Plastics in the Brain

Plastics have become an omnipresent feature of the modern world. Since their mass production in the 20th century, plastics have become an integral part of nearly every aspect of people’s daily lives and of our industries. However, effective disposal methods of plastics have remained elusive; only a fraction of manufactured plastics are recycled, with 12 million tons of plastics ending up in the world’s oceans alone every year. Over time these plastic items break down, forming nanoplastics (plastic items that range in size from 1 to 1,000 nanometers). The effects of these nanoplastics on animals is still largely unknown. Therefore, researchers working for the American Chemical Society sought to advance the field by examining the Bioeffects of Inhaled Nanoplastics on Neurons and Alteration of Animal Behaviors through Deposition in the Brain.

Before experimenting with live organisms, the researchers determined which concentration and size of nanoplastics would be most likely to reach the brains of mammals. The researchers tested fluorescent polystyrene nanoplastics PS-COOH and PS-NH2 with dimensions of 80, 100, and 200 square nanometers; fluorescent plastics were chosen to facilitate the rapid determination of plastic deposits in organs via imaging. To determine which size and type of nanoplastic would have the highest probability of entering the brain, the researchers used a microfluidic chip. A microfluidic chip is typically a glass or silicon slide with channels and a cell chamber etched into it which can accurately recreate cell to cell and cell-substrate interactions. The researchers injected the nanoplastics into the entrance of the microchannels and seeded neurons in the cell chamber. Overall, 80 nm PS-NH2 nanoplastics had the highest rate of success in entering the cell chamber. Therefore, the researchers opted to use 80 nm PS-NH2, and PS-COOH nanoplastics for further experimentation on mice.

The brains in animals are protected by the blood-brain barrier which is a selective permeability barrier that regulates the movement of substances between the bloodstream and central nervous system. Previous work has demonstrated that aerosolized molecules, especially when inhaled via the nasal cavity, can pass through the blood-brain barrier. Therefore, the researchers designed an airtight box for the mice, with an attached device to feed in a constant supply of air polluted with nanoplastics. A second group of mice were placed in an identical box configuration, but with unpolluted air being filtered in. The trial lasted for a total of seven days. During this period, the behavioral patterns of the mice were tracked. For the mice exposed to the aerosolized nanoplastics, the average speed of these mice decreased, while the speed of the mice exposed to unpolluted air increased each consecutive day. Additionally, the researchers defined a square in the middle of the containment box as “C” and tabulated the number of times the mice in both groups crossed into the box; leaving the edges of the containment vessel and crossing into the box in the center is an indicator of stress in mice. (Figure) The mice exposed to the aerosolized nanoplastics crossed into this space less frequently than the control mice, indicating they were less stressed.

Upon completion of the experiment, fluorescence imaging was used to determine the nanoplastic concentrations in the mice’s organs. The mice’s brains had the highest concentration of nanoplastics, demonstrating that aerosolized nanoplastics can pass through the blood-brain barrier and enter the brain. Additionally, a minimal amount of nanoplastics were observed in the mice’s livers and lungs, while no notable traces were found in their hearts, spleens, or kidneys.

Following the observation of behavioral differences between the mice in the group exposed to the nanoplastic polluted air and those not exposed, the researchers examined the mice to determine precisely what part of the neural system was being impacted by the nanoplastics. Previous experiments have shown that Acetylcholinesterase (AChE) activity is a strong indicator of neurotoxicity in organisms; it is an enzyme that acts to terminate signals between neurons. Therefore, AChE activity in the mice was measured—its activity within the group exposed to nanoplastics was significantly reduced compared to those not exposed. Additionally, the mice exposed to nanoplastics exhibited higher levels of cerebral inflammation compared to those not exposed to nanoplastics. The researchers posited that these two factors, AChE activity inhibition and inflammation, led to the behavioral changes within the mice, supporting the concept that nanoplastic inhalation can cause neurotoxicity in mammals.