Tiny fragments of plastic commonly found in food, water and air may interfere with critical brain cells that regulate puberty and fertility, according to new research that is raising fresh concerns about the health impacts of environmental plastic pollution.
The study, published in the journal Small, found that polystyrene nanoplastics — particles thousands of times smaller than a grain of sand — can enter and disrupt specialized brain cells known as gonadotropin-releasing hormone (GnRH) neurons.
These neurons act as master regulators of reproductive development, controlling the onset of puberty and coordinating fertility throughout life.
GnRH neurons signal the pituitary gland to activate the ovaries or testes. Even minor disturbances in their function can delay puberty, disrupt menstrual cycles, reduce sperm production or impair fertility. When such disruptions occur during early development, the consequences may be long-lasting or permanent.
Researchers reported that polystyrene nanoplastics were able to enter both immature and mature GnRH neurons through an unusual cellular pathway, effectively bypassing the cells’ usual protective entry controls.
Once inside, the particles accumulated within the cells and triggered several harmful changes. Hormone production dropped, movement of immature neurons slowed, and the activity of genes essential for reproductive health was altered.
“These results suggest that polystyrene nanoplastics disrupt key physiological functions of GnRH neurons and may act as novel endocrine disruptors, contributing to the pathogenesis of reproductive disorders,” the authors wrote.
One of the most significant findings was a reduction in the activity of the gene responsible for producing GnRH, leading to lower hormone release in mature neurons.
The study also found that exposure increased reactive oxygen species — a marker of cellular stress — in developing neurons.
Although the stress did not kill the cells, it reduced their ability to migrate. Proper migration during early development is essential because GnRH neurons must travel to precise locations in the brain to establish lifelong reproductive signaling.
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Particle size proved to be a key factor. Very small particles (50 nanometers) were able to enter cells but did not significantly impair movement. Larger particles (500 nanometers) caused stronger disruptions, slowing or even blocking migration of immature neurons. These cells became more rigid and overly “sticky,” reducing their ability to move properly.
Analysis revealed widespread changes in hundreds of genes involved in neuron movement, attachment, brain development and hormone regulation. Many of these gene patterns overlapped with those associated with delayed puberty and hypogonadism in humans.
To explore real-world relevance, researchers compared their laboratory findings with genetic data from patients with pubertal delay and gonadotropin deficiency. They identified rare variants in one gene, NPAS2, in two males with severe delayed puberty. Another gene linked to puberty timing also showed overlap with the cellular findings.
The researchers emphasized that the study was conducted using mouse-derived cell lines commonly used to model GnRH neurons and does not prove that nanoplastics cause infertility in humans. However, they said the results highlight a plausible biological pathway through which plastic pollution could affect reproductive health.
Microplastics and nanoplastics are increasingly detected in human tissues, including placenta, brain tissue, semen, ovaries, follicular fluid and breast milk. They enter the body through ingestion, inhalation or skin contact.
Animal studies have previously linked plastic nanoparticle exposure to disrupted hormone signaling and reduced fertility.
Recent research has also shown that 50-nanometer plastic particles can enter cow eggs and interfere with early reproductive development.
Scientists warn that plastic particles may cause harm not only through direct cellular interaction but also by carrying endocrine-disrupting chemicals that amplify hormonal disruption.
Such effects could impair gametogenesis — the process of producing sperm and eggs — and potentially contribute to declining fertility rates observed in some populations worldwide.
Although polystyrene is widely used in research, humans are exposed to many types of micro- and nanoplastics, including polyethylene and PVC, in various sizes and shapes.
The authors concluded that plastic pollution may represent a previously underappreciated environmental contributor to disorders such as GnRH deficiency, which cannot always be explained by genetics alone.
“Beyond direct effects on GnRH neurons, our findings contribute to broader concerns regarding polystyrene nanoplastics as pervasive environmental contaminants,” the researchers wrote.
They called for more comprehensive studies to assess real-world exposure levels and long-term health risks, as well as strategies to mitigate plastic pollution’s impact on reproductive health.
“A deeper understanding of how these nanoparticles modulate reproductive pathways may ultimately improve the diagnosis and treatment of idiopathic infertility linked to environmental exposures,” the study concluded.