Toxicity of nanoparticles_ challenges and opportunities

Abstract

Nanomaterials (NMs) find widespread use in different industries that range from agriculture, food, medicine, pharmaceuticals, and electronics to cosmetics. It is the exceptional properties of these materials at the nanoscale, which make them successful as growth promoters, drug carriers, catalysts, filters and fillers, but a price must be paid via the potential toxity of these materials. The harmful effects of nanoparticles (NPs) to environment, human and animal health needs to be investigated and critically examined, to find appropriate solutions and lower the risks involved in the manufacture and use of these exotic materials.The vast number and complex interaction of NM/NPs with different biological systems implies that there is no universal toxicity mechanism or assessment method. The various challenges need to be overcome and a number of research studies have been conducted during the past decade on different NMs to explore the possible mechanisms of uptake, concentrations/dosage and toxicity levels. This review article examines critically the recent reports in this field to summarize and present opportunities for safer design using case studies from published literature.

Keywords: Ecotoxic; Mechanisms of uptake; Nanoparticles; Risk assessment; Safer design; Testing protocols.

Fig. 1

A schematic diagram showing the ways in which contaminants in the NMs, NM agglomeration, interactions between the organism and NM coating, release of dissolved ions, or interference from the NM with the assay measurement (i.e., absorbance) can potentially cause inaccurate dosing or artefacts in nano-ecotoxicology assays. Reprinted with permission from the American Chemical Society (Petersen et al. 2014)

Fig. 2

Proposed research prioritization for generating an effective PC ID to form an Intelligent Testing Strategy (Stone et al. 2014)

Fig. 3

Schematics to explain the cellular mechanisms leading to the pro-fibrogenic effects of REOs. The internalization of REOs by macrophages and lysosomal biotransformation, and triggering of events culminating in pulmonary fibrosis. The inserted panel at the bottom shows that the molecular mechanism of lysosomal damage is phospholipid dephosphorylation and nucleation of REPO₄ on the NP surface

Fig. 4

Graphical abstract (Naatz et al. 2017). Reproduced with permission from the American Chemical Society