A systematic review and experimental study of micro/nanoplastic-induced endocrine disruption in rodents: Potential links to autism spectrum disorder.
Fowler Lucas F, Burry T Nadine, Maekawa Alexandre S, Cahill Lindsay S
What this study means for families
This study looked at how tiny plastic particles (microplastics and nanoplastics) might affect hormones and be linked to autism in laboratory animals. Researchers found that plastic exposure consistently lowered certain hormones in male animals and affected brain chemicals and thyroid hormones in developing babies when mothers were exposed. The effects were different between males and females. This research suggests plastic pollution might affect hormone systems that are important for typical brain development.
Summary by AutismInsights from published abstract. This is not a substitute for reading the original paper.
Research summary
This systematic review and experimental study examined how microplastic and nanoplastic (MNP) exposure affects hormones and may relate to autism spectrum disorder in rodent models. The review found that MNP exposure consistently decreased testosterone, luteinizing hormone, and follicle-stimulating hormone in male adult rodents, while effects in females were understudied. The experimental component demonstrated that maternal polystyrene nanoplastic exposure altered inflammatory markers (IL-2, IL-6) and thyroid hormone (T3) in fetal brains, with sex-specific effects on thyroxine (T4) and testosterone in female fetuses. These findings suggest MNP exposure during development and adulthood affects multiple hormone systems implicated in autism, with sex-dependent patterns.
Summary by AutismInsights from published abstract. This is not a substitute for reading the original paper.
Key findings
- 1
MNP exposure consistently decreased testosterone, LH, and FSH in male adult rodents
Confidence: moderateRelevance: Suggests potential reproductive hormone disruption from plastic exposure - 2
Maternal nanoplastic exposure altered inflammatory markers (IL-2, IL-6) and T3 in fetal brains
Confidence: limitedRelevance: Indicates prenatal plastic exposure may affect brain inflammation and thyroid function - 3
Sex-specific effects observed with T4 and testosterone suppressed in female fetuses only
Confidence: limitedRelevance: Highlights sex-dependent vulnerability to plastic-induced hormone disruption
Summary by AutismInsights from published abstract. This is not a substitute for reading the original paper.
Clinical implications
While findings suggest potential links between plastic exposure and hormone disruption relevant to autism, human studies are needed before clinical recommendations. Results highlight the importance of investigating environmental exposures during pregnancy and sex-specific effects in autism research.
Summary by AutismInsights from published abstract. This is not a substitute for reading the original paper.
Limitations
Study is primarily based on rodent models with limited human applicability. Female subjects were understudied with no clear trends emerging. Sample sizes not reported. Experimental study appears to be a single investigation rather than multiple replicated studies.
Summary by AutismInsights from published abstract. This is not a substitute for reading the original paper.
Original 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.
Evidence Grade
limited
Grade assigned by AutismInsights based on study type and published abstract.
Study Details
- Type
- Systematic Review
- Journal
- Hormones and behavior
- Year
- 2025
- PMID
- 40957188
- DOI
- 10.1016/j.yhbeh.2025.105818
MeSH Terms