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Axis-based propagation of nanoplastic toxicity: organ–organ crosstalk and systemic pathophysiological outcomes
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This review examined how nanoplastics cause toxicity not just in individual organs but across organ systems by disrupting interorgan communication pathways, including the gut-liver, gut-brain, and placenta-fetus axes. Evidence indicates that nanoplastics can initiate damage at primary exposure sites like the intestine, which then propagates to secondary organs through established physiological signaling pathways.
Nanoplastics (NPs) are emerging as environmental pollutants with the capacity to penetrate biological barriers, distribute systemically, and cause toxicity to multiple organs. Although early studies have primarily focused on localized organ damage, growing evidence suggests that NPs exert broader biological effects by disrupting interorgan communication through established physiological axes. In this review, we examined NP-induced toxicity through seven critical organ-organ pathways, including the gut-liver, gut-brain, gut-endocrine, liver-kidney, hypothalamus-pituitary-gonadal (HPG), hypothalamus-pituitary-adrenal (HPA), and placenta-fetus. NPs initiate damage at primary exposure sites, such as the intestinal epithelium or hypothalamic neurons, which propagates to secondary organs through hormonal, immunologic, and metabolic signaling. Shared histopathological features, including epithelial or parenchymal degeneration, inflammatory infiltration, and fibrotic remodeling, are consistently observed across axis-linked tissues. Moreover, bidirectional feedback mechanisms within these axes amplify NP-induced dysfunction and promote system-wide pathology. The ability of NPs to cross the placental barrier, accumulate in fetal tissues, and disrupt organ development is of particular concern and suggesting a potential for transgenerational toxicity. Overall, this axis-based framework highlights NPs as systemic toxicants that compromise the integrity of interconnected biological systems. In addition to single-organ perspectives, this review proposes an integrative model for understanding the complex and often indirect effects of chronic NP exposure on organismal health.
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Tiny plastic particles (microplastics and nanoplastics) that we're constantly exposed to through food, water, and air may harm our health largely by disrupting the balance of good and bad bacteria in our gut, according to this review of existing animal research. This gut disruption doesn't stay contained—it can trigger problems throughout the body, including in the brain, liver, kidneys, and reproductive system, by traveling along "gut-organ" communication pathways. While this research is based on animal studies rather than humans, it suggests that protecting gut health could be an important strategy for reducing the potential harms of plastic pollution on our bod
Microplastic-induced multi-organ toxicity: cellular mechanisms and critical roles of organ crosstalk
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This review synthesizes current knowledge on how microplastics cause damage across multiple organ systems, including the liver, brain, lungs, kidneys, intestines, heart, and reproductive organs. Researchers emphasize the critical role of organ crosstalk, where microplastic-induced damage in one organ can trigger cascading effects in others, highlighting the systemic nature of microplastic toxicity.
Micro- and nanoplastics disrupt the gut–liver–brain axis: mechanisms of multi-organ toxicity in animal models
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This review pulls together animal research showing that tiny plastic particles (micro- and nanoplastics) don't just pass through your body harmlessly—they can damage the gut lining, throw off gut bacteria, and trigger inflammation that spreads to the liver and even the brain. The smallest particles (nanoplastics) seem especially good at slipping past the body's protective barriers, raising concern about their effects on human health. Since this is based on animal studies so far, more research is needed to confirm how directly these findings apply to people, but it strengthens the case that everyday plastic exposure deserves closer attention.
Gut-Mediated Systemic Toxicity of Micro- and Nanoplastics: Nanoscale Biointerface Properties, Microbiota-Metabolite Crosstalk, and Evidence Across Gut-Organ Axes
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This review pulls together existing research to show how tiny plastic particles we accidentally eat can disrupt our gut—damaging its protective lining, throwing off our gut bacteria, and triggering inflammation—and then send harmful ripple effects to the liver, brain, kidneys, lungs, and reproductive organs. In other words, the health risks of microplastics may not stay confined to your digestive system; they could potentially affect your whole body. This is a summary of current science rather than new experiments, and it highlights that smaller, more weathered plastic particles appear to pose greater risks, an important insight given how widespread these particles are in our
Nanoplastic Impact on the Gut-Brain Axis: Current Knowledge and Future Directions
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Researchers reviewed the emerging evidence on how nanoplastics may affect the gut-brain axis, the communication pathway between the digestive and nervous systems. Studies indicate that nanoplastic exposure can alter gut microbiota, increase intestinal permeability, trigger oxidative stress and inflammation, and produce neurotoxic and behavioral effects. The review calls for more research given the ubiquitous presence of plastics in the human environment and the potential for nanoplastics to disrupt this critical biological communication pathway.
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