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This is a Systematic Review study (also classified as: Experimental Study).

September 17, 2025Open Access

A systematic review and experimental study of micro/nanoplastic-induced endocrine disruption in rodents: Potential links to autism spectrum disorder

Key Points

Microplastics and nanoplastics have been shown to disrupt endocrine systems in rodent models, potentially linking to autism spectrum disorder.
Research reveals consistent decreases in testosterone, luteinizing hormone, and follicle-stimulating hormone in adult male rodents exposed to micro/nanoplastics.
Experimental data demonstrate maternal exposure to polystyrene nanoparticles significantly alters cytokines and hormones in the fetal brain.
Findings indicate the need for further research on micro/nanoplastic exposure effects, especially regarding female rodents and autism spectrum disorder implications.

Abstract

Recent research shows that microplastic (diameter < 5 mm) and nanoplastic (diameter < 1 μm) exposures can have endocrine-disrupting effects and lead to autism spectrum disorder (ASD)-like behaviours in rodent models. We combine both a (i) systematic literature review and (ii) experimental study to synthesize the potential mechanisms underlying the link between micro-/nanoplastic (MNP) exposure and ASD, focusing on endocrine disruption and articles utilizing rodent models. First, we identify and discuss trends in the literature, outline research gaps, and suggest future directions. Most articles measured gonadal hormones in male adult rodents and consistently reported decreased testosterone (T), luteinizing hormone (LH) and follicle-stimulating hormone (FSH) with MNP exposure. Females were understudied, with no trends emerging in exposure-induced hormone disruption. Second, we present experimental data demonstrating direct effects of maternal polystyrene NP exposure on neuroendocrine systems and inflammatory markers in the fetal brain. Cytokines, interleukin-2 (IL-2) and interleukin-6 (IL-6), and triiodothyronine (T3) were significantly altered in the fetal brain following prenatal exposure to NPs, and thyroxine (T4) and T were significantly suppressed in female NP-exposed fetuses but not in males. Together, these findings demonstrate that MNP exposure during adulthood and early development affect multiple endocrine systems, including those implicated in autism spectrum disorder, in a sex-dependent manner. We synthesize how such results are important to motivate exposure studies in animals and humans and future regulatory guidelines on MNPs.

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