We have discovered functionalized multiwalled carbon nanotubes with reduced protein-binding, cytotoxicity, and immune response and the associated structure-activity relationships using in silico surface molecular diversity design, combinatorial library synthesis, and multiple biological screenings. Our results demonstrated the general utility of the nanocombinatorial library approach in nanomedicine and nanotoxicity research.

The application of nanoparticles in consumer products and nanomedicines has increased dramatically in the last decade. Concerns for the nano-safety of susceptible populations are growing. Due to the small size, nanoparticles have the potential to cross the placental barrier and cause toxicity in the fetus. This review aims to identify factors associated with nanoparticle-induced fetotoxicity and the mechanisms involved, providing a better understanding of nanotoxicity at the maternal–fetal interface. The contribution of the physicochemical properties of nanoparticles (NPs), maternal physiological, and pathological conditions to the fetotoxicity is highlighted. The underlying molecular mechanisms, including oxidative stress, DNA damage, apoptosis, and autophagy are summarized. Finally, perspectives and challenges related to nanoparticle-induced fetotoxicity are also discussed.

Airborne particular matter (PM2.5) contains complex mixtures of pollutants, and their compositions also vary with time and location. Inhalation of PM2.5 may cause a number of diseases, such as bronchial and lung inflammation and lung cancer. So far, how different components of PM2.5 contribute to inflammation and toxicity is still not known. To identify key PM2.5 components that are responsible for inflammation, here we took a reductionism approach and synthesized a model PM2.5 library containing 20 carbon nanoparticle based members with loadings of As­(III), Pb2+, Cr­(VI), and BaP individually or in combination at environment relevant concentrations. We discovered that only carbon nanoparticle–Pb2+ adducts, not other pollutants or adducts, induced inflammation in human bronchial cells by suppressing the expression of a novel long noncoding RNA lnc-PCK1-2:1, while lnc-PCK1-2:1 routinely plays a regulatory role in inhibiting inflammation. This finding was further substantiated by varying Pb2+ loadings on carbon nanoparticles and overexpressing lnc-PCK1-2:1. The success of this approach opens an avenue for further elucidation of molecular mechanisms of PM2.5-induced inflammation and toxicity.