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Lactating exposure to microplastics at the dose of infants ingested during artificial feeding induced reproductive toxicity in female mice and their offspring

The Science of The Total Environment 2024 33 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 65 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Yunde Dou, Mengge Zhang, Honghui Zhang, Changlong Zhang, Lijuan Feng, Jingmei Hu, Yuan Gao, Xian-Zheng Yuan, Yueran Zhao, Zhao Han, Zi‐Jiang Chen

Summary

When nursing mice were exposed to microplastics at levels matching what infants ingest from plastic baby bottles, the mothers developed reproductive problems including delayed puberty, irregular cycles, and reduced fertility. Strikingly, their male offspring also showed decreased sperm count and quality, even though they were only exposed through breast milk. This suggests microplastics can cause reproductive harm that passes from mother to child, with males being especially vulnerable.

Polymers
Models

Microplastics (MPs) pollution poses a global environmental challenge with significant concerns regarding its potential impact on human health. Toxicological investigations have revealed multi-system impairments caused by MPs in various organisms. However, the specific reproductive hazards in human contexts remain elusive, and understanding the transgenerational reproductive toxicity of MPs remains limited. This study delves into the reproductive toxicity resulting from lactational exposure to polystyrene MPs (PS-MPs) in female mice, extending the inquiry to assess the reproductive effects on their offspring bred by rigorous natural mating. The MPs dosage corresponds to the detected concentration in infant formula prepared using plastic bottles. By systematically evaluating the reproductive phenotypes of F0 female mice from birth to adulthood, we found that female mice exposed to PS-MPs exhibited delayed puberty, disturbed estrous cyclicity, diminished fertility, elevated testosterone, abnormal follicle development, disrupted ovarian steroidogenesis, and ovarian inflammation. Importantly, the observed inheritable reproductive toxicity manifested with gender specificity, showcasing more pronounced abnormalities in male offspring. Specifically, reproductive disorders did not manifest in female offspring; however, a significant decrease in sperm count and viability was observed in PS-MPs-exposed F1 males. Testicular transcriptomics analysis of F1 males significantly enriched pathways associated with reproductive system development and epigenetic modification, such as male germ cell proliferation, DNA methylation, and histone modification. In summary, real-life exposure to PS-MPs impaired the reproductive function of female mice and threateningly disrupted the spermatogenesis of their F1 male offspring, which raises serious concerns about inter- and trans-generational reproductive toxicities of MPs in mammals. These findings underscore the potential threats of MPs to human reproductive health, emphasizing the need for continued vigilance and research in this critical area.

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