Surface derivatization state of polystyrene latex nanoparticles determines both their potency and their mechanism of causing human platelet aggregation in vitro.

There is evidence that nanoparticles (NP) can enter the bloodstream following deposition in the lungs, where they may interact with platelets. Polystyrene latex nanoparticles (PLNP) of the same size but with different surface charge-unmodified (umPLNP), aminated (aPLNP), and carboxylated (cPLNP)-were used as model NP to study interactions with human blood and platelets. Both the cPLNP and the aPLNP caused platelet aggregation, whereas the umPLNP did not.