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Referee report. For: Neurotoxicity of nanoplastics: A review [version 1; peer review: 2 approved with reservations]
Summary
Researchers reviewed evidence that nanoplastics can penetrate the brain, induce oxidative stress leading to neuronal apoptosis, alter acetylcholinesterase activity and neurotransmitter levels, and produce behavioral changes in animal models, identifying particle size and exposure duration as key determinants of neurotoxic potential.
With the increase in plastic waste in the environment, it is undeniable that humans and most organisms are exposed to plastic particles of various sizes, including nanoplastics (NPs). Humans are at risk owing to various routes of entry, including ingestion, inhalation, and dermal contact. While the toxicity of NPs is still debatable due to the scarcity of resources and research, most studies have concluded that NPs may exert toxicity, which exacerbates their neurotoxicity potential. Earlier studies concluded that NPs can cause oxidative stress, which results in apoptosis of neuronal cells. Some studies have shown that NPs can affect fundamental cell functions by inducing physical stress through deposition. Furthermore, studies on in vivo models exposed to NPs have demonstrated behavioral changes that are presumably due to alterations in acetylcholinesterase activity and neurotransmitter levels. This review discusses studies conducted on the neurotoxic potential of NPs and their effects, which are dependent on several parameters, including size and type of NPs, exposure concentration, duration, and various models at risk of NP exposure. Furthermore, speculations on how NPs are related to neurotoxicity are also discussed.