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Thyroid and parathyroid function disorders induced by short-term exposure of microplastics and nanoplastics: Exploration of toxic mechanisms and early warning biomarkers
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Mice exposed to micro- and nanoplastics through both breathing and eating showed disrupted thyroid and parathyroid gland function in just a short exposure period. Microplastics ingested through food were more harmful to the thyroid, while inhaled nanoplastics caused the most damage to the parathyroid, which helps regulate calcium levels in the body. These findings suggest that everyday microplastic exposure could interfere with important hormone systems that affect metabolism and bone health.
Human exposure to micro- and nano-plastics (MNPs) primarily occurs through respiration and diet in the environment. However, the early effects and warning signs of MNPs exposure on vertebrates are unclear. Here we used intratracheal instillation and intragastric infusion to establish mouse models for MNPs exposure to systematically investigate the toxic mechanisms of MNPs on endocrine organs. Results showed that MNPs induced endocrine disruptions in short-term exposure by both dietary and respiratory pathways. Microplastics (MPs) exposed through dietary route were more toxic to thyroid gland, whereas nanoplastics (NPs) exhibited the highest level of toxicity to parathyroid gland through respiration. The transcriptome and validation of related functional genes revealed that MNPs affected the synthesis of thyroglobulin by interfering with the expressions of PAX8 and CREB. MNPs also impacted the levels of thyroid stimulating hormone, further mediating the secretion of thyroid hormones. Moreover, MNPs modulate the expression of Mafb, thereby exerting regulatory effects on parathyroid hormone (PTH) synthesis and growth development in parathyroid cells. Meanwhile, MNPs interfered with the expression of IP3R in the calcium signaling pathway, indirectly affecting the secretion of PTH. This study reveals the effects and mechanisms of MNPs on thyroid and parathyroid and highlights the significance of early warning of MNPs exposure.
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This review summarizes existing research showing that micro- and nanoplastics can disrupt the endocrine (hormone) system, altering reproductive hormones, thyroid function, and gene expression in lab and animal studies. Exposure to these particles triggered inflammation markers and oxidative stress in hormone-producing organs, suggesting that widespread plastic pollution may be contributing to rising rates of hormonal and reproductive health problems.
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Dietary exposure to PP and PET micro/nanoplastics in adolescent mice caused thyroid dysfunction by disrupting the gut microbiota-mediated hypothalamus-pituitary-thyroid axis, with gut microbiota transplantation experiments confirming the causal role of microbiome changes.
Microplastics and Nanoplastics Cause Thyroid Dysfunction in Adolescent Mice through the Intestinal Microbiota-Mediated Hypothalamus-Pituitary-Thyroid Axis
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Adolescent mice exposed to PP and PET micro/nanoplastics in diet showed reduced thyroid hormone levels, and fecal microbiota transplantation experiments confirmed that gut microbiota mediated thyroid dysfunction via the intestinal-hypothalamus-pituitary-thyroid axis.
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