12, p=0.001 vs. baseline). Exposure increased the area of particles adherent to RBCs (p<0.001 versus baseline), and this was reduced by wearing a FFP2 mask (p=0.002 versus no mask). Traffic exposure increased the abundance of metal-bearing nanoparticles associated with RBCs. Diesel exhaust particles adhered to RBCs in vitro in a dose-dependent manner. Particles were found adherent to circulating RBCs after intratracheal diesel exhaust particles. Conclusion Adhesion of traffic-related PM to RBCs is a systemic transport mechanism. Quantification of particles on RBCs is a putative practical biomarker of inhaled dose.
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Grigg et al. (2025) studied this question.
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