NANOPLASTICS WORSEN PARKINSON’S SIGNS IN WORMS, HUMAN NERVE CELLS

Exposure to nanoplastics, micro-sized fragments of plastic waste found in the environment, mimicked the signs and symptoms of Parkinson’s disease in tiny worms and in human nerve cells in the lab, a study reported.

Low concentrations of nanoplastics were found to penetrate the walls of the worms’ intestines and spread throughout the body, slowing the animals’ growth and altering their movements. In worms and human cells, nanoplastics also increased the number of toxic aggregates, or clumps, of alpha-synuclein protein, which are thought to contribute to nerve cell death in Parkinson’s.

The researchers say their findings highlight the need for further study into the possible health risks associated with these tiny fragments, given their increasing prevalence in the environment due to widespread use of plastics.

“This [study] underscores the urgent need to understand the interactions of nanoplastics with biological systems and highlights potential environmental and health consequences,” the researchers wrote.

The study, “Nanoplastics exacerbate Parkinson’s disease symptoms in C. elegans and human cells,” was published in the Journal of Hazardous Materials.

Investigating the potential threat of these tiny plastic particles

Parkinson’s disease is thought to be caused by a combination of genetic susceptibility and environmental factors — to include exposure to heavy metals, air pollution, agricultural chemicals, and other toxins in the air, land, and water.

In recent years, there has been a global rise in the production and use of plastics. Plastic waste can break down into tiny fragments called microplastic particles, which are between 100 nanometers (nm) and five millimeters in size. Such waste also can deteriorate into even smaller nanoplastics that are less than 100 nm — about 1,000 times smaller than a strand of human hair.

Because of their tiny size, microplastics or nanoplastics can be unintentionally consumed and accumulate in digestive systems, with nanoplastics even penetrating certain tissues. Some studies now are suggesting links between nanoplastics and neurological disorders, including Parkinson’s and Alzheimer’s disease.

However, according to researchers in South Korea, “the effects and mechanisms of these nanoplastic particles on the development of [Parkinson’s disease] are still uncertain.”

To learn more, the team examined the effects of nanoplastics exposure on human nerve cells and nematode worms called Caenorhabditis elegans, or C. elegans. These tiny worms are widely used in research because roughly 30%-60% of their genes have the same function as human genes. Moreover, C. elegans and humans share several age-associated biological features.

In the lab, the team exposed the worms to different doses of polystyrene nanoplastic beads with a diameter of 25 nm and monitored their ability to swim, a motion called thrashing. The most dramatic reduction in thrashing occurred at a lower dose rather than at higher doses. Seven days of exposure significantly decreased thrashing compared with five days, which had no effect.

“Prolonged exposure to nanoplastics showed more pronounced effects on animal mobility,” the researchers wrote, noting that this suggested that “nanoplastic exposure may affect the neurophysiology in C. elegans.”

In worms, nanoplastics linked to nerve cell degeneration

It is known that weathered plastics can acquire electrical charges on their surface — neutral, positive, or negative — that may lead to different effects. Here, exposure to neutral or negatively charged nanoplastic beads decreased worm body length, while positively charged particles reduced the thrashing frequency.

With short-term exposure (one day), all three types of nanoplastic beads were found in the throat and intestines of the worms; some worms showed more negatively charged nanoplastics in the head region. During long-term exposure (seven days), the beads spread across most worms’ entire head region and penetrated the outside of the intestines.

Using a blue food dye, the researchers confirmed that, in about 13% of worms, nanoplastic beads had penetrated the intestinal walls and spread throughout the worm body, a condition referred to as “leaky gut.” Positively charged particles showed the highest level of gut penetration.

An examination of worm muscle cells showed long-term positively charged nanoplastic exposure led to the fragmentation of mitochondria, the structures within cells that produce energy, perhaps contributing to movement abnormalities, the team suggested.

All three types of nanoplastics were found to worsen the degeneration of the worms’ dopaminergic neurons — nerve cells that produce the chemical messenger dopamine, which dies in people with Parkinson’s, causing disease. In addition, exposure to neutral or negatively charged nanoplastics dramatically increased the number of toxic alpha-synuclein clumps within dopaminergic neurons.

“These findings indicate a potential association between nanoplastic exposure and neurodegenerative alterations seen in [Parkinson’s disease],” the researchers wrote.

Finally, neutral nanoplastic beads were able to penetrate human nerve cells, mostly into the cytosol outside the nucleus, and increased the levels of alpha-synuclein clumps by about 50% over controls.

“As the prevalence of these nanoplastics in the environment continues to grow, understanding their effects on health becomes paramount,” the researchers concluded.

“While our study sets the stage for understanding these interactions, it also underscores the pressing need for more comprehensive studies and increased scrutiny of plastic pollutants,” the te