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Microplastics Disrupt Neuropeptide-Producing Gut Neurons in Pigs, Suggesting Neurotoxic and Inflammatory Effects

evidence
The takeaway

Oral exposure to PET microplastics altered populations of neurons producing substance P, VIP, galanin, and other neuropeptides in the pig gut nervous system, alongside histological damage to intestinal tissue.

Multiple neuropeptide neuron populations disrupted

Microplastics didn't just damage the gut lining — they altered the populations of neurons producing key signaling peptides (substance P, VIP, galanin, CART), suggesting microplastics may interfere with the gut's 'second brain' and its control of digestive function.

What the researchers found

After 28 days of oral PET microplastic exposure in pigs:

- Galanin-positive neurons increased across the gut nervous system

- VIP-positive, CART-positive, and vesicular acetylcholine transporter-positive neurons decreased

- Substance P and neuronal nitric oxide synthase (nNOS) changes varied by dose and by which nerve plexus was examined

- Histological damage was dose-dependent: higher doses (1 g/day) caused more severe villus injury, cellular debris accumulation, mucus buildup, eosinophil infiltration, and hyperemia (excess blood flow)

These neurochemical changes suggest that microplastics can alter the function of the enteric nervous system — the 'second brain' that controls gut motility, secretion, and blood flow.

Why it matters

Humans are exposed to microplastics daily through food, water, and air. The gut's nervous system — containing as many neurons as the spinal cord — controls critical digestive functions through neuropeptide signaling. If microplastics disrupt this system, the implications could extend far beyond the gut, potentially affecting appetite, immune function, pain perception, and the gut-brain axis. This pig model is particularly relevant because pig digestive systems closely resemble those of humans.

How the study worked

Fifteen pigs were divided into three groups: control, low dose (0.1 g PET microplastics/day), and high dose (1 g/day), administered orally for 28 days. Jejunum tissue samples were collected and analyzed using immunofluorescence to identify and quantify neurons positive for specific neurotransmitters and neuropeptides (substance P, VIP, galanin, nNOS, CART, vesicular acetylcholine transporter). Histological examination assessed structural changes in the intestinal wall.

What this study cannot tell us

The study used only 15 pigs (5 per group), which is a small sample for detecting subtle dose-response relationships. The microplastic doses, while designed to approximate human exposure, may not perfectly represent real-world conditions where exposure involves mixed plastic types over a lifetime. The 28-day exposure period may be too short to reveal chronic effects. The study documented neuronal changes but did not measure functional outcomes like gut motility or secretion.

How to read the evidence

This is a preclinical animal study using a pig model, which is considered a good proxy for human digestive physiology. However, the small sample size (5 per group) and relatively short exposure period limit the strength of conclusions. The study demonstrates associations between microplastic exposure and neuronal changes but cannot fully establish the mechanism or functional consequences.

When this study was published

Published in 2024, this is a very recent study at the forefront of microplastic toxicology research, an area of rapidly growing scientific and public health interest.

The bigger picture

This study adds to the growing body of evidence that microplastic exposure has biological consequences beyond simple physical contamination. By showing specific effects on neuropeptide-producing neurons in the gut, it connects the microplastics problem to the neuroscience of the enteric nervous system and the broader gut-brain axis. As microplastic contamination is essentially universal, understanding these neurotoxic effects is crucial for public health.

Questions still open

  • Do the neuropeptide changes in gut neurons caused by microplastics lead to measurable changes in gut function, such as altered motility, secretion, or pain sensation?
  • Are the neurotoxic effects of microplastics reversible if exposure is reduced, or do they represent permanent damage to the enteric nervous system?
  • Do other common microplastic types (polypropylene, polyethylene) cause similar neuropeptide disruptions, or is this specific to PET?

Common questions

What neuropeptides were affected by microplastic exposure and what do they normally do?
Several key gut neuropeptides were affected: Substance P normally mediates pain signaling and inflammation; vasoactive intestinal peptide (VIP) relaxes gut muscles and regulates secretion; galanin modulates gut motility and appetite; and CART peptide is involved in feeding behavior. Changes in these peptide-producing neurons could alter how the gut moves food, responds to inflammation, and communicates with the brain.
Should I be worried about microplastics in my food?
This study adds to evidence that microplastic exposure can have biological effects beyond simply passing through the body. While the health impact for humans is still being studied, reducing exposure is reasonable: avoid heating food in plastic containers, choose glass or stainless steel when possible, and be aware that bottled water and processed foods tend to contain more microplastic particles than tap water and fresh foods.

Read the original research

Oral Exposure to Microplastics Affects the Neurochemical Plasticity of Reactive Neurons in the Porcine Jejunum.

Nutrients, 16(14)

Citation

Gałęcka, Ismena; Całka, Jarosław. (2024). Oral Exposure to Microplastics Affects the Neurochemical Plasticity of Reactive Neurons in the Porcine Jejunum.. Nutrients, 16(14). https://doi.org/10.3390/nu16142268