UC Riverside study links paternal microplastic exposure to metabolic issues in mouse offspring

James B. Milliken, President
James B. Milliken, President - University of California System
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A new study from the University of California, Riverside (UCR) has found that a father’s exposure to microplastics can cause metabolic problems in his offspring. The research, published in the Journal of the Endocrine Society, used mouse models to examine how environmental pollutants may affect future generations.

Microplastics are small plastic particles, less than 5 millimeters in size, that result from the breakdown of consumer products and industrial waste. Previous studies have already detected microplastics in human reproductive systems, but this is the first research to connect paternal exposure with long-term health effects in offspring.

The UCR team fed male mice a regular diet while exposing them to microplastics. Their offspring were then given a high-fat diet to better reveal any potential health effects. Researchers observed that female offspring of exposed fathers were more likely to develop metabolic disorders compared to those whose fathers had not been exposed. All offspring received the same high-fat diet.

“The exact reasons for this sex-specific effect are still unclear,” said Changcheng Zhou, professor of biomedical sciences at UCR School of Medicine and lead author of the study. “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.”

While male offspring did not develop diabetes, they showed a slight decrease in fat mass. Female offspring experienced decreased muscle mass along with increased diabetes risk.

To investigate how these traits were passed down, researchers used PANDORA-seq sequencing technology developed at UCR. They discovered that microplastic exposure changed the composition of small molecules—specifically tRNA-derived and rRNA-derived small RNAs—in sperm. These RNA molecules regulate gene expression 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 induce metabolic disorders in offspring,” Zhou said.

Zhou noted that plastic pollution’s impact may extend beyond those directly exposed: “Our discovery opens a new frontier in environmental health, shifting the focus toward how both parents’ environments contribute to the health of their children,” 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 like microplastics to protect both their health and that of their future children.”

The team plans further research on whether maternal exposure has similar effects and how these risks might be reduced.

The research was conducted by scientists at UCR as well as collaborators from the University of Utah School of Medicine and University of Nevada, Reno School of Medicine. Funding was provided partly by grants from the National Institutes of Health.

The paper is titled “Paternal microplastic exposure alters sperm small non-coding RNAs and affects offspring metabolic health in mice.”



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