Dose and exposure duration |
Nanoparticle’s concentration in the medium multiplied by the exposure duration directly determines the number of nanoparticles in the body cells. |
[207,124] |
Aggregation and concentration |
Data on nanoparticles toxicity as a function of their concentration are not clear-cut. Higher nanoparticles concentrations favor their aggregation. As the size of nanoparticles aggregates is often in the micrometer range, aggregated nanoparticles may not easily enter cells, then their toxicity is decreased/abolished. |
[1] |
Nanoparticle size |
Nanoparticles’ size influences toxicity. For instance, cell penetration and toxicity are higher for small Ag NPs (~10 nm) than for Ag+ ions and larger Ag NPs (20–100 nm). |
[293] |
Nanoparticle morphology |
Nanoparticle’s toxicity varies in function of their aspect ratio. For instance, asbestos fibers of 10 µm in length may cause lung cancer, fibers between 5 and 10 µm may cause mesothelioma, and shorter fibers (2 µm) may cause asbestosis. |
[294] |
Surface area |
Nanoparticle’s toxicity progressively increases with smaller size and larger surface area. Moreover, nanoparticles and microparticles used at the same mass dose have different effects in human cells. |
[1] |
Crystal structure |
Nanoparticles’ crystal structure influences the cellular uptake, oxidative mechanisms, and subcellular localization. For instance, the two TiO2 NPs polymorphs (rutile and anatase crystal structures) display different toxic effects. In the dark, rutile TiO2 NPs (200 nm) cause DNA damage by oxidation and this manages not caused by anatase nanoparticles (200 nm). |
[2] |
Surface functionalization |
Nanoparticles’ surface functionalization (hydrophilicity and surface charge) strongly influences their translocation and oxidation and DNA damage. |
[266] |
Pre-exposure |
The phagocytic activity of cells may be promoted by shorter exposure times or by pre-exposure to NPs at lower doses (to somehow adapt the human body to that nanoparticle). |
[268] |