Nanoparticles: Weighing the Pros and Cons from an Eco-genotoxicological Perspective

Abstract

The exponential growth of nanotechnology and the industrial production have raised concerns over its impact on human and environmental health and safety (EHS). Although there has been substantial progress in the assessment of pristine nanoparticle toxicities, their EHS impacts require greater clarification. In this review, we discuss studies that have assessed nanoparticle eco-genotoxicity in different test systems and their fate in the environment as well as the considerable confounding factors that may complicate the results. We highlight key mechanisms of nanoparticle-mediated genotoxicity. Then we discuss the reliability of endpoint assays, such as the comet assay, the most favored assessment technique because of its versatility to measure low levels of DNA strand breakage, and the micronucleus assay, which is complementary to the former because of its greater ability to detect chromosomal DNA fragmentation. We also address the current recommendations on experimental design, including environmentally relevant concentrations and suitable exposure duration to avoid false-positive or -negative results. The genotoxicity of nanoparticles depends on their physicochemical features and the presence of co-pollutants. Thus, the effect of environmental processes (e.g., aggregation and agglomeration, adsorption, and transformation of nanoparticles) would account for when determining the actual genotoxicity relevant to environmental systems, and assay procedures must be standardized. Indeed, the engineered nanoparticles offer potential applications in different fields including biomedicine, environment, agriculture, and industry. Toxicological pathways and the potential risk factors related to genotoxic responses in biological organisms and environments need to be clarified before appropriate and sustainable applications of nanoparticles can be established.

Keywords: DNA damage; Genotoxicology; Nanoparticles; Nanotoxicology; Risk assessment.

Figure 1. Schematic diagram illustrating (A) transformation of nanoparticles (NPs) in environmental systems and (B) key mechanisms underlying the toxicity of transformed NPs relative to pristine particles.

NPs may encounter physical-, chemical-, or biological-based transformations in different environmental media, i.e., air, soil, and water. The physicochemical traits of NPs in combination with environmental features determines the transformation pathway. During the transformation process, NPs may interact with other co-pollutants and biomacromolecules, thereby resulting in the alteration of physicochemical traits, bioavailability, and differential toxic responses mediated by transformed versus pristine NPs. In an environmental viewpoint, the potential toxicity of transformed NPs not only relies on physicochemical traits (e.g., size and size distribution, charge, coating, aggregation/agglomeration state) but also on the presence of co-pollutants (e.g., heavy metals, organic pollutants etc.) as well as interaction with biomolecules in living organisms (e.g., proteins). MNPs, Magnetic nanoparticles; IS, Ionic strength; OM, organic matter; NOM, natural organic matter.

Figure 2. A scheme representing the potential toxicological effects of nanoparticles (NPs) after environmental transformation.

Environmentally transformed NPs may induce ecotoxicity in terms of cellular, molecular, developmental, or heredity toxicity in airborne, soil, and aquatic organisms. The deleterious molecular effects mediated by the transformed NPs, including membrane shrinkage, mitochondria dysfunction, lysosomal interference, and DNA damage, may differ from those mediated by pristine particles. MNPs, Magnetic nanoparticles; ROS, reactive oxygen species.

Figure 3. A schematic overview indicating main genotoxicity pathways of nanoparticles.

The direct pathway of nanoparticle-induced genotoxicity is mediated by the physical interaction of nanoparticles with genetic components, whilst the indirect pathway is based on the induction of ROS (e.g., hydroxyl, peroxide, and superoxide radicals) and perturbance of replication- and transcription-related proteins. ROS, reactive oxygen species.