A study led by biomedical scientists at the University of California, Riverside, has shown for the first time that a father’s exposure to microplastics (MPs) can cause metabolic dysfunctions in his offspring. The research, conducted using mouse models, highlights a previously unknown pathway through which environmental pollutants affect the health of future generations.
While MPs have already been detected in human reproductive systems, the study, published in Journal of the Endocrine Societyis the first to bridge the gap between paternal exposure to MPs and the long-term health of the next generation (the “F1 offspring”).
MPs are tiny plastic particles (less than 5 millimeters) that come from the breakdown of consumer products and industrial waste. Metabolic disorders refer to a group of conditions—including elevated blood pressure, high blood sugar, and excess body fat—that increase the risk of heart disease and diabetes.
To induce metabolic disorders in F1 offspring, the researchers fed them a high-fat diet. This approach helps reveal effects of paternal exposure that might otherwise remain mild or hidden under normal dietary conditions. A high-fat diet mimics common unhealthy eating patterns, such as the Western diet, and amplifies metabolic risks. Because the fathers themselves were fed a regular diet, the obesity seen in the F1 offspring is due to the diet.
The research team found that female offspring of male mice exposed to MPs were significantly more prone to metabolic disorders than offspring of unexposed fathers, even though all offspring were fed the same high-fat diet.
The exact reasons for this sex-related effect are still unclear. In our study, female offspring developed diabetic phenotypes. We observed upregulation of pro-inflammatory and pro-diabetic genes in their livers—genes previously linked to diabetes. These changes were not seen in male offspring.”
Changcheng Zhou, professor of biomedical sciences at the UCR School of Medicine and lead author of the study
The research team found that while the male offspring did not develop diabetes, they did show a slight but significant reduction in fat mass. Female offspring showed reduced muscle mass alongside increased diabetes.
To understand how the trait was transmitted, the researchers used a specialized sequencing technology called PANDORA-seq, developed at UCR. They found that MP exposure alters sperm ‘cargo’, affecting small molecules that regulate how genes are turned on and off.
Specifically, MP exposure significantly altered the sperm small RNA profile, including tRNA-derived small RNAs (tsRNAs) and rRNA-derived small RNAs (rsRNAs)—types of small non-coding RNAs. Unlike DNA, which provides the “blueprint” for life, these RNA molecules can act like “dimmer switches” for genes, controlling how much or how little a gene is expressed during development.
“To our knowledge, ours is the first study to show that paternal exposure to microplastics can affect sperm small non-coding RNA profiles and cause metabolic disorders in the offspring,” Zhou said.
Zhou stressed that the study suggests that the impact of plastic pollution is not limited to the individual exposed. it can leave a biological imprint that predisposes children to chronic diseases.
“Our discovery opens a new frontier in environmental health, shifting the focus to how both parents’ environments contribute to their children’s health,” he said. “These findings from a mouse study likely have implications for humans. Men planning to have children should consider reducing their exposure to harmful substances such as microplastics to protect both their health and the health of their future children.”
The research team hopes the findings will guide future research into how MPs and even smaller nanoplastics affect human development.
“Our future studies will likely examine whether maternal exposure causes similar risks and how these metabolic changes could be mitigated,” Zhou said.
Zhou was joined on the study by Seung Hyun Park, Jianfei Pan, Ting-An Lin, Sijie Tang and Sihem Cheloufi at UCR. Xudong Zhang and Qi Chen at the University of Utah School of Medicine. and Tong Zhou at the University of Nevada, Reno School of Medicine.
The study was supported in part by grants from the National Institutes of Health.
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