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The Silent Legacy: Paternal and Maternal Exposure to Microplastics and Differential DNA Methylation in Human Oocytes and Zygotes
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This review examined evidence that both paternal and maternal microplastic exposures can alter DNA methylation patterns in human oocytes and zygotes, with potential intergenerational reproductive consequences. The authors found that phthalates and BPA carried by microplastics are likely epigenetic disruptors at the earliest stages of human development, though direct mechanistic evidence in humans remains limited.
The alarming pervasiveness of microplastics in our environment, along with the endocrine-disrupting chemicals (EDCs) they often carry such as phthalates and Bisphenol A BPA) represents a growing and insidious threat to human reproductive health. While epidemiological studies have linked these compounds to negative reproductive outcomes, we still lack aclear picture of their direct molecular impact. Specifically, how does parental exposure shape the epigenetic landscape of the very first stage of human life, the pre-implantation embryo? This study seeks to bridge this gap by investigating whether quantifiable exposure to microplastic-related EDCs in parents correlates with altered DNA methylation patterns in human zygotes. We designed a prospective observational cohort study involving couples undergoing IVF/ICSI treatments. We will measure concentrations of specific EDCs (BPA, phthalates, PFAS) in follicular fluid and seminal plasma using the highly sensitive technique of liquid chromatography-tandem mass spectrometry (LC-MS/MS). On non-viable or supernumerary zygotes (at the 2-Pronuclear stage), we will perform single-cell whole-genome bisulfite sequencing (scWGBS) to map the entire epigenetic landscape. Our analysis will then identify differentially methylated regions (DMRs) by comparing embryo from parents with high versus low EDC exposure, while statistically controlling for potential confounding factors. We anticipate detecting EDCs in a large proportion of the biological samples. Our primary expected outcome is the identification of specific genomic regions in the zygotes where DNA methylation is significantly associated with parental EDC levels. We hypothesize a trend towards hypomethylation a reduction in methylation in the promoter regions of genes critical for development (e.g., HOXA10, DNMT1), with EDC concentration acting as a key predictor. This research aims to provide the first direct human evidence that parental exposure to microplastics and EDCs can leave a targeted epigenetic “signature” on the zygote. We propose this “silent legacy” mechanism, where environmental toxins alter the embryonic epigenome, could fundamentally compromise implantation success and long-term developmental health. These findings would carry profound implications for the fields of assisted reproduction and public health policy.
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Reproductive toxicity and transgenerational effects of microplastics: Evidence from experimental models and underlying epigenetic mechanisms
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Tiny plastic particles have been found in human reproductive fluids, and this review of animal research shows they can harm fertility in both sexes and may even affect the health of future children and grandchildren—not just people directly exposed. Scientists think microplastics may cause these lasting effects by altering "chemical switches" on DNA that get passed down through generations, changing how genes turn on and off without changing the DNA itself. While the animal evidence is concerning, more human studies are needed to confirm these effects happen the same way in people.
Beyond genetics: can micro and nanoplastics induce epigenetic and gene-expression modifications?
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This review gathers existing research on whether micro and nanoplastics can cause epigenetic changes, which are modifications that alter how genes work without changing the DNA itself. Although studies are still limited, the evidence so far shows that both short-term and long-term plastic particle exposure can trigger these gene-level changes in various organisms. This is concerning because epigenetic changes can potentially be passed to future generations and may contribute to disease.
Micro- and nanoplastics: Emerging environmental threats to the Developmental Origins of Health and Disease
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This review examines how micro- and nanoplastic exposure may contribute to chronic health conditions through the lens of developmental origins of health and disease. Evidence suggests that microplastics accumulate in human metabolic and reproductive tissues and may induce physiological and epigenetic changes that could potentially be inherited by future generations, though research into these mechanisms is still in early stages.
Environmental Xenobiotics and Epigenetic Modifications: Implications for Human Health and Disease
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This review examines how environmental pollutants, including microplastics, can change gene activity through epigenetic modifications without altering DNA itself. These changes to how genes are turned on and off can contribute to cancer, brain diseases, and developmental problems, and may even be passed down to future generations. The research highlights that microplastics and other common pollutants could have long-lasting health effects that go beyond direct chemical toxicity.
Reproductive and developmental implications of micro- and nanoplastic internalization: Recent advances and perspectives
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This systematic review documented the detection of micro- and nanoplastics in human semen, placenta, and ovarian follicular fluid, and found evidence linking exposure to impaired sperm quality, disrupted ovarian function, and adverse pregnancy outcomes. In animal models, MNPs caused developmental toxicity and transgenerational effects, with oxidative stress, inflammation, and epigenetic modification identified as key mechanisms.
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