Nano- and neurotoxicology: An emerging discipline

Abstract

The present critical review analyzes the question of how nanoparticles from continuously growing industrial production and use of nanomaterials may impact human brain health. Available evidence suggests incomplete effectiveness of protective barriers of the brain against nanoparticles translocation to the brain. This raises concerns of potential effects of manufactured nanoparticles on brain functions, given that nanoparticle's potential to induce oxidative stress, inflammation, death by apoptosis, or changes in the level of expression of certain neurotransmitters. Most concerns have not been studied sufficiently and many questions are still open: Are the findings in animals transposable to humans? What happens when exposure is chronic or protracted? What happens to the developing brain when exposure occurs in utero? Are some nanoparticles more deleterious, given their ability to alter protein conformations and aggregation? Aside from developments in nanomedicine, the evidence already available fully justifies the need to specifically evaluate the interactions between nanoparticles and the nervous system. The available data clearly indicates the need for original dedicated experimental models and tools for neurotoxicological research on the one hand, and the need for epidemiological studies of neurodegenerative diseases in manufactured nanoparticle-exposed populations, on the other. A combination of nanotoxicology with neurology in a novel discipline, with its specific tools and methods of investigation, should enable answering still unresolved questions.

DNA damage in BV‐2 cells: An important supplement to the neurotoxicity of CdTe quantum dots

“…That makes them ideal for in vivo imaging and immunofluorescence (Minami et al, 2012;Zhang, 2013). Additionally, QDs were discovered to be quickly transported from the nose to the brain primarily by olfactory uptake and via fast axonal transport (Bencsik, Lestaevel, & Canu, 2017). Thus, it is essential to evaluate the biosafety of CdTe QDs in the central nervous system (CNS).…”

Reference ranges of oxidative stress biomarkers selected for non-invasive biological surveillance of nanotechnology workers: Study protocol and meta-analysis results for 8-OHdG in exhaled breath condensate

“…Despite a paucity of epidemiological data regarding the health effects of engineered nanomaterials (ENMs) , both human and animal experiments reported that ENMs elicited activation of inflammatory and oxidative stress responses that could be monitored in different biological matrices as preclinical alterations (Bencsik et al 2018;Schulte et al 2019). Such preclinical alterations may function both as indicators of early effects before J o u r n a l P r e -p r o o f clinical manifestations may occur and as indirect markers of exposure, although with a low specificity for ENMs (Schulte et al 2019).…”

“…Nevertheless, the choice of appropriate biological matrix for a biomarker validation for non-invasive biological J o u r n a l P r e -p r o o f monitoring in occupational setting has a paramount importance. For ENMs, the respiratory tract is the primary route of exposure in occupational settings, thus the respiratory system plays a central role in the toxicokinetic and toxicodynamic profile of ENMs (Bencsik et al 2018;Schulte et al 2019). ENMs may enter other human organs and generate toxicity after they are absorbed into the bloodstream through the respiratory systems (Mu et al 2014).…”

Predisposition to Alzheimer’s and Age-Related Brain Pathologies by PM2.5 Exposure: Perspective on the Roles of Oxidative Stress and TRPM2 Channel

“…There is growing evidence to show that exposure to polluted ambient air is also injurious to the brain (Brockmeyer and D'Angiulli, 2016;Clifford et al, 2016;Power et al, 2016;Babadjouni et al, 2017;Cohen et al, 2017;Sripada, 2017;Underwood, 2017;Bencsik et al, 2018). Among other air pollutants, the fine particulate matters (PM) with an aerodynamic diameter of <2.5 µm (PM2.5), which include ultrafine PM with a size of <200 nm (PM0.2) and nanometersized PM (nPM) or nanoparticles (NPs), has attracted particular attentions for their potential damage to the brain because they more readily enter the brain; they can penetrate the olfactory epithelium and, alternatively and/or additionally, travel deep into the airways and lungs, infiltrate into the blood circulation, and finally cross the blood-brain barrier (BBB) (Heusinkveld et al, 2016;Maher et al, 2016;Underwood, 2017;Bencsik et al, 2018). Such tiny particles in ambient air can be mainly derived from diesel exhaust (DE) and traffic/combustion-related air pollution, and also increasingly result from manufacturing, application, and subsequent release of nanomaterials (Bencsik et al, 2018).…”

“…Among other air pollutants, the fine particulate matters (PM) with an aerodynamic diameter of <2.5 µm (PM2.5), which include ultrafine PM with a size of <200 nm (PM0.2) and nanometersized PM (nPM) or nanoparticles (NPs), has attracted particular attentions for their potential damage to the brain because they more readily enter the brain; they can penetrate the olfactory epithelium and, alternatively and/or additionally, travel deep into the airways and lungs, infiltrate into the blood circulation, and finally cross the blood-brain barrier (BBB) (Heusinkveld et al, 2016;Maher et al, 2016;Underwood, 2017;Bencsik et al, 2018). Such tiny particles in ambient air can be mainly derived from diesel exhaust (DE) and traffic/combustion-related air pollution, and also increasingly result from manufacturing, application, and subsequent release of nanomaterials (Bencsik et al, 2018). In general, the smaller their size, the greater their capacity of inducing oxidative stress and thus the more severe the resulting cytotoxicity is (Underwood, 2017).…”